Age affected: Piglets pre-weaning, weaners, human risk.
Causes: Many strains of rotavirus; poor hygiene.
Effects: Inappetence, diarrhoea, vomiting, stunting.
Rotaviruses are double stranded RNA viruses with the RNA arranged in 11 segments. They have a characteristic wheel shaped appearance and can be classified by their viral proteins and nucleic acids into groups. Groups A, B, C and E have been found in pigs. Group A is usually the first to infect a piglet and is most common in pre-weaning diarrhoea. Rotaviruses are relatively resistant, surviving 60°C for 30 minutes in faeces and 7-9 months at 12-20°C and are stable between pH 3 and 9.
Rotaviruses may be cultured in calf and kidney cells but require exposure to trypsin and agitation for continued subculture. Infection occurs in piglets which have not taken colostrum and when maternal antibody in milk declines from 2 weeks onwards. Infection is oral and the virus replicates in the cells lining the middle small intestine from upper jejunum to lower ileum.
Replication is most intense 24-96 hours after infection but later becomes restricted to villus tips. Mature absorptive cells are shed and villous atrophy, crypt hyperplasia and villous fusion occur. Lactase levels fall but lactose digestion may not be affected. The resulting failure to absorb nutrients leads to diarrhoea containing virus particles. Recovery may be complete within 7 days.
Mode of transmission
Infection is oral, and results from the consumption of feed or water contaminated with rotavirus particles. These may be freshly voided in faeces or persisting in the environment from earlier contamination with infected faeces. As the virus can survive for 6-9 months, carry over of infection from one batch of pigs to another is possible and contaminated implements, clothing and transport may all represent sources of infection.
Transfer of infection from farm to farm is normally by means of infected pigs, either clinically affected or carriers, but can result from the contamination of water, feed and bedding, or transport in contaminated vehicles. Infection may also be transmitted on the feet or in the gut contents of birds.
The incubation period is 18-24 hours after which depression, inappetence and reluctance to move are noted. Vomiting may be seen. A few hours later, profuse diarrhoea develops and, in milk-fed pigs, this is yellow with floccules floating in a whey-like fluid, while in others it may be yellow or dark grey. There is a rapid loss of condition. Inappetence continues for 24-72 hours after which appetite returns. Clinical signs regress 4-6 days after infection but loose yellow faeces may persist for 7-14 days. Thirty-three percent of affected young pigs may die in field outbreaks.
Weaned pigs may also be affected, but in them no diarrhoea or only transient diarrhoea (mean duration 3 days) results when rotavirus is demonstrated in the faeces. The difference in disappearance of immunity means that individuals in a group do not all develop the disease at once and disease may continue for days of weeks in the group. Rotavirus diarrhoea may recur as immunity to one type does not prevent infection with others. The effects on growth rate range from nothing, to at least 5 days to 25 kg.
The ubiquity of rotavirus infection should lead to its consideration as a component of most diarrhoeas of sucking and recently-weaned piglets. There are commercial reversed passive latex agglutination tests (RPLA) and immunochromatic tests for virus which can be used on-farm. Unfortunately, up to 25% of outbreaks of diarrhoea in pigs may contain rotavirus particles and mixed infections are common so that it is up to the clinician to decide the importance of rotavirus in each case. Passive antibody levels persist for 2-7 weeks and active antibody levels increase from 5-8 weeks.
Pathological findings suggesting rotavirus include dehydration in piglets, a stomach filled with milk and a small intestine distended with creamy fluid contents. The villi lining the last three quarters of the small intestine are stunted and are visible using a hand lens or dissecting microscope.
There is no necrosis on the epithelium in uncomplicated rotavirus infections. The presence of rotavirus can be confirmed by the electron microscopical examination of faeces or colon contents for the characteristic particles or by polyacrilamide gel electrophoresis to detect the characteristic double-stranded RNA. These two methods detect all groups of rotavirus. Modifications of the Polymerase Chain Reaction (RT PCR) can detect viral nucleic acid and are widely used in multiplex PCR examinations for common enteric viral infections.
Treatment and prevention
There is no specific treatment. Bacterial and protozoal complications should be controlled. Fluid replacement using glucose:glycine electrolyte solutions may be of value and water should always be available. Growth depression in weaned pigs is reduced if high protein rations are given, but milk protein is better than vegetable protein.
Prevention may be achieved by stimulating maternal immunity by feed-back of faeces from affected piglets at least 14 days prior to farrowing (not legal in many countries) or by vaccinating. Vaccines are currently not available in many countries. Live vaccines given intramuscularly or orally have been described and may contain serotypes A1 and A2 human rotavirus, or viral proteins from serotypes 4 and 5 for protection against both serotypes. Performance may improve from vaccination of the sow 4 and 2 weeks prior to farrowing followed by oral or intramuscular vaccination of piglets at 2 or 4 weeks.
Viral excretion may not be prevented by dead vaccines and transient diarrhoea may occur. Protection against other rotavirus serotypes or groups may be poor. Cow colostrum containing antibodies to bovine rotavirus protects if fed to piglets. Disinfection can be carried out using hypochlorite on clean surfaces and proprietary disinfectants such as a mixture of surfactant, organic acid, oxidising agents and buffers.