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Diseases of

Pacific

Coast Conifers

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Agriculture Handbook No. 521

Forest Service

U.S. Department of Agriculture

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Diseases of Pacific

Coast Conifers

Technical Coordinator:

Robert V. Bega

Pacific Southwest Forest and

Range Experiment Station

Berkeley, California

Agriculture Handbook No. 521

July 1978

Forest Service

U.S. Department of Agriculture

Library of Congress Catalog Card No. 77-600044

For sale by the Superintendent of Documents, U.S. Government Printing Office

Washington, D.C. 20402

Stock Number 001-000-03727-7
Bega, Robert V., technical coordinator

1978 Diseases of Pacific Coast conifers. U.S. Dep. Agrie, Agrie.

Handb. 521, 204p., illus.

This handbook provides basic information needed to identify the

common diseases of Pacific Coast conifers. Hosts, distribution, damage, disease cycle, and identifying characteristics are described for 31

needle diseases; 17 canker, dieback, and gall diseases; 23 rusts; 8 root

diseases; 15 forms of mistletoe; and 18 forms ofrot. Diseases in which

abiotic agents are contributory factors are also described. Also included are: color and black-and-white illustrations; a descriptive key

to field identification for each major group of diseases; a glossary; and

host plant and disease causal agent indexes.

Oxford: 44/45 — 1747 Coniferae (79)

Keywords: Diagnosis, abiotic diseases, needle diseases, cankers,

dieback, galls, rusts, mistletoes, root diseases, rots.

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FOI.L.OW THE LABEL

U.S. »CrAIIMENT OF ASIICUITUH

Acknowledgments

We thank our many colleagues in the Forest Service, U.S. Department ofAgriculture; Canadian Forestry Service; California, Colorado,

Oregon and Washington Departments of Forestry; Oregon,

Washington, and Colorado State Universities; Universities of Arizona, California, Idaho, Montana, Utah and Washington; St. Johns College, New Mexico; and the Los Angeles County Fire Department, who

gave unsparingly of their time by providing photographs, critically

reviewing the manuscript for technical accuracy, suggesting improvements, and testing its suitability for use by field personnel.

ii
CONTENTS

Page

INTRODUCTION 1

1. ABIOTIC DISEASES 5

2. NEEDLE DISEASES 42

3. CANKERS, DIEBACKS, AND GALLS 69

4. RUSTS 91

5. MISTLETOES 121

6. ROOT DISEASES 142

7. ROTS 157

GLOSSARY 189

INDEX TO HOST PLANTS,

WITH SCIENTIFIC EQUIVALENTS 195

INDEX TO DISEASE CASUAL AGENTS 198

111

DISEASES OF PACIFIC COAST

CONIFERS

INTRODUCTION

by

ROBERT V. BEGA*

This handbook was designed to bring under one cover the basic

information needed to identify some ofthe common diseases of Pacific

Coast conifers. Although written primarily to help identify conifer

diseases of the Pacific Coast States, it should be useful throughout

Western North America, where most of these diseases also occur.

The information contained in this handbook is intended to serve a

comparatively broad group that is interested in such activities as

resource management, conservation, forestry, tree farms, outdoor recreation, and growing ornamental trees. Except for a number of texts

written on forest and plant pathology, most ofthe available literature

is in the form of bulletins, monographs, articles, and shorter contributions issued from time to time through a variety ofpublication outlets.

A tree disease is primarily a disturbance ofthe normal functions of a

tree or the deterioration of its parts. Therefore, it is fundamental to

recognize the parts of the tree that are attacked by disease-producing

agents and the kinds of disease common to them. When attempting to

diagnose a particular conifer disorder, the ability of some diseasecausing agents to adapt and successfully attack must be kept in mind.

The roots of a tree, for example, require infection and establishment of

an organism under conditions widely differing from those to be found

surrounding the leaves of the same tree. An organism causing a disease of living tissues may possess a different mode of attack than one

which produces a heart rot in the dead tissues of the heartwood.

Agents of Tree Disease

Agents ofdisease can readily be classified as (a) abiotic, non-organic,

non-living agents, such as air and soil pollutants, ice, snow, wind,

frost; and (b) biotic or living organisms, such as mistletoes, bacteria,

and fungi. Viruses are not included in either of these classes simply

because there have been, as yet, no proven virus diseases of western

conifers.

Climate, soils, and vegetation vary greatly from the Pacific Coast to

the Rocky Mountains. The cool, humid conditions of the Northwest

contrast with the arid conditions of southern California. Aside from

host specificity and biologic competition, the important factors in-

* Principal Plant Pathologist, Pacific Southwest Forest and Range Experiment Station, Forest Service, U.S. Department of Agriculture, Berkeley, Calif.
fluencing the prevalence and vigor ofdisease pests are environmental,

including the duration of critical levels of temperature and moisture,

the type and aeration of soils, and human influence on these factors.

The same disease may, and usually does, have different degrees of

intensity depending on the locale ofthe host. For example, the canker

fungus Botryophaeria ribis has never been found attacking the giant

redwood in its natural habitat. However, when the host is moved

outside its natural zone, thisfungus and several others (e.g., A. mellea)

attack the redwood not only readily but quite destructively.

Human influence is a definite factor affecting most of the diseases

being considered in this publication and must be considered in diagnosing a disease and evaluating the damage it caused. In work where

trees are growing, every effort should be made to keep environmental

changes to a minimum. Construction work — particularly road making, land leveling for housing development, campgrounds, and picnic

sites — are frequently a source ofinjury to trees. Apart from mechanical damage by construction machinery, roots can be injured ifthey are

severed or if they are covered with excessive amounts of soil. Overdevelopment in previously undeveloped areas may damage trees in an

even more indirect way, such as ground water pollution or depletion.

Conversely, humans must also be protected from trees in recreation

sites — particularly campgrounds, picnic areas, and summer home

sites. Control of hazardous trees is of prime importance in both existing and planned recreational sites. Trees that fail because ofdisease or

other agents can destroy lives and property.

The proper understanding of both host and disease-causing agent

involves consideration of the surroundings. The effect of most abiotic

agents is to some extent relative. One tree might grow quite healthfully under conditions that would cause disease or even death in

another tree, even of the same species. In many cases, the degree and

rate of change in the environment are more importantthan the actual

level which conditions of the environment reach. For example, a tree

planted in a hole in a pavement may grow quite well, but an established tree may die for lack ofsoil oxygen when a pavementis laid over

its roots. This question of degree and rate of environmental change

must be kept in mind in all considerations of injuries due to abiotic

agencies. Many examples are cited in this publication in which abiotic

factors ofthe environment greatly influence the origin and subsequent

development of biotic-caused diseases.

This publication is organized primarily for use in field diagnosis

and, except for the chapters on rusts and mistletoes, it describes

symptoms based on the part ofthe tree attacked. Even the descriptive

keys in the Rust and Mistletoe chapters, however, have been designed

to focus first on specific parts of the tree. A cross index lists terms

relating hosts to pathogens.

Control recommendations are not discussed in this publication except in special instances because of the continued change in control

methods and changes in materials approved for control. As the environment undergoes changes, and as tree values continue to change

from timber to recreation and esthetic values, specific control recommendations will also change. Many disease control methods can now
be applied because the growth in value of trees permits more costly

control measures to be adopted.

Tree Disease Diagnosis

Diagnosis ofplant diseases is the art ofidentifying a disease from its

symptoms, signs, and patterns. The symptoms (expressions of the

diseased host), signs (evidences of the cause), and patterns of occurrence provide the clues on which the investigator bases his diagnosis.

The following guide may be helpful in diagnosing tree disease:

1. Determine as accurately as possible the part ofthe plant that

is actually affected. The death of only 1 year's needles indicates a needle disease; ofscattered whole branches — a canker

disease; of the whole tree — a root disease, drought, or fire.

Note the pattern of the disease in the trees. Is the damage

limited to the south side, to the lower, or to the upper crown?

2. Note what species are affected. Are there any individuals that

are affected less or which are free from the problem? Also note

the condition of other adjacent plants.

3. Note the pattern of occurrence. What areas show the problem

worse? How do these areas differ from those areas free from

the problem? Are these problem areas in any particular environmental zone or related to a particular cultural activity?

4. If the cause of the disease is not immediately evident, look

first for the simplest effects, such as animal damage, frost,

lightning, other climatic influences, simple injuries, fire, or

other obvious causes of the problem.

5. Look for the presence of fungi, insects, or other parasites.

Observe accurately, and try to judge whether the organisms

found are the main cause ofthe trouble orjust secondary. For

example, insects will frequently move in as secondaries on

trees weakened by disease.

6. If the whole tree is dead or suffering and nothing is found

above ground to indicate the cause of the disease, expose the

roots and root crown for examination.

7. If you are still unsure, learn about the recent history of the

problem and the area. Is the problem of recent origin and

when was it first noted? What cultural practices have been

carried on in the area, such asthe use of herbicides, fertilizers,

irrigation or flooding, road salting, and air pollution? Do the

environmental records indicate the recent occurrence of any

unusually severe conditions?

Descriptive Keys

The descriptive keys found in each chapter are based on the host and

the causal agent. In each key, letters are followed by either a letter for

alternatives or for the causal agent that fits the specimen. Thus, each

step leads to another step and its alternatives, until a name is reached.
Success in diagnosing a specimen by these keys depends largely on an

understanding ofthe characteristic used. In many cases, this publication illustrates the key characteristics. If at any point in the key you

are undecided aboutthe way to proceed, follow through on the alternatives and compare the specimen with illustrations and descriptions

found in the text or in the references cited.

An example is the key on rots:

A* on incense-cedar, juniper, or redwood B

B^ on incense-cedar C

C^ A brown pocket dry rot.(Pocket dry rot) Polyporus amarus

C^ A white stringy root or butt rot.(Fomes root and butt rot)

Fomes annosus
1. ABIOTIC DISEASES

by

PAUL R. MILLER*

Each tree that is a subject for disease diagnosis has an environmental history. Certain factors in that history may be an individual cause

of abiotic or noninfectious disease. Some injuries caused by abiotic

agents may predispose the tree to certain infectious diseases. The

environmental history of trees at a given location is the result of the

varying influences of solar radiation, temperature, water, atmospheric gasses, chemicals, wind, fire, topography, geologic substratum,

and soil. The almost instantaneous events like lightning and fire, the

extremes of such dynamic factors as temperature and water, and the

relatively persistent influences of geologic substratum and soils show

the wide range in the time spans during which the individual causes of

abiotic disease may have an active influence on trees. For example,

frost injury develops suddenly, accumulation of chloride salts near

roadways occurs continuously in several consecutive seasons, and the

dwarfing oftrees due to toxic serpentine soils is an influence which is

always present. Abiotic factors may exert direct effects singly, simultaneously, or sequentially with respect to one another.

Most of the record of events or circumstances causing abiotic tree

diseases is present atthe site as symptoms on needles, twigs, branches,

and main stems and roots, or in terms ofthe immediate surroundings

ofthe subject trees. In some situations, it may be useful to consult past

weather records. The following key to abiotic diseases uses several

characteristics of the main stem, branches, twigs, and needles in the

upper and lower halves of the crown and also the inner and outer

(branch tips) portions ofthe crown. The four major sections (A^ A^, A^,

A*) in the key each start with stylized descriptions of a tree crown and

use the gross appearance of the tree as a means for selecting an entry

point into the key. The key identifies animal damage and provides a

cross reference to the appropriate chapter when the symptoms encountered could also be caused by an infectious disease.

The most important abiotic diseases included in the key are discussed in greater detail in the remainder of this chapter.

*Plant Pathologist, Pacific Southwest Forest and Range Experiment Station, Forest

Service, U.S. Department of Agriculture, Berkeley, Calif., stationed at Riverside, Calif.
Key to Abiotic Diseases

Main stem erect, leaning or prostrate, sometimes broken. Injuries

to top, middle, or lower sections of main stem and sometimes

branches, usually 4 to 10 annual needle whorls retained, needles

of all ages not abnormally shortened B

B^ Tree leaning or prostrate C

C* Main stem sometimes bent or broken. Excessive snow or

avalanche, logging activities, and failure at a rust canker

or beaver girdle.

C^ Main stem prostrate, large roots torn from the soil.

Windthrow and butt rot.

B^ Tree erect, damage to main stem D

D* Only top section of main stem affected E

E* Top broken F

F* Top has uneven, splintered break and upper

branches broken, fallen to ground, tree dead or

often after several years multiple leaders develop: Excessive ice or snow accumulation.

F^ Top and upper branches broken, prominent furrow in bark or sapwood spiraling from top to

bottom; lower portion of stem sometimes shattered lower down: Lightning damage.

E^ Top not broken G

G^ Top of crown has dead needles and branches

with lower limit a complete girdle on the main

stem: Porcupine or occasional squirrel damage;

sometimes a rust canker (Chapter 4) orPhomopsis canker (Chapter 3).

G^ Top of crown has dead needles and branches

with a variable lower limit, no visible mechanical injury H

H^ Investigate for bark beetle infestation.

H* Very low winter temperatures or sun

scorch.

H^ Drought or high water table.

D^ Mainly basal section of main stem affected I

P Tree severely debarked, and deeply gouged, usually

on one side: Mechanical damage, e.g., earth moving,

logging, or snow removal equipment; sometimes

struck by a falling tree.

P A narrow circumferential strip debarked with girdle

extending into heartwood, tooth marks visible:

Beaver activity.

P Slightly debarked, smooth area 1 to 2 feet long on one

side ofmain stem often up to 20 feet above the ground:

Blasting by ice crystals where surface of the snowpack and stem intersect.

P Partially debarked, mostly one side, usually extends

from 3 to 8 feet above the ground, claw marks evident:
Bear damage. Small patches debarked no higher than

snow level, tooth marks evident: Ground squirrel or

rabbit damage.

P Cracks in the lower stem, larger trees, especially true

firs: Frost cracks.

P Large, calloused lesion or canker, widest just above

ground level and tapering upward mostly on the uphill or leeward side ofstem, heartwood exposed, sometimes charred: Fire damage.

P Same as P, but no charring: Armillaria rot.

P Lesion on south side, small thin barked tree, often

Douglas-fir: Heat canker or bark scorch.

D^ Damage occuring anywhere on main stem J

J^ Swellings or hip cankers anywhere on main stem.

Investigate for dwarf mistletoes, (Chapter 5), or rust

canker (Chapter 4). If not present, then stem may

have been formerly cracked by wind but not broken or

girdled by a cable or wire, often remaining under the

bark.

J^ Resin bleeding at any level. No obvious wound: Bark

beetle pitch tubes, bullet holes, Armillaria (if base of

tree).

J^ Resin blisters on stems of white fir or Douglas-fir:

Nonpathological.

Main stem usually erect, may or may not be injured, usually 4 to

10 annual needle whorls, needle lengths of all ages usually not

abnormally shortened. All or restricted portions of the crown

exhibit needles uniformly brown or reddish brown K

K^ Generally all of the tree crown has damage to all ages of

needles; sometimes buds, and small stems may also be dead

L

L^ Affected trees often occur in distinct horizontal belts

along slopes, but current-year needles eventually fall off,

alternate cold and warm temperatures: Red belt.

L^ Affected trees occur singly or in definite small groups

M

M^ Exposure of roots by excavation.

M^ Burial of roots, silting, or asphalting.

M ^ High water table, beaver ponds or new stream

channels.

M* Fire; heat-killed foliage, minimal burning.

M^ Make inspection for major root rot infection or bark

beetle infestation (Chapter 6).

M* Accumulation of chloride salts along roadways.

M^ Borate or chlorate soil sterilants.

M® Drought (severe).

M' Trees very close to industrial site or rail siding:

Chlorine, hydrogen chloride, or ammonia gas; accidental release.

M*® Only needles of pines (often Jeffrey) show tip
dieback, mainly older needle whorls: Needle miners.

L^ Affected trees uniformly distributed over landscape ...N

W In spring, buds, new shoots, and full length ofemerging needles are dead or brown. In fall, succulent

shoots and needles still growing are affected. Damage most intense in low spots or depressions: Frost

damage.

N^ Damage in late winter or early spring, needles of all

ages are brown or intensely brown flecked: Winter

kill.

K^ Mainly the upper portion of the crown exhibits brown

needles O

O^ Only upper crown was in the lower part ofthe belt on

a slope where warm and cold temperature alternate

in winter: Red belt.

O^ Condition visible usually in late summer, often continuing into next spring: Drought.

K^ Mainly the lower portion of the crown exhibits brown

needles P

P^ Cold air accumulation in very shallow layer near the

ground in winter, site usually flat or slight depression: Winter kill.

P^ Only the lower crown was in the upper part of a belt

on a slope where warm and cold temperatures alternate in winter: Red belt.

P^ Ground fire, scorched needles on lower crown, bark

near ground charred.

P* Herbicide damage, only lower crown sprayed.

K* Mainly one side of crown, upper or full length shows

brown needles; sometimes needles and smaller branches

are absent Q

Q^ Trees isolated or on edge ofstand, usually midwinter:

Sun scorch.

Q^ Windward side oftree affected, usually early spring:

Parch blight.

Q^ Trees exposed to salt spray up to 100 m inland along

the coastline after gale.

Q* Flagform tree: Branches, and needles blasted by ice

and snow particles or salts.

Q® Trees along roadside with injury only to needles:

Drift of contact herbicides, deicing salt, or injury to

needles, and smaller branches removed: Impact of

snow plume from rotary snow plow.

K^ Mainly the outer portions of the entire crown or the

youngest (current-year) needles are normal length, or

sometimes shorter R

R^ Partial brown tip dieback, symptoms most severe in

late summer progressing from the current year to

older needles and from top to bottom of crown: Soil

drought.
R^ Complete brown dieback of current-year needles:

Frost injury or high temperature.

R^ Complete brown dieback ofcurrent-year needles, also

evidence ofinsect mines, usually white fir: Defoliator

insects.

Main stem usually erect, may or may not be injured, usually 4 to

10 needle whorls, needle lengths of all ages usually not abnormally shortened. All or restricted portions of the crown exhibit

needles with general chlorosis, chlorotic mottle, discrete brown

flecks, partial brown tip dieback, bands of brown, fading green,

white bleaching or purple discoloration. Needles may droop or

needles and shoots may be twisted S

S^ Chlorosis or yellowing of needles T

T^ Destruction of chlorophyll by normal low winter temperatures imparts a brassy yellow-green color to conifers:

Winter yellows.

T^ Exposure of needles to low concentration spray of contact

herbicide.

T^ Chronic exposure to ozone with 0.10 to 0.15 ppm daily

peaks.

T* Chronic exposure to sulfur dioxide.

T^ Exposure to low concentrations of borate or chlorate

applied to soil.

T* High water table (greenish-yellow).

T^ Nitrogen deficiency.

S^ Chlorotic mottle of needles U

U^ Older needle whorls exhibit most mottle; mottle most

intense at needle tip and progresses to the base of the

needle: Caused by chronic exposure to ozone with daily

peaks greater than 0.12 ppm.

U^ Mottle present at basal portions in all ages of needles:

Usually is associated with insect punctures or scale infestation.

S^ Discrete necrotic flecks on needle surfaces facing skyward,

with or without chlorotic mottle or tip dieback: Winter fleck,

associated with exposure to snow and low temperatures.

S* Brown tip dieback, "tipburn," extent on needles variable ..V

V^ Narrow chlorotic margin delimiting necrotic and healthy

tissue: Soil drought.

V^ Sharp boundary between necrotic and healthy tissue

W

W* Injury by high concentrations of air pollutants: Hydrogen fluoride, hydrogen chloride, chlorine, ammonia, sulfur dioxide, or ozone.

W^ Potassium deficiency — rare.

W^ Rapid chloride salt accumulation near roadway,

both tip and banded necrosis.

W* Low temperature or frost injury.

W^ Current-year foliage most affected: Severe injury by

borate or chlorate soil sterilants.

W*^ High temperature injury; Douglas-fir or white fir.
W^ Needle miners, typically Jeffrey pine or Rocky

Mountain ponderosa pine.

S^ Brown tip dieback with darker bands evident at 1 to 2 cm

intervals within the brown tissue: Gradual accumulation of

chloride salts.

S^ Whole needle fading from green to tan X

X^ All oftree crown involved. Inspect for bark beetle infestation or for root infection hyFomes annosus orArmillaria

mellea (Chapter 6).

X^ Random needles involving all or parts of crown — inspect

for infection by needle cast fungi, e.g., Lophodermium,

Elytroderma, Rhabdocline (Chapter 2).

S ^ Needles bleached yellow-white: Foliar application of aminotriazol.

S ® Purple discoloration of older foliage followed by withering:

Phosphorus deficiency.

S ^ Purple discoloration of younger foliage and tops of smaller

trees and seedlings: Prolonged exposure to moderately cold

temperatures.

S^" Drooping or curved needles: Associated with rapid transpiration in the absence of available soil moisture.

S" Severely twisted needles and shoots: Foliar application of

hormone weed killers, lightning.

Main stem usually erect and uninjured, top surfaces or upper

branches may be injured and needles of all ages reduced in

number, more frequently one to three annual whorls present;

needles normal or more often, shortened with chlorosis, chlorotic

mottle or tip dieback Y

Y* Affected trees uniformly distributed over landscape, sometimes in a strip, but not related to similar sites. Upper crown

has fewer needles of all ages than lower crown, upper surface

of branches has wounds or scars, numerous terminal buds

missing, green foliage on ground: Hail damage.

Y^ Affected trees are dwarfed, occur uniformly over the landscape and are often separated from normal appearing vegetation by a sharp boundary: Serpentine soil toxicity.

Y^ Affected trees randomly distributed over landscape, not related to particular site conditions Z

Z^ Tree is large, over-mature, low vigor results in fewer

annual whorls retained and shorter needles throughout

the crown with no pronounced foliage discoloration:

Natural senescence.

Z^ Trees of all ages, most frequently ponderosa, Jeffrey,

Coulter, or Monterey pines, and big-cone Douglas-fir, retain one or two needle whorls in upper crown and one in

lower crown; needles have intense chlorotic mottle and

sometimes tip necrosis, needles often shortened and in

late summer fall easily from the stem. Branches of lower

crown dead or dying: Chronic ozone injury.

Z^ Chronic damage by defoliator insects, e.g., Douglas-fir

tussock moth.

10
Y^ Affected trees distributed individually or grouped in recognizable patterns A®

A®^ Pole-sized western white pine on dry sites; leaders and

needles shortened, needles yellow, symptoms progress

downward and inward; resin bleeding associated with

flat or depressed area in bark: Pole blight.

A^ Trees recently damaged by red belt or summer drought,

after older needles have fallen off and before a sufficient

number of seasons have elapsed to allow recovery.

A®^ Trees infected by a root disease fungus, e.g., Fomes annosus or Armillaria mellea (Chapter 6).

A®* Trees damaged by salt accumulation.

Effects of Low Winter Temperatures

Winter Killing, Winter Injury

Extremely low temperatures can kill the needles, buds, twigs, and

the inner bark of conifers. Needles are usually completely brown

regardless of age (fig. 1-1), however, irregular brown and green tissues

may result in less severe cases of injury. Discrete brown flecks mainly

on the upper needle surface commonly occur with greatestintensity on

the older needles which are exposed to the sky and snow deposition (fig.

1-2, lower). Minima ranging from -31 to -45° F caused extensive damage to ponderosa and Jeffrey pine east of the Sierra Nevada crest.

Affected treesrecovered unless the inner bark tissues ofthe main stem

had been injured.

The severity oflow temperature injury varies between and within a

species; for example, differences in winter injury have been observed

among white fir seedlings depending on seed source. In eastern

Washington, ponderosa pine receives greater injury than Douglas-fir

during midwinter low temperature episodes. Injury to needles of coast

redwood seedlings resulted during an 8-day period when the temperature remained between -5 and -1° C. Inland plantings ofMonterey pine

especially above 1,500 feet elevation in southern California are badly

damaged when temperatures remain below freezing for several hours

during 1 or 2 consecutive days.

Top kill — Top kill of Coulter pines in southern California results

from freezing of inner bark tissue down to about 5 inches in diameter

when a quick drop in temperature to approximately 20° F followed an

abnormally warm period of 11 days; this particular damage is called

spiketop. Similar injury has been observed on ponderosa pine in northern California. Spiketop may also be caused by drought, lightning,

bark beetle attack, defoliator insects, or the mistletoes (fig. 1-3).

Frost crack — Frost cracks are frequent in older white fir trees,

particularly those on the east slope ofthe Sierra Nevada, and on grand

fir in northern Idaho and Montana. During periods of sudden cooling

the wood cylinder shrinks more in a tangential than a radial direction,

resulting in cracks that usually do not extend more than 20 feet above

11
'JJJÍ'^ÍJ'

F-700206

Figure 1-1. A Monterey x knobcone pine hybrid severely injured by belowfreezing temperature in midwinter.

K.525000

Figure 1 -2. Discrete necrotic flecks on a ponderosa pine needle associated with

winter conditions only, particularly snow deposition.

12
F-526001

Figure 1-3. Top kill ofJeffrey pine associated with drought. Similar "spiketop"

appearance may be caused by cold temperature, lightning, insects, or mistletoe.

the ground. Callustissue forms over the surface ofthe crack in the first

year. The crack is split and healed again successively through the

seasons until it heals completely. Frost cracks are often the source of a

watery exudation from the bole ofwhite fir. This exúdate is often called

"slime flux." Large callus growths that project some distance out from

the normal circumference of the trunk are called "frost ribs."

Frosts in Spring and Autumn

Tolerance offoliage, small branches, and main stems to cold temperature depends on "hardiness", which in turn is closely correlated with

the time of year. Low temperatures above freezing and short photoperiods induce frost hardiness. The changes in plant cells which are

associated with frost hardiness include increases in both osmotic pres13
sure and cell protein content. Freezing injury is most often caused by

ice crystal formation within the cell and less frequently by dehydration oftissue by extracellular ice crystal formation. Increases in osmotic pressure and cell protein content may inhibit intracellular formation of ice crystals. The sudden occurrence of below freezing temperatures (frosts) in spring or early autumn can severely damage unhardened tissues, actually killing young shoots and needles.

Autumn frost injury — Any succulent shoot tips and current-year

needles will be injured if growth is still in progress. A partial list of

conifers in order ofincreasing frost sensitivity includes lodgepole pine,

Jeffrey pine, ponderosa pine, incense-cedar, sugar pine, and white fir

in California. Recovery can be expected the following spring.

Frostlesions form on the main stems ofsmall Douglas-firs as a result

of a sudden drop in temperature before tissues have hardened off.

Later the sapwood is exposed when the dead bark tissue cracks and

falls off. Eventually the lesion is calloused over, but in the meantime

decay fungi may enter the area.

Spring frost injury — Spring frost causes differing amounts of damage to conifers depending on the stage of growth and development at

the time of injury. Before bud break, some buds may be killed. After

bud break, there is damage to the new leaves and soft succulent shoots.

The brown, dead portions usually remain on the tree and a new shoot is

produced (fig. 1-4). Trees that are repeatedly injured by frosts are

characterized by long, dead main stems with a dense growth ofneedles

developing at the base forming a bushy appearance (fig. 1-5). Frost

injury thatis notsevere enough to cause death ofsucculenttissue often

results in crooked shoots. Spring frost damage may vary considerably

on the same species because it is dependent on the stage of development ofthe new tissue. For example, the more advanced growth atthe

lower elevational range of a species would resultin greater injury than

at the upper limits where the stage of development is in an earlier

phase.

After an abrupt temperature drop to -10° C in mid-April in New

Mexico, the order of increasing sensitivity in several species was

alligator juniper, Douglas-fir, ponderosa pine, white fir, and limber

pine. Limber pine was the most severely damaged because its growth

was the most advanced in its lower elevational range.

Both spring and autumn frost injury is likely to be localized where

topographic conditions cause the pooling of cold air. These depressions

are referred to as "frost pockets."

Winter Temperature, Sunlight, and Wind Interactions

Red belt — The occurrence of trees with variable lengths of their

crowns from the tip downward that display dead, reddish-colored needles and thlat are distributed in well-defined bands varying from less

than 20 and up to 1,000 yards wide on slopes and benches is a condition

called "red belt." Extensive damage may develop when an unseasonably warm spell in winter is followed by a sudden drop in temperature.

14
F-700207

Figure 1-4. Frost-injured white fir in spring show dead young shoots and

needles. The shoots and needles will remain on the tree through summer.

15
^CV r. nf.»

F-700208

Figure 1-5. Repeated frost iixjury to bishop pine planted out ofits natural range

results in numerous dead branches and ragged tree crowns.

The belt is formed because of a warm temperature inversion layer

thatimpinges at varying elevations along the slope, depending on time

of day. The valley bottoms are constantly filled with cold air, but the

sudden occurrence of warm dry foehn winds (Chinook or Mono winds)

form a relatively thin layer of warm air on top that does not mix

downward. At night, normal cold air drainage down the slopes fills the

valley to a greater depth and raises the warm air layer above its

daytime level. Trees exposed to unseasonably warm air by day receive

cold air at night. This alternation of warm and cold air exposure with

the soil usually frozen causes injury because daytime transpiration

removes moisture from the needles more rapidly than it can be replaced by roots in frozen soil. Older needles fall off, leaving only

current-year needles on living branches.

Winter drying or sun scorch — When bright sunny days follow a

period of below freezing temperatures, several western conifer species

— typically western red cedar — experience conditions causing the

leader and several of the youngest branch whorls to die. Usually the

south, southeast, orsouthwestsides ofmostly small trees on the border

16
F-700209

Figure 1-6. Young shoots and needles of Jeffrey pine, particularly those on the

sunny side, have been desiccated. This occurred during sunny, warm winter

days when roots and stems were too cold for adequate water transport.

of denser stands, or sometimes the entire exposed crown of isolated

trees show reddish-brown needles (fig. 1-6). Lower portions of the

crown where needles are covered with snow never show injury.

The localization ofinjury on the sunny side ofthe trees suggests that

rapid thawing in the bright sun and transpiration without replacement of water because roots and bole are very cold or frozen causes

irreversible desiccation of the needles. After repeated incidents, the

more sensitive species such as lowland grand fir and incense cedar will

develop a bushy appearance (fig. 1-7). Limber pine native to high

elevation sites near timberline has a permanent prostrate form because of continuous injury to new growth (fig. 1-8).

Parch blight - Brief episodes of dry winter (Chinook) winds occur

occasionally in western Washington and Oregon. The winds originate

east ofthe Cascades. During these episodes the needles of Douglas-fir

on the eastern edge of single exposed trees, and particularly trees on

the eastern edge ofstands, become brown. Even last year's shoots may

be killed. The soil is not frozen at the time but apparently transpira17
F-700210

Figure 1-7. An incense-cedar has an unusual bushy form because of repeated

desiccation of the top not protected by snow.

tion losses exceed the rate of water absorption possible by roots in a

cold soil. Injured trees recover almost completely by the following

summer.

Minor Effects of Low Winter Temperatures

Winter yellows — One of the least harmful effects of cool winter

temperatures is the winter yellowing or chlorosis of conifer needles. A

breakdown of chlorophyll begins with the first frost; foliage exposed to

direct sunlight shows the most severe sjmiptoms, namely, a brassy

yellow-green. Giant sequoia often turns to a bronze color. The

chlorophyll content is restored and the needles become green after the

first weeks of warm weather in spring.

Purple top — Ponderosa pines and western white pines grown in

exposed nursery beds show a purple discoloration of the youngest

18
F-7002110

Figure 1-8. Prostrate growth of this limber pine near timberline was caused by

repeated freezing and desiccation of upper needles and branches not protected by snow.

foliage. The tops may eventually become brown and die; surviving

seedlings have a bushy appearance.

Necrotic fleck — Discreet tan flecks only on needle surfaces facing

skyward are a common occurrence on conifers throughout the West

(fig. 1-2, lower). Histological evidence has eliminated fungi as a cause

and implicated low temperatures. Circumstantial evidence suggests

that exposure to snow is a prerequisite for injury to develop. Flecks are

most numerous on the oldest needles, but do not seem to contribute to

early senescence.

High Temperature and Radiation Injury

Needle scorch — Leaves or needles that have developed under cool

conditions may be injured by sudden temperature increases. For

example, needle tip browning results in the latter part of a generally

cool spring on coast redwood, Monterey pine, and juniper when temperatures suddenly reach 100° F.

19
\ Ê'/Ji//I'

WEäjh ^H

'^^¿^ffu^^ÊÊ^^^

1 F-700212

Figure 1-9. Needles of this ponderosa pine have bent at the end of the fascicle

wrap where tissue is soft and immature.

Shoot tip dieback — The new developing shoots of Douglas-fir and

white fir are particularly sensitive to a sudden rise in temperature in

May and early June. This injury may be confused with spring frost

damage because the shoot tips droop, turn red-brown, and later break

off

The effects of prolonged high temperatures during spring, summer

and fall in conjunction with soil moisture deficiency and dry winds

may result in extensive top dieback in large trees of several species

(fig. 1-3). This condition resembles bark beetle damage, but lack of

beetle galleries and the involvement of firs, incense-cedar, and pines

together appear to disqualify insects as the cause.

Needle droop — Sudden and excessively rapid transpiration may

result in abrupt needle droop caused by collapse ofthe tissue near the

base of young succulent needles. This condition may be followed by

death of current-year needles. The condition is observed on pines in

California (fig. 1-9).

Heat canker or bark scorch — On rare occasions, the southwest sides

of the main stems of young western white pine, Douglas-fir, spruces,

and true firs will develop cankers during the first few years after the

stand is thinned. In Douglas-fir, there is a yellowish to reddish discoloration followed by a slight sinking of bark tissue. Later, the bark

cracks and scales off Healing is generally very slow.

20
An apparently benign effect of high air temperature is sugar exudation by needles of Douglas-fir reported in eastern Washington. Sugar

exudation and subsequent growth of sooty mold fungi on needle surfaces are commonly observed on conifers infested by aphids.

Soil Moisture Deficiency

Drought — Soil-drought conditions usually develop first on gravels

and sands that can hold very little water or on sites where shallow soils

overlay rock or gravel. For this reason, drought-damaged trees usually

occur in groups. Conifers that are undergoing only moderate moisture

stress will shed older needles prematurely — often accompanied by

needle tip and small twig dieback. Under more severe stress the

needles ofthe leader and upper branch whorls turn light tan, advancing from tip to base of each needle with a narrow, band of yellow tissue

between green and tan portions. Drought stress symptoms progress

from the top down and the outside in. The symptoms remaining on

surviving trees in subsequent years include dead tops, fewer needle

whorls and shortened needles in the whorls formed following the

drought years. The growth of trees that survive drought is retarded.

With some conifers, reduced diameter and height growth appear 1 year

after the drought. Generally, seedlings and saplings are more severely

affected and often killed because they have less extensive root systems

than larger trees.

During severe drought conditions in California in 1929 and 1960,

Douglas-fir and incense-cedar were killed or injured on poorer sites but

ponderosa pine, sugar pine, and white fir on similar sites were less

seriously affected. Small incense-cedar and Douglas-fir were the first

to show drought symptoms. Western white pine were more seriously

affected by drought than nearby Douglas-fir and lodgepole pine. Italian stone pine, aleppo pine, Italian cypress, and Arizona cypress were

highly drought tolerant; Jeffrey and Coulter pines were slightly

drought tolerant and Monterey pine was not drought tolerant in comparative tests. Knobcone pine, Torrey pine, single-leaf pinyon pine,

and digger pine successfully occupy dry sites.

Pole blight — This disease is confined to pole-sized western white

pine north of the Clearwater drainage in the Idaho panhandle and

extending northward into parts of Montana, Washington, and British

Columbia. Affected trees occur randomly first, later coalescing into

limited patches. The first evidence ofinjury is a radial growth followed

by reduced leader and branch growth. Older needles drop and remaining needles are shortened and yellow. The disease spreads downward

and inward until the whole crown is affected. Resinous stem lesions,

appearing as flattened areas on the stem, are a common symptom.

After extended dry and warm weather, western white pine does not

regenerate rootlets fast enough to replace those lost due to moisture

stress. The decline ofthe crown is a secondary reaction that reflectsthe

effects of a degenerated root system. Dry sites, i.e., those with low soil

moisture storage capacities and recharge potentials encourage pole

blight development.

