Isolation of picornavirus from feces and semen from an infertile bull.

Virus was isolated from semen and fecal samples from a bull with orchitis, testicular degeneration, aspermatogenesis, and loss of libido. Both isolates were classified as picornavirus, bovine enterovirus serotype I, on the basis of physical, chemical, and serologic characteristics. Veterinary practitioners that may suspect viral infection as a cause of bovine infertility should submit both semen and fecal samples for virus isolation and identification.     

Responses of immune and nonimmune adult rhesus macaques (Macaca mulatta) to adenovirus SV-20.

Adenovirus SV-20 (ASV-20) was inoculated subcutaneously into adult rhesus macaques (Macaca mulatta), and various immunologic parameters were studied. Similar changes were observed in macaques that had anti-ASV-20 serum-neutralizing antibodies prior to inoculation and in those lacking detectable antibodies. There were absolute decreases in numbers of peripheral blood lymphocytes (PBL), erythrocyte-rosetting lymphocytes, complement-receptor lymphocytes, and Fc-receptor lymphocytes. These changes were most significant (P less than 0.05) on postinoculation days (PID) 3 and 7. Mitogenic responsiveness to concanavalin A, phytohemagglutinin, and pokeweed mitogen in cultured PBL from immune and nonimmune macaques was depressed on PID 3, 7, and 14. Ultraviolet-inactivated ASV-20 caused moderate suppression of phytohemagglutinin-induced mitogenesis when viral particles and lectin were added simultaneously to PBL cultures. Plasma cortisol (hydrocortisone) values were not significantly altered following inoculation of ASV-20. High titers of anti-ASV-20 antibody developed by PID 7 in nonimmune macaques, and previously immune macaques showed a booster effect in the same time period. Antibody titers were still increased 120 days after inoculation. There was no clinical evidence of an adverse effect of ASV-20 infection in these macaques.     

Prolactin and colibacillus-induced fluid transport in ligated intestinal segments.

Two experiments, using the ligated intestinal segment technique, were conducted to determine whether the pituitary hormone prolactin (PRL) could reduce Escherichia coli-induced fluid loss into the small intestine of 2- to 3-week-old pigs. Inoculation of 10(6) to 10(8) enteropathogenic E coli organisms into ligated jejunal segments caused a significant accumulation of luminal fluid within 12 hours. In the first experiment, intraluminal inoculation with 0.5 mg of ovine PRL along with the bacteria did not have any effect on fluid accumulation. Systemic IV treatment of the animals with 1.0 mg of ovine PRL at 3-hour intervals, beginning either immediately after or 9 to 10 hours before intestinal ligation, did not significantly (P less than 0.05) reduce fluid accumulation as compared with control animals. In the second experiment, IM administration of 100 microgram of thyrotropin-releasing hormone (TRH) at 3-hour intervals, beginning 6 hours before intestinal ligation, significantly (P less than 0.05) increased circulating PRL concentrations, as measured by radioimmunoassay. However, TRH treatment did not reduce the accumulation of luminal fluid in E coli-inoculated segments.