MARKET DISEASES

OF POTATOES

AGRICULTURE HANDBOOK NO. 479

Agricultural Research Service

UNITED STATES DEPARTMENT OF AGRICULTURE
PRECAUTIONS

Pesticides used improperly can be injurious to man, animals, and plants.

Follow the directions and heed all precautions on the labels.

Store pesticides in original containers under lock and key—out of the

reach of children and animals—and away from food and feed.

Apply pesticides so that they do not endanger humans, livestock, crops,

beneficial insects, fish, and wildlife. Do not apply pesticides when there

is danger of drift, when honey bees or other pollinating insects are

visiting plants, or in ways that may contaminate water or leave illegal

residues.

Avoid prolonged inhalation of pesticide sprays or dusts; wear protective

clothing and equipment if specified on the container.

If your hands become contaminated with a pesticide, do not eat or drink

until you have washed. In case a pesticide is swallowed or gets in the eyes,

follow the first aid treatment given on the label, and get prompt medical

attention. If a pesticide is spilled on your skin or clothing, remove

clothing immediately and wash skin thoroughly.

Do not clean spray equipment or dump excess spray material near ponds,

streams, or wells. Because it is difficult to remove all traces of herbicides

from equipment, do not use the same equipment for insecticides or

fungicides that you use for herbicides.

Dispose of empty pesticide containers promptly. Have them buried at a

sanitary land-fill dump, or crush and bury them in a level, isolated place.

NOTE: Some States have restrictions on the use of certain pesticides.

Check your State and local regulations. Also, because registrations of

pesticides are under constant review by the Federal Environmental

Protection Agency, consult your county agricultural agent or State

Extension specialist to be sure the intended use is still registered.
PREFACE

This handbook is an extensive revision of and supersedes

Miscellaneous Publication 98, "Market Diseases of Fruits and

Vegetables: Potatoes," by G. B. Ramsey, the late J. S. Wiant, and

M. A. Smith. This handbook is one of a series designed to aid in the

recognition and identification of market diseases, to provide

information on factors and organisms causing the diseases, and to

give control measures for reducing economic losses caused by these

diseases during marketing.

These handbooks are intended for use by market inspectors,

research workers, shippers, receivers, carriers, and others concerned

with maintaining quality of fresh fruits and vegetables during

marketing.

Other publications in this series are—

28 Market Diseases of Tomatoes, Peppers, and Eggplants. (Rev.,

Feb. 1968.)

155 Market Diseases of Beets, Chicory, Endive, Escarole, Globe

Artichokes, Lettuce, Rhubarb, Spinach, and Sweetpotatoes.

(Apr. 1959; reprinted. May 1967.)

184 Market Diseases of Cabbage, Cauliflower, Turnips, Cucumbers, Melons, and Related Crops. (Sept. 1961.)

189 Market Diseases of Grapes and Other Small Fruits. (Reprinted, Apr. 1966.)

303 Market Diseases of Asparagus, Onions, Beans, Peas, Carrots,

Celery, and Related Vegetables. (Sept. 1966.)

376 Market Diseases of Apples, Pears, and Quinces. (Rev., May

1971.)

398 Market Diseases of Citrus and Other Subtropical Fruits. (Rev.,

May 1971.)

414 Market Diseases of Stone Fruits: Cherries, Peaches, Nectarines, Apricots, and Plums. (Rev., Dec. Í972.) 3 :

:r^
CONTENTS

Page

Bacterial diseases 2

Bacterial soft rot (slimy

soft rot) 2

Blackleg 5

Brown rot (southern bacterial wilt) 7

Red xylem and pinkeye ... 9

Ring rot 10

Fungus diseases 12

Armillaria rot 12

Black dot 13

Black SCUYÎ (Rhizoctonia) . . 14

Charcoal rot 16

Early blight (alternaria

tuber rot) 17

Fusarium tuber rots 19

Fusarium wilts 23

Gray mold rot (Botrytis) . . 25

Late blight 26

Leak 30

Phoma tuber rot (gangrene,

buttonhole rot) 31

Pink rot 33

Powdery scab 34

Scab 36

Sclerotium rot (southern

blight) 38

Silver scurf 40

Skin spot 43

Verticillium wilt 44

Wart 46

Xylaria tuber rot 47

Virus diseases 48

Corky ring spot 48

Net necrosis

(leaf roll) 49

Purple top wilt 51

Page

Spindle tuber 52

Tuber necrosis (alfalfa) .... 52

Yellow dwarf 52

Other virus diseases 53

Nematodes and their injury ... 53

Golden nematode 53

Root knot (nematode gall) . 54

Rot nematode 55

Insects and their injury 56

Potato tuberworm 56

Spotted cucumber beetle . . 56

Tuber flea beetle 57

Wireworm 57

Nonparasitic disorders and

injuries 58

Blackheart 58

Browning 59

Bruising 59

Chemical injury 60

Enlarged lenticels 61

Freezing injury 62

Greening 64

Heat injury (scald) 65

Heat or drought necrosis . . 67

Hollow heart 67

Internal black spot 68

Internal brown spot 71

Jelly-end and glassy-end rots 72

Knobbiness and other

malformations 73

Mahogany browning 74

Mechanical damage and

cracking 75

Russeting 76

Stem-end browning 77

Vine killing 78

References 79

Washington, D.C. Issued March 1978

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

Washington, D.C. 20402 - Price $2.15

Stock Number 001-000-03516-9
MARKET DISEASES OF POTATOES

By Wilson L. Smith, Jr., Horticultural Crops Marketing Laboratory,

Northeastern Region, and Jack B. Wilson,* formerly Market Quality

Research Division, Agricultural Research Service

The white potato (Solarium tuberosum L.) is the most important

commercial member of the nightshade family (Solanaceae). Three

other important members of this family are the tomato (Lycopersicon esculentum Mill.), the pepper (Capsicum frutescens L.), and

the eggplant (S. melongena L.).

The potato tuber is a storage organ that develops from a swelling

at the end of a rhizome or underground stem. When potatoes are

harvested before they are fully mature, they are often called "new"

or *'early potatoes." Such potatoes have a thin tender skin, which is

easily feathered or rubbed off during harvesting and handling. They

discolor and wither rapidly at skinned places and are more

susceptible to decay than mature tubers. For this reason the early

crops are not suitable for long storage.

The late or main crop of potatoes, which comes chiefly from the

Middle Atlantic and Northern States, is not harvested until the vines

are mature or dying and the tuber skin is firm, tough, and corky.

These tubers are not easily injured. If free of serious diseases and

stored under proper conditions at about 40° F^ and 85 to 90

percent relative humidity, they change very little within 3 to 6

months.

Many people handle potatoes carelessly as if they were dead.

Fortunately both immature and mature tubers can develop protective and healing tissues when wounded. Under moderate temperature and humidity conditions the cells about and underneath

injuries change chemically and physically so that they are impervious to water and resistant to infections. The walls of the cells

become corky and additional layers of new cells are formed under

and about the wound. This stops loss of tissue moisture and affords

as much protection against decay-producing organisms as did the

original skin.

Under optimum conditions this corky, protective tissue develops

within 24 to 48 hours after the injury. However, at 50° F and

below and above 95° healing does not take place rapidly enough to

offer much protection against wound parasites. For this reason it is

' Now Director, North Atlantic Area, Northeastern Region.

^ For ° C, see conversion table inside back cover.
2 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

advisable whenever possible to hold newly harvested potatoes at

moderate temperatures and at as high a humidity as possible for a

few days to permit wound healing before storage at low temperature.

The quality of potatoes depends not only on the variety and

maturity but also on how they are harvested and handled

immediately afterward. When tubers are badly cut and bruised

during harvest, they discolor, wither, and decay much more rapidly

than uninjured tubers, particularly early potatoes harvested during

hot weather. Heat injury or scald of tubers left exposed in the field

before picking up often greatly damages the early potato. Extreme

heat causes death of cells with subsequent breakdown and decay by

various organisms. Sublethal temperatures predispose the tubers to

infection by soft rot bacteria.

Sometimes part of the northern late-potato crop is injured by

low temperatures before and during harvest. Mild or severe types of

freezing injury also predispose tubers to bacterial soft rot when

they become warm. Unless tubers that have been injured by

freezing are graded out before storage, they may be invaded by any

one of several decay-producing organisms. Handling operations that

avoid both mechanical injuries and temperature extremes are

necessary therefore to maintain good-quality potatoes £ind reduce

losses.

During transit and storage it is not necessary to refrigerate

p)otatoes at very low temperatures. In fact, potatoes are of better

cooking quality when they are held at 50° to 60° F than at 36° to

40° as usually recommended for storage. However, the latter

temperature range is advisable for long storage periods in order to

hold in check sprouting and development of decay.

BACTERIAL DISEASES

Bacterial Soft Rot (Slimy Soft Rot)

Erwinia carotovora (L. R. Jones) Holland and Other Bacteria

Bacterial soft rot is one of the most serious postharvest diseases

of potatoes. It may cause severe losses during storage, transit, or

marketing. No variety is immune to attack. The disease occurs

wherever potatoes are grown in the world.

Symptoms

Soft rot first appears as tiny tannish or water-soaked spots on the

potato skin. These spots rapidly enlarge and as the tissue beneath
MARKET DISEASES OF POTATOES 3

decomposes, a soft blisterlike area develops on the surface of the

tuber. Often a slimy or watery exúdate oozes from breaks in the

paper-thin skin of the blister (pi. l,A),On light-skin potatoes this

blister is surrounded by a brown margin; on red-skin potatoes the

margin usually is black. With slight pressure on the blister the

decomposed flesh beneath will squirt out.

When the tuber is freshly cut, the decomposed flesh usually is

creamy, but it will soon turn pink and finally brown to black (pi.

1, B). The flesh is mushy, but not watery, and sharply separated

from healthy tissue by a black border. The odor at this stage is

almost normal. As the disease progresses, black mushy decay may

consume most of the potato and the skin above the decay collapses.

Then foul-smelling chains or strings of decomposing flesh and

bacteria will ooze out (slimy soft rot). Finally under drying

conditions the mushy tissue dries to a chalky-white foul-smelling

mass (pi. 1, C and £)).

Bacteria that cause soft rot also invade lenticels of potatoes

swollen by long exposure in wet soils or deep washing vats. Infected

areas around the lenticels may be up to one-fourth inch in

diameter, slightly raised above the normal skin, and dark brown to

black, particularly on red-skin varieties (pi. 1, E). Flesh beneath

these areas normally is firm and appears yellowish to cream color or

water-soaked. When such tubers are held at high temperatures, the

infected flesh becomes mushy and typical bacterial soft rot

develops. At low temperatures or under drying conditions these

lenticel infections usually dry up, leaving a shallow spot with

normal skin color but with a chalky-white deposit under the skin

(pi. 1, Fand G).

Causal Factors

The soft rot bacteria attack a wide variety of truck crops and are

common in the soil. During harvesting and packing, the tissues are

contaminated with these bacteria by means of soil, tools, hiinds, or

wash water. Not only are the bacteria present as contaminants in

the field but they cause active rots there, and much of the rot

developing in transit and storage actually originates in the field.

Since the soft rot bacteria invade potato tubers chiefly through

injuries, practically all infections are in tissues weakened or killed

either by heat injury, freezing, mechanical injury, and enlarged

lenticels or by lesions caused by other diseases. Soft rot almost

invariably appears in potato tubers injured by heat in the field

during harvesting and loading. Not only killing temperatures of

122° F and above but also sublethal temperatures of 109° to 113°
4 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

predispose potato tubers to soft rot. Lethal temperatures can occur

in potato flesh when air temperatures are no higher than 90°. Both

field and laboratory tests have shown that potatoes dug, hauled,

graded, and sacked while hot are much more likely to become

infected and eventually to decay than similar potatoes handled at

moderate temperatures. Even potatoes subjected to sublethal

temperatures develop less soft rot if they are not handled until after

they become cool again.

Causal Organisms

Bacterial soft rot of potatoes can be caused by Erwinia

carotovora (L. R. Jones) Holland and E, atroseptica (van Hall)

Jennison. Since these organisms can liquify pectin materials, it has

been suggested that they be placed in the newly created genus

Pectobacterium (Waldee) instead of Erwinia. This suggestion,

however, has not been generally adopted. The Erwinia species are

gram-negative rods about 0.6 by 1.5 ß with four to six short,

inconspicuous, peritrichous flagella. Although both species cause

soft rot of potatoes, only E. atroseptica produces blackleg. On

synthetic media the two species can be readily differentiated. E.

carotovora will utilize 5 percent of ethyl alcohol and dulcitol and 1

percent of sodium hippurate, sodium malonate, and sodium urate as

growth factors; E. atroseptica will not. E. atroseptica produces

more acid from maltose than E. carotovora.

Species of Pseudomonas and Bacillus also cause soft rot of

potatoes. The Erwinia and the Pseudomonas species differ in that

the latter has polar flagella, will not ferment lactose, and will give a

blue-white fluorescence in media containing aspargine. The Bacillus

species differ from both of these genera since they are gram-positive

rods about 0.8 by 2-3 /i, often contain spores, form long chains of

cells, and grow under anaerobic conditions. Certain species of

Clostridium are also found on rotted tubers. They are rods about

0.5-8 by 3-7 /x, which grow usually under anaerobic conditions.

Generally they produce the foul odor associated with rotted

potatoes.

The Erwinia and Pseudomonas species can grow and produce soft

rot of potatoes from about 32° F to slightly above 90°. The

optimum for growth and infection is from 70° to 80°. The Bacillus

species on the other hand have optimum growth from 86° to 97°

and will develop up to about 122°. Usually they are secondary

invaders following the Erwinia or other organisms and may be

partially responsible for the foul odor of the decayed tubers.
MARKET DISEASES OF POTATOES 5

Bacterial soft rot organisms can spread from diseased to healthy

tubers during transit, storage, or marketing.

Control

As with many other storage diseases, the control of bacterial soft

rot begins in the field. It is necessary to control such field diseases

as late blight, brown rot, ring rot, and blackleg, which produce

lesions in tubers through which infection by the soft rot organisms

may occur. Furthermore, the tubers must be protected during

harvest from bruising and exposure to excessive heat or to freezing.

Rotting tubers should be sorted out in packing. If possible, potatoes

that have been washed should be dried before being stored or

shipped. Ventilation and moderately low temperature during transit

and storage are essential in controlling bacterial soft rot.

Storing tubers near 60° F for the first 4 to 5 days will allow

injured surfaces to heal and will restrict the entrance of bacterial

organisms. After healing, tubers should be stored at 40° in

well-ventilated bins. Moderate refrigeration of early potatoes during

transit in hot weather is beneficial, since decay does not develop as

rapidly at 60° and slightly below as at higher temperatures.

References: 14, 36, 41, 55, 62, 123, 134, 135, 148, 151, 182, 183,

187, 198, 212, 214, 215, 217, 234, 245, 249, 250, 269, 270, 274,

283, 317,

Blackleg

Erwinia atroseptica (van Hall) Jennison

Blackleg occurs wherever potatoes are grown. Its name comes

from the jetblack lesion produced on the basal part of the stems.

Tuber rots and discoloration of the vascular system make this an

important market disease. It can be serious from a seed-certification

standpoint, since infected seed pieces cause losses in stand and

yield.

Symptoms

The blackleg organism enters tubers through the stolons and

produces various symptoms.

The most pronounced symptoms appear on tubers infected about

midseason. Jetblack slightly sunken lesions develop at the stem end,

with blackened skin extending about half the length of the tubers

(pi. 1, H). Normally the skin of intact tubers is dry and thin pieces

may be peeled off. Internally the infected flesh of freshly harvested
6 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

tubers is at first cream color, then grayish, and finally black. It has

the mushy texture of bacterial soft rot. Such infections spread from

the stem end through the heart of the tuber in irregularly shaped

patterns. A dark border separates the infected from the healthy

flesh.

When infected tubers have remained for long periods in the fields

or when they are stored, the blackened skin at the stem end breaks

apart and the discolored flesh disintegrates, leaving irregular cavities

with blackened walls, which may extend through the center of the

tuber (pi. 2, B). These cavities differ from those caused by

blackheart since they are always near or connected with the stem

end. They differ from those produced by fusarium rots since no

fungal growth is present.

In late-season infection, slight grayish-black skin lesions form at

the stem end. The flesh beneath these lesions is yellowish to tan, is

slightly water-soaked, and does not extend deep into the tubers (pi.

1, H; pi. 2, A). Regardless of the stage of tuber infection, a

brownish discoloration of the vascular system often occurs (pi. 2,

B).

The blackleg organism also may infect the lenticels, causing them

to be slightly simken and brownish to black. If the relative

humidity is low, the rot around the lenticels is apt to be dry; if it is

high, the rot will be moist. Lesions vary from one-eighth to

one-fourth inch in diameter. Tissues beneath the lesion are

brownish, disorganized, and usually dry; they extend about

one-sixteenth of an inch into the healthy tissue. Sometimes the

entire tuber is affected, but usually only one side.

Causal Factors

The exact conditions for severe outbreaks of blackleg are not

known. The disease is tuberborne and may be transmitted from

infected to healthy seed pieces by the cutting knife. Generally the

disease develops most rapidly during cool, wet weather. Usually

tubers infected early in the growing season decay before harvest, so

that storage and seed-piece decay arise from late-season infections

on tubers showing only slight blackleg symptoms. The seedcorn

maggot {Hylemya platura (Meigen)) is reported to spread this

disease in the field from infected to healthy plants.

Causa/ Organism

The blackleg organism Erwinia atroseptica (van Hall) Jennison is

closely related to E. carotovora, which causes bacterial soft rot of
MARKET DISEASES OF POTATOES 7

potatoes. The former is often called Pectobacterium carotovorum

var. atroseptica (van Hall) Dowson. It usually does not spread from

diseased to healthy tubers during storage, but it will remain

dormant in tubers during storage and later cause serious seed-piece

decay and plant losses. For a brief description of this organism, its

distinction from E. carotovora, and its temperature requirements,

see Bacterial Soft Rot.

Control

The best control for blackleg is to use certified seed. Since the

disease-producing organism can be transmitted on a cutting knife,

carefully avoid tubers with blackleg symptoms when seed pieces are

cut. Tuber and lenticel rot can be controlled by low temperature

and proper ventilation.

References: 16, 49, 110-112, 129, 171, 179, 183, 198, 218, 242,

270, 294, 296.

Brown Rot (Southern Bacterial Wilt)

Pseudomonas solanacearum E. F. Sm.

Brown rot may attack all varieties of potatoes with varying

degrees of severity. In addition, it attacks eggplant, pepper, tomato,

tobacco, peanut, and many other plants. It is primarily a disease of

crops in the South Atlantic and Gulf Coast States from Maryland to

Texas. For this reason, it is often referred to as southern bacterial

wilt. However, the disease has been reported as far north as

Massachusetts, Pennsylvania, Ohio, Michigan, Illinois, and Idaho.

Brown rot is principally a field disease, but it is sometimes

serious in market shipments of the early or new potatoes from the

South. The discoloration or slight decay of the vascular ring may

result in reduced prices. Also, the potatoes may be invaded by

secondary organisms and decay completely. Since practically none

of them are stored, the disease is of little importance as a storage

rot.

Symptoms

The external symptoms of brown rot may be a slight depression

on the tuber where it was attached to the stolon or a grayish-brown

patch on the surface (pi. 2, C). Sometimes no external symptoms

develop. When infected tubers are cut at the stem end, a moist

brown discoloration and a slight softening of the water-conducting
8 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

tissues can be seen (pi. 2, D), Frequently, though not invariably,

yellowish-white sticky masses of bacteria ooze from the discolored

vascular area without applying any pressure. At this stage there is

no odor. Later, as the bacteria work toward the center of the tuber,

the entire interior becomes soft and brown and only a thin crust of

tissues holds the tuber together. If the rot reaches this advanced

stage while the potatoes are in transit, adjacent tubers are likely to

become smeared with the rotted content. In the later stages of the

disease, secondary organisms gain entrance, the tissues become

creamy in consistency, and a foul odor results.

The symptoms of brown rot are similar to those of ring rot.

However, when a diseased tuber is cut, the presence of brown rot is

indicated if white sticky droplets of bacteria ooze from the vascular

ring and the decay tissues in the immediate vicinity of the ring are

brown to black. Tubers affected with ring rot show no bacterial

ooze from the vascular ring, but cheeselike decayed tissues can be

forced out of the ring area by squeezing the tuber.

Causal Factors

The bacterium causing brown rot occurs in the soil. The disease is

most severe in potato crops grown on newly cultivated land.

Warm, moist weather favors the spread of the disease. It develops

at 77° to 97° F. Most rapid development is at about 90°. As the

temperature is reduced, growth is retarded until it is practically

stopped at 55°. Decay in transit is greatest in shipments of potatoes

that have been dug during hot weather and not precooled

sufficiently.

