Equine Influenza
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Subtypes
- Two subtypes of Equine Influenza have been described:
- H7N7 (Equine 1), which was prevalent in the UK between 1963-1977
- H3N8 (Equine 2), or the European strains, have been circulating since 1965
- Some drift has occurred, causing outbreaks of North-American-like strains of H3N8 in 1998 (EU) and 2003 (South America)
Pathogenesis
- Aerosol and fomite transmission infects the epithelium of the upper respiratory tract, resulting in cell necrosis
- This manifests a bronchiolitis and serous exudation
- 1-3 day incubation period
- Excretion of the virus in nasal secretions peaks at 3-4 days and finishes by 10 days
- Clinical signs:
- Harsh dry cough
- Pyrexia (103-106F)
- Depression
- Loss of appetite
- Enlarged submandibular lymph nodes
- Secondary bacterial infection can follow defective muco-ciliary transport, eg Streptococcus zooepidemicus
Diagnosis
- Virus isolation: Deep nasal swabs (12 inches) deposited into 10ml of transport medium and transported at 4C
- Antigen detection via ELISA: tests for type A nucleoprotein
- Serology provides a retrospective diagnosis by Haemagglutination Inhibition (HI):
- Acute and Convalescent (2 weeks post-acute) samples are tested from the same animal
- 4-fold increase of HI must be shown to confirm diagnosis
Control
- Isolate coughing horses to minimize spread
- Vaccination:
- All vaccines include H7 and varieties of the current circulating strains of H3
- Inactivated egg-grown vaccine is produced with alhydrogel as an adjuvant
- Live vaccines using purified haemagglutinin do not require adjuvants
- UK Jockey Club rules regarding timing:
- Horses must be certified as completing a vaccination course of 3 injections at least 8 days prior to racing
- The course consists of a primary inoculation followed by a second within 21-92 days and a third after a further 150-215 days
- Boosters are given annually to maintain immunity, and in the event a year is missed the initial course of three jabs must be repeated
- Causative agent: Orthomyxoviridae
- Rhinitis,
- Pathogenesis:
- Inhalation -> replication in epithelial cells of upper and lower airways (attaches via haemaglutinin spike and gains entry into cell) -> neuramidase alters efficiency of mucociliary apparatus
- Sloughing of the affected area
- Severity of signs will depend on dose of virus
- Acute tracheobronchitis with coughing, and fever
- May be accompanied by secondary bacterial infections
- No viraemia
- In severe cases may cause bronchointerstitial pneumonia
- Secondary invaders are usually Streptococci