21
Soil Moisture Excess

Damage by excess soil moisture is confined to specific sites. Problems occur along the shoreline of new reservoirs or beaver ponds and

along new river channels formed by flooding (fig. 1-10). The water

table may be raised where highway embankments impede normal

drainage.

Overwatering of conifers in ornamental plantings is also a common

problem. Damage is caused by the depletion ofthe oxygen supply to the

roots and the problem is more severe on poorly drained and poorly

aerated clay soils than on sandy soils (fig. 1-11). The death of native

conifers in newly established lawns is a common problem.

The injury may be discovered at any stage ranging from greenish

yellow or brown foliage throughout the crown to dead snags. Excess

soil moisture may also encourage the "water mold" fungi, which causes

serious root rots — particularly in ornamental plantings on former

agricultural soils.

There may be some demonstrated differences in species response to

high water table. For example, lodgepole pine may persist longer

under these conditions than ponderosa pine.

F-700213

Figure 1-10. These Jeffrey pines were killed by excess soil moisture when the

water table was changed by a new beaver pond.

22
F-700214

Figure 1-11. A chronic problem of poor drainage over a period of year has

caused yellowing and stunting of this juniper. Root rot fungi often are involved in such cases, thereby increasing damage and death.

Mineral Excess

Excess Salt

Roadside environment — Mineral excess in needle tissue results

from salt absorption through the roots or by direct foliar contact. The

uptake of chloride salts by the roots of roadside trees is a common

problem wherever sodium chloride and calcium chloride are applied to

icy highways in the winter (fig. 1-12). In the Lake Tahoe Basin of

California and Nevada, the average distances from the edges of highways to trees showing different salt damage ratings were: no damage

41 feet, light damage 21 feet, moderate damage 20 feet, and severe

damage 15 feet. The final result of accumulation of salt in the tips of

conifer needles is needle tip dieback. The cause can be confirmed by

analysis of leaf tissue and soil for chloride content. The dead tissue is

reddish brown and may occupy as little as 2 or 3 cm ofthe needle tip or

as much as two-thirds of the needle. The increased salt content of the

soil also decreases water uptake by trees, thus inducing an artificial

drought. Highway maintenance programs sometimes use borate salts

for weed control along roadsides (see Injury from Herbicides). Many

roadside trees are killed by chloride and borate salts.

Irrigation water — Careful observations have been made of ponderosa pines receiving salty irrigation water in ornamental plantings.

The symptoms were chronic foliar chlorosis and needle tip dieback

initiated by a 3- to 5-mm band of resin-infiltrated tissue that caused

23
F-700215

Figure 1-12. Absorption of chloride salts from de-icing comi>ounds applied to

highways can cause severe needle necrosis, as shown by this Jeffrey pine.

the distal needle tissue to become brown. This process was repeated

and the bands still remained visible as darker areas. Severely affected

trees were randomly distributed, retained only the current-year needles and some trees died.

Coastal environment — Salt damage may be expected in locations

along the coast where trees have been planted on land fill, e.g., a

marina. Eventually, the roots grow down to the salty water table. The

damage is characterized by reddish brown needle tip dieback, the

living needle tissue is yellow, and needle length is reduced.

Salt spray can severely damage conifers and other trees at some

distance from the beach or ocean front. Following a storm with high

winds along the California coast, only the windward side of trees had

brown needles and damage was observed up to 1/4 mile or more from

the beach. Occasional storm-related salt injury causes no lasting damage. A more common foliar damage to coast redwood has been attributed to salt spray. The flag form of cypresses and other conifers may

24
F-700216

Figure 1-13. The prostrate forms of Torrey pines growing on the bluffs immediately above the ocean may have resulted from both wind pressure and

gradual absorption of windborne salts by foliage.

not be as much a result of wind pressure as of constant salt absorption

causing death of needles, buds, and twigs (fig. 1-13).

Excess fertilizer — Nitrogen compounds can cause a "burning" of

needle tips. This disorder is usually limited to Christmas tree plantations and nurseries, or other locations where trees receive intensive

care. It may also be confused with injury by selective herbicides

applied in excess to the soil. Recovery from excess nitrogen injury may

be expected to be more rapid than recovery from herbicide injury.

Sewage effluent — Trees growing near places of habitation may

receive sewage water from drainage fields or treatment plants. After

an initial growth stimulation, trees show symptoms resembling those

caused by soil sterliants (boron) appear in the second year; some trees

can be expected to die thereafter. Jeffrey pine, sugar pine, and white fir

trees have been killed in the vicinity of leach lines.

Soil Parent Material

Serpentine soils — Soils derived from igneous rocks of the same

name occupy thousands of acres in Lake, Napa, Marin, and Sonoma

counties, and in some Mother Lode counties of California, as well as in

the Siskiyou mountains of Oregon. In Lake County, a sparse kind of

chaparral, including digger pine, is present on the soils derived from

serpentine. An abrupt line dividing vegetation types often marks the

transition from serpentine soils to soils derived from other parent

materials.

25
The dwarfing oftrees on serpentine soils is attributed to high levels

of magnesium that prevent absorption of calcium, further inducing a

nutrient imbalance with respect to nitrogen, phosphorus, and some

trace elements.

Mineral Deficiency

Deficiency of the major nutrients, nitrogen, phosphorus, and potassium might be expected if trees are planted on land formerly used to

grow crops. Nitrogen deficiency shows as chlorosis ofthe older needles,

and stunted growth. Phosphorus deficiency results in a purple discoloration and withering of older foliage. Potassium deficiency causes

chlorosis and needle tip dieback of older needles.

Herbicide Injury

Chemical herbicide applications are usually associated with particular land-use situations, including the control of brush around

dwellings, on fuelbreaks, and along roadsides, railroad tracks, and

powerline rights-of-way. Damage to desirable species atthe edge ofthe

control area is usually caused by direct but accidental application or by

drift of the spray droplets on foliage and root absorption when herbicides are applied to the surface near adjacent trees.

The symptoms of herbicide injury to conifers are numerous but not

as well known as those on herbaceous plants. Some categories of

symptoms to expect include: Twisting of needles and shoots and necrosis (hormone-type herbicides such as 2,4-D, 2,4,5-T, picrolam) (fig.

1-14); severe stunting (thiocarbamates); chlorosis and necrosis by

root-absorbed herbicides (aminotriazole, triazines, substituted ureas,

monuron, arsenics, borates, and chlorates); yellow-white bleaching

(aminotriazole); and desiccation (weed oil) (fig. 1-15).

Sometimes herbicides that are absorbed by roots on one side of the

tree will damage only that foliage supplied by those roots. Rootabsorbed herbicides usually cause death or lasting damage in the most

severe cases. Conifers usually recover from hormone-type herbicides

with little lasting damage.

Herbicides like simizine used to control weeds selectively in Christmas tree plantations may cause injury to Monterey pines if soils are

sandy.

Injury From Air Pollutants

Particulates — Solid particles such as flyash, road dust, or dust from

cement plants are often harmful to conifers in the immediate vicinity

of the source. Injury results because light is prevented from reaching

the needle surface, thereby reducing the photosynthetic activity ofthe

tree. In some cases, the cement dust or flyash may have toxic compo26
^

F-700217

Figure 1-14. Damage by 2,4-D spray drift occurring after needle elongation

caused yellowing and drooping of the old needles of Jeffrey pine.

nents that injure the needle tissue directly. Both effects result in

premature defoliation ofthe tree. Damage can be expected only in the

immediate vicinity ofthe source because all but the smallest particles

settle out rapidly.

Gaseous pollutants — Gaseous air pollutants are dispersed over

much wider areas than particulate pollutants. Sources may be classified as: (1) point sources — the stack of a power generating plant or

factory, (2) an area source — a metropolitan complex, and (3) a line

source — a heavily traveled highway.

Topography and local meteorological conditions are important factors that determine the degree to which pollutants concentrate in the

atmosphere. These two factors define air basins, which are regions

where communities share a simlar air mass and meteorologial conditions.

The meteorological conditions most responsible for concentration of

air pollutants include the radiation temperature inversion, which is

typical of inland valleys, and the marine temperature inversion, in

27
F-700218

Figure 1-15. Injury to incense-cedar as a result of direct spray application of

weed oil.

28
coastal valleys. The distinctive feature ofthe temperature inversion is

a warmer layer of air sandwiched in between a cool air layer near the

ground where pollutants concentrate and the cool, relatively clean air

above. The prevailing windspeed and direction determine the horizontal transport of the pollutants while the structure of the vertical

temperature profile determines the vertical dispersion of pollutants.

Low windspeed enhances concentration of pollutants. Both the inland

flow of marine air and the daytime upcanyon or upslope flow on

sunheated mountain slopes transport pollutants concentrated beneath

the inversion layer to forested areas.

Ozone — The most important cause of air pollutant damage to

conifers in California is ozone (O3). Ozone damage is most severe in the

southern California mountains; on the westside of the southern

Sierra Nevada, injury has been slight and concentrated mainly east of

Fresno. Ponderosa pines moderately and severely injured by ozone are

more frequently attacked and killed by bark beetles.

Ozone is the major plant-damaging constituent of photochemical

oxidant air pollution (smog). The source of this pollution is mainly

automobiles and to a lesser extent industrial sources. Ozone is not

emitted directly from automobiles or chimneys, butrather is formed by

a complex chemical reaction in the atmosphere. Two primary pollutants, nitrogen dioxide and hydrocarbons (gasoline vapor) react with

sunlight to produce ozone.

The distribution ofozone-damaged trees is typically near the border

of an air basin (e.g., between coastal and desert areas) and in the

predominant summer downwind direction from heavily populated

areas. Damage is present as far as 80 miles east of the Los Angeles

metropolitan area. The distribution of affected trees at a particular

site is quite random. This indicates a high degree of variability in

sensitivity within the species.

Ponderosa and Jeffrey pines are the ñrst species to show injury and

the amount of injury under field conditions to these pines can be

identified with five descriptive categories.

1. None — four or more annual needle whorls retained, with no

evidence of yellow or chlorotic mottle on any needles.

2. Possible injury — four or more annual needle whorls retained, but

oldest whorl(s) displays distinct chlorotic needle mottle (fig. 1-2, upper), and sometimes may be easily pulled from the stem.

3. Slight injury — three or four annual needle whorls retained, with

distinct chlorotic mottle on older needle whorls accompanied by premature needle abscission ofoldest needles. The length ofrecent annual

shoot growth may be reduced. Lowest branches show the most defoliation.

4. Moderate injury — two to three annual whorls retained, with

intensification of other symptoms described under '^slight injury."

5. Severe injury — one or two annual needle whorls retained in late

summer, both with shortened yellow mottled needles with or without

tip necrosis of the current and 1-year-old needles (fig. 1-16). Older

needles fall easily from the stem. Chronic suppression ofshoot growth

is evident. Apical dominance is often diminished resulting in a flat29
F.7002I9

Figure 1-16. Ponderosa pine needles injured by ozone show how the chlorotic

mottle advances from tip to base and is always more intense on older needle

whorls.

topped crown. Lower and mid-crown branches are dead (fig. 1-17).

Ozone injury to white fir develops according to the same sequence of

events.

In fumigation trials, the order of decreasing ozone sensitivity of a

number of western conifers where higher score ranges indicate more

severe damage were 15 down to 10 — western white pine, Jeffrey x

Coulter hybrid, red fir, Monterey x knobcone hybrid and ponderosa

pine; 9.99 down to 5 — Coulter pine, Douglas-fir, Jeffrey pine, ponderosa pine (Rocky Mountain), white fir, big-cone Douglas-fir, and

knobcone pine; 4.99 down to 1.5 — incense-cedar, sugar pine, and giant

sequoia.

Monterey pine in Christmas tree plantations in southern California

may have up to 10 percent of the trees severely injured by ozone;

surrounding trees usually show some detectable injury (fig. 1-18).

Sulfur dioxide — Historically, sulfur dioxide has been a serious local

problem in the Western States notably at Redding, Calif; Anaconda,

Mont.; and in the upper Columbia River Valley ofWashington. Sulfur

dioxide is a serious problem in areas where sulfur containing coal and

oil is burned or where smelters process sulfide ores (copper, zinc, lead,

iron).

30
F-700220

t igure 1-17. During winter, only shortened current-year needles remain on this

ponderosa pine severely damaged by ozone, and infested with bark beetles.

On conifer needles, sulfur dioxide causes a reddish brown discoloration that often does not cover the entire needle but occurs in bands

beginning at the needle tip. Middle-aged and older needle whorls are

injured first and branches die progressively from the bottom ofthe tree

to the top. Damage can occur anytime — even during mild winter

weather. Less severe doses cause a chlorosis and premature abscission

of older needles. Winter injury and drought symptoms usually cause a

31
F-700221

Figure 1-18. In densely planted Monterey pine Christmas tree plantations,

ozone damage is found in all degrees.

brown discoloration of the entire needle but not as reddish as sulfur

dioxide injury; symptoms appear in spring or late summer, respectively. Drought affects current-year's needles and the upper crown

first; winter injury involves older needles as well, and is present

throughout the crown.

The order of decreasing sulfur dioxide susceptibility of selected

western conifers is: Grand fir, subalpine fir, western red cedar, western hemlock, Douglas-fir, western white pine, ponderosa pine,

lodgepole pine, western larch. Engelmann spruce, western juniper,

and Pacific yew.

Hydrogen fluoride — Fluoride damage to western conifer species

was a difficult problem in the vicinity of Spokane, Wash., during the

1950's and more recently at Columbia Falls, Mont. Hydrogen fluoride

is emitted from aluminum ore reduction plants, phosphate fertilizer

plants, brick kilns, and glassworks.

The current-year's needles of conifers are the most sensitive to

fluoride. Needle tip dieback begins while new needles are elongating

in the spring, but the same needles become relatively resistant to

further damage later in the season. Needle tips first become chlorotic

and then turn brown. The needle tip dieback on older needles does not

represent new injury but mainly injury which was received during

elongation; these needles are usually shed. Foliar analysis for fluoride

content is an excellent diagnostic method for confirming the cause if

done by a laboratory with adequate experience. Serious errors result

from poorly cleaned laboratory glassware. Ponderosa pine was virtually eliminated from some sites as the dominant species near Spokane,

Wash. Other sensitive species include: Western larch, lodgepole pine,

32
and Douglas-fir. Grand fir, blue spruce, and white spruce are less

susceptible while arborvitae and juniper are tolerant.

Minor air pollutants — The air pollutants of minor importance are

ammonia, chlorine, and hydrogen chloride. The first two pollutants

are only present during brief episodes when containers in storage or

transport accidentally burst or develop a serious leak. Hydrogen

chloride results from incineration of polyvinyl chlorides. Ammonia

and hydrogen chloride cause needle tip necrosis of all ages of needles.

Chlorine causes both tip necrosis and various amounts of chlorotic

mottle not unlike severe ozone injury.

Effects of Fire

Conifers are most susceptible to fire damage early in the growing

season when stem and shoot growth is active. The factors that determine tree survival after fire are the amount of bud and twig kill,

foliage kill, and bark and cambium kill. Extensive heat kill of the

foliage may occur without much damage to buds and twigs (fig. 1-19).

A tree that overwinters with no live needles may survive unless high

temperatures have killed the cambium tissue of the main stem. Several years after the fire, bark scaling is common on surviving thin bark

species. Thicker bark has greater insulating capacity to protect the

cambium from injury. Bark thickness varies from species to species

and even within a species. The decreasing bark thickness and order of

decreasing fire resistance of some selected western conifers is Sierra

redwood, Douglas-fir, sugar pine, red fir, white fir, white pine, western

red cedar, and lodgepole pine. Young trees of nearly all species are

highly susceptible to ground fires (fig. 1-19).

Figtire 1-19. Young trees are usually killed or extensively damaged by ground

fires. This young plantation of sugar and Coulter pines shows heat kill of

foliage that was not consumed by fire; older trees with thicker bark and no

foliage close to the ground may survive fire.

33
F-700223

Figure 1-20. The large fire scar on this ponderosa pine is easily recognized by

the charred heartwood remaining. Bole damage may vary from severely

hollowed basal sections to flattened or depressed areas in the bark on one

side of the stem, usually on the uphill side or leeward side of the tree with

respect to the run of the fire.

Cambium injury is ordinarily heaviest on the lee side ofthe tree with

respect to the direction of run ofthe fire and on the uphill side oftrees

located on slopes. Killed patches of cambium are widestjust above the

ground and taper upward; however, charred heartwood is usually still

present as confirming evidence ofthe cause ofthe canker-like area (fig.

1-20).

Lightning Injury

The most common evidence of lightning injury to taller trees is the

tearing offofbark and a thin layer ofwood in a narrow strip, extending

spirally around the trunk from the top ofthe bole to the butt (fig. 1-21 ).

The tree top may be killed immediately; bark beetles often invade the

34
F-700224

Figure 1-21. Symptom of lightning injury is typically a narrow strip of bark

removed in a spiral course down the bole. This ponderosa pine had a powerline attached to the bole, which served as a ground. The strip usually continues to the soil.

tree. Thisjagged furrow is easily distinguished from the ribs or cracks

resulting from freezing or drought. Some trees, particularly white fir,

are completely shattered. Either the top is broken or a large section of

the lower bole "explodes" (fig. 1-22). Occasionally small circular

groups of conifers may be killed by a diffuse electrical discharge without showing any outward signs of mechanical injury except for a

foliage scorch.

Injury by Mechanical Factors, Snow, and Ice

Heavy snow accumulations often bend or break the stems ofyounger

conifers. Severely bent stems straighten after a few years, but snow

bending can significantly reduce height growth the year after injury.

35
F.700225

Figure 1-22. Lightning often causes severe damage and kills trees. This white

fir essentially "exploded" on being struck.

36
F-700226

Figure 1-23. The flat-topped crowns ofolder pines are usually a sign of extreme

age, but repeated removal of the top by heavy snow and ice loads causes the

same appearance as shown in this small ponderosa pine.

Extremely heavy accumulations of ice are common on ponderosa

pine and other dominant conifers along exposed ridgetops in the

southern California mountains. This results in broken tops as well as

broken smaller branches throughout the crown. Many of the larger

trees have broad, flat-topped crowns while the boles of pole-sized trees

have many curves and distortions caused when lateral branches become terminal leaders (fig. 1-23). In areas where rotary snow plows are

used, for example, along the Trans-Sierra highways in California,

needle, twig, and branch damage and removal is common. The repeated impact of the snow plume can result in a tree with only half a

crown along the lower and mid-sections of the stem on the side facing

the road (fig. 1-24).

After a new fall of wet, heavy snow up to 3 or 4 feet deep, the snow

settles immediately. The settling process tears small buried branches

away from the bole which later may hang by a strip of bark.

37
F-525002

Figure 1-24. Red fir severely debranched on one side due to the impact of the

snow plume thrown by a rotary plow. This condition is common on several

species along major all-weather highways in the Sierra Nevada.

At higher elevations where deep snow is persistent, the freezing and

thawing in the top layer produces large ice crystals under some conditions. High winds drive these crystals against the bark and the wood

may be exposed in a 2- to 3-foot-long section on one side of the stem.

This injury appears at heights up to 20 feet above the ground depending on snow depth.

Hail

Hail causes defoliation, bud injury, and bruising or lesions on the

upper side of stems and young cones. The trees are most severely

damaged when new growth is in progress. The worst bruising occurs on

upper branches and those on the windward side oftrees. Immediately

after the storm, many green needles and small shoots have fallen to the

ground. Several years after a hail storm, the most obvious evidence is

dead tops and one-sided crowns. Damage is sometimes confined to

long, narrow strips through the forest. The species most severely

38
damaged by hail is Douglas-fir; while white fir, incense-cedar, sugar

pine, and ponderosa pine receive less injury.

Wind

Topography, timber cutting practices, and land developments are

important factors that determine the extent of windthrow or blowdown. Damage is usually heavy on ridgetops and upper slopes, but

downslope winds can cause extensive damage. Winds at 40 to 50 miles

per hourstreamline or flow with the contour ofthe slope on the lee side,

especially where the mountain barrier is atright angles to the wind. In

the most severe situation, a clear-cut area on the windward side ofthe

slope offers no barrier to the wind blowing into a timbered area on the

lee side of the slope. As a result, winds blow with greater force along

the contour of the lee slope than elsewhere and windthrow is more

frequent.

Other associated factors that favor windthrow in decreasing order of

importance are: Root and butt rot, particularly where roots on the

leeward side fail under compression, shallow soils, and wet, poorly

drained soils. The tree may also break at any point along the main

stem, for example, at rust cankers, a beaver girdle, or where the bole is

hollowed by fire. Swellings may develop at places where the stem was

cracked but failed to break.

Some dominant trees that undergo constant wind rock tend to develop much sturdier root systems than those in the interior of a stand.

Itis common for individual treesleftstanding in a heavily cutover area

to be windthrown within the first 2 years after the cut. Blowdowns

create longer term problems like fire danger and bark beetle infestations. Extensive blowdowns have been reported frequently in the

Pacific Northwest and in the Sierra Nevada.

Human Activities

The use of heavy earth moving equipment can cause damage by

severely debarking the stems or by severing large portions of the root

system during excavation. These stressed trees are more susceptible to

windthrow, stem decay, and bark beetle attack. The burial of the root

systems by earth fill, asphalt pavement, or the deposition ofsilt on root

systems downhill from construction sites will diminish the normal

oxygen supply to the roots and may killthe trees in a single season (ñg.

1-25).

The growth rates of larger conifers observed in public campgrounds

throughout California have not revealed any changes over a 30-year

period that could be directly related to recreational use. Young conifers, however, were susceptible to damage by recreation impact. No

seedlings ofthe smallest size category were observed at any ofseveral

recreation sites and larger seedlings, saplings, and poles had generally

decreased in number.

39
F.700227

Figure 1-25. Incense-cedars killed by the anaerobic conditions induced when

the dirt, rocks, and chunks of asphalt were dumped over the roots.

Selected References

Anonymous.

1967. Forest pest conditions in California — 1967. Calif. Forest Pest Action Council,

Calif. Div. of Forestry, Sacramento, Calif, 20 p.

Anonymous.

1968. Forest pest conditions in California — 1968. Calif. Forest Pest Action Council,

Calif Div. of Forestry, Sacramento, Calif, 16 p.

Bentley, Jay R., D. A. Blakeman, and S. B. Cooper.

1971. Recovery of young ponderosa pines damaged by herbicide spraying. USDA

Forest Serv. Res. Note PSW-252, 7 p.. Pacific Southwest Forest and Range Exp.

Stn., Berkeley, Calif

Jacobson, Jay S., and A. Clyde Hill (eds.).

1970. Recognition of air pollution injury to vegetation: A pictorial atlas, 102 p. Air

Pollution Control Assoc, Pittsburgh, Pa.

40
Leaphart Charles D., and Albert R. Stage.

1971. Climate: A factor in the origin of pole blight disease oiPinus montícola. Dougl.

Ecology 52(2):229-239.

Lund-Huie, K., and D. E. Bayer.

1968. Absorption, translocation, and metabolism of 3-amino-1,2,4-triazole in Pinus

ponderosa and Abies concolor. Physiol. Plant. 21:196-212.

Magill, Arthur W.

1970. Five California campgrounds . .. conditions improve after 5 years recreational

use. USDA Forest Serv. Res. Paper PSW-62,18 p.. Pacific Southwest Forest and

Range Exp. Stn., Berkeley, Calif.

Miller, Douglas R.

1970. In Key and guides to the damaging forest pests of California. USDA Forest

Serv., Calif. Reg. (unpublished manuscript).

Miller, Paul R., and Arthur A. Millecan.

1971. Extent of oxidant air pollution damage to some pines and other conifers in

California. Plant Dis. Rep. 55(6):555-559.

Oliver, William W.

1970. Snow bending ofsugar pine and ponderosa pine seedlings — injury not permanent. USDA Forest Serv. Res. Note PSW-225, 3 p.. Pacific Southwest Forest and

Range Exp. Stn., Berkeley, Calif.

Perry, T. O., and G. W. Baldwin.

1966. Winter breakdown ofthe photosynthetic apparatus of evergreen species. Forest

Sei. 12:298-300.

Scharpf, Robert F., and Michael Srago.

1974. Conifer damage and death associated with the use ofhighway deicing salt in the

Lake Tahoe Basin of California and Nevada. USDA Forest Serv., Calif. Reg.,

Forest Pest Control Tech. Rep. 1, 16 p.

Scheffer, Theodore C, and George G. Hedgecock.

1955. Injury to Northwestern forest trees by sulfur dioxide from smelters. U.S. Dep.

Agrie, Tech. Bull. 1117, 49 p.

Staley, John D., Jack Altman, and Robert A. Spotts.

1968. A sodium linked disease ofponderosa pine in Denver, Colorado. Plant Dis. Rep.

52:908-910.

Stewart, Dennis, Michael Treshow, and Francis M. Hamer.

1973. Pathological anatomy of conifer needle necrosis. Can. J. Bot. 51(5): 983-988.

Wagener, Willis W.

1949. Top dying of conifers from sudden cold. J. For. 47:49-53.

Wagener, Willis W.

1960. A comment on cold susceptibility of ponderosa and Jeffrey pines. Madrono

15:217-219.

Wagener, Willis W.

1961. Guidelines for estimating the survival of fire damaged trees in California.

USDA Forest Serv. Misc. Paper 60, 11 p.. Pacific Southwest Forest and Range

Exp. Stn., Berkeley, Calif.

Walker, R. B.

1954. Ecology of serpentine soils. II. Factors affecting plant growth on serpentine

soils. Ecology 35:259-266.

Westing, Arthur H.

1969. Symposium on soil and water pollution damage to plants — plants and salt in

the roadside environment. Phytopathology. 59:1174-1191.

41
2. NEEDLE DISEASES

by

RICHARD S. SMITH, JR.*

Most conifers depend upon a 2- to 11-year complement of needles for

maximum growth and development. When a large portion of these

needles are killed, they are not replaced — and the growth ofthe tree is

reduced. Complete defoliation is usually fatal.

Many agents are responsible for needle death. Older needles die

naturally and are cast after a certain number ofyears on the tree.Some

insects such as mites, scale, and aphids may kill needles. Abiotic

factors, such as air pollution, herbicide sprays, salt injury, overfertilization, high temperature, drought, and winter injury (red belt),

kill needles or parts ofthem. Rust fungi may also cause needle diseases

(Chapter 4). Root diseases (Chapter 6) may cause needles to yellow and

die prematurely.

This chapter concerns needle diseases caused by fungi otherthan the

rust fungi. Most ofthese diseases are identified by the fruiting bodies

of the casual fungi which are found on the dead needles or dead

portions of partially killed needles. These fungi often have life cycles

which are timed with the growth and development ofthe host and may

require 1, 2, or more years to complete.

Sporulation, spread, and infection of these fungi are frequently

restricted to a specific season, such as spring, summer, or fall, and

successful infection depends on whether conditions are favorable at

the time. For example, in some needlecasts infection is frequently

restricted to the newly developing needles, and sporulation is timed to

coincide in spring with needle development. These rather rigid requirements for infection in some species result in only an occasional

year of heavy infection on 1 year's set of needles. Consequently, the

host is usually not completely defoliated and is not killed, but its

growth rate may be reduced.

* Plant Pathologist, formerly with the Pacific Southwest Forest and Range Experiment Station; now with the California Region, Forest Service, U.S. Department of

Agriculture, San Francisco, Calif.

42
Descriptive Key

A^ Needles and twigs enveloped in a brown felt-like mat of fungus —

on lower branches or small or bent trees below snow line. . Brown

J^elt Blight (Herpotrichia nigra, Neopeckia coulteri)

A Needles not in brown felt-like mat — with various types offruiting

bodies on needle surface ß

^ Needle diseases of Spruce C

* Needle diseases of Fir 1................... D

Needle diseases of Douglas-fir .'..............'^^^^ Needle diseases of Cupressaceae ................I

Needle diseases of Pine J

B

B^

B^

B^

B^

Spruce

C^ On Brewer spruce — needles with black elliptical

fruiting bodies in rows on either side of middle rib

JLfOphodermium crassum

C2 On Sitka spruce — needles with black elliptical

fruiting bodies in rows on either side of middle rib

Lophodermium picea

True fir

D^ On bristlecone fir E

D^ On other firs '^Z''^Z'^^^^^^^

E^ Fruiting bodies brownish-black, large,

extending down the middle ofthe needle

for almost its whole length

JLirula nervisequia

W Fruiting bodies greyish-black, elliptical, appearing in two rows, on each side

. . of mid rib Lophodermium decorum

i^ruitmg bodies on needles of all ages, appearing as oval disc-like

structures breaking through the lower epidermis in two rows one

on either side of the mid rib Snow mold, Phacidium abietis

Fruiting bodies brownish-black, large, elongate extending down

center of lower surface of 2-year-old or older needles G

G* Pycnidial fruiting structures appear as a single brownish line down the center groove of upper surface of

needle

•• Lirula abietis concoloris

G Pycnidia needle colored to light brown appearing as two

wrinkles or rows, one on each wing, along the upper

needle surface Virgella robusta

43
Douglas-fir

H^ Fruiting bodies brown cushion-like elongate

structures developing on lower needle surface on

either side of mid rib

Douglas-fir needle cast Rhabdocline spp.

H^ Fruiting bodies small, black, spherical; appearing

as soot-like streaks on undersurface of needle

along each side of mid rib

Swiss Needle Casi Phaeocryptopus gaumanni

Cupressaceae

Fruiting bodies appear as small shiny black elliptical fruiting

bodies on leaves ofjuniper and incense-cedar Lophodermium

juniperi

Fruiting bodies, olive brown to black, circular to elliptical breaking

through upper leaf surface. Fruiting bodies later dropping out to

leave a deep pit Cedar Leai Blight Didymascella thujma

or Didymascella tetraspora

Pines

J^ Infection perennial in twigs, resulting in necrotic flecks in

inner bark; in a red flagging of almost all 1-year-old needles of

infected twigs in the spring; and a brooming and upturning of

infected twigs Mytroderma deformans

J2 Infection not perennial in twigs; separate infection of each

needle required; no brooming K

K^ Infected needles with bright red bands or spots with

black fruiting bodies on 1- , 2- , or 3-year-old needles

Scirrhia pini

K^ Infected needles not as above L

L^ Fruiting bodies on infected needles exposed by the

splitting ofthe epidermis along stomatal lines and

tearing at the ends ofthe fruiting body to form two

door-like epidermal flaps which remain hinged at

the side; exposed spore layer brown

Naemacyclus niveus

I? Fruiting bodies opening by a narrow slit, elliptical

to elongate, black to brown M

M^ Host in the White pine group N

M^ Host in the hard pine group ^

W Fruiting body light brown to concolorous with the needle surface Lophodermella arcuata

W Fruiting body black -O

O' Fruiting body shiny black with irregular black crust-like

growth of fungus tissue Bifusella linearis

44
O^ Fruiting body without associated crust-like growth P

P^ Fruiting bodies shiny black, elliptical, associated pycnidia brown, on needles of singleleaf pinyon pine

Bifusella pini

P* Fruiting bodies large black, associated pycnidia black

on whitebark and limber pines Bifusella saccata

P^ On other white pines Q

Q* Fruiting bodies shiny black, elliptical, occurring

subcuticularly in groups on outer surface of needles; group of fruiting bodies separated from adjacent groups by distinct black lines bisecting the

needle Lophodermium nitens

Q^ Fruiting bodies dull to shiny black, elliptical, occurring in rows on all surfaces of 3-year or older

needles. Infected needles often remain on tree and

turn grey Lophodermium pinastri complex

R* Fruiting body light brown to concolorous

with needle surface S

R^ Fruiting body black T

S^ Fruiting bodies oval and concolorous, on ponderosa and lodgepole

pine Jjophodermella cerina

S^ Fruiting bodies elongate, concolorous to brown on ponderosa and

knobcone pine Lophodermella mórbida

T* Fruiting bodies often found in dead areas of live green needles U

T^ Fruiting bodies found on completely dead or faded needles

V

U* Fruiting bodies in dead areas of live green needles ofPinus

radiata or P. attenuata. . .

either Davisomycella lacrimiformis

or Davisomycella limitata

U^ On lodgepole pine, fruiting bodies in dead areas and separated from green areas by an orange-brown band which remains even after the whole needle dies

Davisomycella montana

V^ Fruiting bodies, elongate, black W

V^ Fruiting bodies elliptical, dull to shiny black, occurring

in rows on all surfaces of 3-year-old needles. Infected

needles often remain on the tree and turn grey

Lophodermium pinastri

W^ Fruiting bodies elongate, black, wide — one-third to one-half the

width of the needle, variable in length, occurring on lighter colored zones on dead 3-year-old needles

Davisomycella medusa

W* Fruiting bodies elongate, thin, occurring on dead 1-year-old needles, not found in lighter colored zone

LJlytroderma deformans

45
Brown Felt Blight

Herpotrichia nigra

Neopeckia coulteri

Hosts

The brown felt blight is a foliage disease of conifers caused by two

similar fungi, Herpotrichia nigra and Neopeckia coulteri. In North

America, A/^. coulteri attacks the foliage of pines only, while i/. nigra

attacks conifers other than pines. Macroscopically, these two fungi are

indistinguishable; their effects on the hosts are identical, and their life

cycles are quite similar. So, traditionally, these two fungi have been

treated together. These fungi are commonly but erroneously referred

to as "snow mold."

Distribution and Damage

Brown felt blight is distributed worldwide, and generally found

throughoutthe coniferous forests ofNorth America. The two fungi are

usually found only at the higher elevations of mountainous regions,

where enough snow falls to meet the unique requirements of these

fungi.

The disease develops only under cover ofsnow; therefore, its attacks

are limited to smaller trees and the lower branches oflarger trees that

are buried under snow in the winter. These fungi envelop twigs and

needles in a dark brown, felt-like growth. Needles within the felt are

infected and killed. This disease may on occasion kill seedlings and

saplings that are covered by snow, but it has little effect on trees once

they reach pole size. The damage done in the forest is minimal, but it

has attimes been a serious problem in snow-covered forest nurseries.

Disease Cycle

Infection of the host branch occurs under the snow during winter.

The exact mode ofinfection is unknown, butit has been suggested that

it originates from infested litter on the forest floor. Under cover of

snow, the fungus envelops the branch in a gray mycelium. After

snowmelt and exposure, the fungusfelt stops growing and turns a dark

brown. The following summer, the mycelium remains inactive. The

second winter, fruiting bodies (perithecia) develop on the felt under the

snow. The fruiting bodies remain immature while the infected twig is

on the tree, but ripen in late summer on the fallen twigs. Their role in

the infection cycle is uncertain.

46
Field Identification

This disease is easily identified in the field by the dense, dark brown

mat ofmycelium that envelops the needles and twigs (fig. 2-1). Small,

black, spherical fruiting bodies can be seen on the second-year mycelial mats.

Figure 2-1. The brown fungus mat ofthe Brown Felt Blight covering the ends of

branches of a red fir (top) and a sugar pine (bottom.)

47
Spruce Needle Casts

Lophodermium crassum

Lophodermium piceae

Two minor needle casts of spruce are found in the Western United

States. Lophodermium crassum has been reported on Brewer spruce,

in Siskiyou County, California. Lophodermium piceae has been found

on sitka and Engelmann spruces.

InL. piceae, the black, elliptical, fruiting bodies occur in longitudinal rows on either side of the middle ridge of the outer faces of the

needles. The areas occupied by one or a group of fruiting bodies are

separated from one another by heavy black lines extending through

the needle and along which the needle readily breaks. L. crassum is

very similar. These two species can be separated only by a cross

sectional view of the fruiting bodies. L. piceae is intraepidermal; L.

crassum is subepidermal.

Bristlecone Fir Needle Cast

Lirula nervisequia ssp. conspicua

A disease similar to the other true fir needle casts and caused by

Lirula nervisequia is found on bristlecone fir in Monterey County,

Calif. The fruiting bodies are brownish-black, large, elongate structures extending down the middle ofthe undersurface ofthe needle for

most of its length. Appearing only rarely, this fungus does little damage.

