Resistance-plasmid- and protease-independent murine virulence of a multiple-drug-resistant strain of Serratia marcescens.
The multiple-drug-resistant Serratia marcescens isolate SH 186 (serotype 06/014:H12, bacteriocin type 18) carried a 44 megadalton, nonconjugative resistance (R-) plasmid as demonstrated with 'curing' experiments and the DNA agarose gel electrophoresis technique. 'Cured' variants, which had lost part of or the entire R-plasmid, proved as virulent for outbred NMRI mice (intraperitoneal route) as the wild-type parent strain. Therefore, the virulence of this S. marcescens strain was plasmid-independent. Protease-deficient variants of this strain as well as protease-negative variants of two additional S. marcescens strains displayed comparable murine virulence. None of 19 representative S. marcescens strains, including isolate SH 186, gave rise to guinea pig keratoconjunctivitis (negative Anton-Sereny tests), i.e., were non-invasive; NMRI mice pretreated with either cyclophosphamide (leukopenia), type II carrageenan (blockade of macrophages) or with zymosan (depletion of complement) revealed essentially unaltered susceptibility to S. marcescens. However, mice pretreated with cyclophosphamide followed by zymosan were significantly more susceptible for 4 tests strains of S. marcescens, including isolate SH 186. Thus, neutrophil granulocytes and complement were required for murine defense against intraperitoneal infection with S. marcescens.
D000818:Animals; D001424:Bacterial Infections / Q000382:microbiology*; D005260:Female; D006168:Guinea Pigs; D006801:Humans; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D010447:Peptide Hydrolases / Q000235:genetics; D011815:R Factors; D012706:Serratia marcescens / Q000187:drug effects / Q000201:enzymology / Q000235:genetics / Q000472:pathogenicity*; D014774:Virulence
D010447:Peptide Hydrolases