Transmissible Gastro-Enteritis (TGE)
Occurrence: Worldwide, absent/notifiable in some countries.
Age affected: All ages.
Causes: Transmissible gastroenteritis virus.
Effects: Illness, watery diarrhoea, pre-weaning mortality.
TGE is caused by a coronavirus which produces extensive cell damage (CPE), syncytia and round refractile cells in cell culture. It is sensitive to heat and is inactivated after 45 minutes at 50°C. The half-life at 37°C is less than 2 hours. Some strains are very sensitive to light, but it is extremely stable when frozen. One serotype of TGE virus exists but there are minor differences between isolates.
Infection is by ingestion or inhalation. The virus multiplies in the cells lining the small intestine and mature absorptive cells are lost, leading to shortening of the villi, and to reduction of the ability to digest food and to absorb products of digestion. Osmotic diarrhoea results and piglets die from dehydration. Specific IgA antibody in the colostrum and milk of immune sows protects piglets against infection. Serum antibody develops within 7-8 days of infection and may persist for at least 6 months in finishers and 16 months to 2 years in sows. Virus can still be demonstrated in the lung 104 days after infection and in the gut for at least 104 days. Virus shedding in the faeces may not, however, be easily detectable more than 14 days after infection.
Mode of transmission
Infection is oral, from virus present in the faeces of infected pigs. As the diarrhoea in affected pigs is so profuse and watery, the faeces can be distributed widely within a herd by contact and also by aerosol and spread within a building is extremely rapid. Recovered pigs carry and shed the virus for weeks. The virus can survive for long periods when frozen and remains stable in neutral conditions. Transmission between farms is usually by the movement of infected pigs, but transport, contaminated clothing and aerosol spread have all been documented and mechanical spread by bird movement can occur.
TGE begins as an explosive outbreak of diarrhoea which involves pigs of all ages within a few days in non-immune herds. The diarrhoea is profuse, watery and yellowish green in colour sometimes with a foetid odour and containing curds of undigested milk. Vomiting may occur in piglets under 3 weeks of age. Affected pigs become dehydrated, resulting in death in piglets within 24-48 hours and in agalactia in sows.
The disease has an incubation period of 1-2 days and occurs within 3-4 days of birth in susceptible piglets. In a non-immune herd where water is not available to the piglets, mortality between days 0 and 7 is 100%, 50% between 8-14 days and 25% between 15-21 days and is rare in piglets aged 3 weeks or more. Affected adults usually recover within 7-10 days. Abortions and a reduced conception rate have been recorded in sows. Where the disease is enzootic, pigs aged between 10 days and 6 weeks develop diarrhoea and growth depression. Only growth depression may occur in finishing pigs. Where wet feed is given with no supplementary water, weaned pigs may die from salt poisoning and these clinical signs may be superimposed on those of TGE.
The pattern of the outbreak, the clinical signs of diarrhoea throughout the herd, deaths in the young piglets and the pathological findings lead to suspicion of TGE or Porcine Epidemic Diarrhoea (PED). Viral nucleic acid can be identified in faeces by the Polymerase Chain Reaction (RT PCR for TGE alone or in multiplex PCRs including rotavirus and PED) and antibody can be detected in the sera of recovered pigs using tests which distinguish it from Porcine Respiratory Coronavirus, PRCV, very closely related to TGEV, and PED.
Dead piglets are dehydrated but in good condition. Freshly killed animals are required to confirm diagnosis. The stomach is distended with curdled milk and the small intestine is distended with foamy yellow fluid and is thin-walled. Yellowish deposits or urate crystals may be seen in streaks in the kidney medulla. Gastritis may be present. The mesenteric lymph nodes may be enlarged.
Villous atrophy may be seen in the small intestine. Intestinal mucosa is best mounted in saline and viewed x 10 under a dissecting microscope. Microscopic examination of the intestine confirms the villous atrophy. Virus can be demonstrated in frozen sections of small intestine using a specific fluorescent antiserum or monoclonal antibody using immunoperoxidase, or by detection of viral nucleic acid in fixed tissue. Virus can be isolated from mesenteric lymph node, tonsil and small intestine which may be frozen.
Treatment and prevention
There is no treatment. Affected piglets can be supported using electrolyte replacer solutions. Early weaning, high environmental temperatures and hygiene may all help reduce mortality. Cross sucking of litters onto immune sows may also help. Water should be freely available to weaned pigs. Antimicrobials may control infections by other enteric pathogens. Prevention of entry to farms relies on isolation, exclusion of unnecessary visitors or contaminated lorries and use of showers or disinfectant dips for visitors.
Pigs remain carriers for 104 days and should not be purchased during epizootics of TGE, but may be safe after 40 days. Entry may still occur by bird or wind transmission (up to 1.6km). When an outbreak occurs, sows due to farrow within 14 days should be maintained in isolation. Sows which are more than 14 days from farrowing can be infected with intestinal contents from dead pigs (where legal) and may develop immunity in time to protect their litters. An all-in, all-out policy should be operated in finishing and farrowing houses in herds where the disease is enzootic. Disinfection and control of rodents and birds may break the cycle of infection. Vaccines do not protect completely and are not available in all countries.