Nearly one-half of the patients who presented to the emergency department with diarrhea had a definite or plausible pathogen in their stool specimens. We were unable to develop a model that was substantially better than physician judgment in identifying patients for whom bacterial culture would yield positive results. The unexpectedly high rate of C. difficile toxin warrants further examination.

Antibiotic use during E. coli O157:H7 infections is associated with a higher rate of subsequent HUS and should be avoided.

No abstract

The bacterial diarrhea prevalence is similar to that in other ambulatory studies, although the spectrum differs. Exclusion criteria for stool testing in diarrhea remain elusive. Studies to determine the etiology of unexplained diarrhea and cost-effective algorithms for diarrhea diagnosis, are needed.

The extent to which antibiotic-resistant bacteria are excreted by humans who have not been exposed to antibiotics is not known. Children, who rarely receive fluoroquinolones, provide opportunities to assess the frequency of fecal excretion by fluoroquinolone-naïve hosts of fluoroquinolone-resistant gram-negative bacilli. Fresh nondiarrheal stools from children were processed by screening them on agar containing ciprofloxacin to recover ciprofloxacin-resistant gram-negative bacilli. Resistant isolates were identified, and ciprofloxacin MICs were determined. Resistant Escherichia coli isolates were also analyzed for urovirulence-associated loci. Thirteen (2.9%) of 455 stools yielded ciprofloxacin-resistant E. coli (seven children), Stenotrophomonas maltophilia (four children), and Achromobacter xylosoxidans and Enterobacter aerogenes (one child each). Neither the subjects themselves nor members of their households used fluoroquinolones in the 4 weeks preceding collection. Six of the seven resistant E. coli isolates belonged to phylogenetic groups B2 and D, in which extraintestinal pathogenic E. coli bacteria are frequently found. All resistant E. coli isolates contained at least three putative E. coli virulence loci. Most ciprofloxacin-resistant bacteria were resistant to additional antibiotics. Potentially pathogenic bacteria that are resistant to therapeutically important antimicrobial agents are excreted by some humans, despite these persons' lack of exposure to the particular drugs. The sources of these resistant organisms are unknown. This underrecognized reservoir of drug-resistant potential pathogens poses public health challenges.

P1 and ABO antigens and bacterial stx genotypes might influence the risk of developing hemolytic uremic syndrome (HUS) after Escherichia coli O157:H7 infections. We determined ABO status and P1 antigen expression in 130 infected and 17 uninfected children, and we determined the stx genotype of the infecting isolate. P1 expression was weakly and directly related to HUS risk (P=.04), but this risk did not extend to the group with the greatest P1 expression. P1 expression remained constant as HUS evolved. The ABO frequency was similar in all groups. These associations were not affected by the stx genotype. stx1(-)/stx2(+) E. coli O157:H7 strains were more commonly associated with HUS than were stx1(+)/stx2(+) strains (P=.21), and 1 child with HUS was infected with a rare stx1(+)/stx2(-) isolate. In the present study, ABO antigens and stx genotypes were not major determinants of the outcome of E. coli O157:H7 infections, and P1 expression did not protect against the development of HUS.

The role of platelet-activating factor (PAF), a phospholipid inflammatory mediator, in Escherichia coli O157:H7-associated hemolytic uremic syndrome (HUS) is unknown. PAF is synthesized by diverse cells and is degraded by PAF-acetylhydrolase (PAF-AH). Deficient PAF-AH activity results from a G-->T transversion at position 994 of exon 9. We examined children infected with E. coliO157:H7 to determine if PAF levels or the PAF-AH ( G994T) mutation reflects the risk of developing HUS. Plasma PAF concentrations were determined using chloroform/methanol extraction, thin layer chromatography purification, and scintillation proximity assay in 10 patients with uncomplicated infection (UI), 10 infected patients who subsequently developed HUS (pre-HUS), 5 HUS patients, and 8 healthy controls. The PAF-AH ( G994T) allele frequency was determined in 52 UI children, 15 with HUS, and 11 controls. Wilcoxon rank sum tests were performed to test differences in location (median) of pairs of groups. PAF levels were higher in the UI ( P=0.04) and pre-HUS ( P=0.01) groups than in healthy controls. No subject had the PAF-AH ( G994T) allele. Thus, elevated plasma PAF levels occur in E. coliO157:H7-infected children, even without HUS, but diminish when HUS develops. The PAF-AH ( G994T) allele does not contribute to the risk of developing HUS.

The frequency of Shiga toxin (Stx)-producing Escherichia coli (STEC) in the urinary tract, which can precipitate the hemolytic-uremic syndrome, is unknown. We tested 597 urinary E. coli isolates by Stx immunoassay and found no STEC. The routine screening of urinary E. coli for the ability to produce Stx is not warranted.