The effect of aspirin on bovine platelet function and thromboxane A2 (TXA2) production in stimulated platelets was evaluated. A single dose of aspirin (100 mg/kg of body weight) was administered orally to Holstein cows, and blood samples were obtained before and at regular intervals for 7 days after treatment. The production of TXA2 was assessed by measuring the stable metabolite thromboxane B2, using a specific radioimmunoassay. Within 4 hours of aspirin administration, the production of TXA2 was significantly (P less than 0.05) decreased, irrespective of whether collagen, adenosine diphosphate, or platelet activating factor was used to initiate platelet aggregation. Despite the inhibition of TXA2 release from the stimulated platelets, platelet function, assessed by initial rate of aggregate formation and extent of aggregation, was unaffected by aspirin administration. The extent of aggregate formation in response to collagen, adenosine diphosphate, or platelet activating factor was independent of the amount of TXA2 released from platelets before and after aspirin treatment. The results suggested that TXA2 formation is not the primary biochemical pathway involved in the aggregation of stimulated bovine platelets.

Immunodeficiency in neonatal and young pigs was studied in terms of T-cell function. Generalized T-cell deficiency did not exist in young pigs on the basis of the in vitro response of blood mononuclear cells to a polyclonal T-cell mitogen, phytohemmagglutinin. However, immunodeficiency that extended from birth up to 4 weeks, was observed in serum antibody concentration and in vitro proliferative responses of blood mononuclear cells from young pigs exposed to a low antigen dose of a T-cell dependent antigen, egg white lysozyme. The low in vitro proliferative response to lysozyme was not attributable simply to a lack of interleukin-2 production, because supplementation with human interleukin-2 did not enhance the in vitro cellular response. Also, pokeweed mitogen-stimulated B cells from young pigs up to the age of 5 to 6 weeks produced immunoglobulin concentration, which also was not affected by the addition of human interleukin-2 to the in vitro cultures. The blood mononuclear cells obtained from pigs within the first 5 to 6 weeks after birth and incubated with monoclonal antibodies reactive to all T cells (MSA4), helper T cells (74-12-4) or suppressor/cytotoxic T cells (76-2-11) did not yield consistent excess of suppressor/cytotoxic T cells. This observed immunodeficiency cannot be attributed to a simple lack of functional T cells or to an excessive number of suppressor/cytotoxic T cells, but may be a property of the ability of specific T-cell clones to respond t o low concentration of T cell-dependent antigens or may be attributable to the induction of a suppressor T-cell population in response to in vitro stimulation with the polyclonal T-cell-dependent pokeweed mitogen system.

The uptake of colostral IgG and IgM, their serum half-lives, and the rates of endogenous synthesis of IgG and IgM were evaluated in 6 newborn foals fed bovine colostrum (principals) and 6 foals allowed to suckle their dams (controls). The principal foals were fed 400 ml of bovine colostrum (IgG, 10,000 mg/dl and IgM, 200 mg/dl) at 2-hour intervals, from 2 to 20 hours after foaling (total dose, 4 L). Serum IgG and IgM concentrations were determined by single radial immunodiffusion from birth to 98 days of age. At foaling, principal foals had no detectable serum equine IgG, but 1 control foal had serum equine IgG of 185 mg/dl. AFter ingestion of colostrum, there was no significant difference in the maximal serum bovine IgG concentration (range, 1,350 to 3,300 mg/dl) in the principal foals, and maximal serum equine IgG concentration (range, 500 to 6,000 mg/dl). The calculated biological bovine and equine IgG half-life in the principal and control groups was 9.4 and 26 days, respectively. Endogenous IgG synthesis was first detected in 1 principal foal at 3 days of age, but was detected first between 28 and 42 days in the other principal foals. Starting on day 56 there was no significant difference in serum equine IgG concentration between groups. At foaling, foals in both groups had low equine IgM concentrations. In the control foals, there was marked individual variation in the increases in equine IgM concentration (range, 5 to 73 mg/dl) after ingestion of colostrum. With the exception of day 49 after foaling, there was no statistical difference between groups for serum IgM concentration after day 3, and both groups had parallel rates of IgM synthesis. Bovine IgM was undetectable at foaling and maximal serum concentration ranged from 200 to 350 mg/dl following ingestion of colostrum. The calculated bovine and equine IgM half-lives were 8 and 5 days, respectively. The coefficients of absorption of bovine IgG and IgM were 30.9 and 84, respectively, in the principal foals. In the control foals, the coefficient of absorption of equine IgG and IgM was 35 and 30, respectively. One principal foal was excluded from the study because it died of aspiration pneumonia at 2 days of age.

