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Serratia spp. have been isolated from superficial abscesses, wounds, ocular or urethral discharges, lung, and liver of marine mammals. Although it is now an established pathogen, at one time Serratia marcescens was believed to be completely innocuous. In England and Wales, Serratia bacteremia reports increased by 13.2% between 2000 and 2001. Patients with urinary tract infections (UTIs) and indwelling catheters or colonized or infected respiratory tracts are the most common reservoirs; spread occurs primarily via the hands of hospital personnel. Serratia bacteremia is relatively uncommon; S. marcescens accounted for only 2% of bloodstream infections reported to the National Nosocomial Infections Surveillance System (NNIS). Cholangitis, osteomyelitis, ruptured diverticuli, and premature ruptured membranes have also been reported as sources of bacteremia. S. fonticola fails to produce DNase, lipase, or gelatinase, all hallmark traits of the genus Serratia. The majority of pigmented strains belonged to environmental serotype O6:K14 and were serum resistant, a trait previously determined to be associated with this serotype and not believed to be important in human serratia infection. Strains that are initially susceptible rapidly become resistant during antimicrobial therapy. The current literature indicates that 88 to 93% of serratiae are susceptible to ciprofloxacin. Susceptibilities to various cephalosporins and other antimicrobials are reported.
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