Decreased virulence of a gls24 mutant of Enterococcus faecalis OG1RF in an experimental endocarditis model.
In the current study, the gls24 disruption mutant TX10100, previously shown to be more sensitive to bile salts and attenuated in a mouse peritonitis model, showed an approximately fivefold higher 50% infective dose than wild-type OG1RF in a rat endocarditis model. When administered as a mixture, TX10100, unlike a downstream glsB mutant, was significantly outnumbered by OG1RF in vegetations, organs, and blood, despite being inoculated in greater numbers. These results indicate that gls24 is important in the pathogenesis of enterococcal endocarditis.
Nannini
Esteban C
EC
Center for the Study of Emerging and Re-Emerging Pathogens, University of Texas Medical School at Houston, 6431 Fannin, MSB 2.112, Houston, TX 77030, USA.
Teng
Fang
F
Singh
Kavindra V
KV
Murray
Barbara E
BE
D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics* / Q000378:metabolism*; D004697:Endocarditis, Bacterial / Q000097:blood / Q000382:microbiology*; D013293:Enterococcus faecalis / Q000145:classification / Q000235:genetics* / Q000472:pathogenicity*; D006360:Heat-Shock Proteins / Q000235:genetics* / Q000378:metabolism*; D007668:Kidney / Q000382:microbiology; D009154:Mutation / Q000235:genetics; D051381:Rats; D013154:Spleen / Q000382:microbiology; D014774:Virulence / Q000235:genetics
D001426:Bacterial Proteins; C412463:Gls24 protein, Enterococcus faecalis; D006360:Heat-Shock Proteins