ABSTRACT
PURPOSE: In this study, the culturable halophilic and halotolerant bacterial diversity was determined in Aran-Bidgol as a thalassohaline seasonal hypersaline lake in Iran. METHODS: Thirty water, soil, sediments, coastal mud, multi-color brines and salt crystals samples were extracted and cultured using different media and incubation conditions. Totally 958 isolates were obtained and 87 isolates were selected for further studies, based on morphological, physiological and biochemical tests, representing different morphotypes. RESULTS: Based on 16S rRNA gene sequence analyses, the isolates exhibited 94.6-100% sequence similarity to the closest known species of the genera Bacillus, Halomonas, Oceanobacillus, Salinicoccus, Thalassobacillus, Ornithinibacillus, Halobacillus, Salicola, Virgibacillus, Aerococcus, Arthrobacter, Idiomarina, Paraliobacillus, Staphylococcus, Acinetobacter, Aneurinibacillus, Brevibacillus, Brevundimonas, Chromohalobacter, Gracilibacillus, Jeotgalicoccus, Kocuria, Marinilactibacillus, Marinobacter, Microbacterium, Paenibacillus, Paracoccus, Piscibacillus, Pseudomonas and Sediminibacillus and also, comparison of ARDRA patterns among the sequenced strains, using AluI, Bst UI and Hpa II enzymes showed that these patterns are in accordance with the phylogenetic position of these strains. CONCLUSION: The PCR-RFLP analyses suggested that ARDRA possess a functional potential for distinguishing halophilic bacteria to be used for further studies in elementary steps of isolation to reduce the tedious duplication of isolates.
ABSTRACT
BACKGROUND: High levels of multidrug resistance are usually associated with mobile genetic elements that encode specific resistance genes. Integrons are important genetic elements involved in spreading antibiotic multi-resistance. In special cases, large exogenous segments in bacterial genomes form genomic islands, and one of the functions of these genomic islands is antibiotic resistance. Due to geographical heterogeneity in antibiotic resistance pattern, it is mandatory to determine resistance patterns that are region-specific rather than generalized. OBJECTIVES: The objective of this study was to detect class 1 and 2 integrons in clinical isolates of Haemophilus influenzae. PATIENTS AND METHODS: Antibiogram tests were carried out for twenty clinical isolates collected from different patients admitted to the Milad hospital. The PCR reactions were performed using universal primers specified for Int1 and Int2 genes attributed to class 1 and 2 integrons. Also amplification of integrase genes related to genomic islands was investigated by designing specific primers. RESULTS: Of the twenty isolates, all (100%) were resistant to clindamycin, chloramphenicol and tetracycline, 95% to amoxicillin, 50% to ceftriaxone, 45% to ciprofloxacin and 5% to azithromycin. Also, all isolates (100%) were sensitive to trimethoprim/sulfamethoxazole. Class 1 and 2 integrons were not detected in any of the isolates; however the integrase gene attributed to genomic islands was identified in twelve isolates. CONCLUSIONS: Antibiotic resistance gene cassettes may be carried on integron or other genetic elements. The purpose of this study was to detect integron or genomic islands involved in antibiotic resistance profile of the isolates of H. influenzae collected in this study.
ABSTRACT
The attaching and effacing (A/E) bacterial pathogens enteropathogenic Escherichia coli and enterohemorrhagic E. coli and the related mouse pathogen Citrobacter rodentium colonize their hosts' intestines by infecting the apical surfaces of enterocytes, subverting their function, and they ultimately cause diarrhea. Surprisingly, little is known about the interactions of these organisms with goblet cells, which are specialized epithelial cells that secrete the protective molecules Muc2 and trefoil factor 3 (Tff3) into the intestinal lumen. C. rodentium infection leads to dramatic goblet cell depletion within the infected colon, yet it is not clear whether C. rodentium infects goblet cells or if this pathology is pathogen or host mediated. As determined by immunostaining and PCR, both the number of goblet cells and the expression of genes encoding Muc2 and Tff3 were significantly reduced by day 10 postinfection. While electron microscopy and immunostaining revealed that C. rodentium directly infected a fraction of colonic goblet cells, C. rodentium localization did not correlate with goblet cell depletion. To assess the role of the host immune system in these changes, Rag1 knockout (KO) (T- and B-cell-deficient) mice were infected with C. rodentium. Rag1 KO mice did not exhibit the reduction in the number of goblet cells or in mediator (Muc2 and Tff3) expression observed in infected immunocompetent mice. However, reconstitution of Rag1 KO mice with T and B lymphocytes from C57BL/6 mice restored the goblet cell depletion phenotype during C. rodentium infection. In conclusion, these studies demonstrated that while colonic goblet cells can be subject to direct infection and potential subversion by A/E pathogens in vivo, it is the host immune system that primarily modulates the function of these cells during infection.
