ABSTRACT
BACKGROUND: Plasmid-mediated quinolone resistance is an increasing clinical concern, globally. The major objective of the present study was to identify the qnr-encoding genes among the quinolone non-susceptible K. pneumoniae isolates obtained from two provinces in Iran. METHODS: A total of 200 K. pneumoniae isolates were obtained from hospitals of Qazvin and Tehran, Iran. The identification of bacterial isolates was carried out by standard laboratory methods and API 20E strips. Susceptibility to quinolone compounds were examined by standard Kirby-Bauer disk diffusion method according to the CLSI guideline. PCR and sequencing were employed to detect qnrA, qnrB and qnrS-encoding genes. RESULTS: Of 200 K. pneumoniae isolates, 124 (62%) were nonsusceptible to quinolone compounds among those 66 (53.2%) and 58 (46.8%) isolates showed high and low-level quinolone resistance rates, respectively. Out of 124 quinolone non-susceptible isolates, qnr-encoding genes were present in 49 (39.5%) isolates with qnrB1 (30.6%) as the most dominant gene followed by qnrB4 (9.7%), and qnrS1 (1.6%) either alone or in combination. CONCLUSIONS: This study, for the first time, revealed the high appearance of qnrB1, qnrS1 and qnrB4 genes among the clinical isolates of K. pneumoniae in Iran. Therefore, the application of proper infection control measures and well-established antibiotic administration guideline should be strictly considered within our medical centers.
ABSTRACT
Multi-drug therapy (MDT) and Leprosy Elimination Campaigns (LEC) are the major strategies for eliminating leprosy. We report the results of a LEC conducted in 2006 in Qazvin. A total of 1987 individuals (1379 household contacts of 319 registered leprosy patients and 608 people from 3 endemic villages with a high prevalence of leprosy) were examined for detection of new cases of leprosy. All new cases were given MDT and were reviewed after a year. There were 256 suspected cases of leprosy, 13 of whom were confirmed as new cases (7 were classified as multibacillary leprosy). None had visible deformity nor was < 20 years old. All patients completed the recommended MDT course. The few cases detected suggest that in low prevalence areas, a long-term approach of integrated leprosy services and disability management may be more appropriate than LEC as a leprosy elimination strategy.
Subject(s)
Communicable Disease Control/methods , Endemic Diseases/prevention & control , Leprosy/prevention & control , Outcome Assessment, Health Care , Adult , Communicable Disease Control/organization & administration , Drug Therapy, Combination , Humans , Iran/epidemiology , Leprostatic Agents/administration & dosage , Leprosy/drug therapy , Leprosy/epidemiology , Leprosy, Multibacillary , Mass Screening , Middle AgedABSTRACT
Multi-drug therapy [MDT] and Leprosy Elimination Campaigns [LEC] are the major strategies for eliminating leprosy. We report the results of a LEC conducted in 2006 in Qazvin. A total of 1987 individuals [1379 household contacts of 319 registered leprosy patients and 608 people from 3 endemic villages with a high prevalence of leprosy] were examined for detection of new cases of leprosy. All new cases were given MDT and were reviewed after a year. There were 256 suspected cases of leprosy, 13 of whom were confirmed as new cases [7 were classified as multibacillary leprosy]. None had visible deformity nor was < 20 years old. All patients completed the recommended MDT course. The few cases detected suggest that in low prevalence areas, a long-term approach of integrated leprosy services and disability management may be more appropriate than LEC as a leprosy elimination strategy
Subject(s)
Leprosy , Incidence , PrevalenceABSTRACT
Catecholase and cresolase activities of mushroom tyrosinase (MT) were studied in presence of some n-alkyl carboxylic acid derivatives. Catecholase activity of MT achieved its optimal activity in presence of 1.0, 1.25, 2.0, 2.2 and 3.2 mM of pyruvic acid, acrylic acid, propanoic acid, 2-oxo-butanoic acid, and 2-oxo-octanoic acid, respectively. Contrarily, the cresolase activity of MT was inhibited by all type of the above acids. Propanoic acid caused an uncompetitive mode of inhibition (K(i)=0.14 mM), however, the pyruvic, acrylic, 2-oxo-butanoic and 2-oxo-octanoic acids showed a competitive manner of inhibition with the inhibition constants (K(i)) of 0.36, 0.6, 3.6 and 4.5 mM, respectively. So, it seems that, there is a physical difference in the docking of mono- and o-diphenols to the tyrosinase active site. This difference could be an essential determinant for the course of the catalytic cycle. Monophenols are proposed to bind only the oxyform of the tyrosinase. It is likely that the binding of acids occurs through their carboxylate group with one copper ion of the binuclear site. Thus, they could completely block the cresolase reaction, by preventing monophenol binding to the enzyme. From an allosteric point of view, n-alkyl acids may be involved in activation of MT catecholase reactions.
Subject(s)
Agaricales/enzymology , Carboxylic Acids/pharmacology , Catechol Oxidase/metabolism , Enzyme Activation/drug effects , Enzyme Inhibitors/pharmacology , Monophenol Monooxygenase/metabolism , Agaricales/classification , Molecular StructureABSTRACT
Buruli ulcer is a chronic and progressive necrotizing ulcer for which there is no medical treatment. Historically, a soluble toxin (factor) derived from the causative Mycobacterium ulcerans was found to induce the massive necrosis of skin and s.c. tissue seen in this condition. However, the persistence of the disease is thought to be caused by a lack of any immune response. We therefore investigated whether the factor was related to immunosuppression. A protocol to partially purify the factor was developed, and its effects on immune competent cells were tested. The factor produced >95% inhibition of LPS-induced release of TNF and IL-10 from human monocytes and caused a loss of adherence of these cells without cell death. The factor also blocked the production of IL-2 from activated T lymphocytes. The factor had no effect on TNF-induced cytotoxicity, but abrogated TNF-induced NF-kappa B activation. Surprisingly, a synergy was observed between the factor and phorbol ester-directed NF-kappa B activation. The factor had no effect on IL-1- or LPS-induced NF-kappa B activity, indicating selective activity of the factor. The factor did not inhibit the degradation of I kappa B alpha induced by TNF, indicating that the target for its activity lies within an undefined part of the TNF signaling mechanism. The data indicate that the localized immunosuppression associated with Buruli ulcer relates to the activity of the released factor, and this may provide a target for future therapeutic strategies for this intractable disease.