Toxoplasma gondii, goats, prevention of abortion and neonatal death by vaccination with nonpathogenic coccidium Hammondia hammondi

Babesia bovis, cattle, kinetics of specific indirect fluorescent antibody test titers and total serum IgG and IgM values after vaccination and challenge exposure, nonspecific suppression of total IgG and IgM values coinciding with period of peak parasitemia

Schistosoma japonicum, diagnosis, formalin fixed tissue section used with indirect fluorescent antibody test and intraoval precipitin reaction

Interferon (IFN)-γ has been shown to be associated with immunity to Marek’s disease virus (MDV). The overall objective of this study was to investigate the causal relationship between IFN-g and vaccine-conferred immunity against MDV in chickens. To this end, 3 small interfering RNAs (siRNAs) targeting chicken IFN-g, which had previously been shown to reduce IFN-γ expression in vitro, and a control siRNA were selected to generate recombinant avian adeno-associated virus (rAAAV) expressing short-hairpin small interfering RNAs (shRNAs). An MDV challenge trial was then conducted: chickens were vaccinated with herpesvirus of turkey (HVT), administered the rAAAV expressing shRNA, and then challenged with MDV. Tumors were observed in 4 out of 10 birds that were vaccinated with HVT and challenged but did not receive any rAAAV, 5 out of 9 birds that were administered the rAAAV containing IFN-γ shRNA, and 2 out of 10 birds that were administered a control enhanced green fluorescent protein siRNA. There was no significant difference in MDV genome load in the feather follicle epithelium of the birds that were cotreated with the vaccine and the rAAAV compared with the vaccinated MDV-infected birds. These results suggest that AAAV-based vectors can be used for the delivery of shRNA into chicken cells. However, administration of the rAAAV expressing shRNA targeting chicken IFN-γ did not seem to fully abrogate vaccine-induced protection.

Early epidemiological information indicated that bovine spongiform encephalopathy (BSE) originated from scrapie in sheep. The question arose if scrapie in North America would induce a BSE-like disease in cattle. Six years ago, we reported that brain tissue from sheep with scrapie caused a neurologic disease when injected directly into the brains of cattle, but the disease induced was different from BSE as it occurs in the United Kingdom and Europe. Here, we report that cattle fed raw brain or meat and bone meal and tallow prepared from sheep with scrapie remained normal for 8 years after exposure. This work indicates that cattle are highly resistant to North American scrapie by the oral route.

Systemic administration of dexamethasone led to a significant reduction in the size of the tuberculin reaction in response to intradermal injection of bovine purified protein derivative in 18 cattle experimentally sensitized to Mycobacterium bovis (P < 0.01) and 8 cattle naturally infected with M bovis (P < 0.001). The reaction in 6 of the 7 M bovis-infected cattle that received dexamethasone was classified as negative for the standard interpretation of the single intradermal comparative tuberculin test. Significantly fewer BoCD2+ (P < 0.05) and BoCD4+ T cells (P < 0.001) were present at the reaction site and in blood of dexamethasone-treated cattle, compared with untreated control cattle. Significantly fewer cells expressing the interleukin-2 receptor and WC1+ gamma delta T cells (P < 0.001), and a significantly greater number of cells expressing the ACT2 antigen (P < 0.05) were found at the reaction site in dexamethasone-treated cattle than in controls. The number of BoCD8+ T cells at the reaction site and in blood was not significantly affected by administration of dexamethasone. In vitro production of interferon-gamma by lymphocytes incubated with bovine purified protein derivative also was significantly lower (P < 0.01) in the dexamethasone-treated cattle.

The microscopic brush border membrane adherence assay was used to determine resistance (nonadherence) and susceptibility adherence) of Chinese pigs (n = 289) to the K88ac+ strain of Escherichia coli-mediated disease. This study estimates prevalence of resistance to diarrheal disease in multiple family lines (no common ancestry for a minimum of 3 generations) for the Chinese Meishan, Fengjing, and Minzhu breeds. Results of in vitro assays indicate that pigs of the Meishan breed are highly resistant (nonadherent) to K88ac+ E coli-mediated disease. The gene conferring susceptibility to K88ac+ E coli-mediated disease exists at low frequency in pigs of the Minzhu breed. Minzhu-type (crossbred) pigs of both phenotypes (susceptible and resistant) were identified in ratios consistent with a 1-locus gene model. Given that all susceptible pigs were from 1 site, frequency of susceptibility within this Minzhu population is estimated at 8%. Inheritance within the Fengjing breed is still unclear because a weakly adherent phenotype, as well as the resistant phenotype, was identified. The weakly adherent phenotype was observed in pigs derived from multiple family lines. Expression of the weakly adherent phenotype in terms of susceptibility to disease is not known at this time.

