Transmissible gastroenteritis (TGE) is an acute, rapidly spreading, viral disease of swine of all ages, characterized by diarrhea and vomiting. High mortality in piglets under two weeks of age is common with mortality decreasing with age. There also is an endemic form of the disease, seen in herds with partial immunity or concurrent porcine respiratory coronavirus (PRCV) infection, with less severe signs and much lower mortality.
Transmissible gastroenteritis (TGE) occurs naturally only in swine. Among previously unexposed swine, all age groups are susceptible. TGE occurs throughout the year but incidence may be higher in the colder months. TGE occurs in many major swine-raising countries but is seen infrequently in Europe.
In the United States, outbreaks that were likely TGE were seen as early as 1943 but the first documented outbreaks were reported in 1946. Subsequently, the disease was identified in many other countries.
Serologic surveys indicate that TGE is widespread throughout the US. Although initial outbreaks are acute, a less severe, endemic form now persists in some herds. TGE can cause up to 100% neonatal mortality during the initial stages of an outbreak and is therefore unlikely to be misdiagnosed in a previously naïve herd.
In Europe, and more recently in the US, TGE is seldom seen because a natural mutant of TGE virus, porcine respiratory coronavirus (PRCV) presumably stimulates immunity to TGE.
The etiologic agent of TGE is a coronavirus (TGEV). Most isolates are enteropathic. Virus is labile at about 72° F (22° C), but quite stable when frozen. A closely related virus, porcine respiratory coronavirus (PRCV), is present in many countries, including the United States. Canine coronavirus and feline infectious peritonitis viruses are related to TGEV.
The PRCV is derived from TGEV by deletion of the S-gene. It has lost its tropism for enterocytes but has increased tropism for the lungs. It can cause a mild respiratory disease in swine although most infections are subclinical. Serologically, TGEV and PRCV cross-react but tests are available to distinguish between them. TGEV can be destroyed by many disinfectants, e.g. iodides, quaternary ammonium compounds, phenol and sodium hypochlorite.
Swine that survive TGE develop antibodies against the virus but continue to excrete virus in their feces or nasal secretions for at least two to eight weeks; some individuals have been shown to excrete virus intermittently for up to 18 months. TGE virus has been isolated from intestinal and lung homogenates for up to 104 days. Infected sows can transmit virus in their milk or feces to their piglets. Although feces are the major source of infection, virus probably is spread aerogenously, at least for short distances. In feeding operations or multiple farrowing operations, where animals from multiple sources are intermixed, carrier animals often are a source of exposure to TGE virus. Other animals and insects known to act as mechanical carriers of virus for various lengths of time and distance include dogs, cats, foxes, starlings and flies.
The virus is resistant enough that fomites readily transmit the virus. Once introduced, virus may persist on premises, especially during the colder months. Conversely, premises depopulated for a few days during hot summer months may then be free of virus.
When virus is introduced into a herd of naïve swine, all age groups are affected and the disease assumes epidemic characteristics. Once premises are infected and there is a constant source of immunologically naïve pigs because of frequent or continuous farrowing or frequent introduction of susceptible animals, TGE may persist as a chronic disease in the herd. Infection often persists in successive groups of pigs entering a contaminated nursery.
Factors other than virulence of the virus and host resistance seem to play little part in susceptibility to infection. Outbreaks often occur on premises with excellent husbandry, nutrition and sanitation.
The virus enters the pharynx via the oral or nasal route, is swallowed and reaches susceptible epithelial cells of the small intestine. In neonates or young pigs, infection of those cells with destruction or loss of function is accompanied by patchy atrophy of intestinal villi most noticeable in the jejunum and ileum. The lesions lead to malabsorption of nutrients. Inability to hydrolyze lactose in dam’s milk leads to an osmotic flow of fluids into the intestinal lumen. This results in diarrhea and dehydration. Death is related to dehydration, metabolic acidosis and abnormal cardiac function caused by hyperkalemia. In very young pigs, the relatively high proportion of absorptive enterocytes and the relatively slow regeneration time of epithelial cells to cover denuded villi, coupled with the limited ability to maintain homeostasis, results in very high mortality.
In acute outbreaks, the incubation period is very short, 18 hrs to three days. In baby pigs the disease spreads rapidly to affect all susceptible pigs. Signs include profuse diarrhea, frequent vomiting, rapid dehydration, shivering and marked thirst. The pigs weaken rapidly and usually die within one to two days. Pigs suckling immune dams may remain well as long as they receive adequate antibody in the dam’s colostrum and milk. Pigs infected after 4 weeks of age often survive.
The chronic or endemic form of TGE often is seen in pigs from herds where some dams are immune and others have a limited immunity. Onset of clinical signs varies, depending on when lactogenic immunity fails and leaves them susceptible, but is usually later in lactation or early in the postweaning period (two to five weeks of age). Signs can be rather mild, especially in well-doing pigs, and usually include diarrhea, dehydration, unthriftiness and runting.
