An avirulent live Salmonella choleraesuis culture (SC-54) was evaluated for use as an effective vaccine in preventing salmonellosis caused by S choleraesuis in pigs. Eighty-two pigs, 3 to 4 weeks old, were randomly assigned to 1 of 2 treatment groups, which were designated as either vaccinates or controls. After vaccination, all pigs were examined for fecal shedding of S choleraesuis, rectal temperature, and 10 clinical variables. Significant difference was not detected between vaccinated and nonvaccinated pigs for 14 days (phase I) after intranasal administration of the vaccine. Efficacy and duration of immunity were examined by intranasally challenge exposing respective pigs from either treatment group with a virulent field isolate of S choleraesuis at 2, 8, or 20 weeks after vaccination (phases II-IV). Pigs were again evaluated for 14 days after challenge exposure, and 10 clinical variables and rectal temperature were monitored. Surviving pigs were euthanatized and evaluated for gross lesions, and samples of 7 organs were collected. These organ samples were homogenized, and level of S choleraesuis infection was determined. After virulent challenge exposure during phases II-IV, the clinical status of the SC-54 vaccinates was significantly (P < 0.05) superior to that of nonvaccinates for rectal temperature, feces consistency, behavior, appetite, body condition, and mean score for the 10 clinical variables. Quantitative bacteriologic culture of the tonsil, lung, liver, spleen, mesenteric lymph nodes, ileum, and colon samples indicated consistent reduction of organ colonization in vaccinates; bacteria numbers in the mesenteric lymph nodes, lungs, and ileum were significantly (P < 0.05) reduced. Gross lesions in pigs indicated reduction of pneumonia in vaccinates. Pigs also had consistent weight gain throughout all phases of the study after challenge exposure, although the differences were not significant. In conclusion, a single intranasally administered dose of SC-54 given to 3- to 4-week-old pigs proved to be safe and efficacious and to provide protection to pigs at least 20 weeks after initial vaccination.

Persistence of the vaccine RH strain of Toxoplasma gondii was studied by bioassay and histologically in 14 pigs. Pigs were euthanatized 2, 4, 7, 8, 14, 15, 21, 29, 36, 42, 52, 57, and 76 days after IM inoculation with 100,000 T gondii tachyzoites. Viable T gondii tachyzoites derived from the RH strain were isolated by bioassay in mice inoculated with tissues of pigs euthanatized up to 14 days after vaccination. Except for fever, pigs vaccinated IM with the RH strain remained clinically normal. Two other pigs inoculated IV with 100,000 T gondii tachyzoites of the RH strain became ill, and 1 pig was comatose by 4 days after inoculation. These findings indicate that route of inoculation may influence the response of pigs to T gondii. To evaluate protective immunity in pigs vaccinated with the RH strain, 16 age-matched pigs were allotted to 4 groups (A-D) of 4 pigs each. Eight pigs (groups A and C) were vaccinated IM with 100,000 RH strain tachyzoites and 8 pigs (groups B and D) were nonvaccinated controls. Pigs of groups A and C were challenge-inoculated orally with a lethal dose of T gondii oocysts (100,000 oocysts) 81 days after vaccination, pigs of groups B and D were inoculated similarly 220 days after vaccination. The concentration of T gondii at 3 days after challenge inoculation of pigs vaccinated 81 days earlier was reduced 100,000-fold in mesenteric lymph nodes, compared with that in a nonvaccinated pig euthanatized at 3 days after challenge inoculation. Another nonvaccinated pig became comatose and had to be euthanatized at 7 days after challenge inoculation, numerous tachyzoites were in its mesenteric lymph nodes, intestines, and liver. The vaccinated pigs generally remained clinically after challenge inoculation with oocysts. Toxoplasma gondii was not isolated by bioassays from tissues of 5 of 8 vaccinated pigs, but was recovered from all nonvaccinated pigs. Results indicate that protective immunity persisted in pigs for at least 7 months after vaccination with the nonpersistent RH strain of T gondii.

