United States

Department of

Agriculture

Animal and

Plant Health

Inspection

Service

Foreign Animal

Disease Report

Summer 1998
We are initiating a plan to reconstruct the FAD report completely. Therefore, your

questions, comments, and suggestions would be very much appreciated. Please send

them to

Dr. Quita P. Bowman, Editor

USDA, APHIS, VS

4700 River Road, Unit 41

Riverdale, MD 20737–1231

or

e-mail : qbowman@usda.gov

Thirty days before moving, send address changes and, if possible, mailing label from

latest issue to

Distribution Management Section

USDA, APHIS, MSD, PDMB

4700 River Road, Unit 1

Riverdale, MD 20737–1231

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The opinions expressed by individuals in this report do not necessarily represent the

policies of the U.S. Department of Agriculture.
Contents

03 Emergency Programs Activities

Field Investigations—1996

Field Investigations—1997

Regional Emergency Animal Disease Eradication

Organization (READEO) Update

07 FAD Update

10 FAD Review: Bovine Spongiform Encephalopathy

Etiology

Epizootiology

BSE and CJD—Human Health Concerns

Actions Taken in the United Kingdom in Response to nvCJD

Infectivity of Tissues, Products, and Body Fluids

Clinical Signs

Diagnosis

Treatment, Prevention, and Control

European Union (EU) Actions

U.S. Actions

References

26 Vesicular Stomatitis Virus Outbreak—Update 1997

32 Risk Analysis of Potential Control Options for the 1997

Nonpathogenic Avian Influenza Outbreak in Pennsylvania

Background

Methods

Discussion

41 Foot-and-Mouth Disease in Taiwan—1997 Overview

Clinical Disease

Laboratory

Epidemiology

Swine Vesicular Disease (SVD)

The Agriculture Sector in Taiwan

Taiwan’s Swine Industry Prior to the Outbreak

Economic Impacts of the Outbreak

References

Acknowledgments

51 Chronology of Hog Cholera Outbreak in the Dominican Republic

Introduction

Chronology

USDA Intervention

1
55 Epidemiologic Study: The Oklahoma City Bombing—Working Dogs

Who Responded and Their Associated Injuries and Illnesses

56 Emerging Animal Diseases Update

The Acute Porcine Reproductive and Respiratory

Syndrome (PRRS)

Salmonella typhimurium DT104

63 FAD Training and Education

Emerging Disease Course Summary

Veterinary Services, Emergency Programs

Planned Training for 1998

66 Emergency Programs Staff and Current Major Projects

2
 Emergency Programs Activities

The primary responsibilities of the U.S. Department of Agriculture’s (USDA) Animal

and Plant Health Inspection Service (APHIS) are to protect American agriculture and

its livestock from the ravages of disease, to prevent the quality of our food supply from

being degraded, and to minimize the economic impact of disease and disasters on

American agriculture. The principal responsibilities of the Emergency Programs unit in

APHIS’ Veterinary Services (VS) are to ensure prompt evaluation of suspect

outbreaks, and, when a foreign animal disease is diagnosed, to coordinate a prompt

and thorough eradication of an outbreak.

The mission of Emergency Programs is to prevent destructive and harmful effects on

the health of animals and human populations in the United States from epizootics of

foreign and emerging animal diseases and from natural and technological disasters,

such as hurricanes, floods, nuclear fallout and chemical fallout. To accomplish this, VS

has developed and maintained a high level of expertise and preparedness and leads

and coordinates rapid response efforts to safeguard the well-being of our animal

populations and enhance public health.

During fiscal year (FY) 1996 (October 1, 1995–September 30, 1996), veterinary

medical officers from USDA, APHIS, VS, and State departments of agriculture

conducted 420 investigations of suspicious foreign animal diseases in the United

States to explore the possibility that an exotic disease might have been introduced.

Seventy-four investigations were conducted in the Central Region, 100 in the Northern

Region, 50 in the Southeastern Region, and 196 in the Western Region. These

diseases or conditions included abortion, avian diseases, acute death, central nervous

system (CNS) disorders, myiasis and ascariasis, mucosal disorders, respiratory

disorders, septicemia, and vesicular conditions. VS personnel also performed

surveillance activities in regard to bovine spongiform encephalopathy (BSE). These

figures do not include the field investigations done for vesicular stomatitis in FY 1996.

During FY 1997, 718 foreign animal disease (FAD) investigations were conducted (316

routine FAD investigations and 402 investigations for vesicular stomatitis). Chart 1

illustrates the number of investigations for FY 1997 by the condition investigated.

These values do not include vesicular investigations from May 18 to September 30,

1997. That notwithstanding, the majority of investigations were for vesicular conditions

(122) with encephalitic and CNS conditions (66) next most frequent.

Chart 2 shows the number of routine investigations by species for FY 1997. The

largest number of investigations for suspected FAD’s was 129 for bovines, and

equines came in second with a total of 88 investigations. Other species investigations

were as shown.

Field Investigations—1996

Field Investigations—1997

3
Chart 1

Chart 2

129

15 18 21 45

88

Bovine

40.8%

Porcine

4.7%

Other

5.7%

Ovine/Caprine

6.6% Avian

14.2%

Equine

27.8%

Surveillance for FY 1997

Routine FAD Investigations*—By Species

October 1, 1996, to September 30, 1997

*Does not include vesicular investigations

from May 18, 1997, to September 30, 1997.

Total: 316

1

122

5

2

7

23

4

9

13

66

31

33

0 20 40 60 80 100 120 140

Viremia of Carp

Vesicular

Spontaneous abortion

Septicemia

Respiratory, severe

Other

Myiasis/Ascariasis

Mucosal

Excess acute death

Encephalitic/CNS

BSE Surveillance

Avian DZ/acute death

Routine FAD Investigations*—By Condition Investigated

October 1, 1996, to September 30, 1997

*Does not include Vesicular investigations

from May 18, 1997, to September 30, 1997.

4
Chart 3 presents the numbers of routine field investigations for suspected FAD’s that

have occurred over the past 10 years, reported by fiscal year. Total investigations for

1995 increased by over 300 percent with a total of 981 investigations for vesicular

stomatitis virus (VSV) alone. The number of routine FAD investigations increased in

1996, during which 181 investigations for VSV took place. There was a decrease in

routine FAD investigations in 1997 and an overall increase in the total number of

investigations as the result of the VSV outbreak during the year.

Chart 3

Reorganization—As part of the USDA’s overall efforts to colocate, restructure, and

“right-size,” APHIS is restructuring VS from four regions to two. In anticipation of this

restructuring, VS has decided to take a proactive posture and immediately begin the

restructuring of the READEO from four organizations to two. This will enable VS to

have a stable emergency response posture, should an exotic or new animal or poultry

disease emerge during the VS restructuring. The agency will benefit significantly

through cost reductions by maintaining only two organizations rather than the previous

four and will better be able to allocate reduced training dollars.

Regional Emergency

Animal Disease Eradication Organization

(READEO) Update

213 260 217 203 258 230 299 283 270

420

316

981

181 402

0

500

1,000

1,500

1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997

Surveillance for FY 1997

Routine Field Investigations For Suspected Foreign Animal Diseases

Number of 

investigations

Fiscal Year

VS 1997 outbreak investigations

VS 1995 outbreak investigations

Routine FAD investigations

5
Dr. Tom Holt, Assistant Regional Director for VS, Northern Region, has been named

director for the eastern READEO, and Dr. Jan Huber, Assistant Regional Director for

VS, Central Region, has been named director for the Western READEO. VS has also

taken this opportunity to enhance the previous READEO structure. Each READEO

will have a new position of assistant READEO director. The previous structure of field

operations and technical and administrative support has been maintained, although

some of the subunits have been shifted among the three units. Another addition to the

READEO is the early response team (ERT)—an FAD diagnostician, an epidemiologist,

and a pathologist from the National Veterinary Services Laboratories (NVSL). This

team will be called upon to assist the Regional Director, Area Veterinarian-in-Charge,

and the State official when an emergency animal disease situation is being evaluated

with the possibility of activating the READEO.

6
FAD Update

This update consolidates information from the Office of International Epizootics (OIE)

bulletins dated January through April 1997. Countries reporting disease outbreaks

are listed below the appropriate disease heading followed the by month and year of the

outbreaks and the total number of outbreaks for that period. The notation “+” indicates

that the presence of disease was reported without information on the number of

outbreaks. A number followed by “+” indicates that specific outbreaks were reported

during some months, whereas the distribution and occurrence of outbreaks were

unknown during other months.

Foot-and-mouth disease (FMD)

Virus not typed

Bangladesh 10–12/96 +

Bhutan 3,4,9/96 2

Burkina Faso 8–12/96 8+

Cambodia 12/96–2/97 3

Georgia 8/96, 1–2/97 12

Ghana 7–12/96 19+

Hong Kong 11/96 1+

India 10/96 124

Kirghizstan 2/97 4

Laos 12/96–2/97 6

Mali 11,12/96–1/97 3+

Myanmar 11/96, 1–2/97 7

Pakistan 1–7/96,1–2/97 24+

Philippines 12/96 3

Qatar 1,3/97 12

Saudi Arabia 11/96 +

Senegal 12/96–1/97 6

Uganda 10,11/96 +

United Arab Emirates 3,4,6,11/96 4

Virus O

Afghanistan 6/96 +

Bhutan 1,2,7,10,11/96 6

Bolivia 12/96–1/97 3

Brazil 2/97 1+

Colombia 12/96-1/97 7+

Ecuador 1/97 1+

Georgia 7,9–12/96 19

Hong Kong 12/96, 2/97 1+

India 9,11,12/96–1/97 696

Iran 6/96–2/97 132+

Kuwait 3/97 +

Malaysia (peninsular) 4,12/96–3/97 14

Nepal 10–12/96 55+

Oman 11,12/96 11+

Pakistan 8–12/96, 3/97 8+

Palestinian Territories 1/97 3

Peru 3/97 1

Philippines 1–3/97 117+

Sri Lanka 1/97 24

Taipei China 3/97 1,300

Tanzania 7/96 +

Thailand 12/96–3/97 9

Turkey 12/96–3/97 9

Uganda 4–7,9,12/96 +

Vietnam 10/96, 2–3/97 8

Virus A

Albania 5/96 10

Bhutan 7/96 1

Bolivia 1/97 2+

Colombia 12/96–2/97 6+

Ecuador 2/97 1+

India 9,11,12/96–1/97 696

Iran 6/96–3/97 132+

Kenya 2/96 +

Pakistan 8–12/96 8+

Virus C

India 9,11,12/96–1/97 526

Kenya 2/96 +

Pakistan 10–12/96 3+

Virus SAT 2

Kenya 1–4/96 +

Uganda 4–9,12/96 +

Virus Asia 1

India 9,11/96, 1/97 514

Malaysia (peninsular) 4,5/96,12/96–2/97 15

Nepal 10–12/96 55+

Pakistan 8–12/96 8+

7
Vesicular Stomatitis

Virus not typed

Costa Rica 12/96–1/97 10

Honduras 2,4–5,7–11/96 15

Peru 12/96, 2–3/97 7

Virus Indiana

Colombia 12/96–2/97 90

Mexico 1/97 2

Panama 1–2/97 4

Peru 11/96, 1/97 10

Venezuela 1,2/97 5

Virus New Jersey

Colombia 12/96–2/97 90

Costa Rica 2/97 1

Ecuador 12/96 3

Honduras 6/96, 1–2/97 12

Mexico 1–12/96 33

Panama 3/97 1

Peru 1/97 8

Venezuela 10,11/96, 1–3/97 12

Swine Vesicular Disease

Italy 1,2/97 3

Rinderpest

Kenya 12/96 3

Pakistan 1–12/96—2/97 +

Saudi Arabia 11,12/96 +

Tanzania 1/97 +

Peste des Petits Ruminants

Bangladesh 12/96 +

Burkina Faso 10/96 1

Central African Republic 3/96 1+

Cote d’Ivoire 1,2/97 +

Ghana 7–12/96 45

Guinea 10/96,12/96–3/97 +

India 4,10/96,12/96–1/97 20

Nepal 10–12/96 3+

Oman 11,12/96 14

Palestinian Territories 1/97 1

Saudi Arabia 9,11,12/96 +

Senegal 3/97 1

United Arab Emirates 4,5,7/96 3

Contagious Bovine Pleuropneumonia

Angola 10/96 4

Bangladesh 10–12/96 +

Burkina Faso 8–12/96 17

Cote d’Ivoire 1,2/97 +

Ghana 9/96 2

Guinea 10/96,12/96–3/97 9+

Mali 11/96–3/97 7

Namibia 12/96–2/97 2+

Pakistan 4–12/96 +

Qatar 3/97 2

Uganda 4–12/96 +

Lumpy Skin Disease

Ghana 7–9/96 7

Guinea 10/96,12/96–3/97 +

Madagascar 10,11/96 12

Senegal 1/97 1

South Africa 1–3/97 112

Swaziland 12/96–1/97 +

Uganda 5–12/96 +

Zimbabwe 11,12/96 6

Rift Valley Fever

Mozambique 12/96–2/97 +

South Africa 3/97 1

Uganda 7/96 +

Bluetongue

Guinea 10/96,12/96–3/97 +

India 9–12/96—1/97 487

Mozambique 12/96–2/97 +

Pakistan 1–12/96 +

Saudi Arabia 9,12/96 +

South Africa 1–3/97 17

United States 12/96–3/97 +

Sheep Pox and Goat Pox

Algeria 1–3/97 11

Bangladesh 10–12/96 +

China 11/96–1/97 5

Georgia 2/97 1

Greece 12/96–1/97 19

India 10–12/96—1/97 101

Iran 6/96—1/97 71

Kazakhstan 10/96 1

Kirghizstan 8,9/96,12/96–2/97 8

Libya 11,12/96 +

Mozambique 12/96 +

Oman 1/97 5

Pakistan 12/96–2/97 4+

Palestinian Territories 1/97 4

Qatar 3/97 3

Russia 11/96 1

Saudi Arabia 11,12/96 +

Tunisia 11/96–1/97 9

Turkey 12/96–3/97 12

United Arab Emirates 1,9,11/96 3

African Horse Sickness

Mozambique 12/96–2/97 +

Senegal 1/97 1

South Africa 1/97 2

Zimbabwe 1–5/96 8

African Swine Fever

Cote d’Ivoire 1,2/97 +

Italy 2–4/97 4

Mozambique 12/96–2/97 +

Senegal 2/97 1

South Africa 4/97 2

Uganda 4,5,8,10–12/96 +

8
Classical Swine Fever (Hog Cholera)

China 11/96–1/97 28+

Colombia 2/97 1

Cuba 1/97 5

Czech Republic 2/97 1

Federal Republic of

Yugoslavia (Serbia

and Montenegro) 11/96–2/97 13

Germany 1–4/97 35

Honduras 6/96,9/96–1/97 4

Hong Kong 10/96 1

India 9/96–1/97 57

Indonesia 10–12/96 +

Italy 1–4/97 13

Korea 12/96–2/97 9

Laos 10–12/96 +

Madagascar 10,11/96 2

Malaysia (peninsular) 12/96–4/97 2

Mexico 1–3/96,6/96–1/97 27

Myanmar 12/96 +

Netherlands 2–4/97 162

Peru 11/96–2/97 2

Philippines 7–9/96 +

Russia 11/96 4

Slovakia 1–3/97 15

Spain 4/97 10

Sri Lanka 12/96 1

Taipei China 1,2/97 15

Venezuela 11/96 1

Vietnam 10–12/96 +

Highly Pathogenic Avian Influenza

Laos 10–12/96 +

Myanmar 11,12/96 +

Pakistan 1–12/96 +

Newcastle Disease

Virus not characterized

Algeria 4/97 10

Bangladesh 10–12/96 +

Central African Republic 10/96 1

Colombia 2/97 2

Cote d’ Ivoire 1,2/97 +

Fedral Republic of

Yugoslavia (Serbia

and Montenegro) 11,12/96 2

Ghana 7–12/96 129

Great Britain 12/96–4/97 9

Guinea 10/96,12/96–3/97 +

Honduras 3,5,6/96 3

Hong Kong 10/96 1+

India 9/96–1/97 222

Indonesia 10–12/96 +

Iran 6–12/96—1/97 287

Jordan 10–12/96—3/97 +

Korea 1–3/97 13

Laos 10–12/96 +

Madagascar 10,11/96 13

Malaysia (peninsular) 12/96, 2/97 3

Myanmar 10–12/96 +

Namibia 1,3/97 3

Nepal 10–12/96 11+

Northern Ireland 2,3/97 21

Norway 12/96 1

Pakistan 1/96–2/97 4+

Philippines 7–9/96 +

Russia 12/96 1

Saudi Arabia 9–12/96 +

South Africa 1,3/97 3

South America 1/97 2

Sri Lanka 12/96–1/97 10

Swaziland 1,2/97 5

Turkey 1,2/97 3

Uganda 5–9,11/96 +

Unites Arab Emirates 1–3,6/96 4

Vietnam 10–12/96 +

Zimbabwe 11,12/96 7

Velogenic Virus

Denmark 9/96 1

Great Britain 1/97 5

Kenya 11,12/96 2

Korea 12/96 2

Mexico 2,3,5,6,8/96 13

South Africa 2/97 4

Uganda 10,12/96 +

Mesogenic virus

Mexico 1,2,9/96 7

Israel 4/97 1

Lentogenic virus

Mexico 8,9,11/96 5

(Compiled by Ms. Christine Allen, secretary, and Dr. Richard Pacer, epidemiologist,

USDA, APHIS, International Services (IS), Riverdale, MD, (301) 734–8892)

9
Foreign Animal Disease Review:

Bovine Spongiform Encephalopathy

Bovine spongiform encephalopathy (BSE), widely known as “mad cow disease,” is a

chronic, degenerative disease affecting the CNS of cattle. It is one in a family of

diseases known as the transmissible spongiform encephalopathies (TSE’s).

