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1.
Iranian Journal of Medical Microbiology. 2007; 1 (2): 27-34
em Persa | IMEMR | ID: emr-82913

RESUMO

The Study of E.coli and Klebsiella resistance to wide spectrum antibiotics and molecular evaluation of resistance in these bacteria were examined. Treatment with wide spectrum antibiotics against bacteria can lead to resistance. The antimicrobial resistance can be seen in two types: 1] chromosomal alterations which could result in changes in structure of receptors of specific drugs. Most of this mutation can cause the absence of a penicillin binding proteins [pbps] and 2] is plasmid resistance. Plasmid genes can usually produce enzymes which result in destruction of antibiotics. An example is extended spectrum B-lactamase [ESBLs] which causes resistance to the third generation of cephalosporin, monobactams and new penicillin. ESBL plasmids are derived from TEM-1, TEM-2 and SHV-2. It has been recognized that because of point mutations in these plasmids, there are about 90 types of TEM and 25 types of SHV. The reason for the formation of point mutations within the ESBL plasmids is due to high consumption of broad spectrum antibiotics. In a cross-sectional study, 218 specimens from patients were collected and after identification of bacteria, the percentage of ESBLs among the isolates was calculated. For this purpose combined disk method and double disk method are used .Then TEM and SHV plasmids from 23 specimens of E.coli and Klebsiella were examined using plasmid extraction kit and PCR. The result of this study showed; the antibiotic resistance in 10% of E .coli was chromosomal and 50% were plasmids. The remaining isolates were sensitive. In Klebsiella, 12.8% of resistance was chromosomal and 62% were due to plasmids and remaining isolates were sensitive. The results from PCR showed; in E .coli 52.8% of the isolates were TEM positive and 84.6% were SHV positive and 69.2% were positive for both TEM and SHV. For Klebsiella 80% were TEM positive and 80% were SHV and 60% were positive for both TEM and SHV. The rate of ESBLs in Iran is higher than the results in similar studies in other countries .This could be because of the overuse of third generation of cephalosporin. For the purpose of having proper treatment using antibiotics, medical education and laboratory detection of ESBLs could be effective to choose choice antibiotics


Assuntos
Humanos , Klebsiella pneumoniae/efeitos dos fármacos , Resistência Microbiana a Medicamentos , beta-Lactamases , Estudos Transversais , Reação em Cadeia da Polimerase
2.
Govaresh. 2004; 9 (3): 176-180
em Persa, Inglês | IMEMR | ID: emr-104560

RESUMO

Helicobacter pylori commonly is associated with gastritis: but only sometimes it causes clinically significant diseases such as gastric and duodenal ulcer. The development of disease depends on the virulence of the infecting H. pylori strain, the susceptibility of the host, and environment co-factors. The cytotoxin associated protein encoded by cagA gene is an important virulence factor that is produced by some H. pylori strains, and has been used as virulence marker in some populations. The aim of the study was to examine the prevalence of cagA gene in the isolated strains of H. pylori from patients with dyspeptic disease and to investigate the association of cagA gene and the severity of H. pylori related diseases in Iran. In this study, biopsy specimens were obtained from the antrum of 180 patients. After isolation of H. pylori and its DNA by standard methods, polymerase chain reaction [PCR] technique was used for detection of cagA bacterial gene. 92 out of the 180 patients had H. pylori strains. 70% were cagA gene positive. All patients with peptic ulcer [100%] and 44 out of 72 [61%] patients with non-ulcer dyspepsia were cagA positive [p<0.01]. There was significant difference in frequency of cagA gene in peptic ulcer disease and non-ulcer dyspepsia [p<0.01]. It showed that the risk of PUD in patients with cagA+ H. pylori infection may be higher than in those with cagA- H. pylori infection


Assuntos
Helicobacter pylori/patogenicidade , Prevalência , Proteínas de Bactérias , Biópsia , Reação em Cadeia da Polimerase , Úlcera Duodenal/etiologia , Úlcera Duodenal/parasitologia , Úlcera Duodenal/genética , Úlcera Gástrica/etiologia , Úlcera Gástrica/parasitologia , Úlcera Gástrica/genética , Úlcera Péptica/etiologia , Úlcera Péptica/parasitologia , Úlcera Péptica/genética , Gastrite/etiologia , Gastrite/parasitologia , Gastrite/genética
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