Bacterial infections of the equine genital tract

Abstract

SummaryBacterial infections of the genitial tract are the major cause of reproductive failure in the mare. The variety of bacteria involved has been carefully established in the past and is approved in recent studies. There are approved laboratory procedures for etiologic diagnostics of bacterial infections of the female equine genital tract. Innovative molecular based approaches aim at elucidating, for instance, potential transmission modes of opportunistic pathogens like Pseudomonas aeruginosa, or at analysing genital microbial communities (microbiomes). The latter approach may provide new and more dynamic insights into the pathogenesis of genital infections since alteration of microbiomes is known to be associated with several pathogenic conditions.

Infection and Infertility in Mares

“…The antigenicity of the Mprotein-like is mainly responsible for the mounting of a protective immune response. Bacterial toxins promote deterioration of complement and exacerbate uterine inflammation [64][65][66].…”

Vaginal bacterial microbiota of an endangered donkey breed: a comparison between Asinina de Miranda (Equus asinus) jennies with and without reproductive problems

“…Bacteria which are capable to establish endometritis are considered to di er from the physiological genital microbiota by several tracts that promote colonizing and causing damage to equine endometrium. e concept that some virulence mechanisms are su cient to explain why a bacterium can cause endometritis may oversimplify the complex nature of the disease [4,5,6,7].…”

“…Understanding the role played by virulence factors can help elucidate the understanding of the pathogenesis of infection and can be used to identify points of treatment or vaccination. Known virulence factors of S. zooepidemicus include M-like proteins and superantigens [4,10,11,12,13] e designation M-like protein usually refers to proteins that bind brinogen and have antiphagocytic activity. e antiphagocytic of these proteins appears to be associated with their ability to inhibit deposition of the complement component C3b on the bacterial surface and their ability to bind brinogen which then inhibits the phagocytosis.…”