In June 2001, the Los Angeles County Department of Health Services/Public Health conducted a cohort study of an outbreak of acute febrile gastroenteritis among 16 of 44 healthy attendees of a catered party. The median age of the attendees who became ill was 15.5 years. Symptoms included body aches (in 88% of attendees), fever (81%), headache (81%), diarrhea (63%), and vomiting (56%). Illness was associated with ingestion of precooked, sliced turkey (P=.000004). Six stool specimens yielded Listeria monocytogenes. Leftover turkey yielded L. monocytogenes, 1.6x10(9) cfu/g. All isolates were serotype 1/2a and had matching molecular fingerprints. Clusters of suspect cases were identified among attendees at 2 other catered events, but no additional cases were confirmed. This is only the third reported outbreak of L. monocytogenes-associated gastroenteritis in the United States. In cases of febrile gastroenteritis for which routine cultures for enteric pathogens are negative, clinicians should suspect listeriosis and should consider asking laboratories to retain stool specimens to expedite testing for Listeria organisms.

Botulism results from consumption of preformed toxin or in vivo toxin elaboration in wounds or intestine. Of U.S. food-borne botulism cases since 1950, the majority were due to toxin A, but a significant number of suspect cases were never confirmed by culture or toxin detection. We report here a possible case of food-borne botulism attributed to toxin F production by a Clostridium baratii organism isolated from food consumed by the patient. The isolation of a toxin-producing Clostridium species other than Clostridium botulinum from food and stool requires deviation from the usual laboratory protocols, which may account for the lack of complete laboratory confirmation of clinically diagnosed cases.

While evaluating quinolone resistance in a sample of Campylobacter isolates recovered from patients with campylobacteriosis in Los Angeles County, California, in 1998, we discovered that the second most frequently isolated species was Campylobacter upsaliensis (6 [4%] of 155 isolates). The ability of laboratories to recover this species may be dependent on the culture conditions and the media used. Three dogs living in the households of 2 of these 6 patients had C. upsaliensis isolated in their stool specimens.

An epidemiological and microbiological investigation of a cluster of eight cases of Legionnaires' disease in Los Angeles County in November 1997 yielded conflicting results. The epidemiological part of the investigation implicated one of several mobile cooling towers used by a film studio in the centre of the outbreak area. However, water sampled from these cooling towers contained L. pneumophila serogroup 1 of another subtype than the strain that was recovered from case-patients in the outbreak. Samples from two cooling towers located downwind from all of the case-patients contained a Legionella strain that was indistinguishable from the outbreak strain by four subtyping techniques (AP-PCR, PFGE, MAb, and MLEE). It is unlikely that these cooling towers were the source of infection for all the case-patients, and they were not associated with risk of disease in the case-control study. The outbreak strain also was not distinguishable, by three subtyping techniques (AP-PCR, PFGE, and MAb), from a L. pneumophila strain that had caused an outbreak in Providence, RI, in 1993. Laboratory cross-contamination was unlikely because the initial subtyping was done in different laboratories. In this investigation, microbiology was helpful for distinguishing the outbreak cluster from unrelated cases of Legionnaires' disease occurring elsewhere. However, multiple subtyping techniques failed to distinguish environmental sources that were probably not associated with the outbreak. Persons investigating Legionnaires' disease outbreaks should be aware that microbiological subtyping does not always identify a source with absolute certainty.