Lophodermium Decorum

In the Western United States, Lophodermium decorum is found on

shaded and weakened needles of grand fir. This rare fungus is easily

differentiated from the other true fir needle casts by its two rows of

short, elliptical, brown to grayish-black, fruiting bodies on the lower

needle surface, one row on each side ofthe midrib. A similar but as yet

unnamed species ofLophodermium has been reported on bristlecone

fir.

48
F-700230

Figure 2-2. Snow blight of white fir caused by Phacidium abietis. The dark

brown oval fruiting bodies are arranged in two rows along the lower needle

surface.

Snow Blight

Phacidium abietis

Snow blight caused by the fungus Phacidium abietis has been found

on the needles ofwhite fir in the southern Cascade Mountains and the

northern Sierra Nevada in California. At times, it has reached

epidemic proportions in northern Idaho and eastern Oregon, killing

reproduction of lowland white fir, alpine fir, and Douglas-fir. The

fungus attacks all ages of needles during winter while under cover of

snow. After the snow has melted, the infected needles remain on the

tree and turn brown. Only those needles covered by snow during

winter are attacked. In summer and fall, dark brown round to oval

disc-like fruiting bodies break through the lower epidermis of the

needle. The fruiting bodies are arranged in two rows — one on either

side of the midrib (fig. 2-2). They mature and release spores from

August to October. The following year the needles remain attached to

the host and turn gray. The fruiting bodies fall away, leaving a cavity

in the lower needle surface much like that which occurs in the cedar

leaf blight.

True Fir Needle Casts

Lirula abietis-concoloris

Virgella robusta

Hosts

In the Western United States, Lirula abietis-concoloris and Virgella

robusta have been found on white, grand, Noble, Pacific silver, and

California red firs.

49
Distribution and Damage

Both fungi are found throughout western North America generally

wherever their hosts occur. As with many other needle casts, they

appear sporadically and in many areas infrequently.

As a rule, these diseases are of little economic importance in the

forest. Since they occur sporadically and attack only one year's complement of needles, they seldom kill a significant proportion of the

host'sfoliage. Only ifseveral successive years ofinfection were to occur

would they defoliate trees and greatly affect host growth and vigor.

Their most serious effect is to damage Christmas trees. The unsightly

browning and premature dropping of the infected needles make the

tree unsalable.

Disease Cycle

Little information is available on the life history ofthese fungi. Field

observations suggest a 2-year or longer life cycle, with infection occurring on young, developing needles, and fruiting structures maturing

on these needles during the summer 2 or more years later.

Field Identification

Both fungi may be identified by the presence oftheir elongate, dark

brown to black fruiting bodies (hysterothecia) (figs. 2-3, 2-4) on

2-year-old or older straw colored needles. These fruiting bodies extend

down the center of the lower needle surface for almost its full length.

Infection is usually confined to 1 year's set of needles.

These fungi may be distinguished from each other by the arrangement ofpycnidial fruiting bodies on the upper surface ofthe needles. In

V. robusta, the pycnidia form two distinct concolorous rows or wrinkles

— one on each wing of the infected needle (fig. 2-3). In L. abietisconcoloris, the pycnidia form a single brown line or occasionally a

double row ofdots in the groove down the center ofthe needle (fig. 2-4).

Douglas-Fir Needle Cast

Rhabdocline pseudotsugae

Rhabdocline weirii

Hosts

The two hosts ofDouglas-fir needle cast are Douglas-fir and big-cone

Douglas-fir.

50
P-.700231

Figure 2-3. Virgella robusta on the needles of white fir. The needle on the left

shows the heavy dark hysterothecium on the lower surface ofthe needle, and

the needle in the center shows the two rows of concolorous to brown pycnidia

on the upper needle surfacece.

F-700232

Figure 2-4. The fruiting bodies oí Linda abietis-concoloris on white fir. The needle on the right shows the heavy dark hysterothecium on the lower needle

surface. The needle on the left shows the single row of brown pycnidia down

the center of the upper needle surface.

51
Distribution and Damage

The Douglas-fir needle cast, the single most important needle disease of Douglas-fir, is caused by any of two subspecies ofRhabdocline

pseudotsugae or three subspecies ofR. weirii. Inasmuch as the main

differences between these species and subspecies of fungi are microscopic, this handbook treats the disease, and its causal fungi, as one.

The disease, originally native to the Douglas-fir regions of western

North America, is now also found in eastern North America and

Europe. In California, it has been found in most native Douglas-fir

stands, where it appears sporadically.

This disease appears on needles 1 year old or older. R. pseudotsugae

is found only on 1-year-old needles, while R. weirii is found on older

needles as well. And R. weirii subspecies obovata occurs only on needles 2-years-old or older. A single attack usually results in only partial

defoliation of the host. Trees subjected to several consecutive years of

attack may be completely defoliated and killed or severely restricted in

growth. In California, where these conditions rarely occur, the disease

is more unsightly than damaging. The greatest damage results from

an attack on potential Christmas trees since the partial defoliation

makes them unsalable for a few years. This disease is most severe on

younger trees up to pole size. Mature trees when attacked usually are

only slightly affected.

Disease Cycle

Fruiting bodies, on the undersurf ace ofneedles infected the previous

year, mature in May or June and ascospores are released at this time.

These spores, carried by air currents, land on and infect this year's

young developing needles. The fungus continues to develop in the

newly infected needle that summer and fall. The first symptoms appear early that first winter as slightly yellowish spots at the site of

infection. During the winter these spots become larger and more distinct. By spring the spots have changed to a deep red-brown color, and

many ofthe spots have merged. In late spring, elliptical fruiting bodies

(apothecia) appear on the undersurface of the needle on either side of

the midrib. These mature and sporulate in May or June and the

infected needles are cast during the following summer. It is suggested

thatthose subspecies appearing on needles 2 years old or older attack

current year's needles, but have a 2- to 3-year developmental cycle in

which necrosis occurs and fruiting bodies appear a year or two later.

Field Identification

The best time for identifying this disease is in late spring, when the

needles are still retained and the red-brown needle spots and developing fruiting bodies are visible. During the summer, generally all ofthe

needles are cast, and the only field symptom isthe absence ofneedles of

1 year's growth of the host.

52
The disease is characterized by the red-brown needle spots and the

long brown cushion-like fruiting bodies (apothecia) which develop on

either side of the midrib on the underside of the infected needles (fig.

2-5). At maturity, the epidermis covering the fruiting bodies splits

irregularly, exposing an orange to orange-brown spore-bearing surface.

F.700233

Figure 2-5. Douglas-fir needle cast caused byRhabdocline ssp. The light colored

fruiting bodies of ñ. pseudotsugae are located in the red-brown spots on the

underside of an infected needle, as shown on the needle on the left.

53
Swiss Needle Cast

Phaeocryptopus gaumanni

The Swiss needle cast caused by the fungus Phaeocryptopus

gaumanni damages Douglas-fir in Asia, Europe, and parts of North

America. Along the Pacific Coast, where both the host and fungus are

native, the disease causes little or no damage. The fungus attacks the

host's needles, causing them to yellow, brown, and finally drop. In

Europe, the current year's needles are infected and they die and are

cast over a 1- to 3-year period. In the Pacific Coast area, the current

and last year's needles show no signs ofinfection. Only needles 3 years

or older show such signs. The small fruiting bodies push their way

through the stomata in fall and winter and mature in the spring.

Spores are released in May and June. The numerous small black

spherical fruiting bodies appear as soot-like streaks on the undersurface of the needle along each side of the midrib.

Lophodermium Juniperi

In the Western United States, Lophodermium juniperi occurs on

junipers and incense-cedar. There is little indication that it is parasitic. The fungus forms small, shiny, black elliptical fruiting bodies on

the leaves ofthe host. Itis quite common on many ornamentaljunipers

in city plantings.

Cedar Leaf Blight

Didymascella thujina

Cedar leaf blight is a needle disease of the genus Thuja caused by

Didymascella thujina. Native to North America and introduced into

Europe, this disease is severest on seedlings and the lower branches of

older trees. The foliage is attacked and in severe cases appears as if

scorched by fire. In spring, circular to elliptical olive-brown to black

fruiting bodies are formed in the upper surfaces of infected leaves.

These are exposed by the rupture of the covering host epidermis. In

late autumn, many young infected twigs drop off. On the remaining

leaves, the presence ofthe disease is easily recognized by the deep pits

which remain in the leaves after the fruiting bodies drop out. The

disease is of little or no economic importance in the Western United

States.

54
Elytroderma Disease

Elytroderma deformans

Hosts

Elytroderma disease of pines caused by the fungus Elytroderma

deformans (Weir) Darker is considered to be the mostimportant needle

cast of ponderosa and Jeffrey pines in western North America. Its

perennial nature and capacity to infect the hosttwigs, which is unique

among the needle casts, enables it to maintain its populations even

under adverse environmental conditions.

Although mainly a disease of ponderosa and Jeffrey pines, Elytroderma disease has been found on knobcone, lodgepole, and pinyon

pines.

Distribution and Damage

Elytroderma disease is limited to North America — mainly west of

the Rockies. It is scattered throughout most of the pine forests of

California and has reached epidemic proportions in certain specific

environments, such as around lakes and along stream bottoms. Its

concentration around lakes such as Tahoe, Almanor and Manzanita

Lakes results in considerable impact on recreation and esthetic forest

uses.

This fungus causes the premature death of 1-year-old needles, and a

brooming and deformation ofinfected twigs and branches. The effect of

the disease depends on the proportion of the host crown which is

diseased. There is little effect upon the host until more than two-fifths

of the twigs are blighted. The disease is most severe on seedlings,

saplings, and poles with poor crowns. Although direct killing of mature trees by this disease is infrequent, moderate to severe infection

predisposes the host to other diseases and to bark beetle attack.

Disease Cycle

Spores of the causal fungus are released in late summer and early

fall from fruiting bodies borne on infected needles. Air currents carry

the spores to the current years's needles of a susceptible host. Under

suitable conditions, the spores germinate and infect the needles. The

fungus spreads throughout the needles and into the twigs without

initially killing the needles. The following spring the infected needles

die and turn a red brown and fruiting bodies which mature in late

summer begin to form. The infection within the twigs spreads into the

growing tips and buds, where it causes a brooming and deformation of

future growth. New needles formed each year from infected buds are

infected as they form. These needles stay green their first year, die in

spring of their second year, and produce fruiting bodies in late sum55
F-70Ü234

Figure 2-6. (Top left): A seedling infected by Elytroderma déformons

shows the reddening of last

year's needles and a brooming of

the infected terminal. The current year's developing needles

are green.

F-700235

(Top right): Brown necrotic flecks

in the inner bark of an older twig

of ponderosa pine infected with

E. deformans.

F-700236

(Bottom): The fruiting bodies of £. deformans appearing on brown needles in

June are elongate, narrow, dull black, and scattered on all needle surfaces.

56
mer. Thus, E. deformans produces a new crop of spores each year for

many years from the same infection.

Field Identification

Elytroderma disease is relatively easy to identify in the field. The

most conspicuous symptoms are reddening of the infected foliage in

spring, the development of witches' brooms (fig. 2-6 — top left), and

necrotic flecks in the inner bark of older infected twigs (fig. 2-6 — top

right). The infected needles lose their brightred-brown color gradually

through the summer. The brooms tend to be more compact and globose

than those caused by dwarf mistletoe, and the ends of the twigs turn

up. The brown necrotic flecks that appear in the inner bark of twigs

infected for more than 3 years is quite characteristic. Their presence is

one of the best evidences for confirming this disease. The fruiting

structures of the fungus that appear on infected needles in June are

elongate, narrow, dull black, and scattered on all surfaces ofthe needle

(fig. 2-6 — bottom).

Red Band Needle Blight

Scirrhia pini

(Dothistroma pini)

Hosts

Scirrhia pini (imperfect stage — Dothistroma pini) attacks some 30

species, varieties, or hybrids ofpines. In the West, it has been found on

bishop, ponderosa, western white, lodgepole, knobcone, and Monterey

pines and the Monterey x knobcone hybrid.

Distribution and Damage

Red band needle blight is distributed worldwide. In western North

America, it has been reported from north coastal California north into

British Columbia and east to Idaho. In northern California, it is confined mostly to a few localized infection centers along the Pacific Coast.

This disease is considered to be the most destructive needle disease

of pines on a world basis. Its recent discovery along the Pacific Coast,

therefore, aroused considerable concern.

The fungus attacks the needles ofsusceptible pines, causing them to

die and drop off. All ages of needles are susceptible. Under favorable

environmental conditions, this disease can completely defoliate the

host and eventually kill the infected trees. Monterey pine, although

severely affected when young, becomes resistantto this disease after it

becomes 20 to 30 years old.

57
F-700237

Figure 2-7. The red band needle blight caused by Scirrhia pini showing the red

banding around the infected needles.

Disease Cycle

Fruiting bodies (pycnidia) are produced in abundance on infected

needles. In the presence of free water, these pycnidia liberate spores

which are splashed or blown to uninfected needles. Under the right

environmental conditions, the spores infect the new needles. The fungus grows within the needle tissue, killing the distal portion of the

needle. Again, under favorable conditions, new pycnidia and spores

are produced. Dead needles remain attached to the host and produce

spores for about a year.

Field Identification

The first noticeable symptoms are yellow to tan spots appearing at

the site of infection. These spots turn a brownish-red and enlarge to

produce the characteristic red band around the needle (fig. 2-7). This

58
red banding of the infected needle is highly useful for diagnosing the

disease. Small black fruiting bodies develop in the center of the red

bands. The portion of the needle distal to the infection dies, while the

uninfected base of the needle may remain green for some time.

Sugar Pine Needle Cast

Lophodermella arcuata

Hosts

The sugar pine needle cast caused by the fungus Lophodermella

arcuata has been reported on sugar and western white pines from

Idaho and Oregon. In California, it has been found only on sugar pine.

Distribution and Damage

This disease is found generally throughout the West where sugar

and western white pines grow. It appears more prevalent in Oregon

and the northern part ofCalifornia than in southern California, where

it is found only in canyon bottoms.

This disease attacks only the current year's needles, and a single

attack results in only partial defoliation ofthe host. Repeated consecutive infections, as have occurred in certain local areas, have led to

reduced tree growth and vigor, and occasional mortality.

Disease Cycle

This fungus infects newly developing foliage. Infected foliage remains green an entire year until the following spring (April to May),

when the needles die and turn brown. This browning occurs before bud

break, giving heavily infected trees a scorched appearance. At this

time, there is no sign ofthe fruiting bodies. Fruiting bodies appear in

mid-June and mature in July and August. The needles are cast in mid

to late summer after spores are discharged.

Field Identification

This disease can be identified in the field by the gray-brown to brown

(almost the same color as the needle), elongate to elliptical fruiting

structures, which develop on all surfaces of last year's dead needles.

Bifusella Linearis

The fungus,Bifusella linearis, causes a needle cast of 2- to 3-year-old

needles of western white, limber, and whitebark pines in the Western

59
United States. This disease ranges south from British Columbia to the

higher mountains of California and east into Idaho. Because of its

limited distribution, small host range, and restriction to older needles,

the fungus is not considered to be a serious pest. The fungus forms

shiny black, elongate, fruiting bodies ofvariable lengths on the surface

of 2- to 3-year-old needles. Frequently associated with the fruiting

bodies are black crust-like growths offungus tissue (sometimes including pycnidia) that are irregular in size and outline (fig. 2-8). These

crust-like formations are the most distinctive characteristic of this

disease in the field.

Figure 2-8. The fruiting bodies ofBifusella Unearis on the needles oflimber pine.

Note the black crustlike formation with its irregular margin.

60
Singleleaf Pine Needle Cast

Bifusella pini

Bifusella pini occurs only on singleleaf pinyon pine in western

Nevada and southern California. It forms long, shiny, black, elliptical,

fruiting bodies (hysterothecia) on all surfaces of needles 4 years and

older (fig. 2-9). Pycnidia, which are also formed, vary from brown dots

to long irregular brown blotches on needles 3 years of age or older.

F-700239

Figure 2-9. The long shiny black fruiting bodies of Bifusella pini on the two

needles of singleleaf pinyon pine on the right and the brown pycnidia on the

needle of the left.

61
F-700240

Figure 2-10. The fruiting bodies ofBifusella saccata on whitebark pine.

Bifusella Saccata

The fungus Bifusella saccata has been found on whitebark pine in

California and limber and pinyon pines in Colorado. It has been reported only from elevations above 9,000 feet in the southern Sierra

Nevada. Because of its limited distribution and small host range, this

disease is not considered to be economically important. This fungus

forms large, long, shiny, black fruiting bodies on the dead tips of green

needles (fig. 2-10).

Lophodermium Nitens

Lophodermium nitens is found in both eastern and western North

America. In California, it is common on the needles of sugar pine,

fairly common on western white pine, and rare on whitebark pine. The

fruiting bodies are shining, black, elliptical, blister-like structures on

the outer surface of the needles. They mature on dead fallen needles

and occasionally on the tips of partially green attached needles. These

fruiting bodies occur singly or in clusters. Each cluster is separated

from adjacent clusters above and below by a very distinct black line

bisecting the needle and along which the needle readily breaks (fig.

2-11).

62
F-700241

Figure 2-11. Lophodermium nitens on the needles of sugar pine. Note the shiny

black blister-like elliptical fruiting bodies and the fine black lines which

cross the needles.

Lophodermium Pinastri Complex

In the Western United States, several similar but different species of

needle cast fungi have in the past been lumped together and all called

Lophodermium pinastri. This treatment of several species as one has

caused much confusion in understanding the taxonomy and biology of

L. pinastri. This complex contains a number ofhard to separate and yet

unnamed species. It is now under study and revision. Pending any

changes, this handbook treats these species as a group ofsimilar fungi

that resemble L. pinastri.

The needle diseases caused by species of Lophodermium are found

throughout the world and on many species of pine. In the Western

United States, they have been found on digger, Jeffrey, Coulter, knobcone, lodgepole, Monterey, ponderosa, sugar, western white, and

whitebark pines. The diseases they cause are common, but do little or

no damage to their hosts. In general, the fruiting bodies of most of

these fungi appear on all surfaces of 3-year-old or older needles as dull

to shining black, elliptical structures which tend to occur in lines or

rows (fig. 2-12). Mature fruiting bodies open by a conspicuous longitudinal slit. The infected needles often remain on the tree for several years

after dying and turn gray.

63
F-700242

Figure 2-12. Needles of ponderosa pine infected by one of the fungi in the

Lophodermium pinastri complex. The fruiting bodies are small, black, irregular in size, and scattered over the needle surface.

Lophodermella Cerina

The fungusLophodermella cerina causes a needle blight oflodgepole

and ponderosa pines in California from Modoc County south to Fresno

County. The disease has been severe and damaging in certain areas for

several years. The fruiting bodies of this fungus are short, oval, light

brown to buffstructures which are easily overlooked on necrotic pine

needles. Af first, they are slightly darker and then the same color as

the needle spot on which they occur. They develop in groups in buff to

tawny waxy spots on live green or dead reddish-brown needles. The

short concolorous fruiting body is the most distinctive characteristic of

this fungus.

Lophodermella Mórbida

Hosts

Lophodermella mórbida is found on ponderosa pine in Oregon and

Washington and knobcone pine in northern California.

Distribution and Damage

This disease is found only in the mild, moist climate west of the

Cascade crest in Oregon and Washington and the western slopes ofthe

64
F-700243

Figure 2-13. Lophodermella mórbida on ponderosa pine. The light to dark brown

fruiting bodies occur in rows along the infected needles.

Coast Range of northern California. It attacks the current year's

needles, which become necrotic in late summer or early fall and then

drop off the second summer. A single year's attack results in only

partial defoliation, but repeated attacks, as have occurred in ponderosa pine in Oregon, result in complete defoliation and death of the

tree. This pathogen has been described as a highly aggressive needle

cast fungus.

Disease Cycle

Needles ofthe current year are infected in June and become necrotic

as early as the end ofJuly. Pycnidia begin to appear in October, and

light brown hysterothecia are faintly evident by mid-November. Ascospores are mature and ready for discharge by mid-June ofthe following year. Infected needles are cast shortly thereafter.

Field Identification

This disease is characterized by light brown (concolorous) immature

hysterothecia which darken as they mature. These elongate fruiting

bodies (1 to 6 mm long) occur in an interrupted linear or occasionally

double-rowed series that may extend the full length ofthe needle (fig.

2-13). The pycnidia are light brown, round to elongate structures, 0.25

mm in diameter and up to 3.5 mm long.

65
F-700244

Figure 2-14. Davisomycella montana on lodgepole pine. The shiny black fruiting

bodies are grouped in light straw-colored areas bordered by an orangebrown band.

Davisomycella Limitata

Davisomycella Lacrimiformis

The two fungi Davisomycella limitata and D. lacrimiformis cause

identical diseases of Monterey pine. The latter also attacks knobcone

pine. The fruiting bodies are black, elliptical to oblong, often confluent

and scattered on dead areas on still green living needles.

D. limitata has been found in central coastal California. D. lacrimiformis has been reported from the coastal mountains ofCalifornia

and Oregon. Both diseases appear to be of little economic importance.

Lodgepole Pine Needle Cast

Davisomycella montana

The lodgepole pine needle cast caused by the fungus Davisomycella

montana has been reported in Idaho, Oregon, and California. Although widespread throughout California, the disease does not appear

to cause much damage to its host except in a few localized areas. This

disease is characterized by the appearance of fruiting bodies on dead

brown areas on 2-year-old needles. The dead areas are frequently

found on green needles and are separated from the green tissues by an

orange-brown zone or band. This orange band remains visible even

after the needle dies and turns brown. The fruiting bodies appear as

shiny, black, raised, elliptical blisters scattered on all surfaces of the

dead areas (fig. 2-14). These fruiting bodies mature during the period

from July to September.

66
Medusa Needle Blight

Davisomycella medusa

Hosts

The medusa needle blight is found on lodgepole, Jeffrey, and ponderosa pines.

Distribution and Damage

This needle disease is widely distributed throughout the ponderosa-Jeffrey pine forests east of the Cascades in Washington, Oregon,

and northern and central California. It becomes a serious pest in local

areas on individual trees, often causing a marked decrease in growth.

It characteristically occurs in relatively pure open stands and tends to

be most pronounced on medium to poor sites. It also tends to become

more intense after a drought.

Life Cycle

Fruiting bodies (hysterothecia) mature on infected needles in June,

and spore discharge occurs in summer and fall. These spores are wind

blown to nearby pines, where they infect the current year's needles.

The disease remains latent for 2 to 4 years within the infected needles

before a greenish-white fading of the infected foliage occurs. The

fruiting bodies of the fungus then appear on the affected needles as

elongate, blackish raised blisters.

Field Identification

The best time for identifying this disease is in late spring to early

summer. The elongate, black, raised, fruiting bodies are one-third to

one-halfthe width ofthe needle and variable in length (fig. 2-15). They

appear on greenish-white to straw-colored zones, which are lighter in

color than the rest of the needle. These zones, occupying one-fifth to

one-third the length of the needle, may occur on any portion of the

needle, but are found more commonly near the base.

h K-700245

Figure 2-15. Davisomycella medusa on the needles of ponderosa pine. Elongate,

raised, black fruiting bodies appear in the light-colored zones ofthe infected

needles and are more numerous towards the base of the needle.

67
Selected References

Boyce, J. S.

1940. A needle-cast of Doublas-fir associated withAdelopus gaumanni. Ph5^opathology 30: 649-659

Boyce, J. S.

1961. Forest pathology, Ed. 3, 572 p., illus., McGraw-Hill Book Co., Inc., New York

Brandt, W. B.

1960. The Rhabdocline needle cast ofDouglas-fir. New York State Univ. Coll. Forest.,

Tech. Publ. 84, 66 p.

Childs, T. W.

1968. Elytroderma disease of ponderosa pine in the Pacific Northwest. USDA Forest

Serv. Res. Paper PNW-69, 45 p.. Pacific Northwest Forest and Range Exp. Stn.,

Portland, Oreg.

Darker, G. D.

1932. The Hypodermataceae of conifers. Arnold Arboretum Contrib. 1:1-131

Darker, G. D.

1966. A revision of the genera of the Hypodermataceae. Can. J. Bot. 45:1399-1444

Funk, A., and A. K. Parker

1966. Scirrhia pini N. Sp. the perfect state ofDothistroma pini Hulbary. Can. J. Bot.

44:1171-1176

Morton, H. L., and R. F. Patton

1970. Swiss needle cast of Douglas-fir in the Lake States. Plant Dis. Rep. 54:612-616

Parker, A. K.

1967. Rhabdocline needle cast ofDouglas-ñr,Rhabdoclinepseudotsugae.In important

forest insect and diseases of mutual concern to Canada, the United States, and

Mexico, p. 207. Queen's Printer and Controller of Stationary, Ottawa.

Parker, A. K., and D. G. Colis.

1966. Dothistroma needle blight of pines in British Columbia. Forest. Chron. 2:160-

161.

Parker, A. K., and J. Reid

1969. The genus Rhabdocline Syd. Can. J. Bot. 47:1533-1545.

Peace, T. R.

1962. Pathology of trees and shrubs. 753 p., illus., Oxford Univ. Press, London

Reid, J., and R. F. Cain

1962. Studies on the organisms associated with "snow blight" of conifers in North

America. IL Some species of the genera Phadicium, Lophophacidium, Sarcotrichila, and Hemiphacidium. Mycologia 54:481-497

Scharpf, R. F., John Staley, and F. G. Hawksworth

1970. A needle cast, the first known disease ofbristlecone fir in California. Plant Dis.

Rep. 54:275-277

Simms, H. R.

1967. On the ecology oíHerpotrichia nigra. Mycologia 49:902-909

Staley, J. M. and H. H. Bynum

1972. A new Lophodermella on Pinus ponderosa and P. attenuata. Mycologia 64:722-

726

Sturgis, W. C.

1913. Herpotrichia and Neopeckia on conifers. Phytopathology 3:152-158

Thyr, B. D., and C. G. Shaw

1964. Identity of the fungus causing band disease on pines. Mycologia 56:103-109

Wagener, W. W.

1959. The effect of a western needle fungus (Hypoderma medusa Dearn.) on pines and

its significance in forest management. J. For. 57:561-564

Wagener, W. W.

1967. Red band needle blight of pines—a tentative appraisal for California. U. S.

Forest Serv. Res. Note PSW-153. 6 p.. Pacific Southwest Forest and Range Exp.

Stn., Berkeley, California

68
3. CANKERS, DIEBACKS, AND GALLS

by

ROBERT F. SCHARPP=

This chapter describes tree diseases known as cankers, diebacks,

and galls. The term canker as discussed here refers to any localized

necrotic area or spot on branches or trunks of trees caused by certain

species of fungi. Dieback refers to rapid girdling or tip killing of twigs

and branches that are caused mainly by canker fungi. Galls, commonly called burls, are pronounced swellings on trees caused by fungi,

bacteria, mistletoes, insects, or other agents.

In many instances, initial infection by a fungus results in a localized

canker that subsequently girdles a branch, causing dieback. Often

dead branches are the only symptoms ofthe disease — particularly in

small branches that are girdled and killed quickly with no apparent

canker development. In other instances, both dieback and cankers

occur on the same tree.

Cankers vary considerably in appearance and occurrence. They may

be sunken orslightly swollen, circular or elongate in shape. Some show

little or no healing, whereas others are progressively callused over so

that concentric rings are formed. Cankers are either annual orperennial.

Annual cankers occur sporadically — for one year or one season

only. They are caused directly by unusually severe weather conditions

(see Chapter 2 for a description of cankers caused by adverse climate)

or by a particular sequence of climatic conditions that favor the attack

of trees by certain weakly parasitic fungi. Thus, annual cankers usually occur only during a year following periods of unusual weather

conditions. Dead tissues eventually slough off annual cankers and the

affected area becomes covered with callus in much the same way a

wound is healed. Prolonged growth of annual cankers often results in

dieback.

Perennial cankers are caused by biotic agents that remain active in

trees more than 1 year. Sometimes fungi causing perennial cankers

* Plant Pathologist, Pacific Southwest Forest and Range Experiment Station, Forest

Service, U.S. Department of Agriculture, Berkeley, Calif.

69
kill branches and trees, but more often they weaken and deform the

hosts. Usually the circumferential growth of the tree exceeds the

growth in canker size, thus preventing the tree from being girdled and

killed. Perennial cankers often result in sunken, resinous, unhealed

wounds on branches or trunks. See chapters 5 and 6 for descriptions of

cankers caused by rust fungi and mistletoes. Perennial cankers caused

by other organisms are described here.

In general, cankers do not constitute a serious disease problem in the

coniferous forests of the West. With few exceptions they seldom reach

epidemic proportions. Cankers are considered most serious in plantations and on ornamental or high-value trees. Occasionally, larger trees

with trunk cankers constitute a hazard in some high-use areas because

these trees are weakened or decayed atthe canker site and may break

during high winds.

Descriptive Key

1. On Monterey Cypress Seridium cardinale

2. On Coastal Redwood Coryneum sp.

3. On Giant Sequoia or Incense-Cedar...Soiryosp/iaer/a ribis

4. On Douglas-fir

A* Fruiting bodies disc or cup-shaped when fresh,

shriveled when dry B

A^ Fruiting bodies small globose, black, mostly embedded

in the bark of larger dead branches

JDiaporthe lokoyae

B^ Center of cup yellow to orange; outer margin

hairy Dasyscyphus sp.

B^ Fruiting bodies small (1 to 1.5 mm diameter),

black; formed on twigs or branches dead for about

1 year Dermea pseudotsugae

5. On True Firs

A^ No branch dieback, spindle-shaped branch swellings

often bearing leafless greenish shoots

Dwarf mistletoes-(Chap. 5.)

A^ Branch dieback resulting in reddish brown

flags Cytospora abietis

A^ Branch and twig dieback but no conspicuous

red-brown flags B

B^ Dieback of current year's growth only

Sydowia polyspora

B^ Dieback on all ages of wood C

C* Fruiting bodies yellow to orange colored; cup-shaped when fresh or moist,

brown to black outer surface, hairy

margin (2 to 8 mm diameter)

Dasyscyphus sp.

C^ Fruiting bodies black; cup shaped

70
when fresh or moist D

D* Fruiting bodies (1 to 2mm diameter) Cenangium ferruginosum

jy Fruiting bodies very small (0.5 to

1mm in diameter)

Grouesiella abieticola

6. On Pines

A* Wood of cankered areas showing blackish stain

B

A^ Wood of cankered areas not showing blackish stain

D

B^ Sunken trunk cankers common and conspicuous

Atropellis piniphila

B^ Sunken trunk cankers not conspicuous, infection

mainly on branches and needles C

C^ Noticeable disc-shaped black fruiting

bodies 2 to 4mm in diameter on dead or

dying branches Atropellis pinícola

C^ Fruiting bodies not disc-shaped and conspicuous

(1) Diplodia pinea^

(2) Dothichiza pythiophila^

D* Branch swelling often present E

D^ Branch swelling not present F

E^ Small leafless orange-green shoots arising

from swelling

Dwarf mistletoe (chap. 5)

E^ Yellow-orange spore bearing pustules arising from swelling Rust (chap. 4)

F* Fruiting bodies cup-shaped when moist,

yellow or orange, outer margin hairy, 2 to 8

mm diameter Dasyscyphus sp.

F^ Fruiting bodies small, globose when fresh

or moist, black 1 to 2 mm in diameter

Cenangium ferruginosum

^These two fungi are difficult to differentiate under field conditions and must be

examined in the laboratory for positive identification.

71
Atropellis Canker

Atropellis pinícola

Atropellis piniphila

Atropellis pinícola

Hosts

Sugar pine is the most common host, but the fungus also occurs on

western white, ponderosa, and lodgepole pine.

Distribution and Damage

Although commonly found in the West, this organism primarily

infects only branches of young, suppressed, or weakened trees or

shaded, suppressed, lower branches oflarger healthy trees. Except for

young sugar pines in Oregon and California, trees seldom are killed or

severely damaged. Thus, this fungus poses little threat to vigorous

trees in well-managed stands.

Field Identification

Typical symptoms and signs of infection by Atropellis pinícola include branch flagging, the presence of black fruiting bodies 2 to 4 mm

in diameter on living or dead branches (fig. 3-1) and a blackish stain of

the wood under the dead bark (fig. 3-2). The dry fruiting bodies are

shriveled, irregular shaped structures. Fresh or moist fruiting bodies

are cup-shaped.

Atropellis piniphila

Hosts

Lodgepole pine.

Distribution and Damage

A. piniphila is a fungus that causes a perennial canker of lodgepole

pines in the Pacific Coast States and Western Canada. Its southernmost distribution along the coast is the northern Sierra Nevada.

72
F-700246

Figure 3-1. Dried, shriveled, fruiting bodies of Atropellis pinícola arising from

the bark of a twig of sugar pine.

F-700247

Figure 3-2. Black stain of the infected wood of a branch of sugar pine infected

with Atropellis pinicola.

73
The organism appears to be restricted in occurrence by rather specific

écologie factors. Infection is often limited to trees growing on cool,

moist sites, such as those in wet meadows and around lake shores.

Field Identification

The most obvious symptom of infection is the presence of large,

sunken, perennial, resin-soaked cankers on the trunks and branches of

infected trees (fig. 3-3). Noticeable black, disc-shaped fruiting bodies 2

to 5 mm in size are usually present on the sunken bark surface. A

bluish-black stain of the wood at the canker site is also an apparent

symptom for identifying this disease.

Although bole cankers cause severe trunk deformation with an

increase in infection age, only occasionally do they girdle and kill

trees.

F-525003

Figure 3-3. Sunken cankers formed on lodgepole pine as a result ofinfection by

Atropellis piniphila.

74
Botryosphaeria Canker of Giant Sequoia

Botryosphaeria ribis

Hosts

Giant sequoia, incense-cedar.

Distribution and Damage

This fungus is common on giant sequoia and occasionally on

incense-cedar planted outside of the natural range of these species.

This organism is particularly damaging when giant sequoia is grown

in the warmer lower elevational regions in the West. Trees in ornamental plantings frequently are attacked after the trees are several

years old. The fungus progressively kills branches and may severely

damage or kill trees.

Field Identification

Initial symptoms of infection are scattered dieback of twigs and

branches. With time, the fungus builds up and spreads throughoutthe

crown. Occasionally tops are killed. Recently killed branches appear

as reddish brown flags (fig. 3-4). Branches dead for longer periods are

grey-brown and bare of much of their foliage. Infected branches often

exude drops of pitch.

_. _, F-700248

Figure 3-4. Severe branch flagging of giant sequoia caused by Botryosphaeria

ribis.

75
Cenangium Canker

Cenangium ferruginosum

Hosts

Common on Jeffrey pines, but also occurs on other pines and true

firs.

Distribution and Damage

This organism occurs throughout the West and is most common on

trees up to pole size. Considered a weak parasite, this organism seldom

kills trees. Suppressed or weakened lower branches are most commonly infected, but trees growing under poor conditions or weakened

from other causes may be more severely attacked.

Field Identification

Symptoms and signs of Cenangium include dead or dying lower

branches usually 2 cm or less in diameter, and the presence of small,

black fruiting bodies 1 to 2 mm in diameter on the dead branches. The

fruiting bodies are cup-shaped when fresh or moist and shriveled when

dry (fig. 3-5). Unlike A írope//íS pinícola, no black stain ofthe infected

wood is associated with this fungus.

F-700249

Figure 3-5. Clustered black fruiting bodies oí Cenangium ferruginosum arising

from within the bark of a branch of Jeffrey pine.

76
Redwood Canker

Coryneum sp.

Hosts

Coast redwood

Distribution and Damage

This fungus has been found in native stands ofredwood north ofSan

Francisco. For the most part, it occurs only spottily, and appears to be

most common on trees on poor sites for redwood. For example, trees

growing on warm, dry southern slopes in Mendocino County, Calif

have occasionally suffered severe branch killing and some top kill.

Smaller ones are most commonly infected, and usually the lower

branches are attacked first. Butthis fungus has been observed killing

branches in the tops of old-growth redwood.

Field Identification

Symptoms of this disease are nearly identical to those of Monterey

cypress caused by the cypress canker. In fact, there is some evidence

thatthe redwood canker fungus and the cypress canker fungus may be

the same species. Further studies are needed, however, to determine

the actual host-disease relationships between these two canker fungi.

