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Ovine brucellosis by Brucella ovis is a highly prevalent disease in Argentina. This study aimed to evaluate the pathogenicity of B. ovis and the serological response in ewes during late pregnancy and in their offspring. Six adult ewes were distributed in two groupsG1 (pregnant females, n = 4) and G2 (nonpregnant females, n = 2). Three pregnant ewes at 15 days prepartum and one nonpregnant eve were inoculated with B. ovis. Sera of sheep and their offspring were analyzed by different serological tests. Samples of cervicovaginal mucus, placenta and milk were studied by bacteriology. A Brucella genus-specific PCR assay was carried out in placenta and milk samples. Placenta samples were hystopathologically processed. g1 females gave birth to live lambs, but one died hours postpartum. Serological techniques employed detected antibodies in serum of inoculated pregnant animal 5 days postchallenge. sera of female controls G1 and G2 remained negative throughout the study. Cervicovaginal mucus of infected ewes in G1 and G2 yielded negative results to bacteriology, but B. ovis was isolated from milk. The PCR assay was positive for the placenta and milk from inoculated pregnant ewes. Histopathology revealed necrotic suppurative placentitis in one placenta. However, although results demonstrated that B. ovis can invade the placenta and mammary gland, this bacterium did not cause abortion when it was inoculated intravenously at 15 days prepartum. B. ovis infection induced an early humoral response in pregnant ewes, but their lambs remained seronegative, indicating that there was no transfer of antibodies in infancy. Placenta colonization and milk excretion of B. ovis involves a potential source of infection for lambs, which could play a role as latent carriers of infection.

A villitis is a focal or multifocal inflammatory reaction of chorionic villi with infiltration of mononuclear cells and usually is associated with fibrinoid necrosis. The aetiology of villitis could be a transplacental infection of the fetus, especially with virus (VIV), in normal placentae however, the presence of villitis is referred as villitis of unknown ethiology (VED). This study was designed to characterize villitis lesions of 11 placentae, four VIV and seven VED, ultrastructural descriptive comparisons of both types of villitis are discussed. Biopsies were processed with the conventional optic and electronic microscopy techniques. Our ultrastructural observations confirmed the presence of virus in four placentae whereas no virus or bacteria were found in seven placentae. Microvilli were absent or markedly diminished, this finding was associated to the presence of fibrinoid necrosis in the stroma and clinically to intrauterine growth retardation, 4 preterm pregnancies and one obitus. Trophoblast alterations were found in both types of villitis, basal membrane thickness, is some cases associated to electrodense material similar to calcium deposites, vascuolization and the presence of edema in the stroma was observed. In some cases we noted the presence of focal fibrin deposits associated to necrosis zones in the stroma, calcium precipitates and mielinic bodies. Fetal vessels obliteration and intravascular thrombi were found in the syncitiotrophoblast placentae with viral particles CMV or rubivirus associated to an increment in Hofbauer cells and basal membrane calcifications. From our ultrastructural observations, we conclude that both types of villitis are associated to a typic immunologic reaction that induce lose of trophoblast microvilli, mononuclear infiltration and edema. This placental alterations reduce dramatically the maternofetal exchange of gases, nutrients and other active peptides and could be the cause of fetal growth retardation, inmadurity or death.