Foot and Mouth DiseaseSamra Nourine

DVM 10th Semester, IUB

FMD also called as aftosa, aphthous fever, and hoof and mouth disease.

FMD is a highly contagious viral disease, primarily of cattle, sheep, swine, and goats, but also affecting other artiodactylid domestic and wild animals.

It is characterized by vesicular lesions and, subsequently, erosions of the epithelium of the lips, gums, soft palate, narries, muzzle, coronary bands, interdigital spaces, teats, and rumen pillar.Degenerative necrotizing lesions may have been observed in the myocardium of calves.

Etiology

Foot-and -mouth disease is associated with an aphthovirus (family Picomaviridae) which occurs as seven major serotypes: A, 0, C, Southern African Territories (SAT) 1, SAT 2, SAT 3 and Asia 1. However, there are a number of immunologically and serologically distinct subtypes with different degrees of virulence, especially within the A and 0 types. As there is no cross-immunity between serotypes, immunity to one type does not confer protection against the others. This presents difficulties to vaccination programs. Newer techniques for identifying subtypes involve enzyme-linked immunosorbent assay (ELISA), reverse transcriptasepolymerase chain reaction (RT-PCR) and nucleotide sequence analysis.1

Structure of Apthovirus

Aphthovirus has an icosahedral symmetry and a diameter of 24nm. The outer capsid consists of 32 capsomeres and surrounds a single-stranded molecule of RNA of approximately 8000 bases and molecular weight 2.8 X 106 daltons. This RNA codes for a single large polyprotein which is cleaved into eight nonstructural proteins (L, 2A, 2B, 2C, 3A, 3B, 3C and 3D) and the four structural proteins (VP1, VP2, VP3 and VP4), 60 copies of which make up the outer capsid. The RNA base sequence is extremely variable, which is reflected in variations in the amino acid sequence of the proteins for which it codes. The structural characteristics of the outer capsid proteins of the virus stimulate an immune response in the infected host animal. Thus mutations in the genome which change the structure of these proteins can reduce the ability of a vaccinated or previously infected animal to resist challenge with mutated virus.

Epidemiology

DistributionFoot-and-mouth disease is endemic throughout sub- Saharan Africa as far south as Tanzania, and also Equador, Bolivia, Peru, part of Brazil, Columbia and Venezuela in South America and most of the Middle and Far East.

Canada, Central and North America,Australia,New Zealand, Japan, Argentina, Chile and South Korea are free of FMD. Most of Europe is also free of FMD, but suffers occasional outbreaks of disease in spite of strict import regulations. From 1992 routine vaccination against FMD ceased in all countries of the European Union and has since also stopped in Eastern Europe, other than parts of Russia.

In Southern Africa FMD virus is usually restricted to wildlife in the game parks, although it rarely escapes into cattle areas bordering the parks.

Types O and A of FMD virus are the most widespread, especially in S. America, the Middle East and Asia; types SAT 1, SAT 2 and SAT 3 are generally restricted to Africa, although they have periodically spread into the Middle East; Asia 1 occurs in the Far East and India, although it also has spread into the Middle East. Type C only rarely causes outbreaks in Asia and has all but disappeared.

Susceptible animals

FMD affects cattle, pigs, sheep, goats, deer, and other cloven-hoofed animals. Other animals that have been found susceptible include hedgehogs, armadillos, nutrias, elephants, capybaras, rats and mice. Foot-and-mouth disease does not affect horses.

Transmission

Foot-and-mouth disease is spread by direct contact, such as when a healthy animal touches, rubs, or licks an animal that is sick. The virus may also spread by aerosol depending on environmental temperature and humidity. Animals may also become infected from eating (oral) contaminated feed or by contact with contaminated objects (fomites). FMD virus can be carried on clothes, shoes, vehicles and even in the nasal passages of people that have had contact with infected animals.

Public health problem

Infections in humans are extremely rare. Mild blister like lesions can occur. FMD is not considered to be a public health problem.

Risk factors

Host factors Some strains of the virus are limited in their infectivity to particular species. There are

strains that are much more virulent for pigs (so-called porcinophilic strains), some for buffalo, and some even for tropical breeds of cattle, which generally react only mildly to endemic strains

Immature animals and those in good condition are relatively more susceptible and hereditary differences in susceptibility have also been observed.