Influence of supplemental Se on humoral immune response was measured in 60 weaned beef calves with marginal blood Se status. Calves were fed a Se-deficient diet consisting of corn silage, corn grain, and soybean meal. Blood Se concentrations, primary and secondary humoral immune responses to hen egg lysozyme inoculation, and weight gain were determined in a 70-day trial. Calves fed 20 mg of Se/kg of mineral mixture ad libitum had lower antibody responses (P less than 0.02), compared with calves fed 20 mg of Se/kg of mineral mixture and given 0.1 mg of Se and 0.22 IU of vitamin E/kg of body weight, IM, or with calves fed 80, 120, 160, or 200 mg of Se/kg of mineral mixture. Calves fed 80, 120, 160, or 200 mg of Se/kg of mineral mixture had higher (P less than 0.001) blood Se concentrations on day 70, compared with calves fed 20 mg of Se/kg of mineral mixture and given 0.1 mg of Se and 0.22 IU of vitamin E/kg of body weight, IM. Selenium supplementation had no effect on weight gain.

A study was conducted to establish baseline data on Brucella abortus infection induced in 5 strains of mice (CBA/NJ, BALB/c, CD-1, C3H/HeN, and C3H/HeJ). The strains were compared on the basis of immunologic, histopathologic, and bacteriologic responses. There were 4 treatment groups for each strain of mice: (1) vaccinated with homologous lipopolysaccharide and challenge exposed to B abortus strain 2308; (2) not vaccinated but challenge exposed; (3) vaccinated but not challenge exposed; and (4) not vaccinated and not challenge exposed. Results indicated that mice can be used for comparative studies on the pathogenesis and immunogenesis of B abortus infections; strains of mice may vary in their responses to Brucella infection, regardless of their vaccination status. Bacteriologic and immunologic responses in mouse strains BALB/c, CD-1, C3H/HeN, and C3H/HeJ, but not those of CBA/NJ, were extrapolative among strains.

Results of a double agar gel immunodiffusion (Ouchterlony) test that contained a polysaccharide (poly-B) antigen of Brucella melitensis strain B115 were compared with those of 5 other serotests. To determine the sensitivity and specificity of the immunodiffusion, standard tube, 2-mercaptoethanol, Rivanol, card, and complement fixation tests, sera obtained from 1,328 vaccinated, infected and seronegative cattle, 56 of which had been examined bacteriologically, were used to evaluate the humoral response to Brucella sp. The poly-B antigen confirmed infection in 87.5% of the 56 cattle from which Brucella abortus biotype 1 had been isolated, and in 96.6% (205/212) of a group of cattle suspected to be infected on the basis of results of conventional serotests. Likewise, sera from 4 groups of vaccinated cattle did not react with poly-B antigen, whereas they did not react in conventional tests. The poly-B antigen was more specific in detecting infected cattle even in a group of vaccinated adults. A useful strategy to identify infected cattle might be screening, using a combination of the Rivanol and card tests together with the agar-gel immunodiffusion test containing poly-B antigen.

Purified O chain of Brucella abortus was passively attached to polystyrene to differentiate antibody responses of cattle vaccinated with B abortus strain 19 from those of naturally infected cattle. In the indirect assay, using O polysaccharide as antigen, a single serum dilution was used and mouse monoclonal antibody to bovine L chain conjugated with horseradish peroxidase was the detection reagent. Measurable antibody was not found in sera of vaccinated cattle, except for 3 sera from cattle that were persistently infected with strain 19. Sera from 25 cattle infected with pathogenic strains contained antibody on the basis of results of indirect enzyme immunoassay, using smooth lipopolysaccharide or O chain as antigens, or results of competitive enzyme immunoassay, using the O-chain antigen. Results in sera from calves with experimentally induced Yersinia enterocolitica serotype 0:9 infection or inoculated with a low dose of B abortus strain 2308 were comparable with those in sera of cattle that were vaccinated with strain 19. The data correlated with those from competitive enzyme immunoassay, using one serum dilution and horseradish peroxidase-conjugated mouse monoclonal antibody to smooth lipopolysaccharide. On the basis of results of the indirect enzyme immunoassay, all sera (except those samples obtained before inoculation) contained antibody to smooth lipopolysaccharide.

