Pathogenesis of Placentitis in the Goat Inoculated with Brucella abortus. I. Gross and Histologic Lesions

Abstract

Abstract. Pregnant goats were given Brucella abortus intravenously or in uterine arteries, and tissues from the uterus and placentae were examined at various post-inoculation intervals to study mechanisms of placental infection. Placentitis was present by 5 days post-inoculation and abortions occurred within 11 days. B. abortus was identified in placentae by light microscopy and immunoperoxidase techniques. B. abortus was first seen in erythrophagocytic trophoblasts of the placentome. Subsequently, high numbers of B. abortus were seen in periplacentomal chorioallantoic trophoblasts. Trophoblast necrosis, chorioallantoic ulceration, and large numbers of B. abortus in chorionic villi were present in later stages of infection. These results suggest that entry and replication of B. abortus in trophoblasts precede placentome and fetal infection and that trophoblasts are the source of B. abortus for these tissues. Experimental caprine brucellosis closely resembles bovine and ovine brucellosis and it provides a model to study the intracellular development of B. abortus in trophoblasts.Brucella abortus has a marked predilection for the ruminant placenta. In acute infections of pregnant cows, up to 85% of the bacteria are in cotyledons, placental membranes, and allantoic fluid. Materials and MethodsTwenty 2-to 3-year-old pregnant alpine crossbred goats in their last third of gestation were given various amounts of Brucella abortus (strain 2308 supplied by Dr. B. Deyoe, National Animal Disease Center, Ames, IA) in jugular veins, uterine arteries, or the uterine lumen (Tables 1, 2). Goats were maintained in isolation until necropsy. Four pregnant goats were not inoculated and served as controls. All goats lacked serum antibodies to B. abortus (card and tube agglutination test) and no clinical evidence of brucellosis was apparent in the herd history.Jugular vein inoculations were done by injecting varying amounts of B. abortus into either the right or left jugular vein (Table 1). Uterine artery inoculations were done following ventral laporatomy on goats anesthetized with 2 to 4 mg/kg ketamine hydrochloride (Ketaset, Bristol Laboratories, Syracuse, NY) and 0.1 mg/kg xylazine (Rompun, Haver-Lockhart, Shawnee, KS). Gravid uteri were removed from the abdomen, the middle uterine arteries were exposed, and various amounts of B. abortus (Table 1) suspended in phosphate buffered saline were injected into one or both species. One goat was inoculated into the uterine lumen with lo6 B. abortus after an unsuccessful attempt at inoculating the uterine artery. At first, random dosages were selected to evaluate the effect of dose upon lesion development. Later, most goats received lo9 B. abortudml of diluent (Tables 1, 2). All goats appeared clinically normal after inoculations and were observed twice daily until necropsy.Goats were necropsied from 2 to 23 days post-inoculation. At necropsy, gravid uteri were exposed by ventral laparot-219

Epizootiology of Brucella Infection in Australian Fur Seals

“…Our finding of inflammatory lesions in fetal tissues suggests that infectious agents are likely involved in some instances of gestational failure. Suppurative lesions consistent with Brucella or other bacterial infection (Anderson et al, 1986;Neta et al, 2010) were seen in four individuals: one fetus had placentitis, two had pericarditis, and the fourth had lymphadenitis. However, the diffuse, interstitial pneumonia with a mononuclear infiltrate seen in six individuals is not typical for Brucella, for which suppurative pleuritis and bronchointerstitial pneumonia are expected to be the predominant lesions (Neta et al, 2010).…”

Comparisons of brucellosis between human and veterinary medicine

“…Release of erythritol from the placenta into the circulatory system causes translocation of brucellae out of lymph nodes and migration to reproductive tissues. The new focus of infection is invasion of the chorionic villi, extending into the cotyledons on the fetal side of the placenta [59,60]. There, bacterium can replicate to a very high level (10 13 bacteria/gram of tissue) and induce infiltration of inflammatory cells, necrosis of trophoblast, and lead to vasculitis [61,62].…”

“…There, bacterium can replicate to a very high level (10 13 bacteria/gram of tissue) and induce infiltration of inflammatory cells, necrosis of trophoblast, and lead to vasculitis [61,62]. This ultimately leads to compromised fetal-maternal metabolic exchanges, resulting in fetal loss [59]. Fetal and placental tissues and associated fluids expelled in abortion events are the main transmission in animal populations [56].…”

Brucella alters endocytic pathway in J774 macrophages

“…Graciela N. arenas, 1, * Diego J. Grilli, 1 Luis e. Samartino, 3 Javier Magadán 2 and Luis S. Mayorga have not yet been clearly elucidated. It has been suggested that increased susceptibility to infection at late stages of pregnancy could be explained by the presence of erythritol in these tissues.…”

“…This suggests that Brucella replicates in the ER lumen using translocation proteins for its metabolism. 3,4 Although Brucella abortus infection of fetal tissues and its multiplication therein happen early in pregnancy, miscarriage frequently occurs during the second half of pregnancy. The reasons determining this course of events Brucella is a facultative intracellular bacterium which causes chronic infections in mammals by surviving and replicating within host cells.…”