Foreign Animal Diseases of Concern
A. Jacques Fuselier, DVM, DABVP
Large Animal Track
2012 ISVMA Conference Proceedings
The United States is currently in a vulnerable position. Our beef and pork exports are
increasing annually, as well as our food imports. A major reason for this is our safe food
supply and being free of many diseases that are of concern to our global trade partners.
The introduction of one of these foreign animal diseases to the United States would be
economically damaging. Moreover, the Department of Homeland Security (DHS) is
concerned about agroterrorism and bioterrorism.
The purpose of this talk is to serve as a refresher on several foreign animal diseases of
concern. Veterinarians are essentially our nation’s first line of defense and early
recognition of these diseases is necessary to contain the disease and minimize the
negative effects that will follow. Although all of the foreign animal diseases are important,
for the purpose of this discussion, we will focus on the diseases of most concern for our
livestock industry.
African Swine Fever (ASF)
African Swine Fever is a highly contagious viral disease of pigs. If it were to be
introduced into the US, it could severely damage our pork exports valued at 2 billion
dollars a year. This disease is essentially clinically indistinguishable from Classical
Swine Fever and many of our domestic swine diseases. The most likely route of entry
into the US will be through uncooked garbage or meat brought in by visitors from an
endemic country. This disease could spread rapidly in this country because of our
intensive swine industry and the extensive swine movements.
African Swine Fever virus is the only member of the genus asfivirus of the family
Asfarviridae. It has properties of a pox virus and is the only DNA virus transmitted by
arthropods. Highly virulent strains cause peracute and acute disease with mortality
reaching 100%. The low virulent strains are of most concern. These strains cause
chronic disease with low mortality and infected pigs can transmit virus for up to 1 month.
Recovered pigs may be life-long carriers. This virus remains stable at a pH range of 4-13
and can survive for 15 weeks in chilled pork products and 15 years in frozen carcasses.
It also survives for at least 1 month in pig pens and 15 weeks in putrefied blood.
Disinfectants found to be effective are Virkon 1% and bleach.
Transmission
Domestic and wild pigs, except African wild swine, are susceptible. Transmission is
through oronasal contact (most common), feeding uncooked garbage with infected meat,
Ornothodoros soft ticks, and fomites. The virus has been found to live in soft tick
colonies for up to 8 years.
Pathogenesis
The primary route of infection is through the upper respiratory tract. The incubation
period ranges from 5 to 15 days. Virus replication occurs in the tonsils and lymph nodes
of the head and neck, followed by rapid, generalized infection. The reason for the
hemorrhagic lesions is not well understood but suspected to be from viral disruption of
the clotting mechanisms.
Clinical Signs
With peracute infections, pigs are just found dead. Acute disease results in nearly 100%
mortality. Clinical signs before death usually include high fevers, bloody diarrhea,
erythema, anorexia, and death. Animals that suffer the acute form of this disease never
really lose body condition. The chronic form of this disease is the most concerning from
a disease-spread standpoint. This presentation is associated with the low virulence
strain and survivors may be life-long carriers. These animals present with overall low
mortality, stunted growth, skin ulcers, and pneumonia. The chronically infected pigs will
have an intermittent fever and lose body condition throughout the illness.
The post-mortem signs commonly associated with all forms of ASF are enlarged dark
red to black, friable spleen, as well as enlarged and hemorrhagic renal and
gastrohepatic lymph nodes. Post-mortem signs commonly found with chronic, low
virulence strains include pericarditis, consolidated lung lobes, necrotic dermal lesions,
swollen joints, and generalized lymphadenopathy.
If a case of ASF is suspected, the veterinarian should contact the Federal Area
Veterinarian in Charge (AVIC) and the state veterinarian. Samples that will be submitted
include serum, whole blood (heparin and EDTA), tonsil scraping, and fresh and fixed
samples of spleen, tonsil, kidney, and distal ileum. There is no vaccine for this virus.
Rapid detection, testing and slaughter is essential to control an outbreak.
Heartwater
Heartwater is a tick-borne disease of cattle, sheep, goats, and wild ruminants. It is
caused by the Gram-negative rickettsia Ehrlichia ruminantium (previously Cowdria
ruminantium). This disease is common on a few islands of the Caribbean and SubSharan Africa and is a definite threat to the Gulf Coast region of the US. Heartwater is
characterized by neurologic signs, high fever, hydrothorax, hydropericardium, pulmonary
edema, brain edema, and death.
Transmission
Although many ruminants are susceptible to this disease, variable susceptibility does
exist. For example, zebu cattle have a low susceptibility and very young (less than a
month old) animals are resistant. Transmission is via Amblyomma spp. Ticks. An
important characteristic is that trans-stadial tick infection is common. Vertical
transmission via colostrum is also likely. Cattle egrets are known to spread ticks around
the Caribbean. It is possible for these migratory birds to bring infected ticks from the
Caribbean to the US. We have competent tick vectors and wildlife hosts to support this
disease. Importation of mammals, reptiles and valuable hides from Africa and the
Caribbean adds to the risk of introducing infected ticks into the US.