Causal Organism

Brown rot is caused by Pseudomonas solanacearum E. F. Sm.

The bacteria are gram-negative rods 0.5 to 1.5 ju- They are motile

with a polar flagellum. On agar the colonies have irregular margins

and usually are small, smooth, glistening, and opalescent. At first

they are white but later turn brownish. In broth a slight pellicle is

formed and the broth turns brown. In culture the optimum

temperature is between 95° F and 99° with a minimum of 50° and

a maximum of 106°.

Control

Diseased tubers should not be stored or shipped even though

infection may be only in its initial stages, because they rot very
f

MARKET DISEASES OF POTATOES 9

quickly at 55° F and above. As it is practically impossible to

discover and remove all tubers with brown rot in its early stages,

potatoes from affected fields should be used immediately or

shipped to nearby markets. Temperature during shipment should be

below 55°.

References: 66, 67, 115, 203, 267, 268.

Red Xylem and Pinkeye

Pseudomonas fluorescens (Trevisan) Migula

These diseases of potatoes are reported chiefly from the northern

potato-growing areas. The discolored vascular ring and shriveling

around the eyes may cause serious losses. These diseases are

particularly pronounced in 'Katahdin' tubers.

Symptoms

Red xylem is most common in large tubers. A sunken but not

discolored lesion occurs at the stolon scar and a cavity lined with

blackened tissue may extend from this scar into the center of the

tuber. The vascular ring has a thin reddish-brown line, and

sometimes a network of discolored strands extends into the cortex

(pi. 2, E). Red xylem is distinguished from stem-end browning and

net necrosis since the last two discolor the phloem strands. Also,

Katahdin is among the most susceptible varieties to red xylem and

yet resistant to stem-end browning and net necrosis.

Pinkeye is characterized by pinkish blotches near the eyes and

mostly aroimd the blossom end of the tubers because of the pink

underlying tissue. The internal tissue is firm to corky, and pink to

reddish-brown and black areas and cavities may occur. During

storage the discolored tissues under the eyes dry out, turn light

brown, and finally become wrinkled and cracked (pi. 7, E and F),

The xylem tissue of the affected tubers is about the same color as in

red xylem. Pinkeye may be confused with late blight, but it does

not have the brick-red granular tissue characteristic of blight.

The cause of these diseases is not truly known.

Causal Organisms

Red xylem and pinkeye are reported to be caused by Pseudomonas fluorescens (Trevisan) Migula, a bacterium commonly found

in the soil. It apparently does not survive in stored tubers. Pinkeye

in particular often is associated also with a fungus, Verticillium
10 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

alboatrum,^ which causes wilting of the plants and vascular

discoloration of tubers. Pinkeye is also associated with the disease

caused by Rhizoctonia solani. Generally pinkeye occurs when the

soil is very moist and is absent when it is dry.

P. fluorescens is a gram-negative rod about 1.5-2 by 0.5-0.8 ¡JL

with a polar flagellum. The rods occur singularly or in pairs. On agar

plates the colonies are white to translucent, circular, and slightly

raised. In a liquid medium the growth is at the surface with a

pellicle formation. On agar the growth is filiform and slightly

iridescent in reflected light. Growth temperatures range from about

43° to 99° F with an optimum neair 80°. Strong fluorescence occurs

when the organism is grown on medium with asparagine.

Control

No control methods are known

References: 20, 90, 91, 95, 98, 100, 141, 158, 242.

Ring Rot

Corynebacterium sepedonicum (Spieck. and Kotth.) Skapt. and

Burkh.

Ring rot is probably the potato grower's most feared disease and

continues to be one of the most destructive since its discovery in

Germany early in the 20th century. It was first reported in North

America in eastern Canada in 1931 and in Maine in 1932. Because it

is easily disseminated, it has since appeared in rapid succession in

various parts of Canada and the United States until by now it is in

all the major potato-producing States. It has caused extremely

heavy losses.

Tubers with ring rot are commonly found at the terminal

markets, and occasionally this disease is responsible for serious

market losses. Extensive decay due to secondary invasion of soft rot

bacteria also contributes to market losses.

Symptoms

The chief symptom of ring rot on tubers is a characteristic

odorless decay, which is confined at first to the immediate vicinity

of the vascular ring. This decay can readily be seen by slicing the

tuber crosswise near the stem end. In the early stages of infection

^ See Verticillium Wilt.
MARKET DISEASES OF POTATOES 11

the vascular ring is cream to pale lemon yellow and approaches the

color of the normal ring of a healthy tuber, but in later stages the

ring is brownish. The affected areas of ring rot-infected potatoes are

soft with a cheesy consistency (pi. 2, F and G). The bacterial cheesy

material can readily be forced out of the affected vascular ring

tissue by squeezing the tuber or by gently pressing a blunt stick or

pencil against the vascular ring at the cut surface of the tuber. In

more severely affected tubers the diseased tissue can readily be

pushed aside, leaving a narrow cavity or cleft that extends down

into the tuber and runs part way or entirely around the vascular

ring (pi. 2, H). Dehydration follows with advanced lesions becoming

dry and powdery. When these areas are invaded by soft rot bacteria,

a soft mushy consistency may replace the dry powdery condition.

Vascular cavities may extend to the pith or cortex and result in

canker lesions on the tuber surface.

Causal Factors

The disease is spread by infected seed potatoes. The bacterium

lives from season to season chiefly in tubers. It can survive in dried

slime on crates, pallet boxes, bins, harvesting and grading equipment, and sacks. Contaminated cutting knives and harvesting

equipment are chief sources of primary inoculum, with the causal

bacterium invading the tubers through harvesting and handling

bruises.

When the disease reaches the surface of the tuber near the eyes, a

characteristic cracking affords an entrance for secondary soft rot

bacteria, which spread through the vascular ring and eventually

affect the entire tuber. The presence of secondary rots may result in

a variety of discoloration symptoms near the vascular ring £ind

thereby mask the symptoms of ring rot. Brown rot and ring rot

symptoms are similar, and sometimes the two diseases are difficult

to distinguish (see Brown Rot).

The incubation period for ring rot may be from 2 to 3 months.

Consequently, infected tubers with no visible evidence of the

disease at harvest may develop positive symptoms in storage.

Although healthy tubers can be infected through fresh wounds that

penetrate as deeply as the vascular ring, there is generally little, if

any, spread from diseased to healthy tubers during storage. Ring rot

develops in the tubers most rapidly at 64° to 72° F and only

slightly at 37°.

Causal Organism

Ring rot is caused by Corynebacterium sepedonicum (Spieck.

and Kotth.) Skapt. and Burkh. It is a nonmotile rod 0.3-0.4 by
12 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

0.8-1.0 M. On agar the colonies are thin, smooth, translucent, and

glistening white. They seldom exceed 3 mm in diameter. The

organism grows best at 68° to 73° F with a minimum of 39° and a

maximum of 88°.

Control

The best way to prevent ring rot is to plant disease-free tubers.

Potatoes known to contain any appreciable amount of ring rot

should be moved early and promptly into marketing channels to

prevent losses from advanced stages of ring rot and from secondary

bacterial soft rot, which frequently follows. Storage at 38° F will

control further development of ring rot and associated soft rots

during the holding period.

Such varieties as Teton, Saranac, and Merrimack are resistant to

bacterial ring rot.

References: 24, 29, 30, 39, 40, 103, 143, 159, 163, 170, 193, 230,

240, 265, 266, 272, 275, 279, 280.

FUNGUS DISEASES

Armillaria Rot

Armillaria mellea (Vahl. ex Fr.) Kummer

Armillaria rot of potatoes has been reported from California,

Florida, Michigan, Oregon, Washington, Wisconsin, Wyoming,

British Columbia, and Australia.

Symptoms

The fungus that induces this rot produces dark-brown to black

rhizomorphs or threads, which penetrate the corky layer of the

tuber and generally adhere to the skin at various points« Affected

tubers often have hard, brown, corky areas, which are roughened,

shrunken, usually shallow, but sometimes they extend into the flesh

a considerable distance. The diseased internal tissues are light brown

and interspersed with convoluted, white, brown-edged plates of

fungus mycelium.

Causal Factors

This disease only affects potatoes planted on newly cleared land

rich in humus, and it is of little economic importance.
MARKET DISEASES OF POTATOES 13

Causal Organism

A fungus, Armillaria mellea (Vahl. ex Fr.) Kummer, causes this

disease. The mushroom stage is not seen on harvested potatoes. The

fungus grows most rapidly in culture at 67° and 81° F. After long

periods the greatest development of rhizomorphs in nonsterile

potting soil was at the lowest temperatures.

Control

Control measures after harvest are not needed.

References: 8, 150, 156.

Black Dot

Colletotrichum atramentarium (Berk, and Br.) Taub.

Although black dot is considered a minor disease of potatoes, it

occurs in many potato-growing areas in the United States, Canada,

Europe, Australia, and South Africa. Its symptoms, which overlap

those of other potato diseases, make accurate evaluation of its

importance difficult.

Symptoms

The fungus progresses down the stolons to the tubers in the soil.

A common symptom is the adherence of sections of the affected

stolons to the tubers at harvest. Sclerotia of the fungus are scattered

or in patches on the surface of mature tubers, where their

appearance is sometimes coincidental with silver scurf (pi. 3, A),

Causal Organism

The causal fungus Colletotrichum atramentarium (Berk, and Br.)

Taub, has a branching, septate, slightly colored mycelium, which

produces black sclerotia up to one-half mm in diameter. Acervuli,

which are formed on the sclerotia, contain numerous prominent

black setae or hairs, which are septate, tapered to the tip, and about

80 to 350 M long. Conidiophores are 10 to 30 ¡x long, cylindrical,

tapering to slightly clávate, sometimes curved, occasionally

branched, and may be nonseptate to three septate. In mass the

conidia are usually pink; individually they are hyaline or colorless,

continuous, sometimes slightly curved, and sometimes attenuated at

the basal end and round at the apical end. They are from 3 by 17 to

7.5 by 22/x.
14 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

Control

No specific control measures are recommended.

References: 63, 210.

Black Scurf (Rhizoctonia)

Pellicularia filamentosa (Pat.) Rogers

Black scurf is one of the several phases of rhizoctonia disease. It

is one of the most common diseases of potato and is distributed

worldwide. The causal fungus is responsible for other diseases on

many species of cultivated plants, including beans, beets, cabbage,

carrots, peas, and tomatoes. Damage to potato tubers results in

poor appearance and a reduced market quality.

Symptoms

The most common symptom of black scurf on potato tubers is

small, hard, coal-black bodies called sclerotia, which are tightly

appressed to the tuber skin (pi. 3, B). These sclerotia are the resting

or overwintering bodies of the fimgus and range from as small as a

pinhead to as large as a half pea.

Another symptom of this disease on potato tubers is the

development of small, hard, sunken pits about the size of a pea.

This condition is the result of lenticel penetration by the fungus.

These areas can generally be lifted out with the point of a knife.

Although this injury is common, it rarely causes serious losses. Still

another symptom is a russeting of the tuber surfaces similar to that

caused by the shallow form of common scab. This is often referred

to as russet scab and commonly occurs in heavy soils. The disease

impairs the appearance of potato tubers, particularly when they are

washed, and thereby reduces their acceptance as table stock

potatoes.

Following injury by the potato flea beetle {Epitrix cucumeris

(Harris)), the causal fimgus often produces deep cracks and furrows

by invading the insect channels and punctures. Also, holes made by

wireworms may be invaded and result in deepened pits and

channels.

Although the disease seldom causes a tuber rot, a dry, punky

decay has been reported at the stem end of tubers. Sometimes

Rhizoctonia may be associated with other fungi or bacteria and a
MARKET DISEASES OF POTATOES 15

jellylike rot may occur in tne succulent pointed ends of the Russet

Burbank variety.

Causal Factors

The causal fungus comprises a large number of physiologic races,

or strains, which differ considerably in their environmental requirements. The disease is more severe in cool than in warm seasons.

Frequently stems and roots that have few sclerotia in the summer

are covered with them when the weather becomes cool. Therefore

sclerotia may be abundant if tubers remain in the soil for a long

period in the fall. This is particularly a problem in the northern

potato-growing aresis.

Rhizoctonia occurs in most soils and may live saprophytically on

decaying plant debris when a living host is not available. Both the

pathogen in the soil and the sclerotia carried on the seed tuber may

be responsible for propagating the disease. However, there is

evidence that the fungus is less virulent when propagated from

sclerotia.

Causal Organism

Black scurf is caused by the basidiomycete Pellicularia filamentosa (Pat.) Rogers described originally as Hypochnus solani by

Potouillard in France in 1891. EarUer the imperfect stage of this

organism was termed Rhizoctonia solani Kuehn. The two were

identified as different stages of the same organism early in the 20th

century. The imperfect stage, which produces the black sclerotia on

the tubers, occurs more frequently than the perfect stage. However,

there is evidence that strains of the fungus from spores are more

pathogenic than those from sclerotia.

The imperfect stage of the fungus, which grows well on artificial

media, produces when young a hyaline mycelium, which becomes

brown as the culture ages. The mycelial branches are constricted at

the juncture with the main hyphae, and as the culture becomes

older, the branches assume a right-angle relation to the main

hyphae. On some media and under certsdn conditions the mycelium

becomes tufted, dividing into short, ovate cells that eventually

make up brown sclerotia.

The cardinal temperatures for the fungus in culture are an

optimum of 77° to 86° F, a minimum of 46°, and a maximum of

88° to 95°. The sclerotia germinate at 46° to 86° with the optimum

at 73°. The optimum for basidiospore germination is 70° to 77°.
16 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

Control

No completely effective control measures can be recommended

for this disease. No resistant varieties are available, and chemical

control is not totally satisfactory.

References: 38, 54, 94, 188, 258, 262, 284,

Charcoal Rot

Macrophomina phaseoli (Maubl.) Ashby or Botryodiplodia phaseoli

(Maubl.) Thirumalchar

Charcoal rot develops in potatoes grown in warm areas. In the

United States serious losses from this disease occur on the market

on potatoes from California, Georgia, Mississippi, Missouri, Tennessee, and Texas. Serious losses from this disease have been reported

from India.

Symptoms

Externally charcoal rot appears first as black moderately firm

areas near the stem end of tubers and as cloudy blotches around the

eyes and lenticels. Eventually the entire skin of an infected tuber

may blacken. Sometimes infected areas around the eyes and lenticels

dry and form a slightly sunken, dark, dry rot. When the fungus

progresses throughout the tuber, a semiwatery breakdown of the

tissues occurs. Internally the freshly cut flesh is grayish or tannish

yellow, but it soon changes to pinkish buff, then brown, and finally

black (pi. 3, C). A dark or black border often separates diseased

from healthy tissue. Small cavities mostly near the stem end

sometimes occur. The infected flesh is firm, but with slight pressure

yellowish-gray water can be squeezed from the affected areas. The

decay appears somewhat like leak, but affected tissues are not as

watery as leak and usually wounds are not visible.

Causal Factors

Charcoal rot occurs most often when heavy, poorly drained soils

are waterlogged or excessively wet. Since high temperatures of the

wet soils increase the development of this disease, the northern

potato crop should remain free of the disease. Soil containing the

organism and sticking to eyes or lenticels may make conditions

favorable for infection.
MARKET DISEASES OF POTATOES 17

Causal Organism

Charcoal rot is caused by Macrophomina phaseoli (Maubl.)

Ashby, which recently was classified Botryodiplodia phaseoli

(Maubl.) Thirumalchar. This organism will not infect potatoes

below 43° to 50° F. The optimum for infection is between 89° and

97° and the maximum near 108°. On artificial media the colonies

of this organism are at first grayish white but turn a blackish mouse

gray at maturity. Young hyphae are hyaline and contain granular

material. Older hyphae are brown gray. When pycnidia are

produced, the pycnospores are at first one-celled and hyaline, but

later they become two-celled and reddish brown. The organism does

not spread from diseased to healthy tubers during storage or transit.

Control

Low storage or transit temperatures will prevent the development

of charcoal rot, but when tubers are moved to higher temperatures,

decay follows rapidly. Forced-air circulation will lower storage

temperatures rapidly and help to dry the surface of the tubers.

References: i5, 35, 79, 233, 285, 286, 301.

Early Blight (Alternaria Tuber Rot)

Alternaría solani (Ell. and G. Martin) Sor.

Although the early blight pathogen was first described by Ellis

and Martin in 1882 and the disease was extensively studied by

Jones in Vermont during 1891-1903, the tuber rot phase was not

described until 1925 by Folsom and Bonde in Maine.

The disease is general in potato-growing areas, but the tuber rot

phase is sometimes more serious in the northern late-season crop

areas, where potatoes are harvested and stored during cool, humid

weather. Early blight tuber rot is a serious storage and market

disease and often predisposes tubers to secondary infection by

other pathogens such as the Fusarium species.

Symptoms

Early blight lesions on tubers are dark brown to black, of several

different shapes including circular to oblong, and about one-fourth

to 2 inches in diameter. Often they are slightly sunken and have

raised purplish borders (pi. 3, D), The lesions on a tuber vary from
18 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

one to many. The affected areas may be similar to those caused by

the late blight organism, but early blight areas are shallower and

sharply set off from the healthy tissue by a layer of cork. The decay

does not spread irregularly into healthy tissue as does late blight.

The flesh of the tubers one-eighth to one-half inch deep beneath the

lesions is black and often surrounded by a yellowish zone (pi. 3, E).

The lesions may cover the eyes of the tubers and kill the sprouts.

No fungus sporulation is evident over the tuber lesions. Cracks may

develop on older tubers.

Causal Factors

The causal fungus overwinters as mycelium and conidia in the

soil and on potato tubers. Initial plant infection occurs on vines in

the field. Fungus spores are abundantly produced in leaf lesions

when rain or dew is frequent and when it is about 78° F in the

field. If the disease is uncontrolled in the field, the tubers become

inoculated with spores during harvest. Unbruised as well as bruised

tubers are subject to infection from this inoculation at harvest since

the spores, which germinate under favorable temperature and

moisture conditions in storage, can penetrate directly. However,

under dry storage conditions, which prevent spore germination,

infection is held in check and spread to unbruised tubers is imlikely.

Bruised tubers are most likely to develop decay under moist

conditions at about 55° to 60° F. The optimum for decay

development is about 60°, the minimum 41° to 45°, and the

maximum 77°.

Causal Organism

Early blight is caused by Alternaría solani (Ell. and G. Martin)

Sor., which was earlier called Macrosporium solani Ell. and G.

Martin. A. solani is classified in the order MoniUales of the class

Fungi Imperfecti.

The mycelium is septate, branches, and darkens with age. Conidia

have long beaks and are uniform and dark. They are borne singly or

in chains of two in pure culture on relatively short, dark

conidiophores. The conidia are formed from buds that arise from

the terminal cell of the conidiophore. The conidia range from 12 by

120 to 20 by 296 M- The fungus produces an abundant yellowish to

reddish pigment, which diffuses through the substrate of artificial

media. Conidia are sparse in uninjured pure culture, but abundant

sporulation can be stimulated by wounding the mycelium or by
MARKET DISEASES OF POTATOES 19

exposure to ultraviolet light. Pure cultures vary considerably in

their virulence, growth rate, and sporulation.

The mycelium of the fungus remains viable in dry infected leaves

for more than a year and conidia remain viable for up to 17 months

at 68° to 70° F. They germinate within 1 to 2 hours in water at

43° to 93°. At an optimum of 82.5° to 86° germination will occur

in 35 to 45 minutes. Cardinal temperatures for growth in pure

culture are optimum 79° to 82°, minimum 34° to 36°, and

maximum 99° to 113°.

Control

Chemical control of vine infections in the field is necessary to

prevent tuber infection. Also, vine killing before harvest will reduce

chances of tuber inoculation from infected vines.

Careful harvesting and handling will reduce tuber disease spread.

Maintaining storage temperatures below 41° F will stop decay

development in storage. Forced-air ventilation will reduce or

eliminate the free moisture that is necessary for spore germination

and the resulting spread of infection in storage.

References: 23, 38, 89, 113, 228.

Fusarium Tuber Rots

Fusarium spp.

Fusarium tuber rots probably cause greater storage and transit

losses, particularly in late potatoes, than any other postharvest

disease of potatoes. Although some types of this rot may develop

on potatoes in the soil causing a stem-end decay, most infections

occur through wounds during the harvesting and storing of this

crop. The tuber rots develop in storage or in transit to market.

