Transmissible Gastroenteritis in Pigs

The causal coronavirus infects and destroys villous epithelial cells of the jejunum and ileum, which results in severe villous atrophy, malabsorption, osmotic diarrhea, and dehydration. The incubation period is ~18 hr. The infection spreads rapidly by aerosol or contact exposure. Severe epidemics are more common during winter because of survival of the virus in colder temperatures.

In nonimmune herds, vomiting often is the initial sign, followed by profuse watery diarrhea, dehydration, and excessive thirst. Feces of nursing pigs often contain curds of undigested milk. Mortality is nearly 100% in piglets <1 wk old, whereas pigs >1 mo old seldom die. Gestating sows occasionally abort, and lactating sows often exhibit vomiting, diarrhea, and agalactia. Diarrhea in surviving nursing piglets continues for ~5 days, but older pigs may be diarrheic for a shorter period.

In large herds with endemic TGE, clinical signs are variable, depending on the level of immunity and magnitude of exposure. Immunity from antibody in the sow’s milk usually is sufficient to protect piglets until they are 4–5 days old. As the antibody level in milk decreases, infection and mild disease may occur. Depending on the level of immunity and exposure, diarrhea may be mild in some litters but severe in others. If passive protection is sufficient to protect pigs throughout the nursing period, diarrhea often develops during the first few days after weaning.

Clinical signs in the epidemic form of TGE usually justify a presumptive diagnosis. In the mild endemic form, laboratory procedures are required. Histologic and immunofluorescent examinations of the small intestine to demonstrate typical lesions and the presence of TGE viral antigen provide confirmatory evidence. In some outbreaks, hemagglutinating encephalomyelitis (see Porcine Hemagglutinating Encephalomyelitis) may cause similar signs.

There is no specific treatment. Increasing farrowing room temperature to minimize loss of body heat and providing electrolyte solutions to combat dehydration are helpful. Administration of swine immunoglobulins has been reported to be beneficial. Weaning older nursing pigs that are consuming creep feed may reduce mortality.

Protective immunity depends on presence of antibody in the small intestine. Passive protection of piglets is provided by continual nursing of immune sows. Active, protective immunity develops after infection of the intestinal mucosa with virulent TGE virus. Active infection of the intestine with virulent virus provides protective immunity for 6–18 mo due to a secretory IgA response. Vaccination of naturally immune sows boosts immunity sufficiently to protect neonates and is particularly useful in endemically infected herds. Vaccination of swine in herds free of TGE may not be economically beneficial because vaccines do not induce complete immunity.

Planned infection of pregnant sows at least 2–4 wk before farrowing in herds known to be infected with virulent virus usually provides adequate immunity. This may be accomplished by mixing ground, TGE virus–infected intestine and feces in the gestation ration. Because of the obvious hazards associated with this procedure, it should be undertaken only if a later epidemic in the farrowing house seems inevitable. The infectious material should be used only in the same herd from which it was collected, and the tissues should be as free as possible from other pathogens of pigs. TGE virus can be eliminated from herds without total depopulation by maximizing immunity with planned infection of the sow herd; an “all-in/all-out” management of farrowing, nursery, and grower rooms; and good sanitation.

Because TGE virus is easily spread during an epidemic by people, animals, and fomites, special care should be taken to prevent spread to unexposed groups of pigs and to neighboring herds.