Classical Swine Fever

Description

Classical swine fevetr is a highly contagious disease of swine, caused by a Togavirus. The disease may be actue, sub-acute, chronic or persitent and is indistinguishable both clinically and pathologically in the field from African Swine Fever. The acute form is characterised by severe depression, high fever, superficial and internal haemorrhages, and high morbidity and mortality. The chronic form is characterised by anorexia, pyrxia and depression. Transplacental infection results in persistently infected piglets which constitute a major sources of virus spread in endemic situations.

Prognosis

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