Worldwide, there have been more than 170,000 cases of BSE since it was first

diagnosed in 1986 in Great Britain. BSE has had a substantial impact on the livestock

industry in the United Kingdom. The disease has also been confirmed in native-born

cattle in Belgium, France, Ireland, Luxembourg, the Netherlands, Northern Ireland,

Portugal, and Switzerland. However, more than 98 percent of all BSE cases have

occurred in Great Britain. BSE is not known to exist in the United States.

Owing to the nature of the disease, it is difficult to develop all-inclusive guidelines that

would establish BSE-free status for a country. Currently, OIE has criteria to assist

countries in evaluating the status of trading partners. This code was adopted in May

1997.

The lack of a preclinical screening test that definitively detects all BSE infection adds

to the complexity of verifying the absence of the disease. Hence, an active and

aggressive surveillance program is essential in any country wishing to claim freedom

from BSE. Because many outside factors influence reporting, it is rarely possible to

claim freedom from BSE on the basis of passive surveillance alone. In addition, the

OIE guidelines take into account certain risk factors that may be present in countries.

These risk factors include the importation of infected cattle feed contaminated with the

BSE agent (Schreuder et al. 1997), the presence of other animal TSE’s, and feeding

practices, among others. For the same reason, it is virtually impossible to obtain a

true picture of disease prevalence in a country where BSE has been detected.

TSE’s are caused by a transmissible agent that is yet to be fully characterized. They

share the following common characteristics:

• A prolonged incubation period of months or years;

• A progressive debilitating neurological illness that is always fatal;

• The presence of scrapie-associated fibrils (SAF’s) when detergent-treated extracts

of brain tissue from animals or humans affected by these diseases is examined by

electron microscope;

• Pathological changes, such as vacuolation and astrocytosis, that appear to be

confined to the CNS; and

• The absence of any detectable specific immune response in the host.

The lack of antibody formation in BSE-infected animals has inhibited the development

of a live animal diagnostic test. Listed below are other TSE’s.

Creutzfeldt–Jakob Disease (CJD) is a sporadic presenile dementia that affects

humans. It occurs at an annual incidence of about one in a million of the population.

About 90 percent of the cases are sporadic and have no known source of exposure.

Five to 10 percent of the cases are familial and are associated with certain inherited

gene mutations. An extremely small number of cases result from iatrogenic transmission through such mechanisms as corneal transplants, contaminated pituitary

growth hormone injections, or the use of poorly disinfected brain electrodes (Brown

1988a, b).

Creutzfeldt–Jakob

disease

10
New-variant Creutzfeldt–

Jakob disease (nvCJD)

Kuru

Gerstmann–Sträussler–

Scheinker syndrome

Fatal familial insomnia

Twenty-four cases of nvCJD have been identified in the United Kingdom and France

between 1994 and 1996. Unlike sporadic CJD, the cases were unique because the

patients were younger than usual, the clinical manifestation was different, and the

patients displayed a new neuropatho- logical profile. The Spongiform Encephalopathy

Advisory Committee (SEAC) in the United Kingdom concluded that, although there

was no direct scientific evidence of a link between BSE and CJD, on the basis of

current data and in the absence of any credible alternative, the most likely explanation

is that nvCJD is linked to exposure to BSE before the introduction of the specified

bovine offal ban in 1989 (Will et al. 1996).

An extremely rare human disorder characterized by trouble sleeping and disturbances

of the autonomic nervous system. An inherited mutation in the PrP gene has been

identified as the precipitating factor of this disease (Tateishi et al. 1995).

A rare familial syndrome of humans caused by an inherited mutation in the PrP gene

affecting about 50 extended families. The syndrome is characterized by loss of

coordination and dementia (Prusiner 1995).

A disease of the Fore tribe in the eastern highlands of Papua New Guinea. The

disease is characterized by a loss of coordination followed by dementia. The infection

was thought to spread through the practice of cannibalism and exposure to high-risk

tissues such as brain. Since cannibalism was discontinued, kuru has essentially

disappeared.

CWD was first discovered in 1967 and reported by Williams and Young (1980) and

originally was confined to mule deer and Rocky Mountain elk held in captivity in

Colorado and Wyoming (Williams and Young 1982). CWD has more recently been

confirmed in free-ranging cervids in Colorado and Wyoming, such as mule deer, whiteand black-tailed deer, and elk. CWD has also been diagnosed in ranch-raised elk in

South Dakota. The disease is characterized by emaciation, changes in behavior, and

excessive salivation.

A naturally occurring TSE first reported in domestic cats in 1990 (Wyatt et al. 1990).

More than 70 cases of FSE have been diagnosed in the United Kingdom since 1990.

In addition, one case of has been identified in Norway (Bratberg et al. 1995) and one

in Liechtenstein. Cats with the disease display locomotor disturbances, behavioral

changes, and hypersensitivity to sudden movements or noises (Wyatt et al. 1991).

Current evidence suggests that the disease in cats is most probably linked to BSE.

Chronic wasting disease

(CWD)

Feline spongiform

encephalopathy

11
An insidious degenerative disease affecting the CNS of sheep and goats. The disease

is also called la tremblante (French: trembling), Traberkrankheit (German: trotting

disease), or Rida (Icelandic: ataxia or tremor). Scrapie was first recognized as a

disease of sheep in Great Britain and other countries of Western Europe more than

250 years ago. Scrapie has been reported worldwide and affects most sheepproducing regions. Australia and New Zealand are commonly accepted to be scrapie

free. The disease has been recognized for over two centuries in England, Wales, and

Germany (Parry 1983). The first U.S. case of scrapie was diagnosed in 1947.

An uncommon disease of ranch-raised mink first reported in the United States in 1947

and described by Hartsough and Burger (1965). TME has been reported in Canada,

Finland, Germany, Russia, and the United States. The last U.S. case was in

Wisconsin in 1985 (Marsh and Hadlow 1992). It has been suggested that TME is a

result of feeding either scrapie-infected sheep or infected cattle to mink.

Other cases of spongiform encephalopathy have been reported in kudus, elands,

nyalas, gemsboks, and a few exotic cats. These occurrences are also thought to be

linked to contaminated feed.

The clinical, pathological, and molecular genetic features of BSE, as well as other

TSE’s, have led to speculation on the nature of the etiologic agent and the

pathogenetic mechanisms of the disease. There are three main theories on the nature

of the scrapie agent.

The Virus Theory—In this theory, the virus would have to have unusual biochemical

and biophysical characteristics that would help explain its remarkable physicochemical

properties (Rohwer 1984, Czub et al. 1988, Manuelidis et al. 1988).

The Prion Theory—Here the agent is believed to be composed exclusively of the

host-coded protein (PrPc

), which becomes partially protease resistant (PrPBSE)—most

likely through a posttranslational conformation change after infection. In this theory,

there are no nonhost components of the agent. That is, a specific informational

molecule (nucleic acid such as RNA or DNA) is not present (Prusiner 1982, Bolton and

Bendheim 1988).

The Virino Theory—This theory states that the BSE agent consists of a host-derived

protein coat (PrP is one of the candidates for this protective protein) and a small

noncoding regulatory nucleic acid (Dickinson and Outram 1979, Kimberlin 1982).

Scrapie

Etiology

Transmissible mink

encephalopathy (TME)

12
Comparing the Theories—All three proposed theories have some degree of validity.

Proponents of the virus and virino theories conclude that the existence of different

scrapie strains unequivocally proves the existence of a nucleic acid component of the

infectious agent, which, as in conventional viruses, may undergo mutations

responsible for phenotypic variations. The problem with these two theories is that no

agent-specific nucleic acid has been convincingly identified to copurify with infectivity

(Manuelidis and Manuelidis 1981, Duguid et al. 1988, Oesch et al. 1988, Meyer et al.

1991, Sklaviadis et al. 1993). Moreover, chemical, enzymatic, or physical treatments

that usually inactivate or degrade nucleic acids have no effect on the transmissible

properties of the BSE infectious agent (McKinley et al. 1983; Bellinger Kawahara et al.

1987a,b; Neary et al. 1991). Possible reasons for this lack of effect are that the

amount of nucleic acid of the putative agent is too small to be detected with available

techniques and that its tight bond to the protein protects it from chemical or physical

inactivation. Weakening the virus and virino theories are also the inability to identify

any virus particles under the electron microscope (Bots et al. 1971, Cho and Greig

1975) and the failure of an infected host to generate an immune response. [It should

be noted that small particles resembling virus structures have recently been observed

by electron microscopy (Ozel and Diringer 1994).]

The prion model involves propagation of a protein-only agent (PrPBSE) whereby PrP

can assume various tertiary structures caused by a combination of host genetics and

the introduction of altered (infectious) PrP. Hence, the structure of the infecting PrPBSE

imprints upon the normal cellular precursor (PrPc), which results in a change of shape

to the protease-resistant form. Researchers suspect that mutations in the PrP gene

may render resulting proteins susceptible to “flipping,” and the shape changes account

for what is commonly referred to as “strain” differences. Several explanations for

scrapie strain genetics in the context of the prion theory have been suggested, but not

one has been proven (Prusiner 1991, Weissman 1991). A recent publication suggests

that passaging the agent through different hosts causes the conformational change,

possibly limiting prion diversity (Scott et al. 1997). However, this study could not

eliminate the existence of a mixture of prion strains.

It should be pointed out that the prion theory fails to explain (1) how the PrP of the

infecting agent originally assumed the aberrant structure associated with infectivity and

(2) how the different structures originated as a function of the different strains.

Although numerous scrapie strains can be differentiated in a single host (i.e., sheep),

the PrP associated with these strains has not shown any biochemical and molecular

differences. BSE seems to be caused by a single strain type. This BSE strain is

different from historical or contemporary isolates from sheep or goats with natural

scrapie as determined by study of incubation periods and brain “lesion profiles” in

mice.

Regardless of whether the prion (PrPBSE) is or is not the agent, the partially proteaseresistant form is a marker of infection. Currently several of tests are available to detect

the presence of the PrPBSE.

13
 Different scientific hypotheses concerning the origins of BSE have been advanced.

The epidemiologic data suggest that BSE in Great Britain is an extended, commonsource epidemic involving feed containing TSE-contaminated meat and bone meal as

a protein source. The causative agent is suspected to be from either scrapie-affected

sheep or from cattle with a previously unidentified TSE.

Changes in rendering operations in the early 1980’s—particularly the removal of a

solvent-extraction process that included a steam-heat treatment—may have played a

part in the appearance of the disease and the subsequent amplification of the agent in

the food chain. A ban in Great Britain on feeding animal protein of ruminant origin to

ruminants was enacted in July 1988 (Wilesmith et al. 1992).

In Great Britain, the epidemic peaked in 1992–93, when about, 1,000 cases were

reported each week. In 1997, BSE remained on the decline, with approximately

100 cases reported weekly. Cases that have been detected in other countries appear

to be a result of importations of live cattle or, more significantly, contaminated feed

from the United Kingdom.

There is no evidence that BSE spreads horizontally, that is, by contact between

unrelated adult cattle or from cattle to other species. Results of recent British research

show very low levels of transmission of BSE from affected cows to their offspring.

These results demonstrate about a 9-percent increase in the occurrence of BSE in

offspring of BSE-affected dams as compared with calves born to dams that did not

later demonstrate BSE infection. The study did not ascertain if this was the result of

genetic factors or true transmission. The research did, however, point out that at this

level, if maternal transmission does occur, it will not sustain the epidemic (Wilesmith et

al. 1997).

A TSE has been diagnosed in eight species of captive wild ruminants as well as exotic

and domestic cats. There have been more than 80 cases of feline spongiform

encephalopathy (FSE) in Great Britain, 1 in a domestic cat in Norway, 1 in Northern

Ireland, and 1 in Liechtenstein. The agent isolated from several of these cases using

strain typing in mice is indistinguishable from BSE in cattle, suggesting that FSE is

actually BSE in exotic and domestic cats. This also appears to be true for the other

ruminants. Epidemiologic evidence suggests protein-enhanced feed from ISSEinfected carcasses to be the primary source of infection in these species (MAFF

Progress Report, June 1997).

Some authorities have suggested that 24 cases (as of January 31, 1997) of a variant

form of CJD (nvCJD) in Great Britain (U.K. Department of Health, March 1998) and

France may be linked to exposure to BSE before the introduction of a specified bovine

offal (SBO) ban at slaughter in 1989. The SBO ban excluded from human

consumption brain, spinal cord, and other tissues with potential BSE infectivity.

Epizootiology

14
BSE has been experimentally transmitted to the following species via intracerebral

inoculation: cattle, sheep, goats (Foster et al. 1993), mink (Robinson et al. 1994), pigs

(Dawson et al. 1990), marmosets (Baker et al. 1993), macaques (Lasmézas et al.

1996), and mice (Fraser et al. 1988). Intracranial transmission was attempted in

hamsters but was not successful. BSE has been successfully transmitted via the oral

route to cattle, sheep, goats (Foster et al. 1993), mice (Barlow and Middleton 1990),

and mink (Robinson et al. 1994). Oral transmission has been attempted in swine. The

inoculated swine were euthanized after 84 months of age and had not exhibited any

signs of a TSE. Parenteral and oral transmission have also been attempted in

chickens with no evidence of disease thus far, even 12 months into a second passage.

On March 20, 1996, the SEAC announced the identification of 10 cases of nvCJD. All

of the patients developed symptoms of disease in 1994 or 1995. The following points

describe how these 10 cases differed from other routinely diagnosed cases of CJD:

• The affected individuals were much younger than the sporadic CJD patient.

Typically, CJD patients are over 63 years old. The average patient age for the

variant form of CJD is 27.5 (range of 16 to 42) years. (The term “sporadic” is used

here, after Dr. John Collinge, to indicate classical CJD.)

• The course of the disease in the nvCJD averaged 13 months. Sporadic CJD cases

average a 6-month duration.

• In the 10 victims, electroencephalographic activity was not typical of CJD.

• Although brain pathology was recognizable as CJD, the pattern was different from

sporadic CJD, as manifested by large aggregates of prion protein plaques.

Epidemiologic and case studies have not revealed exposure to a common risk factor.

According to the SEAC, all victims were reported to have eaten beef or beef products

in the last 10 years, but none had knowingly eaten brain material. One of the affected

individuals had been a vegetarian since 1991 (Will et al. 1996).

The SEAC concluded that, although there was no direct scientific evidence of a link

between BSE and nvCJD, on the basis of current data and in the absence of any

credible alternative, the most likely explanation was that the cases resulted from

exposure to BSE before the introduction of control measures—in particular, the SBO

ban in 1989.

Research reported in later 1996 and 1997 has found further evidence to link nvCJD to

BSE. Two significant studies published in the October 2, 1997, edition of Nature led

the SEAC to conclude that BSE agent is highly likely to be the cause of nvCJD.

Dr. Moira Bruce and colleagues at the Institute for Animal Health in Edinburgh,

Scotland, inoculated three panels of inbred mice and one panel of crossbred mice with

BSE, nvCJD, and CJD. Mice inoculated with BSE showed the same pattern of

incubation time, clinical signs, and brain lesions as mice inoculated with tissues from

patients with nvCJD. This finding provides evidence that BSE and nvCJD have the

same signature or are the same “strain.” In addition, sporadic CJD and known scrapie

strains were found not to be similar to nvCJD or BSE (Bruce et al. 1997).

BSE and CJD—Human

Health Concerns

15
The second set of results, published by Dr. John Collinge and colleagues of Imperial

College School of Medicine, London, strongly supported Bruce’s results. Collinge’s

paper reported findings of BSE transmission to transgenic mice expressing only

human PrP (Hill et al. 1997).

Another paper by Collinge et al. in the October 24, 1996, edition of Nature discussed a

molecular analysis of prion strain variation in relation to the etiology of nvCJD.

Collinge and colleagues demonstrated that two of the three forms of CJD (sporadic

and iatrogenic) can be distinguished from one another, after treatment by proteolytic

cleavage, by differing band sizes using Western blot analysis. Types 1 and 2 are

associated with different clinicopathological phenotypes of sporadic CJD, and type 3 is

seen in iatrogenic CJD cases where there is a peripheral route of inoculation.

Iatrogenic cases of CJD with a direct CNS exposure resemble the pattern manifested

by sporadic CJD. The nvCJD, although resembling type 3 to some degree, can be

differentiated from each of the three types by a specific pattern of band intensities.

