The epidemiology of porcine group A rotavirus was studied in commercial herds of pigs in New Zealand. A commercial enzyme-linked immunosorbent assay (ELISA) kit (Dakopatts, Copenhagen) was found to be highly sensitive (100%) and specific (96.8%) for the detection of group A rotavirus in pig faeces when compared to electron microscopy (EM). A highly sensitive and specific ELISA test for the measurement of antibody against group A rotavirus in pigs was also developed. Of 521 faecal samples collected from Massey University Piggery in a cross-sectional survey, 47 (9%) were positive for group A rotavirus by the ELISA test. Only sucking (19.3%) and weaner (14.4%) pigs were shedding rotavirus. Rotavirus was not detected in the faeces of fattener pigs (over two months old) or adult pigs including sows and boars. Three cohort studies revealed that all pigs became infected with group A rotavirus before they were 40 days of age and shed the virus for an average of eight days. Some of the piglets shed rotavirus a second time approximately 10 days after the first period of shedding. All piglets ceased to shed the virus by two months of age. Rotaviral shedding was associated with the occurrence of milk scours in sucking piglets. Diarrhoea in weaner pigs (post-weaning diarrhoea, PWD) was more closely associated with the presence of haemolytic E.coli than with rotavirus in faeces. Infection with group A rotavirus was transmitted from piglet to piglet and from litter to litter. In one cohort of 50 piglets from five litters, shedding of rotavirus was first detected in one litter, then in the second litter two days later, and finally in other litters of piglets. Over a period of 16 days, all piglets in the five litters were infected. Group A rotavirus was also detected in dust, faeces and effluent collected from the farrowing and weaner houses, and from a weaner house which had not been used for three months. Rotavirus was not detected in any of the sows (11) during the period of investigation. Neither was rotavirus detected in fattener pigs (from two months of age to the time of slaughter), nor in the environments where old pigs (fattener and sow houses) were housed. It was not therefore possible to confirm that adult pigs, especially sows, act as carriers for rotaviral infection of young piglets as has been suggested by other workers. All the piglets acquired maternal antirotaviral antibody from their dams and the levels of antibody in piglets' sera were comparable to those in the colostrum of their dams. The maternally-derived antibody was also detected in piglets' faeces. Antibody in sera and in faeces declined rapidly after birth. Rotaviral shedding commenced in each of the cohorts when the geometric mean ELISA antibody titre fell below 1/1600 (equivalent to serum neutralizing antibody titre of 1/8 to 1/16). However, this correlation between antibody titres and protection was not observed in individual litters. In each of the cohorts studied, rotaviral shedding was usually detected initially in one or two piglets of a litter. The infection then spread to other piglets within the same litter and, finally, to piglets of other litters in the same group. Onset of rotaviral infection in particular litters was related to their location in the farrowing unit rather than to the levels of antibody. The shedding pattern of group A rotavirus was studied further in another five New Zealand piggeries and was found to be similar to that observed at the Massey University Piggery. Faecal samples from these piggeries were analyzed by polyacrylamide gel electrophoresis (PAGE) and no common electrophoretype of group A rotavirus was found in these piggeries. More than one electrophoretype of group A rotavirus was detected in three of these piggeries. Faecal samples collected from Massey University Piggery were also analyzed by PAGE and it was found that rotaviruses detected during the first two years of the present investigation had identical electrophoretypes, but one isolate detected in the third year had a distinctively different pattern. Non-group A rotaviruses were also detected for the first time in New Zealand. Nine samples had an electrophoretic pattern similar to that of group C rotavirus and one was similar to that of group B rotavirus. One of the samples containing group C rotavirus was from two litters of piglets with diarrhoea at two to four days of age. In one of these piggeries, five electrophoretypes of rotaviruses representing three groups were detected. These observations indicate that rotaviral infections are important causes of milk scours in piglets, and are probably significant in exacerbating PWD. The epidemiology of rotaviral infections is complicated by a number of factors. These include the continuous transmission of virus from pig to pig and from litter to litter, the survival of the virus in the piggery environment, the incomplete protection afforded by maternally-derived antibody, and the simultaneous circulation of different strains and different groups of rotavirus in one piggery.
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