Title : Exploring association between host factors and different virulence factors of Enterococcus spp. With treatment outcome in Entrococcal BSI. (causing Blood stream infections)
Abstract:
Introduction: Enterococci are normal human of the oral cavity, gastrointestinal tract, and vaginal vault. Although they are relatively a virulent, they evolved as leading cause of nosocomial bacteremia with very high fatality rate of 68% (65) In one large study of nosocomial sepsis due to Gram positive pathogens, enterococci were independently associated with a high risk of death (227).
Enterococci can cause variety of human infections including blood stream Infection. Amongst many species isolated from clinical specimens Enterococcus faecium and E.faecalis are two major species frequently isolated from blood stream infection cases. Majority of infections are caused by E.fecalis.
Evolution of Enterococci from commensal to most frequent pathogen of nosocomial blood stream infections required lot many changes in the Enterococci including adaptation to different environment, evading the host's immune attack and causing toxin mediated damage.
In the present study we have attempted to explore association between the host factors like co-morbidities and virulence factors of Enterococci causing nosocomial blood stream infections.
Virulence genes of Enterococci
Adherence to Host Tissues (Adhesin): Adhesins play a significant role in adhesion to eukariotic cell surface or mucosal serface that makes them remained adhered strongly to remain and proliferate as commensals.
Invasion of Host Tissues: In some cases of nosocomial bacterimia the source of infection is identifiable but in large nuber of cases it is not possible to trace the source and in such case cases the source presumably is Intestinal tract. (1, 234). In some animal studies have hypothesized translocation of Intestinal Enterococci via Phagocytic leucocytes to regional lymphnodes to blood stream. The prior therapy with Cephalosporins kill the normal bacterial flora and allow the growth of Enterococci that are tolerent and evetually dominated the flora. (129, 161, 242) and are consistently associated with development of enterococcal bacteremia (6, 90, 93, 113, 175, 243, 244).
Modulation of Host Immunity: Lipoteichoic Acids od Enterococci are studied for their potency to induce Tumour necrosis factor and Interferons. (221) Enterococcal lipotechoic acid has been found to bring about immunemodulation.
Pheromones: E. faecalis strains are known to secrete Pheromones that are small peptides, comprising only 7 to 8 amino acids. Pheromones have potential to act as chemoatrractants for neutrophils (64).
Protease (Gelatinase): Protease produces by E.faecalis is capable of hydrolyzing gelatin. collagen, casein, haemoglobin and other small biologically active peptides (212) Coque et al. (47) analyzed 95 enterococcal isolates from patients with endocarditis and other nosocomial infections and found that 54% produced protease.
Hyaluronidase: It is suggested that enterococcal hyaluronidase could play a role in invasive disease. No studies, however, address this issue for enterococci.
AS-48: AS-48 is a 7.4-kDa peptide produced by E. faecalis inhibits and lyses a wide spectrum of gram-negative and gram-positive bacteria, including enterococci (80). The significance of this bacteriocin remains uncertain, however, since the prevalence of AS-48-producing strains among human commensal and infection isolates has yet to be defined. No activity of AS-48 against eukaryotic cell membranes has been reported.