In feeder and fattening pigs, signs usually are mild except for diarrhea which is profuse and watery for a few days. Vomiting occurs occasionally. Morbidity is high but mortality is low or absent. Moderate severity is observed in naïve sows and gilts, especially in those that have farrowed recently and are heavily exposed to virus from piglets with TGE. The dams show anorexia, vomiting, diarrhea, depression and may cease to lactate. Recovery usually occurs within 5-10 days.
Gross lesions in baby pigs include marked dehydration, distension of the small intestine with foamy, yellow, odoriferous fluid and scattered milk curds. The intestinal wall is very thin and nearly transparent. The stomach may be empty because of vomiting but sometimes is filled with curdled milk. Chyle seldom is present in mesenteric lymphatics since fat absorption is impaired. There often are yellow or gray urates on the renal papillae. Watery colonic contents, often with undigested milk curd, usually have an acid pH. Microscopic alterations include a marked villous atrophy, perhaps with squamous metaplasia of epithelium, and elongation of crypts in scattered areas of the jejunum and ileum.
In acute outbreaks involving young piglets, a tentative diagnosis often can be made on the basis of the explosive nature of a diarrheal disease accompanied by frequent vomiting and high mortality. The outbreaks often involve all ages of swine but high mortality is confined to small piglets. Lesions, including villous atrophy, also are helpful in diagnosis but not specific. Atrophic villi sometimes can be seen with a hand lens or dissecting microscope.
A specific laboratory diagnosis often can be made using a fluorescent antibody technique applied to fresh sections or scrapings of the jejunum or by immunohistochemistry on formalin-fixed sections. Confirmation of diagnosis requires samples be taken from euthanized pigs in the early stage of the disease. Polymerase chain reaction (PCR), when available, can be performed on feces from acutely affected pigs. This test is particularly valuable in postweaning pigs where fewer viruses are present, lesions are less severe, and disease is further advanced before clinical diarrhea is evident. Virus isolation in tissue culture followed by identification is possible but rarely done. Diseases that must be differentiated include colibacillosis, rotaviral or Strongyloides infection, coccidiosis and, where the disease occurs, porcine epidemic diarrhea.
Preventive measures for negative herds include maintaining a closed herd and implementing strict biosecurity practices. Necessary additions should be from herds that have no recent history of TGE. Additions should be serologically negative before and after a quarantine period of 30 days. The all in/all out system of production with cleaning and disinfection between farrowings is helpful.
An owner may wish to eradicate TGE and maintain a negative herd after infection has occurred. This can sometimes be accomplished by whole-herd exposure to virus and allowing no introductions into the herd for a 60-day period. Alternatively, depopulation during a hot month should be accompanied by thorough cleaning and disinfection. Then, after allowing the facilities to be free of swine for several weeks, restocking with serologically negative stock may be effective.
Attenuated and killed virus vaccines are available. Vaccines usually are used to stimulate immunity in the dams although some also can be given to neonatal piglets. Vaccines are usually administered to dams at intervals prior to farrowing. All the vaccines currently available are most effective when used to stimulate an anamnestic response in previously exposed swine but are generally unable to protect a naïve population in the face of an acute exposure.
In acute outbreaks, pregnant sows and gilts that are two or more weeks from farrowing can be induced to form their own antibodies to TGE to protect their litter by purposefully infecting them with feces or piglet intestinal homogenates from the farrowing house. Antibodies in their colostrum and milk will then provide protection for the most critical time for their piglets. When possible, dams less than two weeks from farrowing should be farrowed separately in isolation.
Endemic TGE may follow an acute outbreak, particularly in larger herds where the whole herd is not simultaneously infected. The virus continues to infect susceptible animals (herd introductions and neonates), persists, and is often is difficult to prevent or eradicate. This form often occurs on premises where there are frequent farrowings or additions. On those premises it may be better to ensure exposure of all swine, especially breeding stock and replacements. Protocols exist for control and/or eradication of TGE in these endemic situations. Basically, all breeding swine should be exposed until they have shown signs of TGE. This can be done by feedback of minced intestine or contents from infected piglets on the premise. Those that do not show signs may have to be individually dosed orally. Vaccination can be an aid in sustaining immunity. All measures are more likely to succeed if a strict all in/all out system is practiced with thorough cleaning and disinfection of facilities between batches of pigs.
Piglets less than three weeks old with TGE seldom respond to treatment. Interventions include weaning, oral electrolytes, and a warm environment. Older swine usually recover spontaneously. Piglets at least one month old before onset usually recover if provided with a nutritious starter feed, warm housing and good care. Antibiotics added to feed or water might be of value in preventing secondary bacterial infections.