Chicken eggs at embryonation day (ED) 18 or newly hatched chicks were inoculated with turkey herpesvirus (HVT), Marek's disease virus (MDV), or virus-free diluent and, at intervals after inoculation, tissue homogenates of virus-exposed and virus-free chickens or chicken embryos were examined for interferon (IFN) activity. Homogenates of lung thymus and spleen specimens from chickens given HVT at ED 18 had IFN activity. Activity of IFN in the lungs was studied further. Homogenates of lung specimens from chickens exposed to HVT at hatching also had IFN activity, although the concentration of IFN was lower than that in chickens given HVT at ED 18. The pathogenic isolates of MDV (JM-(MDV)), but not the atenuated (Md11/75C-(MDV)) or nonpathogenic (SB1-(MDV)) isolates, inoculates at ED 18 also induced high lung IFN activity. Exposure to a combination of HVT and SB1-MDV induced IFN activity comparable with that in chickens given HVT alone. The IFN activity in homogenates of lung specimens from virus-exposed chickens was species specific and heat and pH stable, but was destroyed by trypsin treatment. Occassionally, low IFN activity also was detected in homogenates of tissus specimens from virus-free chickens or chicken embryos. This IFN activity could have been produced constitutively or may have been induced by substances (inducers) in the environment.

Animals recovered from viral diseases represent an important model to study the host cellular and humoral immune responses to the etiologic agents. This is particularly important for African swine fever virus (ASFV) infections in which antibodies have little or no virus-neutralizing effect. Pigs surviving experimental infection with the naturally occurring low-virulent, nonhemadsorbing ASFV/NH/P68 (NHV) isolate did, however, exhibit virus-specific T-cell activities, as measured by a variety of assays. A strong virus-induced, antigen-specific blastogenic response was observed only with blood mononuclear cells (BMC) from ASF-recovered swine, whereas cells from recovered and naive swine responded similarly to the mitogens concanavalin A and phytohemagglutinin. The ASFV-induced blastogenesis was dependent on virus dose and on the presence of adherent cells. Blood mononuclear cells cultured with antigenically related hemadsorbing ASFV isolates of different virulence characteristics, the highly virulent L60 isolate and moderately virulent DRII isolate, exhibited a similar magnitude of blastogenesis to cells infected with the low-virulent NHV isolate. Virus-infected cells proved to be an efficient inducer of interleukin-2 (IL-2) activity to cells from recovered swine, but not from naive swine, whereas T-cell-specific lectins induced production of similar amounts of IL-2 activity from cells of naive and recovered swine. Correlated with the appearance of virus-induced IL-2 activity in the culture supernatant was the induction of promiscuous killing in cells exposed to prolonged (7 days) virus stimulation. This lymphokine-activated killing could be induced experimentally early in the virus stimulatory process (3 days) by the addition of exogenous lymphokines to the cultures. It was concluded that swine inoculated with low-virulent ASFV isolates are a useful model for identifying and characterizing ASFV immune mechanisms in vitro. Furthermore, this ASFV model implicates lymphokines as inducers of nonspecific cell-mediated immunity; in fact, lymphokine-activated killer type responses may contribute to recovery from this viral infection. More important, ASFV-specific blastogenic and cytotoxic T-cells are prime candidates for the cells inducing and/or conferring protective immunity against challenge ASFV infection.

The ability of pseudorabies virus (PRV) to infect and establish latency in pigs with passively acquired (maternal) antibody for PRV was tested by exposing such pigs to the virus and subsequently attempting to reactivate latent virus by administering large doses of dexamethasone. Pigs of each of 4 litters that had nursed gilts with relatively high (512, gilts 1 and 2), moderate (32, gilt 3), and no (less than 2, gilt 4) serum titers of virus-neutralizing (VN) antibodies for PRV were allotted to 3 treatment groups (A, B, C) when they were 2 weeks old. Group-A pigs were separated from littermates and dam and thereafter kept in isolation; group-B pigs were experimentally exposed oronasally to PRV and 1 hour later returned to their dam; group-C pigs were kept with their dam and potentially exposed to PRV by contact with littermates of group B. Sera obtained from pigs at selected intervals until they were 17 weeks old were tested for VN activity and for precipitating activity for radiolabeled viral proteins. All group-A pigs remained clinically normal throughout the experiment. Depending on the initial amount of passively acquired antibody, little or no serum VN or precipitating activity remained by the time these pigs were 17 weeks old. Group-B and -C pigs, with relatively high amounts of passively acquired antibody when exposed to PRV, also remained clinically normal. However, most became latently infected as subsequently evidenced by either dexamethasone-induced or noninduced virus reactivation. Noninduced reactivation may have been initiated by weaning the pigs when they were about 8 weeks old. Group-B and -C pigs with no or moderate amounts of passively acquired antibody when exposed to PRV, had severe clinical signs. These pigs either died or recovered but remained stunted in growth. Virus was reactivated in all of the recovered pigs by treatment with dexamethasone. Quantitative and qualitative changes in serum precipitating activity, especially for viral proteins of relatively low molecular weight (less than 46,000), were a more consistent indication of virus reactivation than were either increased VN titers or virus isolation. Results with litters 1 and 2 clearly indicate that latent infection of young pigs with highly virulent PRV can develop in the absence of clinical signs.