Colostrum-deprived calves (n = 34) were fed various amounts of colostrum, colostrum substitute, or milk replacer to establish a range in titer of passively acquired viral neutralizing antibody in serum. The calves were then challenge exposed intranasally with a virulent, noncytopathic bovine viral diarrhea virus (BVDV-890). After viral challenge exposure, calves were monitored for fever, leukopenia, thrombocytopenia, and diarrhea. In addition, viral isolation and viral titration were performed on specimens of nasal secretions, buffy coat cells, and serum obtained from the calves. Fever and systemic spread of virus were detected in calves that had viral neutralizing titer of 256 or lower. Calves that had viral neutralizing titer lower than 16 developed severe clinical disease manifested by fever, leukopenia, thrombocytopenia, and diarrhea. Seventy and duration of signs of disease decreased as titers of passively acquired viral neutralizing antibody increased. These results indicate that low to intermediate titers of passively acquired viral neutralizing antibody were not sufficient to fully protect calves from virulent bovine viral diarrhea virus.

Passive protection provided by sows inoculated with the virulent Miller strain of transmissible gastroenteritis virus (TGEV), or the ISU-1 strain of porcine respiratory coronavirus (PRCV), or both was evaluated in nursing pigs challenge exposed with virulent TGEV. Four sows (group B) were inoculated with PRCV oronasally twice at 4 and 2 weeks before parturition; 1 sow (group C) was inoculated similarly, but in 2 subsequent pregnancies; and 2 sows (group D) were oronasally primed with PRCV at 4 weeks before parturition, and 2 weeks later were administered a booster inoculation of virulent TGEV. Two additional sows (group E) remained uninoculated and served as seronegative controls, and 1 sow (group A) that had been naturally infected with TGEV served as a seropositive control. The degree of passive immunity transferred by these sows to their litters was assessed by challenge exposing the pigs of sows in groups BE (only the second litter of group C) with virulent TGEV at 3 to 5 days of age. After challenge exposure, clinical signs of infection and mortality were noted and fecal and nasal shedding of virus was assessed by ELISA. The IgA, IgG, and IgM antibody titers to TGEV were quantified in colostrum and milk of the sows by use of an isotype-specific monoclonal antibody-capture ELISA, using biotinylated monoclonal antibodies against each porcine isotype as detecting reagents. A plaque-reduction assay was used to quantify neutralizing antibody titers in serum, colostrum, milk, and fractionated whey (IgG and IgA/IgM). In the sow naturally infected with TGEV (group A), there was a pronounced decrease in IgG antibody titers to TGEV in the transition from colostrum to milk, and IgA TGEV antibodies became predominant, with high titers maintained throughout lactation. The 4 group-B sows partially protected their pigs after TGEV challenge exposure; mean mortality was 67%, compared with 100% in pigs suckling the 2 TGEV seronegative control sows (group-E litters). Although IgA TGEV antibodies were detected in colostrum and milk of group-B sows, IgG TGEV antibodies were the most abundant. The sow of group C had a marked increase in IgA TGEV antibody titers in colostrum and milk after reinoculation with PRCV during the second pregnancy, before TGEV challenge exposure of the litter. Its pigs were passively protected to a high degree after TGEV challenge exposure (27% litter mortality). The sows in group D, primed with PRCV and boosted with TGEV, provided the best passive protection after TGEV challenge exposure of their pigs. Not only litter mortality (27%) but also morbidity was reduced, compared with those factors for the other challenge exposed litters, and the sows did not become ill. In these swine, the high degree of passive protection observed could not be associated with the presence of only IgA TGEV antibodies in the milk, but high IgM TGEV antibody titers also were detected in colostrum and milk. Results of this study suggest that PRCV-inoculated sows are able to partially protect their pigs from TGEV challenge exposure and, on the basis of preliminary data, the degree of protection may increase after multiple PRCV exposures or after secondary exposure to TGEV during pregnancy. Also, an IgA respiratory tract-mammary gland link may exist as evident by the low titer of IgA TGEV antibodies in the milk of PRCV-inoculated sows, but may not be as efficient in inducing lactogenic IgA immunity as is the gastrointestinal tract-mammary gland link.

