Background: Helicobacter pylori (HP) is identified as the most common gastrointestinal (GI) infection agent in the world. According to some findings shepherd's Helicobacterial infection is due to their contacts to sheep. Considering the controversy, the transmission of HP from the milk of small ruminates to humans and the possibility of the Zenotic nature of the disease has not proven yet. Thus, recognition of the routes of transmission of bacterium to human is vital.

Materials and Methods : Using random clustering, 100 samples (81 sheep and 19 goat's samples) were taken from 20 villages of Mashhad suburb during two years. A questionnaire regarding the health status of the shepherds and their family from the point of view GI discomfort was taken. All taken samples were incubated on two specific HP media, HPSPA (Helicobacter pylori Special Peptone Agar) and Columbia Agar including antibiotics. Following centrifugation, DNA extraction was carried out on all precipitated samples. The specific Urease C gene of HP was traced through polymerase-chain reaction (PCR).

Results: Considering the negative results of both PCR and isolation tests, neither culture media nor PCR could prove the existence of HP gene or the Urease C gene for the specific HP in samples. Information showed that 20% of shepherds and 25% of their families and also 10% of both are complaining of GI discomfort, without any clear relation to HP.

Conclusion: The results showed that two incubation procedures could not detect HP or its gene, Urease C. Probably, the reason could be due to some multifactorial agents, essential for the determination of the strategy of prevention and health. Possibility of transmission of the agent from the small ruminants and milk to humans needs further investigation.

Background: Shiga toxin-producing Escherichia coli (STEC), as one of the most important food-borne pathogen, in human may lead to deadly syndromes, like hemolytic–uremic syndrome (HUS). Occurrence of HUS following urinary tract infection (UTI) has been previously reported. The aim of this study was to identify stx1, stx2 and eaeA genes in E. coli strains isolated from urine samples in Alashtar (Lorestan, Iran)

Materials and Methods: A total number of 144 bacterial isolates were collected from three hospitals in Alashtar during a six-month period. One-hundred E. coli isolates were identified using the standard biochemical tests as well as the selective and differential media. The multiplex PCR method was used to evaluate the presence of stx1, stx2 and eaeA genes.

Results: Two out of 100 E. coli isolates carried both stx2 and eaeA genes and one isolate (1%) only sxt1gene. Moreover, the three genes were not found in any of the isolates tested.

Conclusion: Detection of Shiga toxin-producing E. coli (e.g. O157:H7 and non-O157:H7 serotypes), which may lead to life-threatening syndromes such as HUS, from urine samples is of great importance . Further research in this field using the fast and precise molecular methods is recommended.

Background: Quinolone-resistance in Escherichia coli is ordinarily associated with mutations in the gyrA and parC genes. Plasmid-mediated quinolone resistance (PMQR) was increasingly identified in Enterobacteriaceae family worldwide. The aim of this study was to determine the prevalence of qnrA gene among quinolone-resistant E. coli isolates in Khorram Abad, Iran.

Materials and Methods: In this cross-sectional study, one-hundred forty E. coli isolates were collected from urine samples of the patients. Isolates were screened for ciprofloxacin and nalidixic acid resistance using disk diffusion method according to clinical and laboratory standards institute (CLSI) guidelines. Moreover, PCR was used to evaluate the presence of qnrA gene in quinolone-resistant isolates.

Results: One-hundred sixteen (82.8%) and 63 (43%) out of 140 E. coli isolates showed resistance to nalidixic acid and ciprofloxacin, respectively. The results showed that 14 (12.1%) nalidixic acid- resistant and 9 (14.3%) ciprofloxacin-resistant isolates were positive for qnrA gene.

Conclusion: The identification of qnrA gene among quinolone-resistant E. coli isolates shows that the emergence of PMQR in this region requires serious preventive measures.