Genotypic and phenotypic patterns of antimicrobial susceptibility of Helicobacter pylori strains among Egyptian patients

Helicobacter pylori [H. pylori] is currently recognized as one of the most common chronic bacterial infections worldwide. Eradication of bacteria is effective in healing peptic ulcers, preventing ulcer relapses, and potentially decreasing the risk of progression to gastric carcinoma. For successful eradication of bacteria, it is imperative that the clinician be aware of the current antimicrobial susceptibility profiles of isolates within the region. Therefore, the aim of this study is to compare the phenotypic and genotypic patterns of antibiotics' susceptibility to H. pylori strains among Egyptian patients. 60 symptomatic cases were enrolled. H. pylori infection was diagnosed by upper endoscopy as well as biopsy. Antimicrobial susceptibility to H. pylori strains was assessed in all subjects by disc diffusion and Ellipsometer testing [E-testing] methods. Further molecular characterization of genes encoding antimicrobial resistance of isolated strains was done by the polymerase chain reaction [PCR]. For metronidazole and ciprofloxacin, we compared the phenotypic and genotypic patterns of resistance as detected by PCR amplification of the resistance genes. Resistance rates by E-test were 100% and 25% for metronidazole and ciprofloxacin respectively from 16 isolated H. pylori strains. Improving the knowledge of resistance mechanisms, the elaboration of rational and efficacious associations for the treatment H. pylori infection are of high importance especially in determining the therapeutic outcome. Further progress should ultimately focus on the establishment of a cheap, feasible and reliable laboratory test to predict the outcome of a therapeutic scheme

Serum level of transforming growth factor-beta in patients with pulmonary tuberculosis

Pulmonary tuberculosis [TB] is a major cause of morbidity and mortality allover the world. Owing to the complex interaction between the Mycobacterium tuberculosis [MTB] and the specific host cell mediated immune response, the clinical spectrum of TB ranges from a few foci affecting the upper parts of the lungs to intense tissue destruction and caseous necrosis. TGF-beta is one of the inhibitory cytokines that, among other functions, is responsible for deactivation of the T-cell response that is important in host defense against MTB, suggesting its role in the pathogenesis of PTB.The aim of this study was to determine the serum level of TGF-beta1 in patients with active pulmonary tuberculosis [cavitary and non cavitary], in comparison to healthy controls and to chronic obstructive airway disease [COAD] patients as disease controls, as well as investigating the correlation between its level and disease severity. Tuberculous patients were followed up during the course of anti-tuberculous chemotherapy to assess the changes in TGF-beta1 level. Three groups were studied, including 24 pulmonary tuberculosis patients [9 patients were cavitary and 15 patients were non cavitary] that were selected according to the diagnostic standards and classification of tuberculosis. [New York NY: National Tuberculosis and Respiratory disease Association, 1969]. Twenty two patients with [COAD] were taken as a disease control group and 13 apparently healthy individuals with matching age and sex were included as normal controls. All patients were subjected to full history taking, clinical examination, laboratory diagnosis of TB by examination of sputum for the presence of acid fast bacilli [AFB] by film or culture and radiological diagnosis by chest X-rays. Serum from all patients and controls was examined for the level of TGF-beta1 using ELISA technique. Patients with PTB were followed up for the post treatment level of TGF-beta1 3 months after the onset of anti-tuberculous treatment. Statistical analysis for the results showed significant elevation of TGF-beta1 serum level in patients with PTB when compared to normal controls but not when compared to the disease controls. No significant difference was found between TGF-beta1 level on comparing the cavitary and non cavitary groups, or on comparing the pre and the post treatment levels. In conclusion TGF-beta1 is suggested to play an important role in the pathogenesis of pulmonary tuberculosis. Further studies can be done to evaluate the correlation between the TGF-beta1 level and the severity of tuberculous disease, or with the course of anti tuberculous treatment. Controlling TGF-beta1 production may be the key to prevent scarring and fibrosis in progressive pulmonary disease as tuberculosis and chronic obstructive pulmonary disease. Also using anti-TGF-beta1 antibodies may be promising anti-tuberculous agents with their anti-fibrotic actions that may prevent the progress of fibrosis during the course of the disease