Icterus condemnations compose a substantial proportion (41%) of total condemnations of bob veal, the class of veal composed of calves < 3 weeks old and weighing up to 68 kg. At postmortem examination, bob veal condemned because of icterus have generalized yellow discoloration of tissues, which is commonly associated with large, yellow liver (fatty liver), and a paucity of other gross pathologic changes. To establish that the generalized yellow discoloration was attributable to high tissue bilirubin concentrations and to examine the underlying mechanism(s) that might be responsible, blood samples and tissue specimens were obtained from clinically normal and icteric bob veal calves at slaughter. For comparison, blood samples were collected from clinically normal, 1- to 5-day-old Holstein calves being raised on local dairy farms. Hematologic and serum biochemical analyses were obtained for the 3 groups of calves (normal local, normal slaughter, and icteric slaughter), and tissues of slaughter calves were examined for histologic evidence of inflammatory or degenerative changes. Mean +/- SD total bilirubin concentration and creatine kinase (CK) activity in icteric bob veal (3.3 +/- 0.8 mg/dl; 869 +/- 788 U/L), normal bob veal (1.4 +/- 0.7 mg/dl; 486 +/- 890 U/L), and normal local calves (0.5 +/- 0.2 mg/dl; 156 +/- 158 U/L) were significantly different. When data for both normal and icteric bob veal calf groups were combined for analysis, total bilirubin concentration regressed significantly on hepatic lipid scores (P = 0.00003) and CK activity (P = 0.00049). Colostrum consumption was determined by measuring serum total protein concentration and serum gamma-glutamyltransferase activity. Bob veal calves that had not consumed colostrum had significantly higher total bilirubin (P = 0.00005) and CK (P = 0.0008) values. It was concluded that normal and icteric bob veal calves have significant increase in total bilirubin concentration, and icterus of bob veal calves is secondary to unconjugated hyperbilirubinemia. Lack of colostrum consumption was strongly correlated with icterus in bob veal calves.

Mycobacterial culture was performed on colostrum, milk, and feces from 126 clinically normal cows of a single herd with high prevalence of Mycobacterium paratuberculosis infection. Thirty-six (28.6 degrees h) cows were determined to be shedding the organism in the feces. Of the 36 fecal culture-positive cows, M paratuberculosis was isolated from the colostrum of 8 (22.2%) and from the milk of 3 (8.3%). Cows that were heavy fecal shedders were more likely to shed the organism in the colostrum than were light fecal shedders.

Effects of selenium (Se) deficiency and supplementation on production of colostral immunoglobulins by beef cows and transfer of antigen-specific and nonspecific immunoglobulins to their calves were examined. Eighty beef cows, with marginal to deficient Se status (blood Se concentration, 50 micrograms/L), were allotted by breed and age to 1 of 4 Se treatment groups (n = 20/group): no supplemental Se; parenteral administration of 0.1 mg of Se and 1 mg of vitamin E/kg of body weight; ad libitum consumption of 120 mg of Se/kg of salt-mineral mix (SMM); and parenteral administration of 0.1 mg of Se and 1 mg of vitamin E/kg plus ad libitum consumption of 120 mg of Se/kg of SMM. All cows were inoculated IM with lysozyme. Cows consumed Se-deficient pastures or hay (21 to 62 micrograms/kg) during the study that began at mid-gestation and ended at postpartum hour 24. Although the concentration of specific lysozyme antibodies was not affected, cows given 120 mg of Se/kg of SMM (treatments 3 and 4) had higher colostral IgG concentration (P < 0.002) than did Se-deficient cows (treatments 1 and 2). Calves from cows in treatments 3 and 4 had higher postsuckle serum concentrations of IgG (P < 0.01) than did calves from cows in treatments 1 and 2. Colostral IgM and calf serum IgM concentrations did not differ among treatments.