The lesions of rotavirus infection in 1- and 10-day-old gnotobiotic calves.

Age-related resistance to rotavirus disease has been described with some rotaviruses. In the present study, we investigated age-related resistance to rotavirus disease by defining extent of intestinal infection, virus replication, and severity of intestinal lesions in groups of three 1- and 10-day-old gnotobiotic calves of mixed breed inoculated orally with a cloned bovine rotavirus of low virulence for calves (strain C3-160) and in two groups of three uninoculated control calves of mixed breed. One-day-old calves inoculated with rotavirus developed diarrhea 26 hours after inoculation, and their feces contained 10(8.5)-10(9.2) TCID50/g feces; inoculated 10-day-old calves did not develop diarrhea, virus excretion commenced on the second or third day after inoculation, and peak concentrations of virus in feces were 10(5.7)-10(7.9) TCID50/g feces. Calves were euthanatized within 8-30 hours after the attainment of peak virus shedding while they were still shedding virus at peak levels. The mean percentage of small intestinal epithelium that was immunostained for rotavirus was three times greater in 1-day-old calves than in 10-day-old calves, and the large intestine was infected more extensively in 1-day-old calves. Immunostaining for rotavirus was maximal in the mid small intestine. Staining of mucin was substantially less in the epithelium of the small intestines and colon of rotavirus-inoculated 1-day-old calves than in age-matched controls. The mean height of villi was reduced to approximately half that of controls in the mid and distal small intestine of rotavirus-inoculated 1-day-old calves and was unchanged in 10-day-old calves. Mean crypt cell production rates were greater than that in controls in both groups of rotavirus-inoculated calves, indicating increased enterocyte loss. Age-related resistance to disease was not due to an inability of rotavirus to infect and replicate in enterocytes with lethal effects but appeared to be associated with a slowing of the pathogenic process, which occurred because insufficient enterocytes became infected and destroyed for lesions to develop.