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Summary. The infectivity, pathogenicity and immunogenicity of 5 human, 6 calf, 2 pig and 2 foal rotavirus isolates were studied in gnotobiotic calves, piglets and lambs. Three of the human isolates produced subclinical infection in newborn gnotobiotic piglets and the piglets developed neutralising antirotavirus antibody. When challenged with pig rotavirus 2 weeks later, the piglets did not develop diarrhoea, but rotavirus was detected in the faeces. In contrast, piglets inoculated with the other 2 human isolates failed to show evidence of infection and there was no specific antibody detected. These piglets developed diarrhoea when challenged 2 weeks later with pig rotavirus. The 4 human isolates failed to infect gnotobiotic calves and lambs.Two foal rotavirus isolates produced subclinical infection in piglets, but the subsequent protection against a challenge with pig rotavirus lasted less than 15 days. The foal rotavirus isolates failed to infect gnotobiotic calves and lambs.Two ofthe calf rotavirus isolates were extremely pathogenic to newborn pigs. Two other calf isolates infected newborn lambs, one of which developed mild diarrhoea.Ofthe 2 pig rotavirus isolates one induced a subclinical infection in newborn lambs but neither infected calves.These experiments suggest that cross-infection between species is not a property shared by all rotaviruses.

Some aspects of postweaning diarrhoea (PWD) in a piggery during the first week after early weaning were investigated. A haemolytic enterotoxigenic strain of E. coli (O149:K88:H10) was regularly recovered from piglets with PWD while rotavirus was demonstrated on a number of occasions. Prior to weaning piglets were either free of, or shed very few, haemolytic E. coli in their faeces. However, all piglets were excreting haemolytic E. coli between 5 and 7 days after weaning. The role of rotavirus in PWD was unclear. There appeared to be a direct relationship between serum antibodies to rotavirus in the slow at farrowing and those of the piglets soon after birth. The decline of maternal neutralising antibody to rotavirus coincided with the immediate postweaning period (3 to 5 weeks after birth). This was followed by an increase in antibody levels, 5 to 8 weeks after birth. There was no significant difference in the growth rate between affected and unaffected piglets over a period of 120 days. Medication of water during the first week after weaning had no significant effect on the incidence of PWD in the herd. A change in both the weaner diet and the weaning procedure reduced piglet mortality associated with PWD by more than half.

The susceptibility of gnotobiotic, colostrum-derived, or suckling calves to four bovine rotavirus isolates was found to be age dependent. Calves older than 7 days remained clinically normal, although they excreted virus in their feces and subsequently developed antibody against the virus, Enterotoxigenic Escherichia coli, fed to gnotobiotic, colostrum-deprived, or suckling calves ranging in age from a few hours to 26 days old, only caused diarrhea in animals younger than 24 h old. In contrast, diarrhea was consistently induced in 1- and 2-week-old calves infected with both enterotoxigenic E. coli and rotavirus. In general, diarrhea appeared after a rotavirus incubation period of approximately 3 days and was independent of the order in which the two microbial agents were given, the age of the calf, or the level of circulating rotavirus antibodies. The disease episode coincided with the excretion of rotavirus, rather than enterotoxigenic E. coli, in the feces. Infection with enterotoxigenic E. coli became established within 24 h of inoculation, and in older calves enterotoxigenic E. coli was often excreted in very small numbers and for a longer period than rotavirus.

A haemolytic enteropathogenic E. coli (WG) and pig rotavirus were isolated from a field case of postweaning diarrhoea in pigs. Four-week-old gnotobiotic piglets fed on milk diet were found to be extremely susceptible to infection with WG E. coli. Piglets were less susceptible to the infection immediately after the diet was changed from milk to dry food, and were almost completely resistant 4 days after the change to dry food. There was no difference in the clinical response to infection with WG E. coli when the piglets were fed either a high energy diet or low energy diet. Four-week-old piglets fed milk showed mild symptoms of diarrhoea when inoculated with pig rotavirus. Symptoms were more severe when piglets were inoculated immediately after the change from milk to dry food. Piglets inoculated 4 days after the change of diet showed no symptoms of diarrhoea at all. Under the conditions of these experiments the enteropathogenic E. coli produced a more serious disease than did pig rotavirus. Infection of 4-week-old gnotobiotic piglets with both agents given sequentially produced a diarrhoeal disease that was more severe than that produced by each agent separately.