Classical Swine Fever

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:

1. Low Virulence:
   • Transplacental transmission causes abortion, cerebellar hypoplasia, or growth retardation
   • If piglets are born, they are carriers
2. 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