Classical Swine Fever
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This article is still under construction. |
Antigenicity
- Isolates vary in virulence
- Some antigenic variation
- Best defined by monoclonal antibodies, but no serotypes
Hosts
- Pigs
- Wild boar
Pathogenesis
- Virus enters oropharynx and replicates in palatine tonsil
- Viremia 2-6 days post-infection
Two types of strain:
- Low Virulence:
- Transplacental transmission causes abortion, cerebellar hypoplasia, or growth retardation
- If piglets are born, they are carriers
- High Virulence:
- Leukopenia
- Thrombocytopenia
- Generalized vasculitis
- Hemorrhage of lymph nodes, spleen, bladder, larynx, and skin
- Vasculitis in CNS causes tremors, incoordination and convulsions
Chronic disease:
- Infarction causes button ulcers over Peyer's Patches
Epidemiology
- Recovered animals are immune
- Highly contagious
- Transfer via contact, aerosol, or fomites
- Swine fever was once endemic worldwide but has now been eradicated from UK, Australia, NZ, USA, and Denmark following vaccination schemes
Diagnosis
- Immunofluorescence of tissues for virus isolation
- DD: Porcine circovirus 2, African swine fever, or bacterial septicemia
Control
- NOTIFIABLE disease
- Vaccination (live attenuated) in endemic countries:
- Parts of EU are using vaccinated bait to control spread in wild boar population
- Vaccination does not curtail spread: marker vaccine needed to distinguish virus exposure from vaccine-induced antibody
- Pestivirus invades vascular endothelium and macrophages
- Leads to infarcted lesions
- In spleen
- "Button ulcers" in colon and caecum.
- Ulcers are seen as discrete circular areas of haemorrhage and necrosis with dry, yellow centres