Elsevier

Theriogenology

Volume 58, Issues 2–4, August 2002, Pages 791-792
Theriogenology

Route of fetal infection in a model of ascending placentitis

https://doi.org/10.1016/S0093-691X(02)00823-3Get rights and content

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    High concentrations of allantoic fluid prostaglandin E2, and prostaglandin F2α were detected within the 48 hours preceding abortion or delivery.37 Proinflammatory cytokines in the chorioallantois, amnionic fluid, endometrium, cervix, and fetal tissues were higher in the experimentally infected mares, compared with controls.37–41 The placental infection, although typically not affecting the dam, results in an infectious, proinflammatory gestational environment that can lead to impaired fetal growth, fetal sepsis, and early parturition or abortion.

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    While there are regional variations in the bacterial and fungal agents associated with ascending placentitis in mares, β-hemolytic streptococci (Streptococcus equi subspecies zooepidemicus and Streptococcus equisimilis), and coliforms such as Escherichia coli are the predominant microbial isolates worldwide [1,4–6]. In ascending placentitis infection begins at the caudal placental pole (cervical star region), then bacteria spread cranial-ventrally towards the uterine body segments of the chorioallantois and gain access to the fetus either by migrating through umbilical vessels or through fetal fluids [6–8], consequently, reaching the fetus and becoming a potential cause of septicemia and fetal morbidity and mortality. Placentitis is characterized by the production of pro-inflammatory cytokines such as IL-6 and IL-8, and prostaglandins (PGF2α and PGE2) [9,10].

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