TGE virus enters the pig by mouth and multiplies in the villi (finger like structures in the small intestine) and destroys them. This takes place in 24 to 48 hours and is followed by vomiting and a very severe acute diarrhoea with high mortality. When the virus enters the herd for the first time mortality in piglets up to 14 days of age may be 100%. This decreases in pigs over 3 weeks of age but morbidity is high.

The virus multiplies in the intestine and is shed in large numbers in the faeces. Pig faeces therefore are the major source of transmission either directly through the purchased carrier pig or indirectly through mechanical transmission. The virus is killed by sunlight within a few hours but will survive for long periods outside the pig in cold or freezing conditions. It is very susceptible to disinfectants particularly iodine based ones, quaternary ammonia and peroxygen compounds.

Dogs and cats may shed the virus in their faeces for 2 to 3 weeks. Birds and in particular starlings may transmit the disease and management should ensure that feed is not exposed to attract these birds.

Read chapters 2 and 3 on biological control of diseases entering the farm and the precautions necessary to prevent diseases spreading by faeces.

Clinical signs

Acute disease
The most striking feature of TGE when it is first introduced into the herd, is the rapidity of spread. It affects all classes of pig on the farm with evidence of vomiting and diarrhoea. Adult animals show varying degrees of inappetence and usually recover over a 5 to 7 day period. In the sucking piglet the disease is very severe and under 3 weeks of age there is a very acute watery diarrhoea with almost 100% mortality within 2 to 3 days in piglets under 7 days of age due to severe dehydration and electrolyte imbalance. There is no response to antibiotic therapy. The most striking feature is the wet and dirty appearance of all the litter due to the profuse diarrhoea. Disease will persist in the farrowing houses over a period of 3 to 4 weeks until sows have developed sufficient immunity to protect the piglets.

Chronic or endemic disease
In herds less than 300 sows the virus is usually self eliminating provided there are good all-in-all-out procedures in farrowing houses and grower accommodation. In some herds however the virus will persist in the growing herd because piglets at weaning time, still under the influence of the maternal antibody, move into houses where the virus still persists. Once the antibody disappears the pigs become infected allowing the virus to multiply. The pigs then shed the virus, contaminating the weaner rooms and infecting pigs being weaned after them. TGE can become endemic in herds in a mild form with high morbidity but low mortality.

Diagnosis

The clinical picture in acute disease is almost diagnostic. There are no other enteric diseases that would spread so rapidly across all pigs. The ultimate diagnosis of TGE must be made in the laboratory from the intestine of a fresh dead pig using fluorescent antibody tests. Isolation of the virus is also carried out.

Similar diseases

In the acute form epidemic diarrhoea could give a similar picture but it would be less acute and with less mortality in sucking pigs. Where TGE has become chronic then differentiation from the other causes of diarrhoea must be carried out in a laboratory. If the herd has been infected previously with TGE and there are scour problems persisting it is necessary to determine whether the virus is still present or not.

Treatment

• There is no specific treatment for TGE.
• Antibiotic treatment by mouth in individual piglets may reduce secondary infections.
• Provide easy access to water containing electrolyte and an antibiotic such as neomycin. Make this available to the litters twice daily.
• Improve the nursing and environment of the litter by providing extra heat and deep bedding to reduce the weights of infection from the diarrhoea.