Pathogenesis
The incubation period for this disease is 14-18 days. The rickettsia is injected into the
ruminant during tick feeding. The initial bacterial replication occurs in macrophages and
dendritic cells in regional lymph nodes. The bacteria enter the bloodstream and invade
endothelial cells of many organs and tissues. Subsequent multiplication in the
endothelial cells causes cell rupture and release of organisms, which results in
increased vascular permeability. When this organism infects naïve animals, the mortality
rate will range from 40-100%.
Clinical Signs
This disease presents in four different forms: the peracute (Boer goats & Jersey cattle),
acute (most common), subacute, and subclinical forms. Animals with the peracute form
are found recumbent and paddling, followed by sudden death. Sudden death is usually
associated with severe pulmonary edema. Animals with the acute form are febrile,
neurologic, in respiratory distress, and they die within one week. The neurologic signs
include high stepping, ataxia, head pressing, and belligerence. Subacutely infected
animals have pulmonary edema and fever for 10 or more days. These animals either
slowly recover or die. Animals that have partial immunity, as well as newborns, will
develop the subclinical disease, which consists of a transient fever.
Diagnosis, Treatment, and Control
Ticks should be submitted in alcohol for identification. PCR can be performed on whole
blood (EDTA) and fresh lymph nodes, brain, and kidney. All samples should be
submitted to NVSL in Ames, IA.
Tetracyclines have been used to successfully treat heartwater since the 1950s and are
still effective today.
Tick control is essential to controlling this disease. It is important not to implement an
intensive tick control program. This will lead to a naïve population of animals. It is good
to have some exposure to maintain herd immunity. A suggested method is to only dip
the animals if 10 or more ticks or evident on the animals. If this program is implemented,
individual animals showing signs of disease should be treated with tetracycline. There is
a live and an inactivated vaccine available, but no vaccines are approved for use in the
US.
Malignant Catarrhal Fever (MCF)
Malignant Catarrhal Fever is caused by a gammaherpesviruses in the genus Macavirus.
It is a sporadic, often fatal, multisystemic disease of cattle, deer, domestic swine, bison,
and many exotic ruminants. This disease is often characterized by mucopurulent
oculonasal discharge, corneal opacity originating at the limbus, keratoconjunctivitis,
epithelial erosions, and enlargement of the peripheral lymph nodes. This virus is split
into 2 main sub-groups: Ovine herpesvirus 2 (OvHV-2) and Alcelaphine herpesvirus 1
(AlHV-1). The OvHV-2 sub-group is commonly referred to as the sheep form and the
AlHV-1 is known as the wildebeest form. OvHV-2 is endemic to the US. Caprine
herpesvirus 2 (CpHV-2) and MCF of white-tailed deer (MCF of WTD) are other
subgroups found to cause MCF.
Transmission
Sheep and wildebeest are carriers of the virus and do not show clinical signs. Close
contact between carrier and susceptible animals is typically required, but transmission
has occurred in animals several hundred yards away. Young offspring of the carrier
animals are the most important in transmission to susceptible animals. The peak
shedding of OvHV-2 occurs in nasal secretions of 6-9 month old lambs. The spread of
disease has historically been associated with lambing season. Adults usually do not
shed virus unless they are stressed. The AlHV-1 has been detected in nasal and ocular
secretions of wildebeest calves up to 4 months old.
Horizontal transmission between non-carrier animals is unlikely. Forced cohabitation
studies have failed to induce horizontal transmission. As with most herpesviruses, latent
infections with recrudescence could occur. Besides direct contact and aerosol
transmission, MCF can be spread via ingestion of contaminated feed and water, as well
as from arthropod vectors.
Pathogenesis
Following transmission, the virus infects the large granular T-lymphocytes resulting in
severe immune dysfunction. The main dysfunction noted is decreased suppressor
activity resulting in proliferation of T-lymphocytes and increased CD8+ cell activity. This
leads to killing of normal cells. The incubation period for this disease can be as wide as
7-200 days following natural infection. Malignant Catarrhal Fever is known to have low
morbidity (1% to 50% in naïve herds) and high mortality (80-100%). The tissues affected
are mostly the epithelium of the upper respiratory tract, buccal papillae, and lymphatic
structures.
Clinical signs
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Corneal opacity – Starts at the limbus and migrates centrally
Thick nasal exudate
Necrotic muzzle
Necrotic foci of nasal epitheium
Tongue and buccal mucosal erosions
Erosions of the palate
Enlarged peripheral lymph nodes
There are no approved vaccines for MCF in the US. If a case of MCF is suspected, the
veterinarian should contact the Federal AVIC and the State Veterinarian.
Foot and Mouth Disease (FMD)
Foot and mouth disease is a popular topic and important viral disease of animals. As far
as animal diseases, FMD is the most important constraint to international trade.
Additionally, FMD was the first discovered viral disease of animals and currently serves
as the disease that all other foreign animal diseases are measured against.
