Age affected: Piglets pre-weaning.
Causes: Dietary problems; E. coli; poor hygiene.
Effects: White, grey or brown scour, stunting, death.
Rotavirus infection and coccidiosis are the major causes of pre-weaning diarrhoea. Other agents such as E. coli may be involved as colostral protection wanes or when new strains are encountered and clostridia may colonise intestines damaged by other agents. Transmissible Gastroenteritis (TGE) and Porcine Epidemic Diarrhoea (PED) may also occur. Rotavirus Groups A, B C and E have been found in pigs but Group A is usually the first to infect a piglet and is most common in pre-weaning diarrhoea. Rotaviruses are relatively resistant, survive for 7-9 months at 18-20˚C and are stable between pH 3 and 9. 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. Mature absorptive cells are shed and villous atrophy results. The resulting failure to absorb nutrients leads to diarrhoea containing virus particles. Recovery may be complete within 7 days.
The main mode of transmission is from pig to pig. Clinically–affected piglets shed around 10 million particles of rotavirus per gram of faeces and the infectious dose can be as low as 90 particles. Faeces or material contaminated with faeces (feeders, pen furniture, clothing and tools) can transmit the infection. The ability of the virus to persist for up to 9 months allows it to persist for long periods in the piglet environment. The mode of transmission of the coccidian involved (Cystoisospora suis) and of the piglet pathogenic strains of E. coli which can colonise the gut is similar. TGE and PED are very infectious, but persist in the environment for a much shorter time.
Pre-weaning diarrhoea is white or greyish because of the undigested milk present in the faeces and may occur in most litters from 14 days to 3 weeks or age or until weaning. Not all members of the litter develop diarrhoea. Some remain unaffected and others merely pass perfectly-formed white motions. Affected piglets may be depressed, stop sucking and become reluctant to move. Vomiting may be seen. A few hours later, profuse diarrhoea develops and is white or yellow with floccules floating in a whey-like fluid, but may be grey in colour. Dehydration and rapid loss of condition may occur, but many affected piglets appear relatively normal. Appetite returns after 24-72 hours. Clinical signs regress 4-6 days after infection but loose yellow faeces may persist for 7-14 days and the faeces of sucking pigs may remain whitish for a period after recovery. Thirty-three percent of affected young pigs may die in outbreaks where piglets do not have access to water, but mortality is usually much less and uncommonly exceeds 1 piglet per litter. 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.
Inspection of the pen floor, areas between slats, the vicinity of the drinker or the kerb of an outdoor pen reveals whitish or grey diarrhoea or white faeces. Bedding may make detection more difficult. Inspection of individual piglets may then be necessary. Rotavirus is the commonest cause, but is common in piglets of this age group regardless of the presence of diarrhoea. It can be identified in the faeces by the use of latex agglutination tests, user-friendly strip tests, demonstration of the particles by electron microscopy, confirmation of the presence of the RNA by polyacrilamide gel electrophoresis (which identifies it to group) and by nucleic acid methods such as the polymerase chain reaction (PCR). E. coli and the clostridia can be cultured from faecal samples, but confirmation of the presence of coccidia, TGE and PED may require the post-mortem examination of freshly killed piglets and careful examination of the mucosa.
Post-mortem examination of dead piglets confirms the presence of diarrhoea. Animals are frequently dehydrated. The small intestines are thin walled with villous atrophy and filled with fluid, creamy contents. The large intestinal contents are fluid and creamy or greyish and there may be faecal staining on the perineum. Histological examination of the intestines requires the examination of freshly-killed piglets, preferably in the earliest stages of the disease. The agents concerned may then be identifiable in the intestinal lesions, otherwise, the tests described above will reveal the agents present.
The severity of pre-weaning diarrhoea can be reduced markedly by the provision of piglet drinkers. If ion-replacement fluids can be administered through these drinkers and other husbandry factors such as environmental temperature corrected, mortality from this condition can be reduced further. Specific treatment depends upon the agents present. There is no specific treatment for rotavirus, TGE or PED infection. Coccidiosis can be treated (but is best prevented) and those cases where E. coli and clostridia are important can be treated using oral antimicrobial dosers for 3-5 days. Prevention depends upon early treatment for coccidiosis by and E. coli and clostridial infection by vaccination of the sow, ensuring that colostrum is ingested by the piglet. Vaccines have been produced which can immunise the sow against rotavirus and thus protect piglets by colostral immunity, but they are not available in all pig-keeping countries. Rotavirus, coccidian and E. coli survive in the piglet environment, so infection may arise from environmental contamination. All-in, all-out husbandry should be practised in farrowing and rearing accommodation and should include a disinfection step using hypochlorite on clean surfaces and proprietary disinfectants such as a mixture of surfactant, organic acid, oxidising agents and buffers. Phenolic disinfectants are less effective.