Symptoms

The symptoms of fusarium tuber rots vary greatly with different

species of causal fungi. Generally at first the infected tissues are

light brown and become dark brown with age. The decaying tissue

becomes sunken, the skin wrinkles, and tufts of mold may appear at

the eyes, lenticels, wounds, and stem end (pi. 3, F-G). At low

storage temperatures the affected tissues are usually dry and firm,

sometimes even powdery, but at high temperatures they are often

moist and pliable. Secondary bacteria frequently invade the

affected tissues and cause rapid breakdown of the tissues and wet

rot.
20 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

In some types of fusarium tuber rot the causal organism invades

the central part of the tuber, breaking down the tissues and

eventually forming cavities lined with brightly colored fungal

growth. This may be white, yellow, pink, rose, or bluish purple

depending on the species (pi. 3, H). Often the external appearance

of the tuber fails to give a clue as to the extent of internal rot. In

the buttonhole-type rot the external symptom may be a small

circular lesion approximately one-eighth to one-fourth inch in

diameter (pi. 4, A and B), Sometimes it is extremely difficult to

find a break in the skin and the area may be only darkened; paring

reveals a small area of dry rot. These small circular dry areas may

affect much of the tuber skin.

Causal Factors

Many species of Fusarium rot potato tubers and all are soil

inhabitants. Several species may be present in all potato-growing

areas, but one species is often predominant in a given soil or

locality.

Most of the fusaria are wound parasites and consequently

become destructive only after harvest. Rough handling during

harvest, storage, or transit injures the tubers so the fungus can

enter, infect, and cause decay. The mycelium and spores of

Fusarium are commonly in the soil, on the tubers, equipment, and

containers, and on the floors and walls of storage bins.

Since the fungus spores are always present and some skin breaks

generally occur, temperature and moisture conditions determine

whether or not infection develops. These conditions affect both the

causal fungus and the potato. At 40° F wound healing proceeds so

slowly that the host offers little resistance to penetration and

infection. At 60°, on the other hand, wound healing is rapid enough

to inhibit infection. Although most fungus species that cause tuber

rot grow best between 78° and 86°, they can grow slowly and cause

rotting below 50°. Near 40° infected tubers show little or no

progressive decay in storage. However, at 40° the fungus is not

killed but remains dormant in the wounds to become active

whenever the tubers become warm. Consequently, under favorable

conditions (above 70°) for the organism, potatoes may begin to

exhibit visible decay within 4 or 5 days, and more than half of an

average-sized tuber may be decayed in 10 to 15 days.

Causal Organisms

The genus Fusarium is classified in the order Moniliales of the

class Fungi Imperfecti. This is a large and variable genus that is
MARKET DISEASES OF POTATOES 21

sometimes placed in the Tuberculariaceae because some species

produce sporodochia.

The mycelium of this genus is extensive and cottony, often with

some tinge of pink, purple, or yellow. The color often permeates

the artificial media on which the fungus is cultured. Conidiophores

are variable, slender, and simple, or they are stout, short, and

irregularly branched or bearing a whorl of phialides. They may be

single or grouped into sporodochia. Conidia are hyaline, variable,

and principally macroconidia and microconidia. Often they are held

in a mass of gelatinous material. Macroconidia have from two to

several cells and are slightly curved or bent at the pointed ends and

typically boat shaped. Microconidia are one-celled, ovoid or oblong,

and borne singly or in chains.

The Fusarium oxysporum Schlecht group is general throughout

the U.S. potato-growing area, but it is more frequently found in the

South and East. It also causes a stem-end rot of tubers and has been

reported in the Northeast, East, Midwest, Southwest, and Rocky

Mountain region.

F. solani (Mart.) Appel and Wr. var. eumartii (Carpenter) Wr.

has been reported as the cause of stem-end rot from New York to

Maryland and in Colorado, Idaho, Montana, Nebraska, Oklahoma,

Wisconsin, and Wyoming. F. solani var. radicicola (Wr.) Synd. and

Hans, causes a jelly-end rot in the Western States and a black rot of

tubers in the South and East.

F. coeruleum (Lib.) Sacc, F. sambucinum Fckl., and F.

trichothecioides Wr. all cause a dry rot in storage, transit, and

marketing. F. coeruleum is common in the U.S. northern potato

areas and in Europe. It causes most of the fusarium rot on potatoes

in storage and often is associated with other fusaria. The species is

the most vigorous wound parasite of potato tubers. F. sambucinum

is general in the Northern and Central States to Texas and Idaho,

whereas F. trichothecioides has been reported from Ohio and

Michigan to Missouri, Arizona, California, and Washington. This

species sometimes causes a field rot and wilt.

The microconidia of F, oxysporum are abundant and are

produced in false heads. Chlamydospores are present. When grown

on potato-dextrose agar (PDA), the cultures may produce a violet

pigment in the agar. Blue-black sclerotia may be present. The

sporodochia, when present, are from cream to salmon colored.

The microconidia of F. solani var. radicicola are nearly straight

near the base, slightly curved in the upper third of their length,

somewhat rounded to distinctly constricted at the apex, slightly

pedicellate, mostly three-septate, and 31-40 by 4.6-5 ß. The

nonseptate and one-septate microconidia are very common; the
22 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

nonseptate measure 8 by 3 ju. Chlamydospores are common,

terminal and intercalary, and mostly nonseptate and one-septate.

The nonseptate measure 9-10 by 8.7-8.8 ¡i. The aerial mycelium is

well developed. The conidia range from white to olive and the

substratum from pale yellow to olive on agar rich in glucose and on

tuber plugs.

The microconidia of F. coeruleum are nonseptate and about 16

by 4.7 M. Macroconidia are mostly of an even diameter or somewhat

broader near the base, only slightly curved near the apex, somewhat

rounded at the apex, never apically constricted, mostly

three-septate, and 30-36 by 4.5-5.4 ß. Aerial mycelium is usually

medium to well developed, feltlike with age, from white, bluish

white, and olive buff to dusky slate violet on PDA rich in glucose; it

is slate purple on commeal agar. The substratum on PDA rich in

glucose ranges from deep violet to ocher red and in older culture is

violet carmine. Conidia range from orange on strong acid agars to

pale buff, light gray, or blue on neutral media.

F. sambucinum conidia are nearly uniform in diameter, sickle

shaped, gradually attenuated, often somewhat constricted at the

apex, pedicellate, mostly three- to five-septate, 28.5-41 by 4.2-5.2

/x, and are borne on aerial mycelium in sporodochia.

Chlamydospores are rare and not in long chains. The aerial

mycelium ranges from poorly to well developed and no red is in the

mycelium or substratum.

In F. trichothecioides the microconidia are absent. The

macroconidia are of both comma and sickle shapes, with the

comma shape predominating under ordinary cultural conditions, are

mostly one-septate, 14-17 by 4.2-5.4 ß, often nonseptate to

three-septate, and seldom four- or five-septate. The sporodochial

conidia are sickle shaped, three- to five-septate, and 24-42 by

4.5-5.5 jLt. The chlamydospores are few and not prominent. Conidia

are produced in powdery masses on aerial mycelium.

The prevalence of the disease in storage appears to be increasing

as more mechanical harvesters are operated improperly. This

coupled with the perennial stone or clod problems in some

potato-growing areas contributes to small nicks, cuts, and bruises in

the potato tubers, which act as entrance points for the causal

fungus.

Control

Reduction of injury during harvesting, transportation, and

storage is essential to control fusarium tuber rots. This can be

accomplished by eliminating rocks, reducing harvesting equipment
MARKET DISEASES OF POTATOES 23

speeds, using padded equipment, reducing the height of tuber

drops, and warming potatoes before handling. However, even with

the most elaborate precautions some tubers will be bruised. This

emphasizes the necessity of proper curing near 60° F with high

relative humidity during the initial storage period before

temperatures are lowered for holding.

References: i, 6, 7, 31, 45, 93, 105, 146, 147, 178, 186, 187, 196,

220, 227, 229, 242, 255, 272, 290, 307, 315,

Fusarium Wilts

Fusarium oxysporum Schlecht f. sp. tuberosi (Wr.) Synd. and Hans,

and F. solani (Mart.) Appel and Wr. var. eumartii (Carpenter) Wr.

Fusarium wilts have been reported from most potato-growing

areas in the United States as well as Canada, Europe, India,

Australia, and South Africa. These diseases reduce the market

quality by discoloring the vascular system of the tubers. The

usefulness of affected tubers for processing, especially for chip

manufacture, is seriously reduced.

Symptoms

The causal organisms that enter tubers through the stolons cause

different symptoms of the disease.

Tubers infected with Fusarium oxysporum f. sp. tuberosi usually

have no external symptoms, but internally they show different

degrees of discoloration at the stem end. The color of the xylem or

woody vascular ring varies from a slight yellow or brown at the

point of the stolon attachment to a dark brown to black. This

discoloration extends from two-thirds to all the way through the

tubers (pi. 4, C). Sometimes this necrosis also extends to smaller

vascular elements on either side of the vascular ring and may

resemble net necrosis. Frequently the vascular ring becomes hard,

woody, and dark brown, and splinterlike pieces of tissue can be

removed with a knife point.

Fusarium solani var. eumartii first causes a brownish skin

discoloration at the stem end, which later becomes sunken or

wrinkled and even may rot. Below this discolored or rotted area the

vascular ring ranges from a yellowish brown to dark brown and is

water-soaked. The band often extends throughout the tuber and is

from about one-eighth to one-fourth inch wide (pi. 4, D).

Sometimes the water-soaked brownish area causes brown flecking in
24 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

tissue adjacent to the vascular ring. In very mild cases this organism

also may cause a light-brown discoloration of the vascular ring

similar to that caused by F, oxysporum f. sp. tuberosi.

Causal Factors

Organisms causing fusarium wilts can live saprophytically in the

soil on plant debris for many years.

The two types of fusarium wilt occur when potatoes are planted

in contaminated soil or when infected seed pieces are planted.

Tubers from soils with a high moisture content^ave more vascular

discoloration than those from dry soils. Wilt caused by F.

oxysporum f. sp. tuberosi is apt to be in warm soils, whereas wilt

produced by F. solani var. eumartii is in cool soils. Vascular ring

discolorations are present when the tubers are harvested. There is

no spread from diseased to healthy tubers during transportation or

storage, but the killed tissues are subject to invasion by secondary

organisms. The discoloration caused by F. oxysporum f. sp.

tuberosi, however, becomes more intense when tubers are stored at

50° F, and a wet rot may occur when infected tubers are stored at

60° to 70°. The disease caused by F. solani var. eumartii is favored

by high storage temperatures and high relative humidity. At 41° the

disease is completely checked and below 50° there is only slight

growth. Above 50° with high humidity the disease increases.

Causal Organisms

Fusarium oxysporum Schlect f. sp. tuberosi (Wr.) Synd. and

Hans, grows best on artificial medium at comparatively high

temperatures with an optimum for growth between 78° and

89° F, a minimum of 41°, and a maximum of 104°. The optimum

soil temperature for infection of roots is 86° or above. Fusarium

solani (Mart.) Appel and Wr. var. eumartii (Carpenter) Wr., on the

other hand, does not require a high temperature, with an optimum

for growth near 77°, a minimum near 41°, and a maximum between

91° and 95°. The optimum soil temperature for infection of roots is

68° to 77°, the minimum is 53° to 59°, and the maximum is about

86°. The maximum soil temperature for infection by F, solani var.

eumartii therefore is near the optimum for infection by F.

oxysporum f. sp. tuberosi. Sometimes F. avenaceum (Fr.) Sacc. is

also the cause of these wilts.

Control

Control consists of field rotation to reduce fusaria living in the

soil and avoidance of fields known to harbor the organisms. Storage
MARKET DISEASES OF POTATOES 25

below 50° F may lessen the development of vascular discoloration,

which can occur when tubers are stored at higher temperatures.

References: 74, 75, 106, 107, 124, 126.

Gray Mold Rot (Botrytis)

Botrytis cinérea Pers. ex Fr.

Gray mold rot usually occurs on potato tubers in storage, but it

may also appear in the field as a shoot blight and stem girdle.

Although the disease is considered to be minor in nature, it has

been reported in Maine, Connecticut, Ohio, Idaho, and Alaska. The

pathogen causes serious losses on other cultivated crops, such as

lettuce, escarole, endive, globe artichokes, and various fruits. Under

favorable conditions of low temperature and high humidity the

fungus may occur in any region.

Symptoms

In the initial stage of rot a pinkish-buff to brown semiwatery

breakdown of tissue may occur in any part of the tuber (pi. 4, E),

As the rot progresses the tubers become slightly withered and

flabby with grayish mycelium and masses of spores of the causal

fungus appearing at the stem end or near the eyes and in bruised

areas (pi. 4, F). Toward the end of the storage period, black

irregularly shaped sclerotia may appear in the surface growth of the

fungus.

Causal Factors

When a blight of the potato foliage and stems occurs in the field,

tuber infection can apparently result from the fungus growing down

through the stolons into the tuber stem end. This probably

accounts for the commonly occurring stem-end infections. When

potatoes are harvested without killing infected vines, the tubers can

become contaminated. Any inoculated wounded tubers may

become infected when high humidity and low temperature prevail.

However, under the normal temperature-humidity conditions

prevailing in most areas during harvest the bruised tubers can

develop wound periderm or new cells soon enough to prevent

invasion by the fungus.

Causal Organism

The causal organism Botrytis cinérea Pers. ex Fr. is a widespread

facultative parasite, which may comprise many strains. The
26 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

mycelium, which grows rapidly in artificial culture media, is at first

hyaline but becomes gray with age. The conidiophores are long and

slender, arising as branches of the mycelium. They are hyaline at

the tip and gray below the sporiferous region. Several branches

formed just below the tip rebranch one or more times, and the

apical cells enlarge and become round. Short sterigmata arise from

the apical cells bearing clusters of conidia. After the conidia mature,

sterigmata and branches collapse back to the main stalk, where they

are cut off by a septum. A scarlike projection remains on the main

trunk and marks where the branch originated. This process

continues to form new conidiophores and to produce new crops of

conidia. The conidia are hyaline or ash colored and appear gray in

mass. They are continuous and ovate, ranging from 8 by 11 to 11

by 15 ju. Sclerotia may be produced. They are hard, black, irregular

in shape, and about the size of a barley kernel or larger.

Control

Contamination of tubers at harvest can be prevented by vine

killing prior to harvesting. Any tubers exhibiting stem-end infection

at this time should be discarded. Proper curing of tubers at about

55° to 60° F and high humidity for 3 to 7 days before lowering the

storage temperature will allow for wound periderm formation in

mechanically bruised tubers. This recommended normal procedure

will help to control other diseases such as fusarium tuber rots.

References: 86, 116, 232,

Late Blight

Phytophthora infestans (Mont.) d By.

Late blight was first reported about 1830, when the disease

appeared almost simultaneously in the United States and in Europe.

Since then it has been reported in most areas of the world.

Destruction of potatoes by this disease contributed substantially to

the famine in Ireland about 1845.

Late blight is still one of the most important diseases of potatoes.

During wet, cool seasons it may be responsible for serious crop

losses in any potato-growing area. It is commonly found and

sometimes causes serious losses of early potatoes in the Atlantic and

Gulf Coast States, in the Rio Grande Valley of Texas, and in some

potato-growing sections of the Pacific Coast States. Normally,

however, the most serious outbreaks of late blight occur in the late

potato-producing States extending westward from the New England
MARKET DISEASES OF POTATOES 27

States through the Middle Atlantic States to and including the

States bordering the Great Lakes.

Symptoms

On potato tubers, late blight appears as purplish-brown,

reddish-brown, or brown areas, which, as disease development

continues, become distinctively shrunken and darker (pi. 4, G). In

storage, late blight tuber rot is moderately dry, firm, or leathery.

Sometimes severely infected tubers feel "rock like," and thin layers

of the dried infected skin can be peeled with a knife. This rot

usually does not extend more than one-eighth to one-fourth inch

into the tuber flesh. However, in newly harvested potatoes,

particularly those of the early southern crop, the yellowish, brickred, or reddish-brown granular breakdown often penetrates to a

depth of one-half inch or more (pi. 4, H; pi. 5, A). The decay may

also occur in the tissues at the stem end as a broad reddish-brown

ring, and in advanced stages the tuber may become a shriveled mass.

In newly harvested stock or in stock held under very moist

conditions, white tufts of sporangiophores or fungus growth often

appear at the lenticels, skin breaks, or eyes of the tubers.

Another effect of the disease in storage is the wet rot phase,

which is due to the invasion of secondary bacteria following late

blight development. This phase develops rapidly under warm,

humid conditions and causes a very wet, soft, or slimy and

foul-smelling rot. When other fungi, such as species of Fusarium,

follow late blight as secondary pathogens, an odorless dry or wet

rot may occur. The character of this rot depends on prevailing

temperature and moisture conditions.

Causa/ Factors

Tubers are infected in the potato hill by late blight spores washed

by rain from the diseased foliage into the soil. They are also

contaminated with spores of the fungus if they are dug while

diseased vines are still green or if they are piled in the field and

covered with diseased vines.

The powdery scab organism forms sites for entrance of the late

blight organism, particularly if the tubers are resistant to the blight

organism.

The presence of spores on a tuber does not necessarily mean that

the tuber will become infected. Infection develops only if

temperature and moisture conditions are favorable. Under dry

conditions below 40° F or above 86° the fungus spores will not
28 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

germinate. They may lie dormant on or in the tubers for many

months and germinate and produce symptoms only when the

environmental conditions become favorable. As a result, tubers

infected or contaminated with spores of the late blight organism

may appear healthy when they are placed in storage or in transit,

but late blight may be present when they are removed from storage

or on arrival at terminal markets.

During storage above 41° F with high humidity the fungus grows

from diseased tubers and produces spores that can infect healthy

tubers directly through the unbroken skin. At 60° or 71° with high

humidity, lesions on tubers enlarge at the rate of 2 inches in 10

days. If humidity is low during storage or transit, the fungus is not

apt to spread from tuber to tuber.

Potato tubers infected by Phytophthora infestans secrete a liquid

that favors the growth of soft rot bacteria and thereby causes the

wet rot phase. If the invading bacterium is pathogenic, such as

Erwinia carotovora, the wet rot spreads beyond the fungus rot,

whereas if the bacterium is saprophytic, the wet rot is confined to

the zone affected by P. infestans.

Causal Organism

Late blight is caused by Phytophthora infestans (Mont.) d By., a

member of the Phycomycetes.

Sporangiophores, which are hyaline, branched, and indeterminate, arise through the lenticels and eyes of the tuber. The

sporangia are thin walled, hyaline, and oval with an apical papilla or

beak. They range from 21 by 12 to 38 by 23 [i and are borne on the

tip of a hyphal branch (sporangiophore), which, as it approaches

maturity, swells slightly, proliferates, and turns the attached

sporangium to the side as elongation of the sporangiophore

proceeds. The sporangium may germinate directly by means of a

germ tube, but most commonly the germination is indirect with

cleavage within the sporangium, which forms eight biciliate

zoospores that emerge together.

The sporangia are produced at 37° to 79° F with an optimum of

64° to 72°, and a minimum relative humidity of 91 percent with an

optimum of 100 percent. Sporangia germinate directly by means of

germ tubes at 77°, whereas indirect germination by means of

zoospores occurs at an optimum of 54°. Zoospores germinate best

at 54° to 59°. After germination the zoospore germ tubes grow

most readily at 70° to 75°.

The fungus is generally cultured on frozen lima bean agar, on

which it produces white fluffy growth at 68° F.
MARKET DISEASES OF POTATOES 29

Control

When late blight is prevalent in potato vines, harvest should not

begin until the infected tops have been killed by frost or by a

herbicide vine killer, or they have died from natural maturity.

Tubers with any evidence of late blight infection should be

discarded during harvesting and storage.

In storage the holding temperatures should be maintained as

close as possible from 36° to 40° F. The wet rot phase can be

controlled with forced-air ventilation, which prevents the buildup

of moisture in storage. Forced ventilation also aids in maintaining a

uniform temperature throughout stored potatoes. By keeping the

storage environment relatively dry, forced-air ventilation also

prevents sporulation of the late blight fungus and the subsequent

spread of the disease from diseased to healthy tubers.

Washed lots of tubers containing late blight had less rot when

dipped in water at 120° F for 2 minutes and dried in an evaporating

chamber with an air temperature of 133° for 5 minutes than those

dipped in hot water only or washed in cold water.

As with all plant diseases, resistance is the ultimate in control

methods. Several potato varieties resistant to late blight are

available. They can be divided into (1) those possessing some

resistance to the common race of the pathogen and (2) those

immune to the common and certain other races of the pathogen but

susceptible to some races.

In the first group are the varieties Menominee and Sebago.

Although when compared with the varieties Irish Cobbler and

Katahdin, these varieties display considerable resistance, but they

cannot be used without protective fungicides. In the other group

are the varieties Cherokee, Kennebec, and Pungo.

In some areas where late blight is an annual problem, new races

of the fungus may arise suddenly. Under these conditions resistance

will not hold up. Furthermore, resistant varieties are generally

developed on the basis of foliage resistance, which does not

necessarily give resistance in the tubers. Therefore from the

standpoint of marketing problems, the value of resistant varieties is

indirect by preventing foliage blight.

