Pathogenesis of Brucella ovis in pregnant mice and protection induced by the candidate vaccine strain B. Ovis ΔabcBA.

Ovine brucellosis caused by Brucella ovis is a major cause of reproductive failure in sheep. This study aimed to evaluate transplacental infection and pathogenicity of B.ovis wild type strain ATCC 25,840 (WT B.ovis) and the candidate vaccine strain B.ovis ΔabcBA in pregnant mice. A total of 40 BALB/c mice were equally divided into 4 groups: (i) non immunized and uninfected control mice (3/10 mice became pregnant); (ii) non immunized and challenged with WT B.ovis (5/10 pregnant); (iii) inoculated only with B.ovis ΔabcBA (6/10 pregnant); (iv) immunized with B.ovis ΔabcBA and challenged with WT B.ovis (5/10 pregnant). Female mice bred, and five days after visualization of the vaginal plug, they were inoculated intraperitoneally (ip) with 100 µL of sterile PBS, 100 µL of 1 × 106 CFU of B.ovis ΔabcBA, or 100 µL of 1 × 106 CFU of B.ovis WT, according to each group. At the 17th day of gestation, samples of spleen, liver, uterus, placenta, fetus and mammary gland were obtained for bacteriology, histopathology and immunohistochemistry. Non immunized mice challenged with B.ovis WT developed necrotizing placentitis as well as microgranulomas in the liver and spleen. These findings support the notion that B.ovis infection in pregnant mice induces lesions that are similar to those caused by B.abortus in the same animal model. B.ovis ΔabcBA was not recovered from any of the sampled organs, and it did not cause any gross or microscopic lesions, indicating that it is a safe and attenuated strain in this experimental model. In addition, B.ovis ΔabcBA was induced protective immunity as demonstrated by decreased numbers of B.ovis WT in the liver, uterus and fetuses of immunized mice after the challenge with B.ovis WT.

Genotyping of Toxoplasma gondii in a lethal toxoplasmosis outbreak affecting captive howler monkeys (Alouatta sp.).

BACKGROUND: Toxoplasmosis is a zoonotic disease that affects humans and warm-blooded animals. This study describes an outbreak of toxoplasmosis in howler monkeys (Alouatta sp.) and survival of capuchins (Sapajus apella), under the same environmental conditions. METHODS: Howler monkeys were submitted to post-mortem examination. Tissue samples were processed to histopathology and immunohistochemistry to detect lesions and tachyzoites of Toxoplasma gondii. Tissue samples were also frozen and submitted to PCR and genotyping of T. gondii. RESULTS: Typical lesions were observed in several organs including the liver, lymph node, and brain, with intralesional cysts and tachyzoites of T. gondii demonstrated by immunohistochemistry. T. gondii genomic sequences were amplified by PCR, and genotyping characterized the same T. gondii clone in all howler monkeys. CONCLUSIONS: Our results support the notion that some species of neotropical primates are highly susceptible to toxoplasmosis and the hypothesis that capuchins (S. apella) may be resistant.