Environmental & Pathogen Factors The virus is resistant to external influences including common disinfectants and the usual

storage practices of the meat trade. It may persist for over 1 year in infected premises, for 10-12 weeks on clothing and feed,

and up to a month on hair. It is particularly susceptible to changes in pH away from neutral. Sunlight destroys the virus quickly but it may persist on pasture for long periods at low

temperatures. Boiling effectively destroys the virus if it is free of tissue but autoclaving under pressure

is the safest procedure when heat disinfection is used. The virus can survive for more than 60 days in bull semen frozen to -79°C (-l lO°F). In general, the virus is relatively susceptible to heat and insensitive to cold. Most common disinfectants exert practically no effect, but sodium hydroxide or formalin

(1-2%) or sodium carbonate (4%) will destroy the virus within a few minutes.

Economic importance

With the possible exception of bovine spongiform encephalopathy (mad cow disease), FMD is the most feared animal disease in the developed world, even though the mortality rate is low.

This is because it is the most contagious disease of livestock and has a great potential for causing severe economic loss in high producing animals. Losses occur in many ways although loss of production, the expense of eradication and the interference with movement of livestock and meat between countries are the most important economic effects.

Pathogenesis Infection through inhalation, the most efficient method of infection, virus can also gain

entry through ingestion, insemination & inoculation & through contact with abraded skin. Primary viral replication after inhalation takes place in the mucosal & lymphatic tissues

of pharanx Viremia follows primary multiplication with further viral replication in lymph nodes,

mammary glands & other organs as well as the epithelial cells of mouth, muzzle, teats, interdigital skin, & coronary band.

In these areas of stratified squamous epithelium, vesicle formation results from swelling and rupture of keratinocytes in the stratum spinosum.

Clinical Findings

Cattle

Incubation period is from 3-6 days and may vary between 1-7 days. onset is heralded by a precipitate fall in milk yield and a high fever (40-41oC; 104-

106°F), accompanied by severe dejection and anorexia appearance of acute painful stomatitis temperature start to subside abundant salivation with long ropy strings smacking of lips animal chews carefully Vesicles and bullae (1-2 cm in diameter) appear on the buccal mucosa, dental pad and

dorsal one-third of tongue. These rupture with in 24 hours leaving raw painful surface which heals in about one

week The vesicles arc thin walled they rupture easily and contain a thin, straw-colored fluid. Concurrently with oral lesions, vesicles appear on the feet, particularly in the clefts and

on the coronet. Rupture of vesicles causes acute discomfort and the animal is grossly lame, often

recumbent, with a marked,painful swelling of the coronet. Secondary bacterial invasion of foot lesions may interfere with healing and lead to severe

involvement of the deep structures of the foot.

Vesicles may occur on the teats and when the teat orifice is involved, severe mastitis often follows.

Pregnant animals may abort or have stillbirths. Very rapid loss of condition and fall in milk yield occur during the acute period and these

signs are much more severe than would be anticipated from the extent of the lesions. Eating is resumed in 2-3 d as lesions heal The period of convalescence may be as long as 6 months. Young animals are more susceptible and may suffer heavy mortality from myocardial

damage (tiger heart disease), even when typical vesicular lesions are absent in mouth and feet.

A sequel to FMD in cattle, due probably to endocrine damage, is a chronic syndrome of dyspnea, anemia, overgrowth of hair, permanent loss in milk production and lack of heat tolerance. Affected cattle are described colloquially as 'hairy panters'. Diabetes mellitus has also been observed as a sequel in cattle.

Sheep

The chief symptom is a sudden, severe lameness, affecting one or more legs. The animal looks sick, lies down frequently and is very unwilling to rise. Usually, the disease affects all four feet, and when the animal is made to rise, it stands in

a half-crouching position, with the hind legs brought well forward, and seems afraid to move.

Mouth symptoms are not often noticeable. There are blisters on the feet at the top of the hoof, where the horn joins the skin in the

cleft of the foot. They may extend all round the coronet, and when they burst the horn is separated from

the tissues underneath, and the hair round the hoof is damp. Unless complicated by foot rot, the foot is clean and there is no offensive smell. Blisters in the mouth, when they do develop, form on the dental pad and sometimes the

tongue.