Cytospora Canker of True Firs

Cytospora abietis

Hosts

True firs, rarely Douglas-fir.

Distribution and Damage

Cytospora abietis is a damaging, canker-inducing fungus that commonly occurs on true firs throughouttheir natural range in California

and frequently on firs and Douglas-fir elsewhere in the West. A weak

parasite, it attacks only trees that have been debilitated by other

disease-causing agents, drought, fire, insects, and human activities.

One of the important factors that predisposes firs to attack by C.

abietis is dwarfmistletoe (Arceuthobium). Practically all fir stands in

California infested with dwarf mistletoe are attacked by this fungus.

For reasons not fully known, C. abietis more commonly infects

77
branches invaded by dwarf mistletoe. In some stands, nearly a fourth

of all branches bearing mistletoe are infected. Thus, in mistletoeinfected fir stands, considerable branch killing occurs each year as a

result of this canker organism.

Because this fungus is widely found in California's true fir stands

and it occasionally reaches damaging proportions in certain years, C.

abietis constitutes a threat to the management of these tree species.

Field Identification

Numerous brick-red flagged branches, conspicuous in spring and

summer, are the best symptom of the disease (fig. 3-6). Later in the

year the foliage dries and becomes more brown to tan in appearance.

Trees of all ages are attacked. Young trees or tops of young trees are

often killed by the fungus, whereas only branches are killed on larger

trees. Other symptoms and signs of infection are sunken, dead patches

of bark tissue, resin exudation at the canker site, small pimple-like

fungus fruiting bodies imbedded in the dead bark and the presence of

thread-like spore masses exuded from the fruiting bodies (fig. 3-7).

Figure 3-6. Branch flagging of red fir caused by Cytospora abietis.

F-700250

78
^

F-70O2S1

Figure 3-7. Orange, thread-like spore masses exuded from the fruiting bodies

of Cytospora abietis partially imbedded within the bark of red fir.

79
Dasyscyphus Canker of Conifers

Dasyscyphus sp.

Hosts

Douglas-fir, pines, true ñrs.

Distribution and Damage

Apparently, more than one fungus species is involved, and these

attack several conifer species in the West. The disease is spotty in

occurrence and seldom causes serious damage. It appears to be most

serious on Douglas-fir and on high-elevation pine species. Otherwise,

Dasyscyphus species are weak parasites and infect only weakened or

suppressed lower branches and twigs. Occasionally, trunk cankers

may develop on small trees.

Field Identification

The fruiting bodies ofthe fungus are quite distinctive. When fresh or

moist, they are cup-shaped, vary in color from a light cream to orange,

have a fuzzy outer margin, and are about 2 to 8 mm in diameter (fig.

3-8). When dry, they appear as shriveled light-colored bodies on the

dead bark of the infected branch or canker. The wood of the infected

branch at the canker site does not stain black as it does with some of

the other canker fungi.

F-700252

Figure 3-8. Orange, cup-shaped fruiting bodiesformed on branches ofwhite fir

infected hy Dasyscyphus sp.

80
Dermea Canker of Douglas-Fir

Dermea pseudotsugae

Hosts

Douglas-fir.

Distribution and Damage

This disease occurs on Douglas-fir from northwestern California to

British Columbia. Because of the severe damage caused by this organism it poses some management problems. Plantations of young

trees are most severely attacked, but the fungus also develops on

young trees in natural stands. In some plantations surveyed, 10 to 50

percent ofthe trees were killed by this organism in less than 10 years.

Both limb dieback and trunk cankers occur on infected trees. Trunk

cankers often girdle the tree, resulting in top kill and eventually death

of the tree.

Field Identification

Dieback oflimbs, tops, and entire trees is the most obvious symptom

of the disease. Trunk cankers originate from infected limbs and when

fresh have a characteristic reddish margin that disappears when the

tree dies (fig. 3-9). Sexual fruiting bodies (apothecia) do not appear on

freshly killed tissue, but arise on dead bark about a year later. They

appear as tiny, black discs about 1.0 to 1.5 mm in diameter. The bark

beetle Scolytus unispinosus is often associated with cankers.

Phomopsis Canker of Douglas-Fir

Diaporthe (Phomopsis) lokoyae

Hosts

Douglas-fir.

Distribution and Damage

Phomopsis canker of Douglas-fir is most common in the north Coast

Range of California, but is found elsewhere on natural and planted

stands in the State and along the Pacific Coast. It occurs sporadically

and becomes a problem only in years when certain climatic conditions

weaken the host and favor buildup of the fungus. Usually only single

trees or small groups oftrees are affected. The disease is primarily one

81
F-700253

Figure 3-9. Canker caused by Dermea pseudotsugae on trunk of sapling-sized

Douglas-fîr.

of young trees. Trees up to 3 inches in diameter are often killed by the

fungus while larger ones usually survive. On the larger trees, top and

branch killing often occurs. Cankers may also develop on the trunk.

After the initial attack, these often heal in much the same way an axe

wound heals.

The fungus, for the most part, is not a serious problem in natural

forest stands. In nurseries, forest plantations, and in areas planted to

Christmas trees in northern California, however, serious damage and

economic losses have occasionally resulted.

Field Identification

The presence of branch or trunk cankers is one of the best field

symptoms of the disease. Cankers almost always result from the fungus firstinfecting young twigs and branches and then growing into the

adjoining stem. Cankers are usually sunken and several times longer

than they are wide (fig. 3-10). On branches and tree tops girdled by the

82
F-700254

Figure 3-10. Elongate canker on branch of Douglas-fir resulting from infection

by Diaporthe lokoyae.

fungus there is usually a distinct margin between the infected and the

healthy portion ofthe stems. Small, black fruiting bodies (less than 0.5

mm diameter) imbedded in the dead bark may be seen in spring and

early summer on the cankered tissues. Cankers caused by this fungus

are similar to those caused hy Dermea pseudotsugae, but no conspicuous reddish canker margin is present.

Diplodia Canker

Diplodia pinea

Hosts

Pines, rarely Douglas-fir.

Distribution and Damage

This fungus may occur on pines throughoutthe West. In California,

it is found on low elevation and coastal pine species. The fungus is

considered a weak parasite and usually infects only trees that are

planted out oftheir natural environment or are weakened by drought

or other agents. For example, branches weakened by dwarf mistletoe

infection are reported to be commonly attacked and killed by this

organism. The fungus spreads from infected branches into the trunks

oftrees, causing top kill or tree mortality. For the most part, however,

83
vigorous trees suffer only dieback ofweakened branches as a result of

infection by D. pinea.

Disease Cycle

This fungus is one of the few canker and dieback-inducing organisms that also infects needles. Infection takes place through the

stomata of young needles. The fungus then grows through the needles

into young twigs, causing a dieback. Infection by spores may also occur

through wounds or bark cracks on branches. Much ofthe dieback and

cankering of older branches and trunks probably takes place by this

mode of infection.

Field Identification

Dying needles and twigs as well as top dieback and tree mortality

are indicative of infection by D. pinea. The presence of the fruiting

bodies on all infected portions also suggests infection by this fungus.

The fruiting bodies are small (less than 0.5 mm in diameter), black,

globose, and imbedded within the needles or bark of infected stems.

Usually only the beak of the fruiting body protrudes through the

surface of the infected tissues, and these resemble numerous small,

black pinpoint spots. A noticeable black stain of the wood is also

associated with infection by D. pinea.

Dothichiza Canker of Pines

Dothichiza pythiophila

Hosts

Pines.

Distribution and Damage

This fungus is known in California as a weak parasite of pines. It

grows mostly on smaller trees up to about 15 to 20 feet in height. The

disease causes no threat to forest stands, but may damage trees in

plantations or trees grown for ornamental purposes.

Field Identification

This fungus causes both a needle and twig disease. Branches may be

defoliated. Trees may suffer from top dieback and occasionally are

killed back two or three whorls. Infected wood is stained a bluish84
black. Symptoms and signs in the field closely resemble those caused

by Diplodia pinea. Laboratory examination is often necessary to distinguish between these two fungi.

Grovesiella Canker

Grovesiella (Scleroderris) abieticola

Hosts

White fir, grand fir, Pacific silver fir, alpine fir, and red fir.

Distribution and Damage

This fungus grows on Abies along the Pacific Coast from northern

California through British Columbia. Highly sporadic in occurrence, it

is usually not a serious disease-causing agent. Annual cankers and

twig dieback develop as a result of infection and these conditions

usually do not continue for more than one 1 year. Occasionally some

tops are killed. Small trees are most often attacked, butlower branches

of poles sometimes are infected.

Field Identification

The fruiting bodies of this fungus are similar to but somewhat

smaller (0.5 to 1 mm in diameter) than the black, cup-shaped fruiting

bodies ofCenangium thatis also found on firs. The fruiting bodies ofG.

abieticola, although small, are usually very abundant on the dead bark

(fig. 3-11). This organism is seldom found on 1-year-old wood, but

attacks older stems. Canker development is often pronounced, but no

staining of wood accompanies infection.

K-700255

Figure 3-11. Scattered, small, black fruiting bodies on the surface of a branch

of white fir infected by Grovesiella abieticola.

85
Cypress Canker

Seridium (Coryneum) cardinale

Hosts

Principal host is Monterey cypress; occasional hosts are some other

species of cypress, but rarely juniper.

Distribution and Damage

The cypress canker is absent from the native stands in California

and is rare on trees planted immediately along the Pacific Coast. But

the disease is widespread and serious on Monterey cypress planted in

the warmer, drier inland areas. Over the period of about a decade in

the early 1900's, the fungus spread throughout the range of planted

Monterey cypress in the West.

Damage caused by this organism was so severe that planting of

cypress outside of its natural range is discouraged. Why the fungus

suddenly appeared and became epidemic on planted Monterey cypress

is not known, but it is now widespread and well established.

Infection Cycle

Long-distance spread of cypress cankers is by windborne spores,

whereas local buildup and spread within tree crowns is by spores

washed out ofthe fruiting bodies by rains. Most infection occurs atthe

bases of small branches or in branch forks. Both wounded and unwounded tissues are sites for infection.

Cankers grow more rapidly along a branch than around it, and they

usually have a length-width ratio of about 3:1. Infected trees or

branches 2 to 3 years old may be killed within a year, whereas, on

larger trees, infected branches or trunks may remain alive for 5 to 10

years.

Field Identification

Fading and death of twigs, branches, and tops of trees are the most

conspicuous symptoms of infection. Trees of all ages and sizes are

equally susceptible to infection. The presence of cankers (fig. 3-12) is a

sure indication of infection. Resin flow usually accompanies canker

development and as the killed bark tissues dry out, a sunken area

develops. Bark cracking commonly accompanies canker development.

Dark, irregularly-shaped, blister-like fruiting bodies 0.3 to 1.5 mm in

size are produced and break through the bark of the dead tissues.

Cypress bark beetles are often associated with, and hasten the death

of, infected trees.

86
;rp-"Ví^'

F-700256

Figure 3-12. Branch canker on Monterey cypress caused by Seridium cardinale.

Note abundant resin flow and small, black fruiting bodies on bark surface.

Sydowia Tip Dieback of Fir

Sydowia polyspora

Hosts

White fir.

Distribution and Damage

This organism has been reported only in northwestern California. It

has been found primarily in white fir stands managed for Christmas

trees. From the timber management standpoint, damage is negligible,

but losses do occur in firs grown for Christmas trees. In general,

infection of firs is sporadic, and only tip dieback of twigs occurs.

Field Identification

The symptoms and signs of this disease closely resemble those of

Scleroderris abieticola. Butthis organism infects only 1-year-old wood,

causing tip dieback (fig. 3-13). Occasionally, a canker margin may be

found about a third of the way down 2-year-old wood on a branch.

Black, fruiting bodies less than 0.2 mm in diameter appear from under

the bark of twigs that have been dead for a year or more.

87
X^H..

«

F-700267

Figure 3-13. Tip dieback of white fir caused by Sydowia polyspora. Note swollen

branch at canker margin.

Galls

Many galls found on conifers in California are of unknown origin,

but some are caused by bacteria, insects, rust fungi and mistletoes.

Although numerous on some hosts in certain areas, galls are relatively

unimportant forest diseases. They are usually found on scattered trees

rather than on most trees in a stand. They cause relatively little

damage to the trees on which they develop — except for galls that

occasionally occur on the main stem.

Bacterial Gall of Douglas-fir

Bacterial gall of Douglas-fir caused by the bacterium Pseudomonas

pseudotsugae is a disease commonly observed on young Douglas-fir in

northern California and Oregon. Galls are roughly globose and may

become several inches in diameter (fig. 3-14). Tops of young trees may

be killed, but galls on branches or boles of larger trees affect growth

only slightly. The gall-forming bacterium is transmitted by two sucking insects — the orchard cicada and Cooley's chermes — that feed on

Douglas-fir.

88
F-525004

Figure 3-14. Bacterial gall of Douglas-fír caused by the bacterium Pseudomonas

pseudotsugae.

Galls of Unknown Origin

Redwood gall, a gall of unknown origin, develops on coast redwood.

Often huge galls grow on the trunks of old-growth redwood. Because of

their beautifully figured grain, they are highly prized for use in furniture or for novelty items. Galls also occur on branches. Occasional

trees support many of them with little apparent effect on growth or

vigor of the tree.

Other galls of unknown origin also are found on other conifers,

particularly the pines, in the West. Their effect on the growth of trees

is minimal. They are ofno real importance in the management offorest

lands.

Galls caused by rust fungi and mistletoes are covered in Chapters 5

and 6.

89
Selected References

Bega, Robert V.

1964. Diseases of Sequoia. Diseases ofwidely planted forest trees. FAO/IUFRO Symp.

Int. Dangerous Forest Diseases and Insects, Oxford, England, 1964: 131-139.

Boyce, J.S.

1933. A canker ofDouglas-fir associated with Phomopsis lokoyae. J. For. 31:664-672.

Funk, A.

1967. Dermea pseudotsugae n. sp., a causal agent of phloem necrosis in Douglas-fir.

Can. J. Botany 45:1803-1809.

Funk, A.

1973. Phomopsis (Diaporthe) canker ofDouglas-fir in British Columbia. Forest Insect

and Disease Survey Pest Leaflet 60. Canadian For. Serv.; Victoria, B.C.

Hansen, H. N., and R. E. Smith.

1937. A bacterial gall disease of Douglas-fir, Pseudotsugae taxifolia. Hilgardia

10:569-577.

Jackson, Willard L.

1962. Guide to grading defects in ponderosa and sugar pine logs. U.S. Forest Serv.

Pacific Southwest Forest and Range Exp. Stn. 34 p., illus.

Lohman, M. L., and Edith H. Cash.

19A0.Atropellis species from pine cankers in the United States. Wash. Acad. Sei. J.

30:255-262.

Lightle, P.C., and J. H. Thompson.

1973. Atropellis canker of pines. U.S. Dep. Agrie. Forest Pest Leafl. 138, 6 p., illus.

Scharpf, R. F.

1969. Cytospora abietis associated with dwarf mistletoe on true firs in California.

Phytopathology 59:1657-1658.

Sutton, B. C. and I.A.S. Gibson.

1972. Seridium cardinale Commonwealth Mycological Institute, Descriptions of

Pathogenic Fungi and Bacteria. No. 326, 2 p. Kew, Surrey, England.

Wagener, W. W.

1939. The canker of Cupressus induced by Coryneum cardinale n. sp. J. Agrie. Res.

58:1-46

Wright, E.

1942. Cytospora abietis, the cause of a canker of true firs in California and Nevada. J.

Agrie. Res. 65:143-153.

90
4. RUSTS

by

ROBERT V. BEGA*

Rust diseases are caused by obligately parasitic fungi — they develop only on living hosts. Most rusts described in this chapter are

considered "native rusts." Although these native rusts are not known

to have destroyed whole forests of their hosts as has Cronartium

ribicola, an introduced rust, they kill individual trees, reduce wood

quality, and retard tree growth. About 56 species of native rust fungi

are known to attack conifers in the Western United States and about

40 others complete their life cycles on conifers, but are found only on

non-coniferous alternate hosts.

To complete their life cycles, nearly all the major rust fungi on

conifers must alternate between the conifer host and an unrelated type

of host plant. Those that require two different hosts are called

"heteroecious rusts." Most produce four to five different kinds ofspore

stages, as indicated either by name or by the numerals 0 through IV.

Two major rust diseases — western gall rust and possibly a limb rust —

do not require these two unrelated types of host plants, but spread

directly. Rusts requiring no alternate host are called "autoecious

rusts."

Figure 4-1 illustrates the heteroecious type cycle, using C. ribicola

as an example.

Pycnia (0) are the first spore bodies produced on the aecial host.

Pycniospores that serve in sexual fertilization are exuded from the

pycnia and are not known to be infective agents. Sexual fertilization is

required before maturation of the aecial stage (I) which produces

aeciospores that can infect their alternate host as much as 600 to 800

miles distant from their point source. On their alternate hosts, rusts of

most genera produce the repeating or uredinial stage (II) from which

urediniospores are produced. These again are dispersed short distances by wind and infect other individuals ofthe same host species or

reinfect the plant on which they were borne. Later, these infections

produce the telial stage (III), which is composed of teliospores that

remain in place and germinate under the right climatic conditions in a

* Principal Plant Pathologist, Pacific Southwest Forest and Range Experiment Station, Forest Service, U.S. Department of Agriculture, Berkeley, Calif.

91
Figure 4-1. Life cycle of C. ribicola.

few days to produce basidiospores (also called sporidia) (IV). Windborne for short distances, basidiospores infect only the aecial host.

Local climate and land use that favor growth of alternate hosts often

intensify rust diseases. For example, ribes species must be closely

associated with pinyon pine in a favorable regime of moisture and

temperature before infection of pines by pinyon rust (Cronartium

occidentale) can occur. Similarly, concentrations ofComandra species

are needed to trigger outbreaks of comandra rust (C. comandrae).

Western gall rust (P. harknessii), an autoecious rust, will be most

troublesome in localities where high humidity and moderately cool

temperatures prevail or where there are even-age young stands or

plantations. This gall rust can be especially destructive in nurseries

and ornamental plantings. An intricately balanced interaction ofhost,

parasite, and environmental factors determines rust outbreaks. Most

outbreaks often involve a burst of infection during a single season or

even a single moist period and then years may pass with no new

infections occurring. Major outbreaks may come decades apart. Even

with the fungus P. harknessii that spreads from pine to pine, infection

may be sporadic in spite of its simplified life cycle.

92
Among the numerous rustfungithat attack conifers, most are minor

needle rusts that cause partial defoliation only during years favorable

for infection. Some rusts may be more damaging to their alternate

hosts. Several native rusts cause deformities, dieback, and limited

mortality to conifers of little commercial value but of high or potentially high recreational and esthetic value.

The most damaging rusts in the Western United States are: white

pine blister rust on white pines, comandra rust, western gall rust,

stalactiform canker rust, and filamentosum limb rust on hard pines;

broom rust on true firs and spruce; and broom rust of incense-cedar.

Others are a problem only in selected areas, such as Christmas tree

farms and recreational sites.

Descriptive Key

A^ On hard pines B

B* Causes globose woody stem galls or cankers with centralmarginal gall swellings C

C* Galls of hard secondary tissue having annual rings

P. harknessii

(Endocronartium harknessii)

W Causes limb rust or cankers without woody galls D^

D* Causes elongate cankers on tree bole and branches

E

E^ Cankers two to usually many times longer than

broad, aecial filaments pendant

P. stalactiforme

(C. coleosporioides)

E* Cankers usually not more than two times longer

than broad. Aeciospores pear-shaped (under

hand lens) C. comandrae

B^ Causing limb rust only F

F^ Aecia, mostly taller than broad; often more than 2.5

mm tall; bark normal P. filamentosum

(C. coleosporioides)

F^ Aecia, mostly broader than tall; seldom more than 2.5

mm tall; bark rough P. stalactiforme

(C. coleosporioides)

A^ On soft pines G

G* On pinyon pines, aecia to more than 1 cm broad under

bark C. occidentale

G^ On other white pines, aecia less than 8mm broad, spindleshaped branch cankers or diamond-shaped trunk cankers

C ribicola

A^ On incense-cedar and true firs H

H* In brooms on incense-cedar....Gym^iosporan^mm libocedri

W In brooms on true ñrs...Melampsorella caryophyllacearum

93
White Pine Blister Rust

Cronartium ribicola

White pine blister rust, caused by the rust fungus Cronartium

ribicola, is a textbook example of the heteroecious rust fungi found

throughout the world. Its life cycle, symptoms, and climatic requirements are typical of most native western rust fungi described in this

chapter. It differs only in its rate ofspread and the amount of damage

that it causes.

Hosts

C. ribicola can infect nearly all white pines, and is restricted to this

group. Its native North American hosts are: eastern white pine, western white pine, sugar pine, limber pine, white bark pine, bristle cone

pine, foxtail pine, and Mexican white pine. In addition, it infects all

species of its alternate hosts — ribes.

Distribution and Damage

The disease was introduced from Europe into North America on

seedlings of a native North American white pine. It was not native to

Europe, however, butis believed to have been introduced from Asia. Its

introduction to North America from Europe, between 1898 and 1908,

on seedlings of eastern white pine resulted in one of our most serious

disease outbreaks on conifers. White pine blister rust is now widely

found in the Northeastern United States, the Lake State regions, and

the West. After its introduction into British Columbia in 1910, it has

spread throughout most white pine regions of Washington, Idaho,

Montana, Wyoming, Oregon, and California.

In North America, white pine blister rust has caused more damage

and costs more to control than any other conifer disease. Since the

1920's, millions of dollars have been spent on the eradication of the

alternate host, ribes, and thousands of white pine stands have been

severely damaged. In the Western United States and Canada, some

stands have been completely destroyed. When the main stem of a tree

is invaded, death is only a question of time. Frequently, in western

white pine and sugar pine, death results withouttrunk infection — the

branches are killed by numerous infections before the disease reaches

the main stem.

Disease Cycle

The sporidia produced from the teliospores on leaves ofribes species

are windblown short distances, and infect pine needles during late

summer and early autumn. Infection can take place on needles of the

current year, but is more frequent on 2- to 3-year-old needles. One to 2

94
and frequently 3 years after infection, the fungus has penetrated the

needle into the stem and becomes obvious as a yellow or orange discoloration of the bark accompanied by spindle-shaped swellings. Later,

pycnia appear as small blisters on the bark. These blisters then discharge droplets of honey-colored liquid containing pycniospores that

are thought to play a sexual role and are required for the production of

the aecial stage. Aecia produced from aeciospores are the prominent

blisters (fig. 4-2) that burst in spring to disclose masses of orange

spores.

^•< ;• ' ;■■■' '"^-^W

\

F-700258

Figure 4-2. Aecial stage of

Cronartium ribicola on

sugar pine.

Aeciospores can travel long distances — as much as 600 to 800 miles

— to infect young ribes leaves. Within a few weeks of infection, small

yellow uredial pustules appear on the lower leaf surfaces. The resultant urediniospores infect other ribes, but cannot infect pines. This

stage ofthe fungus is the "repeating" stage. The spores are airborne for

only short distances, and infect not only other species ofribes, but also

its own host plant. A large buildup of inoculum occurs within a local

area. Late in summer or early fall, the telial stage is produced. These

are brown hair-like structures which sometimes occur in such numbers as to give a faintly felt-like appearance to the under side of the

leaves (fig. 4-3). These structures then germinate in place under

proper climatic conditions, giving rise to the sporidial stage. The cycle

is then completed.

95
F-700259

Figure 4-3. Ribes leaf

showing uredinial pustules and telial horns of

C. ribicola.

Field Identification

On pine the first noticeable symptoms are tiny yellow spots on the

needle. The spots later turn golden yellow, producing a yellow mottle.

As the fungus invades the twig it too turns yellow. Invasion of

branches then subsequently occurs from the infected twigs. Infection

sites then enlarge to produce the spindle-like swellings. Cankers on

branches and trunks then continue to enlarge from year to year. The

invaded bark first becomes yellow or bronzed. The pycnial stage,

containing an exúdate of pycniospores, then appears. Later aecia are

produced in place of the pycnia, and new pycnia appear in the outer

zone. In spring, the aecia appear as raised blisters. They push through

the bark to the surface and discharge yellow, dusty masses of aeciospores. After the aecia have shed their aeciospores, the bark tissue dies.

As a canker progresses, there will be found a yellow zone, a zone

showing pycnia, a zone bearing aecia, and an inner area of dead bark

where aecia have formed in the previous season. A common symptom

in pines (fig. 4-4) first noticeable to the casual observer is branch

killing or flagging after the fungus has completely girdled the branch

and killed the cambium.

96
F-700260

Figure 4-4. Multiple branch flagging on sugar pine caused by C. ribicola.

97
On ribes, the uredia appear as slightly raised yellow spots on the

lower side ofthe leaves, petioles, and young stems. Telia, which follow

uredia, are darker, and the teliospores are borne in columns up to 2mm

in length. Heavy infection on some ribes hosts such as R. roezli may

cause premature defoliation. In the Western United States, C. ribicola

is frequently confused with C occidentale (see pinyon blister rust). On

ribes, the two fungi cannot be separated macroscopically. This similarity has caused a great deal of confusion in attempts to determine the

distribution of C. ribicola on ribes species in a given year.

Native Limb and Canker Rusts

Cronartium coleosporioides

Taxonomic knowledge of this group of fungi, sometimes referred to

as part ofthe Cronartium coleosporioides complex, is incomplete. This

handbook follows nomenclature based on the imperfect (aecial) stage

of the fungi. This stage is better understood than the perfect stage.

Therefore, little attempt will be made to describe the taxonomic differences because they are based principally on microscopic variations in

the spore stages. Effects on pine hosts are classified for field identification as to whether infection results in cankers, galls, or limb rust. This

classification, however, does not separate the causal fungi; for example, gall fungi all cause cankers, too. Though always originating on the

current season's growth, they may, depending on host species attacked, become systemic and cause cankers or galls on the main stem ofthe

tree.

Two distinct species — stalactiform rust (P. stalactiforme) and

filamentosum rust (P. filamentosum) - cause 'limb rust' on pine.

Stalactiform Rust

Peridermium stalactiforme

Hosts

The principal pine hosts of P. stalactiforme are lodgepole, Jeffrey,

and ponderosa pines. In the Laguna Mountains in San Diego County it

has been found on Coulter pine. Its alternate hosts are in the figwort

family, particularly castilleja species.

Distribution and Damage

The disease occurs from the Southwestern United States and

California, northward into Canada, and eastward into Michigan, and

the Maritime Provinces ofCanada. It is most common along the Pacific

Coast.

98
p. stalactiforme causes cankers on most pine species, butis known to

cause limb rust only on Jeffrey pine from Plumas County southward to

San Diego County in California, and in Washoe, Ormsby, and Douglas

Counties in Nevada. Whether it also causes limb rust in ponderosa

pine is uncertain. P. stalactiforme in the Sierra Nevada usually occurs

on immature pines in concentrated infection centers and often in

obvious relationship to the presence of its alternate host. Most infections are found low in the tree crowns.

In the West, the main damage is from trunk cankers and resulting

cull on lodgepole pine. Stalactiform rust can kill trees by gifdling, but

this is uncommon except in seedlings or where two or more cankers

coalesce. Infected branches are occasionally killed, but no appreciable

growth loss is known.

Disease Cycle

In late summer and fall, the airborne sporidia infect susceptible

pines. Although rarely seen, pycnia may appear the following spring

or one or more years later, depending on the age of the pine and its

environment. Aecia then appear during the same season, but frequently do not mature until early spring of the following year. The

aeciospores are not known to infect pine, but readily infect the telial

host (Castilleja) and can be windborne for greater distances. Uredia

are produced on the telial hosts a few weeks after infection. Urediospores are windborne short distances, and serve to intensify the disease

on other telial hosts or its own nearby host plant. They cannot infect

pine, however. Telia then appear on the host later in the summer and

early fall. The teliospores germinate in place and produce sporidia.

The sporidia then are windborne short distances to nearby susceptible

pines.

Field Identification

Branch swelling, and on most hosts, cankers, that finally become

more than 10 times as long as wide are common. On Jeffrey pine,

fungus growth becomes systemic and limb rust results. It can be

distinguished from the limb rust caused by P. filamentosurn, by bark

roughening, or by ill-defined cankers on branches that are invaded in

contrast to the lack of roughening when P. filamentosum invades.

Monoliform swellings are occasionally found on branches with systemic infections. In stem and branch tissues, the fungus spreads much

slower laterally than longitudinally. Typically on the trunks of older

lodgepole pines, the fungus causes elongated or sunken trunk cankers

up to 30 feet or more long (fig. 4-5). Each year, cankers grow about 7

inches vertically, but only about one-fourth to one-half inch horizontally. Because rodents usually chew the canker margins, aecia are not

easily seen on older trunk cankers. Pine infection in general is more

frequent and more localized when this rust appears than with com99
F-700261

Figure 4-5. Elongate canker caused hy Peridermium stalactiforme.

andra rust or filamentosum limb rust. Symptoms and signs on the

alternate host are typical ofthose described for white pine blister rust.

In Jeffrey pines, stalactiform rust mainly attacks the lower crowns

(fig. 4-6). The fungus spreads slowly and in some trees appears not to

keep up with stem growth. Thus mature infected pines are found, but

usually the fungus has been in them for several decades. Stalactiform

rust, however, has been found occasionally in mid-crowns or upper

crowns of mature trees in southern California.

100
Both p. stalactiforme and P. filamentosum may occur as a limb rust

in the same stands ofJeffrey pine in some areas. Stalactiform rust may

be distinguished from that caused by P. filamentosum by (1) fungus

morphology, notably the lower more confluent aecia and the thick

smooth areas on aeciospore walls ofP. stalactiforme, (2) lack ofperidial

fragments retained on infected twigs from previous year's growth of

aecia, and (3) the constant presence ofrough bark on cankers as well as

symptoms of systemic limb rust.

F-525005

Figure 4-6. Peridermium

stalactiforme nearly always infects the lower

crown of pine and

spreads upward.

101
Filamentosum Rust

Peridermium filamentosum

Hosts

Peridermium filamentosum has the following pine hosts: Apache,

Jeffrey, ponderosa, and Montezuma. One form is heteroecious on Castilleja species of the figwort family. Two other forms, also called P.

filamentosum, appear to spread directly from pine to pine without

requiring the alternate host.

Distribution and Damage

The disease is found in California, the Southwestern United States,

and from western South Dakota and northeastern Utah southward to

Colorado, New Mexico, and Arizona. It has been found in the Sierra

Nevada from Plumas County, California, to northern Baja California,

Mexico.

No intense outbreaks of this rust have been found in species other

than ponderosa and Jeffrey pines. Since little is known ofits epidemiology, its potential importance cannot be fully gauged.

Disease Cycle

The life cycle of P. filamentosum is almost identical to that of P.

stalactiforme. P. filamentosum, however, consists of at least three

races in the Western United States. One race alternates with Castilleja, thereby resembling P. stalactiforme in life cycle. Alternate hosts

are unknown for the other two races. The second race attacks ponderosa pine in Utah and adjacent States. The third is found on Jeffrey

pine. In California, aecia of P. filamentosum begin to emerge in the

Sierra Nevada during early spring atlow elevations, but are produced

mainly in late June and July. Commonly, aecia may be found still

intact in August and retain their spores until September.

Field Identification

P. filamentosum commonly attacks mid-crowns or upper crowns of

mature trees (fig. 4-7). In the Sierra Nevada, it is usually found in

scattered, mature, and over-mature pines, although occasional concentrations occur without apparent reference to topography.

102
F-525006

Figure 4-7. Peridermium

filamentosum nearly always infects the mid or

upper crown of trees

and spreads in both directions.

Hosts

Western Gall Rust

Peridermium harknessii

Throughout its range, P. harknessii (Endocronartium harknessii)

has been found on 22 species, which represent 8 ofthe 9 subsections of

hard pines.

Distribution and Damage

Western gall rust ranges from Mexico and Nebraska to Alaska and

eastward in Canada (with decreasing abundance) to the mid-Atlantic

areas. In California, it is widespread throughout the State, occurring

103
on nearly all of the species of hard pines. It is especially prominent on

Monterey pine in both its natural range and throughout the State

wherever it has been planted, and on lodgepole pine throughout the

Sierra Nevada and southern Cascades.

This rust damages pines by (1) killing seedlings; (2) producing

branch galls so numerous that larger trees may be killed outright or

their growth is diminished by loss ofbranches; and (3) producing trunk

cankers so deforming that they reduce the strength of the tree and

increase the likelihood of wind breakage. Western gall rust is the

native stem rust found most often in the California Disease Survey. All

signs suggest that it will become an even more serious problem in the

West when plantations become more abundant. It is now a serious

problem in Christmas tree plantations and nurseries in the West.

Disease Cycle

In spring, aecia emerge from the living bark ofthe globose galls (fig.

4-8) and the marginal swellings ofthe trunk (hip) cankers. Aeciospores

can directly infect other pines rather than go through an alternate

host. These spores are wind disseminated and may spread the disease

for hundreds of miles.

F-525007

Figure 4-8. Globose galls

are common on Monterey pine infected by

Peridermium harknessii.

104
Field Identification

The disease is characterized by the formation of globose to pearshaped galls as large as 12 inches in diameter on branches and stems of

pine of all ages. Trunk or "hip" cankers are common. Each new pine

infection is followed by formation of well delimited globose galls.

Thereafter, the galls continue to enlarge and produce new spores each

spring until they have girdled and killed the branch or stem. However,

the fungus may survive in cankers for up to 200 years before girdling is

complete (fig. 4-9).

F-525008

Figure 4-9. Old but still

active "hip canker" on

lodgepole pine caused

by Peridermium harknesYellow Witches Broom of Fir

Melampsorella caryophyllacearum

Hosts

The fungus causing yellow witches broom has as its aecial host the

true firs. In the Western United States, these tree species are principally white fir, red fir, grand fir, and sub-alpine fir. Trees ofall ages are

susceptible to the parasite. The alternate hosts are species of

chickweed.

105
Distribution and Damage

M. caryophyllacearum is found on fir species in North America from

Labrador, Newfoundland, west to Alaska, south through Canada to

the Northern United States and in the Western United States, and

from California to Mexico. The disease is abundant in southern Idaho,

western Wyoming, and northern Utah on sub-alpine fir, and in the

south and central Sierra Nevada ofCalifornia on red fir. Elsewhere in

the West, brooms are only occasionally found. Most of the infected

trees have branch brooms and less frequently, trunk burls or spike

tops. Multiple brooms can reduce tree growth, provide infection courts

for heart rots, and even kill trees — particularly seedlings and saplings.

Disease Cycle

M. caryophyllacearum has a tjrpical heteroecious life cycle, alternating between true firs and members of the chickweed family. The

fungus is, however, systemic and perennial not only in firs (the aecial

host) but also on the telial host plants that are perennial species.

Field Identification

The most noticeable characteristic of this disease is the witchesbroom it produces. The brooms are most conspicuous from midsummer to late fall, when their yellowish-orange color reaches a peak

of intensity and stands out in striking contrast to the norçial dark

green foliage (fig. 4-10). Aecia production on the diseased needles

F-700262

Figure 4-10. Witches-broom of white fir caused by Melampsorella caryophyllacearum showing compact growth and light-colored, infected branches.

106
F-700263

Figure 4-11. Light-colored pustules of the yellow broom rust on infected needles of white fir.

contributes to this color. Witches-brooms are upright, typically compact, and have a dense growth of many small and shortened branches

that rarely exceed 3 feet in diameter. The diseased needles are greatly

shortened and thickened (fig. 4-11). In winter, the brooms appear to be

dead as the affected needles shrivel and become dark. In autumn, the

needles drop, leaving the brooms bare until new growth starts. The

new needles are yellowish-green until mid-summer. On the alternate

host — chickweed — the fungus forms the uredinial and telial stages.

The abundance of fir broom rust appears to be related to change in

abundance of alternate chickweed host. Seasonal, climatic differences

are also responsible for outbreaks.

