1887

Abstract

Enterococci are important nosocomial pathogens with multiple intrinsic and acquired resistances to antibiotics. In the past, the majority of infections were caused by ; however, an increase in clinical isolates has been observed in recent years. The enterococcal surface protein (Esp) is expressed on the surface of most clinical isolates and has been shown to be involved in biofilm formation. Here, E1162 and its previously created insertion-deletion mutant of the gene, E1162Δ, were compared in a mouse bacteraemia model. Anti-Esp serum was tested for its capacity to mediate opsonophagocytic killing of E1162 and to protect against bacteraemia. The inactivation of attenuated virulence with reduced numbers of bacteria recovered from the kidneys in animals infected with the mutant compared to the wild-type strain (=0.035). Passive immunization with rabbit polyclonal serum raised against the recombinant N-terminal Esp protein did not protect mice against bacteraemia (>0.05). In contrast, mice passively immunized with polyclonal antiserum raised against lipoteichoic acid (LTA) from had lower numbers of E1162 in the blood compared to mice immunized with normal rabbit serum. These results suggest that Esp contributes to persistence in the host. However, in contrast to LTA, Esp does not seem to be a target for protective antibodies in strain E1162 in mouse bacteraemia.

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2010-09-01
2024-03-28
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