Furthermore, glycoform patterns of the nvCJD were “closely similar to” patterns from

wild-type mice inoculated with BSE and “closely resembled” those from FSE as well as

patterns from macaques inoculated with BSE. However, natural BSE was not

detected through Western blot analysis using the antibodies in the aforementioned

studies (3F4 monoclonal or R073 polyclonal). The use of rabbit antibody to synthetic

human PrP peptide (95–108) with BSE from its natural host, the cow, did generate a

signal and glycoforms closely similar to transmitted BSE and nvCJD (Collinge et al.

1996).

The Health and Safety Executive in the United Kingdom now advises that BSE must

be considered a biological agent (human pathogen) within the meaning of the Control

of Substances Hazardous to Health Regulations 1994 (HSE Press Release, October

1997).

As a result of the identification of the variant form of CJD, the following measures have

been put into place in the United Kingdom (MAFF Progress Report, June 1997):

• In November 1989, entry into the human food supply of any protein derived from

bovine brain, spinal cord, tonsil, thymus, spleen, or intestine was prohibited. These

tissues were referred to as SBO and now are referred to as specified bovine material

(SBM).

• The spinal column and heads of bovine animals over 6 months old, except for the

tongue, are to be treated as SBM. Such materials and their derivatives may not be

used in cosmetic, pharmaceutical, or medicinal products.

• Mammalian meat and bonemeal are not to be incorporated into any feed for any

farmed animals, including fish or horses, or into fertilizer likely to be used on land to

which ruminants have access.

• Meat from animals over 30 months old is prohibited from entering the human or

animal food supply.

Actions Taken in the

United Kingdom in

Response to nvCJD

16
• On July 24, 1996, MAFF announce its intention to introduce controls requiring the

removal of sheep heads from the food chain following a study showing evidence that

BSE could be isolated from spleens of sheep experimentally infected with BSE.

• In September 1996, the Heads of Sheep and Goats Order was put into effect.

• In January 1997, selective cull began. The selective cull targets cattle born on a

farm around the same time as BSE cases born on that farm between July 1989 and

June 1993 that would have been exposed to the same risk of infection by the BSE

agent in feed.

In the naturally infected animals, the BSE agent has been identified in brain, spinal

cord, and retina. Agent identification was by mouse bioassay. The route of inoculation

into the mice was intracranial. The naturally infected animals were adult cattle

exhibiting clinical signs of disease (Fraser et al. 1988).

Experiments with mice that were fed milk, mammary glands, placentas, lymph nodes,

or spleens have failed to transmit the disease within the natural lifespan of the mice or

to establish subclinical infection of the lymphoreticular system (Middleton and Barlow

1993).

Another study is ongoing to examine the pathogenesis of BSE by quantifying the

replication (tissue distribution) of the agent during the incubation period. This study

has identified the agent via mouse bioassay in the distal ileum of experimentally

infected calves. It is thought that the agent may be associated with the lymphoid

tissue of the intestines. The calves were 4 months of age at the time of oral dosing.

First isolation of the agent in the distal ileum was made at 6 months after the

challenge. Subsequent isolations from the distal ileum were made at 10, 14, and 18

months after dosing (Wells et al. 1994). Recently, this study has also disclosed

infectivity in bone marrow and trigeminal and dorsal root gangli (UK MAFF Website).

More than 40 tissues have been examined from cattle using the mouse bioassay. It

appears as if the distribution of the BSE agent is not as diverse as that of the scrapie

agent in sheep. Another consideration that must be noted is the species barrier using

the mouse bioassay. There is a possibility that the agent is present but is found in

such very low levels that the bioassay is not sensitive enough to detect it (MAFF

Progress Report, June 1997).

Cattle afflicted with BSE develop a progressive degeneration of the nervous system.

Affected animals may display changes in temperament, abnormalities of posture and

movement, and changes in sensation. More specifically, the signs include

apprehension, nervousness or aggression, incoordination (especially hind-limb ataxia,

tremor, and difficulty in rising), and hyperesthesia to sound and touch. In addition,

many animals have decreased milk production and/or loss of body condition despite

continued appetite. There is no treatment, and affected cattle die.

Infectivity of Tissues,

Products, and Body

Fluids

Clinical Signs

17
The incubation period ranges from 2 to 8 years. Following the onset of clinical signs,

the animal’s condition gradually deteriorates until the animal becomes recumbent,

dies, or is destroyed. This usually takes from 2 weeks to 6 months. Most cases in

Great Britain have occurred in dairy cows (Frisians) between 3 and 6 years of age

(Wilesmith et al. 1992).

The diagnosis of BSE is based on the occurrence of clinical signs of the disease and

currently must be confirmed by postmortem laboratory testing. Histopathologic

examination of brain tissue collected after the animal dies or is euthanized is the initial

step in the diagnostic process. Bilaterally symmetrical degenerative changes are

usually seen in the gray matter of the brain stem. These changes are characterized by

vacuolation or microcavitation of nerve cells in the brain-stem nuclei. The neural

perikarya and axons of certain brain-stem nuclei contain intracytoplasmic vacuoles of

various sizes, giving the impression of a spongy brain. Hypertrophy of astrocytes

often accompanies the vacuolation (Wells et al. 1987). A diagnosis may also be made

by the detection of scrapie-associated fibrils using electron microscopy.

Supplemental tests are available to enhance the diagnostic capabilities for BSE.

Research has shown that the partially protease-resistant form of the prion protein

(PrPBSE) is found in the brain of BSE-infected cattle. Two tests may currently be used

to detect the PrPBSE. These are immunohistochemistry and the Western blot

technique. In the past, if the brain tissue was not harvested shortly after the animal’s

death autolysis made it very difficult to confirm a diagnosis. Both of these tests allow

for the possibility of confirming a diagnosis of BSE even if the brain has been frozen or

has autolyzed.

The potential live-animal tests, including some in development, are as follows:

• Tests specific for the partially protease-resistant form of the prion protein:

(1) A capillary electrophoresis test, and

(2) A Western blot test with increased sensitivity.

• Tests that identify unique substances of infected animals or humans:

(1) A cyclic voltametric method that describes unique substances in urine, and

(2) An immunoblot test describing unique substances in cerebrospinal fluid.

Tests for PrPBSE in the preclinical cow may not be as successful as they are appearing

to be in scrapie diagnosis because PrPBSE has not yet been detected in peripheral

tissues.

Differential diagnoses for BSE include rabies, listeriosis, nervous ketosis, milk fever,

grass tetany, lead poisoning, and other toxicities or etiological agents that affect the

nervous or musculoskeletal systems of adult cattle.

Diagnosis

18
There is no known treatment for BSE or any of the TSE’s, and there is no vaccine to

prevent these diseases. BSE from foreign sources may be prevented by the

implementation of import regulations prohibiting live ruminants and ruminant products

(especially meat, bone meal, and offal). Because the origin of BSE remains unknown,

preventing a domestic epidemic of BSE would involve, at a minimum, prohibiting the

feeding of ruminant proteins to ruminants. The prevention program of any country

should also include active surveillance for the early detection of BSE. Most countries

have prohibited the importation of cattle and bovine products from countries known to

have BSE. In addition, many countries have taken steps to enact regulations

prohibiting the feeding of ruminant proteins to ruminants. This is true even in countries

such as Australia and New Zealand with no known animal TSE’s.

Agricultural officials in countries known to have BSE have taken a series of actions to

control and, it is hoped, eradicate BSE. These include making BSE a notifiable

disease, prohibiting the inclusion of certain animal proteins in ruminant rations (the

feed bans vary depending on the amount of BSE detected), and the depopulation of

certain groups of cattle thought to be of higher risk owing to epidemiologic findings.

To prevent human exposure to the BSE agent, some countries have established

prohibitions on the inclusion of high-risk material in foods, pharmaceuticals, and

cosmetics.

Several EU member countries have had cases of BSE in native cattle or only in

imports from the United Kingdom. Other countries have reported BSE in both imports

and native cattle, and some member states have not reported BSE.

In June 1994, the EU enacted regulations that prohibit feeding mammalian protein to

ruminants. On March 27, 1996, the European Commission prohibited the export of

most bovine products, including live animals, embryos, meat, meat meal, meat-andbone meal, and other products from the United Kingdom. These restricted products

were those most liable to enter the animal or human food chain or be used in

medicinal, pharmaceutical, or cosmetic products.

In July 1997, the EU adopted legislation restricting the use of “specified risk material”

(SRM). SRM’s include skulls, brains, eyes, tonsils, and spinal cords from all bovines,

caprines, and ovines 12 months of age or older. The category also includes spleens

from ovines and caprines of any age. The SRM’s may not be used in any food, feed,

medicinal products, pharmaceuticals, or cosmetics. This legislation is scheduled to be

effective as of January 1999.

Treatment, Prevention,

and Control

European Union (EU)

Actions

19
An active surveillance program in place for 8 years has not disclosed the presence of

BSE in the United States. USDA, FDA, and industry groups actively work to maintain

this status. The measures APHIS has taken in this regard include prohibitions or

restrictions on certain animal and product imports, ongoing surveillance for signs of the

disease in the United States, preparation of an emergency response plan in the event

that the disease does occur, and ongoing educational efforts. APHIS actively shares

information and coordinates closely with other Federal agencies as well as with the

States, livestock and affiliated industries, veterinary and research communities, and

consumer groups to ensure that the United States has a uniform approach to TSE’s

that is based on sound scientific information.

APHIS has a comprehensive surveillance program in place in the United States to

ensure timely detection and swift response in the event that BSE were to be

discovered here. This surveillance program incorporates both the location of imports

from the United Kingdom and targeted active and passive surveillance for either BSE

or any other TSE in cattle.

APHIS has conducted a traceback effort to locate each of the 496 British cattle that

were imported into this country between January 1, 1981, and July 1989. In July

1989, the United States prohibited the importation of ruminants from countries affected

with BSE. Only 17 of these animals are known to be alive in the United States, and

these animals are being carefully monitored by APHIS personnel on an ongoing basis.

In addition, in cooperation with the States and industry, APHIS has placed five head of

cattle imported from Belgium in 1996 under quarantine, and APHIS makes ongoing

attempts to purchase these animals for diagnostic purposes. No evidence of BSE has

been found in any of these imported animals.

The United States has had an aggressive and active surveillance program for BSE in

place since May 1990. BSE is a notifiable disease, and there are more than 250

Federal and State regulatory veterinarians specially trained to diagnose foreign

animals diseases, including BSE. Several agencies are involved in the surveillance

program, including the USDA’s Food Safety and Inspection Service (FSIS) and the

Health and Human Services Department’s Centers for Disease Control and

Prevention. APHIS leads this interagency effort. The surveillance samples include

field cases of cattle exhibiting signs of neurologic disease, cattle condemned at

slaughter for neurologic reasons, rabies-negative cattle submitted to public health

laboratories, neurologic cases submitted to veterinary diagnostic laboratories and

teaching hospitals, and random sampling of cattle that are nonambulatory at slaughter.

As of February 21, 1998, more than 6,600 brains had been examined for BSE or any

other form of TSE in cattle. No evidence of either condition has been detected by

histopathology or immunohistochemistry.

As of December 12, 1997, APHIS has prohibited the importation of live ruminants and

most ruminant products from all of Europe until a thorough assessment of the risks can

be made. The new restrictions apply to Albania, Austria, Bosnia–Herzegovina, Bulgaria,

Croatia, the Czech Republic, Denmark, Federal Republic of Yugoslavia, Finland,

Germany, Greece, Hungary, Italy, the former Yugoslavian Republic of Macedonia,

Norway, Poland, Romania, the Slovak Republic, Slovenia, Spain, and Sweden.

U.S. Actions

20
This action was taken because, in the past year, the Netherlands, Belgium, and

Luxembourg have reported their first cases of BSE in native-born cattle. There is

evidence that European countries may have had high BSE risk factors for several

years and less than adequate surveillance. Additionally, Belgium reported that the cow

diagnosed with BSE was processed into the animal food chain.

The U.S. Food and Drug Administration (FDA) has recently established regulations

that prohibit the feeding of most mammalian proteins to ruminants. The effective date

of this regulation was August 4, 1997.

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Wilesmith, J. W.; Wells, G.A.H.; Ryan, J.B.M.; Gavier–Widen, D.; Simmons, M. M.

1997. A cohort study to examine maternally associated risk factors for bovine

spongiform encephalopathy. Veterinary Record 141: 239–243.

Will, R. G.; Ironside, J. W.; Zeidler, M.; Cousens, S. N.; Estibeiro, K.; Alperovitch, A.;

Poser, S.; Pocchiari, M.; Hofman, A. Smith, P. G. 1996. A new variant of Creutzfeldt–

Jakob disease in the UK. Lancet 347: 921–925.

Williams, E. S.; Young, S. 1980. Chronic wasting disease of captive mule deer: a

spongiform encephalopathy. Journal of Wildlife Diseases 16: 89–98.

Williams, E. S.; Young, S. 1982. Spongiform encephalopathy of Rocky Mountain elk

18: 465–471.

24
Wyatt, J. M.; Pearson, G. R.; Smerdon, T.; Gruffydd–Jones, T. J.; Wells, G.A.H. 1990.

Spongiform encephalopathy in a cat. Veterinary Record: 513.

Wyatt, J. M.; Pearson, G. R.; Smerdon, T. N.; Gruffydd–Jones, T. J.; Wells, G.A.H.;

Wilesmith, J. W. 1991. Naturally occurring scrapie-like spongiform encephalopathy in

five domestic cats. Veterinary Record [volume unknown]: 233–236.

(Authors: Dr. Linda A. Detwiler, senior staff veterinarian, USDA, APHIS, VS,

Emergency Programs, Robbinsville, NJ, (609) 259–8387, and Dr. Richard Rubenstein,

laboratory head of the Molecular & Biochemical Neurovirology Laboratory, Institute for

Basic Research, Staten Island, NY, (718) 494–5314)

25
Vesicular Stomatitis Virus Outbreak—Update 1997

Vesicular stomatitis is an acute and contagious viral disease that affects horses, cattle,

swine, goats, and humans. Many New World species of wildlife are also susceptible

but rarely affected. Some of these animals include deer, antelope, bighorn sheep,

raccoons, monkeys, sloths, rodents, and bats. This virus has caused sporadic

outbreaks of disease in the United States, Mexico, and Central and South America.

The characteristics of this disease are vesicles in the mouth, on the teats, and on

interdigital areas of some animals. Humans can become infected when handling

affected animals. In people, vesicular stomatitis is a flulike disease; symptoms include

fever and muscle aches and self-limiting blisters that may appear on the hands and in

the mouth.

The causative agent of vesicular stomatitis is a rhabdovirus of the genus Vesiculovirus.

There are two antigenically distinct types of vesicular stomatitis, New Jersey and

Indiana. The Indiana type is further categorized into three subtypes: Indiana 1,

Indiana 2, and Indiana 3. The most virulent and most common of the two types is the

New Jersey strain.

The incubation period for this disease is usually 9 days but can range from 3 to 14

days. After the incubation period, infected animals may have increased temperature

and oral lesions. The muzzle may appear hyperemic, and a serous fluid may drain

from the nose. The animals may also project their tongues from their mouths and

make a smacking noise. The lesions may rupture to form large painful ulcerations,

leading to dysphagia and reluctance to eat. Frothing at the mouth, drooling, agalactia,

weight loss, mastitis, and lameness are observed in some species. Other clinical

signs include depression, local soreness, and general discomfort. Affected animals

often become emaciated.

Vesicular stomatitis can affect all breeds, sexes, and ages of susceptible animals.

There is increasing evidence of biological and mechanical transmission via insect

vectors. Several potential vectors include phlebotomine flies, mosquitoes, and

Culicoides midges. The Indiana strain of vesicular stomatitis has been shown to be

transmitted by phlebotomine sandflies. Vesicular stomatitis usually occurs during the

warmer months or at the end of a rainy season. Most of the previous outbreaks have

occurred in summer months and ceased abruptly with the onset of frosts, except the

outbreaks of 1982–83, which continued during the winter. The seasonality of

outbreaks supports the theory of transmission via an insect vector. Another major

route of infection is believed to be through abraded oral mucosa or skin resulting from

grass seeds or awns. Nonbiting flies that feed on ruptured vesicles may also play a

role in mechanical spread of infection. The virus can remain viable in the environment

for several days, leading to infection. Fomites such as contaminated milking

equipment may also be involved in spreading infection.

Vesicular stomatitis does not generally cause severe morbidity or mortality. But it can

still have a great economic impact on the livestock industry due to import and export

restrictions placed by vesicular-stomatitis-free countries and various States within the

United States that establish movement restrictions to help prevent any exposure to

infected or affected animals. The restrictions vary between the individual States and

countries and are based on their specific interests and needs.

26
The index case of the 1997 vesicular stomatitis virus (VSV) outbreak, an equine in

Cornville, AZ, was confirmed by NVSL on June 5. This outbreak affected Arizona,

Colorado, New Mexico, and Utah. The 1997 epizootic is more geographically confined

than, but similar in location to, the 1985 epizootic. The 1995 outbreak included Texas

and Wyoming as well as the four States currently involved, whereas the 1985 outbreak

included only Arizona, Colorado, and New Mexico.