Effect of estrogen (E2) and progesterone (P4) on uterine antibacterial activity and immunoglobulin concentrations in mares was studied. In 2 in vitro experiments, 6 mixed-breed mares were ovariectomized, and uterine fluid and blood serum were analyzed. Antibacterial assay methods were used to determine inhibitory effects on Streptococcus zooepidemicus of uterine fluid samples collected on days 3, 5, and 8, and serum obtained on day 8 of treatment. Single radial immunodiffusion methods were used to quantify amounts of IgA and IgG in uterine fluid and serum on days 3, 5, 8, and 14 of treatment. Neither E2 nor P4 increased activity of serum and uterine fluid against S zooepidemicus. Numbers of colony-forming units per milliliter of bacteria were significantly (P < 0.01) lower in control Hanks' balanced salt solution with 1.0% gelatin (HBSSG) than in uterine fluids. Bacterial numbers were significantly (50%) greater in uterine fluids and serum than in HBSSG controls for both treatments. Both fluids, especially serum, supported significantly (P < 0.01) more growth of S zooepidemicus than did HBSSG when incubated for 0, 2, and 4 hours. These findings are in contrast to previous reports of antibacterial activity in the uterus of sexually intact mares undergoing an estrous cycle: great reduction of bacterial count in uterine fluid from mares in diestrus, and significant increases in bacterial numbers in uterine fluid or serum from mares in estrus. Treatment comparisons between serum and uterine fluid IgA and IgG concentrations were not significantly different, although overall IgA concentration in the uterus was higher than concentration in serum. The IgG concentration in uterine fluid was higher in P4- than E2-treated mares. However, IgG concentration was significantly (P < 0.01) higher in uterine fluid on day 8 in P4-treated mares than on day 3 or 5. Results of this study indicate that neither immunoglobulin concentration nor hormone treatment has a direct effect on streptocidal activity.

Cell-mediated immunity was evaluated in intestinal, respiratory, and systemic lymphoid tissues of pigs exposed when 11 days old to virulent transmissible gastroenteritis virus (TGEV), attenuated TGEV, or porcine respiratory coronavirus (PRCV), 3 antigenically related porcine coronaviruses with distinct enteric and respiratory tissue tropisms. Mononuclear cells were prepared from mesenteric lymph nodes (MLN), bronchial lymph nodes (BLN), and spleens of pigs and tested for virus-specific responses by use of lymphocyte proliferation assays. Vigorous MLN and BLN proliferation responses to virulent TGEV and PRCV, respectively, at postinoculation days 8 to 24 were strongly associated with prior detection of TGEV in rectal swab samples and PRCV in nasal swab samples. Gastrointestinal disease and intestinal virus replication, assessed on the basis of rectal virus shedding, were almost exclusively found in the virulent TGEV-inoculated pigs, even though virulent TGEV and a high dose of attenuated TGEV elicited the highest proliferation responses in MLN. Pigs exposed to PRCV or attenuated TGEV did not have clinical signs of disease, and only 1 pig given a high dose of attenuated TGEV shed virus in feces. Porcine respiratory coronavirus replicated in the respiratory tract after either oronasal or aerosol inoculation of virus and induced strong BLN, but not MLN, proliferation responses. A high dose of attenuated TGEV (4 X 10(8) plaque-forming units) was more effective than a lower dose of attenuated TGEV (7 X 10(6) plaque-forming units) in eliciting significant lymphocyte proliferation in MLN and BLN. Cellular immune function, assessed on the basis of mitogen-induced proliferation of lymphocytes, was comparable for all 3 sources of lymphocytes and was not adversely affected by exposure to any of the pigs. The tissue tropism of TGEV and PRCV was associated with induction of virus-specific cell-mediated immune responses, as evidenced by substantial lymphocyte proliferation responses in MLN and BLN, mucosa-associated lymph nodes adjacent to the primary sites of virus replication. The failure of PRCV strain ISU-1 to replicate in the intestinal tract correlated with poor virus-specific cellular immune responses in MLN.

Chemotactic locomotion and luminol-dependent chemiluminescence of neutrophils, mitogen-induced lymphocyte blastogenesis, serum cortisol concentration, immunoglobulin quantification, and leukocyte counts were determined to evaluate the effect of a single strenuous exercise in horses. Increased serum cortisol concentration (P < 0.01) and an increased neutrophil-to-lymphocyte ratio P < 0.05) indicated that horses had been stressed. The chemotactic index and peak chemiluminescence production decreased significantly (P < 0.05 and P < 0.01, respectively) 1 day after exercise. Mitogen-induced blastogenesis of lymphocytes and serum immunoglobulin values remained unchanged in response to exercise. Results of this study indicated that a single bout of exercise may transiently impair neutrophil antimicrobial functions and nonspecific defense mechanisms, but not specific immunity in horses.

The relative sensitivity of bovine blood monocytes and macrophages isolated from milk to lipopolysaccharide, with respect to interleukin 1 (IL-1) production, was evaluated. Addition of lipopolysaccharide (0 to 30 microgram/ml) to theculture medium resulted in increases in secreted and intra-cellular IL-1 activity for monocytes and milk macrophages, with maximal stimulation achieved at 30 microgram oflipopolysaccharide/ml of medium. At this concentration of lipopolysaccharide, monocytes released 76% of the total IL-1, whereas milk macrophages released only 26% of the total IL-1 produced within the cell. Secretion of a small quantity of IL-1 was a common property of macrophages isolated from healthy and mastitic quarters. We concluded that limited secretion of IL-1 may render the milk macrophages less efficient in promoting lymphocyte activation.