Comandra Blister Rust

Cronartium comandrae

Hosts

The rust is a typical heteroecious fungus whose alternate hosts in

the Western States are two species of bastard toad flax or comandra.

Aecial hosts are hard pines — principally ponderosa, Jeffrey,

lodgepole, knobcone, and Scots pines. Field evidence, however, shows

that lodgepole and ponderosa pines are especially susceptible while

Jeffrey and knobcone pines are rarely attacked.

107
Distribution and Damage

The fungus is perennial in trunk cankers or branch swellings.

Studies on the chronology of disease outbreaks in California indicate

that infection was abundant for several years, but has become extremely scarce owing principally to extreme fluctuations in the abundance of its alternate host.

The fungus is widely distributed, ranging from Quebec to the

Northwest Territory to British Columbia, and southward to New

Mexico and California. But it has not been found outside of North

America. In the Western United States, the fungus is found in all

States from the Rocky Mountains to the Pacific Ocean. The disease is

now common on lodgepole pine in the Rocky Mountains. In California,

it occurs mainly on ponderosa pine in the Shasta and Klamath River

drainages.

Comandra blister rust has been most damaging to lodgepole pine in

western Wyoming and adjacent States, where mortality continues to

be heavy as a result of an epidemic that started in the late 1940's.

Although significant recent outbreaks have not taken place in

California for many years, the rustis still common in the Shasta River

drainage, where the advanced growth ofponderosa pine from seedlings

to small poles was badly infected in the early 1900's, and many young

trees were killed.

Disease Cycle

Seasonal activity ofthe fungus usually starts in late spring with the

production of whitish-colored spore sacs (aecia) on the pine cankers.

The sacs soon break, releasing many orange-colored spores (aeciospores) that are wind-disseminated to the alternate host, comandra.

About 10 days later, the uredial stage forms on the comandra leaves

and produces urediospores. These spores can infect other comandra

plants. This is the repeating stage of the rust, and serves to intensify

the disease on comandra during the growing season. In early summer,

the uredial stage is followed by the telial stage. Telia may grow up to

nearly one-tenth inch in size. It consists of a mass of teliospores held

together in a gelatinous matrix.

Moisture and mild temperatures are required for germination of all

spore types produced by the fungus and for the subsequent infection of

either host. Since wet seasons favor spread and intensiñcation of

comandra rust, dry seasons discourage it. Not every year in which the

rust is prevalent on the comandra host is the weather favorable for

infection ofpines. The lack ofrecentinfections on pines in California is

due, in part, to unfavorable environmental conditions, but when outbreaks occur they can be damaging.

108
Field Identification

The rust on hard pines is quite similar to blister rust on white pines

in its growth and the damage it causes. On pine, comandra rust causes

slight swellings followed by cracking of the infected bark. Small

branches or seedling stems are usually girdled quickly as the fungus

spreads in the bark and outer wood. Death follows within a few years.

The rust eventually encircles trunks or branches, and soon the bark

and parts distal to the girdle die. When the fungus reaches large

branches or trunks, elongate cankers are formed and copious resin

flow from these cankers is common. Rodents usually hasten girdling

action by removing bark from cankers (fig. 4-12). On trunks of older

F-52.5009

Figure 4-12. Typical large

trunk canker caused by

Cronartium comandrae

on ponderosa pine.

109
trees with comandra rust, little or no swelling is apparent. Frequently,

the symptom is a constriction with the infected bark becoming

roughened. Aecia are seldom produced on the trunk cankers in large

trees — probably because of the thick bark. Symptoms on the comandra host are primarily restricted to leaves and occasionally to stems.

These appear in the spring as yellowish spots (uredia) about the size of

a pinhead. Then, in early summer, brownish hair-like structures or

telia develop. Curling and necrosis of heavily infected comandra

leaves is common in most areas (fig. 4-13).

F-700264

Figure 4-13. Uredinial and telial stages of Cronartium comandrae on bastard

toad flax (Comandra sp.).

Incense-Cedar Rust

Gymnosporangium libocedri

Hosts

One of the most abundant rust fungi on conifers in the Western

United States, G. libocedri, alternates between incense-cedar and

rosaceous shrubs, predominantly serviceberry. It causes only minor

damage except on the leaves and fruits ofserviceberry and hawthorn.

This rust is occasionally found on apple, pear, quince, and mountain

ash.

Distribution and Damage

The disease caused by G. libocedri is found throughout the range of

incense-cedar in the Western United States. It infects incense-cedar of

all ages. It causes witches-brooms and only infrequently kills smaller

branches. When the mycelium penetrates an older twig, it results in

110
the typical witches-brooms, which are numerous and conspicuous.

Badly infected trees may be seriously injured, but we know of no record

oftree mortality. The infection in the main stem of incense-cedar may

result in burls that cause defect in lumber. In northern California, it

has caused some damage to commercial pear orchards. It has also been

reported on pears in Oregon.

Disease Cycle and Field Identification

G. libocedri is a typical heteroecious rust fungus alternating between incense-cedar and several members of the rose family. In contrastto the other major heteroecious rusts described in this chapter, G.

libocedri has its pycnial and aecial stages on rosaceous hosts; it lacks a

uredinial stage, and the telial stage is on the conifer host. In early

spring, infected small branches of incense-cedar trees appear slightly

discolored. On the underside, rarely on the upperside, ofthe green, flat,

scale-like leaves, a number of small brown to brick-colored tufts or

telial cushions appear (fig. 4-14). When they mature, the cushions

become gelatinous during wet periods in spring and finally form conF.700265

Figure 4-14. Telial cushions oîGymnosporangium libocedri on scale-like leaves of

incense-cedar.

spicuous light orange-colored masses that later dry to a thin film (fig.

4-15). The sporidial stage is blown to the rosaceous host, where small,

orange-colored, cup-shaped fruiting bodies appear on the leaves and

petioles, and sometimes on the fruit. These bodies produce the aeciospore, which can again infect the tree.

Witches-brooms caused by G. libocedri are frequently mistaken for

plants ofthe incense-cedar mistletoe. This mistletoe, however, always

hangs down in thick clusters while the bushy witches brooms caused

by the rusts are more or less erect.

Ill
Figure 4-15.

cedar.

F-700266

Gelantinous telial stage of Gymnosporangium libocedri on incensePinyon Rust

Cronartium occidentale

Hosts

The aecial stage ofthis rust isfound on pinyon and singleleafpinyon

pines. The telial stage occurs on ribes species.

Distribution and Damage

The disease is found throughout the Western United States on pines

and ribes. In California, infection on pinyon pine occurs only in a

narrow belt, about 50 miles long by 10 miles wide, stretching north

from the east central border ofCalifornia and Nevada atthe base ofthe

eastern slope of the Sierra Nevada. From this source of aeciospores,

however, annual infection on ribes can be found throughout northern,

central, and north coastal California and southern Oregon. On pine,

multiple branch and trunk cankers are common and occasionally kill

trees. On ribes, damage is restricted to partial defoliation; the plant

seldom dies as a result.

112
Disease Cycle

C. occidentale is a heteroecious rust fungus with a disease and life

cycle identical to that of C. ribicola.

Field Identification

Because the uredinial and telial stages on ribes are macroscopically

indistinguishable from C. ribicola, pest control workers in search ofC.

occidentale may have problems in identification.

The aecial stage on the pine host is less distinct than that of C.

ribicola and native limb and stem rusts. It seldom causes swellings on

either branches or stems; the orange-colored aeciospores are borne in

large irregular cracks in the bark. The aecia themselves are seldom

prominent, often not visible, in contrast with other stem rusts (see C.

ribicola, P. filamentos urn). Rodents often chew on cankers. This

characteristic, however, cannot be used as a definite indicator of rust

infection.

Sweetfern Rust

Cronartium comptoniae

Hosts

The aecial stage is found on lodgepole, ponderosa, Monterey, Jeffrey,

and bishop pines in the West and on several other pines in other parts

of the United States. Its telial hosts are principally sweetfern and

sweetgale.

Distribution and Damage

The disease is common on 2- and 3-needle pines throughout the

Eastern United States and Canada, and in the West from Alaska to

California. Branch and especially trunk cankers deform the tree and

frequently kill it. Young trees are more often attacked than older ones.

Damage can be extensive in nurseries.

Disease Cycle

C. comptoniae is a heteroecious rust fungus and, except for differences in aecial and telial hosts, has a life cycle nearly identical to that

of C. ribicola.

113
Field Identification

The rust on pines usually first becomes evident as elongated swelling on branches of older trees or on the stem of seedlings. These

swellings become evident within 1 to 2 years after infection. They are

most conspicuous in spring when the orange-yellow aeciospores are

formed. Older cankers may vary from deep, vertical fissures to a very

slight depression in the bark.

The uredial stage appears as orange-colored pustules on the underside of the leaves of sweetfern and sweetgale. In autumn, telia are

formed around and within the uredia.

Tarweed Rust

Coleosporium madiae

Hosts

This typical heteroecious rust fungus has its aecial stage primarily

on Monterey pine. Coulter pine, and Jeffrey pine. The telial hosts are

principally the tarweeds.

Distribution and Damage

The rust is found occasionally on its tarweeds hosts from British

Columbia south to central California. It has not been found on its

aecial hosts north of southern Oregon.

The fungus is restricted to needles of its conifer hosts and, except in

occasional wet years when it may build up and cause heavy defoliation,

damage is minimal. On its telial hosts, damage is also minimal.

Field Identification

Aecia occur on all surfaces ofthe needle. They are white, globoid, and

broadly ellipsoid, and usually appear in early spring. On tarweed

leaves, uredinia appear as small, round, golden yellow pustules. Telia

are waxy, compact and orange-yellow when fresh.

Aster Rust

Coleosporium asterum

The uredinial stage of this rust on species of aster and goldenrod is

one ofthe most common rusts in the United States. C. solidaginis is a

synonym. C. asterum usually overwinters on the rosettes of these

species. On its aecial host in the West, it is mostly found on needles of

lodgepole pine, but occurs only sporadically. Damage to the pine hostis

114
usually negligible. Symptoms on pine are discolored spots on needles,

with firm, protruding, light-orange aecial sacs. On aster and goldenrod, the uredinia are round, orange-yellow pustules on the leaves,

while the telia are scattered and reddish-orange with cylindrical

teliospores rounded at both ends.

Rusts on Fir and Douglas-fir

Several needle rusts infect true firs in western North America.

Except for Melampsorella caryophyllacearum, however, most of them

are usually of minor importance and scattered in incidence except in

Christmas tree plantations. The two most common are Pucciniastrum

goeppertianum and Pucciniastrum epilobii. On Douglas-fir and bigcone Douglas-fir, only two rusts have been reported of any significance

in the Western United States: Melampsora medusae and Melampsora

occidentalis. Both alternate between needles ofDouglas-fir and leaves

of poplars and aspens.

Fir Blueberry Rust

(Pucciniastrum goeppertianum)

The hosts are true firs and blueberry. On true fir, P. goeppertianum

forms white tubules on the lower side ofneedles. These tubules contain

orange powdery aeciospores. Frequently, witches-brooms with annual

needles form on true firs. Uredinia are absent on blueberry species.

Telia produce witches-brooms on stems, forming a continuous layer

around the stem with polished reddish-brown surface. Teliospores are

found within the epidermis in single, closely pressed layers.

Fir Willow Weed Rust

(Pucciniastrum epilobii)

This disease is scattered but not uncommon on true fir species

throughout the Western United States. The fungus is also known as

Pucciniastrum pustulatum. The aecia are cylindric, yellow to colorless

pustules on the leaves offir. On the herbaceous willow herbs, uredinia

appear as powdery orange-yellow pustules followed by telia, which are

reddish-brown to blackish-brown cruststhat overwinter in the leaves.

Douglas-fir Rust

(Melampsora medusae)

Distributed throughout the Western United States from Colorado

and Wyoming to British Columbia and Oregon, and into California,

this Douglas-fir rust has also been found in bigcone Douglas-fir in

115
southern California. The fungus is also known as M. albertensis. On

Douglas-fir, the aecia form as tubules 1mm long in two rows — one on

either side ofthe midrib ofthe needle. These tubules contain powdery

yellow spores which, in turn, infect leaves of cottonwood and poplar

species. The uredinial stage of the rust on cottonwood and poplar

species appears as powdery yellow pustules on the lower leafsurface.

Later, these become waxy, orange-brown mats that form under the

epidermis, forming the telial stage.

Rusts on Junipers

A large number ofrusts, primarily in the genus Gymnosporangium,

are found scattered throughout the Western United States and, although oflittle importance in forest stands from a damage standpoint,

they can cause considerable damage to ornamental plantings.

Pear-Juniper Rust

(Gymnosporangium fuscum)

This disease was found for the first time in California in 1960 on

several ornamental juniper plantings and on pear trees in one area.

Although damage can be severe on juniper hosts, the greatest

economic damage occurs on the pear host. The growth and fruit set of

heavily infected trees are reduced and, infected leavestend to fall early

in the season. The fungus also attacks pear fruits.

On juniper, the telial stage appears on branches and twigs, causing

very slight to fusiform swellings several inches long. The perennial

infection in juniper often kills the infected branch or twig in 3 to 4

years. The telia occur in horns, which are small, firm, dark-brown

bodies a few mm across. Under moist conditions, they may swell and

become gelatinous, cylindrical, or conical and compressed and

reddish-brown. Telia horns are composed of teliospores and their

stocks.

On pear, the aecial stage first appears as circular or irregularly

shaped yellow-orange spots up to 2 cm in diameter on the lower surface

ofthe leaves. The stage appears as orange-brown cushions of diseased

tissue, with the aecium an off-white, acorn-shaped tubule 2 to 5 mm

high.

Amelanchier Rust

(Gymnosporangium harknessianum)

This rust is found chiefly on western juniper in California and

central Oregon. Its alternate host is primarily western serviceberry.

On the juniper host, uredinia have not been found. Telia form a

reddish-brown gelatinous masses on juniper leaves. Aecia are found

116
chiefly on western serviceberry fruits, usually over the entire surface.

They are cinnamon-brown, cylindrical tubules, 4 to 7 mm tall.

Inconspicuous Juniper Rust

(Gymnosporangium inconspicuum)

Probably the most abundant Gymnosvoransium on iuniper and on

Saskatoon serviceberry in the Western United States, this rust is

found primarily on Utah juniper and western juniper.

On the juniper host, uredinia have not been found. Telia appear as

golden yellow to brown felt-like structures arising between the scalelike leaves on green twigs or frequently through the bark of woody

twigs. In some parts ofUtah and Nevada, the telial stage is common on

older branches and larger stems. The hosttissue swells slightly, butits

bark appearsto be abnormally rough. Although telia frequently fall off

green twigs after maturation and leave no obvious signs, on woody

bark they are often retained in the cracks so that the disease can be

diagnosed at any time of the year. The fungus can also cause woody

swellings, but these are rarely found. The aecial stage on the serviceberry host is chiefly on the fruits being scattered or crowded over the

entire surface. Aecia appear as pale yellow, oblong cylindrical tubules.

In some areas, fruits may be so heavily infested that it is almost

impossible to find mature ones. Infected fruits are often colored bright

yellow or orange by the rust, so thatthe whole bush may appear atfirst

glance to bear yellow or orange fruit.

Serviceberry Rust

(Gymnosporangium kernianum)

This rust is common on several species of juniper throughout the

Western United States. Its principal conifer hosts are Utah, California, and western junipers. Its principal alternate host is serviceberry

species, but the rust is also found on pear, hawthorn, and quince. On

the conifer host, uredinia are not found. Telia are found developing

between the scale-like juniper leaves as globose witches-brooms

caused by fungus infection. Telia are hemispheric and dark reddishbrown.

On the alternate host, aecia are found principally on leaves and

occasionally on fruits and leaf petioles. The aecia are usually inconspicuous, cylindric, cinnamon-brown pustules. They are sometimes

found in mixed infections among the larger, brighter, more abundant

aecia of G. inconspicuum on the same fruits of serviceberry.

117
Juniper Rust

(Gymnosporangium multiporum)

This rustis a seldom collected species and is ofunknown life cycle. It

occurs on western juniper in California and on one-seed and Utah

junipers in Colorado, New Mexico, and central California. An alternate host for the pycnial and aecial stages is not known. On the juniper

host, uredinia have not been found. Telia develop between the scalelike leaves on green branches. They are chestnut brown with oblong

teliospores.

Nelson's Juniper Rust

(Gymnosporangium nelsonii)

This rust is found frequently throughoutthe Western United States

on creeping, one-seed, western, Rocky mountain, California, and Utah

junipers. Uredinia are not found on the conifer host. Telia, however,

cause conspicuous woody, globose galls ofvarying size on branches and

small stems. The telia are chestnut brown, irregularly flattened, 3 to 5

mm high. The alternate hosts are principally species of serviceberry,

on which the aecia are found on leaves, petioles, and fruits. They are

cylindric, 2 to 4 mm high, with chestnut brown pustules.

Hawthorn-Juniper Rust

(Gymnosporangium confusum)

This disease is found only in one area ofCalifornia, but is common in

Eurasia on several telial and aecial hosts. In a restricted area of

California, it has become well established on Juniperus sabina, its

telial host, and on one-seed hawthorn, which is the aecial host. Telia

develop first as gelatinous horns in spring. When dry, they become

very dark, velvety, reddish-brown. They develop principally in

fusiform cortical swellings on woody branches. Pycnia and later aecia

develop on swellings of the leaves, petioles, succulent stems, pedicels,

and calyxes. Aeciospores are reddish-brown and begin to develop usually in May.

Rusts on Cypress

Two distinctspecies ofrustfungi are found on cypress in the Western

United States: Uredio cupressicola and Gymnosporangium cupressi.

Both occur only rarely.

118
Gymnosporangium cupressi

This fungus has been reported on Arizona and Modoc cypress in the

telial stage, and on serviceberry species in the aecial stage. The telial

stage causes elongate or globoid swellings in cypress often in rows on

larger branches and form irregularly wedge-shaped, chestnut-brown

telial pustules. Although most common on green twigs, all stages of

gall and canker development to ages 100 years or more have been

found. The old cankers resemble the hip cankers of Peridermium

harknessii on pine, with flaring sides of mostly uninfected tissue.

Uredio cupressicola

Only the uredinial stage of this fungus has been found, and only on

Gowan cypress and Arizona cypress variety montana. It has been

found only in California and Baja California. The uredinia ñrst appear

between the scale leaves ofyoung twigs without producing any perceptible swelling. Later, large fusiform swellings are evident on twigs 4

years old or older. Cankers usually kill the twigs within a few years,

but occasionally occur on branches up to 25 years old.

Selected References

Arthur, J. C.

1934, Rev. 1962. Manual of the rusts of the United States and Canada. 438 p.,

Lafayette-Purdue Research Foundation. Rev. ed., Hafner Publ. Co., New York'

Bega, R. V.

1959. The capacity and period of maximum production of sporidia in Cronartium

ribicola. Phytopathology 49 (l):54-57.

Bega, R. V.

1960. The effect of environment on germination of sporidia in Cronartium ribicola

Phytopathology 50 (l):61-69.

Kimmey, James W., and Willis W. Wagener.

1961. Spread of white pine blister rust from ribes to sugar pine in California and

Oregon. U.S. Dep. Agrie, Tech. Bull. 1251, 71 p.

Krebill, R. G.

1965. Comandra rust outbreaks in lodgepole pine. J. For. 63:519-522

Krebill, R. G.

1968. Cronartium comandrae in the Rocky Mountain States. U.S. Dep. Agrie. Forest

Serv. Res. Paper INT-50, 28 p., illus. Intermountain Forest and Range Exp. Stn.,

Ogden, Utah.

McCain, Arthur H., and Dan Y. Rosenburg.

1961. Pear-juniper rust, a disease new to California and the United States. Calif. Dep.

Agrie. Bull. 50, p. 13-19.

Mielke, J. L.

1943. White pine blisterrust in Western North America. Yale Univ. Sch. For. Bull 52

155 p.

Mielke, J. L.

1952. The rust fungus Cronartium filamentosum in Rocky Mountain ponderosa pine.

J. For. 50:365-373.

Mielke, J. L.

1956. The rust fungusCronartium stalactiforme in lodgepole pine. J. For. 54:518-521.

119
Mielke, J. L., R. G. Krebill, and H. R. Powers.

1968. Comandra blister rust of hard pines. U.S. Dep. Agrie. Forest Pest Leafl. 62,4 p.

Peterson, Roger S.

1963. Effects of broom rust on spruce and fir. U.S. Forest Serv. Paper INT-8, 10 p.

Intermountain Forest and Range Exp. Stn. Ogden, Utah.

Peterson, R. S.

1963. Notes on western rust fungi — III Cronartium. Mycologia 54:678-684.

Peterson, R. S.

1965. Notes on western rust fungi — IV. Mycologia 57:465-471.

Peterson, R. S.

1966. Limb rust damage to pine. U.S. Forest Serv. Res. Paper INT-31, 10 p. Intermountain Forest and Range Exp. Stn., Ogden, Utah.

Peterson, R. S.

1967. The Peridermium species on pine. Bull. Torrey Bot. Club 94:511-542.

Peterson, R. S.

1968. Limb rust of pine — the causal fungi. Phytopathology 58:309-315.

Peterson, Roger S.

1967. Studies ofjuniper rusts in the West. Madroño 19:79-91.

Peterson, Roger S.

1967. Cypress rusts in California and Baja California. Madroño 19, 47-54.

Peterson, Roger S., and F. F. Jewell.

1968. Status of American stem rusts of pine. Annual Rev. Phytopath. 6:23-40.

Ziller, Wolf G.

1974. The tree rusts of Western Canada. Canadian For. Serv. Publ. 1329. 272 p.

120
5. MISTLETOES

by

ROBERT F. SCHARPP^

The parasitic flowering plants commonly known as mistletoes are

found throughout North America. Two genera of mistletoes grow in

the Western United States: Phoradendron C'true" mistletoes) and

Arceuthobium (dwarf mistletoes). The "true" mistletoes grow on both

conifers and broadleaf trees; the dwarfmistletoes grow only on conifers. Male and female flowers are produced on separate plants in both

genera.

True mistletoes are large woody plants with mature shoots more

than 6 inches long and one-eighth inch or more in diameter. Foliage is

leafy or scaly. The fruit resembles white or pink globes. On the Paciñc

Coast the true mistletoes on conifers are easily identified. Only two

species and two subspecies are known. They can be distinguished on

the basis of foliage characteristics and the host species.

In contrast, dwarf mistletoes are small plants, with mature shoots

less than 6 to 8 inches long and one-eighth inch in diameter. The shoots

are non-woody, segmented and have scale-like leaves. Seeds produced

in oval-shaped bicolored fruit are forcibly released when ripe.

Although both mistletoes are damaging parasites oftrees, by far the

greatest timber loss in coniferous forests of the West is attributed to

the dwarfmistletoes. Billions ofboard feet oflumber are lost each year

as a result of growth reduction and mortality from these parasites.

They also cause serious damage to high-value, high-use forest recreational areas.

1. True Mistletoes

The true mistletoes are probably more often seen and recognized

than the dwarf mistletoes. Even the leafless true mistletoes usually

appear as conspicuous clumps or balls of foliage growing on conifers

(fig. 5-1). True mistletoes are totally dependent on their hosts, butthey

* Plant Pathologist, Pacific Southwest Forest and Range Experiment Station, Forest

Service, U.S. Department of Agriculture, Berkeley, Calif.

121
F-700267

Figure 5-1. Incense-cedar often becomes severely infected throughout its

crown by the misÛetoe Phoradendronjuniperinum ssp. libocedri.

carry on photosynthetic activity. Thus, much oftheir growth is attributed to their abihty to make foodstuffs from water and certain mineral elements provided by the host. In the absence ofthe aerial portions

of the plant, however, the roots remain alive and continue to grow

within the host branch, eventually producing new shoots and foliage.

Mistletoe flowers are inconspicuous, but the fruits, commonly

known as berries, are readily seen (fig. 5-2). They are about the size ofa

pea (1/8 to 1/4 inch in diameter), when ripe, and grow in clusters.

Usually one seed develops in each berry. The sticky pulp of the berry

surrounding the seed is a preferred food of certain birds. In fact, the

seeds are distributed mainly by birds. Consequently, these mistletoes

tend to be most abundant in the tops oftrees (fig. 5-3). When eaten, the

seeds pass intact through the digestive tract of the birds and are

deposited along with their excrement on tree branches. Thread-like

strands on the seedcoat enable the seeds to adhere to branches, where

they germinate, penetrate, and infect the host.

122
Figure 5-2. Pinkish fruit of the incense-cedar mistletoe.

F-525010

Figure 5-3. Large clusters

of mistletoe, Phoradendron bolleanum ssp.

pauciflorum occur

mainly in the tops of

mature white fir.

123
Both the root and shoot system are initially produced from the

germinating seed. Thereafter, buds produced from the roots break

through the bark to form additional aerial shoots. Woody perennial

stems develop and often persist for many years unless they are broken

off or killed. Often clumps ofshoots and foliage 2 to 3 feet in diameter

are seen in trees.

The true mistletoes on conifers on the Pacific Coast are easy to

identify. Only two species and two subspecies are known. As shown

below, the true mistletoes may be distinguished on the basis offoliage

and host species.

Plants with leaves

1. on Juniperus or Cupressus - Phoradendron bolleanum ssp.

densum

2. onAbies concolor-Phoradendron bolleanum ssp. pauciflorum

Plants leafless

1. on Juniperus - P. juniperinum ssp. juniperinum

2. on Libocedrus - P. juniperinum ssp. libocedri

Cypress — Juniper Mistletoe,

''Dense" Mistletoe

Phoradendron bolleanum ssp. densum

Hosts

Cypress, juniper.

Distribution and Damage

This mistletoe is widespread throughout certain areas of the West.

Its occurrence on Cypress ranges along the coast from the mountains of

northwestern California southward to Marin County. Inland, it ranges

from Butte County, Calif., northward along the western slope of the

Sierra Nevada and into the southern Cascades. This mistletoe is also

found on cypress in central Arizona.

On Junipery the mistletoe extends from Baja California and Arizona

northward along the eastern slope ofthe Sierra Nevada and southern

Cascades. Along the coast, it ranges from San Diego to Monterey

County, Calif.

Many plants may occur on and damage individual trees. But losses

to forests from this particular mistletoe appear minimal.

Field Identification

Clusters of mistletoe foliage occur on branches throughout the host

124
F-525011

Figure 5-4. Branch of

Cupressus infected by

the leafy mistletoe

Phoradendron bolleanum

ssp. densum.

crown. The shoots bear oval-shaped leaves that are usually about 0.1 to

0.2 inch wide and 0.4 to 0.8 inch long (fig. 5-4).

White Fir Mistletoe

Phoradendron bolleanum ssp. pauciflorum

Hosts

White fir.

Distribution and Damage

White fir growing in the Sierra Nevada ft-om Placer County southward and in the mountains of southern California is the host of this

parasite. It also occurs in the Santa Catalina Mountains of Arizona

and the Sierra San Pedro Mártir in Baja California, Mexico.

This mistletoe is for the most part only a serious parasite of larger

and older trees. Many years are required for it to build up and become

damaging to white fir. In some instances, it becomes so dense that tree

tops and sometimes entire trees are weakened and die or are attacked

and killed by bark beetles.

125
Field Identification

This mistletoe is most often observed in the tops ofthe tallesttreesin

the stand. Large clumps offoliage may grow along the trunk ofthe tree

for 20 to 30 feet down from the top (fig. 5-3). Often the tree foliage in

this zone is nearly completely replaced by mistletoe foliage. Spike tops

are also common in white fir stands infected with this parasite. The

dead mistletoe shoots remain attached to the dead top and branchesfor

some years after death.

The leaves are smooth, oval-shaped, about 0.2 to 0.4 inch wide and

0.5 to 1.2 inches long.

Juniper Mistletoe

Phoradendron juniperinum ssp. juniperinum

Hosts

Juniper.

Distribution and Damage

Along the Pacific Coast, this mistletoe ranges from the eastern slope

ofthe southern Cascades in central Oregon, through the upper elevations of the Sierra Nevada, and south into the San Bernardino Mountains of southern California. Elsewhere in the West, it extends from

northern Utah into northern Mexico. Although this mistletoe builds

up to high populations on some trees, the damage it causes to stands

appears to be negligible.

Field Identification

P. juniperinum appears as upright clumps ofshoots in the crowns of

trees. The single characteristic that distinguishes it from P. bolleanum, which also grows on juniper, is the absence of leaves. The

leaves on this particular species are reduced to inconspicuous scales

less than one-sixteenth inch long. Berries are light pink.

126
Incense—Cedar Mistletoe

Phoradendron juniperinum ssp. libocedri

Hosts

Incense-cedar.

Distribution and Damage

This mistletoe is found in the southern Cascades, on the western

slope ofthe Sierra Nevada, and in the mountains ofsouthern California.

For the most part, this mistletoe causes negligible damage to its

host. On older trees, however, it occasionally builds up to high populations. It may weaken a tree, but rarely kills it.

Field Identification

Round, usually pendant, clumps ofmistletoe shoots in the crowns of

incense-cedar identify this organism (fig. 5-1). Like the other subspecies that occur onjuniper, the leaves are inconspicuous scales about

one-sixteenth inch long. This mistletoe occasionally infects tree

trunks and causes some swelling, butthis only occurs in cases in which

the root system of the parasite has been in the trunk for many years

The berries are light pink (fig. 5-2).

2. Dwarf Mistletoes^

Unlike the true mistletoes, dwarfmistletoes depend almost entirely

on food produced by the host; they photosynthesize little material for

themselves. The aerial shoot system, therefore, functions mainly for

reproduction.

Small, inconspicuous flowers are produced in the axils of the shoot

segment (fig. 5-5). Flowers are both insect and wind pollinated. Short

stalks bear fruits that are about 0.1 inch long when ripe (fig. 5-6).

Unlike the true mistletoes, dwarfmistletoes are not disseminated by

birds, but depend on an explosive mechanism for spread. During maturation the fruits swell with water and build up considerable hydraulic

pressure. At maturity the seeds, usually one per fruit, are explosively

discharged by the water pressure in the fruit. Discharged seeds may

travel horizontally for 30 to 40 feet. With the aid of the wind, seeds

iThe genus of dwarf mistletoe has been revised, and many of the species names used

reflect changes in the names of the previously known dwarf mistletoes in California

(Hawksworth and Wiens 1972).

127
F-525012 K-52ñ0i:í

Figure 5-5. Male plant ofArceuthobium occiden- figure 5-6. Shoot from

. , . . . „ „ female plant of Ar- tale bearing mature flowers. *^

ceuthabium accidéntale

bearing mature fruit.

discharged from the tops oftrees may travel as far as 100 feet or more.

Like the true mistletoes, the seeds are sticky. They initially adhere

to the foliage of surrounding branches and trees (fig. 5-7). During

rains, the seeds swell with water, become slippery, and wash down on

and adhere to host branches where germination and infection occur.

The root system of dwarf mistletoe penetrates and grows within the

tree branch in much the same way described for true mistletoes.

Trees respond in several ways to infection by dwarf mistletoe. Usually a localized swelling of the branch occurs (fig. 5-8). Occasionally,

however, pronounced swelling of the main stem of a tree occurs as a

result of the parasite infecting the trunk directly or by growing into

the trunk from an infected branch. With time, these swellings may

grow to a size of twice the normal diameter of the tree trunk. To

compound the problem, decay fungi often enter bark cracks and openings atthe site ofswelling causing heart rot (fig. 5-9 ). Frequently these

decaying trees break at the swelling, causing loss of timber and pre128
-4¡u^

F-525014

Figure 5-7. Seed ofdwarfmistletoe,Arce¡/í/¡o6i¡/m abietinum adhering to needle

of white fir.

K-525015

Figure 5-8. Dwarf mistletoe plant, Arceuthobium abietinum arising from the infected, swollen part of a branch of white fir.

129
F-525016

Figure 5-9. Open, decayed, bole swelling on white fir caused by dwarf mistletoe, Arceuthobium abietinum.

senting a hazard in recreational and high-use areas.

With certain dwarf mistletoe species, branches react to infection by

producing what is commonly known as a "broom." A broom is an

abnormal proliferation of many small twigs on a branch which appear

as a clustered mass of twigs and foliage. Brooms vary in appearance

from ball-shaped to loosely fan-shaped structures. Some brooms remain small (fig. 5-10) whereas others may comprise the bulk of the

foliage on a tree (fig. 5-11).

Many ofthe species of dwarf mistletoe are host specific and occur on

only one species of tree. Others may occur on three or four difí'erent

species of conifers, but only rarely do they cross infect from one genus

of conifer to another. When they do, they usually spread from the

primary host to secondary hosts in stands in which both hosts are

growing close to one another. As a result of their host specificity, the

dwarf mistletoes of the West can best be distinguished from one

another on the basis of host species and host distribution.

130
F-525017

Figure 5-10. Characteristically open, fan-shaped brooms on white fir caused

by the dwarf mistletoe, Arceuthobium abietinum.

F-525018

Figure 5-11. Massive tight brooms develop on Douglas-fir as a result of infection by dwarf mistletoe, Arceui/io6ium douglasii.

131
Descriptive Key

On pines

A^ Pinyon pines A. divaricatum

A^ 2-3-needle pines B.

ßi Digger, Monterey, and bishop pines; occasionally on Coulter

and knobcone pines in the coastal mountains of central

California A. occidentale

W On ponderosa and Jeffrey pines in California, Oregon,

Idaho, and Washington; also on Coulter and knobcone pines

in areas other than those mentioned above.

A. campylopodum

W On lodgepole pine A. americanum

A^ 5-needle pines C.

C^ On sugar pine; rarely western white pine. Plants with

shoots 4- to 6- inches long A. californicum

C^ On limber pines, rarely on whitebark and western white

pines. Small plants (shoots usually less than 2 inches

long). A. cyanocarpum

On fir, hemlock, Douglas-fir, western larch

Al On fir B.

B^ On white fir or grand fir A. abietinum f. sp. concoloris

W Red fir or noble fir A. abietinum f. sp. magnificae

A2 On western and mountain hemlock A. tsugense

A^ On Douglas-fir A. douglasii

A'* On western larch A. laricis

True Fir Dwarf Mistletoe

Arceuthobium abietinum

(f. sp. concoloris) — white fir, grand fir

(f. sp. magnificae) — red fir, noble fir

Hosts

This unique dwarfmistletoe is the only species known that has two

specialized host forms. These forms, although identical in appearance,

are host specific — one infecting only red fir and noble fir and the other

infecting only white fir and grand fir.

The white fir-grand fir form has never been found on red fir or noble

fir. It rarely infects sugar pine in the Sierra Nevada and Brewer spruce

in southern Oregon.

132
Distribution and Damage

The fir dwarfmistletoes are common and widespread on their hosts

through their range in the central and southern Cascades, Sierra

Nevada, and coastal mountains of northern California and southern

Oregon. In California, about 30 percent of the white fir stands and

about 50 percent ofthe red fir stands are infested with this parasite. As

a result of its widespread distribution, dwarfmistletoe constitutes one

ofthe most serious forest disease problems in the management oftrue

firs.

Field Identification

The presence of dwarf mistletoe plants and fusiform branch swellings is a sure sign of infection (fig. 5-8). One ofthe best indications of

infection in fir stands is the presence of branch flagging. Branches

infected by dwarf mistletoe are commonly attacked and killed by a

canker fungus, Cytospora abietis, and flagging results. The brick redflagged branches are most conspicuous in late spring and summer

when the foliage on the killed branch begins to dry. Later in the fall,

the dead foliage turns more gray-brown in color.

Large swellings as a result of invasion of the tree trunk by the

parasite are common on large, old firs (fig. 5-9). These swellings are

often very pronounced and may reach a diameter of twice the normal

size of the trunk.

Some brooming occurs on older infected branches, but is not conspicuous (fig. 5-10). Brooms caused by fir broom rust (see Chap. 4) also

occur on firs in the West and could be confused with those caused by

dwarf mistletoe.

Lodgepole Pine Dwarf Mistletoe

Arceuthobium americanum

Hosts

Lodgepole pine (Pinus contorta ssp. murrayana) is the common host

for this mistletoe, although it has been found rarely on ponderosa pine.