The Disease Reporting Unit was activated in Fort Collins, CO, on June 20, 1997.

Owing to the progression of the outbreak, the Disease Reporting Unit was relocated to

Englewood, CO, on July 14, 1997.

As of January 16, 1998, 703 premises had been investigated for vesicular stomatitis

with 380 case-positive premises identified: 2 in Arizona, 273 in Colorado, 67 in New

Mexico, and 38 in Utah. Table 1 is a summary of investigations outlining the number of

closed investigations with negative and positive results, the number of open

investigations pending and positive (premises still under quarantine), the total number

of investigations and the total positive results and the number of investigations where

the agent was isolated by State. This table is accurate up to January 16, 1998.

Current Situation

27
Table 1—VSV investigations in the United States as of January 16, 1998, by number

of premises

Total Agent

Closed Open investi- Total isoState Negative Positive Pending Positive gations positive lated

Alabama 3 0 0 0 3 0 0

Arizona 2 0 0 0 2 0 0

Arkansas 29 2 0 0 31 2 1

California 5 0 0 0 5 0 0

Colorado 99 273 0 0 372 273 44

Connecticut 2 0 0 0 2 0 0

Florida 1 0 0 0 1 0 0

Georgia 5 0 0 0 5 0 0

Idaho 7 0 0 0 7 0 0

Illinois 5 0 0 0 5 0 0

Indiana 2 0 0 0 2 0 0

Iowa 2 0 0 0 2 0 0

Kansas 8 0 0 0 8 0 0

Kentucky 3 0 0 0 3 0 0

Louisiana 7 0 0 0 7 0 0

Massachusetts 2 0 0 0 2 0 0

Michigan 2 0 0 0 2 0 0

Minnesota 1 0 0 0 1 0 0

Mississippi 1 0 0 0 1 0 0

Missouri 6 0 0 0 6 0 0

Montana 2 0 0 0 2 0 0

North Carolina 2 0 0 0 2 0 0

North Dakota 1 0 0 0 1 0 0

Nebraska 5 0 0 0 5 0 0

New Jersey 3 0 0 0 3 0 0

New Mexico 37 66 0 1 104 67 8

Nevada 1 0 0 0 1 0 0

New York 2 0 0 0 2 0 0

Ohio 2 0 0 0 2 0 0

Oklahoma 17 0 0 0 17 0 0

Oregon 4 0 0 0 4 0 0

Pennsylvania 2 0 0 0 2 0 0

South Carolina 1 0 0 0 1 0 0

South Dakota 1 0 0 0 1 0 0

Tennessee 3 0 0 0 3 0 0

Texas 15 0 0 0 15 0 0

Utah 15 38 0 0 53 38 5

Virginia 6 0 0 0 6 0 0

Washington 3 0 0 0 3 0 0

Wisconsin 3 0 0 0 3 0 0

Wyoming 6 0 0 0 6 0 0

Totals 323 379 0 1 703 380 58

28
0

10

20

18 25 01 08 15 22 29 06 13 20 27 03 10 17 24 31 07 14 21 28 05 12 19 26 02 09 16 23 30 07 14 21 28 04 11

No. of premises released

Vesicular Stomatitis Outbreak 1997

Number of Case-Positive Premises Released From Quarantine

Beginning Sunday 5/18/97

30

50

40

Chart 1 is an epidemiologic curve of all affected States beginning the week of May 18,

1997. It illustrates the number of positive premises per week through the week of

January 11, 1998. There was a dramatic reduction in positive cases beginning the

week of October 19 and decline to zero by the week of November 16.

Chart 2 demonstrates the number of case-positive premises released from quarantine

covering the timeframe from the beginning of the outbreak. The first premises was

released the week of July 6, and the majority of the premises were released between

November 9 and 30.

Chart 1

Chart 2

May Jun Jul Aug Sep Oct Nov Dec Jan

May Jun Jul Aug Sep Oct Nov Dec Jan

0

10

20

18 25 01 08 15 22 29 06 13 20 27 03 10 17 24 31 07 14 21 28 05 12 19 26 02 09 16 23 30 07 14 21 28 04 11

No. of positive premises

Vesicular Stomatitis Outbreak 1997

Epidemiological Curve (All Affected States)

Beginning Sunday 5/18/97

30

50

40

29
Quarantines and Restrictions—Officials of affected States have placed positive

premises under quarantine and instituted various animal movement restrictions.

Quarantines remained in place for 30 days after healing of the last clinical lesion on a

premises. The 10- to 20-mile restricted circle requirements used in the 1995 vesicular

stomatitis outbreak were found scientifically unwarranted and are no longer used.

Immediately following a positive diagnosis of VSV, an epidemiologic investigation was

conducted.

Most States have implemented temporary restrictions regarding importation of

livestock from States affected by vesicular stomatitis. The basic and most common

requirement is a statement on the health certificate similar to the following:

I have examined the animals listed on this certificate and have found

no clinical signs of vesicular stomatitis. To the best of my knowledge,

these animals have not been exposed to vesicular stomatitis, nor have

they been vaccinated with vesicular stomatitis vaccine within the

previous 30 days.

Other restrictions implemented by some States include requirements of permits for

entry, postentry quarantines, negative VSV tests, bans on livestock from affected

premises, and prohibition of VSV-vaccinated animals.

International Restrictions—Some international trade restrictions were implemented

in response to the diagnosis of vesicular stomatitis in the United States. These

restrictions vary from requiring health certificates with statements that the equidae

have not been in any State in which vesicular stomatitis has been diagnosed in the

previous 6 months to declarations that the equidae have not been in contact with

livestock that have been, during the last 30 days, in any State in which vesicular

stomatitis has been diagnosed in the previous 6 months.

Reporting Communications—The USDA–APHIS–VS Emergency Programs staff

provides a weekly report containing information on new cases, quarantines released,

cases closed, virus isolations, and other demographic data. Emergency Programs

also continues to report relevant data on VS to the Office International Des Epizooties

(OIE). Various informative materials have also been widely distributed, including

factsheets on vesicular stomatitis in dairy, beef, equine, and swine, vesicular stomatitis

vaccine and a vesicular stomatitis v. foot-and-mouth disease color card.

Since the outbreak onset, a weekly conference call has been held with APHIS, State,

and Federal officials and industry to discuss issues such as updates, State restrictions,

quarantines, laboratory results, and other related concerns. Industry groups that have

participated include the American Horse Council, Livestock Marketing Association,

National Animal Health Association, National Milk Producers Federation, National Pork

Producers Council, and the National Cattlemen’s Beef Association.

30
No new cases have been reported since the week of November 9, 1997. The Disease

Reporting Unit for vesicular stomatitis was closed on December 12, 1997. The last

premises under quarantine was released on January 20, 1998.

(Authors: Dr. Andrea M. Walker, Tuskegee University School of Veterinary Medicine—

May 1998, summer veterinary intern, Emergency Programs, VS, and Dr. Quita P.

Bowman, senior staff veterinarian, USDA, APHIS, VS, Emergency Programs,

Riverdale, MD, (301) 734–8073, e-mail: qbowman@usda.gov)

31
Risk Analysis of Potential Control Options for the 1997

Nonpathogenic Avian Influenza Outbreak in Pennsylvania

Pennsylvania is currently dealing with an outbreak of nonpathogenic (H7N2) avian

influenza (AI) in commercial egg-layer flocks. At this point, Pennsylvania has identified

more than a dozen infected flocks in the Lancaster County area. In July 1997, the VS

management and the Pennsylvania Department of Agriculture (PDA) requested an

analysis of potential control options.

The objective of this report is to provide decisionmakers with information regarding the

relative consequences and costs of various control options. This analysis may be

useful in framing the problem and for suggesting areas for further exploration. In the

short timeframe for this analysis, we (the APHIS personnel performing this analysis)

consulted with the poultry industry, poultry researchers, and USDA’s Economic

Research Service to obtain best available data. The results in this report apply to the

situation as of August 1997.

We used a state-transition disease model and economic welfare analysis to simulate

the results of four different control options. These options are (1) voluntary controls or

“do nothing,”(2) depopulation–repopulation, (3) quarantine and containment, and

(4) vaccination with quarantine. Also, we modeled several regionalization and exportrestriction scenarios. Brief descriptions of the models are presented below.

Disease-Spread Model—The disease-spread model is an application of statetransition analysis. State-transition analysis involves defining mutually exclusive

categories (“states”) into which animals, herds, flocks, and plants can be divided. We

used a basic three-state infection model: susceptible, infectious, recovered, or

immune. In this analysis the flock was the basic unit of concern. For purposes of the

simulation, flocks in the susceptible state were defined as normal, healthy, and

available to be infected with AI. Flocks in the infectious state have AI virus circulating

among birds and are capable of infecting other flocks. After a flock is infected, it will

be immune to reinfection or removed by depopulation, depending on the scenario

being modeled. If repopulated, these flocks will return to the susceptible state.

Pathways (“transitions”) between the states must also be defined. Pathways are

represented mathematically as the probability of moving from one state to another.

States and pathways serve as the basis for a series of simulations. These simulations

project the spread of a disease or pest over time in hypothetical epidemics and can be

used to compare the relative value of different scenarios.

Information generated from the disease-spread model is combined with physical

impact data such as death or production losses. The resulting output gives an

estimate of the biological consequences associated with the disease spread. The

economic model then uses the calculated biological consequences as input in

estimating the monetary impact on producers and consumers.

For this analysis, the area of risk was defined as all Pennsylvania counties affected by the final

Federal quarantine in 1984. According to the 1982 census, 468 layer premises (>3,200 birds)

were in this area. The model used this number, 468, as the starting number of susceptible

flocks. Each hypothetical flock consisted of 70,000 egg-laying chickens. Each egg layer was

assumed to produce 270 eggs per year (Pennsylvania Agriculture State Statistics 1996).

Background

Methods

32
Flocks move from susceptible to infected to immune and back to susceptible status

based on incidence rates, proportion of flocks becoming immune, proportion of

susceptible flocks vaccinated, and depopulation to repopulation rates. These

proportions were derived by estimating the average waiting time a flock or premises

would spend in the infectious or immune states under various control options. Time in

the infectious state is the time that a flock would be infected with the virus before it

was diagnosed and an action was taken to isolate the flock. Time in immune state is

the time a premises is either vacant or the birds on the premises are no longer

susceptible to infection through vaccination or natural infection. The original rates of

transition were set to approximate the outbreak of 1983–84.

Economic Model—The economic model is an application of economic welfare

analysis. Economic welfare analysis evaluates how market prices and quantities

adjust to changes in disease control measures. It also measures the effects of

disease spread and how consumers and producers are affected by the adjustments in

market prices and quantities. The effects on consumers and producers are measured

in terms of changes in the difference between what consumers are willing to pay and

what they actually pay for products (consumer surplus) plus returns to producers fixed

factors of production (producer surplus).

For the purpose of this analysis, impact on domestic production was measured in

terms of the number of eggs lost owing to disease or depopulation. The analysis

examines economic impacts under high and nonpathogenic scenarios and the different

control options. Output from the disease-spread model was used to help estimate the

number of eggs lost.

Export losses were measured in terms of a single aggregate poultry meat. Therefore,

the estimated consumer benefit may be somewhat overstated because of differences

in consumer preferences for products consumed domestically versus those intended

for export. Modeling the differences in consumer preferences is beyond the scope of

this analysis.

Estimates of regionalized export losses were based on the proportion of total broiler

production in each State. This proportion was applied to estimates of the U.S. impact

if poultry meat exports were eliminated entirely. If a regionalization strategy is implemented, multi-State poultry companies may be able to alter their distribution channels,

minimizing the adverse effects of export restrictions in a given region. The level to which

these adverse effects can be minimized is unknown at this time. If an acceptable

regionalization strategy cannot be established, the full impact of any export bans

would be felt.

Disease Control Scenarios—Several scenarios were developed to examine the

costs and benefits of alternative control options. The scenarios were evaluated using

computer simulation models described above. The scenarios were modeled over a

21-week period starting with one infected flock. The following is a description of each

scenario and assumptions.

33
1. Voluntary Control or “Do Nothing” Approach—After consulting with the PDA,

we considered the do-nothing approach an infeasible option and we did not model its

impacts. The main reason was that, if, in 1997, PDA had not imposed quarantines and

restricted poultry and poultry product movement, spread of infection could have been

substantial. Other reasons are discussed below.

• This scenario would assume that neither State nor Federal authorities will take any

steps to contain or control the situation. Because of the traffic in feed, feed

ingredients, service personnel, maintenance personnel, vaccination, placement, and

catch crews, infection among flocks could be expected to spread rapidly within the

State.

• Without local control, AI would likely be transported out of the State into surrounding

areas. Large poultry-producing States nearest Pennsylvania—specifically the

Delaware, Maryland, Virginia (Delmarva) region—would likely be the first areas

affected. We understand that some of the layer flocks in Maryland share common

feed company sources and vaccination crews with the currently affected area in

Pennsylvania. Feed and feed ingredient trucks serving flocks within the current

quarantine area also serve broiler flocks in the Delmarva region. The estimated

value of the broiler and support industries on the Delmarva is $1.5 billion.

Pennsylvania’s poultry industry is valued at $563.5 million. Virginia produces $773

million worth of poultry and poultry products yearly, and many of their producers

have direct ties and traffic with North Carolina.

• If Pennsylvania did not quarantine the affected area, neighboring States could

impose embargoes on poultry and poultry products moving from Pennsylvania.

Placement of embargoes might send an unintended message to our international

trading partners, potentially resulting in trade restrictions.

• Producers lack the authority to impose and enforce quarantine zones and movement

controls. When nonpathogenic AI was identified in commercial layer flocks in

Lancaster County, the industry requested that a quarantine be placed around an

area approximating a 5-mile radius from the first positive flock. In 1983–84 and

during the current situation, the PDA was able to enlist the Pennsylvania State

Police to enforce the quarantine zone. Establishment of this quarantine zone

provides reassurance to surrounding States and industry.

2. Depopulation Scenario—For this scenario, flocks were moved from the infectious

to the depopulated or removed state after 1 week. This assumption was based on

experience in the 1983–84 outbreak, when active surveillance was devised to sample

flocks on a weekly basis. In 1983, flock owners were instructed to place recently dead

birds in containers near the road. State or Federal personnel collected tracheal and

cloacal swabs from these birds. The swabs were tested for evidence of virus.

Collection personnel established a daily route allowing them to cover a large area

while sampling many flocks. The routine was repeated the following week, providing a

weekly test record for each flock in the quarantine zone (referred to as “dead bird

pickup”). Upon detection of disease in a flock, a quarantine was implemented

immediately to prevent movement of the virus off the premises. Thus, from the time a

flock entered the infectious state until quarantine was generally not more than 1 week.

34
In 1983–84, the offer of indemnity payment also encouraged owners to report illness

as early as possible. Producers were paid only for the live birds on the premises at

the time of field diagnosis and quarantine. With the highly pathogenic AI virus it would

not be uncommon for an owner to experience several thousand bird deaths in a single

day. The owner could expect no compensation for losses that occurred before the

quarantine and diagnosis. This setup encouraged early reporting because doing so

would provide maximum compensation from the authorities. If the flock owner did not

contact authorities, dead-bird pickup would likely identify the infected flock within a 7-

day window. We assumed that placement of the quarantine effectively removes the

flock from infected status and places it into the immune status, where it no longer

poses a risk for other susceptible flocks.

In 1983–84, an infected flock was quarantined at the time of field diagnosis. Soon

after that, birds were destroyed. After depopulation there was an obligatory downtime

during which the premises were cleaned and disinfected. Flock houses were sampled

and must have tested negative on two tests, a minimum of 30 days apart, before

restocking. The final laboratory report releasing the premises from quarantine took a

minimum of 14 days after the last sampling. At this time the premises were eligible for

restocking with new, susceptible egg-laying chickens.

Considering the preceding discussion, we assumed it would require a minimum of 45

days to complete the necessary testing to reach the point of repopulation. Therefore,

theoretical repopulation of flocks occurred 7 weeks after diagnosis. Also, because of

the imperfections of the laboratory tests and the necessary downtime for removing

manure, repairing the caging and electrical systems within a house, and so on, we

further assumed that only 10 percent of the potentially eligible houses would be

repopulated after 7 weeks. Beginning in the eighth week, 10 percent of the houses

found infected in Week 1 moved to the susceptible category. In the ninth week, 10

percent of the flocks diagnosed in weeks 1 and 2 were repopulated and moved into

the susceptible category.

3. Quarantine and Containment of Infected Flocks—We assumed that positive

commercial flocks are detected fairly quickly with the dead-bird pick up procedure

discussed above. The average time the birds were infected and remained infectious

was again assumed to be 1 week. In this scenario, some flocks would become

naturally infected and remain immune for life. The time in immune state was set at

52 weeks, meaning flocks do not reenter the susceptible state through the duration

of the simulated outbreak.

Flocks infected with highly pathogenic AI in 1983–84 lost their table-egg market

because the eggs were destroyed along with the birds during the depopulation.

Flocks infected in the current nonpathogenic AI outbreak may similarly experience

production (morbidity and mortality) losses. Under the plan currently in place in

Pennsylvania, eggs from infected flocks are diverted to an instate pasteurization plant.

