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Antibody responses in serum and semen, and immunoglobulin containing cell (ICC) populations in the genitalia of bulls were compared after inoculating Brucella abortus strain 19 into the seminal vesicles of two bulls (ISV route) and into testes in two other bulls (IT route). Bulls seroconverted as early as 1 week post-infection (PI). Peak serum titres as determined by the serum agglutination test (SAT), complement fixation test (CFT) and ELISA occurred at PI weeks 3, 4 and 5 respectively. Highest titres were in IT inoculated bulls. Seminal antibodies against B. arbotus S19 were demonstrated from 2 weeks PI by both the SAT and the Rose Bengal Test (RBT) and highest titres occurred at PI weeks 3 and 4. Examination of immunoglobulins (Ig) in semen, however, revealed no significant differences of Ig isotypes between infected and control animals at any examination time. When bulls were killed at 7 weeks PI, quantitation of ICC in genital sections stained by the peroxidase-anti-peroxidase method revealed an overwhelming predominance of IgG containing cells in inflamed organs. In all cases IgG1- and IgG2-containing cells were prevalent, and present in approximately equal numbers. IgA-containing cells were second in prevalence in inflamed tissues while IgM cells were always in low percentage. High prevalence of ICC in infected genitalia, associated with elevated specific seminal antibodies but not with increased seminal Ig indicates that most Ig remains localised in tissues and is not transferred into genital secretions.

Bovine spumavirus (BSV) infection is shown to be endemic in some herds in north Queensland. The virus was readily isolated from leukocytes of the majority of mature cattle which were BSV antibody positive (BSV reactors) in the agar gel precipitin test (AGPT). Calves born to dams which were BSV reactors showed no BSV antibody or circulatory leucocyte-associated BSV (CLAB) at birth, but became BSV reactors following ingestion of colostrum, and maintained such evidence of passive immunity until 3–5 months of age. Experimental infection of dams with BSV at 5–7 months of gestation did not cause foetal infection. In groups of young animals at pasture, segregated by age and sex, no evidence of BSV infection occurred, following loss of passive immunity, until 18–24 months of age. At this time, occasional members of some groups (both male and female) became BSV reactors and showed CLAB. At ≈24 months old, following mixing in groups with older cows, and single-sire mating, 34% of heifers became BSV reactors within 10 weeks. A herd survey indicated 85% of 2–3-year-old cows to be BSV reactors; thereafter, the percentage of reactors declined gradually with increasing age. Using BSV grown in cell culture, transmission of infection by throat spray was the most successful route, 7 of 7 (100%) of susceptible cattle becoming BSV reactors within 8 weeks of spraying. Using the intravenous route, only 2 of 5 (40%) susceptible cattle became BSV reactors, and swabbing of cell culture virus into the prepuce or vagina did not result in infection of 4 BSV-susceptible animals. Virus could not be detected by in vitro or in vivo procedures in throat swabs taken from BSV reactors which were CLAB positive. In discussion, epidemiological data are used to support postulates that the spread of BSV infection is associated with intimate contact between individuals, and that the vehicle of infection is saliva. Only saliva from BSV-infected cattle which have no specific antibody is considered to be infectious. Such animals are either those incubating BSV infection before development of an immune response or, more logically to the authors, animals which are BSV tolerant, possibly owing to in utero infection.