Foot and Mouth Disease

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Also known as: FMDV —  FMD

Introduction

This Apthovirus is a small (25nm) +ss RNA virus, unenveloped and has 7 serotypes, namely Oise (O), 'Allemagne (A), 'C (also German), South African Territories (SAT) 1, 2, and 3 and Asia-1.

This disease affects all cloven-hoofed animals, namely cattle, sheep, goats, pigs, deer, elephants and other wild ruminants such as buffalo and kudu etc. It does NOT afferct the horse. The main presentation of the disease is the formation of vesicles.

The disease is NOTIFIABLE in the UK and any animals with the disease, or in contact with the disease have to be destroyed.

The virus replicates primarily in the upper respiratory tract, tonsils, or upper alimentary tract and there is aerosol excretion during this incubation period. This is then followed by a viremia. Virus targets stratum spinosum of stratified squamous epithelia and mucus membranes and secondary vesicles appear after incubation of 2-14 days. Lesions also affect the feet with cutaneous erosions in interdigital cleft, at coronet and bulbs of heals . These feet lesions often take a long time to heal as secondary bacterial infections may ensue and produce true deep ulcerative dermatitis. In the young, without maternal antibody, virus will localize in the heart, particularly the wall of the left ventricle, resulting in multi-focal necrosis of the myocardium and subsequent death. Persistent infection of cattle can occur in unkeratinized lesions, but subclinical carriers do not usually transfer infection except for subclinical buffalo that can transmit the disease.

FMDV causes loss of condition and productivity but is NOT typically fatal. Approximately 5% mortality (usually young animals); older animals recover. The virus is highly contagious and spread is by aerosol, direct contact, saliva, infected swill and fomites. Pigs produce 3000 times more aerosol virus than cows, but cows are much more susceptible to infection than pigs.

In 1967 and 2001 there were major outbreaks in the UK. The disease is still widespread in many parts of world especially S. America and far East.

Clinical Signs

Main clinical signs include pyrexia, depression, separation away from the herd, drooling, excess salivation, anorexia pain while eating as well as smacking of the lips. Lameness is also a key clinical sign and in pigs may often be the first noticeable sign as mouth lesions in this specie are less severe.

Lesions in the mouth and on the tongue have the following characteristics depending on age of lesions.

At 0- 2 days there will be unruptured vesicles.
At 1-3 days newly ruptured vesicles with adherent epithelia at margins will appear.
By 3-7 days there will be ruptured vesicles, loss of epithelia, no marked fibrous margin.
At days 7-10+ open lesions with marked fibrous margin will be present.

Teats on animals that are suckling may also develop vesicles.

In pigs and sheep, lesions are less obvious, but vesicles around nose, mouth, and coronary band are present. Pigs have vesicles on snout, which are quickly traumatised to leave an eroded lesion. Presence of a lesion at coronary band means infection is usually less than a week old. The lesions grow down the claw at a rate of 1mm per week.

In cattle, lesions are seen inside mouth, around muzzle, in the interdigital cleft, around coronary band, and on teats. There will be excessive salivation, anorexia, secondary mastitis and on PM there will be lesions in oesophagus and forestomachs.

Diagnosis

Clinical signs are enough to make a provisional diagnosis. This must be confirmed by ELISA for virus antigen. ELISAs are serotype-specific. This method is soon to be replaced by immunochromatography-bedside ELISA to allow on-farm diagnosis. Virus isolation can also be performed in kidney culture cells, and then serotyped by ELISA. Serology for virus antibody can determine past infection and ELISAs are used to detect subclinical carrier sheep. This cannot be done on vaccinated animals.

RT-PCR has been suggested for on-farm diagnosis, but has flaws such as, RNA is readily degraded by tissue enzymes, RNA must be purified before converting to DNA for PCR, false positives can occur easily by contamination with previously amplified DNA.

Samples should be taken from the vesicle itself and include the vesicle fluid as well as the tissue. These should be placed in transport medium and sent for testing.

Control

Recovered animals show immunity ONLY to the serotype of first exposure, and even this is relatively short-lived, therefore re-exposure to the original serotype after immunity has waned will still result in virus excretion, even without clinical symptoms. Infection by a second serotype will result in clinical disease. It is for these reasons, that vaccination is not practiced in the UK. Further, vaccination would mean a loss of meat export markets.

Prevention in the UK

Imported stock must come from virus-free countries that DO NOT vaccinate. Any meat imported from endemic countries must be de-boned.

ANY sign of lesions in a susceptible animal is NOTIFIABLE to the Divisional Veterinary Officer and local police. Once diagnosis is confirmed, all animals on the premises must be slaughtered and incinerated and the premises fully disinfected. Movement is controlled within a 10-mile radius and follow-up serology must be performed to ensure no spread has taken place on any nearby farms. Ring vaccination with relevant subtype to create a barrier of immune animals (although this was not done in the 2001 outbreak) can be used. There is to be no movement on or off the farm as soon as a case is suspected.

In Endemic Areas disease cannot be prevented by slaughter due to large numbers of carrier stock. Annual inactivated whole virus vaccination using local subtypes is used. This vaccine is inactivated by azuridines, using alhydrogel adjuvant for cows, and oil for pigs. Subunit vaccines are ineffective. The course involves 2 initial injections at 4 months (if dams are vaccinated), followed by boosters every 6-12 months, which induces virus-neutralizing antibodies. Vaccination DOES NOT render meat harmful to consumers, but does affect when it can be exported.

References

Andrews, A.H, Blowey, R.W, Boyd, H and Eddy, R.G. (2004)Bovine Medicine (Second edition), Blackwell Publishing

Brownlie, J (2007) Virology Study Guide, Royal Veterinary College.

Radostits, O.M, Arundel, J.H, and Gay, C.C. (2000) Veterinary Medicine: a textbook of the diseases of cattle, sheep, pigs, goats and horses Elsevier Health Sciences

Taylor, D.J. (2006) Pig Diseases (Eighth edition) St Edmunsdbury Press ltd




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