Transmission:
Foot and mouth disease is a highly contagious viral disease. Transmission occurs with
either direct or indirect contact, via aerosols, fomites, contaminated feed, and direct
penetrating trauma. Contaminated feed (swill feeding) is more common in swine
transmission, whereas direct penetrating trauma is associated with swine to other animal
transmission. Artificial insemination with infected semen can also transmit the virus.
Natural hosts are even-toes ungulates (artiodactyls) including cattle, swine, sheep,
goats, and more than 70 species of wild ungulates. During an outbreak, sheep serve as
maintenance hosts, pigs act as amplifiers, and cattle act as indicators. Swine produce
30-100 times more virus in aerosols than sheep or cattle.
Etiology:
This highly contagious disease is caused by FMD virus (FMDV). FMD virus belongs to
the family Picornaviridae and the genus Aphthovirus. It is a non-enveloped ssRNA virus
with a positive sense genome. There are seven known FMDV serotypes (A, O, C, SAT1,
SAT2, SAT3, and Asia1) and countless subtypes. All of the serotypes are antigenically
distinct, so exposure to one type does not provide cross-protection against another type.
This virus survives well in cold temperatures but is inactivated at prolonged exposure to
temperatures above 122oF. It is quickly inactivated by pH less than 6.0 or above 9.0;
therefore, it is destroyed in tissue after rigor mortis when pH drops below 6.0. Morbidity
may reach 100% but mortality is as low as 1-5% in adults. Mortality in young animals is
20% or greater if they suffer from “tiger heart” or necrosis of the myocardium.
Clinical Signs:
Clinical signs usually appear in 3-5 days when susceptible animals are in contact with
infected animals. Pigs that eat infected garbage usually start showing signs in 1-3 days.
There is a persistent infection in ruminants.
Cattle:
 Initially – pyrexia (103-105oF), shivering, and drop in milk production
 About 3 days into course of the disease – drooling, serous nasal discharge,
kicking of the feet, lameness, and developing vesicles.
 Vesicles develop on tongue, dental pad, gums, palate, nostrils, muzzle,
interdigital space, coronary band, and teats.
 Within 24 hours, vesicles rupture, leaving erosions in its place.
 Pregnant cows abort
 Calves may die
 Takes 2-3 weeks to recover.
Sheep & goats:
 Pyrexia
 Lameness and oral lesions are mild.
 Lame animals have vesicles or erosions on interdigital space and coronary band.
 Agalactia in milking animals
 Abortion in pregnant animals
 Lambs or kids may die
 Vesicles or erosions on dental pad, lips, gums, or tongue
Pigs:
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Pyrexia (104-105oF)
Severe foot lesions and lameness
Sloughing of claws
Vesicles on pressure points of limbs, especially the carpus (knuckling)
Vesicles on the snout and tongue
Higher mortality than in cattle, sheep, or goats.
Sows abort
No drooling
Diagnostics, Treatment, and Control:
Immediately contact the Federal AVIC and State Veterinarian if any vesicular disease if
discovered! Foot and Mouth suspect samples are immediately sent to the Foreign
Animal Disease Diagnostic Laboratory (FADDL) on Plum Island, NY. Samples to be
submitted include vesicular epithelium, heart, vesicular fluid if possible, whole blood,
serum, nasal swabs, oral swabs, and sloughed epithelium or scabs. Sending digital
photographs is also helpful. Extreme care must be taken when collecting samples
because all secretions and excretions are potentially infectious; therefore, clean-up with
appropriate disinfectants is required.
If a FMD outbreak occurs, the following steps will be considered:
 Immediately slaughter infected and contact animals
 The decision to “ring” vaccinate or not
 Thoroughly disinfect vehicles and personnel
 Stop movement of all animals and animal products in the affected area
 Destroy carcasses
 Vaccinate?
 Inform and educate the public and trade partners.
Vaccinating to control an outbreak is a controversial issue. Some trade partners will not
allow “vaccinate to live”. Vaccinate to live means that the vaccinated animals will not be
killed. The concern is that infected ruminants remain persistently infected, so there is
concern that the older vaccine would lead to persistently infected cattle. Science doesn’t
necessarily support this. More countries are in favor of “vaccinate to die” in the face of
an outbreak. This means that vaccinated animals will be disposed of once the outbreak
is under control. Areas that use the vaccinate to die method are considered free in 3
months, whereas the vaccinate to live areas are considered free in 6-12 months.
The newest approved FMD vaccine developed on Plum Island is made from human
adenovirus 5 vector containing FMDV genes. The anti-viral gene for IFNα type I can be
added to provide protection within 3-5 days post vaccine. This vector is replication
defective, so it can infect but not replicate in humans or animals. This new vaccine does
not interfere with detection of natural exposure. It is a better DIVA vaccine than the
previously produced vaccine. Since it is only using select FMDV genes, it can be
manufactured on the US mainland. This vaccine still has the limitation of not preventing
infection, but it does prevent the development of clinical signs and spread of the virus.
References:
Fernandez PJ, White WR. Atlas of Transboundary Animal Diseases. OIE (World
Organisation for Animal Health), 2010
Committee of Foreign and Emerging Diseases of the United States Animal Health
Association. Foreign Animal Diseases, seventh ed. 2008. p261-277