Although protective chemical spraying of the vines is not

generally regarded as a control for blight of tubers, spraying

sometimes effects a very considerable reduction in tuber infection.

In some potato-growing areas the reduction in tuber infection has

been as great as 50 percent.

Late blight control measures may be summarized as follows: (1)

Use resistant varieties, (2) apply protective fungicide sprays in the
30 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

field, (3) do not harvest potatoes until the vines are dead or have

been chemically killed, (4) cull out infected tubers before storage or

transit, and (5) in storage hold potatoes at 36° to 40° F and use

forced-air ventilation.

References: 1, 25, 27, 28, 46, 51, 58, 158, 166, 187, 202, 208,

220, 237, 257, 272, 289, 297, 326,

Leak

Pythium debaryanum Hesse and P, ultimum Trow

Leak may occur wherever potatoes are grown, but it is of most

importance in the North Central States and in California. It may

cause serious losses at harvest, in storage, in transit, and on the

market.

Symptoms

External symptoms of leak are usually around wounds or near

the stem end. The affected area of red varieties becomes metallic

gray and that of the white or dark-skin varieties turns brownish or

water-soaked (pi. 5, B). Sometimes this area is slightly depressed.

Internally the freshly cut affected tissue is grayish cream, but on

exposure to air it turns reddish tan, then brown, and finally inky

black (pi. 5, C). The diseased areas may be separated from healthy

tissue by a dark-brown margin. The blackened tissue resembles

blackheart, but it differs as it is extremely watery and with slight

pressure a yellowish or brownish liquid is readily released. It is this

characteristic that justifies the name leak. When the decay is found

in stored potatoes, large quantities of juice from rotten tubers drip

down on the pile.

Rarely is mold growth visible as in the wet types of fusarium rot,

which may be confused with leak. Sometimes the entire inside of

the potato may rot and leave an outer shell about one-fourth inch

thick, even though only small external lesions are visible. This stage

of the disease is called shell rot.

Causal Factors

Tubers become contaminated in the field. Infection takes place

at harvest through wounds or bruises, which are often very

inconspicuous. Sometimes infection can develop from the stolon.

Hot, unusually wet weather favors the development of this disease.

It is frequently found in tubers with sunburn or scald. Normally
MARKET DISEASES OF POTATOES 31

leak does not spread from diseased to healthy tubers during storage

or transit.

Causal Organisms

Leak is caused by Pythium debaryanum Hesse, P, ultimum Trow,

and probably by other species of Pythium, They belong to the

family Pythiaceae, the most primitive of the Peronosporales.

Mycelium in the Pythiaceae has a diameter of 3 to 4 ju, rarely 7 /x, is

abundantly and irregularly branched, and may be septate at

maturity. On ag£ir or on decaying produce the fluffy snow-white

growth occurs. The sporangium usually is broader than the

mycelium and is symmetrical. The sporangial wall is smooth, and in

germination the sporangium discharges swarm spores into a

thin-walled vesicle, which later ruptures allowing the fully formed

spores to escape. The genus Pythium is closely related to

Phytophthora but differs in the more substantial appearance of the

hyphal contents and the looser branching of the mycelium. The

optimum temperature for growth of these organisms is IT to

87° F, the minimum 39°, and the maximum 104°. Entire tubers

may be rotted in a few days at about 77°, but decay develops

slowly between 40° and 50°.

Control

Losses from leak in storage, in transit, or on the market can be

reduced by careful harvesting and handling methods and keeping

the tubers as cool Eind dry as possible.

References: 3, 19, 109, 127, 153.

Phoma Tuber Rot (Gangrene, Buttonhole Rot)

Phoma solanicola Prill, and Del. and Other Phoma Spp.

Phoma tuber rot, a storage disease at low temperature, is

becoming increasingly more important in England, Ireland, and

Scotland. It also has been reported in the United States, Australia,

and in parts of Europe.

Symptoms

Infections occur first as numerous brownish to gray shallow

depressions on the surface of the tuber (pi. 5, D). These circular

spots may remain small and be corked off. Under favorable
32 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

conditions they may spread superficially over the surface of the

tubers and remain shallow (pi. 5, E), or they may be restricted to a

small surface area but extend deeply into the tuber and extensively

rot the tissue. The internal and external affected areas are separated

from healthy tissue by a dark border. Usually the rotted area is

gray, dry, and hard or bony. It can be removed and leave clean

cavities. The term "buttonhole rot" is applied when the sunken

surface spot extends to the cavities in the flesh of the tubers. Often

these cavities are lined with white fungal growth. Black fruiting

bodies are in this whitish growth or on the tuber surface. Eventually

a tuber may be reduced to a dry shell containing fragments of

rotted tissue.

Causal Factors

Phoma rot does not occur at harvest but develops during storage.

It is an important disease on tubers harvested during a wet growing

season where mud sticking to the tubers contains the organisms and

may result in infection. Cuts, bruises, and other injuries make

excellent entrance points. Development of phoma rot also is

associated with tubers infected with the powdery scab organism.

Causal Organisms

Phoma tuber rot is caused by Phoma solanicola Prill, and Del.

and the related species P. tuberosa (Melhus) Rosenbaum and

Schultz, P. foveata Foister, and P. eupyrena Sacc. P. foveata is

limited to Great Britain and northern Ireland and P. eupyrena

occurs in Europe and the United States. All these organisms

produce decay more rapidly at 40° to 50° F than at higher

temperatures. Decay usually will not develop when tubers are

stored at 70°, possibly because the wound barriers develop rapidly

at this temperature. Some of the decay caused by the dry type

fusaria is believed by some workers to be primarily due to Phoma

spp.

Phoma spp. have hyaline mycelium, which becomes septate and

dark with age. Sclerotia several millimeters in diameter are

produced in agar cultures. Pycnidia are dark and vary considerably

in diameter from 70 to 180 M and 175 to 420 ¡JL. Pycnospores are

hyaline, continuous, oblong, and 1.6 by 3 to 3.8 /i.

Control

Control consists of field rotations. Remove soil and other debris

from tubers before storing. Store at 70° F and high relative
MARKET DISEASES OF POTATOES 33

humidity for 7 to 10 days to stimulate development of wound

barriers before storing at lower temperatures.

References: 4, 50, 84, 94, 197, 205.

Pink Rot

Phytophthora erythroseptica Pethyb.

Pink rot is an important disease of potatoes in several European

countries and in many other regions of the world. In the United

States it is sporadic in areas where the soil normally is relatively

cool. It can be an important rot of potatoes in storage, but it is

rarely found on the market.

Symptoms

External symptoms occur usually at the stem end though

sometimes eyes and lenticels are infected. In white-skin potatoes

the infected area turns dark brown, whereas in red-skin potatoes the

first symptom is a fading of the red. A black band occurs between

the diseased and healthy tissue. Around the eyes and lenticels a

blotchy purplish or black discoloration develops (pi. 5, F\ pi. 6, A).

The skin of the rotted portion is easily sloughed off by rubbing and

exposes slightly darkened tissue with black spots beneath the

lenticels. There is little shrinking of the tubers even though they are

completely rotted. Rotted tubers may feel spongy or rubbery.

When squeezed, droplets of hquid come from eyes and lenticels,

and sometimes the droplets contain gas bubbles. Infected tubers

may give off a pungent odor resembhng formaldehyde.

When infected tubers are freshly cut, the tissue is granular and

dull white with no demarcation line between healthy and diseased

tissue. Within 15 to 20 minutes after cutting, infected tissue turns a

salmon pink (pi. 5, G; pi. 6, B), then brown to black. The flesh of

freshly harvested diseased tubers may be black when dug or turn

black after a day or two at high temperatures. Often blackened

areas are found about one-fourth inch below the surface and

sometimes the central pith is blackened. The moist or watery

condition of this tissue distinguishes pink rot from blackheart.

Sometimes small cavities about one-eighth inch in diameter occur

about one-half inch from the stem end. They do not extend deeply

into the tuber and do not contain fungal mats.

Causal Factors

Pink rot occurs chiefly in cool, wet, poorly drained soils. Wet

soils containing the fungus and adhering to tubers can cause eye or
34 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

lenticel infections during storage. The disease spreads rapidly when

tubers are held under moist conditions in storage but does not

spread if the tubers are kept dry.

Causal Organism

Pink rot is caused by Phytophthora erythroseptica Pethyb. The

organism lives in tubers, field debris, and soil. On artificial media

the organism can grow at 41° F with an optimum for growth near

77° and the maximum near 88°. Under moist conditions tuber

decay develops from 43° to 86° with a maximum amount at 76°. P.

drechsleri Tucker and Pythium debaryanum Hesse also can cause

pink rot of tubers under certain conditions, but neither organism

attacks growing plants. P. erythroseptica differs from many other

Phytophthora species since it will grow at 87° and produce sexual

bodies from sterile hyphae when transferred from pea broth to

distilled water. The oospores are 31 M , and growth is prevented by

1:8 million malachite green. For a more detailed description of

Phytophthora^ see Late Blight.

Control

Elimination of free moisture on tubers during storage will do

much to reduce development and spread of this decay.

References: 18, 32, 42, 43, 108, 154, 155, 175.

Powdery Scab

Spongospora subterránea (Wallr.) Lagerh.

Powdery scab was first reported in 1841 in Germany and by

1885 the disease was widely distributed in Europe. In 1891 it was

found throughout its original habitat of Ecuador, Colombia, Peru,

and Chile. The first report of powdery scab in North America was

in 1913 from specimens in eastern Canada, and the disease was

reported the same year in northern Maine. However, it was thought

to have existed in Maine for 15 years before it was reported.

Powdery scab has been occasionally reported since then from

Alabama, Florida, Maine to Pennsylvania, Minnesota, Mississippi,

Oklahoma, South Carolina, Washington, and Wyoming. In addition

to North America, the disease has since become established in the

U.S.S.R., South Africa, New Zealand, Australia, Rhodesia,

Morocco, Algeria, Kenya, and Madagascar.
MARKET DISEASES OF POTATOES 35

Symptoms

The first symptoms on the potato tuber are faintly brown raised

areas about the size of a pinhead. In about a week these areas

enlarge to about one-fourth inch, the brown disappears, and the

diseased tissue becomes jellylike. In these areas under the skin the

spore balls soon develop. When mature they become yellow brown

to black (pi. 6, C), and the epidermis splits and peels back to expose

the dusty spore mass formed beneath (pi. 6, D). Sometimes these

pustules enlarge to form cankers in the tuber. In storage a dry rot

develops in the pustule areas caused partially by a semisaprophytic

growth of the pathogen and partially by invasion of secondary

facultative parasites. No secondary infection by soft rot bacteria

occurs, but severely affected tubers are likely to shrivel more

rapidly in storage than normal ones.

Causal Factors

Under certain conditions the pathogen persists for undetermined

periods in the soil. However, the fact that the disease has remained

unimportant in the United States is good evidence that the

pathogen is restricted to a rather narrow range of optimum

environmental conditions. Periods of rainy, cloudy weather favor

the development of powdery scab, particularly in poorly drained

soil. Under warm, dry conditions the disease has reportedly failed

to reappear in fields where it had occurred previously. Powdery

scab has developed on tubers planted in infested greenhouse soil

when the temperature was not above 57.2° F and the soil moisture

was relatively high.

Causal Organism

Powdery scab is caused by Spongospora subterránea (Wallr.)

Lagerh. Alexapoulos classified it in the order Plasmodiophorales,

class Phycomycetes, and subclass Plasmodiophoromycetes. It was

first termed Erysiphe subterránea Wallr. in 1842 and later

reclassified as Spongospora solani Brunchorst. This classification

encompasses the group of slime molds that are obligate

endoparasites of vascular plants, algae, and fungi and usually cause

abnormal enlargement of the host cells.

S. subterránea possesses a plasmodium and a type of motile cell

similar to those of the Myxomycètes, the true slime molds. It forms

no fruiting bodies.

Apparently infection originates in the ameboid stage, which

results from the fusion of secondary zoospores. However, it is not
36 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

clear whether penetration of the tuber is directly through the skin

or indirectly through the lenticels. Intracellular plasmodia develop

after penetration by such amebae. Invaded cells are abnormally

enlarged and abnormal cell division may occur. This abnormal cell

growth and division form a wartlike excrescence. Generally lesion

development is checked in the tuber by the formation of a periderm

layer, although in some instances of early harvesting, disease

development may continue to cause a dry rot.

S. subterránea spores germinate rather readily on artificial media,

such as lima bean or potato agar, into single uninucleate amebae. If

growth conditions become unfavorable, the amebae encyst to form

a resting stage. On culture media they seem to produce saprophytic

plasmodia.

Control

No satisfactory control measures have been developed for

powdery scab. Since the disease is of minor importance in the

United States, no resistant varieties have been developed.

References: 5, 25, 94, 118, 164, 199, 205, 231, 257, 263, 297.

Scab

Streptomyces scabies (Thaxt.) Waks. and Henrici

Scab of potatoes has been known for over 100 years in both

America and Europe and is universally distributed throughout the

potato-growing regions of the world. The relationship of the causal

organism to the disease was first shown by Thaxter at the

Connecticut Experiment Station in 1890.

Although yields are generally unaffected, the losses from reduced

marketability of the crop may be very serious. Scabby tubers are

unsightly and wastage from the disease often exceeds the tolerance

for the U.S. No. 1 grade. Tubers may be unsalable when the lesions

are deeply pitted. The keeping quality may be impaired since

rot-causing organisms often enter the scab lesions, particularly the

deep pitted ones. An earthy odor and flavor are commonly present

in affected tubers.

Symptoms

Three phases of the disease are commonly found on potato

tubers—russet scab, shallow or surface scab, and deep or pitted scab.

The severity depends on the resistance of the variety, the
MARKET DISEASES OF POTATOES 37

physiologic race or virulence of the organism, and various cultural

factors.

The first symptom of scab is the appearance of small

reddish-brown spots on the surface of the young tuber. They may

develop into the netted appearance of russet scab, develop more

corky tissue resulting in shallow or surface scab, or develop still

further into deep or pitted scab (pi. 6, E),

Russet scab is merely a roughening, scurfing, or cracking of the

tuber skin, sometimes occurring in locaUzed areas or sometimes

over most of the tuber surface. It resembles the russeting due to

Rhizoctonia and other causes.

Shallow or surface scab consists of superficial roughened areas, at

times raised above but more often slightly below the surface of

healthy skin. The lesions consist of corky tissue caused by abnormal

proliferation of the cells of the tuber periderm as a result of

pathogen invasion. The size and shape of the lesions vary greatly.

They are usually darker than but not greatly different in color from

the normal skin. This phase may grade into the deep scab phase.

Deep or pitted scab may be darker than shallow scab and consists

of lesions ranging from 1 to 3 mm deep (pi. 6, E), As in shallow

scab the tissue around the interior of the pits is corky. This phase of

scab is generally believed to be due to the combined action of the

causal organism, chewing insects, and other pests attracted to

incipient lesions. However, some investigators have reported that

the insects and other pests feed only on dead tissue.

Scab lesions may be in the form of isolated spots of various sizes

and shapes or they may coalesce and form large scabby lesions on

the tuber. Surface cracking generally occurs when the lesions are

extensive.

Causal Factors

The pathogen is a common soil inhabitant and can be transmitted

on seed potatoes. Its development is inhibited by acid soil about pH

5.0 and lower and by alkaline soil higher than about pH 8.

Normally it occurs most severely in soil between pH 5.5 and 7.5. It

does not infect mature tubers; consequently, the disease does not

progress farther on infected tubers and does not spread to healthy

tubers in storage.

Causal Organism

In relatively recent years the organism causing scab was classified

as Streptomyces scabies (Thaxt.) Waks. and Henrici, one of the
38 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

higher or filamentous bacteria in the order Actinomycetales. Earlier

this organism was classed as Oospora scabies Thaxt. and changed to

Actinomyces scabies (Thaxt.) before being placed in its present

nomenclature.

In culture the aerial mycelium of S. scabies is prostrate and

branched with very slender threads. Colonies are compact, are

usually small, and emit a characteristic earthy odor. Sporogenous

hyphae are spiral. Minute spores are produced in chains by

segmentation of hyphae. Septa are at first formed at intervals along

the hyphae with final cleavage occurring when spores in the chain

mature. The spores are roughly cylindrical and hyaline, ranging

from 0.6 by 1 to 0.7 by 2 /x. They germinate by means of one or

two germ tubes.

Cardinal temperatures for growth of S. scabies are an optimum of

IT to 86° F, a minimum of 41°, and a maximum of 104°. Spores

germinate most rapidly at 95° to 104°. Early work showed that the

growth of the organism was inhibited by high acidity, but later

work pointed out that some isolates of the organism grow in culture

at a pH as low as 4.8.

S. scabies is an exceedingly variable organism as shown by

numerous workers who found that most isolates are unstable in

pure culture, producing variants that differ in physiology,

morphology, and pathogenicity. Researchers in the United States

and Europe believe that some of the different strains of the

organism cause the russeting and shallow scab and other strains

cause deep scab. Race 1 and race 2 have been described on the basis

of pathogenicity.

Control

No postharvest control methods are known except to avoid

scabby seed. The ultimate control measure for common scab is the

use of resistant varieties. Some U.S. varieties resistant to the

common scab organism are Blanca, Cherokee, Early Gem,

Menominee, Navajo, Ontario, Plymouth, Pungo, and Redskin. Some

russet-skin varieties, such as Russet Burbank, Russet Rural, and

Russet Sebago, have less conspicuous scab lesions than do

smooth-skin varieties.

References: 2, 22, 38, 136, 158, 167, 173, 184, 185, 236, 297,

Sclerotium Rot (Southern Blight)

Sclerotium rolfsii Saco.

Sclerotium rot occurs in early potatoes in most of the Southern
MARKET DISEASES OF POTATOES 39

States, but mainly in Florida and Alabama. It may be severe on

southern potatoes shipped in the spring and early summer.

Symptoms

Small, partially sunken, circular spots with intact skin about

one-eighth inch in diameter and with diffuse brownish margins

occur anywhere on the tuber but frequently near the stem end and

at the lenticels (pi. 6, F).As the spots enlarge, the skin ruptures and

they became noticeably sunken and yellowish to tan. Internally the

affected flesh at first is sunken, firm, odorless, and colorless. When

the spots enlarge and deepen, the wet, transparent flesh changes to

a chalky white and finally yellow.

The affected flesh has a cheesy or spongy consistency, and

particularly in early infections it can be separated from healthy

flesh with pressure. Later the invaded portions may dry, shrink, and

collapse forming cavities or the rot may be very moist. Potatoes

affected with the wet stage are called melters because of the liquid

released and the nearly complete disintegration of the tubers. As

the disease advances, a coarse white fungal growth containing white

to brown mustard seedlike bodies can be found both externally and

in the internal cavities (pi. 6, G).

Causa/ Factors

The stem portion of potato plants becomes infected near the soil

line during warm, wet weather. As the soil dries, the fungus migrates

below the soil level infecting roots and tubers. Tubers of plants

frequently cultivated, hilled up, or ridged are apt to be invaded by

this organism.

Causa/ Organism

The causal organism is Sclerotium rolfsii Sacc, a soil fungus that

is widely distributed in the Southern States, where it attacks a great

variety of truck crops and other plants as well as the potato. The

presence of the fungus is recognized by a fine, silky, white

mycelium closely appressed to the tubers. Grouping of mold

filaments into coarser strands is characteristic. Later numerous

sclerotia or round bodies, at first white and later brown and

resembling mustard seed, develop in the mycelium. The perfect

stage of this organism is Pellicularia rolfsii (Curzi) E. West. It

consists of basidia produced on mycelial mats on the surface of the

host. The basidia bear hyaline continuous basidiospores.
40 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

This fungus develops most rapidly at 86° to 95° F with a

minimum of about 46° and a maximum near 98°. Growth is slow

below 68°. It infects tubers in the growing stage or by contact

during harvesting or storage.

Control

Early harvesting of tubers to avoid periods of hot, dry weather

may afford some measure of control. After harvest the storage and

transportation of tubers below 46° F will prevent development of

the fungus.

References: 71, 72, 76, 132, 174, 189, 306,

Silver Scurf

Helminthosporium atrovirens (Harz) Mason and Hughes

Silver scurf was first discovered in Austria in 1871. Since then it

has been found in every potato-growing area of the world. The first

report of the disease in the United States was from Connecticut in

1908, when it was called scurf by Clinton. The disease has been

known by various names since its discovery—Fleckenkrankheit,

Phellomyces-Faüle, scab, dry rot, gale argentée (silver scab), and

finally silver scurf, as named by Melhus in 1913.

Silver scurf was considered of little importance and was relegated

to the minor potato disease category. However, with the increased

demand for washed potatoes in the United States, the disease has

become more important to the producer. As with some of the other

potato tuber blemishes, the symptoms of this disease are often

masked by soil particles adhering to the skin of unwashed tubers.

