1887

Abstract

Summary

Over the last 30 years, has become an important cause of nosocomial infection. There have been many reports concerning the identification, antibiotic susceptibility, pathogenicity, epidemiological investigations and typing of this organism. Accurate identification is important in defining outbreaks. The API 20E system has been used widely, but is not individually satisfactory. The growth of in the environment has been investigated in relation to water, disinfectants and plastics such as blood bags. Certain extracellular products are unique to . Pigment (prodigiosin) biosynthesis by has been investigated fully since the emergence of the organism as a cause of infection. Many other aspects of the pathogenicity and virulence of have been studied, including adherence and hydrophobicity, lipopolysaccharide (LPS) and extracellular products. Two modes of adhesion to host epithelial surfaces have been suggested. These are mannose-resistant (MR) pili and mannose-sensitive (MS) pili. LPS, which is responsible for the biological activity of endotoxin, has been investigated fully and 24 somatic antigens have been described. The production of different enzymes by as virulence factors has also been reported, including chitinase, lipase, chloroperoxidase and an extracellular protein, HasA. Antibiotics used to treat serratia infection include β-lactam agents, aminoglycosides and fluoroquinolones and a variety of different resistance mechanisms have been demonstrated. Typing methods used to study the epidemiology of include biotyping, bacteriocin typing, phage typing, plasmid analysis, polymerase chain reaction amplification of enterobacterial repetitive intergenic consensus sequences (ERIC-PCR) and ribotyping. Serological typing has also been used and this method seems to be a suitable first-line typing method for , although some strains remain untypable. RAPD-PCR has also been applied to a small number of isolates and seems to be a promising method, especially for rapid monitoring of an outbreak and tracing the source of initial infection.

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/content/journal/jmm/10.1099/00222615-46-11-903
1997-11-01
2019-12-08
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