ENINGOCOCCAL DISEASE caused predominantly by Neisseria meningitidis serogroups A, B, and C occurs predominantly in young children and remains a substantial cause of morbidity and mortality worldwide. 1,2 In addition to causing endemic disease globally, meningococci, unlike other encapsulated bacteria, cause epidemics. Serogroup B epidemics, problematic in Norway and throughout much of Latin America in the 1980s and 1990s, 1 have recently emerged in New Zealand 3 and the United States. [4][5][6] Response to serogroup B epidemics, unlike serogroup A and C epidemics, is difficult because existing serogroup B vaccines have not been shown to be efficacious on an international scale. [7][8][9][10] Quadrivalent meningococcal polysaccharide vaccine is efficacious against meningococcal disease caused by the A, C, W-135, and Y serogroups. [11][12][13] Serogroup B polysaccharide antigen, however, is poorly immunogenic in humans, 14,15 and the elicitation of antibodies to serogroup B polysaccharide antigen is of concern because this antigen is present in human neonatal neural tissue. 16,17 Therefore, alternative Author Affiliations are listed at the end of this article.
We designed a multiplex PCR for the detection of all categories of diarrheagenic Escherichia coli. This method proved to be specific and rapid in detecting virulence genes from Shiga toxin-producing (stx 1 , stx 2 , and eae), enteropathogenic (eae and bfp), enterotoxigenic (stII and lt), enteroinvasive (virF and ipaH), enteroaggregative (aafII), and diffuse adherent (daaE) Escherichia coli in stool samples.Most Escherichia coli strains are commensal; however, there are several highly adapted clones that have the capacity to cause human illness. Strains that cause enteric infections are designated diarrheagenic E. coli, a group that includes emergent pathogens with public health relevance worldwide (13). Six categories of diarrheagenic E. coli that differ in their virulence factors have been described (13). The most commonly reported diarrheagenic E. coli strains in Chile are enterotoxigenic E. coli (ETEC), which produces one or more enterotoxins that are heat labile LT (LT-1 and LT-2) or heat stable ST (STa and STb) (11); enteropathogenic E. coli (EPEC), which harbors a pathogenicity island that encodes a series of proteins involved in the attaching and effacement lesions of the intestinal microvilli of the host cell (8); and the presence of the large EPEC adherence factor (EAF) plasmid, on which also the cluster of genes encoding bundle-forming pili (bfp) is present (9). Based on these, EPEC strains are classified as typical when they possess the EAF plasmid, whereas atypical EPEC strains do not possess the EAF plasmid (18); Shiga toxin-producing E. coli (STEC) is characterized by the production of two potent cytotoxins denominated Shiga-like toxins 1 and 2 (Stx1 and Stx2) (17) and in some strains the presence of the LEE locus related to the attaching and effacement lesion (7, 16). The three other categories seem to be less prevalent.
In randomized, controlled field trials in Area Norte and Area Occidente of Santiago, Chile, 2 (Norte) or 3 (Occidente) doses of live oral typhoid vaccine Ty21a in enteric-coated capsules conferred protection against confirmed Salmonella enterica serovar Typhi disease (53% efficacy in Norte; 67% efficacy in Occidente) during 3 years of follow-up. There was also a trend in each trial showing protection against S. enterica serovar Paratyphi B disease (56% efficacy in Norte; 42% efficacy in Occidente). To enhance statistical power, an analysis was performed using pooled data from the 2 trials; this pooling of data was justified by the following facts: epidemiologic surveillance and microbiological methods were identical, the trials overlapped during 22 of the 36 months of follow-up in each trial, the estimates of efficacy against paratyphoid B fever in the 2 trials were roughly similar, and the ratio of follow-up of vaccine recipients to control subjects in both trials was ~1 : 1. In the pooled analysis, Ty21a conferred significant protection against paratyphoid B fever (efficacy, 49%; 95% confidence interval, 8%-73%; P=.019).
Several live oral vaccines (polio, bovine rotavirus, CVD 103-HgR cholera) are less immunogenic in developing than in industrialized countries. It was hypothesized that proximal small bowel bacterial overgrowth (common in children in less developed countries but rare in industrialized settings) diminishes the vibriocidal antibody response to CVD 103-HgR. In total, 202 fasting Santiago schoolchildren aged 5-9 years had lactulose breath H2 tests to detect proximal small bowel bacteria 1 day before ingesting CVD 103-HgR. Florid small bowel overgrowth was observed in 10 (5.6%) of 178 analyzable children. In children with florid overgrowth, vibriocidal seroconversion differed little from other children (60% vs. 67%), but the geometric mean titer was lower (160 vs. 368; P=.25). By logistic regression, increased peak breath H2 at small bowel time points was associated with diminished seroconversion (P=.04), as was the interaction of H2 value and weight (children >25 kg had lower seroconversion rates among subjects with heaviest overgrowth).
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