Generation and testing of mutants of Enterococcus faecalis in a mouse peritonitis model.
A previously described mouse peritonitis model was used to study derivatives of Enterococcus faecalis strain OG1RF. The addition of sterile rat fecal extracts (SRFE) lowered the LD50 of OG1RF >10-fold. Hemolysin production caused a 35-fold lower LD50 and a much shorter survival, similar to previous results using a peritonitis model without SRFE. A purine (but not a pyrimidine) auxotroph was considerably less lethal than wild type; gelatinase mutants were also attenuated. A suicide vector was generated with an enterococcal selectable marker in order to disrupt a gene encoding an E. faecalis antigen; the resulting mutant was not attenuated despite a slower growth rate. In conclusion, this model allows attenuated mutants to be detected, corroborates prior reports that hemolysin is a virulence factor, and suggests a role for gelatinase in virulence of E. faecalis in mice; the attenuated purine auxotroph may provide a system for developing vectors for in vivo expression systems.
Center for the Study of Emerging and Re-emerging Pathogens, University of Texas Medical School at Houston, USA.
K V
KV
Singh
X
X
Qin
G M
GM
Weinstock
B E
BE
Murray
D000818:Animals; D004195:Disease Models, Animal; D013293:Enterococcus faecalis / Q000235:genetics*; D005243:Feces; D005260:Female; D018093:Gelatinases / Q000235:genetics; D016908:Gram-Positive Bacterial Infections / Q000235:genetics*; D006460:Hemolysin Proteins / Q000494:pharmacology; D051379:Mice; D009154:Mutation; D010538:Peritonitis / Q000235:genetics*; D051381:Rats
D006460:Hemolysin Proteins; D018093:Gelatinases