Distribution and Damage

A. americanum has the widest range of any North American dwarf

mistletoe, mainly because of the wide range of its principal host. It

occurs throughout the Western United States and Canada. On the

Pacific Coast it occurs on lodgepole pine in the Cascades and Sierra

Nevada. It has not been found on shore pine {P. contorta ssp. contorta)

133
or P. contorta ssp. bolanderi along the coast.

Forest disease surveys indicate that nearly 30 percent of the

lodgepole pine stands in California are infested with this parasite.

Where it occurs, it is damaging and causes considerable growth reduction and mortality to lodgepole pine.

Field Identification

Pronounced brooming of trees is the most conspicuous symptom of

infection. Brooms on older, heavily infected trees often make up nearly

the entire live crown. The presence of dwarfmistletoe plants and some

fusiform swelling of branches also indicate infection.

Sugar Pine Dwarf Mistletoe

Arceuthobium californicum

Hosts

The principal host ofthis mistletoe is sugar pine. It occurs rarely on

western white pine.

Distribution and Damage

This dwarf mistletoe occurs throughout the range of sugar pine in

the west from the southern Cascades, through the Sierra Nevada to the

Cuyamaca Mountains of southern California. It also occurs on sugar

pine in coastal mountains of northern California from about Lake

County to the Oregon border.

Although this mistletoe occurs essentially throughout the natural

range ofsugar pine, it is not as common as dwarf mistletoes on other

species. Forest disease surveys have shown that about 20 percent ofthe

foreststands containing sugar pine are infested with this parasite. The

frequency of dwarf mistletoe is probably lower on sugar pine than on

other host species because sugar pine rarely forms pure stands but

occurs in mixture with other conifer species. Sugar pine seldom comprises more than 50 percent of a stand. This mixed stand situation

undoubtedly limits the spread of the parasite under natural forest

conditions.

Where sugar pine is infected, heavy damage can occur. Numerous

infections may develop and large brooms on older trees are common.

Severe growth reduction results from heavy infection. Weakened trees

are also often attacked and killed by bark beetles.

134
Field Identification

Large compact brooms in the crowns of older trees are the best

symptoms of infection. Numerous individual fusiform branch swellings and the presence of aerial shoots of the parasite are also easily

recognized symptoms and signs of infection.

Western Dwarf Mistletoe

Arceuthobium campylopodum

Hosts

Ponderosa pine, Jeffrey pine, knobcone pine, Coulter pine.

Distribution and Damage

This parasite ranges throughout the forested regions of the West

from Washington and Idaho, through Oregon and California, but it is

not known in the coastal mountains south of Lake County, Calif.

The western dwarf mistletoe is one of the most damaging forest

disease agents in the Western United States. Many commercial pine

stands there have been killed or suffered reduced growth. Jeffrey pine

is considered to be more susceptible to this parasite than ponderosa

pine, but both species are heavily attacked. Coulter pines in southern

California suffer heavy mortality and are among the most seriously

damaged species.

Field Identification

The presence of fusiform branch swellings and aerial shoots of the

plant are conspicuous indications of infection. Brooms may form. On

larger trees, they become well developed and are easily observed.

Swelling as a result oftrunk infection is not as pronounced as that in

true firs. But, in some cases, old trunk infections result in open,

pitch-infiltrated bole cankers.

Limber Pine Dwarf Mistletoe

Arceuohobium cyanocarpum

Hosts

Limber, whitebark, foxtail, and western white pines.

135
Distribution and Damage

This mistletoe occurs on its hosts mainly in the Rocky Mountain

region. In the far West, it occurs only in the southern Cascades, east

side Sierra Nevada, San Bernardino, and San Jacinto Mountains of

California.

Infected trees are often severely damaged and deformed and a high

rate of mortality has been observed.

Field Identification

Infected trees bear numerous infections and the parasite is easily

recognized by the presence of numerous small, densely clustered

shoots. Brooms are formed, but are typically small and compact.

Stands infested by the parasite may show mortality to such an extent

that "ghost forests" result.

Pinyon Dwarf Mistletoe

Arceuthobium divaricatum

Hosts

Singleleaf pinyon pine.

Distribution and Damage

This parasite infects pinyon pines in the Rocky Mountains and on

the east side of the Sierra Nevada and in mountains of southern

California. Damage is usually not severe even when trees are heavily

infected. Tree mortality is slight, although growth is reduced.

Field Identification

Heavily infected trees often bear hundreds of individual branch

infections. Broom formation, however, is not conspicuous.

Douglas Fir Dwarf Mistletoe

Arceuthobium douglasii

Hosts

The principal host is Douglas-fir, but it has been found occasionally

on several species of true fir and spruce in association with infected

Douglas-fir.

136
Distribution and Damage

This parasite occurs on Douglas-fir in the Pacific Northwest east of

the crest of the Cascades. Elsewhere, it occurs on Douglas-fir from

southern British Columbia to central Mexico. Only in southwestern

Oregon and California does it occur along the coast, and then only as

far south as Shasta, Siskiyou, and Trinity Counties.

Douglas-fir is severely damaged by this parasite. Heavily infected

trees are weakened, deformed, and often killed. Because Douglas-fir

often grows in pure stands or is the predominant species, damage to

commercial forests by this mistletoe is often widespread.

Field Identification

Huge brooms are common on older infected trees (fig. 5-11) and are

nearly certain indication of infection by dwarf mistletoe. Young infected trees may be stunted and deformed. The mistletoe plant itselfis

very small and inconspicuous. The aerial shoots often arise from along

infected branches of a broom or from the spindle-shaped localized

infections, but seldom grow to more than 1 inch in length (fig. 5-12).

1

f.

F.525019

Figure 5-12. Small, inconspicuous plants are produced by dwarf mistletoe,

Arceuthobium douglasii on Douglas-flr (male shoots with mature flowers).

137
Larch Dwarf Mistletoe

Arceuthobium laricis

Hosts

Western larch (Larix occidentalis) is the principal host for this

species. Several other conifer species are sometimes infected when

they grow in association with infected larch.

Distribution and Damage

In general, larch dwarf mistletoe occurs throughout the range of

western larch. It is found east of the Cascades in Oregon and

Washington, but does not occur in California. Western larch suffers

severe damage from larch dwarfmistletoe. A high proportion of larch

stands are badly infested and heavy mortality and growth loss is

common.

Field Identification

Pronounced brooming of older trees is the most conspicuous

symptom of infection. Badly infected trees have literally dozens of

brooms that are particularly noticeable in fall and winter after the

deciduous foliage of larch has been shed.

Digger Pine Dwarf Mistletoe

Arceuthobium occidentale

Hosts

Digger pine, Monterey pine; occasionally bishop, knobcone, and

Coulter pines; rare on P, contorta ssp. bolanderi.

Distribution and Damage

Until recently this species of dwarf mistletoe was considered to be

the western dwarf mistletoe, A. campylopodum. However, recent

studies have shown thatthis dwarfmistletoe does notinfect ponderosa

and Jeffrey pines, but is restricted to the lower elevational digger and

coastal pines ofCalifornia. In general, this mistletoe occurs on its hosts

throughout their natural range in the State.

138
Severe damage occurs to trees and stands heavily infected by this

parasite. Trees are reduced in growth, deformed, and often killed.

Digger and Monterey pines are particularly susceptible to infection.

Hundreds of individual infections may occur on trees over a period of

just several years and the upward spread of the parasite on this host

species is known to be very rapid and equal to the height growth of

vigorous trees.

Field Identification

The presence ofnumerous dwarfmistletoe plants and fusiform swollen branches is probably the best symptom of infection. Because ofthe

rapid rate of buildup and upward spread of this parasite, infections

may be seen throughout the crowns of heavily infected trees.

Although some broom formation occurs, brooms never become as

well developed as those caused by western dwarf mistletoe or sugar

pine dwarf mistletoe.

Hemlock Dwarf Mistletoe

Arceuthobium tsugense

Hosts

The principal hosts are western hemlock and mountain hemlock

although some other conifer species (usually pines and true firs) are

occasionally attacked, particularly when they grow in association with

hemlocks.

Distribution and Damage

This mistletoe occurs on western hemlock along with the Pacific

Coast from Alaska to northern California. Inland, it occurs on mountain hemlock in the southern Cascades and as far south as Alpine

County in the central Sierra Nevada.

Forest trees and stands are severely damaged by this mistletoe,

particularly the western hemlock along the Pacific Coast. Severe

growth loss, deformation, and mortality result from heavy infection.

Field Identification

Brooming of older trees is the most noticeable symptom ofinfection.

Brooms are often large and abundant (fig. 5-13). Smaller trees are

often severely stunted. Aerial shoots of the plant are not always

formed particularly under the densely shaded conditions ofthe coastal

forests. Only under open growing conditions or in the tops oftrees does

139
K-Ó25020

Figure 5-13. Large mountain hemlock killed by dwarf mistletoe, Arceuthobium

tsugense. Note the numerous compact brooms formed on branches.

Selected References

Gill, Lake S., and Frank G. Hawksworth.

1961. The mistletoes: a literature review. U.S. Dep. Agrie. Tech. Bull. 1242, 87 p.

Hawksworth, Frank G.

1961. Dwarf mistletoe of ponderosa pine in the Southwest. U.S. Dep. Agrie. Teeh. Bull.

1246, 112 p.

Hawksworth, Frank G., and D. Wiens.

1972. Biology and elassification of the dwarf mistletoes {Arceuthobium). U.S. Dep.

Agrie., Agrie. Handb. 401, 234 p., illus.

Kuijt. Job

195,5. Dwarf Mistletoes. Bot. Rev. 21: 569-627.

Scharpf, Robert F.

1964. Dwarfmistletoe on true firs in California. U.S. Dep. Agrie. Forest Pest Leaf!. 89,

7 p., illus.

Seharpf, Robert F., and F. G. Hawksworth.

1968. Dwarfmistletoe on sugar pine. U.S. Dep, Agrie. Forest Pest Leafl. 113,4 p., illus.

Scharpf, Robert F. and J. R. Parmeter, Jr.

1967. The biology and pathology of dwarfmistletoe, i4rceu//zo6(í/m campylopodum f.

abietinum parasitizing true firs {Abies spp.) in California. U.S. Dep. Agrie. Teeh.

Bull. 1362, 42 p. illus.

140
Walters, James W.

1976. A guide to Mistletoes ofArizona and New Mexico. Bulletin, Forest Service, U.S.

Dep. Agrie. Southwestern Region, Albuquerque, New Mexico.

Wiens, Delbert.

1964. Revision ofthe acataphyllous species ofPhoradendron. Britonnia 16 (1): 11-54.

141
6. ROOT DISEASES

by

RICHARD S. SMITH, JR.*

Root diseases are becoming increasingly more important in the

forests of the Western United States. Each year more areas of root

disease infestation and greater numbers of infected trees are detected

because of increased awareness, more intensive surveys, and better

diagnostic techniques. And, in many areas, forest management practices have increased the incidence and severity of root diseases in the

past and unless control measures are taken, they will continue to do so

in the future.

The major root diseases in western forests are doubly destructive.

They not only kill the trees now growing on the site, but can exist in

dead roots and soils for many years, killing any future trees which

become established within the infested site. Some root disease fungi

remain alive and active in infested sites for more than 50 years. The

losses resulting from these diseases then should include the trees

destroyed initially plus the loss in productivity of the site for the

number of years it is infested.

Four major tree root diseases are found in the Western United

States: annosus root disease, Armillaria root disease, black stain root

disease, and Phellinus (Poria) weirii root disease. The relative importance of each disease, however, varies from area to area. Several lesser

diseases may be important in local areas or in certain periods of a

stand's development.

The diagnosis of root diseases is difficult and can seldom be made

only on above-ground symptoms. The above-ground symptoms of

chlorosis, reduced tree growth, reduced needle length, fading crown,

and finally death are the same for all root diseases. These symptoms

also are similar to those caused by drought, high water table, air

pollution, and bark beetle attack, except that the decline of the tree

affected by root disease or air pollution is usually extended over a

period of 3 to several years and these other causes kill the tree in 1 to 2

years.

* Plant Pathologist, formerly with the Pacific Southwest Forest and Range Experiment Station; now with the California Region, Forest Service, U.S. Department of

Agriculture, San Francisco, Calif.

142
The pattern ofthe dead and dying trees often is helpful in diagnosing

root disease as the cause of a problem. Characteristically, root diseases

start in a tree or stump and spread slowly outward in all directions.

This results in a slowly enlarging group of dead trees, with the oldest

kills at the center and with a fringe of dying and recently killed trees

around the outer edge. Thus, if one finds a pocket of dead trees that

were all killed at once, he would suspect some other cause which would

fit this pattern of kill, such as ground fire, high water table, or insect

attack.

Accurate diagnosis depends upon examination of part or all of the

root crown and major buttress roots. This portion of the tree provides

the most helpful signs and symptoms of each root disease, such as

sapwood stain and decay, mycelial fans, rhizomorphs, resinosis, and

fruiting bodies. It is best to choose a recently killed tree for examination for these below-ground signs. Frequently, these signs are destroyed after a year or two by secondary invaders — both insects and

fungi.

Descriptive Key

A^ Black to chocolate-brown stain or streaks ofstain in the sapwood

of the roots, root crown, and/or lower bole

Black stain root disease

A^ No black stain, stain if present blue, blue-gray, or gray B

B^ Large white mycelial fans between bark and wood of roots

and root crown. Shoestring-like strands (rhizomorphs)

sometimes present on roots and/or under the bark. Associated decay white to yellowish stringy rot sometimes

with fine black zone lines Armillaria root disease

B^ White mycelial fans and rhizomorphs absent C

C^ Bark of roots and root crown separate easily from

wood. Small white flecks of mycelium on inner side of

bark — numerous brown resin canals noted on wood

surface. Small white amorphous fruiting bodies or

buttonlike fruiting body initials may be present on

roots or root crown below soil surface, or shelf-like

cream to light orange colored fruiting bodies inside

hollow stumps. Associated decay white to cream colored, soft and spongy Annosus root disease

C^ Roots and lower bole decayed, leaving a yellow to buff

laminated rot with dark brown mycelial felts often

between sheets of decayed wood and in shrinkage

cracks. Fruiting bodies inconspicuous, crustlike, covered with many small pores, buff with white margin

when young, turning dark brown with age

Phellinus (Poria) weirii root disease.

143
Annosus Root Disease

Fomes annosus

Hosts

Fomes annosus has an extensive hostrange, including most conifers,

some hardwoods, and a few species ofbrush. To date, it has been found

on nearly all native and many introduced conifers in the West.

Distribution and Damage

Worldwide in distribution, F. annosus is also widely distributed

throughout the conifer forests of the Western United States. It has

been found from the dry pinyon-juniper woodland of the Southwest to

the high rainfall cedar-hemlock forests of the Pacific Northwest. This

fungus is indigenous and most abundant in the true fir forests of

California and hemlock forests of Oregon and Washington. It is being

found with greater frequency in the logged pine forests of California.

In Europe and the Southeastern United States, the incidence ofthis

disease has increased directly with increased forest management until

now it is one ofthe major disease problems. Experience indicates that,

without control measures, this disease in the West will follow the same

pattern.

Although most conifers are attacked byF. annosus, the way in which

the host is affected and the type ofresulting damage differ. In pine, the

fungus spreads through the rootsystem, first attacking the inner bark

and sapwood, killing these tissues. Its penetration into the heartwood

is delayed. Within 2 to 6 years after initial infection, the fungus

reaches the root crown and girdles the tree. The tree dies, but the

fungus remains active as a saprophytic wood-decaying organism

within the roots and butt of the dead tree. Thus, in pine, F, annosus

kills the host within a short period.

In true firs, Douglas-fir, and hemlock, the fungus seldom attacksthe

root tissues to the extentthatthe hostis directly killed. In these hosts,

the sapwood and inner bark usually are invaded in the small-tomedium-sized roots. And the fungus is confined to the heartwood and

inner sapwood of the larger roots. Within the heartwood, the fungus

spreads through the roots and root crown into the lower trunk of the

host, where it causes a butt rot of the heartwood. Thus, infection in

these species usually does not kill the host directly, although it may

affect its growth or thriftiness. Losses in true firs fromF. annosus are

mainly the result of butt rot, increased susceptibility to insect attack,

and increased windthrow.

144
Disease Cycle

Thisfungus can survive for as long as 50 years as a saprophyte in the

roots of infected stumps and trees. During favorable periods, the fungus in these stumps and roots forms fruiting bodies which in turn

produce numerous spores. Air currents distribute the spores to new

infection sites. These sites are usually freshly cut stump surfaces of all

conifer species and basal wounds ofhemlock and fir. Spores landing on

a fresh stump surface germinate, infectthe new stump, grow down into

the roots, and eventually colonize the stump and its root system.

Once established in the stump, the fungus grows into the roots of

neighboring trees wherever root contact between the infested stump

and the surrounding trees exists. From these newly established infections atthe site ofroot contact, the fungus spreads through the roots of

the new host to the root crown. The rest of this tree's root system is

colonized and the fungus spreads to its neighbors, again through root

contact. By this method, enlarging infection centers are formed.

Field Identification

In pines, the pattern ofdying within the stand and individualtrees is

often helpful in diagnosing this root disease. The presence of annosus

root disease is indicated by group killings oftrees over a period ofyears

with the oldest deaths atthe center and the most recent dead and dying

trees on the periphery. The presence of a stump atthe center near the

oldest kill suggestsF. annosus root disease. Ifdeath ofindividual trees

were preceded by a period of reduced growth or stunting as indicated

by the terminal height growth and ifthe crowns ofthe dying trees are

thin and chlorotic, a root disease is again suspected.

The presence ofF. annosus fruiting bodies on the infected trees are

the best field evidence ofthisroot disease. These fruiting bodies vary in

size and form from a small button up to a bracket-type conk several

inches wide (fig. 6-1 left) to rather irregular amorphous fruiting bodies

(fig. 6-1 right).The fruiting bodies found on the root crowns of infected

pines range from ¥2 inch to 2 inches across, with a light brown to gray

upper surface and a creamy white lower pore surface. It is usually

necessary to remove the dufffrom around the base ofthe tree to expose

the fruiting bodies, which are characteristically found below the litter

layer. Conks found in the cavities of old hollow heartrotted stumps

(especially fir) are larger — sometimes up to 10 inches wide — and tend

to have a pale orange cast to the pore surface.

Symptoms of this disease may also be found by exposing the roots

and root crown and examining the inner bark. Indications of F. annosus infection in pine are: (a) the bark separates easily from the wood;

(b) the separated surfaces are a light brown to buff and the surface of

the wood is streaked with darker brown lines (fig. 6-2); and (c) the

surface of the inner bark has numerous small silver to white flecks.

These symptoms may be difficult to see when the roots are wet in the

spring. In addition, small white to buff mycelial pads or out-growths

145
111Í

^

^^^^p

' IP W7

j 1

1 ^^1

11

1 '^

J

¡I V \; '-S.

i

mK^k^

K-700269

Figure 6-1. Fruiting bodies ofFomes ofinosi/s. (Left): A small bracket-like conk

formed on the root crown just below the duff. Note the buff

upper surface and white lower surface.

F-700270

(Right): a larger amorphous-type of conk typical of those found

inside stumps. Note the pale orange color of the pore surface.

F-700271

Figure 6-2. A root infected by Fames annosus showing the tan streaking of outer

wood surface and the silver pockets of fungus growth on the inner surface of

the bark. The white pocket rot characteristic ofF. annosus rot is shown in the

piece of wood.

146
are sometimes found between the outer bark scales or on the bark

surface. Infected roots are often heavily infiltrated with resin, and

balls of resin are often found in the soil next to infected roots.

In fir and hemlock, mortality from the disease is infrequent. Therefore, it is seldom necessary to diagnose aF. annosus problem unless it

has been aggravated by windthrow, beetle attack, or other conditions.

The best signs are the presence of fruiting bodies in the hollow roots

and trunk and the type ofwood decay in the roots and trunk. This decay

is described in Chapter 7 on Rots.

Armillaria Root Disease

Armillaria mellea

Armillaria mellea is responsible for the root disease known as Armillaria root disease, shoestring root disease, or oak root disease of

conifer and orchard trees. Widespread throughout the tropical and

temperate regions ofthe world, it haslong been recognized as the cause

of a major root disease and as a widespread forest saprophyte. These

two roles of A. mellea have done much to cloud the picture and our

judgments of its importance.

Hosts

A. mellea has an extremely wide host range, including trees, shrubs,

and herbaceous plants. Most conifers in the West are probably at least

moderately susceptible to this fungus. Some are highly susceptible.

Distribution and Damage

A. mellea is found in mostforest areas, both conifer and hardwood. It

is a major pest on orchard crops in agricultural lands and on ornamental trees and shrubs in many cities, towns, and parks.

The fungus attacks the roots and root crown of trees of all ages,

killing the cambium and inner bark and causing a decay of both

sapwood and heartwood. Itis highly aggressive and damaging in some

young conifer plantations and ornamental plantings. In younger trees,

the pathogen advances rapidly through the inner bark to the root

collar, where it girdles and kills the tree. In older trees, this advance

through the inner bark proceeds much slower and is often blocked by

the host before the fungus reaches the root crown. In cases where

cambial advance is checked, decay of inner wood may continue to

advance. Thus in older, vigorous forest trees, A. mellea often does not

kill its host, although, as a decay organism, it often structurally

weakens the roots and predisposes the tree to windthrow. The virulence of this pathogen is greatly influenced by the environment, host

147
vigor, and the pathogens inoculum potential (food base). Available

information also indicates thatthere are races ofthis fungus that vary

in their virulence to a given host.

Disease Cycle

In general, this fungus lives as a decay organism in the roots, lower

boles, and stumps of either dead or living trees. In some cases, however, it becomes actively parasitic on living trees. Its fruiting bodies

(fig. 6-3), which are typical gill fungi (mushrooms), develop in the fall

in clusters at or near the base of infected dead or dying trees and

stumps. The mature fruiting bodies release many small spores that are

windborne to other infection sites, such as stumps or woody debris on

the forest floor. Infection of living trees by spores has not been demonstrated.

A. mellea is most commonly spread to living trees by rhizomorphs or

root contact (fig. 6-4). Rhizomorphs are specialized fungus structures

that grow out from an established food base to colonize new sites. When

these rhizomorphs, growing through the upper soil and litter layers,

contact the root or root crown of a new host, they penetrate through the

bark and attempt to establish an infection. The disease also spreads

when the roots of an uninfected tree come in contact with an old

infected root or stump and grow into the new host root.

F-700272

Figure 6-3. A cluster offruiting bodies ofArmillaria mellea. Note the light brown

color, the annulus, and the gills attached to the stalk.

148
Field Identification

Occasionally, the fungus can be identified in the field by its fi-uiting

bodies (fig. 6-3), which develop in groups around the bases of infected

trees in fall. These fruiting bodies are light brown to honey colored

mushrooms with a central stalk 3 to 10 inches long. A ring or annulus

is usually found around the stalk. The cap, 2 to 5 inches across, is honey

yellow and may be dotted with dark brown scales. The lower surface of

gills are white to pale yellow and are attached to the stalk. They are of

limited diagnostic value in many areas of the West because of their

infrequent production and their short season of appearance.

The rhizomorphs (fig. 6-4) and mycelial fans (fig. 6-5), which the

fungus produces on the host, are of greater aid in diagnosis. Rhizomorphs may be produced between the bark and the wood, on bark

surfaces below the soil line, and in the litter and soil around the roots

and root crown. They are dark brown to black flattened string-like

structures with a white central core. They may resemble small rootlets, but closer examination will show that they adhere to and penetrate directly into infected root surfaces and that they branch differently than do true rootlets.

Mycelial fans (fig. 6-5) are creamy white flat thin leathery sheets of

fungus growth which develop in the cambial area between the bark

and the wood ofan infected host. The advancing margin ofthese sheets

is fan-shaped and often veined.

F-700273

Figure 6-4. A closeup ofthe rhizomorphs ofArmillaria mellea typically found on

or under the bark of infected roots and root crowns.

149
Figure 6-5. Mycelial fans of Armillaria mellea on an incense-cedar. These

creamy white leathery sheets of fungus grow beneath the bark of infected

roots, root crowns, and lower stems.

Other characteristics used in identifying this disease are resinosis

and type of decay. Excess resin and resin flow is frequently encountered at the root crown in the bark and surrounding soil. The wood

decay caused by A. mellea is a white to yellowish stringy rot that may

be accompanied by fine black zone lines.

Black Stain Root Disease

Verticicladiella wagenerii

Hosts

This disease has been found on Jeffrey, ponderosa, knobcone,

lodgepole, pinyon, singleleaf pinyon, sugar, western white, and eastern white pines, and on Douglas-fir. All other pines tested have been

susceptible. Greenhouse studies and field observation show that white

and red firs are resistant.

Distribution and Damage

The black stain root disease caused by the fungus Verticicladiella

wagenerii is a recently reported disease of conifers. Although this

150
disease is not currently causing greatlosses in commercial forests, the

damage it has done in the non commercial pinyon forests in Mesa

Verde National Park and in southern California indicates that V.

wagenerii is potentially a dangerous pest. The disease is similar to oak

wilt and Dutch elm disease — two very damaging vascular wilt diseases of eastern hardwoods.

This disease is known to exist only in the Western United States. It

is widely but sparsely distributed in two dozen or so general infection

areas in eight western States. The largest ofthese areas is in southern

California, where several thousand acres of singleleaf pinyon pine

forests are infested.

V. wagenerii attacks trees of all ages. It infects the roots, where it

spreads throughout the sapwood of the root system, root crown, and

lower bole. This infection ofthe root system causes a visible decline in

the tree crown. Terminal growth is reduced, needles become shorter

and chlorotic, the number ofneedles produced and retained is reduced,

and finally the host dies. Trees weakened by this disease are predisposed to bark beetle attack. This fungus does not decay the root wood.

Disease Cycle

There are two distinct phases of the spread of this disease — local

spread and long distance spread. Local spread — within an existing

infection center — occurs through root contacts. Infection occurs atthe

site of root contact between an infected and healthy root. Once established in the root, the fungus colonizes the distal portion ofthe root and

grows toward the root crown. From the root crown, it colonizes the

remaining roots. Long distance spread involves the establishment of

new infection centers away from existing ones. How this occurs is not

known.

Field Identification

This disease is relatively easy to identify in the field: It produces a

distinctive sapwood stain in the roots, root crown, and sometimes the

lower bole (fig. 6-6). The stained sapwood is black to dark chocolate

brown, and often is infiltrated with resin. In cross section, the stain

tends to occur in arcs that follow annual rings (fig. 6-7) rather than in

the wedge-shaped patterns characteristic of other sapwood stains.

Blue stain, which is sometimes confused with black stain, has a

wedge-shaped pattern and a bluish gray cast.

151
^^^^^^^Pf ¡¡BÊ^L, ' J^^^^^l

mVI

^^^Hpi^^^pM^kL'^^^^l1 OM

BV^J^

HUML '* iflr " '' ' W^

1p IH''^^H

^^^^B m^jKJ Ui 1j^H Ki^, 1 F-700275

Figure 6-6. The black to dark brown stain of Verticicladiella wagenerii in the

sapwood of the root crown of a western white pine.

F-700276

Figure 6-7. A cross-section of a pinyon pine root infected with Verticicladiella

wagenerii showing how stain tends to occur in arcs which follow the growth

rings.

152
Phellinus Weirii Root Rot

Phellinus (Poria) weirii

Hosts

Phellinus (Poria) weirii occurs most frequently on Douglas-fir and

western red cedar, but also has been found on grand fir, alpine fir,

silver fir, white fir, lodgepole pine, ponderosa pine, western white pine,

western hemlock, mountain hemlock, western larch, Sitka spruce.

Engelmann spruce, and incense-cedar.

Distribution and Damage

The range ofthis root rot extends from Southwestern Canada to the

Northwestern United States.

P. weirii causes both a necrosis ofthe inner bark ofthe roots and the

root crown, and a wood decay of the roots and the lower bole. This

results in growth loss and eventually death of the infected tree.

Windthrow of infected living trees caused by excess root decay is also

common.

This is the most damaging disease to Douglas-fir in the Pacific

Northwest. Itis responsible for an estimated annual loss of 115 million

cubic feet of timber. Available evidence suggests that root disease

centers probably contribute materially to maintaining populations of

Douglas-fir bark beetles between outbreak years.

Disease Cycle

P. weirii is a native inhabitant of many forest stands in the Pacific

Northwest. Initial infection of the current stand of trees starts when

their roots contact P. weirii-miesteà stumps and roots of the previous

stand. The fungus spreads to the surfaces of new roots and penetrates

directly through the bark to the living tissues. Once in the root, the

fungus may develop in the heartwood or sapwood. Spread within a

stand occurs through root contacts between infected and healthy trees.

The fungus does not grow through the soil for any distance. The fungus

forms fruiting bodies, which produce basidiospores, but their role is

unknown. No asexual spores are formed.

Field Identification

Above-ground symptoms of Poria weirii infection are chlorosis, a

reduction in growth, a gradual thinning ofthe crown, and frequently a

crop of distress cones. Live trees with advance root-decay are frequently windthrown.

Incipient decay in the roots and lower bole appears as a red-brown

153
F-700277

Figure 6-8. The buff colored pore surface of the fruiting body of Phellinus

(Poria) weirii.

stain frequently in the outer heartwood. As decay proceeds, the wood

softens, small pits appear, and the annual rings separate to form the

typical yellow laminated rot. Brown mycelium often can be found

between the sheets of decayed wood.

Fruiting bodies, which are infrequent, are found on upturned roots

and on the underside of decayed logs (fig. 6-8). They appear as light

buff-colored crusts with a white margin. The exposed surface of the

fruiting body is covered with many small, uniform-sized regular pores.

As they age, these fruiting bodies turn dark brown.

Minor Root Diseases

Polyporous schweinitzii, the velvet top fungus, commonly causes a

root and butt rot ofconifers. It has, however, been found causing a root

disease of young plantation conifers which on occasion resulted in

154
rather high mortality. The decay of the roots of older trees by this

fungus often predisposes the host to windthrow. See Chapter 7 on

Decays for a description of the velvet top fungus and the decay it

causes.

Phytophthora cinnamomi causes a root disease ofmany tree species,

including conifers. P. cinnamomi is limited by environmental factors;

it requires soils which are warm and moist — two conditions that do

not occur simultaneously in most Western forest lands. Because of

these limitations, P. cinnamomi is usually found in the irrigated

warmer soils of the Sierra Nevada foothills and southern California.

Forest nurseries, Christmas tree farms, parks, and other sites with

summer irrigation are the areas in which P. cinnamomi is most often

found.

Other species oíPhytophthora also produce conifer root diseases. P.

lateralis causes a very destructive root disease of Port Offord cedar in

coastal Oregon. Phytophthora spp., in general, infect and killthe host's

roots. They grow from the roots up through the root crown and into the

lower stems, where they kill the inner bark and cause a browning of

the new sapwood.

Macrophomina phaseoli, which is responsible for charcoal root disease oftree seedlings in forest nurseries, is occasionally found causing

a root disease ofolder planted trees. Itis limited to very warm sites and

is most often detected during periods of moisture stress. The disease

can be identified by the presence of numerous small, spherical, black,

fungus bodies (microsclerotia) in the inner bark and on the xylem

surface of infected roots.

Selected References

Bega, R. V., and R. S. Smith, Jr.

1966. Distribution ofFomes annosus in the natural forests of California. Plant Dis.

Rep. 50:832-836.

Boyce, J. S.

Forest Pathology, Chapter VI — Root Disease. McGraw-Hill Book Co., New York.

Childs, T. W.

1963. Poria weirii root rot. Phytopathology 53:1124-1127.

Driver, C. H., and J. H. Ginns, Jr.

1968. Practical control of Fomes annosus in intensive forest management. Univ.

Wash. College of Forest Diseases, Contrib. 5. 8 p.

Hodges, C. S.

1969. Modes of infection and spread ofFomes annosus. Ann. Rev. Phytopathol. 7:247-

266.

Hodges, C. S., and E. Jorgensen.

1967. Fomes annosus root rot in important forest insect and diseases of mutual

concern to Canada, the United States, and Mexico. A. G. Davidson and R. M.

Prentice, eds. Dep. For. and Rural Develop. Publ. 1180, Canada.

Leaphart, C. C.

1963. Armillaria root rot. Forest Pest Leafl. 78.

O'Reilly, H. J.

1963. Armillaria root rot. Univ. Calif. Agrie. Exp. Stn. Circ. 525 p.

Peace, T. R.

1962. Pathology of trees and shrubs. Oxford Clarendon Press, 723 p.

155
Raabe, D. R.

1962. Host list of the root rot fungus Armi/Zaria mellea. Hilgardia 33:25-88.

Smith, R. S., Jr.

1967. Verticicladiella root disease of pines. Phytopathology 57:935-938

Thomas, H. E.

1934. Studies onArmillaria mellea (Vahl) Quel., infection, parasitism and host resistance. J. Agrie. Res. 48:187-218.

Wagener, W. W., and Marion S. Cave

1946. Pine killing by the root fungus,Fomes annosus in California. J. Forest. 44:47-54

Wagener, W. W., and J. L. Mielke

1961. A staining fungus root disease of ponderosa, Jeffrey, and pinyon pines. Plant

Dis. Rep. 45:831-835.

Wallis, G. W., and G. Reynolds

1965. The initiation and spread oí Poria weirii root rot of Douglas-fir. Can. J. Bot.

43:1-9.

156
7. ROTS

by

ROBERT F. SCHARPP=

Heart rots are caused by fungi that attack and rot (decay) the

nonliving heartwood in the central core of a tree. The living outer

cylinder of wood commonly called sapwood is usually free of attack.

About a dozen different fungus species are considered major heart

rot organisms of conifers along the Pacific Coast. A few of these fungi

are host specific — they attack only a single tree species. Others rot

heartwood of nearly every major conifer and even some hardwoods.

Many heart rot organisms decay only heartwood of living trees,

whereas others also decay heartwood and sapwood of dead trees, deteriorate wood in use, and decompose slash and organic matter in soil.

Heart rots are considered one of the most serious forest disease

problems in the Western United States. Collectively, they are responsible for the loss of millions of board feet of lumber each year. Oldgrowth stands are particularly heavily attacked by heart rot fungi, but

even second-growth stands suffer heavy losses in certain instances.

Rots not only render timber unmerchantable, but reduce the quality of

the wood thatis used. Rot fungi also predispose treesto windthrow and

breakage. This not only causes additional loss of timber, but also

constitutes a hazard in recreational and high-use areas.

As a rule, heart rotfungi do not penetrate sound trees, but require an

opening into the heartwood through which to invade. Any opening into

the heartwood or exposure of dead sapwood next to heartwood is a

potential site for heart rotfungi to become established. Wounds caused

by fire or human activities are common points of entry by these fungi

and may increase the incidence of heart rots in trees. The elimination

of all wounds is, however, not possible. Certain animals, particularly

rodents, birds, and insects, wound trees. Also, wounds associated with

weather, such as lightning, wind, snow, ice, excessive heat and cold,

provide entrance courts for heart rot fungi. But these types of wounds

are considered less important than those caused by human activity

and by fire.

Certain natural openings in trees also provide a means of entrance

* Plant Pathologist, Pacific Southwest Forest and Range Experiment Station, Forest

Service, U.S. Department of Agriculture, Berkeley, Calif.

157
for heart rot organisms. Among these are branch stubs, open knots,

and dead branches. A few heart rot fungi penetrate through living

branches. Some heart rot fungi, particularly the "butt rot" organisms,

may enterthe tree through the roots or through basal fire scars. Fungi,

such SisFomes annosus and Polyporus schweinitzii, are root parasites

as well as heart rot fungi and kill roots before invading the heartwood.

Butt rot organisms also enter the heartwood through roots killed or

injured by other means.

Several systems have been devised to classify the heart rots conveniently. But, for the most part, only three of these are useful for field

identification. One system is based on the type of rot produced; the

second, on the characteristics of the fungus fruiting body; and the

third, on the location of the rot within the tree.