However, when the tubers are washed, the blemishes are exposed

and are often of sufficient severity to reduce the grade of table

stock potatoes and to prevent certification of seed potatoes.

Symptoms

In its early stage the disease appears on the tuber surface as

rather inconspicuous circular or irregular brown lesions, which

often are seen first at the stem end. Although these areas are

difficult to distinguish on dry tubers, they are readily seen on

washed or moistened tubers often as silvery areas, hence the name

silver scurf. This silvery condition is caused by the pathogen, which

penetrates the tubers through the lenticels and epidermis and is

confined to the phellem tissue causing it to loosen. Air trapped
MARKET DISEASES OF POTATOES 41

under the loosened skin causes a reflection of light and the silvery

sheen (pi. 6, H).

As the disease progresses, the lesions become silvery brown and

may coalesce to cover most of the tuber surface (pi. 7, A). The

loosening and sloughing of the outer cork areas of the skin are

responsible for excessive water loss from the tuber. This condition

is followed by shriveling, wrinkling, or even a folding of the

affected areas during storage.

In the early stages of secondary infection in storage the so-called

brown mold stage appears as an olivaceous blackening over the

affected areas. This stage is caused by the production of conidia and

conidiophores of the fungus. Under favorable conditions of

humidity and temperature the entire surface of the tuber may

become dull black and appear sooty.

Causal Factors

The causal organism lives from year to year in the soil and on

infected tubers. The primary disease cycle occurs in the soil from

spores and mycelium produced in the lesions of infected seed

pieces. Potato tubers become more susceptible as they mature in

the soil before harvest. Tests have indicated that the primary disease

cycle is initiated after the tubers have matured and while they lie in

the soil before being dug.

Tubers are highly susceptible during storage. Although the

secondary disease cycle may originate in the field from the primary

lesions, most of the secondary infection, or spread of the disease

from diseased to healthy tubers, occurs in storage. High humidity is

essential for development of the secondary disease cycle. After the

tubers have reached an equilibrium with the ambient air, no new

lesions are formed at a relative humidity of 89 percent or below.

There is little sporulation of the fungus below 95 percent relative

humidity.

Unregulated temperature and humidity conditions in storage,

particularly farm storage, are very favorable to the secondary spread

of the disease. During initial storage after the curing process, when

the storage temperature is slow in dropping to the holding

temperature, there is a rapid succession of secondary disease cycles.

The fungus grows rapidly at 70° to 80° F when the relative

humidity is high.

Causal Organism

The causal organism Helminthosporium atrovirens (Harz) Mason

and Hughes (Spondylocladium atrovirens Harz) is classified in the
42 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

order Moniliales of the class Fungi Imperfecti. It has a septate,

branched mycelium, which is first hyaline but becomes brown with

age. The conidia are borne in whorls from the distal end of the cells

of unbranched conidiophores. Conidiophores are septate, ranging

from 7 to 8 M in width and 150 to 375 M in length. The spores are

dark and vary from 7 by 18 to 8 by 64 ß.

The temperature for growth in culture is 43° to 88° F with the

optimum at 70° to 81°. Although the fungus grows best in culture

with a neutral reaction, it can grow through a wide pH range. In

laboratory cultures the fungus grows best at a relative humidity of

98 percent, with very little or no growth below 90 percent.

The fungus does not fruit as readily in culture as it does on

tubers kept in a moist chamber, but when grown on a green bean

cultural medium, conidia are abundantly produced. The first

growth of mycehum can be seen in about 5 days on agar plates,

with conidia appearing about the 12th day. The fungus grows

slowly both on agar plates and on the host. Two types of mycelium

are common in culture—the normal straight, septate, brown

mycelium and the dark globular cells.

Control

Generally no direct methods are used to control silver scurf. Any

limited control of the disease comes indirectly from methods used

to control other diseases.

The trend toward using forced-air ventilation in potato storage

presents a means of controlling the disease by manipulating the

temperature and relative humidity. Proper manipulation of forced

air will reduce the development and spread of secondary disease

cycles during storage. Forced air is particularly useful for rapid

cooling of the storage after the curing period.

The best way to control any plant disease is to eliminate the

source of primary infection. For silver scurf this is on the potato

seed. Better methods of handling and treating seed are needed to

clean up the infected seed potatoes that often escape detection.

Washing seed potatoes may be a way to prevent undetected

infections.

The most effective control methods are (1) plant only

disease-free seed potatoes, (2) harvest potatoes as soon as possible

after maturity, (3) cool stored potatoes as rapidly as possible after

the curing period, and (4) use forced-air ventilation to control

temperature and relative humidity during the holding or storage

period.

References: 37, 204, 252, 256, 315,
MARKET DISEASES OF POTATOES 43

Skin Spot

Oospora pustulans Owen and Wakef¡eld

Skin spot is a minor disease of potato tubers in the United States.

It has been reported on domestic potatoes in Maine and on

imported potatoes in Pennsylvania and Washington. The report

from Washington was on potatoes shipped from British Columbia.

Skin spot occurs at low temperatures and has been reported only

in the cooler potato-growing regions of the world. It is a disease

that develops in storage and is most destructive when infection

occurs near the eyes of the tubers and hence prevents sprouting of

seed pieces, which results in missing hills. In the United Kingdom

the disease is considered serious on stored seed potatoes and reports

of 20 to 30 percent loss of seed stock due to the disease are

recorded.

Symptoms

This is one of the less conspicuous potato tuber diseases, and

even with severe infection the spots are difficult to detect unless the

tubers are washed. It is not unusual for apparently healthy seed

potatoes in the fall to have such a high incidence of skin spot in the

spring that many tubers fail to sprout. Lesions appear as small,

dark, slightly raised pimples, about one-eighth inch in diameter,

which are usually superficial on the tuber skin (pi. 7, B), The

disease does not cause a rotting of the tuber and the blemishes can

generally be removed by peeling. However, deep penetration of the

tuber has been reported in potatoes that had previously been

treated with a sprout inhibitor. This condition has been attributed

to prevention of the formation of a cork barrier by the tuber. Skin

spot develops extensively under these conditions and renders the

affected tubers unsalable.

Causal Factors

Although slight mechanical injury to tubers at harvest can

promote infection, skin spot can often establish itself without

harvest bruises. Infection takes place about harvesttime through the

eyes, lenticels, and slight bruises and leads to disease development

in storage. This usually is not evident until the tubers are removed.

In the United States some investigators believe the pathogen is a

secondary invader following powdery scab. British investigators do

not share this view. The disease development is considerably

affected by the prevailing storage conditions. Studies in Scotland
44 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

have confirmed that low temperature and high humidity in storage

favor disease development. These workers found that potatoes

stored at processing temperatures in pallet boxes in well-ventilated

storage had less skin spot than potatoes stored in pallet boxes in

similar storage but at a lower temperature.

British reports indicate that varieties differ in their susceptibility

to skin spot, but susceptibility to general surface infection of the

skin and to eye infection is not necessarily correlated. Some

varieties show a much higher incidence of surface infection than

others. However, those varieties high in susceptibility to surface

infection may be less susceptible to eye infection.

Causal Organism

Oospora pustulans Owen and Wakefield, the causal fungus, has a

hyaline septate mycelium, 2 to 4 // in diameter, from which short,

erect, branched conidiophores arise. Conidia are produced by

budding on the conidiophores, where they remain attached to form

a chain of spores.

O. pustulans is not difficult to isolate after thorough disinfection

of the tissue surface. The organism grows well on oatmeal agar and

on cooked tissue of such vegetables as potato, carrots, and parsnips.

In culture, growth is best at room temperature in complete

darkness.

Control

Skin spot can be effectively controlled by storing potatoes in

pallet boxes under relatively dry conditions. Initial storage temperatures should be sufficiently high to properly cure the potatoes.

Combined tuber washing and chemical dip followed by complete

drying is being used commercially in Scotland to control skin spot

on seed potatoes.

References: 34, 64, 73, 83, 114, 128, 213, 224, 263, 297,

Verticillium Wilt

Verticillium albo-atrum Reinke and Berth.

The seriousness of verticillium vrilt varies from season to season.

Generally the disease appears to be increasing both in areas affected

and in severity, partially because some of our most desirable

varieties are highly susceptible to the disease. The disease may

escape detection in the field during some seasons and only becomes
MARKET DISEASES OF POTATOES 45

apparent when the harvested tubers are cut. The only direct effect

of verticiUium wilt on tubers is the internal discoloration, which

makes the potatoes undesirable to the consumer and unacceptable

for certified seed.

VerticiUium wilt is found in the United States chiefly in the

Northeastern and Western States, but it has also been reported in

Arkansas, Florida, Louisiana, Virginia, and West Virginia. It is

considered to be important in eastern Canada, Maine, and western

Oregon and severe in Idaho where yields are reduced.

Symptoms

The xylem or water-conducting tissues in the stem end of tubers

often are yellow red to brown (pi. 7, C and D). This discoloration

resembles stem-end browning, but it differs since often it extends

throughout the vascular ring. Verticülium wilt is found in two of

our most widely grown late varieties, Kennebec and Katahdin,

which are not affected by stem-end browning. Also, internal

discoloration does not always occur in infected tubers.

VerticiUium wilt is often indirectly responsible for tuber

breakdown in storage because of a complex called pinkeye (pi. 7, E

and F). See Red Xylem and Pinkeye.

Causa/ Factors

VerticiUium wilt is spread through infected seed. The disease

apparently predisposes the tuber to infection by the pinkeye

bacterium. Moderate temperatures favor the organism and the

disease does not develop under extremely high temperatures. The

optimum temperature at which it occurs is 77° F, the minimum

41°, and the maximum 86°.

High surface moisture and high storage temperature favor the

development of the pinkeye soft rot breakdown in storage.

Causal Organism

This disease is caused by VerticiUium alho-atrum Reinke and

Berth., which was formerly caUed VerticiUium dahliae Klebahn. The

fungus is classified in the order Moniliales of the class Fungi

Imperfecti. Conidiophores are slender with verticUlate (in whorls)

branches. The conidia are ovoid to eUipsoid, hyaline, one-ceUed,

and borne singly or in smaU apical clusters. The mycehum is septate

and hyaline when young but produces darkened branches or smaU

sclerotia later.
46 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

The maximum temperature for growth of Y. albo-atrum is 86° F.

Spores are unable to germinate at 95°. A slight correlation exists

between the temperature relations of the fungus in pure culture and

its geographical distribution and seasonal occurrence. Strains of the

fungus in the Northern United States have comparatively low

maximum and low minimum temperature points, whereas those in

the Central United States exhibit higher maximum temperature

points although retaining practically the same moderate optimum

temperature point.

Control

No postharvest control measures are possible for verticillium wilt.

However, the disease can be prevented or reduced by using clean

certified seed, rotating potatoes with millet, oats, or corn, and

planting resistant varieties.

The susceptibility of V, albo-atrum to high temperatures suggests

the possibility of heat treatment for infected seed.

References: 6, 20, 38, 90, 158, 242.

Wart

Synchytrium endobioticum (Schilb.) Pare.

Potato wart became known in the United States in 1918, when it

was found in garden plots of several villages in the hard-coal

districts of eastern Pennsylvania. It has since been found in small

scattered coal-mining districts of western Pennsylvania, western

Maryland, western Virginia, and West Virginia. The disease

originated with infected tubers imported from Europe. Because of

strict quarantine regulations it is unlikely that potatoes with this

disease will be found on the market. The potential seriousness of

wart makes it imperative that all field and market inspectors

familiarize themselves with the disease symptoms.

Symptoms

The disease causes spongy outgrowths on the tuber particularly

at the eyes. At first the warts are light brown (pi. 7, G). With age

they enlarge, darken, and eventually become black (pi. 7, H). They

may vary from the size of a pea to that of an entire tuber. Either

few or many warty outgrowths may occur on a potato. Wart can be

slight and easily overlooked on potatoes at harvest but may develop

in infected eye tissue during storage.
MARKET DISEASES OF POTATOES 47

Causal Organism

Potato wart is caused by a fungus, Synchytrium endobioticum

(Schilb.) Perc. This organism lives entirely within the cells of the

potato, where it forms numerous rusty-brown resting spores, which

are globoid and oval and when mature have a thick, rough, outer

wall.

Control

If potatoes with this disease are found, their source should be

determined and the facts reported promptly to the U.S. plant

quarantine authorities.

References: 65, 125, 222.

Xylaria Tuber Rot

Xylaria apiculata Cke.

Xylaria tuber rot is a very minor potato disease. It has been

reported only in southern Florida.

Symptoms

The disease causes a circular, sunken, light-tan dry rot, which

generally is followed by secondary fungi and bacteria.

Causal Factors

The fimgus is a common saprophyte on tree stumps and other

wood debris in the soil of newly cleared land. The disease is found

only on recently cleared land and generally disappears after a few

years of cultivation.

Causal Organism

The causal organism is Xylaria apiculata Cke., an ascomycete.

The fungus produces in the soil slender black rhizomorphs or coarse

threads, which become firmly attached to the potato tubers.

Control

There is no practical control once infection occurs.

References: 33, 251.
48 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

VIRUS DISEASES

The potato is subject to attack by a wide variety of virus diseases.

These include several mosaics, leaf roll, spindle tuber, witches'-

broom, yellow dwarf, purple top, and corky ring spot. Each is caused

by a specific virus or combination of viruses. If the many strains of

the viruses are considered, the number responsible for potato

diseases becomes very large. Virus diseases are caused by nucleoproteins, which can replicate in plants. Only a few of the virus

diseases produce tuber symptoms that are apparent on the market.

Corky Ring Spot

Under the names of sprain and internal rust spot this disease has

been known for many years in the Netherlands, other European

countries, the Indies, and South Africa. It was observed on the

Chicago market in 1944 and 1945 in Washington-grown 'White

Rose' potatoes. In 1946 it seriously damaged tubers in some fields

in Florida and was given the more descriptive name of corky ring

spot.

Symptoms

Affected potato tubers show brown rings, semicircles, loops, and

spots on the surface (pi. 8, A) and similar brown rings, loops, and

spots in the interior tissues (pi. 8, B). The skin often cracks over

some of the brown slightly sunken rings. The surface markings can

usually be traced to similar markings within the tuber, but many

internal brown spots and semicircles appear to be independent of

the surface lesions. The affected tissues are moderately firm and

corky.

The characteristic ringlike external and internal markings of

tubers affected with this disease distinguish it from internal brown

spot and tuber necrosis caused by alfalfa mosaic.

Causal Factors

Tubers from crops infected with corky ring spot may appear

healthy when harvested but develop the disease in storage. The

number of tubers showing symptoms and the size of the lesions

increase as the temperature is raised from 60° to 80° F. No lesions

develop in potatoes stored at 90°.
MARKET DISEASES OF POTATOES 49

Causal Agents

Corky ring spot is a virus disease caused by a combination of two

soilborne viruses. One is an etching virus and the other a necrotic

virus.

Control

'Sebago' and *Red Pontiac' potatoes are very susceptible to corky

ring spot. 'Merrimack/ Tungo/ 'Plymouth,' and 'Hunter' are

resistant.

Storing potatoes below 60° F will retard development of corky

ring spot after harvest.

References: 57, 65, 68-70, 190, 235, 299, 300.

Net Necrosis (Leaf Roll)

Net necrosis is probably the most important virus disease of

potato tubers. Discoloration of the vascular ring and vascular

strands in the flesh of the tuber results in serious market losses.

Particularly for chip manufacture, affected tubers are worthless.

Discoloration of the vascular elements can become more pronounced during storage, transit, and marketing.

Symptoms

No external symptoms of net necrosis occur. The disease is most

readily detected when cuts made near the stem end show a network

of discolored phloem strands (pi. 8, C). The affected strands

become hardened and turn dark brown to blackish. Their appearance varies with the angle the tuber is cut. In cross sections they

show up as dots or streaks, but lengthwise cuts, after removing only

a thin layer of the outer flesh, show a network of brownish phloem

strands (pi. 8, D). These discolored strands may extend throughout

the tuber to the bud end and are found in the heart of the tuber as

well as in the outer flesh. Often it is necessary to cut several sides of

a tuber before discolored strands can be found extending throughout the tuber.

Net necrosis can be confused with several other diseases, possibly

the most important of which is stem-end browning. It differs from

stem-end browning since the discolored phloem strands may

extend throughout the tubers, whereas the discolored strands of
50 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

stem-end browning are limited to not more than one-half inch from

the stem end. Net necrosis also is usually found in large tubers, and

in cross section the cuts show more concentric zones than in

stem-end browning. Net necrosis differs from the fusarium wilts and

vascular browning because the latter are confined to the xylem

strands. It differs from freezing injury, which may produce blue to

grayish strands not distinctly defined. The discolored strands caused

by freezing also are often associated with grayish areas in the flesh.

Causal Factors

Net necrosis occurs in tubers harvested from cool soils. It may or

may not be present at harvest but shows up after the tubers are

stored. Symptoms are more pronounced when soils have a high

potassium content and are masked when soils contain high nitrogen.

Causal Agent

Net necrosis is a tuber symptom of the virus that causes leaf roll

of growing plants. It occurs only when healthy plants of the current

season are inoculated with the virus. Progeny of net necrosis tubers

will produce plants with leaf roll, which in turn produce symptomless tubers. Storage conditions bring out tuber symptoms. Maximum development of symptoms occurs in tubers stored near 50° F.

If tubers are held for 60 days at 32° to 36° or at 70° and then

stored at 50°, symptoms of net necrosis are greatly reduced.

Maximum development of symptoms occurs in 2 to 3 months.

In early shipments net necrosis may increase during transit and

marketing. Such could arise from shipping tubers near 50° F shortly

after harvest or shipping them near this temperature when the

conditioning period at 32° to 36° or 70° was 30 days or less.

Tubers conditioned for 60 days or longer at these temperatures may

therefore have less net necrosis than tubers from the same lot

shipped without proper conditioning earlier in the season.

Control

Use certified seed potatoes and proper control measures for

aphids that spread the virus from diseased to healthy plants.

*Chippewa' and 'Katahdin,' although susceptible to the leaf roll

virus, remain practically free of net necrosis. Whenever there

appears to be extensive spread of the virus during the current

season, reduction in losses from net necrosis can be obtained by

conditioning the newly harvested tubers and holding them at proper
MARKET DISEASES OF POTATOES 51

temperatures. Studies have also shown that long exposure to hot air

or relatively short exposures to hot water will kill the virus in a high

percentage of the tubers.

References: 56, 65, 80, 85, 87, 92, 101, 102, 119, 157, 272, 278,

293, 305, 319.

Purple Top Wilt

Purple top wilt occurs in most areas where potatoes are grown.

On the market it is important as sometimes tubers from infected

plants have vascular discoloration. This discoloration is common in

potatoes grown in Wisconsin, West Virginia, Pennsylvania, Maryland, and Virginia but occurs only rarely in potatoes from Maine,

New York, and Nebraska.

Symptoms

The intense yellowish brown of the vascular strand occurs at the

point of the stolon attachment and extends inwardly and sometimes throughout the tuber (pi. 8, E). Often the necrotic stolons

separate from the stem end leaving a cavity at the point of their

attachment. Browning is most severe in the vascular ring, but often

it extends into the cortex and pith parenchyma. This discoloration

of strands in the cortex and pith parenchyma distinguishes purple

top wilt from other diseases that cause vascular discoloration. In

addition to this symptom, tubers from plants infected with purple

top wilt often are soft and flabby. Infected tubers also frequently

produce weak or hair sprouts.

Causal Organism

Purple top wilt has been considered to be due to a virus that

produces yellows of asters and many other plants. Recently several

studies have shown that the cause of the yellows-type diseases is a

mycoplasmalike organism. Most of them are spherical and range

from 70 to 700 nm. Unlike viruses they can be cultivated on

specialized media. They divide by binary fission and sometimes by

budding. These organisms have been found in the salivary glands

and alimentary tract of insects that transmit the yellows-type

diseases.

Control

There are no postharvest control methods.

References: 59, 65, 145, 172, 200, 219, 254, 261, 325.
52 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

Spindle Tuber

Spindle tuber is likely to be found on market potatoes from

certain sections of the country.

Symptoms

Tubers affected with this disease are characteristically spindle

shaped or cylindrical with the ends, particularly the bud end,

abnormaUy long and pointed (pi. 8, F). The eyes are more

numerous and shallower than those of healthy potatoes, but they

appear conspicuous because of prominent eyebrows. Frequently the

red-skin varieties fade. The smallness and spindle shape lower the

grade of affected potatoes.

Control

Use certified seed. No specific postharvest control method

is known.

Reference: 65,

Tuber Necrosis (Alfalfa)

This disease is caused by the alfalfa mosaic virus and was first

observed in 1946 in California potatoes grown adjacent to alfalfa

plantings.

