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This article is still under construction. |
Hosts
- Reservoir species: wildebeest, sheep, each transferring different forms of the virus
- Innocuous to reservoir hosts
- Dead end hosts: cows, kudu, some deer
Pathogenesis
- Clinical signs in cattle:
- Necrotising lesions in upper respiratory tract and eye: conjunctivitis and corneal oedema / opacity (keratitis or "blue eye" - characteristic feature)
- Fever and diarrhoea with severe oculo-nasal discharge
- Not eating, dull with ulcers on muzzle may spread to rest of face with brown exudate
- Ulcers also on tongue, dental pad, and cheeks that regularly become secondarily infected
- Lymphocyte proliferation progresses in lymphoid tissue and blood until death
- Lymph nodes completely replaced by lymphoblasts - similar to lymphosarcoma
- Also vasculitis with medial necrosis of blood vessels throughout body with infiltration of walls of vessels by lymphocytes.
- Ulcers are due to hypoxia of epithelium resulting from vascular lesions
- Sporadically induce a fatal over-active T cell division, where virus encodes anti-apoptotic protein in dead-end host
- Latent infection that is invariably fatal
- Virus excretion increased during periparturient period
Epidemiology
- Not all that common in UK
- Affects whole body but especially evident clinically in face and mouth
- Sporadic and often seen in animals mixing with sheep (carriers)
- In parts of Africa see long outbreaks (diff serotypes) carried by Wildebeest
- In deer produces very serious outbreaks, probably primarily sheep virus
- Often youngish animal 6 months to 1 year
Control
- Wildebeest should not be stocked in zoos where possible
- Sheep and deer should be housed separately