To assess the effect of ivermectin on immune function (antibody production), male CD-1 mice were inoculated with an antigen the day after SC administration of ivermectin (0.2 mg/kg of body weight or 20 mg/kg). Responses were evaluated 5 days after inoculation of the antigen. Antibody production against sheep RBC, a T lymphocyte-, macrophage-dependent response, was enhanced by ivermectin treatment (P = 0.00049). In contrast, antibody production against dinitrophenyl-Ficoll, a T lymphocyte-independent, macrophage-dependent response, was not altered by ivermectin treatment. Results indicate that the immunostimulatory properties of ivermectin are associated with altered function of T lymphocytes, in particular, T-helper lymphocytes. The immunomodulating effects of ivermectin may provide an alternative approach for treatment of disease problems involving immunosuppression.

Ten colostrum-deprived calves were assigned to 1 of 2 treatment groups (5 calves/group), and fed colostrum that had either low (naturally infected cows) or high (immunized cows) antibody titers to bovine coronavirus (BCV). All calves were inoculated orally and intranasally with virulent BCV when they were 24 to 48 hours old and challenge exposed 21 days later. Blood, feces, nasal secretions, tears, saliva, and bronchoalveolar lavage (BAL) fluids were collected weekly from each calf for 5 weeks after inoculation. The titers to whole BCV or the relative amounts of isotype-specific antibodies to BCV structural proteins were evaluated in these samples by ELISA or immunoblotting, respectively. Both pools of colostrum contained primarily IgG1, IgG2, and IgA antibodies to the E2 and E3 BCV proteins. Calves fed the high-titer colostrum had correspondingly higher amounts of passive IgG1 and IgA antibodies to whole BCV and to the E2 and E3 BCV proteins in serum, feces, and BAL fluid at postinoculation week 1 than those calves fed low-titer colostrum. Active IgG1, IgA and IgM antibody responses in serum and active IgA and IgM antibody responses in most mucosal secretions to whole BCV and to the E2 and E3 proteins were lower or delayed in calves fed high-titer colostrum, compared with responses in calves fed low-titer colostrum. In contrast, increased responses to the BCV N protein were observed in all samples (except in serum and BAL fluid) in the calves fed high-titer colostrum, compared with calves fed low-titer colostrum. Upon challenge exposure, responses to E2 and E3 BCV proteins in serum and BAL fluid were lower in the group fed high-titer colostrum, compared with those in the group fed low-titer colostrum. Our findings indicate that the level of passive immunity in calves at the time of BCV inoculation can influence the development of active antibody responses in serum, feces, and mucosal secretions to whole BCV and to some BCV proteins individually.

T-cell-mediated and humoral immune responses were measured in chickens infected with standard and variant strains of infectious bursal disease virus. One-day-old and 3-week-old chickens were infected with these viruses and then given sheep RBC, killed Brucella abortus strain 19, and Newcastle disease virus. Appropriate serologic tests were used to monitor the primary and secondary responses to the antigens. Lymphoblast transformation assays were performed weekly. The response to the infectious bursal disease virus was determined by virus neutralization tests, microscopic examination of bursas, and bursal to body weight ratios. One-day-old chickens had T-cell-mediated and humoral immune suppression with both strains of virus, compared with controls. The lymphoblast transformation responses indicated that the variant strain was significantly (P < 0.05) more suppressive than the standard strain. Three-week-old chickens had humoral immune suppression with the standard strain, but not with the variant strain. The lymphoblast transformation response was transiently suppressed at this age by the variant strain only. During the first week of infection, 1-day-old and 3-week-old chickens had lower neutralizing antibody titers to the variant strain than to the standard strain.

Cows naturally infected with Brucella abortus developed antibody (Ab) responses to a nonlipopolysaccharide antigen (NLA) purified from B abortus strain 1119-3. Sera from strain 19-vaccinated cows did not have detectable amounts of Ab. Weak lymphoproliferative responses to NLA were observed in blood mononuclear cell suspensions obtained from infected cows. There was no evidence of NLA-specific lymphoproliferation in cell suspensions from healthy cows. Nonlipopolysaccharide antigen binding to bovine blood mononuclear cells was observed by antigen-consumption assays and direct binding of radiolabeled antigen. Cells from infected cows bound less NLA than did cells from healthy cows when assays were conducted with intact blood mononuclear cell preparations (monocytes plus lymphocytes). Monocytes obtained from any group did not bind NLA. Purified B lymphocytes from infected and healthy vaccinated cows bound about 3 times more NLA than did T lymphocytes, but there were no apparent differences between the 2 groups in extent of binding. Results of the study indicate that bovine lymphocytes have binding sites for a NLA purified from B abortus strain 1119-3.