Symptoms

Necrosis in the tuber first develops just under the skin near the

stem end. At this stage the affected areas have a purplish or silver

cast and resemble late blight infection. Later the diseased areas

extend into all parts of the tuber (pi. 8, G and H). The necrotic

tissues are deep brown, very dry, and corky to mealy in

consistency. They may occur in pockets throughout the tuber or on

only one side. In later stages the affected tissues dry out, crack,

become sunken, and resemble a fungus dry rot.

Control

No postharvest control methods are known.

References: 65, 223.

Yellow Dwarf

Potatoes affected with yellow dwarf are seldom found on the

market. Although not all tubers produced on diseased vines show
MARKET DISEASES OF POTATOES 53

external symptoms of the disease, most of them are malformed and

have cracks, which make it possible to grade out the affected tubers

before shipment. Internal discoloration also makes them unsuitable

for table use.

Symptoms

The tubers produced on plants with yellow dwarf are usually

small, irregular, knobby, and cracked. The cracks, which are

one-eighth to one-fourth inch deep, often radiate from the bud end

and resemble growth cracks. They usually heal without infection by

decay-producing organisms. When diseased tubers are cut, rustybrown specks and spots scattered in the pith area and extending

from the bud end halfway to the stem are characteristic symptoms.

Discoloration is seldom found at the stem end.

References: 11, 17, 65, 120, 298.

Other Virus Diseases

Potatoes from plants infected with the tomato spotted wilt virus

sometimes are distorted and show necrotic spotting and cracking.

Potatoes from plants affected with tuber blotch and Canada streak

may have internal discolored, blotchy spots. With tuber blotch

some of these necrotic areas may appear externally as dark sunken

lesions. Neither disease has been reported on potatoes grown in the

United States. Similarly the veinal mosaic virus may cause both

superficial and internal necrotic areas in the tubers of some foreign

varieties of potatoes.

Reference: 65.

NEMATODES AND THEIR INJURY

Golden Nematode

The history of the golden nematode (Heterodera rostochiensis

WoUenwebber) in the British Isles and in continental Europe

indicates that it is a serious threat to the potato industry wherever

it becomes established. Surveys of the U.S. potato-producing

sections have revealed its presence only in New York State. It was

reported first in 1941 in relatively localized districts of Nassau

County, Long Island, N.Y., and was later found in adjoining Suffolk

County. In 1967 the nematode was found in western New York in

Steuben County near the town of Plattsburg.
54 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

Symptoms

The nematode attacks the root system of the potato plant,

causing stunting, midday wilting, early dying of the vines, and a

reduced yield of marketable tubers. Four to six weeks after the

plants are attacked the female nematodes can readily be detected

on the roots with the unaided eye. They first appear as white

spherical bodies, later turning golden brown. No symptoms are

evident on the tuber itself, but the orange or golden-brown

spherical female cysts may be found in soil clinging to the tubers.

Control

Restrictions have been imposed by New York State to prevent

further spread of the nematode and thus to prevent its introduction

into other areas. In districts where it has been introduced, control

becomes very difficult because it can survive long periods in the

absence of a host. Some measure of control has been obtained by

long rotations. Nematode populations may be reduced by applying

certain nematicides. Development of commercially acceptable

varieties resistant to the golden nematode offers much promise in

controlling this disorder.

References: 47, 53, 191, 277, 288.

Root Knot (Nematode Gall)

Root knot (Meloidogyne spp.) has been reported on potatoes

from almost all sections where they are grown commercially.

Affected tubers are occasionally found on the market but are

usually graded out before shipment.

Symptoms

Potato tubers with advanced stages of this disorder appear

roughened, irregular, bumpy, or warty because of galls on the

surface (pi. 9, A). The skin over the gaUs usuaUy remains

unruptured. When such tubers are cut open, the female nematodes

are abundantly scattered through the outer tissues, with most of

them approximately one-eighth to one-fourth inch beneath the

tuber surface. They have whitish, spherical bodies about the size of

a small pinhead, each surrounded by a thin layer of brownish

potato tissue (pi. 9, B). The infected parts of the tubers thus appear

somewhat discolored with some slightly water-soaked spots sur-
MARKET DISEASES OF POTATOES 55

rounding the infected area. Under slight infection, tubers sometimes

show no external symptoms.

Causal Agents

Root knot of potato is caused by several species of the nematode

genus Meloidogyne, Between crop seasons it maintains itself as eggs

or larvae in roots, tubers, or soil. When the nematode larvae come in

contact with the developing tubers, they enter these plant organs,

become sedentary, and begin to enlarge as they feed on the plant

tissue. The female enlarges enormously in diameter so that she

eventually becomes pear shaped and visible to the unaided eye. The

nematodes irritate the tissues, which develop abnormally and form

the galls. Larvae hatching from eggs within the tuber may move a

short distance within the tuber, initiate new galls, and continue to

develop there.

Control

There are no postharvest control measures, but several nematicides afford good field control of root knot. Resistant varieties are

not available.

References: 52, 53, 104, 207, 287, 288, 292.

Rot Nematode

The only known occurrence of the rot nematode (Ditylenchus

destructor Thorne) on potato in the United States was reported in

Idaho and Wisconsin in 1943 and 1953, respectively. Elsewhere on

the North American continent it has been found on Prince Edward

Island and in British Columbia, Canada. In 1946, seed shipped from

Prince Edward Island was intercepted at Long Island, N.Y., and

found infected with the nematode. Apparently none of the infected

seed pieces were planted.

Symptoms

Only tubers are infected. Small gray or brown spots of decaying

tissue on the skin of the tubers are the first symptoms of nematode

attack. Beneath the skin these appear as chalky areas in which the

nematode can be foimd. Affected tissues dry out as the lesions

enlarge and the skin shrinks and cracks. In more advanced stages the

decaying tissues form a shallow, dark-brown layer just beneath the
56 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

epidermis (pi. 9, C) and deeper tissues become bluish gray. Injury

may be serious in the field at the time of digging and most often

increases in severity with invasion of secondary organisms in

storage.

Control

The principal control measure for rot nematode in the United

States is to prevent its spread into new areas in infected seed stocks.

Nematicides have been very satisfactory for field control of this

nematode.

References: 9, 53, 78, 288.

INSECTS AND THEIR INJURY

Several insects attack potato tubers and cause various types of

injury. The following descriptions include the insect injuries that

are most apt to cause economic losses of market potatoes. In most

cases if the injuries are pronounced, the tubers never reach the

market. No postharvest treatments to control these insects are

known.

Potato Tuberworm

The potato tuberworm {Phthorimaea operculelh Zeller) is most

damaging to the tubers after they have been dug. However, exposed

tubers may be injured before digging. The larvae migrate from the

stems and leaves to exposed tubers. Harvested tubers left in the

field overnight may also become heavily infested by larvae moving

from vines to tubers. After the eggs hatch on the tubers either in

the field or in bins or sacks, the larvae at first work under the skin

and later tunnel through the flesh. They often enter at the eyes,

where sawdustlike heaps of material are evidence of their activity.

After transit or storage the infested tubers are frequently riddled

with deeply penetrating channels that make them unmarketable.

The damage by this insect is more severe in certain sections of

California and the Southern States in years of low rainfall.

References: 195, 206,

Spotted Cucumber Beetle

In the early potato-producing areas in the South the larvae of the

spotted cucumber beetle (Diabrotica undecimpunctata howardi
MARKET DISEASES OF POTATOES 57

Barber) sometimes tunnel into the tubers and leave surface holes.

When small tubers are invaded, the remaining channel is rather deep

by the time the tubers are of marketable size. In red-skin potato

varieties the lining of these channels and pockets is red.

References: 195, 206.

Tuber Flea Beetle

The larvae of the following beetles feed on potato tubers and

cause injury: The tuber flea beetle (Epitrix tuberis Gentner) and to

a less extent the western potato flea beetle {E, subcrinita Le Conte)

and the potato flea beetle {E, cucumeris Harris). In feeding on or

near the surface of young tubers they produce pimples (pi. 9, D)

and channels in and under the skin. Deeper feeding results in the

formation of brown splinterlike pegs extending one-eighth to

one-fourth inch into the tuber (pi. 9, E), These corky splinters,

pimples, and channels are so tough and dry that usually no

secondary infections by bacteria or fungi occur.

Injury by the tuber flea beetle is severe in eastern Colorado and

western Nebraska, but it is no longer a pest in most of Oregon and

Washington. The western potato flea beetle causes little damage to

the tubers, although it is associated with the tuber flea beetle. The

potato flea beetle has a wide range, but in the Eastern States where

it is most abundant, it does not usually cause much damage to

tubers.

References: 195, 206,

Wireworm

Wireworm injury caused by the larvae of the snapping or click

beetles (Elateridae) is of several types. The larvae burrow into the

growing tubers, the depth and size of the burrow depending on

their size and length. Large worms attacking tubers late in the

season bore clean-cut round holes rather deep into the tuber (pi. 9,

F). These channels and burrows may be brown and lined with cork

or may become plugged and surrounded by dead tissue caused by

secondary infection with Rhizoctonia,

Holes made in tubers by quackgrass and nutgrass sometimes

appear similar to those made by wireworms. However, the remains

of these grasses in the tuber usually indicate this kind of injury.

References: 195, 206,
58 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

NONPARASITIC DISORDERS AND INJURIES

Blackheart

Blackheart develops in tubers while they are growing or while

they are in transit or storage. It occurs in all varieties of potatoes

from all growing areas. It is important on the market because

normally no external symptoms are apparent, but the blackened

internal tissue makes the tubers worthless for culinary purposes or

processing.

Symptoms

External symptoms of blackheart appear only after affected

potatoes have been stored for long periods and almost the entire

inner tissue is discolored. The skin of such tubers is bluish to gray

blue. The discoloration sometimes covers the entire surface but

normally is restricted to distinct areas.

Internally blackheart may have several symptoms. When freshly

injured potatoes are cut, the affected flesh at first appears normal,

but within minutes various-sized pink areas develop. In about a half

hour these pink areas become jet black with a light grayish-pink

center, which eventually becomes black (pi. 9, G). When freshly cut

tubers show blackened areas, they have been injured for several

days or weeks. The entire central section of the tubers may be

discolored (pi. 9, H) or the black areas may appear as isolated

pockets about one-fourth inch in diameter distributed throughout

the flesh (pi. 10, A). The affected flesh is firm but not crisp, and

usually is not separated from healthy tissue by a definite border.

With prolonged holding the blackened tissue collapses, leaving

hollow cavities with blackened walls.

Causal Factors

Blackheart occurs at any temperature when the supply of oxygen

available to internal tissues is used up faster than it can be supplied.

The affected tissue suffocates and turns black. Conditions causing

blackheart can occur in the field when the soil is flooded or soil

temperatures are extremely high, in storage when aeration is poor,

in transit when tubers are overheated, or in prolonged storage near

32° F. Blackheart can be induced experimentally in nearly 100

percent of the tubers when they are held at 105° to 110° for 24

hours.
MARKET DISEASES OF POTATOES 59

Control

Proper ventilation and temperature control should be provided

during storage and transit to assure air circulation and prevent high

temperatures. Tubers should not be left in hot, light sandy soils

after the vines are dead. In hot weather after harvest the potatoes

should be removed as soon as possible from the fields and placed in

well-ventilated bins.

References: 12, 13, 60, 139, 264, 281,

Browning

Browning, also called chicken skin in Maine, is used to describe

the discolored skinned areas on immature tubers (pi. 10, B). It is

most serious on skinned tubers exposed to the drying effect of

winds in the field, in packing sheds, and in transit in open trucks,

especially if the weather is very warm.

Slight browning is not objectionable except when large areas of

the tubers are involved and excessive wilting results from loss of

moisture. Severe browning affects the appearance and therefore the

market value of potatoes. If browned potatoes are exposed to a

moist atmosphere, the discolored areas become covered with a

sticky bacterial slime and mold and finally may decay.

Control

To prevent browning before shipping, protect tubers from drying

wind in the field by prompt picking and hauling, use tightly woven

bags, cover loaded trucks with tarpaulins, and protect stacks of

potatoes at sheds from sun and wind. Shipping in closed vans or

railcars at about 60° F permits healing of the skinned areas during

transit. Healed potatoes do not turn brown during marketing.

References: 10, 225, 243, 244, 271, 311.

Bruising

Potato tubers bruised in transit are common on the market.

Although there may be occasional slight injury when potatoes are

pressed and rubbed together in the sack, most transit bruising is

caused when the sacks come in contact with the floor racks and the

walls of the railcar or truck. The injury is due to the pressure of the

load, the shifting of bags at points of contact, and the jolting and

jarring while in transit.
60 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

Symptoms

On newly harvested early potatoes the injured tissues are

flattened or slightly sunken and usually conspicuously darkened.

When the bruised tissues are black, they frequently are mistaken for

chemical injury. However, transit bruising can readily be distinguished from chemical injury because there is no external softness or

flabbiness of tissues beyond the borders of the flattened areas and

the tissues deeper than the flattened bruise do not turn black when

the tuber is cut.

Injured tissues of late tubers (pi. 10, C) are likewise flattened or

slightly sunken, but they are seldom markedly discolored. When the

bruised areas are cut transversely, they appear as a shallow layer of

crushed tissue seldom more than one-eighth inch thick. At first the

bruised layer is moist and somewhat tough. As it dries out, it

becomes firm and starchy. In some instances deeper tissues contain

cracks that radiate from the bruise (shatter bruises) (pi. 10, D).

Occasionally in winter shipments transit bruising is mistaken for

freezing injury. The two can be distinguished readily by critically

examining the affected tubers. Bruising symptoms are confined to

the immediate vicinity of the flattened areas, but freezing may be

recognized externally by softened or wrinkled flesh beyond the

bruise and internally by softened or discolored tissues well beyond

the border of the bruise.

Control

Transit bruising can be reduced by using an efficient loading

method, by carefully stowing the load, and by having pads on the

floor racks.

References: 291, 310, 314, 321.

Chemical Injury

Chemical injury to potatoes is rare and almost impossible to

diagnose correctly. The skin of chemically injured tubers may be

bleached. The injured areas are leathery and the tissue beneath is

somewhat flabby. Later the flesh may become brown to black and

dry. Often injured areas are invaded by decay-producing organisms.

Positive diagnosis has been made on tubers injured by incorrect

or prolonged exposures to methyl bromide (pi. 10, E). Affected

tubers may be covered with sunken or saucer-shaped lesions about

one-eighth inch deep and ranging from minute spots to about
MARKET DISEASES OF POTATOES 61

one-fourth inch in diameter. Sometimes these lesions coalesce and

cover large areas of the skin. The skin is not discolored. Beneath the

affected skin dry corky tissue extends less than one-eighth inch into

the flesh.

Enlarged Lenticels

Enlarged lenticels detract from the appearance of the tubers and

may serve as entrance points for soft rot bacteria and other decay

micro-organisms.

Symptoms

Lenticels normally are inconspicuous on tubers, but under high

moisture conditions they rise about one-sixteenth inch and form

numerous whitish protuberances over the tuber surface (pi. 10, F).

H tubers are held in moist atmospheres, these elevated areas remain

whitish, but when the tuber dries, they become skin color, open,

and somewhat depressed. They make excellent openings for

micro-organisms, particularly soft rot bacteria. Once infection

occurs, soft decayed tissue develops around the lenticels. If these

infected tubers are held at moderate temperatures, the decay

usually dries, leaving moderately large round areas over the tuber's

surface. Sometimes these areas contain white starchy material.

When the tubers are held at excessively high temperatures, decay

may cause considerable damage.

Causal Factors

Enlarged lenticels may occur when tubers are harvested from

heavy and water-saturated soils, when they are submerged too long

in deep washing vats, or when they are packaged wet and held in

moistureproof containers for long periods. Lenticel enlargement

also can occur when the plants are growing if carbon dioxide

concentrations in the soil increase to 5 percent even though

adequate oxygen is present.

Control

Avoid potatoes from wet areas of fields. Do not leave tubers in

deep washing vats longer than necessary. Do not package them

while wet and then only in ventilated bags. Avoid conditions that

may cause carbon dioxide accumulation.

Reference: 269.
62 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

Freezing Injury

Freezing injury or frost necrosis can cause serious losses in any

area of the world where below freezing temperatures are prevalent

during the harvesting, storing, or shipping of potatoes. The greatest

danger exists in northern areas, where early frosts or freezes are

likely during harvest and where temperatures are extremely low

during storage or when potatoes are removed from storage and

shipped to market.

Symptoms

Since symptoms of freezing injury may overlap those of tuber

diseases and disorders and since there is sometimes no external

evidence, information about a given lot of potatoes usually is

necessary for a correct diagnosis.

Tissues at the stem end of the tuber are more sensitive to freezing

than those at the bud end, and the differentiated vascular cells, such

as tracheae, sieve tubes, and tracheids, are more sxisceptible than are

the parenchymatous cells. Because of this difference in cell

sensitivity to cold, any freezing during storage and transit may

manifest any or all the necrotic patterns known as ring necrosis,

blotch, or net necrosis.

Ring necrosis consists of internal discoloration, particularly in

the region of the vascular ring, and is more common at the stem end

of the tuber (pi. 10, G). Blotch necrosis usually forms irregular

areas of various sizes, ranging from opaque blue gray to black (pi.

10, H). This type of freezing injury is more difficult to identify

than the other two types. Net necrosis causes blackening of the

vascular elements of the tuber inner phloem, and a netlike pattern

results when these vascular elements, which are scattered throughout the tuber within the vascular ring, blacken from freezing injury

(pi. 10, G; pi. 11, A). The net of freezing injury usually has blotches

associated with it and so differs from the net necrosis caused by the

leaf roll virus. Generally the symptoms of freezing progress from

the ring to net to blotch type as the freezing period lengthens.

Often the different types of symptoms will overlap. The various

internal symptoms of freezing injury may not occur unless the

tubers are bumped, jarred, or dropped during the freezing period.

When freezing injury occurs prior to harvest, it is often referred

to as field frost (pi. 11, B). This condition can usually be diagnosed

by bluish-gray blotches beneath the skin of the more uniformly

soft, flabby, or watery areas, which generally are on one side of the

tuber.
MARKET DISEASES OF POTATOES 63

Since the different types of symptoms overlap, it is often

necessary to look further for clues as to where and when freezing

occurred. Frozen tubers scattered throughout the load when

received on the market indicate that freezing happened in the field

or during storage, whereas frozen tubers only along the floor and

sidewalls of the railcar or truck indicate transit freezing.

Tubers frozen solid collapse promptly on thawing and become

soft and watery. The flesh is cream color or white and the eyes are

often black. Such tubers are frequently called leakers. However,

moisture on a tuber is not necessarily a sign of freezing, since cold

tubers soon condense water from the air on their surface when

brought into moist air with a temperature higher than their own.

When extensive areas of a tuber are frozen, the affected tissues

usually become invaded with bacteria, which cause sticky, slimy,

foul-smelling rots under moist conditions. In dry air, such as in

forced-air ventilated storage, the frozen tissues may become dried,

tough, and leathery or may lose moisture and become granular with

chalky masses of starch and tissue remnants.

Sweetness of potatoes does not indicate freezing as is commonly

believed. Potatoes held for protracted periods at 40° F or lower,

which is not low enough to form ice, gradually acquire a sweet

taste. This condition is not due to freezing but is due to the

conversion of tuber starch to sugar more rapidly than it can be used

in respiration. Potatoes in this condition are not suitable for

cooking, especially for frying, because of the sweet taste and since

caramelization of sugar causes an undesirable color. The sweetness

of some potatoes can be corrected by raising the holding temperature to about 60° for a week or more.

Causal Factors

Varieties of potatoes differ in their reaction to low temperatures.

Some show serious internal discoloration after prolonged storage at

several degrees above their actual freezing point, whereas others may

not show injury even when exposed to 29° F, the average freezing

point of most varieties. The freezing point of a given variety tends

to become lower as the season progresses. Tubers stored for several

weeks at low temperatures will stand about 1° lower without

freezing than similar tubers stored at 50° or above.

Long exposure of tubers to temperatures just below the freezing

point or moderately long exposure to very low temperatures usually

results in killing of all the tuber tissues, with both internad and

external symptoms becoming apparent after thawing. Moderately

short exposure just at the freezing point or short exposure far
64 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

below the freezing point usually results in death of only the most

susceptible tissues, and internal symptoms may not be apparent

unless the tuber is cut.

Individual tubers in a given lot of potatoes differ as to the point

they can undercool before ice forms, even though the temperature

to which the tissue rises immediately after undercooling in each

may be the same. When the temperature drops rapidly, the degree

of undercooling before ice formation and freezing is generally less

than when the temperature drops more gradually. Undercooled

tubers may recover without injury if they are not agitated during

this period.

When used for seed purposes, tubers with considerable discoloration from freezing often give poor stands, but those tubers with

slight injury seldom affect stands.

