Rotaviruses cause diarrhea in nursing and postweaned pigs, affecting primarily the small intestine. If uncomplicated, diarrhea is accompanied by high morbidity and low mortality.
Rotaviruses are ubiquitous in swine populations throughout the world. Rotavirus infections occur in many species, including man. Although rotaviruses are related antigenically, porcine rotaviruses infect only swine.
In 1969, rotaviruses were identified in calves. Subsequently, they were detected in other animals, including swine and humans. Rotaviral infections are important because they are common and reduce productivity.
There are at least 7 antigenically distinct serogroups of rotaviruses (A, B, C, D, E, F, G) of which 4 (A, B, C, E) affect swine. There are also antigenically dissimilar subgroups or serovarieties within groups. Most is known about the more common group A rotaviruses. Group A is by far the most prevalent but type C has been associated with outbreaks. Immunity is not cross-protective between serogroups and is incomplete between serovarieties.
Rotaviruses are very stable in the environment. They are resistant to temperature changes, many chemicals, various pH levels, and many disinfectants. Recommended disinfectants for cleaned surfaces include formaldehyde and chlorine-based disinfectants including chlorox.
It is likely that all large swine herds are infected and rotaviruses circulate constantly in them. Neonatal and susceptible young growing pigs are exposed to virus shed by carriers, including sows, or that is present in their environment. They may develop clinical or subclinical disease but most pigs recover with at least some becoming carriers. The resistance of rotaviruses in the environment assures their survival on swine-raising premises during short periods of depopulation. The possibility of interspecies spread of rotaviruses has not been studied extensively.
Rotaviral infection can occur concurrently with other diarrheal diseases of young pigs, e.g. with transmissible gastroenteritis, colibacillosis, or salmonellosis. Combined infections with other agents cause more severe clinical signs and lead to higher mortality.
The pathogenesis of type A rotaviral infection in pigs is much the same as for transmissible gastroenteritis (TGE). Exposure to virus is fecal-oral. The virus is swallowed and reaches the small intestine. Virus invades intestinal epithelial cells on the tips of the villi and damages or destroys many of them. The result is villous atrophy with fusion of some villi. Villous destruction can be subtle, segmental, or severe but generally is less severe than with TGE.
Destruction of villous epithelium and villous fusion result in impaired intestinal function and reduced disaccharidase activity. Disaccharides accumulate in the intestine. An osmotic movement of fluid into the intestinal lumen, along with malabsorption, leads to diarrhea. Death is an unusual outcome but probably is related to multiple factors including malnutrition, dehydration, imbalance of electrolytes and cardiac failure. The pathogenesis of types B, C and E rotaviral infections are likely similar to that of type A.
The onset and severity of signs depends on dose ingested and amount of protective antibody in the dam’s colostrum and milk. Outbreaks on specific premises often occur repeatedly when the piglets reach an age at which lactogenic immunity is no longer adequate to protect against the degree of exposure.
Diarrhea appears, usually white to yellow in color, and generally continues for a few days until the pigs develop an active immunity. There is moderate dehydration. Vomiting occurs but is not a major clinical sign. Morbidity is variable but mortality usually is low or none when good housing and husbandry is present. Signs, morbidity and mortality are enhanced if there is concurrent disease, poor husbandry or exposure to cold.
Pigs that die are dehydrated and may show fecal staining of the perineal area. The intestinal wall is thin, flaccid and rather transparent. The small intestine and colon contain yellow or gray fluid and debris. Microscopic lesions are largely confined to villi of the terminal jejunum and ileum; the duodenum is not spared as with TGE. Microscopy reveals villous atrophy with some fusion of villi as well as epithelial hyperplasia in crypts.
Necrosis of apical enterocytes is followed by squamous and cuboidal metaplasia as lesions resolve.
History, signs and gross lesions are helpful but not diagnostic. A variety of laboratory techniques are available to establish a firm diagnosis. Electron microscopy can be used to identify virions in the intestinal content or viral particles in affected epithelial cells. Fluorescent antibody technique and immunohistochemistry can demonstrate rotavirus in the epithelial cells. Using light microscopy, the typical lesions of villous atrophy and glandular hyperplasia may be useful in diagnosis. Rotaviral antigens in fresh fecal samples or intestinal fluid sometimes can be detected using an enzyme-linked immunosorbent assay (ELISA) test.
Virus shedding is much greater during early stages of the disease so samples should be obtained from acutely affected pigs.
There are no proven specific therapies for rotaviral infection in young piglets. However, good husbandry and supportive therapy, including electrolytes in drinking water, can be of value. A dry, warm environment and good nutrition are important in reducing severity of outbreaks. Antibiotics are not effective for rotaviral infections but may be indicated for concurrent bacterial diseases.
The all in/all out system with thorough cleaning and disinfection between farrowings and a high standard of sanitation reduces exposure of piglets to rotavirus. A shorter farrowing period is less likely to lead to a build up of rotaviruses in the farrowing house. Similarly, all in/all out population of nurseries will decrease the dose and lessen the effects of rotavirus infections postweaning. Rotavirus as a consistent cause of diarrhea in post-weaned pigs would implicate poor sanitation, and disinfecting between groups of pigs would be warranted. Decreasing dose by scrupulous sanitation is high priority for breaking the cycle of disease.
Both modified live virus and killed rotavirus vaccines are available. Dams can be vaccinated at intervals prior to farrowing to stimulate them to produce antibody in their colostrum and milk. The antibody should protect their piglets until piglets have time to develop their own immunity. Booster vaccinations are given before subsequent farrowings, sometimes after farrowing. Alternatively, some swine raisers intentionally expose their new breeding stock to resident stock, or to their feces, prior to breeding. In this way added stock will develop immunity to indigenous rotaviruses being shed by older stock. Most rotavirus vaccines are combined with vaccines for control of other diarrheal diseases. Most are made to control only type A rotaviral infection.