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FMD FMDV
Morphology
- Very small (25nm) +ss RNA virus, unenveloped
- 12 capsomeres (1 per vertex)
- 5 subunits per capsomere
- 1 molecule of virus protein (VP) per subunit
- 4 virus proteins (VP1-VP4)
- VP1 is the attachment protein
Antigenicity
- FMDV was the first animal virus in which serotypes were isolated
- To date, there are (important in bold):
- Oise (O)
- Allemagne (A)
- C (also German)
- South African Territories (SAT) 1, 2, and 3
- India (Asia-1)
- Each serotype has at lease three subtypes
- Serotype and subtype can be quickly identified by ELISA using guinea pig antisera
- All isolates are virulent
Hosts
- Cloven-hoofed animals, EXCLUDING the horse
- Cattle
- Sheep
- Goats
- Pigs
- Deer
- Elephants
- Wild ruminants: buffalo, kudu, impala, etc
Pathogenesis
- Primary replication in the upper respiratory tract, tonsils, or upper alimentary tract
- Aerosol excretion during this incubation period
- Viremia
- Virus targets stratum spinosum of stratified squamous epithelia and mucus mebranes
- Secondary vesicles appear after incubation of 2-14 days
- Appearance of lesions by age:
- 0-2 days: unruptured vesicles
- 1-3 days: newly ruptured vesicles with adherent epithelia at margins
- 3-7 days: ruptured vesicles, loss of epithelia, no marked fibrous margin
- 7-10+ days: open lesions with marked fibrous margin
- Lameness
- Also produces 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
- Teats on animals that are suckling may also develop vesicles
- In the young, without maternal antibody, virus will localize in the heart and cause death by myocarditis
- FMDV causes loss of condition and productivity but is NOT typically fatal
Pathogenesis by species
- Pigs and Sheep:
- Lesions less obvious, but vesicles around nose, mouth, and coronary band
- Pigs have vesicles on snout, which are quickly traumatised to leave an eroded lesion
- Lesion at coronary band means infection is usually less than a week old
- Lesions grow down claw at a rate of 1mm per week
- Cattle
- Lesions are seen inside mouth, around muzzle, in the interdigital cleft, around coronary band, and on teats
- Excessive salivation, anorexia, secondary mastitis
- PM: lesions in oesophagus and forestomachs
Epidemiology
- Highly contagious virus that is spread by aerosol, saliva, infected swill, direct contact, and fomites
- Pigs produce 3000 times more aerosol virus than cows
- Cows are much more susceptible to infection than pigs
- Persistent infection of cattle can occur in unkeratinized lesions, but subclinical carriers do not usually transfer infection
- Subclinical buffalo CAN transmit the disease
- 1967 + 2001 major outbreaks in UK
- Still widespread in many parts of world especially S. America, far East
- Foot and Mouth disease is NOT a highly fatal disease: approximately 5% mortality (usually young animals); older animals recover
Diagnosis
- Clinical signs for provisional diagnosis
- Confirmed by ELISA for virus antigen
- ELISAs are serotype-specific
- Should soon 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
- ELISAs used to detect subclinical carrier sheep
- Cannot be done on vaccinated animals
- RT-PCR has been suggested for on-farm diagnosis, but has flaws:
- 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
- May see animals that have discoloration of tongue due to having had FMD
- In these cases take scraping of retropharyngeal region, put scrapings in transport medium and send for testing
Control
- Recovered animals show immunity ONLY to the subtype of first exposure, and even this is relatively short-lived
- Re-exposure to the original serotype after immunity as waned will still result in virus excretion, even without clinical symptoms
- Infection by a second serotype will result in clinical disease
- For these reasons, 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
- Meat imported from endemic countries must be de-boned
In an Outbreak
- 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
- Further disinfection of the premises
- Movement is controlled within a 10-mile radius
- Follow-up serology must be performed to ensure no spread has taken place
- Ring vaccination with relevant subtype to create a barrier of immune animals (although this was not done in the 2001 outbreak)
In Endemic Areas
- Disease cannot be prevented by slaughter due to large numbers of carrier stock
- Annual Inactivated whole virus vaccination using local subtypes
- Inactivated by azuridines, using alhydrogel adjuvant for cows, and oil for pigs
- Attenuated virus reverts to virulence
- Subunit vaccines ineffective
- Expensive
- 2 initial injections at 4 months (if dams vaccinated), followed by boosters every 6-12 months
- Induces virus-neutralizing antibodies
- Vaccination DOES NOT render meat harmful to consumers, but does affect when it can be exported
Pathology
Gross
- Initially - hyperaemia of mucosa (e.g. catarrhal inflammation) then within 12 hours produces fluid filled vesicles on dorsum of tongue, may be other places
- Small vesicle coalesce to produce big ones -i.e. Bullae
- Very quickly rupture; epithelium appears dirty grey in colour because of necrosis - sloughed skin, very good for diagnosis
- Leave painful, hyperaemic epithelium
- Looks like "ulcer "with ragged edge but not a true ulcer as stratum germinativum retained and will rapidly heal completely in about 2 weeks unless becomes secondarily infected
Microscopic lesions
- Degeneration of prickle cells
- Cells "balloon" as fill with fluid and then die to produce vesicle containing straw coloured or clear fluid
For more information
- Caused by Apthovirus
- Main presentation are vesicles
- May also involve skeletal and heart muscle
- Grossly:
- Yellow streaks and grey foci
- Histologically:
- Segmental myofibre necrosis
- Infiltration of lymphocytes and neutrophils