Caseous lymphadenitis (CIA) caused by Corynebacterium pseudotuberculosis is a worldwide disease of sheep and goats and is characterized by development of pyogranulomas in lymph nodes and lungs. Control of this disease by vaccination remains controversial, although toxoid vaccines are now commercially available in some countries. To determine the efficacy of acquired immunity to control CLA, the effect of primary infection on subsequent challenge exposure was investigated. Adult seronegative ewes were primarily inoculated with a streptomycin-sensitive strain of C pseudotuberculosis on the external part of the left ear and thereafter challenge-exposed by inoculation of the streptomycin-resistant strain 19R in the right ear. This protocol indicated that primary infection with at least 10(7) viable bacteria induced strong protection against subsequent challenge exposure; the ewes with primary infection did not develop lesions as a result of challenge exposure, whereas immune-naive ewes developed numerous pyogranulomas in the right car, in lymph nodes draining the inoculation site, and in the lungs. However, ewes with primary infection remained carriers of the disease as a result of primary inoculation. These results offer experimental support for development of more effective vaccination to control CLA, in sheep and goats, and this model indicates that animals with primary infection can be used as positive controls for protection when testing a candidate vaccine against CLA.

Porcine blood mononuclear cells (BMC) were exposed to prepartum concentration of estrogen in gilts before acquisition (in vivo), and their subsequent reactivity (in vitro) was explored. In a cross-over experimental designed study, 6 ovariectomized gilts were injected once with 3.75 mg of estradiol-17beta benzoate in arachidic oil or with arachidic oil only during 2 experiments. The ability of their BMC to proliferate in response to stimulation with phytohemagglutinin, concanavalin A, and pokeweed mitogen was assayed in cultures of blood and in cultures of purified BMC. After 2 days of mitogen stimulation, activity of accessible interleukin 2 was quantified in supernatants obtained from cultures of purified BMC and supernatants of blood cultures stimulated with pokeweed mitogen. Also, production of immunoglobulins by purified BMC in response to polyclonal stimuli was measured. Three days after treatment with estradiol, the proliferative response was suppressed in blood cultures stimulated with concanavalin A (P < 0.05) and phytohemagglutinin (P < 0.07). Effects of estradiol treatment were not found in any of the assays performed with purified BMC. We, therefore, assumed that in vivo exposure to estradiol can affect the function of porcine BMC; however, this was only evident when the in vitro assays were performed on blood cultures.

Concanavalin A (conA) blast proliferation as a quantitative measure of lymphoblast proliferative capacity by blood mononuclear cell supernatants was measured in cattle naturally infected with Mycobacterium paratuberculosis and in healthy control cattle. Blast cell proliferation was significantly reduced in infected animals, compared with control cattle when blood mononuclear cells were stimulated with conA. Proliferation was significantly greater than media control when M bovis purified protein derivative and johnin were used to stimulate cells from the infected group. After sensitizing control and affected cattle with M paratuberculosis bacterin (live M bovis and keyhole limpet hemocyanin in Freund's incomplete adjuvant), infected animals had no difference in blast cell proliferative capacity with the mycobacterial antigens and cona stimulation, whereas healthy animals had significantly increased blast proliferation in response to all the sensitizing antigens. The blast cell proliferative capacity in infected animals with keyhole limpet hemocyanin stimulation was increased significantly after sensitization; however, it remained significantly less than that in the sensitized control group. These data indicate that cattle naturally infected with M paratuberculosis probably produce suboptimal interleukin-2 (IL-2) activity in response to a potent IL-2 inducer (conA) and fail to optimize IL-2 activity when sensitized with a potent immunogen (keyhole limpet hemocyanin).