The first system recognizes two general types ofrots, the brown rots

and the white rots. Brown rots develop as a result of the selective

utilization of carbohydrates (primarily cellulose) by the fungus, leaving behind the brownish lignin component ofwood. Brown rotted wood

usually is dry and fragile and tends to crumble readily or break into

various sized cubes. Most brown rots form a solid column of rot, but

some appear in pockets, such as those caused hyPolyporus amarus and

Poria sequoiae. A few brown rotfungi produce a stringy, brown rotthat

in some cases is similar to that produced by certain white rot fungi.

The white rots are produced by fungi that attack both the carbohydrate and lignin components ofwood. They may be further divided into

(1) pocket rots, (2) white stringy rots, (3) yellow stringy rots, and (4)

others, depending on their appearance and texture.

For some species, the type ofrot is a distinctive characteristic, as for

example, the pocket rot caused hy Polyporus amarus. In other cases,

however, the type of rot produced by a given species is not distinctive

and only suggests the fungus responsible.

The second classification system used to identify heart rot fungi in

the field is based on the fruiting body, more commonly known as a

"conk" or "sporophore." These spore-producing bodies vary in form

from fleshy, typically mushroom-shaped structures to woody "brackets" found on trees. Color, texture, and the nature ofthe spore producing surface are other examples of characteristics used to identify the

fruiting bodies ofthese heart rot fungi. Itis usually possible to identify

the heart rot species by observing the characteristics of the fruiting

body and the type and location of decay associated with it.

The third classification system is based on the location of the rot in

trees. Some fungi cause primarily root and butt rots; others cause

trunk rot; and others attack roots, butts, and trunks. This system is

used merely as a convenient method of classifying the heart rot fungi

based on their general location within the tree. It is used along with

other systems to help determine which rot fungi are involved.

Problems arise in trying to identify a specific heart rot fungus. Often

heart rots occur without the presence of fruiting bodies. And, often

more than one type of rot is present in a tree. The "early" stage of

decay, known as incipient rot, is not easily recognized and may be

confused with "wetwood," stain, or other heartwood discoloration.

Recent studies have shown that for many heart rot conditions in trees,

158
a succession or community of wood-invading organisms is necessary.

Bacteria as well as wood rotting fungi and otherfungi that do not decay

wood may be involved. Therefore, in trying to determine the type of

decay and the organism(s) responsible for the rot, use the characteristics ofboth the rot and the fruiting body in helping to decide on the rot

organisms involved. More than one rot organism may be associated

with a particular heart rot condition. Use of all the features available

in examining treesfor heart rot will increase the observers' chances for

correct identification.

Some of the Important Rots of Conifers

of the Pacific Coast

Trunk Rots

1. Brown Trunk rot —Forties officinalis

2. Brown crumbly rot — F. pinícola

3. Red ring rot — F. pini

4. Juniper pocket rot — F. juniperinus

5. Brown top rot — F, roseus

6. Brown stringy rot — Echinodontium tinctorium

7. Red rot — Polyporus anceps

8. Pocket dry rot — P. amarus

9. Pouch fungus — P. volvatus

10. Oyster mushroom — Pleurotus ostreatus

Root and Butt Rots

1. Femes root and butt rot —Fomes annosus

2. Brown cubical rot — Polyporus basilarus

3. Red-brown butt rot — P. schweinitzii

4. Brown cubical rot — P. sulphureus

5. Red root and butt rot — P. tomenotsus

6. Laminated root rot — Phellinus (Poria) weirii

7. Shoestring root rot — Armillaria mellea

8. Lacquer fungus — Ganoderma oregonense

Butt and/or Trunk Rots

1. Brown cubical rot — Poria sequoiae

2. White ring rot — P. albipellucida

3. Mottled rot —Pholiota adiposa

4. Yellow pitted rot — Hericium abietis

5. Scaly cap fungus —Lentinus lepideus

159
Descriptive Key

A^ On incense-cedar, juniper or redwood B

B^ On incense-cedar C

C^ A brown pocket dry rot (Pocket dry rot) Polyporus

amarus

C^ A white stringy root or butt rot (Fomes root and butt

rot) Fomes annosus

B2 On Juniper (Juniper pocket rot) Fomes juniperinus

B^ On coast redwood D

D^ Advanced decay, a brown pocket rot

(Brown cubical rot) Poria sequoiae

D2 Advanced decay, a white ring rot (White ring rot)

Poria albipellucida

A^ On other conifer hosts E

E^ Advanced decay brown, cubically cracked (Brown rot)....F

F^ Fruiting body large, white, mushroom shaped; upper

surface scaly, lower surface with gills (Scaly cap fungus) Lentinus lepideus

F^ Fruiting body not as above; lower surface with pores,

not gills G

G^ Fruiting bodies on the soil or on the base of the

tree H

H^ Fruiting body brown to greenish and

velvet-like in texture when fresh; often

clustered. Typically a root and butt rot

(Reá-hro'wnhuiÍYOÍ)Polyporusschweinitzii

H2 Large, fleshy annual, bracket-type, fruiting

bodies; bright sulphur yellow when fresh,

chalky white when old (Brown cubical rot)

Polyporus sulphureus

G^ Fruiting bodies occurring anywhere on the tree

J

J^ Perennial woody chalky white fruiting

bodies, very bitter to taste (Brown trunk rot)

Fomes officinalis

J2 Large rubbery to woody bracket-type fruiting

bodies; dark upper surface, reddish margin,

buff to cream colored pore surface (Brown

crumbly rot) Fomes pinícola

E^ Advanced decay not distinctly brown and cubically cracked;

usually white to light brown, in pockets, spongy or stringy

(White rots)... K

K^ Advanced decay as small white pockets in the

heartwood (occasionally sapwood of trees) L

L^ Pockets white, fibrous M

M^ Fruiting bodies on tree trunk often clustered, light to dark brown, bracket-type.

160
woody, with pores on lower surface (Red

ring rot) Fomes pini

M^ Fruiting bodies produced atthe base oftrees

or on soil, brown to light tan; hairy zonate

upper surface. Root and butt rot (Red root

and butt rot) Polyporus tomentosus

K^ Advanced decay white to yellowish, stringy or spongy,

pockets not conspicuous N

N^ Rot confined to roots and butt of tree. Fine,

black zone lines present in rotted wood.

White mycelial fans often present between

bark and wood and black rhizomorphs often

associated with the rot. Fruiting bodies

mushroom-shaped with gills on the lower

surface, honey-colored and occurring in

clusters from the decayed wood or soil atthe

base of the tree (Shoestring root rot) AmiU

laria mellea

N^ Rot usually always associated with roots

and butt of the tree. No zone lines or

rhizomorphs present. Fruiting bodies irregular in shape and varying in size from

small button-shaped structures to large

conspicuous brackets (Fomes root and butt

rot) Fomes annosus

L^ Pockets of rot empty; fruiting bodies creamywhite, coral-like (Yellow pitted rot) Hericium

abietis

K^ Advanced decay yellow to yellowish-brown O

O^ Wood in advanced decay separating into distinct

laminations along growth rings. Root and butt

rot (laminated root and butt rot) Phellinus weirii

O^ Distinct separation of wood along growth rings

not obvious P

Pi Yellow to yellow-brown stringy rot in

heartwood, tree trunk usually hollow.

Fruiting bodies large, black, bracket-type,

woody with a toothed undersurface and a

brick-red interior (Brown stringy rot)

Echinodontium tinctorium

P2 Decayed heartwood having a dark colored,

streaked or mottled appearance. No

rhizomorphs. Yellowish brown mycelial

strands present in the advanced decay.

Fruiting bodies mushroom-shaped, yellow,

with gills on lower surface and often arising

in clusters from the decayed wood or base of

the tree (Mottled rot) Fholiota adiposa

161
Brown Rots

Quinine Fungus — Brown Trunk Rot

Fomes officinalis

Hosts

Douglas-fir, pines, western larch, spruce, hemlock, rarely true firs.

Distribution and Damage

This fiingus is known in both Europe and North America. In the

Western United States, it has traditionally been considered to be an

important trunk rot of old-growth conifers. It is found most commonly

on Douglas-fir and larch, but attacks pines and some other species as

well. The incidence of this organism in second-growth forests, however, is not well known. It is believed that wounds, broken tops, and

branch stubs are common entrance points for the fungus. It may also

occasionally enter fire scars.

Field Identification

Rot — The rot caused by this fungus is almost indistinguishable

from the cubical brown rot caused hyPolyporus sulphureus. Unlike the

sulphur fungus, however, the rot only occasionally occurs in the butt

and is mainly found in the trunk and upper bole of the tree. Another

characteristic that distinguishes it from P. sulphureus is the bitter

taste of fresh mycelial felts present in the decayed wood. Thus, it has

been named "Quinine fungus."

Fruiting body — The fruiting bodies do not commonly occur on trees

attacked by the fungus. When present, they are pendant, woody, perennial, and often hoof-shaped structures that may range in size from

several inchesto more than 2 feetlong (fig. 7-1). The fruiting bodies are

white and leathery when young, but chalky and crumbly when old.

Like the mycelial felts, they also have a bitter taste.

162
F.700278

Figure 7-1. Woody, perennial fruiting body ofFames officinalis growing from the

base of a Douglas-fir stump.

163
Red Belt Fungus — Brown Crumbly Rot

Fomes pinícola

Hosts

Pines, firs, Douglas-fir, western hemlock, western larch, spruce,

western red cedar.

Distribution and Damage

This ftingus is one of the most common wood rot organisms in

western coniferous forests. Although itis mainly a decomposer ofdead

and down timber, it has also been known to cause heart rot in living

trees. The mode of entrance for this fungus is mainly through wounds

and broken or dead tops. Decay in living true firs from the red belt

fungus has also been found associated with the large open bole swellings caused by dwarf mistletoe.

Field Identification

Rot — The rot caused by this fungus is somewhat lighter than that

caused by some of the other crumbly brown rots. It may vary in color

from a yellow brown to slightly reddish. Cubical cracking is common

(fig. 7-2) and the shrinkage cracks are usually filled with white fungus

felts.

Fruiting body — Fruiting bodies are commonly found associated

with this rot (fig. 7-3). They are leathery to woody, perennial brackettype structures that, when young, appear as a leathery round white

fungus mass. As they develop, the upper surface turns dark gray to

black; whereas, the fresh lower pore surface remains white to creamy

in color. A conspicuous reddish margin develops between the two

surfaces; thus, the name "red belt fungus." Fruiting bodies of this

organism are among the most common ones seen on dead and fallen

coniferous trees. They generally range from about 4 to 18 inches

across.

164
F-5250^1

Figure 7-2. Characteristic, advanced, brown

rot caused by Fames

pinícola.

F-700279

Figure 7-3. Commonly observed fruiting body of the red belt fungus. Fames

pinicala, growing on a white fir log.

165
Scaly Cap Fungus

Lentinus lepideus

Hosts

Pines.

Distribution and Damage

This fungus is of worldwide distribution and in the Western United

States is a heart-rot organism. It also decays dead and down wood. As a

heart-rot organism, it does not appear to be limited to any particular

part ofthe tree. It has been observed rotting roots as well as heartwood

in the upper portion of the bole. It is common on pines in the high

elevations and on the eastern slope of the Sierra Nevada.

Field Identification

Rot — Advanced decay is dark brown, cubically cracked, almost

black where exposed. Thin, white mycelial fans occur in shrinkage

cracks. Rotten wood is said to have an anise or turpentine odor.

Fruiting body — Of all of the important brown heart rots of the

Pacific Coast, this is the only one caused by a typical, mushroom-type

fungus(fig. 7-4). The fruiting bodies are often large and range from 2 to

12 inches in diameter, are borne on a stalk, are leathery, and have a

white gilled lower surface. The top of the cap is composed of a whitish

surface overlaid with darker tan to brown scales; thus, the name,

"scaly cap." The dry fruiting bodies become quite hard and brittle.

F-525022

Figure 7-4. Mushroom-like fruiting body of the "scaly cap fungus," Lentinus

lepideus.

166
Pocket Dry Rot

Polyporus Amarus

Hosts

Incense-cedar.

Distribution and Damage

Polyporus amarus causes a common heart rot of incense-cedar

throughoutits natural range. More than a third ofthe volume, or about

5 billion board feet, of the merchantable incense-cedar is cull from rot

caused by this fungus. Pocket dry rot is most common in trees on good

growing sites and less common in trees on marginal sites near the

eastern limit of incense-cedar. Trees less than 150 years old are relatively free of rot, whereas in trees 200 years or older, the incidence of

decay increases rapidly. Fire scars, large open knots, and branch stubs

are the most common entry point for the fungus.

Field Identification

Rot —Polyporus amarus produces a characteristic brown pocket rot

not unlike the brown cubical rot od redwood (fig. 7-5). The initial stage

ofthe rot appears as a brownish discoloration of the heartwood. Eventually elongated pockets, usually several times longer than wide,

develop. The wood within the pockets is broken down into a dry, dark

brown, crumbly residue, separated by cross and longitudinal shrinkage cracks. Although pockets may coalesce with one another, the

margin between rotten wood and sound wood remains sharp. The

pockets never become so numerous that the entire central cylinder of

heartwood is decayed, as happens when brown cubical rot decays

redwood.

F-525023

Figure 7-5. Pocket dry rot

of incense-cedar caused

by Polyporus amarus.

167
K-7ÜO280

Figure 7-6. Fruiting body oí Polyporus amarus on the trunk of an old-growth

incense-cedar.

Fruiting body — The fruiting bodies furnish certain evidence of

extensive pocket dry rot. Usually one fruiting body is produced (rarely

two) and then only on trees with extensive rot (fig. 7-6). When fresh

they are soft, moist bracket-type structures with a yellow undersurface

and tan top. They have a smooth margin and often appear somewhat

hoof-shaped. Old fruiting bodies darken in color and become dry and

firm. They appear annually — and only in late summer and fall. Eaten

by insects, they may be destroyed in a short time. As a result, they are

only occasionally seen on trees with pocket dry rot.

"Velvet Top" Fungus — Red-Brown Butt Rot

Polyporus schweinitzii

Hosts

Douglas-fir, pines, true firs, larch, spruce, incense-cedar, western

red cedar, and rarely hemlock.

Distribution and Damage

The velvet top fungus occurs throughout the world where conifers

are native or grown. Hardwoods are seldom attacked. This fungus is

168
most common on Douglas-fir along the Pacific Coast. The fungus

generally enters trees through basal fire scars and is known mainly as

a butt rot organism, but also is a root parasite. Although it has been

reported as a trunk rot, it almost always is confined to the root system

and lower 8 to 10 feet of the tree bole. Timber losses are not precisely

known, but are considered high both because the valuable buttlogs are

badly decayed and because infected trees are predisposed to

windthrow.

Field Identification

Rot — Incipient decay from this fungus is not easy to recognize.

Advanced decay is a typical brown rot. Rotted wood characteristically

appears reddish-brown and tends to form large cubes and cracks across

the grain. Thin, white resinous fungus mats may appear in the shrinkage cracks. Dry decayed wood may be easily crumbled into a fine

powder.

Fruiting body — The fruiting bodies of this fungus may appear

either on the soil around the base of an infected tree or from the butt of

the tree itself. Depending on the site of development, they may be

either brackets or mushroom-like in structure. Brackets tend to form

on exposed wood, whereas the stalked mushroom-type fruiting bodies

usually appear on the soil (fig. 7-7). The fruiting bodies have a soft

velvety top that, when fresh, is usually reddish-brown in color and

encircled by a yellowish margin. Concentric lines are also present on

the top surface. The lower spore producing pore surface varies from

dark green to light brown. The fruiting bodies are produced annually

and, when old, dry up, darken, and closely resemble cow dung.

Tf n n E' F-700281

tigure 7-7. Fruiting body ofPolyporusschweinitzii on the soil at the base ofan infected Douglas-fír.

169
Sulphur Fungus — Brown Cubical Rot

Polyporus sulphureus

Hosts

Douglas-fir, true firs, pines, hemlock, spruce, larch and western red

cedar.

Distribution and Damage

The sulphur fungus most commonly is found on hardwoods in other

regions, but in the West does cause considerable rot in some conifers,

particularly true firs. The organism generally enters through basal

fire scars and wounds on conifers and primarily causes a butt rot.

Although the sulphur fungus is not considered a major slash decay

organism, it is often seen on stumps, logs, and dead trees.

Field Identification

Rot — Advanced decay is similar to that caused by red-brown butt

rot. Decayed wood is dark to reddish brown, cubically cracked, and is

easily crumbled. Usually, white mycelial felts are present in the

shrinkage cracks. These may be very thin or range up to one-quarter

inch thick. Felts may also be a foot or so wide and several feet long.

Fruiting body - Clustered, annual, shelf-like fruiting bodies are

typical ofthis organism (fig. 7-8). When fresh, they are soft and fleshy,

with a bright yellow-orange upper surface and a bright sulphur yellow

lower pore surface. Old fruiting bodies are hard, brittle, and chalky

white.

F-700282

Figure 7-8. Fresh Fruiting body of Polyporus

sulphureus emerging

from the stump of an old

red fir.

170
Brown Cubical Rot

Poria Sequoiae

Hosts

Coast redwood.

Distribution and Damage

This rot is distributed throughout the natural range of coast redwood. Among the two major rots in redwood, it is the most common and

causes the most cull. About 10 billion board feet of cull in redwood is

attributed to heart rots of which more than 75 percent is caused by

Poria sequoiae. Surveys have shown that by far the greatest amount of

rot occurs in old-growth redwood, particularly in trees with basal fire

scars or broken tops. Second-growth redwood may suffer some loss

fromP. sequoiae, but fortunately the rotis nottransferred from stumps

to stump sprouts.

Field Identification

Rot — Initial stages ofrot range from a dark brown stain ofthe inner

heartwood to scattered pockets of brown charcoal-like "dry rot" which

shrinks and cracks into cubes (fig. 7-9). In the advanced stages, the

pockets of rot are so numerous that nearly the entire central and, to

some degree, the outer cylinder of heartwood is rotted.

Figure 7-9. Pockets of brown rot in redwood caused by Poria sequoiae.

F-700283

171
FruitingBody—The spore-producing structure is unlike the typical

bracket or mushroom-shaped fruiting bodies produced by most of the

rot fungi. Instead, the entire fruiting body develops as a thin, white

mantle or crust composed offungus strands and a spore-producing pore

surface. The fruiting bodies often are no more than 2 inches long and 1

inch wide and most frequently are found in fire scars, bark crevices,

and on the ends of down logs.

White Rots

Shoestring Fungus Shoestring Root Rot

Honey Mushroom (Soft Spongy Rot)

Armillaria mellea

Hosts

Most conifer species in the west.

Distribution and Damage

Armillaria mellea is more commonly considered a root disease fungus rather than a rot organism. Therefore, details of the fungus, its

distribution, occurrence, and structure of the fruiting body are described in Chapter 6.

Field Identification

Rot — Advanced rot caused by the shoestring fungus is white or light

yellow, soft and spongy, often stringy, marked by numerous black zone

lines and confined to the roots and/or butt ofthe tree. Often the rot is

accompanied by white mycelial fans (fig. 6-5) under the bark. Black

rhizomorphs (shoestring-like fungal strands) usually also are present

(fig. 6-4).

Fruiting Body — For a detailed description of the fruiting body, see

Chapter 6 on root diseases.

172
Indian Paint Fungus — Brown Stringy Rot

Echinodontium tinctorium

Hosts

True firs, hemlock, rarely Douglas-fir and spruce.

Distribution and Damage

This decay ftingus is distributed throughout the Western United

States on firs and hemlock and is considered to be the most serious

heart rot organism on these tree species. In some old-growth stands,

losses of 25 to 50 percent or more of the gross board foot volume have

been recorded. The Indian paintfungus may enter treesthrough trunk

scars, dead tops, and other wounds, but most infections probably enter

through branches. As a result, the rot is most common in the midtrunk region, butit may also extend into the butt or down from the top.

Trees up to 40 years old are essentially free of brown stringy rot

because in trees this young, limited heartwood has developed.

Field Identification

Rot — The name brown stringy rot is confusing in that the Indian

paint fungus attacks both lignin and cellulose components of

heartwood. The fungus is, therefore, a white rot organism.

The first noticeable evidence of rot is a yellowish to golden tan

discoloration of the heartwood. The invaded wood is also somewhat

softer than uninvaded heartwood at this stage. Next, the heartwood

turns pale reddish-brown, and rust-red streaks appear following the

grain. Wood with advanced rot becomes soft, stringy, and may vary

from yellow-brown to tan to rust-red. Brown to rust-red streaks or

areas are also present. Rotted wood often tends to separate along the

annual rings. In the very late stages of decay, the stringy mass of

rotted wood may disintegrate, leaving a hollow in the tree (fig. 7-10).

Fruiting Body — The fruiting bodies ofthe Indian paint fungus are

quite distinctive and receive their name because certain Indian tribes

ground the brick red interior into a powder for use as a red pigment

(fig. 7-11). The woody, perennial, hoof-shaped bodies range from a few

inches to more than a foot in width, and are quite common on infected

trees. The upper surface is dull black and rough (fig. 7-12), whereasthe

undersurface is usually level but set with hard, coarse teeth or spines.

The toothed surface is gray when fresh but turns black when old.

Fruiting bodies develop on the bole, usually on the underside of

branches or branch stubs. Heart-rot often extends about 16 feet above

and 16 feet below a fruiting body. Trees with one or more fruiting

bodies usually have extensive decay.

173
Figure 7-10. Brown, stringy rot ofwhite fir caused byEchinodontium tinctorium.

F-700284

Figure 7-11. Reddish interior of the fruiting body oíEchinodontium tinctorium.

174
F-525025

Figure 7-12. Black,

woody fruiting body of

Echinodontium tinctorium on white fir.

Fomes Root and Butt Rot

Fomes Annosus

Hosts

Occurs on most conifer species in the West.

Distribution and Damage

This organism occurs throughout the coniferous forests in the West.

Although it is primarily known as a root disease organism, it also acts

as an important butt and trunk rot on some species. F. annosus is

particularly common on true firs in California and on hemlock in the

Pacific Northwest and is considered a damaging butt rot organism in

old-growth stands. The fungus commonly enters through fire scars,

dead or broken tops, and other wounds. The rot column, although

usually in the butt and root systems, may occur anywhere in the

heartwood. The fungus spreads from one tree to another by root grafting or from infected roots contacting non-infected roots.

Field Identifîcation

Rot — Incipient decay from Fomes root and butt rot is not readily

recognized. Discoloration may or may not be present, and heartwood

remains firm and hard. In the advanced stage, the decayed wood is

white, spongy, and may contain elongated white pockets (fig. 6-2). No

175
rhizomorphs are formed as they are with a similar decay caused by

Armillaria mellea. .. ,.

FruitingBody - The fruiting bodies of F. annosus vary considerably

in shape and size. Their shape is indefinite. They may appear as small,

round, button-shaped structures growing under or protruding from the

bark at the base of trees or as rather conspicuous irregularly shaped

bracket-like bodies on the butts and roots of trees. Often they occur

deep within hollow stumps of true firs and may develop to become

almost a foot in width. When fresh, they are dark brown to gray on the

upper surface and creamy white to pale orange on the lower pore

surface (fig. 6-1).

Juniper Pocket Rot

Fomes Juniperinus

Hosts

Western junipers.

Distribution and Damage

This fungus is found on western juniper throughout its natural

range in the Western United States. The extent of decay in juniper

stands throughout the Far West is not known. However, studies m

stands of western juniper in Modoc County, Calif, have shown that

about 40 percent of the trees 12 inches and greater in basal diameter

were infected with juniper.pocket rot. Consequently, utilization of

western juniper for pencil stock is uneconomical.

Field Identification

Rot—Fomesjuniperinus may occur as either a butt or a trunk rot,

depending on the location of the entrance court for the fungus. Incipient decay first appears as a yellowish discoloration. Wood with

advanced decay contains numerous large pockets, lined with

yellowish-white fibers, and fungus mats and strands. These pockets

often join to form fairly long tubes of stringy rot.

Fruiting Body — Fruiting bodies (fig. 7-13) are fairly common m the

Far West and when present indicate extensive heart rot. The upper

surface of the woody hoof-shaped fruiting bodies is dark brown to

nearly black and usually contains numerous deep cracks. The lower

pore surface is light brown, and the interior is reddish-brown.

176
F-700285

Figure 7-13. Woody, perennial, fruiting body of

Famesjuniperinum.

Red Ring Rot or White Pocket Rot

Fomes Pini

Hosts

Douglas-fir, pines, true firs, larch, spruce, hemlock, western red

cedar, and rarely incense-cedar.

Distribution and Damage

Red ring rot occurs throughout the coniferous forests of the world,

and in the West is considered to be the single most damaging heart rot

organism. Coastal Douglas-fir is the tree most commonly infected.

Other coniferous trees species along the coast as well as conifers in the

mountains of the West are also attacked. Millions of board feet of

timber a year are lost or degraded as a result of rot caused by this

organism.

Red ring rot attacks second-growth as well as old-growth trees.

Nearly all infections become established through living and dead

branches or branch stubs. Open wounds rarely act as entrance points

177
for this fungus. Thus, red ring rot may be one ofthe most serious heart

rot problems in future forest stands.

Field Identification

Rot — Incipient decay appears as a discoloration ofthe heartwood. In

pines, a pink to reddish color is present. Pronounced reddish-purple to

olive discoloration appears in Douglas-fir.

Wood with advanced decay is often reddish and contains sharply

margined small spindle-shaped pockets containing white, soft, fibers

(fig. 7-14). Mostly heartwood is affected, but sapwood is also invaded.

Dark colored zone lines may also be observed in decayed wood. In cross

section, the pockets may be evenly distributed throughout the wood

(soft pines) or appear in rings (Douglas-fir, hard pines). The ring-like

attack of heartwood is the result ofthe fungus attacking certain groups

of annual rings and more readily destroying early wood rather than

late wood.

F-.52.'i026

Figure 7-14. White pocket

rot of Douglas-fir caused by Fomes pini.

Fruiting Body — The perennial, woody fruiting bodies are the best

indicators of decay. But they vary considerably in size, shape, and

texture. One should be aware ofthis variability in identifying F. pini.

Fruiting bodies may range from about 2 to 10 inches in width and be

thin and bracket-like or thick and hoof-shaped (fig. 7-15). The lower

pore surface is usually a rich, rusty brown, the pores ranging from

nearly round to maze-like. The upper surface is darker brown or dark

gray, and is usually marked with several concentric furrows.

Often a velvety margin separates the two surfaces. On living trees,

the fruiting bodies nearly always arise from knots or branch stubs.

Sometimes only punky knots bearing the inner portion of the fruiting

body remain on the tree. These punky knots may subsequently be

overgrown with new wood, becoming swollen knots that are the only

symptom of decay.

178
F-525027

Figure 7-15. Typical

bracket-like fruiting

bodies of Fomes pini on

Douglas-fir.

Coral Fungus — Yellow Pitted Rot

Hericium abietis

Hosts

True firs, Engelmann spruce, hemlock.

Distribution and Damage

This fungus is an important decay organism oftrue firs in the Pacific

Northwest, particularly in the mountains of eastern Oregon and

Washington. It also occurs in the Rocky Mountains and in northern

California but is rare elsewhere along the Pacific Coast. The rot may

develop in the butt or upper portions ofliving trees, or in stumps, fallen

trees, and snags. The coral fungus probably enters living trees through

wounds and dead branches.

Field Identification

Rot — The advanced stage ofthis rot is similar to that caused by red

ring rot butthe elongate pockets formed are empty of noticeable white

fibers. The color of the wood does not change noticeably.

Fruiting Body — The fruiting bodies are soft, creamy white, corallike, and characterized mainly by the presence of numerous "spines" or

"teeth" which produce spores (fig. 7-16). The fruiting bodies are shortlived and not readily recognized when shriveled and dry.

179
F-700286

Figure 7-16. Fruiting

body oíHericium abietis,

the cause of yellow pitted rot.

Laminated Root Rot

Phellinus (Poria) Weirii

Hosts

Douglas-fir and western red cedar are the conifer species most frequently damaged. For additional hosts attacked, see Chapter 6 on root

disease.

Distribution and Damage

This fungus occurs throughout the Pacific Northwest. Although

Phellinus weirii is known mainly as a root disease organism, it does

decay tree roots and butts. Heavy losses occur not only from tree

mortality but also from blowdown as a result of root decay.

Field Identification

Rot — Early decay by this organism appears as a red-brown stain in

the outer heartwood. As the decay develops the wood softens, small pits

appear and the annual rings separate to form the characteristic laminated rot (fig. 7-17). At this stage the rotted wood is yellow to buff

colored with dark brown mycelial felts often found between the laminations and in shrinkage cracks.

Fruiting body — For a description ofthe fruiting body, see Chapter 6

on root disease.

180
Figure 7-17. Laminated rot of Douglas-fir caused by Phellinus weirii.

F-700287

Yellow Cap Fungus — Mottled Rot

Pholiota adiposa

Hosts

Red fir, white fir, grand fir.

Distribution and Damage

This fungus is found on both hardwoods and conifers in the United

States, but in the West it is primarily a problem on true firs (Abies). In

California and parts of Oregon, it is considered to be a major heart rot

organism in old-growth true fir stands. Young, unwounded trees are

seldom infected. Fire scars, other basal wounds, and dwarf mistletoe

bole cankers are the sites of infection for mottled rot. As a result, most

ofthe rot occurs in the lower bole, but has been found to extend 50 to 60

feet above the ground.

Field Identification

Rot — The fungus produces a mottled appearance in the wood in the

advanced stage of rot. Early decay appears as a light cream to yellowish discoloration in heartwood. As the rot progresses the areas

181
darken and brownish streaks develop, forming small widely scattered

holes or pockets resembling insect burrows.

Yellowish-brown fungus strands fill the holes and shrinkage cracks.

These strands may be best observed ifthe wood is split along the grain.

Older trees with decay of long standing usually have a hollow butt.

Fruiting body — Other than shoestring root rot, mottled rot is the

only major white rot of conifers caused by a gill bearing, mushroomlike fungus (fig. 7-18). The yellow cap fungus fruits in the fall, usually

after the first rains. The fresh fruiting structures consist of a yellowish

central stalk and a cap that varies from yellow to yellowish brown on

the upper surface and yellow on the lower gill surface. The tops of the

caps are sticky and slightly scaly. The mushrooms often occur in

clusters and may appear on the trunk or from the base ofinfected trees.

They are also commonly seen on stumps, down trees, and on the ends of

cull logs. Old fruiting bodies dry and shrivel and turn black. They often

persist for a year or more in this condition.

F-700288

Figure 7-18. Mushroom-like fruiting bodies of Pholiota adiposa on white fir.

182
False Velvet Top Fungus —

Red Root and Butt Rot

Polyporus tomentosus

Hosts

Pines, spruce, larch, hemlock, Douglas-fir, true firs.

Distribution and Damage

The fungus occurs on conifers throughout the West but is most

commonly found on hosts in the Pacific Northwest and the Rocky

Mountains. It appears to be less often found in the drier, arid regions of

the Pacific Southwest.

Field Identification

Rot — The advanced stage ofthis rot closely resembles that caused

by the red ring rot fungus. Many narrow pockets filled with white

fibers occur in the heartwood. Affected wood usually becomes stained

dark reddish-brown to tan but retains its structural integrity as in the

case with wood affected by red ring rot. This fungus causes primarily a

root and butt rot and is seldom found more than a few feet above the

ground in tree trunks.

Fruiting body — The fruiting bodies of this fungus resemble those

produced by the velvettop fungus but are much smaller (usually about

2 to 3 inches in diameter) and lighter in color. The upper surface is

brown to tan, zonate and slightly hairy in texture. The lower surface

contains pores and is usually light brown. The fruiting bodies almost

always occur on the ground in small clusters where they arise from

diseased roots. Occasionally they occur at the base of a tree.

White Ring Rot

Poria Albipellucida

Hosts

Coast redwood, western red cedar.

Distribution and Damage

Except for brown cubical rot, white ring rot is the only other rot of

any consequence associated with native stands of redwood. Whereas

brown cubical rot is fairly evenly distributed throughout the natural

range of redwood, white ring rot increases in severity from south to

north. For instance, less than 10 percent of old-growth trees in Sonoma

183
County, Calif, were attacked by this fungus, but in Del Norte County,

Calif, nearly 75 percent of old-growth trees contained white ring rot.

Western red cedar along the Pacific Coast is also often attacked by this

fungus, and it is believed that the incidence of rot in redwood is

correlated with the amount ofwestern red cedar in the stand. Entrance

courts for this fungus are wounds, mainly fire scars and dead or broken

tops. Like brown cubical rot, white ring rot does not move into stump

sprouts from rotted stumps.

Field Identification

Rot — Incipient rot looks like normal heartwood except for a dark

brown discoloration. As the decay progresses, the heartwood softens

and turns lighter brown. Wood with advanced decay is soft and

cinnamon-brown and often separates along the annual rings. Minute,

elongated pits occur in the wood surfaces between these separations.

These pitted surfaces may become somewhat hairy with whitish wood

fibers as the rot continues (fig. 7-19). Wood in the final stage of decay

appears as a stringy, fibrous mass.

Fruiting body — Fruiting bodies of this organism have never been

found associated with decayed wood ofredwood. The fungus was identified solely from laboratory cultures obtained from rotted wood. Fruiting bodies are found on western red cedar slash in the Pacific Northwest.

F-525028

Figure 7-19. White ring

'^ rot (Poria albipellucida)

along the checked surface of a redwood log.

184
Heart Rots of Minor Importance

Fomes roseus, the cause of brown top rot in Douglas-fir, true fir,

spruce, and some pines, occurs occasionally in northwestern California

and in the Pacific Northwest. As the name implies, the rot often occurs

in the uppermost part ofthe bole. This fungus is most common on dead

trees and wood in service, but can cause a brown cubical rot in the

heartwood of Douglas-fir. Wood in the advanced stage of decay is soft,

yellow to yellowish-brown in color and breaks into irregular shaped

cubes. The fruiting bodies are bracket-like, woody, have a pinkish rose

colored lower pore surface and a rough black zoned upper surface (fig.

7-20).

Polyporus basilaris causes a brown cubical pocket rot in the butts of

Monterey cypress (Cupressus macrocarpa). It occurs in natural stands

in California and nearly everywhere Monterey cypress has been

planted along the Pacific Coast. Trees 65 years and older are highly

defective, 80 percent and more with rot. Trees less than 26 years old

are practically rot-free. One to several fruiting bodies may be present

and these usually arise from branch stubs. Entrance of the fungus is

thought to be through dead branches. Fruiting bodies are usually

small (1 to 2 inches across) and leathery, bracket-like and vary from

grayish brown to black in color.

Ganoderma oregonense, commonly called the lacquer fungus because of the shiny, reddish, lacquer-like upper surface of the fruiting

body, primarily decays dead timber, but occasionally causes a soft,

spongy white rot of living trees (fig. 7-21). The distinctive annual,

Figure 7-20. Fruiting body of Fomes roseus, the brown top rot fungus.

F-700289

185
F-700290

Figure 7-21. White spongy rot of red fir caused by Ganoderma oregonense.

F-700291

Figure 7-22. Large distinctive fruiting body of Ganoderma oregonense.

bracket-type fruiting bodies have a cream colored lower pore surface

and are produced in the fall and often grow to be a foot or more across

(fig. 7-22). The lacquer fungus attacks Douglas-fir, spruce, hemlock,

186
F-700292

Figure 7-23. Small, leathery fruiting bodies of the pouch fungus Polyporus volvatus, on a white fir log.

and some pines along the Pacific Coast, and true firs throughout their

natural range in California. Red fir is the most commonly attacked fir

species.

Pleurotus ostreatus, the oyster mushroom, occasionally causes a

white, flaky rot of the sapwood and heartwood of conifers in the West,

but is most common on hardwoods. Infection usually occurs through

open wounds and the fungus has been observed invading true firs at

the site of old open dwarf mistletoe bole infections. The white, fleshy,

shelf-like mushrooms are smooth on the upper surface with gills on the

lower surface, and often arise in clusters. The gills on the lowersurface

characteristically extend down along the stalk.