Infected flocks were released from quarantine when the flock no longer exhibited

clinical signs and was negative on two tests (30 days apart) for AI. Flock owners are

then permitted to reenter the table-egg market; therefore, infected flocks lose their

table-egg market only for a short period. However, if this pasteurization market

35
becomes saturated, flock owners may be unable to recoup any salvage value for their

eggs, thus significantly increasing their cost.

4. Vaccination with Quarantine—Research has shown that clinical signs and

production losses can be mitigated by use of vaccine. However, research also shows

that vaccinated birds can become infected with field strain virus. Vaccinated birds or

flocks can be expected to shed less virus, to develop less severe clinical signs, and to

experience fewer production losses than unvaccinated birds or flocks. Some of the

literature notes a 1–2 log-factor decrease in the amount of virus shed by

experimentally challenged vaccinated birds.

The vaccination scenario was simulated by vaccinating 60 flocks (assuming

70,000 birds per flock) over the initial 4-week period. This is approximately the

number of flocks capable of being vaccinated once with the 4 million doses of vaccine

ordered by PDA.

The key parameter for vaccine use is its efficacy in reducing flock-to-flock transmission

of field virus. We are not aware of any research or data on this topic. In the absence

of this information, and for example purposes, we simulated four levels of vaccine

efficacy: 0 percent, 25 percent, 50 percent, and 75 percent. These levels were

implemented in the model by starting with varying numbers of flocks in the immune

state, assuming that 1 million birds per week will be vaccinated. For example, the

75 percent effective scenario starts with 45 (60 × 0.75) flocks in the immune state

during the first 4 weeks of the simulation.

In Pennsylvania, there is a current proposal to place unvaccinated sentinel chickens in

vaccinated flocks. These sentinel birds will be tested regularly to determine if field

strain virus has entered the flock. If there is evidence of infection, the flock will be

treated as an infected flock. When a vaccinated flock is found infected with field strain

virus, it will be managed as any other infected flock. Eggs will be diverted to

pasteurization if there is market available. Therefore, we modeled the economic

impacts with and without total loss of table and pasteurization egg markets.

Vaccinated flocks or naturally infected were assumed to be immune for the remaining

flock life. We assumed quarantine was effective in reducing flock spread and set the

model for only 1 week’s waiting time in the infectious state to match the other

scenarios.

Results—The simulated number of infected flocks and economic impact of

“quarantine only” compared with “quarantine with depopulation” are shown in table 1

for highly pathogenic and nonpathogenic AI. Figure 1 shows the course of the

simulated epidemics compared with the actual for 1983–84. The morbidity and

mortality (M&M) impacts for the nonpathogenic scenarios are based on data provided

by PDA for the current outbreak. For nonpathogenic AI, the economic losses are

shown with and without total loss of table and pasteurization egg markets. For the

quarantine and vaccination scenarios, any morbidity and mortality occurring during the

time of flock quarantine were included in the market loss calculation.

36
Table 1—Simulated number of AI-infected flocks and economic impact of quarantine

and depopulation control options in Pennsylvania layer flocks

(N = 468 at-risk flocks [>3,200 birds] in the 1983–84 quarantine zone)a

Quarantine only Depopulation and quarantine

Time in infectious state 1 week b,c 1 weekb,c

Time in immune state 52 weeks 7 weeks, 10% exit each week

after

Number of infected flocks 262 281

Losses for highly pathogenic AI ($ million)

Producer loss $17.2 plus $27.2 plus

export impactsd export impactsd

Consumer loss $55.6 plus $89.6 plus

export impactsd export impactsd

Net loss $72.8e plus $117.4e plus

export impactsd export impactsd

Losses for nonpathogenic AI ($ million) M&Mf / M&M plus Market Lossg

Producer loss $4.0 / $17.2 $27.2h

Consumer loss $13.1 / $55.6 $89.6

Net loss $17.1 / $72.8e $117.4e

_________________________________________________________________________

a

Under the depopulation option, incidence rate and number of flocks

infected were based on the 1983–84 Pennsylvania outbreak.

b

Assumes early detection procedures.

c

Assumes 100-percent effectiveness of flock quarantine in reducing

virus spread.

dExpected export losses result from conversion to highly pathogenic AI.

See impacts in table 3 for various regionalization scenarios.

e

Government costs were not included because they are similar for both

scenarios with the exception of indemnity, which is a transfer cost from

Government to industry. Detailed data are available from the authors.

f

M&M = morbidity and mortality, which are based on mortality and egg

losses for the 1997 virus reported by the Pennsylvania Department of Agriculture.

g

Market loss due to infection with field virus and loss of table and pasteurization

egg market if pasteurization market is saturated. Under current conditions, it is

estimated that approximately $3.4 million of the market losses shown could be

salvaged or regained in the pasteurization market.

h

Figures in this column do not include export-related impacts because

nonpathogenic AI does not usually influence poultry exports.

37
The simulated number of infected flocks and economic impact of vaccine for

hypothetical efficacy is shown in table 2. Economic losses are reported with and

without total loss of all egg markets. Table 3 shows the projected annual export losses

Table 2—Simulated number of infected flocks and economic impact (excluding export

losses) of vaccine use with different assumed efficacies for reducing flock-to-flock

spreada

Vaccine efficacyb Zero 25% 50% 75%

Infected flocks 262 236 210 184

Losses ($ millions) M&Mc / M&M including market lossd

Producer losse $1.4/$17.2 $1.3/$15.7 $1.3/$13.5 $1.3/$12.0

Consumer loss $1.2/$55.6 $1.1/$50.8 $1.0/$43.6 $0.8/$38.7

Net loss $2.6/$72.8 $2.4/$66.5 $2.3/$57.0 $2.1/$50.7

a

Export losses could result from use of vaccine and must be added

to all scenarios. See impacts in table 3 for various regionalization scenarios.

b

Assumes 60 flocks (70,000 birds/flock) started in immune state during first

4 weeks of outbreak. Efficacy refers to reducing flock-to-flock spread, not clinical signs.

c

M&M = morbidity and mortality, which are based on mortality and egg losses

for the 1997 virus reported by the Pennsylvania Department of Agriculture.

d

Market loss due to infection with field virus and loss of table and pasteurization

egg market if pasteurization market becomes saturated. Under current condtions,

it is estimated that approximately $3.4 million of the market losses shown could be

salvaged or regained in the pasteurization market.

e

Includes production losses due to handling of birds and costs of vaccine

administration (4 million birds vaccinated twice at $0.12 each = $1 million)

plus about 2 days of low-level production losses under the nonpathogenic scenario.

1 3 5 7 9 11 13 15 17 19 21 23

2 4 6 8 10 12 14 16 18 20 22 24

Cases

40

30

20

10

0

Number of weeks

Actual

Simulated, with depopulation

Simulated, with quarantine

Figure 1—Avian influenza. Simulated epidemic curves for quarantine and

depopulation and 1983–84 outbreak.

38
if Pennsylvania vaccinates for AI or the virus converts to highly pathogenic form. Four

different potential regionalization scenarios are shown. For the purpose of this

evaluation, the estimated impacts of these scenarios were based on the total impact to

the United States due to a complete loss of poultry meat exports weighted by the

proportion of broiler production occurring in each region. Note that these losses are

on an annual basis, and export restrictions are expected to last more than 1 year.

Table 3—Projected annuala export losses if Pennsylvania (PA) uses AI vaccination or

the virus converts to Highly Pathogenic under four potential regionalization scenarios

(in millions of dollars)

PA + PA + Delmarva

PA only Delmarva + S.E. U.S.A. Rest of U.S.A.

Producer lossb $21.5 $166.5 $863.5 $1,300.0

Consumer gainc $19.4 $154.0 $799.0 $1,200.0

Net loss $ 1.6 $ 12.4 $ 64.4 $ 96.7

a

Annual export losses shown above should be multiplied by

the number of years trade sanctions would remain in place

(probably between 2 and 3 years).

b

These losses were based on proportion of all poultry meat

production that comes from respective regions. It is likely that,

should Pennsylvania be embargoed, production from other States

can be shifted to fill that market, decreasing the loss.

c

Restrictions on exports of poultry in a highly pathogenic AI

situation yield consumer gains because the supply of domestic

poultry in the marketplace goes up drastically, causing retail

prices for chicken to fall.

This analysis focused on the disease production impacts in commercial layer

operation, as well as potential impacts in the export markets for U.S. poultry meat. We

looked for benefit of vaccine use in three areas: (1) reducing producer losses,

(2) decreasing the likelihood of conversion to highly pathogenic virus, and (3) decreasing the number of number of infected flocks. Compared with the high cost of potential

export market loss, the benefits appear minimal.

The efficacy of vaccine at reducing flock-to-flock spread is the key variable affecting

the outcome of this analysis. No data were available on this topic. However, there is

agreement in the literature and expert opinion that vaccination will not prevent the

circulation of field virus among flocks. Vaccination will reduce the amount of virus

shed from field-strain-infected birds. The impact of this reduction on the probability of

flock-to-flock spread is expected to be slight because of the large amount of virus

excreted by 70,000 vaccinated birds. We had planned to model the likelihood of the

virus converting from nonpathogenic to highly pathogenic. Instead, we estimated

Discussion

39
economic impacts for high and nonpathogenic scenarios without assigning

probabilities. We could find no data applicable to the probability of conversion for

individual birds or flocks. If vaccination decreases the number of birds infected, it may

decrease the number of opportunities for random molecular changes in the virus. The

mechanism that triggers conversion is currently unknown. Also, experts generally feel

that the H7N2 virus in Pennsylvania is stable and unlikely to convert to a highly

pathogenic strain. This opinion suggests that vaccine use would have little impact on

the emergence of highly pathogenic AI.

The time a flock spends in the infectious state is a critical variable because it affects

the number of flocks that can spread disease at any one time. According to field

experience and expert opinion, flocks stay infectious for an average of 4 weeks.

However, the time flocks spend in the infectious state was set to 1 week for all

scenarios. This assumption allows us to examine the impact of depopulation and

vaccine efficacy without an added variable.

(Authors: Dr. H. Scott Hurd, analytical epidemiologist, USDA, APHIS, VS, Centers for

Epidemiology and Animal Health (CEAH), Fort Collins, CO, (970) 490–7869; Ken

Forsythe, agricultural economist, USDA, APHIS, VS, CEAH, Fort Collins, CO, (970)

490–7955; Dr. Susan C. Trock, regional epidemiologist, USDA, APHIS, VS, Northern

Region, Albany, NY, (518) 453–0103)

40
Foot and Mouth Disease in Taiwan—1997 Overview

On March 14, 1997, a hog farmer near the port city of Hsinchu in the Prefecture of

Hsinchu notified his local livestock disease control center that he had a sow in a

farrowing crate that had vesicular lesions on the feet and snout. Claws had also

sloughed. His was a midsized farm with about 2,000 hogs, and that sow was in the

middle of the farrowing house. The farm was operated by the farmer and his wife, and

no animals had been introduced onto the farm in the last month.

No people other than the farmer and his wife had entered the farrowing house in the

past several weeks. The management was considered to be good but sparrows did fly

in and out of the animal buildings. Morbidity in the subsequently infected herd was

very high, and the mortality in young stock neared 100 percent.

The incubation period was short and appeared to be approximately 1 to 4 days. Only

swine were affected. The disease was characterized by vesicles on the feet, snout,

teats and tongue. Vesicles were commonly observed on the snout, and it was not

uncommon to examine several hundred pigs from several pens and observe fluid-filled

vesicles on their snouts. The vesicular fluid was clear to slightly cloudy. Vesicles were

commonly observed on the teats.

Many of the vesicles on the feet had ruptured, leaving raw, hemorrhagic, ulcerated

lesions around the coronary band, between the claws, and on the soles. Sloughed

claws, were very common, as were abortions. Adults very quickly became emaciated

because their feet were so sore they would not move to eat or drink.

Morbidity often reached 100 percent in adults and piglets. Neonatal mortality was

commonly associated with acute myocarditis and malnutrition and related to other

undiagnosed unthrifty conditions in neonates.

Specimens were collected from the index farm on March 14, 1997, and sent to the

Taiwan Provincial Research Institute for Animal Health in Tanshui, Taiwan. Laboratory

workup was completed over the weekend, and all other swine diseases were

excluded. The foot-and-mouth disease (FMD) diagnostic kit was opened, and on

March 19 a diagnosis of FMD was tentatively confirmed as types O1 and Asia 1.

On March 20, 1997, OIE was notified of the outbreak. Samples from Taiwan were

sent to the OIE/World Reference Laboratory for FMD, Institute for Animal Health,

Pirbright, UK, for further evaluation. Employing indirect enzyme-linked immunosorbent

assay (ELISA) and cell-culture techniques, the Laboratory identified FMD type O.

To determine if the Taiwan strain was naturally adapted to swine, various experiments

were initiated at the Laboratory. Experimental pigs inoculated with the Taiwan FMD

isolate became ill with generalized FMD. Four normal pigs and four normal cattle

were placed in contact with the FMD pigs for 2 hours. The contact-exposed pigs

developed generalized FMD. The contact-exposed cattle remained normal. Further

animal studies at the Laboratory indicated that the Taiwan FMD isolates are naturally

adapted to pigs and are considered porcinophilic strains of FMD.

Index Case

Clinical Disease

Laboratory

41
FMD disease was previously diagnosed in Taiwan in 1913–14 and again in 1924–29.

The exact mode of entry remains unknown for the 1997 outbreak. This information

may become available after exhaustive epidemiologic studies. The disease may have

entered Taiwan via (1) smuggling of live pigs, (2) smuggling of pig meat products,

(3) legal importation of live pigs, (4) legal importing of pig meat products, (5) smuggling

of animal biologics, (6) legal importing of animal biologics, (7) legal and illegal moving

of people, or (8) intentionally introducing the disease agent.

Although the laboratory diagnosis was being made on the index farm in Hsinchu

Prefecture, clinical cases of an FMD-like disease were being found on hog farms in

Tainan and Pingtung Prefectures, about 200–300 km south of the index farm. This fact

suggests that FMD was present in Taiwan long before the official date of March 20,

1997. Currently, however, there is no scientific information available to support that

hypothesis.

The index farm was also located near a port city that was well known for the smuggling

of pigs, especially the black-skinned pigs, which are highly valued by many local

markets. The index farm was also situated near legal and illegal slaughterhouses.

On March 17, FMD was clinically diagnosed on a second hog farm in the Hsinchu

Prefecture. On March 18, FMD was also diagnosed on a hog farm in the Prefecture of

Taoyuan, bringing the number of affected farms to three. Unfounded comments have

suggested that when FMD was diagnosed on the index farm, the disease was also

present on 25–30 other hog farms.

During March 1997 and the preceding several months, Taiwan had initiated a control

and eradication program for hog cholera that included the collection of at least 100,000

blood samples from 17 livestock disease control centers around the island. In a recent

preliminary study to determine any prior serologic evidence of FMD, approximately

550 samples were tested in April and May 1997, and all were negative for FMD.

Japan and South Korea set February 21, 1997, as the official date of FMD infection in

Taiwan for import reasons. Comments and news articles suggest that FMD was

present on the island as early as October 1996 or in the late summer of 1996. There

is currently no scientific evidence to support this conclusion.

SVD is well recognized in Taiwan. It is characterized by vesicular lesions on the snout,

teats, and feet, including the interdigital space. SVD is clinically indistinguishable from

other vesicular diseases, especially FMD.

Reports from Taiwan suggest that SVD can easily be easily recognized based on

clinical lesions and that laboratories were not routinely employed to diagnose SVD. It

is very possible, on the basis of this reliable information, that early cases of FMD may

have been misdiagnosed as SVD. Serologic evidence of SVD was detected at the

World Reference Laboratory.

Epidemiology

Swine Vesicular Disease

(SVD)

42
FMD moved very rapidly throughout Taiwan, as the data indicate. For example, on

March 20, 70 farms were officially infected. Within 8 days, 1,175 farms were infected.

The disease appeared to infect an additional 200–300 farms per day. At the moment,

no explanation can be given to account for the lightninglike speed at which this

disease moved throughout the island.

FMD infection in Taiwan was confined to swine despite observations of cattle and other

small ruminants in very close proximity to infected hogs. No infection was ever

reported in other species, including zoo animals.

Therefore, contributing factors to the introduction and very rapid spread of FMD in

Taiwan have been associated with (1) very high swine density (Taiwan has been

reported to have the world’s highest density of hog farms), (2) garbage feeding,

(3) hog farms located in close proximity to slaughterhouses, (4) the absence of a

vaccination program (although the disease has been absent for almost 70 years),

(5) frequent social farm visits, and (6) lack of complete laboratory confirmation of

vesicular diseases.

Figures available as of June 17, 1997, indicated that 6,144 farms were affected,

involving 1,011,421 FMD-infected pigs, 184,231 dead pigs, and 3,850,536 pigs killed.

Depopulation and Disposal—Immediate steps to be taken on an FMD-infected farm

include the following:

• Stop shipping pigs immediately.

• Kill all infected pigs.

• Spread lime around infected areas and hallways.

• Spread alkali flakes in sewage around pens and sterilize pigpens with a strong acid

or alkali solution.

