ABSTRACT
We describe the features of 13 cases of Pseudomonas aeruginosa folliculitis (eight of which occurred sporadically and five of which resulted from two family outbreaks) that developed subsequent to the use of commercial synthetic sponges for bathing. On the basis of O serogrouping and pyocin typing and subtyping, the strains recovered from the skin lesions were found to be identical to those isolated from household shower water and sponges. P. aeruginosa folliculitis is commonly caused by the serogroup O:11; The serogroups described in this study are rare causative agents of this type of skin infection. We believe that this is the first report of P. aeruginosa folliculitis due to serogroups O:3 and O:16.
Subject(s)
Community-Acquired Infections/microbiology , Equipment Contamination , Folliculitis/microbiology , Pseudomonas Infections/microbiology , Pseudomonas aeruginosa/isolation & purification , Water Microbiology , Adult , Baths , Child , Child, Preschool , Humans , Serotyping , Skin/microbiologyABSTRACT
Comparative studies of a gentamicin-sensitive strain (P28-0) of Pseudomonas aeruginosa and a gentamicin-resistant mutant (P23-800) have been carried out. No aminoglycoside-modifying enzymes were detected in extracts of the mutant. Electron microscopy of thin sections and the loss of O-antigenicity suggested that resistance of the mutant to gentamicin was related to an alteration in the outer membrane. Analysis of the lipopolysaccharide (LPS) components of the cell walls revealed significant differences. The LPS from strain P28-0 was typical of wild-type P. aeruginosa strains of Habs serotype O6, with quinovosamine and aminogalacturonic acid as O-specific aminocomponents. The LPS from the resistant mutant lacked the O-specific polymer, but had a core oligosaccharide similar to that of the parent strain. Both LPS were rich in phosphorus, part of which was present in triphosphate residues. Although the 31P nuclear magnetic resonance spectra of the LPS differed in some respects, these differences did not seem to correlate with the disparity in sensitivity to gentamicin of the two organisms.