Polyporus anceps or red rot often occurs in ponderosa, Jeffrey, and

Coulter pines in southern California. It is rare elsewhere along the

Pacific Coast, but is common and damaging on pines in the Southwest

and Rocky Mountains. This fungus acts as both a decomposer of dead

wood and as a heart rot. In living trees, the fungus frequently enters

through broken tops causing considerable rot ofthe upper boles. It can

also enter through bole wounds and large dead limbs. Advanced decay

is a white pocket rot—not unlike that caused by the red ring rot

organism Fomes pini. Wood infected by red rot does not remain firm,

but tends to crumble and disintegrate when handled. Fruiting bodies

are rarely found on living trees, but occur mostly on the underside of

down logs or on slash. They appear as white to light brown colored

crusts of irregular shape on down trunks and branches. Detection of

the rot in living trees is difficult.

Polyporus volvatus, the pouch fungus, is not a heart-rotting fungus

but causes a greyish white rot of the sapwood of most conifers in the

187
West. It is only included because it occurs so frequently in the forest

and is often mistaken for a heart rot organism. For the most part, it

only occurs on dead trees and snags within 1 to 2 years after the tree's

death. But, it has been observed on dead portions ofliving trees and on

Douglas-fir weakened by bark beetle infestation. The small, leathery

white fruiting bodies are produced in abundance within a short time

after the tree is attacked (fig. 7-23). One of their distinguishing features is that the lower spore bearing surface is covered by a fungus

sheath except for a single hole through which insects enter, feed, and

then exit and move on to spread the fungus. This unique adaptation to

spread by beetles and other insects accounts for the rapidity with

which it invades dead and dying trees.

Selected References

Bailey, H. E.

1941. The biology of Polyporus basilarus. Torrey Bot. Club Bull. 68:112-120.

Boyce, John Shaw

1961. Forest pathology. Ed. 3, 572 p., illus. McGraw-Hill Book Company, Inc., New

York

Etheridge, D. E., H. M. Craig, and S. H. Farris

1972. Infection of western hemlock by the indian paint fungus via living branches.

Environment Canada, For. Ser. Bimonthly Res. Note 28:3-4

Fritz, Emanual, and Lee Bonar

1931. The brown heart rot of California redwood. J. For. 29(3):368-380.

Hadfield, James S., and David W. Johnson

1977. Laminated root rot. A guide for reducing and preventing losses in Oregon and

Washington Forests. Forest Service, U.S. Dep. Agrie. Pacific Northwest Reg.

Bull.

Kimmey, James W.

1950. Cull factors for forest tree species in northwestern California. U.S. Forest Serv.,

Calif. Forest and Range Exp. Stn., Surv. Rel. 7, 30 p., illus.

Kimmey, James W.

1958. The heart rots of redwood. U.S. Dep. Agrie, Forest Pest Leafl. 25, 4 p., illus.

Kimmey, James W.

1965. Rust-red stringy rot. U.S. Dep. Agrie, Forest Pest Leafl. 93, 8 p., illus.

Kimmey, James W., and H. H. Bynum

1961. Heartrots ofred and white firs. U.S. Dep. Agrie, Forest Pest Leafl. 52,4 p., illus.

Kimmey, James W., and Paul C. Lightle

1955. Fungi associated with cull in redwood. Forest Sei., 1(2):104-110.

Meinecke, E. P.

1914. Forest tree diseases common in California and Nevada. A manual for field use.

U.S. Forest Serv. Manual, 67 p., illus.

Partridge, Arthur D. and Daniel L. Miller

1974. Major decays ofwood in the Inland Northwest. Univ. Natural Resources series,

No. 3, 125 p. illus. Idaho Research Foundation Inc., Moscow, Idaho.

Wagener, W. W.

1929. Lentinus lepideus Fr.: A cause of heart rot of living trees. Phytopathology

19:705-712.

Wagener, Willis W., and Robert V. Bega

1958. Heart rots of incense-cedar. U.S. Dep. Agrie, Forest Pest Leafl. 30, 7 p. illus.

Wagener, Willis W., and Ross W. Davidson

1954. Heart rots in living trees. Bot. Rev. 20:61-134.

188
GLOSSARY

Aerial Shoot — Stem-like portion of dwarfmistletoe outside the host

bark whose primary function is to reproduce.

Alternate Host — One or the other oftwo unlike hosts of a heteroecious fungus, i.e., some rust fungi.

Annual Canker — A canker that occurs only during one period of

time ofthe year or season, usually caused by adverse environmental

conditions or organisms.

Apothecium(ia) — A cup or saucerlike sexual fruiting body that

produces ascospores.

Aseocarp — A sexual or perfect fruiting body of the Ascomycete,

which produces its spores within an ascus.

Ascospores — A spore produced in an ascus (see ascus).

Ascus(i) — A sac-like cell of the perfect stage of the Ascomycetes in

which ascospores—usually eight—are produced.

Asexual Stage — A stage in the life cycle of a fungus in which spores

are produced without a previous sexual fusion; also called imperfect

stage.

Autoecious Life Cycle — A fungus that completes its life cycle on one

host, e.g., some rust fungi.

Basal Shoot Scar — See basal cup.

Basal Cup — The cup-like remnant on the bark of an infection that

remains visible long after the disintegration of an aerial shoot.

Biotic Factors — The living organisms in an ecosystem and their

relationship with other organisms.

Bicolored — Two colors (relating to the fruit ofdwarfmistletoe which

are bicolored).

Blight — A loose term for a disease causing rapid death or dieback.

Bole — A tree stem once it has grown to substantial thickness—

roughly capable of yielding saw timber; similar to trunk stem.

Bracket Type Fungus — Laterally attached, shelf-like fungus fruiting bodies occurring on trees; mostly of the wood decay type.

Broom — See witches-broom.

Brown Rot — A light to dark brown decay of wood that is friable and

rectangularly checked in the advanced stage, caused by fungi that

attack mainly the cellulose and associated carbohydrates; residue is

chiefly lignin.

Burl — A hard, woody, abnormal outgrowth in a tree, more or less

rounded in form. Usually resulting from the entwined growth of a

cluster of adventitious buds—sometimes from an old wound.

Butt Rot — A rot characateristically conñned to the butt or lower

trunk of a tree.

189
Canker — A definite, relatively localized, necrotic lesion primarily of

the bark and cambium.

Cellulose — A complex carbohydrate occurring in most all plant

material. A major component of wood.

Colonize — To establish an infection within a host or part of a host.

Concolorous — Of the same color as.

Confluent — Running into one another, merging.

Conk — The large, often bracket-like fruiting bodies of wood destroying fungi (Basidiomycetes).

Cubical Cracking — The characteristic of woods in an advanced

stage of brown rot to break up into distinct cubes.

Cull Factor — A calculated percentage ofthe amount ofmerchantable

wood lost from a tree as a result of decay or other defect.

Decay — The decomposition of wood by fungi

Decline — The gradual reduction in health and vigor as a tree is in the

process of dying slowly.

Decomposer — Organism that physically and chemically breaks

down dead organisms into simpler compounds and elements.

Defect — Any imperfection in a tree that reduces the volume ofsound

wood or lowers its durability, strength, or utility value.

Dieback — The progressive dying, from the tip downward, of twigs,

branches, or tops.

Discoloration — A change in hue or color.

Disease — The alteration of the function or the form of a plant from

normal.

Disease Cycle — The chain ofeventsin the development ofa disease.

Dry Rot — A decay of the brown rot type, caused by specialized fungi

able to conduct moisture from an available source and extend their

attack to wood previously too dry to decay.

Duff— The litter and partially decomposed litter on the forest floor.

Early Wood — The less dense, larger-celled portion of an annual

growth ring formed during the early part of the growing season.

Elliptical — Shaped like an ellipse, oblong with regularly rounded

ends.

Endemic — A disease which is at its usual normal balanced level

within a region to which it is indigenous. Not epidemic or rampant.

Entrance Courts — The point of invasion of a disease organism into

its host.

Environment — The sum total of all the biotic (living) and abiotic

(non-living) factors affecting an individual's surroundings.

Epidemic Disease — A disease that occurs periodically, widely, and

rapidly, and reaches injurious levels.

Exúdate — Matter which oozes out or is secreted out.

Facultative Parasite — An organism normally saprophytic but capable of changing to a parasitic life.

Fade — To change foliage color slightly in the early process of dying.

Usually changes occur from a dark green toward a lighter graygreen.

Flagging — Displaying dead brown branches known as flags among

the rest of the living crown.

190
Flags — Conspicuous dead branches with foliage remaining as a

result of rapid killing by adverse abiotic conditions or disease

agents.

Form — A description below the subspecies or variety level but which

is still distinguished on morphological grounds.

Fruiting Body — Any of a number of kinds ofreproductive structures

which produces spores.

Fungus — One of a group oforganisms considered by some authorities

to be lower plants which lack chlorophyll.

Fungus Mat — Dense, leathery mass of fungus mycelium often

formed in decayed wood by certain wood rotting fungi.

Fusiform Swelling — A swelling on a host branch or stem that is

typically widest near the middle and tapers toward each end. Syn.

spindle-shaped swelling.

Galls (Burls) — Pronounced swellings on woody plants caused by

certain insects and disease organisms.

Germinate — The beginning of growth by a seed or spore.

Gill Fungi — Those fungi whose fruiting bodies are mushroom shaped

and which bear gill-like plates on the underside of the cap.

Gills — Blade-like, spore-bearing structures on the lower surface of

the fruiting bodies of certain fungi.

Globose — Spherical.

Hard Pine — Any pines of the subgenus Pinus (Diploxylon).

Heart Rot — A decay characteristically confined to the heartwood.

Heartwood — The inner layers of wood that in the growing tree have

ceased to contain living cells and in which the reserve materials

(e.g., starch) have been removed or converted into more durable

substances.

Heteroeeious Life Cycle — A fungus that must pass different stages

of its life cycle on unlike hosts, i.e., some rust fungi.

Hoof-Shaped — Appearing like a hoof; e.g., the bracket-type fruiting

bodies of certain wood decay fungi that are flat on the bottom and

rounded on the sides and top.

Host — The plant on or in which a pathogen exists.

Host Range — All the hosts that a particular pathogen attacks.

Host Specific — Disease organismsthat attack only certain species of

hosts.

Hysterothecium(ia) — A specialized fruiting body of needle cast

fungi which is usually elongate, covered, and opens at maturity by a

long slit.

Immune — Unable to be attacked by an organism.

Incidence — Rate of occurrence.

Incipient Rot — The early stage of wood decay in which the wood is

invaded and may show discoloration but is not otherwise visibly

altered.

Incipient Decay — See incipient rot.

Infection — The act of a pathogen establishing itself on or within a

host.

Infection Site — The area in which the pathogen ñrst established

itself on or in the host.

191
Infest — To be present in such numbers within an area as to be a

source of danger.

Inner Bark — The active layer of tissues (phloem and cambium)

between the wood (xylem) and the suberized bark.

Inoculum — The spores or tissues of a pathogen which infect a host or

crop.

Inoculum Potential — The general mass of the pathogen (including

spores and tissues) and its relative virulence which are available for

infection.

Late Wood — The denser, smaller celled portion of an annual growth

ring formed during the latter part of the growing season.

Life Cycle — The stage or series ofstages in fungi between one spore

form and the development of the same spore again.

Lignin — A substance impregnating the cell wall in woody tissue;

along with cellulose, it is the principal component of wood.

Litter — See duff.

Microsclerotium — A tiny (microscopic) sclerotium.

Mortality — The loss from death.

Mycelial Fans — Similar in structure to mycelial felts but fanshaped.

Mycelial Felt — A mass offungusfilamentsthat are arranged in a flat

plane and resemble a thin felt-like paper or cloth.

Mycelial Pads — Small mats of compacted mycelia that are often

formed by fungi on or in the host.

Mycelial Strands — A mass or group offungus filaments that appear

as visible strands to the naked eye.

Mycelium(ia) — A mass of hyphae that forms the vegetative

filamentous body of a fungus.

Necrosis — Death of plant cells usually resulting in darkening ofthe

tissue.

Necrotic Spot (Area) — A dead area on a living plant. Often caused

by biotic and abiotic diseases.

Needle Cast — A disease of conifers in which the needles are killed

and shortly thereafter fall from the tree.

Needle Complement — The normal or usual number ofneedlesthat a

conifer of a particular species will bear.

Needle Spotting — A needle disease characterized by isolated circular or elongate lesions.

Obligate Parasite — A parasite incapable of existing independent of

live host tissue.

Parasite — An organism living on and nourished by another living

organism.

Parasitic — Living on or in another organism and deriving nourishment therefrom.

Pathogen — An organism which causes a disease.

Pendant — Hanging, pendulous.

Perennial — Continuing growth from year to year.

Perennial Canker — The recurrent yearly killing back and healing

over of the bark and cambial tissue of woody plants by certain

disease organisms.

192
Perithecium(ia) — A closed, flask-like sexual fruiting body containing asci and ascospores produced by certain Ascomycetes.

Pocket Rot — A characteristic pattern ofrot caused by certain fungi.

The rot occurs in distinct, scattered pockets within the heartwood of

a tree rather than in a distinct column.

Pore Surface — The surface of the fruiting body of certain wood

decaying fungi (polyporaceae) that consists of small openings or

pores.

Predispose — To make susceptible

Predisposition — The effect of one or more environmental or biotic

factors which makes a plant vulnerable to attack by a pathogen.

Primary Host — See principal host.

Principal Host — The main host for a particular disease organism.

This term is used particularly with regard to the main host species

infected by dwarf mistletoes.

Pustule — Blisters caused by certain disease fungi, often maturing

into the spore-bearing structures of the disease organism.

Pycnidium(ia) — An asexual type of fruiting body, typically flasklike, that produces asexual spores or conidia.

Resinosis — The unnatural and profuse flow or accumulation ofresin

from conifers injured or attacked by insects and disease.

Resistant — Able to withstand without serious injury attack by an

organism or damage by a non-living agency but not immune from

such attacks.

Rhizomorphs — A specialized thread- or cord-like structure made up

of parallel hyphae with a protective covering.

Root Crown — The upper-most portion ofthe root system where the

major roots join together at the base of the stem.

Root Grafting — The union of the roots of two different trees as a

result of physical contact.

Rot — The physical and chemical deterioration of wood caused by

wood rotting fungi.

Rot Column — The vertical column of rotted wood within the

heartwood of a tree invaded by heart rot fungi.

Saprophyte — An organism using dead organic material as food.

Sapwood — The outer layers of wood which in the growing tree

contain living cells and reserve materials.

Secondary Host — A host species attacked less commonly than the

principal host.

Sexual Stage — The stage in the life cycle of a fungus in which spores

are formed after sexual fusion. Syn. perfect stage.

Scale-Like Leaves — A scale-like structure thatis morphologically a

leaf often reduced in size (as bud scale, various bracts).

Sclerotium — A firm, frequently rounded, often black mass ofhyphae

often acting as a resting body.

Shoot Scar — See basal cup.

Soft Pine — Any pines of the subgenus Strobus (Haploxylon).

Spindle-Shaped Swelling — See fusiform swelling.

Spores — The final reproductive structure of the fungi and other

lower plants.

Sporulation — The act of producing and liberating spores.

193
stain — The dark brown to black discolorations of wood caused by the

presence of certain fungi; not to be confused with wetwood.

Susceptible — Unable to withstand attack by an organism or damage

by a non-living agency without serious injury.

Symptoms — The noticeable evidence of disturbances in the normal

development and life processes of the host plant.

Teeth — See toothed surface.

Toothed Surface — The tooth-like texture of the spore-bearing surface ofcertain wood decay fungi, e.g., indian paint fungus. See teeth.

Upward Spread — See vertical intensification.

Vertical Intensification — The spread upward of dwarf mistletoe

within a tree. Syn. upward spread.

Virulent — Vigorously pathogenic.

Wetwood — A discolored, water-soaked condition ofthe heartwood of

some conifers presumably caused by bacterial fermentation. Often

associated with distinctive odor, gas production, and an exudation

called slime flux.

White Rot — Decay caused by fungi that attack all chief constituents

of wood and leave a whitish or light colored residue. Wood is often

fibrous or spongy in texture.

Witches-Broom — An abnormally profuse, dense mass of host

branches and foliage. Syn. broom.

Wilt — The collapse of a plant or part of a plant due to a loss of cell

turgidity.

Xerophytic — Adapted to dry conditions.

Xylem — The woody tissue oif the stem, branches, and roots.

Zone Lines — Narrow, dark brown or black lines in a decayed wood

caused by fungi.

194
INDEX OF HOST PLANTS,

WITH SCIENTIFIC EQUIVALENTS

Host Tree Page

Arborvitae, Thuja orientalis L 33

Apple, Pj/rz/s ssp .................110

Aspen, Populas tremuloides Michx .,....,.llb

Aster, Aster ssp 1 i^

Bastard toad flax, Comandra umbellata Nutt .107, 110

Blueberry, Vaccinium ssp ' n^

Chickweed, Stellaria spp 3^95 j^Qg ^Qrj

Comandra, Comandra spp 92 107' lOs' 110

Cottonwood, Popí/Z¿/s spp ' ' ' nß

Cypress Family, Cupressaceac 24, 86, 118, 124

Arizona cypress, Cupressus arizonica Greene '. '....2l' 119

Gowan cypress, Cupressus goveniana Gord '.119

Italian cypress, Cupressus sempervirens L ..!...'...21

Modoc Cypress, Cupressus bakeri Jeps .............^........119

Monterey cypress, Cupressus macrocarpa Hartw. ......86, 185

^ouglas-ñr, Pseudotsuga menziesii (Mirh.) Franco 7 9 11

14, 17, 20, 21, 30, 32, 33, 39, 49, 50, 54, 77, 80, 81, 83, 88,'115,116

136,144,150,153,162,164,168,170,172,173,175,177,180 183

185, 186, 188 , , ,

Big-cone Douglas-fir, Pseudotsuga macrocarpa

(Vasey) Mayr... 10, 30, 50^ 1^5

i:<igwort, bcrophularia spp 93 IQ2

Firs, A6/es spp 20 76 77

80, 115, 136, 139, 144, 162,164,'l68;*l'70rÏ727l*737l75, 177 179

183, 185, 186, 187 , , ,

Alpine ñr, Abies lasiocarpa (Hook.) Nutt 49, 85, 153

Bristlecone ñr, Abies bracteata D. Don ...........'. ....48

Grand ñr, Abies grandis (Dougl.) Lindl 32 33 48

49, 85, 105, 132, 153, 181 ' '

Lowland grand ñr, Abies grandis (Dougl.) Lindl 17, 85, 132

Noble ñr, Abies procera Rehd '49' 132

Pacific silver ñr, Abies amabilis (Dougl.) Forbes...........49, 85,' 153

^eá¥\Y, Abies magnifica A. MMYV 30 33 38

49, 85, 105, 106, 132, 181 ' '

Subalpine ñr, Abies lasiocarpa (Hook.) Nutt 32, 105, 106

White iiY, Abies concolor (Gord. & Glend.) Lindl .'...7, 9, H

195
13,14,20,21,25,30,33,35,36,39,49,85,87,105,106,107,125,132

153, 181

Goldenrod, Solidago spp 114

Hawthorn, Crataegus spp HO, 117

One-seed hawthorn, Crataegus monogyna Jacq 118

Hemlock, Tsuga spp : 139, 144

162, 168, 170, 172, 173, 175, 177, 179, 183, 186

Mountain hemlock, Tsuga mertensiana (Bong.) Carr 139, 153, 162

Western hemlock, Tsuga heterophylla (Raf.) Sarg 32, 139,

153, 162, 164

Incense-cedar, Lièocedrz/s decurrens Torr 14, 17, 18

21, 28, 30, 39, 40, 54, 75, 93,110, 111, 112,127,153,167,168,172

175, 177

Indian paint-brushes, Casi/Zfeja spp 98, 99, 102

Juniper, Juniperus spp 23, 33

54, 86, 116, 117, 124, 126, 172, 176

Alligator juniper, Juniperus deppeana Steud 14

California juniper, Ji/mperas caZi/bm/ca Carr 19, 117, 118

One-seed juniper, Jz/mperz/s monosperma (Engelm.) Sarg 118

Rocky Mountain juniper, Juniperus scopulorum Sarg 118

Savin, Juniperus sabina L 118

Utah juniper, Jí/72¿perí/s osteosperma (Torr.) Little 117, 118

Western juniper, Jí¿^¿perz/s occidentalis Hook 32, 117, 118

Larch, LaWx spp 168, 170, 172, 175

Western larch, Larix occidentalis Nutt 32, 138, 153

162, 164, 177, 183

Mountain Sish, Fraxinus dipetala Hook & Arn 110

Pear, Pyrits communis L 110, 116, 117

Fines, Pinus spp 57, 76, 80, 83

84, 139, 144, 162, 164, 166, 168, 170, 172, 175, 177, 183, 185, 186

Aleppo pine, Pinus halepensis Miller 21

Apache pine, Pinus engelmannii Carr 102

Bishop pine, Pmi/s muricata D. Don 16, 57

113, 138

Bristlecone pine, Pinus aristatu Engelm 94

Coulter pine, Pinus coulteri D. Don 10, 11, 21, 27

30, 33, 63, 98, 114, 135, 138, 187

Digger pine, P¿nz/s sabiriana Dougl 21, 25, 63

138

Eastern white pine, Pinus strobus L 94, 150

Foxtail pine, Pinus balfouriana Grev. & Half 94, 135

Italian stone pine, Pinus pinea L 21

Jeffrey pine, Pinusjeffreyi Grev. & Balf 7, 10, 11

13,14,21,22,24,25,29,30,55,67,76,98,99,100,102,107,113,114

135, 150, 187

Jeffrey-Coulter hybrid, P. jeffreyi x coulteri 30

Knobcone pine, Pinus attenuata Lemm 21, 30, 55

57, 63, 64, 66, 107, 135, 138, 150

Lodgepole pine, Pmi¿s contorta Dougl.. 14, 21, 22

32,33, 55,57,63,64, 66,61,72,98,99,104,107,108,113,114,150

153

196
Limber pine, Pinus flexilis James 14, 17 19

59, 62, 94, 135

Mexican white pine, Pinus flexilis var. reflexa Engelm 94

Monterey x knobcone hybrid, Pinus radiata x attenuata 12, 30, 57

Monterey pine, Pinus radiata D. Don 10, 11, 19

21, 26, 30, 32, 57, 63, 66, 104, 113, 114, 138

Montezuma pine, Pinus montezumae Lamb 102

Pinyon pine, Pinus edulis Engelm 55, 62 92

112, 150

Ponderosa pine, Pm¿¿5 po^d^rosa Laws 10, 11, 12

14,18,20, 21,22, 29,30, 31,32,34,35, 37,39, 55, 57, 63, 64, 67, 72

98, 99, 102, 108, 109, 113, 133, 135, 150, 153, 187

Rocky Mountain ponderosa pine, Pinus ponderosa

\3X. Ponderosa Laws 10 11 14

30, 32

Scots pine, Pinus sylvestris L 107

Singleleaf pinyon pine, Pinus monophylla Torr. & Engelm 21

61, 136, 150

Sugar pine, Pmz/s lambertiana Dougl 14, 21, 25

30, 33, 39, 59, 62, 68, 72, 94, 95, 97, 134, 150

Torrey pine, Pinus torreyana Parry 21, 25

Western white pine, Pinus monticola Dougl 11, 18, 20

21, 30, 32, 33, 57, 59, 62, 63, 72, 94, 95, 97, 134, 150, 153

White pines 92, 93

Whitebark pine, Pinus albicaulis Engelm 59 62

63, 94, 135

Poplars, Popí/Zí/s spp 115, 116

Port-Orford-cedar, Chamaecyparts lawsoniana (A. Murr.) Pari....155

Quince, Cydonia spp 110, 117

Redwood, Seq'z/oia spp 18 19 24

30, 33

Coast redwood. Sequoia sempervirens (D. Don) Endl 19

24, 77, 89, 171, 183

Giant redwood, Sequoia gigantea (Lindl.) Decne 2, 18

30, 33, 75

Giant sequoia. Sequoia gigantea (Lindl.) Decne 2, 18

30, 33, 75

Sierra redwood, Sequoia gigantea (Lindl.) Decne 2, 18

30,33,75

Rihes,Ribes spp 92, 94, 95

96, 98, 112

Serviceberry, Amelanchier spp 110, 116

117, 118, 119

Saskatoon seryiceherry/amelanchier alnifolia (Nutt.) Nutt 117

Western serviceberry, Amelanchier florida Lindl 116, 117

Spruces, Picm spp 20, 136, 162

164, 168, 170, 172, 173, 175, 177, 183, 185, 186

Blue spruce. Picea pungens Engelm 33

Brewer spruce, P¿cea breweriana S. Wats 48

197
Engelmann spruce, Picea engelmannii Parry 32, 48

153, 179

Sitka spruce. Picea sitchensis (Bong.) Carr 48, 153

White spruce, Picea glauca (Moench) Voss 33

Sweetfern, Comptonia spp 113, 114

Sweetgale, Myrica spp 113, 114

Tarweeds, Hemizonia spp 114

Thuja, Thuga spp 54

Western red cedar, Thuja plicata Donn 16, 32, 33

153, 164, 168, 170, 172, 175, 177, 180, 183

Western yew, Taxus brevifolia Nutt 32

Willow, Salix spp 115

198
INDEX TO DISEASE CAUSAL AGENTS

Disease Page

Amelanchier rust 110, 116, 117, 119

Aminotriazole damage 10

Ammonia gas 7^ 9^ 33

Annosus root disease 142, 144

Arceuthobium spp 121 127

Arceuthobium abietinum 77 132

(f. sp. concoloris) 77^ 132

(f. sp. magnificae) 77' 132

Arceuthobium americanum I33

Arceuthobium californicum , I34

Arceuthobium campylopodum 135, 138

Arceuthobium. cyanocarpum I35

Arceuthobium divaricatum 136

Arceuthobium douglasii 136

Arceuthobium. laricis 138

Arceuthobium, occidentale 138

Arceuthobium tsugense I39

Armillaria mellea 2 142 147

172, 176

Armillaria root disease 7 147

172, 176

Asphalting 39^ 40

Aster rust 7^ 39^ 114

Atropellis canker 72, 76

Atropellis pinicola 72, 76

Atropellis pinipila 72

Avalanche damage 6, 35

Bacterial gall of Douglas-fir '.88

Banded needle necrosis 10, 23, 31

Bark injuries 6 7 14

20, 21, 33, 34, 38

Bark scorch 7^ 20

Bear damage 7

Beaver girdle 6

Bifusella linearis 59

Bifusella pini gl

199
Bifusella saccata

62

Black stain root disease142, 150

Bole injuries6, 7, 13

33, 35, 36, 39

Borate damage (herbicide)7, 9, 23

Botryosphaeria canker of giant sequoia75

Botryosphaeria ribis2, 75

Branch injuries10, 16, 30

31, 37, 38

Bristlecone fir needle cast48

Brown crumbly rot164

Brown cubical rot162, 170

Brown cubical rot of Cypress185

Brown cubical rot of redwood167, 171

Brown felt blight46

Brown top rot185

Brown stringy rot173

Brown trunk rot162

Bud injuries8, 10, 14

19, 20, 33, 38

Bullet damage7

Cable girdle7

Cedar leaf blight54

Cenangium canker76

Cenangium ferruginosum76

Charcoal root disease155

Chlorate damage (herbicide)7, 9, 26

Chloride salt accumulation7, 9, 10

11, 23, 24

Chlorine7,9,33

Chlorosis9, 10, 11

23, 26, 31, 32

Chlorotic mottle9, 10, 29

30,33

Chronic ozone injury9

Coleosporium asterum114

Coleosporium madiae114

Coleosporium solidaginis114

Commandra blister rust92, 93, 100

107, 109, 110

Contact herbicides9, 26

Coral fungus,179

Coryneum sp77

Coryneum cardinale86

Cronartium coleosporioides98

Cronartium comandrae92, 107

109, 110

Cronartium comptoniae113

Cronartium occidentale92, 98, 112, 113

Cronartium ribicola91, 92, 94

95, 96, 97, 98, 113

200
Curved needles

9, 10, 21

Cypress canker86

Cypress-juniper mistletoe124

Cytospora abietis77, 133

Cytospora canker of true firs77, 133

Dasyscyphus canker of conifers80

Dasyscyphus sp80

Davisomycella lacrimiformis66

Davisomycella limitata66

Davisomycella medusa61

Davisomycella montana66

Defoliator insects9

De-icing salt7, 8, 23

Dense mistletoe124

Dermea canker of Douglas-fir81, 83

Dermea pseudotsugae81, 83

Diaporthe lokoyae81

Didymascella thujina54

Digger pine dwarf mistletoe138

Diplodia canker83, 85

Diplodia pinea83, 85

Dothichiza canker of pines84

Dothichiza pithyophila84

Dothistroma pini57

Douglas-fir dwarf mistletoe136

Douglas-fir needle cast50

Douglas-fir rust115

Drooping needles10, 20, 27

Drought damage6, 7,8

11, 21, 31

Dry site11, 21

Dust effects26

Dwarf mistletoe57, 128

Dwarfed26

Echinodontium tinctorium173

Elytroderma deformans55

Elytroderma disease55

Endocronartium harknessii103

Excavation damage7, 39

False velvet-top fungus183

Filamentosum rust93, 98, 100, 102

Fir blueberry rust115

Fir needle casts49

Fir willow weed rust115

Fire damage7, 8, 33

Flagform8, 24

Fomes annosus144, 158, 175

Fomes juniperinus176

Fomes officinalis162

Fomes pini177, 187

201
Fontes pinícola

164

Fomes root and butt rot144, 175

Fomes roseus185

Frost cracks7, 11, 35

Frost damage8, 9, 13, 14

Ganoderma oregonense185

Grovesiella canker85

Grovesiella (Scleroderrus) abieticola85

Gymnosporangium confusum118

Gymnosporangium cupressi118, 119

Gymnosporangium fuscum116

Gymnosporangium harknessianum116

Gymnosporangium inconspicuum117

Gymnosporangium kernianum117

Gymnosporangium libocedri110, 111, 112

Gymnosporangium multiporum118

Gymnosporangium nelsonii118

Hail damage10, 38

Hawthorn-juniper rust118

Heat canker7, 20

Hemlock dwarf mistletoe139

Hericium abieti^179

Herpotrichia nigra46

High temperature9, 19, 20

High water table6, 7, 9, 22

Honey mushroom2, 147, 172

Hormone herbicides10, 26, 27

Hydrogen chloride7, 9, 33

Hydrogen fluoride damage9, 32

Ice crystals (windblown, main stem)6, 38

Ice damage6, 35

Incense-cedar mistletoeIll, 127

Incense-cedar rust110

Inconspicuous juniper rust117

Indian paint fungus173

Juniper mistletoe126

Juniper pocket rot176

Juniper rust118

Lacquer fungus185

Laminated root rot153, 180

Larch dwarf mistletoe138

Lentinus lepideus166

Lightning damage6, 10, 34

35, 36

Limber pine dwarf mistletoe135

Lirula abietis-concoloris49

Lirula nervisequia ssp. conspicua48

Lodgepole pine dwarf mistletoe133

Lodgepole pine needle cast66

Logging damage6, 39

202
Lophodermella arcuata

59

Lophodermella cerina64

Lophodermella mórbida64

Lophodermium crassum48

Lophodermium decorum48

Lophodermium juniperi54

Lophodermium nitens62

Lophodermium piceae48

Lophodermium pinastri63

Low temperature damage6, 9, 10

11, 14, 18

Macrophomina phaseoli155

Mechanical damage6, 25, 37, 39

Medusa needle blight67

Melampsora albertensis116

Melampsorella caryophyllacearum105, 106

115, 133

Melampsora medusa115

Melampsora occidentalis115

Mottled rot181

Native limb and canker rusts98, 99

Natural scenescence10

Necrotic flecks8, 9, 12, 19

Needle drop7, 10, 16

21, 24, 27, 29 38

Needle fade6, 7,9

10,22

Needle miners8

Needle scale infestation10

Needle tipburn9, 25, 33

Needle tip dieback7, 8, 9,

10, 17, 22, 23, 24, 25, 26, 32, 33

Nelson's juniper rust118

Neopeckia coulteri46

Nitrogen deficiency9, 26

Oyster mushroom186

Ozone injury9, 29, 31, 32

Parch blight8, 17

Pear-juniper rust116

Peridermium filamentosum98, 99, 101

102, 103

Peridermium harknessii92, 103

104, 105, 119

Peridermium stalactiforme98, 99, 100

101, 102

Phacidium abietis49

Phaeocryptopus gaumanni54

Phellinus weirii142, 153, 180

Pholiota adiposa181

Phomopsis canker of Douglas-fir6, 81

Phomopsis (Diaporthe) lokoyae81

203
Phoradendron spp 121

Phoradendron bolleanum ssp. densum 124, 126

Phoradendron bolleanum ssp. pauciflorum 125

Phoradendron juniperinum ssp.juniperinum 126

Phoradendron juniperinum ssp. libocedri 127

Phosphorus deficiency 10, 26

Phytophthora cinnamomi 155

Phytophthora lateralis 155

Pinyon dwarf mistletoe 136

Pinyonrust 92, 112

Pleurotus ostreatus 187

Pocket dry rot 167

Pole blight 11, 21

Polyporus amarus 158, 167

Polyporus anceps 187

Polyporus basilarus 185

Polyporus schweinitzii 154, 158, 168

Polyporus sulphureus 162, 170

Polyporus tomentosus 183

Polyporus volvatus 187

Porcupine damage 6

Poria albipellucida 183

Poria sequoiae 158, 167, 171

Poria weirii 142, 153, 180

Poria weirii root rot 153, 180

Pouch fungus 187

Pseudomonas pseudotsugae 88

Pucciniastrum epilobii 115

Pucciniastrum goeppertianum 115

Pucciniastrum pustulatum 115

Purple discoloration 10, 18, 26

Quinine fungus 162

Rabbit damage 7

Red band needle blight 57

Red belt 7, 8, 11

14,42

Red belt fungus 164

Red brown butt rot 168

Red ring rot 177, 187

Red root and butt rot 183

Red rot 187

Redwood canker 77

Redwood gall 89

Resin bleeding 7, 11

Resin blisters 7

Rhabdocline pseudotsugae 50

Rhabdocline weirii 50

Road salt damage 7, 23, 24

Root diseases 10, 39, 142

Root injuries 22, 39, 40

Rotary snow plow damage 8, 37, 38

204
Salt spray

8, 24, 25

Scaly cap fungus166

Scirrhia pini57

Scleroderris abieticola85

Serpentine soil10, 25

Seridium (Coryneum) cardinale86

Serviceberry rust117

Shoestring fungus147, 172

Shoestring root rot2, 147, 172

Short needles10, 24, 29, 31

Silting7, 39

Singleleaf pine needle cast...61

Snow blight49

Snow damage6, 9, 19, 35, 37

Soft spongy rot172

Soil drought8, 21

Soil sterilants9, 25, 26

Spring frost8, 13

Spruce needle casts48

Squirrel damage6,7

Stalactiform rust93, 98, 99

100, 101

Stem swellings7, 39

Sugar pine dwarf mistletoe134

Sugar pine needle cast59

Sulfur dioxide9, 30

31, 32

Sulphur fungus162, 170

Sun scorch6, 8, 16

Sweetfern rust113

Swiss needle cast54

Sydowia polyspora87

Sydowia tip dieback of fir87

Tarweed rust114

Top injuries6, 11, 13

16, 20, 21, 37

True fir dwarf mistletoe132

Twig injuries8, 14, 15

17, 20, 21, 26, 33, 37, 38

Twisted needles10, 26

Twisted shoots10, 26

Uredio cupressicola118, 119

"Velvet top" fungus154, 168

Verticicladiella wagenerii150

Virgella robusta49

Western dwarf mistletoe135

Western gall rust92, 93

103, 104

Wind effects6, 8, 17

25, 38

Windthrow6, 39

205
Winterkill 8, 11, 31

Winter yellows 9, 18

White fir mistletoe 125

White pine blister rust 91, 92

93, 94

White pocket rot 177

White ring rot 183

Yellow cup fungus 181

Yellow pitted rot 179

Yellow witches-broom of fir 105, 133

^ U.S. GOVERNMENT PRINTING OFFICE: O 1979—246-760

206



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