• Strictly control infected areas.

• Consider adding organic acid to the hog drinking water.

• Vaccinate as soon as possible.

The proper and rapid depopulation and disposal of millions of hogs can present grave

economic, manpower, animal care, and environmental challenges. The speed and

efficiency of depopulation are directly related to the speed and efficiency of disposal.

Very high water tables and other environmental concerns in Taiwan complicated these

procedures.

Electrocution was the means of choice for depopulation. The disposal methods were

dependent upon local and regional conditions, including EPA regulations. Once EPA

officials formulated their burial, incineration, and rendering procedures, depopulation

and disposal continued at a smooth pace.

Because of the immensity of the task, there was an initial lack of supplies, equipment,

and manpower that caused a significant delay in the prompt and timely depopulation

and disposal of infected pigs. The military made a substantial contribution toward

manpower needs in the area of depopulation and disposal. The military recorded

43
50,732 military person-days and the use of 3,277 military vehicles. Many stressrelated problems were evidenced in the military recruits working on this detail. Some

military conscripts employed in depopulation activities reported problems associated

with psychological distress and anxiety requiring medical leave. This is most

understandable, if one considers the magnitude of the depopulation and disposal

effort. When military recruits completed their tour of duty, they returned to the barracks

for a 10-day quarantine period. A peak depopulation capacity of 200,000 hogs per day

was achieved.

The delay in depopulation posed a serious problem because the longer an infected

hog farm remained intact, the greater the opportunity for spread of the FMD virus

through the air, fomites, and animal and people traffic became. This must also be

evaluated in view of the very high density of hog farms in Taiwan, where one can stand

on a main road or backroad in Pingtung Prefecture (a very high-density Prefecture)

and identify numerous pig farms (10) located about 200–300 m apart along a severalkm stretch of road.

Indemnity—Much of the information provided to APHIS requires translation which was

not available at this writing. Farmers could apply to their livestock disease control

center or local agriculture office for indemnity payment for FMD-infected hogs. The

indemnity price was based on production costs set at New Taiwan Dollars

(NTD)$2,400 for a 100-kg pig and NTD$350 for pigs less than 25 kg. For registered

breeding stock, the indemnity price was set at NTD$4,800. Initially, this indemnity

price was very high and significantly more than that for a healthy pig, which caused

some farmers to collect and introduce FMD-infected pigs to their uninfected farms.

This would enable them to collect the much higher indemnity price for the FMDinfected pigs. This disparity was quickly rectified.

Disposal plans called for the burial in large municipal landfills of approximately

80 percent of the hogs. Fifteen percent were rendered, and percent were burned.

Burning consisted of open burn and incineration. A capacity of approximately

200,000 pig carcasses per day was achieved. In water resource protection areas,

only incineration or open burning was used.

On April 11, 11 industrial portable kerosene incinerators arrived in Taiwan. The

capacity of the incinerators was 2.5 or 40 metric tons (t) per day. A day represented

24 hours of operation. One site visited in Pingtung Prefecture contained several

2.5- and 40-t incinerators surrounded by telephone poles with floodlights for aroundthe-clock operation. It would require several 24-hour days of operation to complete

disposal on most of the farms visited.

Vaccination—Animal disease emergency planning procedures in place in Taiwan for

many years included the maintenance of an FMD vaccine bank. The emergency

planning procedures also involved the completion of several FMD test exercises over

the past several years.

At the outset of the epidemic, 40,000 doses of trivalent FMD vaccine (O1, A24, Asia 1)

were in the repository. This vaccine was immediately dispersed to the east side of the

44
island and elsewhere to vaccinate all susceptible zoo animals and valuable hogbreeding stock.

Because of a preliminary FMD diagnosis of both O and Asia, an order for a bivalent

vaccine was placed. The bivalent vaccine (O1 and Asia 1) of approximately 526,000

doses arrived on March 26 and 27. This vaccine was immediately disbursed free of

charge for islandwide use.

In mid-March, officials purchased 3 million doses of a bivalent vaccine, O and Asia, to

be used on the eastern side of the island in valuable zoo animals and hog-breeding

farms. A significant portion of the vaccine was given free to small farmers. To prevent

the spread of the disease by vaccination crews, trained, experienced farmers under

veterinary supervision were permitted to administer the vaccine. An order for

13 million doses of a monovalent FMD vaccine O was received on May 3, 1997, and

distributed free of charge to farmers.

Initially, all FMD-infected hogs were destroyed. When enough vaccine became

available, all pigs (including those with the disease) were vaccinated. About 17–21

million doses of vaccine were administered. Additional material on vaccination is in

the process of translation.

Cleaning and Disinfection—The cleaning and disinfection process is one of the most

critical and essential aspects of recovery after an FMD epidemic. Various protocols for

these procedures were supplied by the local livestock disease control Centers, other

government agencies, livestock journals, and private industry. These procedures

included the standard textbook sterilization disinfectants used against the FMD virus.

Onfarm procedures included scrubbing and spraying with disinfectant twice a week.

Large tonnages of New Formula Farm Fluid, Farm Fluid S, and Virkon S were airlifted

to Taiwan as needed. The Japanese Pig Producers also donated disinfectant.

Abundant material is available on this subject matter but requires translation.

Restocking—A five-step procedure was initiated to restock hog farms infected with

FMD. Step I, ii stipulates that farms applying for reintroduction must have no reported

cases of FMD in a month within 6 km of their surroundings. Farms with only partial

slaughter are required to have two doses of FMD vaccinations and no reported cases

of FMD in 2 weeks.

Other pertinent points include part III, number 3, which states that applicants must hire

inhouse or contract a veterinarian to be in charge of health management and disease

reporting for the farm. Part III, number 4 states that reintroduced pigs must come from

FMD-free farms, must weigh more than 25 kg, and must be effectively vaccinated

against FMD and hog cholera. Part III, Environmental Protection Regulations, is quite

specific and pertains mostly to wastewater pollution control and waste disposal.

Part V addresses violations and includes fines up to NTD$150,000 for reintroducing

pigs without permission. In addition, no compensation will be given if farms are

reinfected with FMD or any other serious disease. Increased surveillance of actions

likely to pollute rivers and the environment was included.

45
The Agriculture Sector in

Taiwan Taiwan’s major agricultural commodities are hogs, rice, poultry, shrimp, eels, squid,

tuna, sugar, and bananas. In 1996, agricultural exports were worth approximately

U.S.$5.48 billion and represented nearly 5 percent of Taiwan’s total exports. Exports

of live animals and poultry, frozen meat, and pork chops comprised 29 percent of total

agricultural exports (U.S.$1.61 billion). Japan has been Taiwan’s principal market for

agricultural exports (57 percent of total agricultural exports), followed by Hong Kong

(20 percent) and the United States (7 percent).

The livestock sector in Taiwan has seen sharp growth in production in the last several

decades. Meat output increased tenfold from 1952 to the early 1990’s. By the mid1990’s, livestock accounted for over a third of the total value of Taiwan’s agricultural

production.

The two leading livestock sectors in Taiwan are the hog and poultry sectors. Taiwan is

self-sufficient in poultry production and exceeds domestic needs in hog production.

Taiwan has small cattle and dairy industries (over 90 percent of the country’s beef

needs are met through imports).

Before the FMD outbreak, hog production was the leading agricultural product in

Taiwan, and was worth U.S.$2.6 million in 1994, which was well above the value of the

rice (U.S.$1.5 million) and poultry (U.S.$1.1 million) industries. More than 14 million

swine were slaughtered in both 1995 and 1996, yielding more than 1 million t of

product each year.

Pork, the preferred meat in Taiwan, accounts for about 60 percent of total meat

consumption. Per-capita consumption averaged 37 kg in 1991. Because Taiwanese

consumers prefer fresh pork, hogs for domestic consumption are typically slaughtered

at night and sold in wet markets the following day. Before to the outbreak, about

20 processing plants provided meat for the domestic market. Hogs move from the

farm to slaughter via auction markets. In the auction markets, hogs are sold

individually. The auctions run on a daily basis with a relatively small daily volume of

sales. A small but growing percentage of hogs (22 percent in 1991) are raised under

contract and go directly from the farm to the packing plant.

Exports have been important to the Taiwanese swine industry. Prior to the outbreak,

nearly 40 percent of the hogs destined in Taiwan were raised for the export market,

and exports were worth U.S.$1.5 billion. (The USDA’S National Agricultural Statistics

Service reports that only 3 percent of total U.S. pork production is exported.) Meat

products constitute the majority of Taiwanese exports and totaled nearly 270,000 t in

1995 and 1996. Most of these exports were shipped to Japan, where Taiwan captured

44 percent of the market in 1996.

Exports of fresh, chilled pork had been increasing, reaching nearly 40 percent of total

exports by the mid-1990’s. Before the FMD outbreak there were approximately

20 processing plants in Taiwan of export quality (i.e., they met the standards and

requirements set by Japan). In addition to meat products, several thousand live swine

were exported annually before the outbreak.

Taiwan’s Swine Industry

Prior to the Outbreak

46
Taiwan was among the top 15 producers of pork and pork products worldwide in 1996.

Approximately 270,000 t of pork products were exported from Taiwan in 1995 and

1996, leading to Taiwan’s status as the third largest exporter of pork products

worldwide. Most of these exports were sent to Japan.

Hog production in Taiwan developed during the last 3 decades from a sideline farm

activity to a major enterprise. By 1995, the number of hog farms with more than

1,000 head jumped to 9 percent of all hog farms, whereas those farms with fewer

than 200 head dropped to 65 percent of the total.

Hog density in Taiwan is extremely high. Eighty-three percent of the hog population is

concentrated in the southwestern portion of the country. Swine density is approximately 6,500 hogs/mi2

 there. By comparison, in Sampson County, NC (one of the top

swine-producing counties in the United States), swine density is approximately

1,800 hogs/mi2.

Because of the high concentration of hogs in Taiwan, hog waste and environmental

pollution have been a problem. Water quality regulations have been adopted in recent

years, and efforts have been made to implement onfarm manure treatment. By 1993,

86 percent of farms had implemented manure treatment regimens. A controversial

plan prepared in 1991 called for the end of pork exports to reduce the size of the hog

herd to better match environmental carrying capacity. This plan was not enacted.

To support the development of the livestock sector, the Taiwanese Government operates an integrated disease-prevention system, including an inspection system for

imported meat. In addition, the government oversees the production and use of veterinary medication. Routine monitoring of the livestock population is also carried out.

In the 1990 “Council of Agriculture Yearbook,” Taiwan considered itself free of FMD,

rinderpest, and African swine fever. Prior to the 1997 FMD outbreak, hog cholera and

pseudorabies were the major diseases of concern to hog producers, and Taiwan had

been working toward the eradication of hog cholera.

The most significant economic impacts of the FMD outbreak will be those related to

the loss of export markets, particularly the fresh pork market in Japan, possibly for as

many as 4 to 5 years. Because nearly 40 percent of the hog population was raised to

meet export demand, significant structural impacts will take place to adjust production

to a new market carrying capacity. It is too early to tell what these adjustments will be.

Indications are, however, that prices will be more unstable and that farms and

processors will leave the market.

Within 1 week of the outbreak, hog prices had dropped 60 percent, falling from

NTD$4,500 per 100 kg (about U.S.$167) to NTD$1,700 per 100 kg (about U.S.$63).

These price decreases resulted from the immediate loss of export markets and an

initial sharp drop in domestic consumption. With hog production costs estimated at

NTD$4,100 per 100 kg (about U.S.$152), even farms without FMD infection were

affected.

Economic Impacts of the

Outbreak

47
Hog prices rebounded, regaining preoutbreak levels by mid-May. To encourage pig

prices to recover, the Taiwanese Government provided low-interest loans and storage

subsidies. A survey taken in Taiwan in July showed higher-than-expected hog

numbers, which resulted in another drop in hog prices in late August and early

September. At that time, prices fell again to NTD$3,000 per 100 kg (approximately

U.S.$111).

The Taiwanese Government conducted a survey in July showing a total of 21,891

swine farms nationwide, which represented a decrease of 14 percent from the 25,357

reported in November 1996. In addition, the survey indicated a total of 8,533,476 pigs

on these farms, which was down 20 percent from November 1996 (10,698,366 pigs).

A standing herd of 7 million pigs is seen as sufficient to meet the needs of the

domestic market. Numbers in excess of 7 million are likely to put downward pressure

on prices. Production estimates for 1997 suggest an annual hog slaughter of 11.7

million head, which is a decline of 20 percent from the 1996 level of 14.6 million head.

Taiwan’s processing capacity has fallen. After the outbreak, seven of the meat

packers exporting to Japan closed or downsized, including a plant run by Cargill.

Early estimates released in March suggested that as many as 50,000 persons might

become unemployed as a result of the outbreak. These same early estimates

projected the impact on swine-related industries at U.S.$6.9 billion.

The Taiwanese Government’s goal is to have no additional FMD outbreaks from July

1997 through June 1998. Taiwan then hopes to reach FMD-free-with-immunization

status by June 2000. From July 2000 to June 2001, Taiwan intends to eradicate FMD

and reach FMD-free-without-immunization status.

To meet these goals, regulations controlling repopulation efforts were issued and

farmers were allowed to begin restocking in July. Under these regulations, farmers will

need to apply for a permit to be allowed to restock. Conditions for the permit include

ensuring that the farmer has disinfected his or her premises, that the farm has a

contract with a veterinarian, and that the farm is equipped with wastewater and wastedisposal devices. Owing to new regulations regarding watershed areas, permits may

not be issued for farms located in fragile watershed districts. Indications are that

farmers began restocking herds prior to July in response to good hog prices.

Taiwan’s export market will be affected for many years. Japanese import requirements

prohibit unprocessed pork being imported from an area infected with FMD unless the

disease has been eradicated and vaccines have not been used for at least 2 years.

These requirements may exclude Taiwan from the Japanese fresh pork market for at

least 5 years.

Taiwanese officials are negotiating with Japan regarding the possibility of Japan

accepting processed pork such as hams, sausages, and similar products. It was

unlikely that such exports would occur in 1997. The United States, Denmark, and

Canada have replaced Taiwan in the Japanese market. Exports of pork from the

United States to Japan are projected to total 185,000 t in 1997 compared with

142,000 t in 1996. About 93,000 t of U.S. exports are projected to be chilled pork,

which is increase from 77,000 t in 1996.

48
Exports from Denmark are projected at 135,000 t in 1997, which is up from 119,000 t

in 1996, whereas exports from Canada are projected to increase from 39,000 t in 1996

to 55,000 t in 1997. The U.S. share of the Japanese market is expected to grow from

22 to 40 percent by 1998.

Taiwan Ag Info Center, Web site.

USDA, Foreign Agricultural Service Attaché Reports, various.

Taiwan Agricultural Yearbook 1996. Department of Agriculture and Forestry, Taiwan

Provincial Government.

Wu Huang, Sophia. October 1994. Environmental challenges and prospects for

Taiwan’s hog industry in the 1990’s. International Agriculture and Trade Reports, Asia

and Pacific Rim. Washington, DC: U.S. Department of Agriculture, Economic

Research Service.

North Carolina Department of Agriculture, Web site.

Tsai, Reyfong; Williams, Gary W. Taiwan’s livestock and feedgrain industries, TAMRC.

International Market Research Report No. IM-2-93. October 1993.

Morgan, J. Brad. July 1995. Packing/processing relationships. (Report commissioned

by the National Pork Producers Council).

Hayenga, Marv, agricultural economist, Iowa State University. Personal

communication.

Hurt, Chris; Plain, Ron. Comparative live hog production and its economic

consequences. Purdue University.

Amount allocated to fight FMD deemed not enough. May 1997. Taiwan Central News

Agency.

Impact of FMD on economy assessed. March 1997. Taiwan Central News Agency.

Halley, Millie, agricultural economist, United States Department of Agriculture

Economic Research Service. Personal communication.

Brennan, Terry. September 19, 1997. U.S. producers in hog heaven: Japanese open

pork market. Journal of Commerce.

Sources of Information

49
USDA, National Agricultural Statistics Service, Agricultural Statistics, 1996.

Dunn, C. S.; Donaldson, A. I. August 16, 1997. Natural adaptation to pigs of a

Taiwanese isolate of FMD virus. Veterinary Record 141: 174–175.

Office International des Epizooties, 1997, 10(12)53; 10(13)53; 10(14057).

King, J. M; Hsu, F. S; Hong, C. B; Lee, R.C.T. 1976. An atlas of general pathology.

Taipei, Taiwan: Council for Agriculture, Planning and Development: 16–18.

Pig Disease Information Center, University of Cambridge. March 22, 29, and 30, and

August 6, 1997. Asia and Pacific disease reports (OIE).

Antec International Web site.

Acknowledgments

We would like to acknowledge the assistance of Dr. Wesley Garnett, Jr., and Ralph

Iwamoto, APHIS, USDA, International Services. The assistance of Debra Henke of the

American Institute in Taiwan is greatly appreciated.