Control

Freezing injury to potatoes may be avoided by providing

adequate protection from temperatures below 29° to 30° F. In very

cold climates or during very cold weather supplemental heat must

be applied during storage and in transit. During storage this heat

must be distributed through ducts of a forced-air ventilation system

to prevent freezing of tubers in some areas of the building.

Adequate insulation must be present in buildings used for potato

storage, particularly in the northern areas.

References: 152, 241, 316, 318, 320-323,

Greening

Potatoes exposed to light either before or after harvest gradually

turn green at the surface owing to the development of chlorophyll.

Greening that occurs before harvest is often called sunburn.

Greening after harvest in markets or retail stores is called light bum,

light struck, or simply greening. Greened potatoes are an unnatural

color and may cause serious market losses. In addition, affected

potatoes often have a bitter taste, which makes them unpalatable

and possibly dangerous to eat since the alkaloid solanine is usually

associated with the greened areas. Solanine is considered poisonous

if taken in sufficient dosages.

Symptoms

Some potatoes develop greening after exposure to light for a day

or two. The discoloration progresses from a light yellow to a
MARKET DISEASES OF POTATOES 65

definite green (chlorophyU) and is generally restricted to layers

immediately below the skin. If exposure to light is prolonged,

chlorophyll develops deeper in the tissue and the bitter taste

associated with solanine results.

Causal Factors

All potatoes will green to some extent, especially when exposed

to direct sunlight. Greening occurs initially in the field when tubers

are insufficiently covered with soil (pi. 11, C), or it may be induced

by exposure to incandescent or fluorescent light during grading and

in retail stores (pi. 11, D), Usually immature tubers green more

readily than mature ones. Greening develops more rapidly at warm

than at cool temperatures. Light intensities as low as 5 foot-candles

produce greened tubers, and as light intensities increase, greening

increases. The amount of greening is also directly proportional to

the duration of light exposure. Although greening may increase

under artificial light in retail stores, Httle if any solanine is

synthesized under such light.

Control

Store potatoes in the dark and protect them from exposure to

light during marketing. Avoid displays near windows or under

strong fluorescent lights. Light-resistant packaging is valuable in

preventing retail greening, together with package rotation and

holding reserve stock in the dark.

References: 117, 121, 122, 142, 168, 177, 324.

Heat Injury (Scald)

Heat injury occurs most frequently in the early and intermediate

crops of potatoes harvested on hot days from April or May through

August. The breakdown of tubers due to heat injury and the

subsequent decay in the injured tissues cause excessive shipping

losses. Most of the potatoes injured by heat in the field become

infected by soft rot bacteria. Extensive development of this decay,

usually referred to as slimy soft rot, is one of the best evidences

that market potatoes were excessively warm at some period during

harvesting or marketing.

Symptoms

In severe cases of heat injury the exposed surfaces of tubers

become watery and blistered and juice may ooze from the lenticels.
66 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

Those with less severe heat injury may not show external symptoms

of tissue breakdown for several hours. With exposure to dry air the

damaged tissues not infected by bacteria lose moisture and become

simken, flat, and leathery. The condition often resembles field

freezing injury (pi. 11, E). When first cut, the heat-injured tissues

may appear white to gray, but after exposure to air they become

brown and finally black as in blackheart. The skin of colored

varieties is sometimes bleached if potatoes have been exposed to

bright sunlight.

The term "scald spot" has been used to describe oval or irr^ular,

sunken, brown areas on the skinned parts of freshly harvested

tubers (pi. 11, F). When the flesh beneath this spot has a grayish to

purplish watery breakdown with sometimes a purplish black

discoloration on and just under the skin, the injury is called deep or

sunken scald.

Causal Factors

It is not possible to judge by air temperature alone whether

potatoes will be injured by heat during harvest, for on a moderately

hot day the heat accumulated by tubers at their exposed surfaces

may kill the tissues. The surface tissues of exposed tubers will often

be between 20° and 30° F higher than the air temperature. As high

as 135° has been recorded on the sunny side of tubers left exposed

in the field on a hot day. The thermal death point of potato tissue

is believed to be near 122°. Below this point potato tissues are not

likely to break down because of death by heat alone. Such

temperatures are, however, definitely dangerous to freshly dug

potatoes because they are affected physiologically in such a way as

to predispose them to attack by soft rot bacteria.

Prolonged exposure of tubers on or near the surface of the soil to

excessively high temperatures will cause deep or sunken scald. Scald

spot is caused by short exposures to high temperatures or by

exposures to drying winds.

Control

To avoid heat injury, protect potatoes from prolonged exposure

to the sun when harvested during hot weather, especially above

90° F. Within 15 to 30 minutes after tubers are dug, they should be

hauled to the packing shed. Heat injury can occur while the

potatoes are on the truck if it is left standing in the sun. Covering

the load with a tarpaulin gives some protection against the sun and

also prevents drying and browning of bruised and skinned areas of
MARKET DISEASES OF POTATOES 67

tubers when hot winds and low humidity prevail. If mechanized

harvesting is not used, it may be advisable in hot weather to dig the

potatoes late in the afternoon, allow them to cool on the ground

overnight, and pick them up early the following morning.

Since potato tubers may be injured by heat without showing

external evidence of breakdown of tissues for several hours or days,

use caution in shipping potatoes suspected of having been thus

injured. If it is possible to hold the potatoes several days before

grading and loading, a great deal of decay in transit can be avoided.

Shipping the potatoes under refrigeration at 55° to 65° F can also

minimize possible losses from the bacterial soft rot that always

follows as a secondary effect.

References: 214, 217, 225, 272.

Heat or Drought Necrosis

Symptoms

Heat or drought necrosis causes slate-gray to golden-yellow or

brown discoloration of the water vessels of the affected tubers. It is

most pronounced in the vascular system and may occur at either

the stem end or the bud end. It also is in the tissues between the

vascular ring and the tuber surface. Discolored tissue near the

surface makes the skin appear dark, but generally there are no

external symptoms.

Causa/ Factors

Heat or drought necrosis occurs on tubers grown in light soils in

hot, arid areas. It is especially likely to appear on tubers left in the

soil after the vines begin to die.

Contro/

There are no postharvest control measures.

References: 20, 65, 328.

Hollow Heart

Hollow heart is a disorder of potatoes grown anywhere in the

world. It can occur in potatoes growing in the field or on tubers

during transit or in storage. It causes serious losses and at times

seriously affects the marketability of potatoes.
68 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

Symptoms

The term "hollow heart" describes cavities that form near the

center of very large tubers (pi. 11, G). These cavities may vary

greatly in size and usually have radial cracks extending in many

directions from the central cavity. The cavities usually are lined

with first a pinkish and later a light-brown to brown dead tissue.

The exact cause of this type of hollow heart is not known, but it is

believed to be due to some type of abnormal condition that causes

too rapid growth or an abnormal type of growth of the tuber.

A second type of hollow heart occurs when the tubers are

exposed to very high temperatures in the fields before harvest, at

the packing sheds before shipment, or during transit if they become

excessively hot (pi. 11, H). The tubers contain from one to many

small cavities distributed throughout the flesh. They may be near

the center of the tuber but frequently are about a half inch beneath

the skin. They are rarely over one-half inch in diameter and are

lined with jetblack tissue. The condition is due to suboxidation

caused by high temperatures and probably was preceded by

blackheart. Tubers with this type of hollow heart symptom have

been reported from Alabama, Arkansas, California, and Mississippi.

A third type of hollow heart is associated with chilling injury (see

Mahogany Browning). Tubers held for long periods at or near 32° F

develop both mahogany browning and blackheart. During this

holding period the blackheart tissue may collapse leaving a cavity

lined with jetblack dead tissue (pi. 11, H).

Control

Close spacing of seed pieces in the rows is reported to decrease

chances of excessively large tubers and hence reduce chances of

normal field hollow heart. After the vines are dead or removed

during hot weather, the tubers should be harvested as promptly as

possible to avoid high soil temperatures because of no vine covering.

During storage and transit proper air circulation wül prevent

buildup of excessively high temperatures and remove possible

suboxidation. Storage of tubers at 40° F and above will prevent

chilling injury.

References: 139, 140, 160, 176, 308, 309,

Internal Black Spot

Internal black spot (black spot) of potatoes was first described in

England in 1913. In Europe it is known as bruise, blue discolora-
MARKET DISEASES OF POTATOES 69

tion, bluing, and blue spotting. It was first reported in the United

States on Long Island, N.Y., in 1940. Since then it has been

reported in Maine, New York, New Jersey, Pennsylvania, the Red

River Valley of Minnesota, North Dakota, California, and Washington. It occurs in almost any region where potatoes are stored. The

disorder has caused losses of over a million dollars a year on Long

Island alone.

Symptoms

The black spots are generally limited to the outer one-fourth to

three-eighths inch of tuber flesh and extend from the vascular ring

outward. Occasionally the deeper tissues are affected. The spots are

largely concentrated on the stem end half of the tuber and are

generally on the shoulders, which are most Ukely to be bumped and

bruised during handling. These spots are generally beneath the

unbroken skin where they are not visible, even when the tuber is

washed (pi. 12, A). This is due to a normal, uncolored thin layer of

cortical cells about one-sixteenth inch thick between the discolored

spots and the skin. The spots develop from a slight jolt or bruise

during handling. At first they are pink, then after 4 to 6 hours they

become dark red, and finally after 12 to 18 hours they are coal

black. Later after the area begins to dry out, it shrinks and becomes

slate gray (pi. 12, B). The spots are usually circular and range from

a barely visible grayish tint to gray spots one-half to three-fourths

inch in diameter.

External symptoms are readily visible in more severe cases of

black spot. They result from a rapid drying out of the blackened

tissues and the thin overlying layer. Consequently, the surface of

the tuber over the black spots becomes irregularly sunken to a

depth of from one-sixteenth to one-eighth inch. At first the

blackened tissue is of nearly normal texture, but later it dries out

and becomes starchy. Eventually it becomes sharply delimited

through the formation of a thin boundary of cork tissue. This

condition is generally referred to as pressure bruise or pressure spot.

Causa/ Factors

Black spot appears in susceptible tubers only after they have

been bruised and usually only after the tubers have been removed

from storage and passed over a grader. Normal handling and grading

operations are sufficient to produce the discoloration by the time

the potatoes reach the market.

Susceptibility of tubers to black spot seems to be dependent on
70 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

(1) cultural and environmental conditions under which the plants

grow in the field, (2) the stage of tuber maturity at harvest, (3) the

environmental conditions in storage and in transit to market, and

(4) the duration of the storage period. Therefore the presence or

absence of black spot on any single lot of potatoes indicates the

degree of susceptibility or resistance at that specific time and for

that specific lot.

Turgidity of tubers is a factor in their resistance to pressure

bruise and black spot. There is an apparent optimum condition of

turgor at which potato tubers are resistant. As water is lost during

storage or in marketing and turgor of the tubers decreases, they

become more susceptible to black spot. However, as the water loss

continues, the cells reach a certain point of dryness at which the

tubers become rubbery and once again are resistant. Black spot is

apparently due to changes in physical structure and response of the

tuber cells to impact.

The pressure bruise and black spot complex is becoming more

common in modem potato storage facilities designed to maintain

higher holding temperatures for processing potatoes. These facilities

are equipped to force air through the stored potatoes so as to

regulate temperatures, but they cause a greater than normal loss of

tuber moisture. Unless carefully regulated, this condition plus the

higher holding temperature increases the susceptibility of the tubers

to internal black spot.

Although a close relationship exists between pressure bruise and

internal black spot, either condition can appear without the other.

The flattened or indented areas known as pressure bruise are not

commercially important without black spot, for these areas tend to

round out and become inconspicuous in the market channels.

However, if the tubers are susceptible or predisposed to black spot,

a slight pressure or bump on these areas will cause internal

discoloration or black spot.

In the western potato-growing areas, a condition referred to as

deep black spot is attributed to high soil temperatures. When

coupled with tuber bruising, it causes a physiological rot. The

bruised area at first appears as a black spot on the surface followed

by a rot that penetrates to the center of the tuber. This is not true

of internal black spot, for it does not cause a tuber rot.

Considerable research has been conducted to determine the

effect of fertilization on black spot development. Because of

conflicting and inconsistent results with nitrogen, potassium, and

copper, it is impossible to prove a specific relationship between the

elements and internal black spot.
MARKET DISEASES OF POTATOES 71

We know that certain conditions can result in internal black spot

in susceptible tubers, but the basic cause or causes are unknown.

Control

Avoid conditions during storage, transit, and marketing such as

rapid flow of dry air, which may result in excessive loss of tuber

moisture. After storage at low temperatures, warm the tubers to

55°-60° F before grading and packaging them.

References: 33, 48, 61, 144, 165, 201, 211, 221, 238, 239, 253,

259, 260, 295, 302-304, 312, 313.

Internal Brown Spot

Internal brown spot has been noted on market potatoes from

several regions. It was particularly prevalent in the Long Island and

New Jersey crops in 1944,1948,1949, and 1953.

Symptoms

Affected potatoes have dry, firm, corky, light reddish-brown

spots or blotches scattered throughout the flesh. There are no

external symptoms. The spots vary from minute flecks to threefourths inch or more in diameter and are irregular and indefinite in

outline. Usually they are from one-fourth to one-half inch (pi. 12,

C). Most of the spots are at the bud or eye end and are seldom

found much beyond the middle of the tuber. Internal brown spot is

very severe and appears most commonly in large, long, and

irregularly shaped tubers.

Causa/ Factors

Internal brown spot develops before the potatoes are dug. It does

not increase in severity or extent in storage. It is a physiological

disorder that seems to result from extremely high temperatures and

drought during the last part of the growing season.

Control

The Pontiac, Kennebec, Katahdin, and Mohawk varieties are

relatively resistant to internal brown spot. There are no postharvest

control measures.

References: 77, 96, 97, 169, 327.
72 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

Jelly-End and Glassy-End Rots

Both jelly-end and glassy-end rots result in serious losses during

harvesting, storage, transit, and marketing. Losses often are due to a

soft watery breakdown. Sometimes apparently sound tubers make

black potato chips and disintegrate during canning or other

processing. Jelly-end and glassy-end rots have been considered

distinct disorders, but because of strong similarities they are now

considered the same.

Symptoms

Jelly-end or glassy-end rot always occurs at the stem end of

tubers and often shows no external symptoms. When external

symptoms occur, the stem end is soft and the skin wrinkled (pi. 12,

D). The rotted flesh varies from colorless or glassy translucent to

straw color and various shades of brown or black (pi. 12, E and F).

The rotted tissue is fragile and easily broken apart, has a jellylike

consistency, is devoid of fibrous texture, and is very watery. A

sharp line of demarcation forms between affected and healthy

tissue. During storage, water evaporates from affected areas, leaving

a shriveled clump of epidermal tissue collapsed at the stem end.

Both jelly-end and glassy-end rots are most frequently found in

tubers that have made secondary growth. The disorders differ

mainly in the growing regions and on the varieties of potatoes they

affect.

Jelly-end rot appears principally on long russet-type potatoes

grown in California and the north-central region (pi. 12, E). It is

found most frequently in tubers with malformed secondary growth,

such as those with constricted stem ends (bottleneck), those with

constrictions near the middle (dumbbell shaped), and sometimes

long pointed types.

Glassy-end rot is found in round-type potatoes grown in the

eastern and northeastern regions. It frequently occurs at harvest on

bottleneck or dumbbell-shaped tubers and on tubers with abnormal

stolon growth from the bud end (pi. 12, G and H). Small tubers

present on these stolons at harvest do not have glassy-end rot

symptoms.

In the long russet-type tubers the glassy condition extends 1 to 2

inches from the stem end. With the round-type tubers the glassiness

may extend throughout the primary but not the secondary tuber.

These glassy areas are devoid of starch. Absence of starch can easily

be detected by failure to develop a deep purple color in the flesh

when slices from the tubers are placed in potassium iodide
MARKET DISEASES OF POTATOES 73

solutions. Both types of potatoes form a mushy translucent jelly

when they are boiled.

Causal Factors

Jelly-end or glassy-end rot is caused by weather conditions that

temporarily stop or inhibit the development of young tubers,

followed by their rapid growth. Conditions that may cause this

disorder include very high temperatures, drought followed by rainy

periods, and vine defoliation, each of which may result in secondary

tuber development. Growth of secondary tubers and increased

glassiness may occur after the vines are dead. The disorder does not

become more pronounced in storage or transit. Glassy tubers in

storage, however, may lead to wet spots or in transit to spotted

sacks caused by the breakdown of the glassy areas and release of

water. Both conditions are ideal for development of bacterial soft

rot and other disorders.

Control

Irrigation started early in the growing season and continued until

near harvest will help prevent secondary growth. Plant early

maturing varieties or plant regular varieties late so that crops have

passed or not reached critical stages of tuber production before

severe weather fluctuations occur.

No postharvest control is known. Tubers from lots containing

large amounts of glassy-end or jelly-end should not be processed.

References: 99, 180, 181, 216, 226, 248, 273.

Knobbiness and Other Malformations

Knobby or malformed tubers often occur, particularly in the

long Russet Burbank-type varieties. These malformations or protuberances result in serious grade reduction.

Symptoms

Knobby tubers have secondary lateral growth from a few tuber

eyes. This growth produces knoblike protuberances and sometimes

new tubers form on the original ones (pi. 13, A).

Offtype or malformed tubers may have constrictions near the

stem end (bottle shaped), or they may have constrictions near the

middle (dumbbell shaped), or they may be normal with pointed

ends.

No active decay occurs with any of these malformations.
74 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

Causal Factors

The specific cause of knobby tubers is not definitely known.

Such factors as the following contribute to knobbiness and other

malformations: High soil moisture, stem girdling by mechanical

means or pathogenic organisms that interfere with water transport

in the vines, and partial or complete vine defoliation by hail or

other physical means, especially when tubers are partially formed.

Control

No control methods are known.

References: 21, 26, 162, 276, 282.

Mahogany Browning

Mahogany browning was once a very important storage and

marketing disorder of some potato varieties, but because of better

storage conditions it has become rather rare. However, it can cause

serious losses under certain conditions.

Symptoms

Normally no external symptoms appear until the tubers are very

severely affected internally or when they are stored for very long

periods near 32° F. Under such circumstances the skin becomes

bluish gray to purple, is wrinkled or cracked, and has numerous

sunken pitted areas. Such tubers may be confused with those

infected with the late blight organism, particularly because of the

reddish-brown flesh beneath the discolored skin (pi. 13, B) and

because they are hard or rocklike. The reddish brown of mahogany

browning may occur anywhere in the flesh of the tuber, whereas

late blight usually is limited to the outer one-half inch of the flesh.

Symptoms of this disorder vary with different varieties. Katahdin, Chippewa, and Pungo show many manifestations of mahogany

browning. The first symptom is a diffuse grayness occurring

anywhere in the flesh. Sometime at this stage a water-soaked area or

brownishness appears just under the skin. Later a firm, almost

granular reddish-brown discoloration either replaces the gray or is

surrounded by grayish areas (pi. 13, B). No sharp lines of

demarcation separate this firm tissue from the unaffected flesh. In

very advanced stages some blackened areas resembling blackheart

develop in the reddish or gray flesh. Eventually the flesh in these
MARKET DISEASES OF POTATOES 75

blackened areas disintegrates, leaving hollow cavities with blackened

walls.

With such varieties as Sebago and Kennebec, which apparently

are less susceptible to chilling injury, symptoms are less pronoimced. First symptoms are yellowing and firming of affected

flesh followed by the development of black areas. The flesh in these

blackened areas later collapses forming cavities. Sometimes between

the blackened areas the diffuse gray and reddish-brown discolorations typical of mahogany browning appear (pL 13, C).

Causal Factors

Mahogany browning is an injury caused by low temperatures. It

occurs when tubers are stored at 32° to 34"* F for at least 3 months.

With longer storage the internal symptoms become more intense

and external symptoms appear. Mahogany browning should not be

considered a form of freezing injury since it occurs at well above

the freezing point of the tubers.

Control

Do not store potatoes below 40° F. Sometimes during storing the

tuber temperature drops to near 32°. Under such circumstances it is

advisable to warm them to 65° for a short period and then return

them to 40° storage to avoid mahogany browning. Storage walls

and bins should be properly insulated so that tubers near the walls

will not be exposed to unreasonably low temperatures. Forced-air

circulation should be used to keep temperatures uniform.

References: 88, 133, 139, 140.

