Pathogenesis of placentitis in the goat (Capra hircus) inoculated with Brucella abortus

A caprine model of ruminant brucellar placentitis was developed and used to determine the pathogenesis of placental infection and to characterize changes in trophoblasts infected with Brucella abortus. Tissues from the uterus and placentae were examined by light and electron microscopy at various post-inoculation intervals. B. abortus was identified in placentae by immunoperoxidase and immunogold cytochemistry. Placentitis was present by 5 days post-inoculation and abortions occurred by 11 days. Histologically, brucellae were first seen in placentomal erythrophagocytic trophoblasts and periplacentomal chorioallantoic trophoblasts. Necrosis of trophoblasts, chorioallantoic ulceration, and large numbers of brucellae in chorionic villi were present in later stages of infection. This study indicated that entry and replication of brucellae in trophoblasts precede placentome and fetal infection and that trophoblasts are the source of brucellae for these tissues;Ultrastructurally, brucellae were first seen in phagosomes of erythrophagocytic trophoblasts and in the rough endoplasmic reticulum of chorioallantoic trophoblasts. After intracellular bacterial replication caused trophoblast necrosis, large numbers of brucellae were in connective tissue of chorionic villi, placental vasculitis was present, and placentomal trophoblasts were separated from maternal syncytial epithelium. This study indicated that bacteremic brucellae are endocytosed by erythrophagocytic trophoblasts, brucellae likely replicate in trophoblastic rough endoplasmic reticulum, and that placental vasculitis is important in the pathogenesis of abortion;Trophoblasts in normal and brucellae-infected placentae were characterized by electron microscopic morphometry. Volume and surface density of normal rough endoplasmic reticulum decreased six-fold in brucellae-infected trophoblasts as compared to normal trophoblasts. The remainder of rough endoplasmic reticulum in infected trophoblasts was hypertrophied and distended by intracisternal brucellae. This decrease in normal rough endoplasmic reticulum and the corresponding hypertrophy of brucellae-filled rough endoplasmic reticulum indicates that B. abortus replicates in trophoblastic rough endoplasmic reticulum