(Authors: Dr. Terrance M. Wilson, senior staff veterinarian, USDA, APHIS, VS,

Emergency Programs, Riverdale, MD, (301) 734–8073 voice, (301) 734–7817 fax,

e-mail: twilson@aphis.usda.gov; and Ms. Carol Tuszynski, agricultural economist,

USDA, APHIS, VS, Centers for Epidemiology and Animal Health, Fort Collins, CO,

(970) 490–7893 voice, (970) 490–7899 fax, e-mail: ctuszynski@aphis.usda.gov)

50
Chronology of Hog Cholera Outbreak

in the Dominican Republic

Hog cholera (HC), or classical swine fever (CSF), was first reported on the island of

Hispaniola in Haiti in the fall of 1996. The disease spread rapidly with high mortality. A

vaccination program was developed using both the Minnesota and Chinese strains of

the virus. High mortality was associated with the Minnesota strain because no

neutralizing sera were used with the vaccine. Vaccine with the Chinese strain was

donated by a private French group. Approximately 50 percent of the swine population

may have been vaccinated in Haiti. The first positive serology on the other end of

Hispaniola, in the Dominican Republic, was reported in March 1997. Viral antigen was

detected in June 1997. These early detections were found near the border with Haiti.

In November 1996, the Dominican Republic received official notification that several

HC outbreaks had occurred in Haiti. This prompted the Dominican Ministry of

Agriculture to initiate an HC epidemiologic surveillance program.

In March 1997, 8 of 29 samples submitted to the Central Veterinary Laboratory were

seropositive for HC. The seropositive samples were from Hondo Valle, Elías Piña

Province, and originated from two separate locations. The positive samples were sent

to NVSL for (BVD) differentiation.

On May 7, 1997, one of nine samples from the Elías Piña Province was tissue positive

for HC. This sample came from a dying animal, which was one of the eight positive

pigs found in March.

In June 1997, 6 of 115 samples submitted were seropositive. Five of the six cases

came from the northwestern part of the country. Tissues were collected from two of

these cases and were positive on ABC–AP for HC antigens. Ministry records indicate

that at least three of these five animals were found to be seropositive on June 12, 1996,

in the community of Mariano Cestero, Municipio de Restauración, Province of Dajabón.

The sixth seropositive animal came from Las Matas de Farfan, San Juan Province.

In July 1997, 19 of 69 cases were seropositive. Two of the 19 samples came from a

kill plant in the National District Province. Traceback on these two cases was not

conclusive. The other 17 seropositive cases were from the Province of Elías Piña (34

submitted). In mid-July 1997, the entire pig population of the Elías Piña Province was

depopulated. A 20-km hog-free zone was thus formed along a portion of the Haitian

border. The depopulation operation was carried out the last 2 weeks of July, but

stragglers continued to be sacrificed through mid-October. A total of 6,412 pigs were

sacrificed from the Elías Piña Province.

In August 1997, 13 of 761 samples were seropositive. Four seropositive samples

came from San Cristobal, San Cristobal Province. Five seropositive samples came

from Neiba, Bahoruco Province (86 submitted), and four seropositive samples came

from various areas in the Province of Valverde (257 submitted).

Introduction

Chronology

51
In September 1997, 18 samples of 1,031 submitted to the central laboratory were

seropositive. Eight of 11 tissue samples submitted were positive for viral antigens. In

the National District Province, seven samples were seropositive (77 submitted), and

two tissue samples were positive (4 submitted). In the Northwest Region: one

seropositive case was submitted from Mato Nuevo, Mao, Province of Valverde (70

submitted), and one seropositive sample from the Dajabón area (32 submitted). The

southern region of the country had nine seropositive samples. Six seropositive

samples were from Neiba, Province of Bahoruco (95 submitted). One seropositive

sample was submitted from Polo, Barahona Province (18 submitted). Finally, two

seropositive samples were submitted from Duvergé, Independencia province (20

submitted). From August 14 to September 23, a total of 77 were sacrificed, burned,

and buried in Neiba to try and stop the spread of the disease.

In October 1997 (exclusive of October 31 data), 47 samples of 1,131 samples

submitted to the central laboratory were seropositive. Fourteen of 42 tissue samples

submitted were positive (the total number of tissues submitted is not accurate because

“single-owner lot samples” from slaughterhouses were counted and processed as one

tissue sample. A more accurate estimate of total tissue samples submitted would be

80). See tables 1 and 2.

Approximately 300 pigs were depopulated from Bavaro, La Altagracia Province, by

mid-October. Ninety-nine pigs were sacrificed from the Villa Mella Barrio, National

District Province on October 24 and 25, 1997. Tables 1 and 2 summarize the HCpositive tissue (14) and serum samples (47) and their sources throughout the

Dominican Republic in the first 30 days of October 1997.

Table 1—HC-positive tissue samples (14) from the Dominican Republic, October 1–

30, 1997

Positive Total Premises

samples samples Source location positive Date

3 6 Vavaro, La Altagracia Province 1 10/2

2 4 Barahona, Barahona Province 2 10/7

3 20 Villa Mella, National District Province 3 10/8, 10/14

4 4 San Ysidro, National District Province 1 10/10

1 1 Haina, San Cristobal Province – 10/8

1 2 Cesda, San Cristobal Province 1 10/16

52
Table 2—HC-positive serum samples (47) from the Dominican Republic, October 1–

30, 19971

Positive Premises

samples Source location positive Date

9 Bauaro, La Altagracia Province 4 10/2, 8, 16, 24

4 Los Rios, Villa Jaragua, Bahoruco Province 2 10/2

9 Vicente Noble, Barajona Province 2 10/7, 30

5 Galvan and Barahona, Barahona Province unk. 10/21

4 Los Matas de Farfan, San Juan Province 2 10/8

2 Villa Mella, National District Province 2 10/14, 27

1 San Isidro, National District Province 2 10/16

1 Los Tres Brasos, Santo Domingo, National

District Province 1 10/21

1 La Bomba, Dajabón Province 1 10/30

1 Dajabón Province 1 10/24

1 Los Ingenitos, Santiago Rodriguez Province 1 10/24

2 Mao, Valverde Province 1 10/24, 30

1 Haina, San Cristobal Province 1 10/10

2 Boco de Nigua, San Cristobal Province 1 10/27

3 Independencia Province 1 10/30

1 Moca, Espillat Province2 1 10/30

1

The total number of samples submitted from each province is not known

because a power outage occurred at the lab on October 31.

2

In the herd of 38 animals, only 1 pig tested positive for HC.

The Dominican Republic contacted USDA on August 27, 1997, for technical assistance

and equipment. Since the first serologic evidence of this outbreak was found in March

1997, APHIS had several other representatives in the Dominican Republic before this

action team. We have examined the methods of pig farming and marketing and the

activities of the Ministry of Agriculture in its campaign to control and eradicate HC. In

addition, assistance has continually been provided by various means.

Several APHIS personnel have been to the Dominican Republic, on permanent

assignment or detailed as consultants, to provide technical support and expertise:

Permanent Assignment

Osvaldo Perez, International Services, Dominican Republic

Consultants

Jose Diez—VS, Area Veterinarian-in-Charge, Puerto Rico

Douglas Gregg—VS, veterinary medical officer, Foreign Animal Disease

Timothy Deveau—VS, veterinary medical officer, Wisconsin

A. C. Welsch—VS, veterinary medical officer, New Jersey

USDA Intervention

53
Action Plan Team

Ed Arza—VS, Area Veterinarian-in-Charge, Georgia

John Belfrage—VS, epidemiologist, CEAH

Mark Schoenbaum—VS, Regional Epidemiologist, Central Region

Adrian Guzman—port veterinarian, Puerto Rico

Juan Lubroth—VS, Diagnostic Head, Foreign Animal Disease Diagnostic Laboratory

Robert Tanaka—International Services, veterinary medical officer, Virgin Islands

Edward Rossy—VS, veterinary medical officer, Puerto Rico

Eloisa Jones—International Services, veterinary medical officer, Riverdale, MD

Mark Teachman—VS, Emergency Programs, veterinary medical officer, Riverdale,

MD—CSF in the Dominican Republic liaison

(Authors: Dr. A. C. Welsch, veterinary medical officer, USDA, APHIS, VS, New Jersey

Area Office, (609) 259–8387; Dr. Timothy Deveau, veterinary medical officer, USDA,

APHIS, VS, Wisconsin Area Office, (608) 270–4000)

54
Epidemiology Study : The Oklahoma City Bombing—

Working Dogs Who Responded and Their

Associated Injuries and Illnesses

An epidemiologic study entitled “Injuries and Illnesses in Working Dogs Used During

the Disaster Response After the Bombing in Oklahoma City” was conducted by USDA,

APHIS, VS, EP personnel and VS employees from the Centers for Epidemiology and

Animal Health, Animal Disease Information and Analysis unit, working in conjunction

with the Injury Prevention Service, Oklahoma State Department of Health. The study

was published in vol. 212, issue 8 (April 15, 1998) of the Journal of the American

Veterinary Medical Association. See pages 1202–1207 under the Disaster Medicine

section heading.

(For more information, please contact Dr. Roberta Duhaime, veterinary medical officer,

Pennsylvania Area Office, VS, APHIS, USDA, (717) 782–3442, e-mail:

rduhaime@aphis.usda.gov)

55
Emerging Animal Diseases Update

During 1996, swine producers began reporting outbreaks of high sow abortions and

preweaning mortality. The severity of the syndrome and the current clinical picture

mirror that of the original porcine reproductive and respiratory syndrome (PRRS) when

it first hit the United States in 1989. For this reason, the syndrome was named acute

PRRS. If this disease continues to spread, the pork industry will experience significant

economic losses. Should acute PRRS reach the same level of herd infection as

original PRRS, producer surplus would decrease by $583 million per year. Consumer

surplus would decrease by $121 million per year. In the United States, direct losses

due to conventional PRRS (cPRRS) have ranged from $50 to $250 per sow in the

herd. Data from the National Animal Health Management Study’s Swine ’95 study

showed that 68.5 percent of hog operations had cPRRS virus on the premises in 1995.

Also, the hog and pork export market is severely threatened by the existence and

spread of any undefined pathogen.

The pork industry and the U.S. Government have responded aggressively to this new

emerging disease problem. NVSL and the National Animal Disease Center (NADC) in

Ames, IA, and other veterinary diagnostic laboratories have begun diagnostic and

research efforts directed toward understanding acute PRRS. In December 1996, the

National Pork Producers Council and the American Association of Swine Practitioners

called upon VS to help investigate the epidemiology of acute PRRS.

During the week of December 16–20, 1996, APHIS–VS sent an early response team

to southeastern Iowa to conduct an investigation of acute PRRS. The team

investigated operations where swine were experiencing acute PRRS and operations

that had not reported acute PRRS. The team’s analysis suggests that clinical signs

and laboratory findings in affected herds were consistent with conventional PRRS as

initially defined in the United States in 1989 and 1990. The PRRS virus was isolated

from some premises. The team did not identify risk factors for increased abortions and

deaths in the area.

On December 24, 1996, the American Association of Swine Practitioners surveyed its

members to estimate the number of acute PRRS-affected swine herds in the United

States and Canada over the previous 15 months. Affected herds were defined as

those with (1) acute onset, (2) clinical signs over a 2- to 4-week period, (3) high

mortality (>5 percent) in sows and boars, and (4) high rates of abortion (>10 percent)

occurring in all stages of parity and gestation (Zimmerman et al. 1997). Results of the

survey show that at least 138 herds may have been affected with acute PRRS.

Veterinary Services, the National Pork Producers Council, the American Association of

Swine Practitioners, and other members of the swine industry are now implementing

an investigative study of acute PRRS epidemiology. This is the first collaborative effort

by these groups in response to an emerging animal health issue and may be the new

model of cooperative studies for the future. Planning began in January 1997. Data

collection began in May. The goals of the study are (1) better characterization of the

role of the agent involved and (2) identification of management factors that put

producers at risk for acute PRRS. This report describes the study and provides an

update on data collected to date.

The Acute Porcine Reproductive and Respiratory

Syndrome (PRRS) Investigative Study—an Update

56
There are three current theories on the causes of acute PRRS, including (1) a change

in management or herd immunity that alters the clinical expression of conventional

PRRS virus, (2) a change in the conventional PRRS virus, or (3) emergence of a

previously unidentified risk factor.

To address these hypotheses, this study will have three parts: (1) a prospective casecontrol study, (2) a retrospective case-control study, and (3) multiple add-on or

followup studies. The prospective part will investigate current outbreaks (starting May

1997) of acute PRRS using case herds selected from submissions to designated State

veterinary diagnostic laboratories. The retrospective study will collect data from case

herds that have previously reported outbreaks through the American Association of

Swine Practitioners’ survey.

Followup projects will be implemented by various universities. The followup studies

will assess the longer range production impacts, provide a better characterization of

the virus, or perform other detailed investigations. Producer and practitioner

participation in these studies is voluntary and completely confidential.

The case-control study design offers significant benefits for studying a disease such as

acute PRRS. The approach works well for a disease whose occurrence is relatively

rare. Sample size requirements are relatively low, and the design can be used to go

back and retrospectively study outbreaks that have already occurred (Cole 1979).

Prospective Phase—For the prospective part, producers from any State can submit

samples for consideration through their veterinarian. However, samples must be

submitted to the seven participating veterinary diagnostic laboratories (VDL’s). The

laboratories are located in Nebraska, Iowa, South Dakota, Minnesota, North Carolina,

Indiana, and Illinois. These States’ laboratories were selected because the States

account for most of the U.S. hog population (table 1). In addition, these States were

concerned about acute PRRS and were willing to cooperate in finding cases of the

disease.

The herd selection methods will be different for case and control premises but should

represent the same population of potentially affected producers. Case herds will be

identified when an operation with high abortion or preweaning mortality submits

samples through its veterinarian to one of the seven participating VDL’s. The receiving

diagnostician will proceed with the laboratories’ normal abortion workup. If the

diagnostician suspects that a herd qualifies for the study, the diagnostician will notify

the designated VDL contact. The VDL contact will conduct a screening survey over

the phone by talking with the submitting veterinary practitioner. The survey will be

completed on an APHIS site on the World Wide Web. Each laboratory has been

issued a unique access code to prevent unauthorized data entry. No data will be

accessible via the World Wide Web. Using Internet technology will allow immediate

feedback to the diagnostician and veterinarian as to whether the herd in question

qualifies as a case. If the herd qualifies, the project coordinators in Fort Collins, CO,

are immediately notified by e-mail to begin additional data collection.

57
Table 1—Hog populations and number of operations in States with diagnostic

laboratories participating in the acute PRRS investigative study1

Number of operations

Breeding Total With < With > Total

State inventory sows Total 100 sows 100 sows operations

Thousand

hogs Percent Thousand Percent

Iowa 1,250 28.6 21.0 4.6 16.4 38.8

North

 Carolina 1,000 22.9 6.0 4.0 2.0 4.7

Minnesota 540 12.3 11.0 5.0 6.0 14.2

Illinois 520 11.9 8.8 2.9 5.9 13.9

Indiana 460 10.5 8.5 4.2 4.3 10.2

South

 Dakota 155 3.5 3.5 1.2 2.3 5.4

Nebraska 45 10.3 8.0 2.6 5.4 12.8

Total 4,375 100 66.8 24.5 42.3 100

U.S. total 6,663 — 157.45 96 61.5 —

Percent — 65.7 — — — 68.8

1

Based on the Hogs and Pigs Report, Dec. 27, 1996, published

by USDA’s National Agricultural Statistics Service.

58
Case herds are currently defined as those with abortion rates greater than 3 percent if

less than 7 days into the outbreak, 8 percent if 7 to 10 days, or greater than 12 percent

if the outbreak lasts more than 10 days. A case herd may also have preweaning

mortality greater than 25 percent within last 28 days. Also, if the diagnostician

considers this herd to have acute PRRS, an investigation will be performed. To qualify

for the prospective phase, case herds must still be experiencing these production

problems. Control herds will need to meet the same criteria as a case herd without

reporting an abortion episode with rates greater than 5 percent for any 1 month within

the last 15 months or preweaning mortality greater than 25 percent. Case and control

herds must also have computerized production records they are willing to share and

have more than 50 sows on March 1, 1997.

Control herd selection will begin after case identification. The APHIS, VS, veterinary

medical officer (VMO) assigned to the district involving a case herd will be notified.

The VMO will visit the veterinarian. He or she will generate a list of all swine clients in

the practice. From this list, the VMO will randomly select client names using a random

numbers table. The VMO will conduct a quick screening survey and select another

name if the herd chosen does not qualify. The practitioner will contact the producer

asking permission to arrange a farm visit.

The farm visit will involve a management survey, conducted by the VMO, and blood

and tissue collection by the practitioner. Data collection will be the same on case and

control farms. Additionally, on case farms, fresh tissues (lung, spleen, and kidney) and

thoracic fluid or serum will be collected from recently aborted piglets. Serum samples

will be collected from 30 randomly selected sows or gilts and 15 neonatal (< 24 hours

old) piglets (maximum of 3 piglets/litter). Sows will be rebled 3 to 4 weeks later to

evaluate changes in serum antibody levels. All samples will be sent to NVSL. Serum

samples will be tested for the presence of PRRS virus and stored for later use, as

needed. Neonatal piglet serum and fetal tissue samples will undergo virus isolation

procedures to isolate PRRS or any other potential viral agent.

