Foot and Mouth Disease

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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
  1. Initially - hyperaemia of mucosa (e.g. catarrhal inflammation) then within 12 hours produces fluid filled vesicles on dorsum of tongue, may be other places
  2. Small vesicle coalesce to produce big ones -i.e. Bullae
  3. Very quickly rupture; epithelium appears dirty grey in colour because of necrosis - sloughed skin, very good for diagnosis
  4. Leave painful, hyperaemic epithelium
  5. 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

DEFRA


  • Caused by Apthovirus
  • Main presentation are vesicles
  • May also involve skeletal and heart muscle
  • Grossly:
    • Yellow streaks and grey foci
  • Histologically: