BACKGROUND: Despite the use of prophylactic chemotherapy and vaccination, coccidiosis is still one of the most devastating diseases in poultry industry. Understanding the immune mechanism helps researchers to prevent this parasitic infection more effectively. OBJECTIVES: The purpose of this study was to evaluate the antibody response in chickens, induced by a live attenuated vaccine (Livacox Q), before and after challenge, by means of ELISA. METHODS: One hundred and twenty one-day-old male Ross 308 broiler chicks were randomly divided into 4 groups of 30 birds. In 4th day of age, half the birds were orally vaccinated. The challenged groups received the infective dose at 14th day of age via oral administration. Besides recording weight gain, lesion score and oocyst count in 21st day old birds, humoral immunity was assessed by means of ELISA on serum samples taken from 7 and 21day-old birds. Results: Three days post vaccination, the average of optical density (OD) showed significant difference between vaccinated (0.553) and unvaccinated (0.686) birds (p≤0.05). In 21 day-old birds, the OD of unvaccinated-unchallenged (negative control) groups (0.331) differed significantly with vaccinated-unchallenged (0.663) birds. The average of lesion score in vaccinated-challenged birds (2.22) showed significant dissimilarity with unvaccinated-challenged groups. No difference and correlation were observed in comparing average of weight gain and oocyst count with serum optical density among treatment and control groups. ConclusionS: The results indicated that ELISA can be used for evaluating immunity uniformity of a flock after vaccination. Besides inducing antibody responses comparable to challenge with wild oocysts, vaccination with live attenuated coccidiosis vaccines may have inhibitory effects in intestinal lesion scores which are responsible for pathogenesis and economic loss during coccidial infections.

Immunoglobulin E is produced in response to parasitic nematodes that undergo blood and tissue migrations. Results of our previous studies indicated that IgE and IgG respond to Dirofilaria immitis in experimentally infected dogs. To determine the association between treatment with the larvicide, diethylcarbamazine (DEC), and antibody responses and to examine the potential influence of infection with a nonfilarid intestinal nematode on isotype-specific immune responses, we monitored, by use of isotype-specific ELISA, separate IgE and IgG responses against D immitis in 4 groups (A-D) of 8 dogs experimentally coinfected with D immitis and Ancylostoma caninum. All dogs were monitored from 2 weeks before inoculation with D immitis, through postinoculation (PI) week 20. Group-B dogs received a daily regimen of 6.6 mg of DEC/kg of body weight. Group-C dogs received 4.95 mg of oxibendazole/kg daily. Group-D dogs received DEC and oxibendazole, equivalent to the daily doses given to dogs of groups B and C. All dogs given oxibendazole had no A caninum at necropsy. Of the groups receiving DEC, 3 group-B dogs each had 1 to 2 D immitis at necropsy. When results of chronologic IgE determination for all groups were statistically compared, only groups B and C had significant (P = 0.0148 and P << 0.00005, respectively) increases in IgE values. Group-C dogs had the highest IgE values from PI week 10 until the end of the study, whereas IgG values were statistically identical to those of group-A dogs. Group-B dogs given only DEC and having the least number of D immitis of all groups, had IgE values that peaked at PI week 6; values were significantly (P = 0.0002) higher than those for all other groups. In Group-B dogs, IgG values increased significantly (P << 0.00005) only at PI week 20 and were significantly (P << 0.00005) decreased after PI week 6, compared with values for all other groups. Group D containing 6 dogs infected with 1 to 18 D immitis found at necropsy had IgE values betwee.

Vaccina virus (VV) infection induces specific antibodies and cytotoxic T cells in various animal species. Therefore, helper T cells also should be induced that stimulate the humoral and cellular immune responses. We determined such helper T-cell activity in 2 species after VV infection. Rabbits and rhesus macaques were infected with the Copenhagen strain of VV or with recombinant VV expressing retroviral proteins. Animals of both species developed antibodies and specific proliferative T-cell response. This reactivity could be enhanced by booster infection with VV. The proliferating macaque cells were CD4+ and major histocompatability complex class II-restricted. These data confirm the broad immunogenicity of VV. Expression of additional polypeptides expressed from a recombinant VV does not lead to altered immune response to VV antigens. However, strength of the helper T-cell response, as well as clinical reactions, differed between macaques and rabbits. Infection with recombinant VV as delivery vectors offers the opportunity for combined vaccination against recombinant proteins and does not diminish cellular and humoral immune responses to VV itself.