Data on farrowing and weaned pig production will be collected for the baseline time

period of January through February 1997 and the time period of the outbreak. This

production data was used to reclassify herds as cases or controls for analysis. Data

entry and analysis will be conducted at the Centers for Epidemiology and Animal

Health (CEAH) in Fort Collins, CO.

Retrospective Phase—For the retrospective part of the study, members of the

American Association of Swine Practitioners responding to the Association’s survey

will be telephoned. They will be asked to provide names of producers they believe

have experienced acute PRRS in 1996 or 1997. Practitioners reporting they had not

seen acute PRRS will be asked to provide names of two producers to serve as

controls. All producers will be given a short telephone interview. The questions asked

will be similar to those asked in the on farm management survey of the prospective

phase. Analysis will be conducted at CEAH in the same manner as the prospective

phase of the study.

59
To aid in the prevention and control of acute PRRS, results will be disseminated to

producers and practitioners through as many venues as possible.

Cole, Philip. 1979. The evolving case-control study. Journal of Chronic Diseases 32:

15–27.

Zimmerman, J.; Epperson W.; Wills, R. W.; McKean, J. D. 1997. Results of the recent

survey of the membership of AASP for outbreaks of sow abortion and mortality. Swine

Health and Production 5(2): 74–75.

(Author: Dr. H. Scott Hurd, analytical epidemiologist, USDA, APHIS, VS, Centers for

Epidemiology and Animal Health, Fort Collins, CO, (970) 490–7869)

A multiple-antibiotic-resistant strain of Salmonella serotype typhimurium known as

Definitive Type (phage type pattern) DT104 is being recognized as an emerging

pathogen in the veterinary and human health world on both sides of the Atlantic.

In Humans—S. typhimurium DT104 was first reported in the United Kingdom in 1984

and has been reported in the United States, Canada, and many other European

countries. This organism is now the second most prevalent strain of Salmonella

isolated from humans in England and Wales (Threlfall et al. 1992, DT104 Workshop

Minutes 1997). The number of reported isolates of DT104 in England and Wales has

increased from 259 in 1990 to 3,837 in 1995 (Thelfall et al. 1992). Of particular

importance in this increase has been the epidemic spread of DT104 with a multiple

antimicrobial resistance pattern (R-type) to ampicillin, chloramphenicol, streptomycin,

sulfonamides, and tetracycline (ACSSuT). In England and Wales, the proportion of

DT104 that was R-type ACSSuT increased from 27 percent in 1990 to 79 percent in

1993 and decreased to 54 percent in 1995 (Threlfall et al. 1992). Molecular studies

have demonstrated that in this strain, resistance genes are chromosomally encoded.

This is of concern because removal of the selective pressure, as in plasmid-mediated

resistance, is expected to have no effect on reversion to susceptibility. Of additional

concern is the increasing additional resistance of DT104 to trimethoprim and

ciprofloxacin (a fluoroquinolone).

In the United States, the proportion of S. typhimurium isolates from the Centers for

Disease Control and Prevention (CDC)-selected county studies that were R-type

ACSSuT increased from 2 percent in 1980 to 4 percent in 1985, to 9 percent in 1990,

and to 12 percent in 1995 (DT104 Workshop Minutes 1997). Studies are under way to

determine how many of these isolates are DT104. National CDC studies in 1995 (all

50 States) and 1996 (14 State and local health departments) found that 28 and 33

percent, respectively, of S. typhimurium isolates were R-type ACSSuT (DT104

Workshop Minutes 1997). In both studies, approximately 85 percent of isolates

phagetyped were DT104. To date, no additional resistance to trimethoprim or

fluoroquinolones has been reported among DT104 isolates in the United States.

References

Salmonella typhimurium

DT104

60
The clinical features associated with infection with DT104 R-type ACSSuT suggest that

these infections may be more severe than other nontyphoid Salmonella infections.

These outcomes include increased hospitalization and mortality rates. Epidemiologic

studies in the United Kingdom suggest DT104 infections are associated with

foodborne exposure, including processed and unprocessed foods of animal origin, or

domestic and farm animal contact (particularly animals with diarrhea such as cattle

and cats) (DT104 Workshop Minutes 1997).

In Animals—S. typhimurium DT104 has been isolated from a wide range of wild,

companion, and food animals (DT104 Workshop Minutes 1997).

In the United Kingdom, from 1993 to 1995, the prevalence of reported DT104 R-type

ACSSuT isolations increased in cattle, poultry, and sheep to become the most

common Salmonella serotype and phage type (DT104 Workshop Minutes 1997). The

proportions of Salmonella DT104 isolates from cattle received at the national

veterinary diagnostic laboratory were 44 percent in adult cattle and 45 percent in

calves during 1993; this increased to 56 percent and 68 percent, respectively, in 1995

(DT104 Workshop Minutes 1997). Of the 110 Salmonella isolates from cats in the

United Kingdom received by the Laboratory of Enteric Pathogens during 1991–95,

78 (71 percent) were serotype typhimurium, and 40 (51 percent) of those were DT104

R-type ACSSuT (Wall et al. 1996).

In the United States, retrospective examination by the diagnostic laboratory at

Washington State University of S. typhimurium isolates obtained from cattle in the

Pacific Northwest showed none submitted in 1983–86 were R-type ACSSuT compared

with 12 percent of isolates obtained between 1987 and 1990, and over 60 percent in

1991–96. Selected isolates have been phagetyped as DT104 (DT104 Workshop

Minutes 1997). Although differences in sample source, species, and animal clinical

status limit interpretation and comparison of prevalence data, the proportion of S.

typhimurium isolates from national USDA 1995 and 1996 studies that were R-type

ACSSuT increased from 10 percent in 1995 to 15 percent in 1996 (DT104 Workshop

Minutes 1997). Studies are under way to determine how many of these isolates are

DT104. Of 549 S. typhimurium isolates submitted to USDA from October 1996 to midFebruary 1997 from various species nationwide, 143 (26 percent) were R-type

ACSSuT and 90 (16 percent) of these were DT104 (DT104 Workshop Minutes 1997).

The clinical features associated with infection with DT104 R-type ACSSuT suggest that

these infections may be more severe (higher morbidity and mortality rates) than other

nontyphoid Salmonella infections. Animals may also serve as asymptomatic carriers

of DT104. Long-term carriage has been observed in multiple species, particularly in

cats and cattle.

A single case-control study of risk factors for DT104, R-type ACSSuT infection in cattle

in Great Britain identified the following factors with an increased risk of infection:

introduction of new additions to a herd; purchase of cattle from dealers, close

confinement, inadequate or nonexistent isolation facilities for sick cattle, a high

population density of feral cats, and access of birds to feed storage facilities (Evans

61
and Davis 1996). Possible modes of cat acquisition of this infection are through eating

contaminated human food or by preying on rodents infected with DT104. Cats may

then serve as a source of the organism for humans through contact or for cattle though

feed contamination.

Prevention and Control of DT104 Infections—To address this emerging public and

veterinary health problem, representatives from the United States (CDC, USDA, Food

and Drug Administration, and various academic institutions), Canada, the United

Kingdom, and the Netherlands attended a workshop held in Atlanta, GA, in May 1997.

The workshop’s goals were to review the available data on DT104, and to identify

research (laboratory and epidemiology) needs, available resources, and potential

areas for collaboration. The workshop recommended the appointment of an

interagency project team of public and animal health agency representatives to

coordinate activities involving DT104. USDA’s Food Safety and Inspection Service is

leading a working group in assessing the situation with DT104 in the United States and

developing objectives to be addressed by the interagency team.

Evans, S.; Daris, R. 1996. Case control study of multiple-resistant Salmonella

typhimurium DT104 infection of cattle in Great Britain. Veterinary Record: 557–558.

Salmonella typhimurium DT104 workshop minutes. May 1, 1997. Atlanta, GA.

Threlfall, E. J.; Frost, J. A.; Ward, L. R.; Rowe, B. 1996. Increasing spectrum of

resistance in multi-resistant Salmonella typhimurium. Lancet 347: 1053–1054.

Wall, P. G.; Threlfall, E. J.; Ward, L. R.; Rowe, B. 1996. Multiresistant Salmonella

typhimurium DT104 in cats: a public health risk. Lancet 348: 471.

(Author: Dr. Thomas M. Gomez, senior staff veterinarian, Emergency Programs, VS–

CDC Liaison, Atlanta, GA, (404) 639–2213 voice, (404) 639–2212 fax, e-mail:

tmgl@cdc.gov)

References

62
FAD Training and Education Emerging Disease

Course Summary

A training course on emerging diseases was held from April 28 to May 1, 1996, in

Atlanta, GA. The course, jointly sponsored by Emory University, the Armed Forces

Institute of Pathology and CDC, was entitled, “Emerging Infections: Clinical and

Pathologic Update” and presented numerous topics of current interest from both

clinical and pathological perspectives. Topics covered were diverse and included

plague, ehrlichiosis, borreliosis, microsporidiosis, Hantavirus, viral hepatitis, Ebola

virus, streptococcal disease, bartonellosis, cryptosporidiosis, amebiasis, and

Helicobacter pylori. A comparative medicine theme was a resounding refrain, with

physicians and veterinarians as participating speakers. Presentations on the following

topics included information on approaches to the pathologic diagnosis of infectious

diseases with emphasis on morphology and molecular biology:

• Human ehrlichiosis in the United States

• Pathology of Ehrlichia and other rickettsial infections

• Lyme disease

• Pathology of human Borrelia infection

• Hantavirus pulmonary syndrome

• Ebola virus hemorrhagic fever

• Ebola virus infection in nonhuman primate models

• Zoonoses and emerging pathogens: the role of veterinary medicine

• Emerging fungal infections: cryptococcosis, fusariotoxicosis, and Penicilliosis

marneffei

• Laboratory diagnosis of cryptococcosis, fusariotoxicosis, and P. marneffei

• Pathology of infection with cryptococcosis, fusariotoxicosis, and P. marneffei

• Epidemiologic and clinical features of cryptosporidiosis: What have we learned

since Milwaukee?

• Pathology and diagnosis of cryptosporidium infections

(For more information please contact Dr. Corrie C. Brown, Department of Pathology,

College of Veterinary Medicine, University of Georgia, Athens, GA, (706) 542–5842

voice, (706) 542–5828 fax)

The primary mission of VS is to protect U.S. agriculture and the livestock industry by

preventing the introduction of foreign animal diseases. To that end, VS is committed to

ensuring the highest level of competence of foreign animal disease diagnosticians,

veterinary medical officers, and accredited veterinarians in their ability to diagnose

foreign animal diseases. Formal and informal training courses are being scheduled as

time and funding permit. The following courses and seminars were conducted in 1996,

1997, and the first half of 1998.

• Animal Identification Coordinators Workshop—July 16–18, 1996, Richmond, VA.

Four lectures on FAD’s were presented.

• Wildlife seminar on FAD preparedness, August 13–15, 1996, College of Veterinary

Medicine and Southeastern Cooperative Wildlife Disease Unit, University of Georgia,

Athens. The course was designed primarily for trained FAD diagnosticians.

Veterinary Services and

Emergency Programs

63
• FAD’s satellite TV seminar, September 5, 1996, Washington, DC, with numerous

downlink sites throughout the United States. This course was also primarily

designed for trained FAD diagnosticians.

• Military FAD course at the Foreign Animal Disease Diagnostic Laboratory (FADDL),

September 16–26, 1996, Plum Island, NY. This course was contracted by the U.S.

Army.

• FAD awareness training (a continuing education course) for the Virginia Academy of

Food Animal Practitioners, November 9, 1996, Harrisonburg, VA.

• The second annual FAD seminar via satellite was held on April 17, 1997. In

cooperation with Organizational and Professional Development, Emergency

Programs, APHIS, USDA, and Home Team Sports of Bethesda, MD, the seminar

was an excellent continuing education program. The program was beamed to about

1,000 people at 68 downlink sites (3 outside the United States) and included USDA

regional participation, 12 colleges of veterinary medicine, 5 veterinary science

departments, and industry colleagues. The program included 6 hours of instruction.

The objectives of the seminar were (1) to incorporate revised procedures for

investigating a suspected FAD into day-to-day work; (2) to describe the current world

situation on FMD, HC and BSE; (3) to discuss on-the-farm investigations in the

United Kingdom and the impact of BSE on the British and American farmer; and

(4) to visualize the impact of emerging diseases on the state of American agriculture.

Several program topics were presented by a wide range of experts. The afternoon

session was followed by a panel discussion.

• A 2-week FAD training course for Federal veterinarians was held from April 28 to

May 9, 1997. The first week of the course was conducted at the NVSL, Ames, IA,

and the second week was held at Plum Island, NY. Twenty-four Federal

veterinarians, six from each region, were participants in the course. Two trained,

experienced FAD diagnosticians, Drs. T. Schiefer and T. Vardy, assisted with the

course. Speakers were drawn from various sources to include universities and

Federal veterinarians. The course objectives were to be able (1) to conduct and

report a suspected FAD investigation properly; (2) to recognize clinical signs and

lesions, identify the species affected, and draw upon knowledge of the causative

agent of the foreign animal diseases discussed; (3) to provide a differential diagnosis

to include relevant domestic diseases; (4) to collect a probang specimen and take a

tonsillary biopsy from a pig properly; (5) to conduct a systematic postmortem of the

avian, porcine, and bovine species; (6) to collect correct diagnostic specimens,

properly preserve and package the specimens, and prepare them for shipment to

the laboratory; (7) to prepare essential paperwork properly; and (8) to recognize the

importance of vectors in FAD’s. The course was very well received, and we would

like to thank all the speakers and support staff at NVSL and Plum Island for their

support, especially the animal caretakers.

Special thanks are extended to Drs. Schiefer and Vardy.

64
• Wildlife seminar on FAD preparedness, June 1997, College of Veterinary Medicine

and Southeastern Cooperative Wildlife Disease Unit, University of Georgia, Athens.

The course was designed primarily for trained FAD diagnosticians.

• Military FAD course at the FADDL, September 1997 Plum Island, NY. This was a

course contracted by the U.S. Army.

• FAD’s Satellite TV Seminar, February 11, 1998, from 10 a.m. to 5 p.m. with

numerous downlink sites throughout the United States. This course was also

primarily designed for trained FAD diagnosticians.

• Spanish language FAD training course at FADDL on Plum Island, NY, February 9 to

13, 1998.

• State VMO FAD training course at FADDL, March 23 to April 3, 1998.

• Federal VMO FAD training course at FADDL, June 8 to 19, 1998.

• Military Veterinary Corps, VMO FAD training course at FADDL, August 17 to 28,

1998.

We would like to hear your comments and suggestions for future topics and speakers.

We are anxious to include a cross section of VS and APHIS personnel as speakers as

well as field VMO’s.

(For more information on FAD training, please contact Dr. Terrance Wilson, USDA,

APHIS, VS, Emergency Programs, Riverdale, MD, (301) 734–4917 voice, (301) 734–

7817 fax, e-mail : twilson@aphis.usda.gov)

Planned Training for 1998

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Emergency Programs Staff and Current Major Projects

• Dr. Joseph Annelli, chief staff veterinarian (director, domestic and international

liaison for all animal health emergency issues)

• Dr. Quita Bowman, senior staff veterinarian (national animal health emergency

management system coordinator, project manager—Secretary’s Advisory Committee

for Foreign Animal and Poultry Diseases, Animal Agriculture Coalition industry

liaison, Editor—FAD Report)

• Ms. Ida Ceesay, veterinary program assistant (program support for training, FAD kit

correlation and distribution, office automation)

• Dr. Linda Detwiler, senior staff veterinarian (BSE technical advisor for USDA and

APHIS, TSE Working Group coordinator, finalization of BSE Response Plan)

• Dr. Thomas Gomez, senior staff veterinarian (emerging and zoonotic diseases,

CDC/public health liaison)

• Ms. Dianna Herbert, veterinary program specialist (special projects, weekly reports

for disease, budget)

• Dr. Karen James, senior staff veterinarian (Assistant Chief, avian influenza—Hong

Kong H5N1 coordinator, contagious equine metritis coordinator)

• Ms. Sheila Miller, lead secretary (office manger, correspondence coordinator)

• Ms. Karola Oliver, veterinary program assistant, FAD surveillance, logistical

support, program information assistance, office automation)

• Ms. Cheryl Reed, veterinary program assistant (manager of maximizer data, travel

coordinator)

• Dr. Mark Teachman, senior staff veterinarian (classical swine fever in Dominican

Republic liaison, manager FEDS data base, OIE reporting)

• Dr. Larry White, senior staff veterinarian (READEO coordinator, State emergency

board coordinator, CEAH coordinator, project manager CD-ROM development)

• Dr. David Wilson, senior staff entomologist (Cattle Tick Fever Program, ARS/VS

data bank on biology, surveillance and vectors)

• Dr. Terrance Wilson, senior staff veterinarian (FAD training coordinator, military

liaison emergency management system, biological terrorism)

• Ms. Dawn Youngling, veterinary program assistant, manuscript editing for FAD

report, program support for Secretary’s Advisory Committee for Foreign Animal and

Poultry Diseases, office automation)

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