Mechanical Damage and Cracking

Mechanical damage to potato tubers during digging, handling,

storage, and transporting probably causes more losses than any

other factor. Losses can be direct from excessive damage or indirect

by providing an entrance point for tuber-rotting organisms. A

survey of wastage in Great Britain revealed that almost one-third of

the potatoes removed from the field had been mechanically

damaged to the extent that they were unfit for marketing and

another one-third had some minor mechanical damage that could

predispose them to tuber rots. Only 4.6 percent by weight of the

total crop was absolutely free of damage. A similar situation no

doubt exists sometimes in the United States.
76 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

Causal Factors

Cracking or bruising of potatoes can be caused by many

conditions. Growth cracks in tubers are generally associated with an

imeven water supply or incorrect use of fertilizers or both (pi. 13,

D). These conditions cause an uneven rate of tuber growth with the

resultant cracking of the rather tough skins. Pressure bruises from

heavy loading in transit, particularly on tubers next to the floor

racks, may cause cracks. These cracks may be severe and readily

visible on the exterior or in less severe cases may be seen only after

cutting the tuber. They do not extend uniformly through the tuber

but present a shattered or netlike pattern in the area where

excessive pressure has been applied.

Curved thumbnail cracks, which become conspicuous after

grading of cold-stored crisp tubers, particularly after some drying

out, result from glancing impacts of tubers with other tubers or

from digging and handling equipment (pi. 13, E). This condition,

which occurs anytime from harvest to removal from storage, is the

result of mechanical shock in tubers that have developed a high

internal pressure from increased water absorption. The amount of

mechanical shock necessary to induce this cracking may be

extremely slight.

Other cracking may be in the form of digger cuts or shattering

during harvest operations. Deep cracks appearing suddenly during

digging are caused by harvesting when the tubers are immature or

when soil and air temperatures are too low.

Control

Handle potatoes gently at all times. Postpone digging until tubers

are mature. In cold weather delay harvesting until late morning so

the soil will have time to warm up.

Potatoes should be warmed before they are removed from

storage, graded, or handled in any way.

References: 20, 82, 93,130,131,146,149,187,188, 209, 291, 310, 314,

315.

In addition to natural russeting of such varieties as Russet

Burbank and Russet Rual, there are blemishes and discolorations of

smooth-skin varieties known as soil scurf, sand scurf, russet scab,

and russeting. In many instances these blemishes resemble the

russeting caused by the Rhizoctonia fungus on the tuber surface or
MARKET DISEASES OF POTATOES 77

the superficial lesions caused by the common scab organism

Streptomyces scabies.

Causa/ Factors

The exact cause of much of this russeting is unknown. However,

the fact that by careful examination some Rhizoctonia can be

found on the skin of practically all tubers has suggested that this

fungus may cause most of these problems. Some studies have

indicated that other causes may be responsible. A very serious type

of russeting that sometimes occurs in Missouri, Kansas, and

Nebraska has been reduced by some soil sterilizing agents, indicating that an organism might be responsible for the problem. Since

this condition is usually more prevalent in sandy soils, it has been

referred to as sand scurf. It is usually more serious in soil previously

planted to potatoes, also indicating that an organism might be

involved.

Any irritation or injury to the skin of growing tubers may lead to

scurfy or scabby eruptions and corky discoloration, which might be

called russeting. Under some conditions, tubers growing in contact

with fertilizers in the soil may have rough skins that resemble

russeting. Although russeting does not lead to decay in storage or in

transit, the marketability of seriously russeted tubers is greatly

affected.

References: 94, 252, 329.

Stem-End Browning

Stem-end browning, which causes discoloration of the vascular

system, can be considered an important disorder of potatoes and is

often confused with net necrosis. It occurs mostly in Maine, New

Hampshire, and Vermont but may be found in many other

potato-growing regions. The vascular discoloration decreases the

value of the tubers for general cooking and especially for chip

manufacture. Symptoms of stem-end browning become more

pronounced during storage.

Symptoms

No external symptoms of stem-end browning occur. When a thin

slice is removed from the stem end of affected tubers, a dark-brown

to blackish discoloration appears in the xylem and phloem strands

radiating from the point of a stolon attachment (pi. 13, F). The

discoloration rarely extends more than one-fourth to one-half inch
78 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

from the stem end (pi. 13, G). The depth of discoloration of the

strands usually distinguishes this disorder from net necrosis.

Causal Factors

The cause of stem-end browning is unknown. Some evidence

indicates that the disorder is more common when potatoes are

grown for several years in the same fields with increased amounts of

fertilizers, particxilarly those with high chloride and potassium

content. There is also some evidence that it is caused by a virus.

Stem-end browning may or may not be present when tubers are

harvested. Maximum development occurs when tubers are stored at

50° F for about 100 days. Its incidence is greatly reduced by

storing tubers from 32° to 35° or at 70° for about 60 days before

permanent storage near 50°. The disorder is reported to occur when

soil temperatures at harvest are too high for the development of net

necrosis. Normally it is most apt to affect small potatoes. Green

Mountain and Irish Cobbler are considered the most susceptible

varieties to stem-end browning, whereas Katahdin and Chippewa are

resistant.

Control

Conditioning potatoes for 60 days at 32° or 70° F before

permanent storage near 50° will greatly reduce stem-end browning,

which develops during constant storage at 50°.

References: 87, 92, 246, 247.

Vine Killing

Killing potato vines a week or two before harvest has become a

common practice in most potato-growing areas. Often tubers from

these plants have varying degrees of vascular discoloration. Such

discoloration can be confused with that caused by wilt diseases and

by freezing and lessens the value of tubers, particularly for the

potato chip industry. In this respect vine kiUing can be considered

an important physiological disorder of potatoes.

Symptoms

Affected tubers have no external symptoms. Internally they have

a brownish vascular discoloration, most pronounced at the stem end

but often extending throughout the tuber (pi. 13, H). When the
MARKET DISEASES OF POTATOES 79

vessels extending to each eye are affected, the peeled tubers exhibit

a network of discolored vessels that resembles net necrosis. It

differs from net necrosis since the discolored vessels do not extend

to the inner flesh of the tubers and the browning is not as dark.

Vascular discoloration from vine killing resembles that of verticillium wilt but differs usually in being dull brown rather than reddish

brown.

Causal Factors

Any factor causing premature death of the vines, even frost or

droi^ht, can discolor the vascular ring. Certain chemical and

mechanical methods of vine killing cause this disorder. Discoloration is more apt to occur when the vines are rapidly rather than

slowly killed, when they are immature at the time of killing, and

when plants are deficient in moisture when they are killed. The

discoloration does not increase during storage and apparently does

not make the tubers more susceptible to decay.

Control

No postharvest control methods are known.

References: 44, 81, 137, 138, 161, 192, 194.

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MARKET DISEASES OF POTATOES 81

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84 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

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1933. Botrytis cinérea as a cause of potato tuber rot.

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MARKET DISEASES OF POTATOES 85

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1958. Pseudo monas fluorescens in relation to certain diseases of

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1940. Potato tuber net-necrosis and stem-end browning studies in

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1953. Storage behavior of Kennebec potatoes infected by

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86 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

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1944. A phythiaceous stem-end rot of potatoes. (Abstract)

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1961. Heat inactivation of leafroll virus in potato tuber tissues.

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1943. A study of the control of the yellow-dwarf disease of

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MARKET DISEASES OF POTATOES 87

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1960. Mechanical damage to potatoes I. European Potato Jour 3-

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1927. Physiology and parasitism of Sclerotium rolfsii Sacc.

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1942. A new form of low-temperature injury in potatoes. Amer.

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1953. Factors influencing bacterial soft rot of potatoes. Indian

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1950. Factors influencing invasion of potato by Erwinia carotovora.

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1957. Control of common scab of potatoes. Amer. Potato Assoc.

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1947. Observations on the use of potato vine killers in the Red River

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88 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

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1969. Reducing chilling injury of potatoes by intermittent warming.

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1967. Production of pectic enzymes by Pseudomonas fluorescens

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1959. Potato greening under artificial light. N.Y. (Cornell) Agr.

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1940. Suggestions for control of bacterial ring rot of potatoes. Mont.

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1959. Studies on internal blackspot of potatoes. N.Y. (Cornell) Agr.

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1947. Aster yellows and its vector on potatoes. Phytopathology 37:

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1968. Are traditional hours of harvesting potatoes obsolete? Maine

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1966. Soil, air and tuber temperatures and bruise resistance. Maine

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1967. Some studies on pre-storage washing of Maine potatoes.

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1969. Effect of soil temperatures at harvest on the bruise resistance

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1935. Soft rot of potatoes caused by Pythium ultimum Trow. Sei.

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MARKET DISEASES OF POTATOES 89

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1937. Armillaria dry rot of potato tubers in British Columbia. Amer.

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1950. Heat inactivation of leaf-roll virus in potato tubers. Ann. Appl.

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1944. Efficacy of the rotary knife in the control of potato ring rot.

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1942. Incidence of hollow heart in potatoes as influenced by

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1944. Tuber maturity hastened by killing the vines. Idaho Agr. Expt.

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1945. Influence of certain factors on second growth on Russet

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1943. Location and movement of the causal agent of ring rot in the

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1915. A contribution to the life history of Spongospora subterránea.

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1967. Laboratory assessments of the susceptibility of potato tubers

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1968. Infection of potato tubers by common scab (Streptomyces

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1949. Investigations on cause and prevention of greening in potato

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1945. Physiological internal necrosis of potato tubers in Wisconsin.

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1941. Temperatures affect development of ring rot. Wis. Agr. Expt.

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90 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

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1964. Recent research in Romania on blackleg and bacterial sott rot

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1946. Purple-top wilt of potatoes. W. Va. Agr. Expt. Sta. Bui. 326,

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1939. Pathogenic races of Actinomyces scabies in relation to scab

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1936. Viability of sclerotia of Sclerotia rolfsii after passage through

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1934. Identification of Phytopthora species. W. Va. Agr. Expt. Sta.

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1942. A histological study of hollow heart of potatoes. Amer. Potato

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1960. Greening and solanine development of white potatoes m

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1964. Bacterial hard rot of potato. European Potato Jour. 7: 45-56.

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1960. Second-growth phenomena. European Potato Jour. 3:

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1964. Observations on the induction of second-growth in potato

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1955. Efficiency of various methods of washing Red River Valley

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MARKET DISEASES OF POTATOES 91

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1951. The rapidity of vine killing by herbicides in relation to internal

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1958. Some factors affecting the occurrence and development in

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1966. Some major points from 22 years of experience in breeding

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MARKET DISEASES OF POTATOES 93

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94 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

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MARKET DISEASES OF POTATOES 95

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96 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

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1955. Relation of soft rot development to protective barriers m Irish

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1943. Studies on the morphology, physiology, serology, longevity,

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1958. Abnormalities in the potato due to water uptake and

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1968. The golden nematode handbook. U.S. Dept. Agr. Agr. Handb.

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1944. Observations on phloem necrosis of potato tubers. Canad.

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1942. A stem-end rot of potato tubers caused by Rhizoctonia solani.

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1953. Pycnidial stage of charcoal rot inciting fungus with a

discussion on its nomenclature. Phytopathology 43: 608-610.
MARKET DISEASES OF POTATOES 97

(286)

1955. Incidence of charcoal rot of potato in Bihar (India) in relation

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1942. Distribution of the root-knot nematode in high ridge plantings

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1961. Principles of nematology. 553 pp. McGraw Hill Book Co

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1965. Control of potato-storage diseases as affected by airflow,

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1962. Effect of storage on postharvest physiology of potatoes used

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(291) Twiss, P. T. G., and Jones, M. P.

1965. A survey of wastage in bulk-stored maincrop potatoes in Great

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1933. The root-knot nematode. Calif. Agr. Expt. Sta. Cir. 330, 35

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(293) Upriti, G. C, and Nagaich, B. B.

1968. Inactivation of potato leaf roll virus in tubers by hot water

treatment. Amer. Potato Jour. 45: 373-377

(294) Van Den Boom, T.

1967. Studies on the conditions needed for the occurrence of potato

black leg. Phytopath. Ztschr. 58: 239-276.

(295) Vertregt, N.

1968. Relation between black spot and composition of the potato

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(296) Waldee, E. L.

1945. Comparative studies of some peritrichous phytopathogenic

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1952. Diseases of vegetable crops. 529 pp. McGraw-Hill Book Co.,

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1939. Yellow dwarf of potato in Wisconsin. Jour. Agr Res 59-

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1959. Corky ring spot of potato, a soil-borne virus disease Wis Agr

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1958. A soil-borne virus associated with the corky ring spot disease

of potato. Nature 181: 1146.

(301) Watson, R.D.

1944. Charcoal rot of Irish potatoes. Phytopathology 34: 433-435.
98 AGRICULTURE HANDBOOK 479, U.S. DEPT. OF AGRICULTURE

(302) Weaver, M. L. . ^^ r^u ^

1969 Theories for black spot susceptibility in potatoes: Old and

new. Rpt. of 18th Nati. Potato Util. Conf., Corvallis, Oreg.,

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(303) Roberts, J., George, J. E., and others.

1965. Harvesting potatoes into water in a water-tight truck bed.

Amer. Potato Jour. 42: 147-162.

(304) and Steen, H. A. A a u f

1966. Deep black spot in Russet Burbank potatoes. Amer. hoc. wort.

Sei. Proc. 89: 464-471.

(305) Weber, G.F. ,, , i^o

1923. Potato diseases and insects. Fla. Agr. Expt. Sta. Bui. lb«:

103-163.

1943. Southern blight, Corticium rolfsii of potato tubers.

Phytopathology 33: 615-617.

(307) Weiss, F., Lauritzen, J. I., and Brierley, P.

1928. Factors in the inception and development of fusarium rot m

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(308) Wenzl, H. . . ^ .. 4.

1965. Potato hollow heart. The form of the cavities as a function ot

the shape of the tubers. Pflanzenschutzberichte 32 (11-12):

185-191.

(309)

1965. The histological distinction of three types of hollow heart in

potato tubers. Ztschr. f. Pflanzenkrank. (Pflanzenpath.) u.

Pflanzenschutz 72: 411-417.

(310) Werner, H. O.

1931. The cause and prevention of mechanical injuries to potatoes.

Nebr. Agr. Expt. Sta. Bui. 260, 35 pp.

(311) White, M.

1951. Comparison of weight losses and defects in early Irish potatoes

shipped by van and open truck and value of water chlorination

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1945. Internal black spot of Long Island potato tubers. Amer.

Potato Jour. 22: 6-11.

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1951. Effect of temperature on black spot in Long Island and Red

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(314) Williams, C. M.

1963. King Edward potatoes, impact and mechanical damage at

lifting time. Amer. Potato Jour. 40: 332.

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1967. Storage of fall flumed potatoes. (Abstract) Amer. Potato Jour.

44: 341.

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1966. Salvaging field frosted potatoes. Maine Agr. Expt. Sta. Farm

Res. 14: 31-34.

(317) and Johnston, E. F.

1967. Reducing the incidence of bacterial lenticel infection to fall

washed Maine potatoes. (Abstract) Amer. Potato Jour. 44:

342.
MARKET DISEASES OF POTATOES 99

(318) and Johnston, E. F.

1967. Studies on the feasibility of rehandling to salvage from field

frosted potatoes. (Abstract) Amer. Potato Jour. 44: 342

(319) Wilson, J.H.

1951. Expressions of symptoms of leaf-roll virus in potatoes. Ann.

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(320) Wright, R. C.

1929. Influence of freezing of seed potatoes on viability and yield.

U.S. Dept. Agr. Tech. Bui. 119, 10 pp.

(321)

1939. Bruising, freezing, and chemical injury of potatoes in transit.

U.S. Dept. Agr. Tech. Bui. 668, 23 pp., iUus.

(322) and Diehl, H. C.

1927. Freezing injury to potatoes. U.S. Dept. Agr. Tech. Bui. 27, 24

pp., illus.

(323) and Taylor, G. F.

1921. Freezing injury to potatoes when undercooled. U.S. Dept

Agr. Bui. 916, 15 pp., illus.

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1960. Effect of season, storage temperature, and temperature during

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potatoes. Amer. Soc. Hort. Sei. Proc. 75: 529-536.

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1943. Purple top wilt of potatoes caused by the aster yellows virus.

Amer. Potato Jour. 20: 177-183.

(326) Zan, K.

1962. Activity of Phytophthora infestons in soil in relation to tuber

infection. Brit. Mycol. Soc. Trans. 45: 205-221.

(327) Zimmerman-Gries, S.

1947. Internal rust spot of potatoes. Palestine Jour. Bot. Rehovot

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(328)

1964. The occurrence of potato heat-necrosis symptoms in Israel and

the use of affected tubers as seed. European Potato Jour 7-

112-118.

(329) and Blodgett, E. G.

1963. Some skin defects of potatoes in Israel. European Potato Jour

6: 191-200.

Agriculture Handbook 479, U.S. Dept. of Agriculture Plate 1

Bacterial diseases: A-G, Bacterial soft rot: A, Bacterial ooze; B, internal

decay; C, advanced breakdown; D, dried infection; E-G, lenticel infection : E, Swollen stage; F-G, dried stage. H, Blackleg.
/^¡culture Handbook 479, U.S. Dept. of Agriculture Plate 2

Bacterial diseases: A-B, Blackleg: A, Early field or harvest symptoms; B, late

storage decay. CD, Brown rot. E, Red xylem. F-H, Ring rot:. F-G, Early

stage : F, Not squeezed; G, squeezed; H, advanced stage.
Agriculture Handbook 479, U.S. Dept. of Agriculture Plate 3

Fungus diseases: A, Black dot. B, Black scurf. C, Charcoal rot. D-E, Early

blight (alternarla tuber rot). F-H, Fusarium tuber rot: F-G, Stem-end

infection;//, advanced decay.
Agriculture Handbook 479, U.S. Dept. of Agriculture Plate 4

Jk^

E

&

F

Fungus diseases: A-B, Fusarium tuber rot, buttonhole type. C-D, Fusarium

wilt: C, Oxysporum type; D, eumartii type. E-F, Gray mold rot

(Botrytis). G-H, Late blight.
Agriculture Handbook 479, U.S. Dept. of Agriculture Plate 5

Fungus diseases: A, Late blight. ß-C, Leak. D-Ê, Phoma tuber rot.

F-G, Pink rot, western russet-type tubers.
Agriculture Handbook 479, U.S. Dept. of Agriculture Plate 6

H

Fungus diseases; A-ß, Pink rot, eastern round tubers. CD, Powdery

scab. E, Scab. F-G, Sclerotium rot. H, Silver scurf.
Agriculture Handbook 479, U.S. Dept. of Agriculture Plate 7

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Fungus diseases: A, Silver scurf. ß, Skin spot. CD, Verticillium wilt. E-F,

Pink eye. G-//, Wart: G, Early stage; //, advanced stage.
Agriculture Handbook 479, U.S. Dept. of Agriculture Plate 8

Virus diseases : A-B, Corky ring spot: A, Early stage; B, after storage. C-D,

Net necrosis. E, Purple top wilt. F, Spindle tuber. G-H, Tuber necrosis.
Agriculture Handbook 479, U.S. Dept. of Agriculture Plate 9

Nematodes and their injuries: A, Root linot. B, Root knot, internal view

showing encysted female. C, Rot nematode. Insects and their injuries: DJB, Tuber flea beetle. F, Wireworm. Nonparasitic disorders and injuries: GH, Blackheart.
Agriculture Handbook 479, U.S. Dept. of Agriculture Plate 10

'. A

Nonparasitic disorders and injuries: A, Blackheart due to field heat. B,

Browning. C, Floor bruising. D, Shatter bruising. E, Chemical (methyl

bromide) injury. F, Enlarged lenticels. G-H, Freezing: G, Ring type; H,

blotch type.
Apiculture Handbook 479, U.S. Dept. of Agriculture Plate 11

Nonparasitic disorders and injuries: A-B, Freezing: A, Internal netting; B,

field frost. CD, Greening: C, Field; D, retail display. E, Heat injury. F,

Heat, deep scald. G-H, HoUow heart: G, Field; H, high temperatures and

long storage at 32° F.
Agriculture Handbook 479, U.S. Dept. of Agriculture Plate 12

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Nonparasitic disorders and injury: A-B, Internal black spot. C, Internal brown

spot. D-F, Jelly-end rot of long russet potatoes. G-H, Glassy-end rot of

round potatoes showing starchy areas stained with iodine and abnormal

stolons from tubers.
Agriculture Handbook 479, U.S. Dept. of Agriculture Plate 13

Nonparasitic disorders and injuries: A, Knobby tubers. B-C, Mahogany browning: B, 'Katahdin' tuber; C, 'Kennebec' tuber. D, Growth crack. E, Air

cracic. F-G, Stem-end browning. H, Vine killing.

Aus. GOVERNMENT PRINTING OFFICE ; I978 0-2I2-827

Conversion Table

°F °C °F °C

30 -1.1 80 26.7

32 0 85 29.4

35 1.7 90 32.2

40 4.4 95 35.0

45 7.2 100 37.8

50 10.0 105 40.5

55 12.8 110 43.3

60 15.6 115 46.1

65 18.3 120 48.9

70 21.1 125 51.8

75 23.9

Conversion:

°C = °F-32x5/9

°F = °Cx9/5+32