Pigs

The chief symptom in pigs is sudden lameness. The animal prefers to lie down and when made to move squeals loudly and hobbles

painfully, though lameness may not be so obvious where the pigs are on deep bedding or soft ground.

The blisters form on the upper edge of the hoof, where the skin and horn meet, and on the heels and in the cleft. They may extend right round the hoof head, with the result that the horn becomes detached.

At a later stage new horn starts to grow and the old hoof is carried down and finally shed. The process resembles the loss of a fingernail following some blow or other injury.

Mouth symptoms are not usually visible, but blisters may develop on the snout or on the tongue.

Pathology

The epithelial cells of the stratum spinosum of the skin undergo ballooning degeneration. As the cells disrupt and oedema fluid accumulates, vesicles develop which coalesce to form the aphthae and bullae that characterize FMD. The cells of the squamous epithelium of the rumen, reticulum and omasum may also become involved. In young animals the virus invades the cells of the myocardium and macroscopic grey lesions may be seen particularly in the wall of the left ventricle, giving it a striped appearance (tiger heart). Cells of the skeletal muscles may also undergo hyaline degeneration.

Necropsy Findings

The lesions of FMD consist of vesicles and erosions in the mouth and on the feet and udder. The erosions often become ulcers especially if secondary bacterial infection has occurred. In some cases, vesicles may extend to the pharynx, esophagus, fore stomachs, and intestines as well as trachea and bronchi.

The teats and mammary gland are often swollen.

In the malignant form and in neonatal animals, epicardial hemorrhages with or without pale areas are also present. Grossly, the ventricular walls appear streaked with patches of yellow tissue

interspersed with apparently, normal myocardium, giving the typicaJ 'tiger heart' appearance. If the animal survives, there is replacement fibrosis and the heart is enlarged and flabby.

Histopathology

Histologically, vesicles start as foci of progressive swelling, necrosis and lysis of infected keratinocytes in the deeper layers of the epidermis and accumulation of fluid in the space. This is followed by necrosis of overlying keratinocytes and rupture of vesicles to form erosions that may extend deep into the dermis to form ulcers, especially on the feet. There is only mild leukocytic infiltration around the erosions and ulcers.

Similar changes in mammary gland epithelium lead to acinar necrosis and mild interstitial cellular infiltration.

Heart (and occasionally skeletal, muscle) lesions in the malignant form are characterized by severe hyaline degeneration, necrosis and occasional calcification of myocardial fibers and marked interstitial infiltration by mononuclear cells.

In addition, pancreatic islet and acinar degeneration has been reported in chronically infected cattle.

Diagnosis Initial diagnosis is usually on the basis of clinical signs, with or without a history of

contact between the herd and an infected animal or reports of FMD in the vicinity. Laboratory diagnosis includes Virus isolation, serology and RT- PC R detection.

Differential diagnostic list

Vesicular stomatitis Vesicular exanthema Swine vesicular disease Rinderpest Bovine viral diarrhea

(Center for food security and public health, Iowa State university-2011)

Treatment

As FMD is a viral disease so there is no specific treatment for this disease only symptomatic treatment can be performed.

Anti-pyretics Antibiotics Protective dressing on inflamed areas to prevent secondary bacterial infection.

Prevention and control

The initial measures in the global strategy for dealing with FMD are early detection and warning systems and prevention and rapid response measures and mechanisms in place. This contributes to monitoring the occurrence, prevalence and characterisation of FMD viruses.

Protection of FMD free countries, areas or zones is enhanced with stringent import and cross-border animal movement controls and surveillance.

It is essential for livestock owners and producers to maintain sound biosecurity practices to prevent introduction/spread of the virus. Measures that are recommended at the farm level include:

control the introduction of new animals to existing stock; control over access to livestock by people and equipment; maintain sanitation of livestock pens, buildings, vehicles and equipment ; monitor and report illness; Appropriate disposal of manure and dead carcasses.

 

Contingency planning for potential outbreaks will identify the elements included in a response effort to eradicate the disease, such as:

humane destruction of all infected, recovered and FMD-susceptible contact animals; appropriate disposal of carcasses and all animal products; surveillance and tracing of potentially infected or exposed livestock; strict quarantine and controls on movement of livestock, equipment, vehicles, and; Thorough disinfection of premises and all infected material (implements, cars, clothes,

etc.)