dThis study aimed to evaluate the Brucella ovis ⌬abcBA strain as a vaccine candidate in the murine model. BALB/c mice were subcutaneously or intraperitoneally immunized with a single dose or three doses of the B. ovis ⌬abcBA strain and then were challenged with wild-type B. ovis. Single or multiple immunizations provided only mild protection, with significantly smaller numbers of wild-type B. ovis CFU in the livers of immunized mice but not in the spleens. Encapsulation of B. ovis ⌬abcBA significantly improved protection against experimental challenges in both BALB/c and C57BL/6 mice. Furthermore, immunization with encapsulated B. ovis ⌬abcBA markedly prevented lesions in the spleens and livers of experimentally challenged mice. These results demonstrated that the encapsulated B. ovis ⌬abcBA strain confers protection to mice; therefore, this strain has potential as a vaccine candidate for rams. Brucella ovis is a facultative, intracellular, Gram-negative coccobacillus (1) that causes economic losses due to its potential to induce reproductive failure in sheep (2, 3). The most important lesions caused by B. ovis in rams are epididymitis and seminal vesiculitis (4), and B. ovis occasionally causes abortion in ewes (5, 6).In spite of attempts to develop safe, effective vaccines (7-10), there is no available vaccine specifically against B. ovis. The ideal vaccine against B. ovis must prevent infection and clinical signs or at least reduce the risk of infection and transmission (11). Rev-1, a live attenuated Brucella melitensis strain, is the most commonly used vaccine against B. melitensis, and it also protects against B. ovis (12). However, the Rev-1 strain retains pathogenic potential, so it is capable of infecting humans. It may cause abortions in ruminants, it may interfere with serological tests, and it is resistant to streptomycin (13,14).Mice have been extensively used as a model for brucellosis, which is very important due to the limitations of experimentation with larger animals (15-18). The murine model has allowed studies for the development of safe, effective brucellosis vaccines (15,19,20).Inactivation of a predicted abcEDCBA-encoded ATP-binding cassette (ABC) transporter of B. ovis (21), which is located in B. ovis pathogenicity island 1 (BOPI-1), results in strong attenuation of this pathogen in the murine model (22). Although the substrate of this ABC transporter is not known, it is required for expression of B. ovis virulence proteins, including Omp31, Sod, and the virB-encoded type IV secretion system (23), which is required for B. ovis intracellular survival and in vivo persistence (17). Furthermore, a B. ovis ⌬abcBA strain is capable of triggering humoral and cellular immune responses like the wild-type strain in rams; importantly, however, the mutant strain is not excreted in semen and urine (24). Therefore, this mutant strain has great potential as an attenuated vaccine strain. However, considering that the ⌬abcBA mutant strain is attenuated at very early stages during infection, resulting in p...

This study aimed to evaluate protection induced by the vaccine candidate B. ovis ΔabcBA against experimental challenge with wild type B. ovis in rams. Rams were subcutaneously immunized with B. ovis ΔabcBA encapsulated with sterile alginate or with the non encapsulated vaccine strain. Serum, urine, and semen samples were collected during two months after immunization. The rams were then challenged with wild type B. ovis (ATCC25840), and the results were compared to non immunized and experimentally challenged rams. Immunization, particularly with encapsulated B. ovis ΔabcBA, prevented infection, secretion of wild type B. ovis in the semen and urine, shedding of neutrophils in the semen, and the development of clinical changes, gross and microscopic lesions induced by the wild type B. ovis reference strain. Collectively, our data indicates that the B. ovis ΔabcBA strain is an exceptionally good vaccine strain for preventing brucellosis caused by B. ovis infection in rams.

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Salmonella enterica serotype Typhimurium is able to expand in the lumen of the inflamed intestine through mechanisms that have not been fully resolved. Here we utilized streptomycin-pretreated mice and dextran sodium sulfate (DSS)-treated mice to investigate how pathways for S. Typhimurium iron acquisition contribute to pathogen expansion in the inflamed intestine. Competitive infection with an iron uptake-proficient S. Typhimurium strain and mutant strains lacking tonB feoB, feoB, tonB or iroN in streptomycin pretreated mice demonstrated that ferric iron uptake requiring IroN and TonB conferred a fitness advantage during growth in the inflamed intestine. However, the fitness advantage conferred by ferrous iron uptake mechanisms was independent of inflammation and was only apparent in models where the normal microbiota composition had been disrupted by antibiotic treatment.