[Antibiotic resistance of clinical isolates of acinetobacter baumannii in hospitals of Kermanshah, Iran during one year]

Acinetobacter spp. are non-fermenting gram-negative coccobacilli that have emerged in recent three decades as major causes of nosocomial infections. Acinetobacter baumannii is the most common pathogen causing a wide spectrum of infections. Acinetobacter infections are difficult to treat, due to both the intrinsic resistance of the pathogen and its ability to readily acquire new resistance mechanisms. A total of 84 Acinetobacter strains isolated from clinical samples were identified at the species level by biochemical tests. Then their susceptibility to 23 antibiotics and synergism among some of them were determined using disk agar diffusion testing. Antibiogram results were interpreted by using CLSI standard tables. The highest rate of drug resistance [92-98%] was observed to ampicillin, cefpodoxime, cefotaxime and ceftriaxone. Tigecycline, colistin and polymyxin B with the least resistance [3-14%] were identified as the most effective antibiotics. Non-fermentative bacteria such as Acinetobacter always are known as examples of drug-resistant bacteria. The results of the present study also indicate a high level of resistance to different antibiotics. Difference in the rates of Acinetobacter resistance to antibiotics based on geographical areas was observed

[Detection of mutation in codon 315 katG gene as a gene marker associated with isoniazid resistance, in mycobacterium tuberculosis strains isolated from patients in Isfahan and Tehran by PCR-RFLP method]

Drug resistance to tuberculosis is continuously increasing and is a significant threat to tuberculosis control programs because afew effective drugs are present against Mycobacterium tuberculosis. Although isoniazid [INH] is the most effective drug against tuberculosis, resistance to this drug also develops readily. Mutations in katG, specially the Ser315Thr substitution, are responsible for isoniazid resistance in a large proportion of patients with tuberculosis. However, the frequency of the katG Ser315Thr substitution varies among population samples. This study provided molecular characterization of isoniazid resistance of M. tuberculosis strains and extended our knowledge about molecular basis of M. tuberculosis drug resistance that is widely applicable for rapid drug resistance detection. Using 1% proportional method, the sensitivity of 126 strains isolated from patients in Isfahan and Tehran to isoniazid was determined. The katG mutations in codon 315 associated with isoniazid resistance among isoniazid resistant isolates was determined by PCR-RFLP. In this way, 355 bp PCR products were digested by MspI. Out of 126 isolates of M. tuberculosis, 32 [25.4%] strains were determined as INH resistant. Resistance rate was 22.6% [19 strains] in Isfahan and 31% [13 strains] in Tehran. Overall, 72% of isoniazidresistant isolates could be identified by analysis of just katG 315 loci. The PCR-RFLP using MspI restriction enzyme that detects katG Ser315Thr substitution could be identified in 72% of isoniazid-resistant strains. Elucidation of the molecular characterization of isoniazid resistance in M. tuberculosis has led to the development of different genotypic approaches to the rapid detection of isoniazid resistant in clinical isolates

Detection of s315t mutation in the katg gene associated with isoniazid resistance in mycobacterium tuberculosis isolated from isfahan and tehran by PCR-RFLP

Drug resistance to tuberculosis is increasing continuously and is a significant threat to tuberculosis control programs because there arc few drugs effective against Mycobacterium tuberculosis. Although isoniazid is most efficient in killing the tuberculosis bacilli, resistance to this drug also develops most readily. Mutations in katG, in particular the Ser 315 Thr substitution, are responsible for isoniazid resistance in a large proportion of tuberculosis cases. However, the frequency of the katG Ser 315 Thr substitution varies with population samples. This study provided the first molecular characterization of isoniazid resistance of M. tuberculosis strains and extended our knowledge of molecular basis of M. tuberculosis drug resistance that are widely applicable for rapid drug resistance detection. Using 1% proportional method, the sensitivity of 126 strains collected from Isfahan and Tehran to isoniazid was determined. The katG mutations in codon 315 associated with isoniazid resistance among isoniazid resistant isolates were determined by PCR-RFLP. In this way, 355 bp PCR products were digested by Mspl of 126 isolates of M. tuberculosis, 32 [25.4%] strains were determined as INH resistant. Resistance rate was 22.6% [19 strains] in Isfahan and 31% [13 strains] in Tehran. In total, 72% of isoniazid-resistant isolates could be identified by analysis of just katG 315 loci. The PCR-RFLP with Mspl that detect katG Ser315Thr substitution identified more isoniazid-resistant strains with mutations at codon 315 in the katG. Elucidation of the molecular basis of isoniazid resistance in M. tuberculosis has led to the development of different genotypic approaches for the rapid detection of isoniazid resistance in clinical isolates