Diarrhoea continues to be one of the most common causes of morbidity and mortality among infants and children in developing countries. To investigate the incidence, antimicrobial resistance and genetic relationships of enteropathogenic Escherichia coli (EPEC) in children with diarrhoea, a total of 612 stool specimens were collected in Tehran, Iran, and cultured to isolate strains of EPEC. The disc diffusion method was used to determine the susceptibility of the isolates according to the Clinical and Laboratory Standards Institute (CLSI) guidelines. The presence of eae, stx and bfp-A genes was determined by PCR. The genetic relationships between EPEC isolates were determined by pulsed-field gel electrophoresis (PFGE). Out of the 412 strains of E. coli obtained from 612 diarrhoeal stool specimens, 23 (5.6 %) were identified as EPEC, of which seven (30.4 %) were classified as typical strains of EPEC and 16 (69.6 %) were classified as atypical. Out of the 23 EPEC isolates, 69.5 % were resistant to ampicillin, 39.1 % were resistant to tetracycline and cotrimoxazole, 30.4 % were resistant to cefpodoxime, ceftazidime, ceftriaxone and aztreonam, and 26.1 % were resistant to imipenem. The isolates were classified into 21 pulsotypes by PFGE profiles. The present study shows that typical and atypical EPEC isolates displayed considerable heterogeneity in PFGE profiles and EPEC infections were only sporadic in Tehran. Overall 69 % of isolates were resistant to at least one of the antibiotics tested. INTRODUCTIONEnteropathogenic Escherichia coli (EPEC) is one of the major causes of diarrhoea among children in developing countries (Hernandes et al., 2009;Moura et al., 2009). The pathogenesis of EPEC depends on the locus of enterocyte effacement (LEE), a chromosomal pathogenicity island. The LEE contains a number of different genes, including eae, which has an essential role in inducing a characteristic lesion formation in the intestinal epithelium, termed an attaching and effacing (A/E) lesion (Elliott et al., 1998;Vallance & Finlay 2000;Kaper et al., 2004). The eae gene encodes intimin, a 94 kDa outer-membrane protein that is responsible for the intimate adherence between bacterial and enterocyte membranes (Vallance & Finlay, 2000;Trabulsi et al., 2002). EPEC strains are classified as typical or atypical, according to the presence or absence of the E. coli adherence factor plasmid (EAF) that carries the bfpA gene, which encodes the bundle-forming pili (Hernandes et al., 2009). The most typical EPEC strains belong to the classic O : H serotypes and are eae-and bfpA-positive (Ochoa et al., 2008). The atypical EPEC isolates are eaepositive and bfpA-and stx (the gene encoding shiga-like toxin)-negative. EPEC are among the most important pathogens infecting children under 2 years of age in the developing world (Ochoa et al., 2008). Recent studies indicate that atypical EPEC is more prevalent than typical Abbreviations: EPEC, enteropathogenic Escherichia coli; LEE, locus of enterocyte effacement; PFGE, pulsed-field gel electrophore...

An increased prevalence of immunoglobulin (Ig) A deficiency has been documented in a number of autoimmune diseases; however, its association with type 1 diabetes mellitus (DM1) is a subject of debate. This study was performed to evaluate serum IgA levels in a group of pediatric patients with DM1. Three hundred patients with mean age of 12.6 ± 6.7 years were enrolled in this study. Serum IgA and other immunoglobulins levels were measured using enzyme-linked immunosorbant assay. Mean serum IgA level of patients was 271.0 ± 141.4 mg/dl. Only two patients had IgA deficiency (IgA < 10 mg/dl), who were two boys with ages of 9 and 10 years. Although associated autoimmune disorders were found in a number of patients with DM1, no other autoimmune disorder was detected in these two patients with IgA deficiency. Serum levels of all other immunoglobulins were normal. Serum IgA levels did not significantly differ by grouping the patients according to age variation, sex distribution, disease duration, and associated disorders. There was no significant correlation between IgA levels and hemoglobin A1c. This study showed the prevalence of IgA deficiency in Iranian patients with DM1 as 0.7% (1:150), which is much higher than reported prevalences in general populations. Further studies are needed for better understanding the possible etiologies of increased IgA deficiency in DM1 and its effects on diabetes control.

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