The adulteration of wax foundation is, for many reasons, a growing problem of modern beekeeping not only in Europe but also around the world. Wax foundation contaminated with stearin addition leads to a brood die-off, while paraffin addition negatively affects the strength of combs. It is tenable that such adulterated wax foundation reduces bees’ immunity. The aim of the study was to determine the activities of two bee immune enzymes, lysozyme and phenoloxidase, in the haemolymph of worker bees which had emerged from combs with wax foundations contaminated with stearin or paraffin.

Small ruminant lentivirus (SRLV) causes caprine arthritis-encephalitis in goats and maedi-visna disease in sheep. Transmission is via ingestion of colostrum and milk from infected dams or long-term direct contact between animals. Lifelong seroconversion can occur several weeks after infection via ingestion. However, sub-yearling lambs that ingest contaminated colostrum may be able to clear the infection and become seronegative. Whether a similar phenomenon occurs in goats remains unknown. Therefore, the serological status of goats was studied longitudinally from the moment of natural exposure to colostrum and milk of SRLV-positive dams through the age of 24 months.

OBJECTIVE To evaluate cell-mediated and humoral immune responses of calves receiving 2 doses of a dual-adjuvanted vaccine containing inactivated bovine herpesvirus type 1 (BHV1) and bovine viral diarrhea virus types 1 (BVDV1) and 2 (BVDV2) before and after exposure to BHV1. ANIMALS 24 Holstein steers negative for anti-BHV1 antibodies and proliferative cell-mediated immune responses against BHV1 and BVDV. PROCEDURES Calves were randomly assigned to 3 groups. The vaccinated group (n = 10) received 2 doses of vaccine on days 0 and 21. Control (n = 10) and seeder (4) groups remained unvaccinated. Calves were commingled during the study except for the 3-day period (days 53 to 55) when seeders were inoculated with BHV1 (1.04 × 107 TCID50, IV) to serve as a source of virus for challenge (days 56 through 84). Rectal temperature and clinical illness scores were monitored, and blood and nasal specimens were obtained for determination of clinicopathologic and immunologic variables. RESULTS After BHV1 challenge, mean rectal temperature and clinical illness scores were lower for vaccinates than controls. In vaccinates, antibody titers against BHV1 and BVDV2, but not BVDV1, increased after challenge as did extracellular and intracellular interferon-γ expression, indicating a T helper 1 memory response. Additional results of cell marker expression were variable, with no significant increase or decrease associated with treatment. CONCLUSIONS AND CLINICAL RELEVANCE Calves administered 2 doses of a killed-virus vaccine developed cell-mediated and humoral immune responses to BHV1 and BVDV, which were protective against disease when those calves were subsequently exposed to BHV1.

OBJECTIVE To measure immunologic responses of snakes after experimentally induced infection with ferlaviruses. ANIMALS 42 adult corn snakes (Pantherophis guttatus) of both sexes. PROCEDURES Snakes were inoculated intratracheally with genogroup A (n = 12), B (12), or C (12) ferlavirus (infected groups) or cell-culture supernatant (6; control group) on day 0. Three snakes from each infected group were euthanized on days 4, 16, 28, and 49, and 3 snakes from the control group were euthanized on day 49. Blood samples were collected from live snakes on days −6 (baseline), 4, 16, 28, and 49. Hematologic tests were performed and humoral responses assessed via hemagglutination-inhibition assays and ELISAs. Following euthanasia, gross pathological and histologic evaluations and virus detection were performed. RESULTS Severity of clinical signs of and immunologic responses to ferlavirus infection differed among snake groups. Hematologic values, particularly WBC and monocyte counts, increased between days 4 and 16 after infection. A humoral response was identified between days 16 and 28. Serum IgM concentrations increased from baseline earlier than IgY concentrations, but the IgY relative increase was higher at the end of the study. The hemagglutination-inhibition assay revealed that the strongest reactions in all infected groups were against the strain with which they had been infected. Snakes infected with genogroup A ferlavirus had the strongest immune response, whereas those infected with genogroup B had the weakest responses. CONCLUSIONS AND CLINICAL RELEVANCE Results of this experimental study suggested that the ferlavirus strain with the highest virulence induced the weakest immune response in snakes.