ABSTRACT
An abrupt and persistent 30% increase in the rate of nosocomial infections was detected at a university teaching hospital after a prolonged period with a relatively constant nosocomial infection rate. Demographic data, risk factors for nosocomial infection, features of reported cases of nosocomial infection, and policy and procedure changes were evaluated for the periods of 1 January 1997 to 30 April 1998 (endemic period) and 1 May to 31 December 1998 (epidemic period). An extensive outbreak investigation revealed no evidence of a true outbreak of nosocomial infection. The apparent outbreak involved all four major body sites, began during the same month that an antibiotic management programme was started, involved the same adult medical and surgical units where antibiotics were being controlled, and occurred months before any significant change in antibiotic usage. A greater proportion of nosocomial infection during the epidemic period was reported by the nosocomial infection surveillance nurses, based on a treating physician's diagnosis rather than on specific clinical criteria. In an attempt to justify existing antibiotic prescribing practices after the implementation of an antibiotic management programme, clinicians altered the threshold at which they documented the presence of nosocomial infection. This change in documentation produced a large pseudo-outbreak of nosocomial infection.
Subject(s)
Anti-Bacterial Agents/adverse effects , Cross Infection/etiology , Disease Outbreaks , Drug Utilization Review , Anti-Bacterial Agents/administration & dosage , Cross Infection/diagnosis , Cross Infection/drug therapy , Data Collection , Hospitals, University , Humans , VirginiaABSTRACT
The lipopolysaccharide (LPS) structure of Salmonella typhimurium has been correlated with the virulence of wild-type strain LT2. Mutants of LT2 with truncated polysaccharide portions of LPS are less virulent than strains with a complete LPS structure. Polyclonal T cells and monoclonal T-cell hybridomas were more reactive to heat-killed rough mutants than to heat-killed smooth strains, as measured by interleukin-2 (IL-2) production. Using a large panel of strains with truncated LPS molecules, we found that T-cell reactivity decreased with certain lengths of polysaccharide. The decreased response was not due to differential phagocytic uptake, IL-12 production, or major histocompatibility complex class II surface expression by macrophages. Also, LT2 did not mediate any global suppression since addition of LT2 did not diminish the response of T cells specific for antigens unrelated to Salmonella. In an experiment in which processing times were varied, we found that antigens from rough strains were processed and presented more quickly than those associated with smooth strains. At longer processing times, epitopes from LT2 were presented well. We hypothesize that the slower antigen processing and presentation of wild-type Salmonella may be caused by masking of surface antigens by the longer polysaccharide portion of smooth LPS. This blocking of effective antigen presentation may contribute to the virulence of Salmonella.
