Enterococcal surface protein contributes to persistence in the host but is not a target of opsonic and protective antibodies in Enterococcus faecium infection.
Enterococci are important nosocomial pathogens with multiple intrinsic and acquired resistances to antibiotics. In the past, the majority of infections were caused by Enterococcus faecalis; however, an increase in Enterococcus faecium clinical isolates has been observed in recent years. The enterococcal surface protein (Esp) is expressed on the surface of most E. faecium clinical isolates and has been shown to be involved in biofilm formation. Here, E. faecium E1162 and its previously created insertion-deletion mutant of the esp gene, E. faecium E1162Deltaesp, were compared in a mouse bacteraemia model. Anti-Esp serum was tested for its capacity to mediate opsonophagocytic killing of E1162 in vitro and to protect against E. faecium bacteraemia. The inactivation of esp attenuated E. faecium virulence with reduced numbers of bacteria recovered from the kidneys in animals infected with the mutant compared to the wild-type strain (P=0.035). Passive immunization with rabbit polyclonal serum raised against the recombinant N-terminal Esp protein did not protect mice against E. faecium bacteraemia (P>0.05). In contrast, mice passively immunized with polyclonal antiserum raised against lipoteichoic acid (LTA) from E. faecalis had lower numbers of E. faecium E1162 in the blood compared to mice immunized with normal rabbit serum. These results suggest that Esp contributes to E. faecium persistence in the host. However, in contrast to LTA, Esp does not seem to be a target for protective antibodies in E. faecium strain E1162 in mouse bacteraemia.
Division of Infectious Diseases, Department of Medicine, University Medical Center, Hugstetter Str. 55, 79106 Freiburg, Germany.
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Sava
Department of Medical Microbiology, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands.
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Heikens
Division of Infectious Diseases, Department of Medicine, University Medical Center, Hugstetter Str. 55, 79106 Freiburg, Germany.
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Kropec
Division of Infectious Diseases, Department of Medicine, University Medical Center, Hugstetter Str. 55, 79106 Freiburg, Germany.
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Theilacker
Department of Medical Microbiology, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands.
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Willems
Division of Infectious Diseases, Department of Medicine, University Medical Center, Hugstetter Str. 55, 79106 Freiburg, Germany.
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Huebner
D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood* / Q000276:immunology; D016470:Bacteremia / Q000382:microbiology*; D001426:Bacterial Proteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D016984:Enterococcus faecium / Q000378:metabolism*; D005260:Female; D016908:Gram-Positive Bacterial Infections / Q000382:microbiology*; D007106:Immune Sera / Q000276:immunology; D007116:Immunization, Passive; D008565:Membrane Proteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D009895:Opsonin Proteins / Q000276:immunology*; D011817:Rabbits
D000907:Antibodies, Bacterial; D001426:Bacterial Proteins; D007106:Immune Sera; D008565:Membrane Proteins; D009895:Opsonin Proteins; C116707:enterococcal surface protein, esp