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S Chowdhry

Publications and source records attributed to S Chowdhry.

11 recordsLinked to original sources

High incidence of treatment failure of Neisseria gonorrhoeae isolates to ciprofloxacin in male gonococcal urethritis in Delhi.

Several treatment failures and widespread antimicrobial resistance to ciprofloxacin have been documented, subsequent to its initial recommendation in 1989 as a single dose alternative therapy for gonorrhoea. Still, it continues to be part of various treatment schedules in National STD control guidelines including India. This prompted us to study the current status of this drug in the treatment of gonorrhoea. Thirty-five male patients with gonococcal urethritis were included in the study. The susceptibility to penicillin, tetracycline, ciprofloxacin and ceftriaxone was determined by Kirby-Bauer disc diffusion method and minimum inhibitory concentration (MIC) of ciprofloxacin by agar plate dilution method. The clinical and bacteriological response was assessed on day 5 after treatment with single dose ciprofloxacin, 500 mg. The sensitivity pattern of Neisseria gonorrhoeae was observed to be: ceftriaxone 100%, azithromycin 100%, tetracycline 65.7%, penicillin 40% and ciprofloxacin 5.7% by disc diffusion method. The MIC for ciprofloxacin was below 0.06 microg/mL (sensitive) in one (2.5%) isolate only. On the fifth day a large number of treatment failures (88.5%) were seen with ciprofloxacin while none was noted one week after re-treatment with ceftriaxone. The location of endemic quinolone-resistant N. gonorrhoeae (QRNG) in New Delhi has increased alarmingly, resulting in an extremely high proportion of therapeutic failures, and thus requiring appropriate alterations in the presently recommended treatment regimens.

Anti-Infective Agents↗

Rising quinolone resistance in Neisseria gonorrhoeae isolates from New Delhi.

BACKGROUND & OBJECTIVES: Treatment for gonorrhoea with fluoroquinolones is recommended. However, reduced susceptibility and treatment failure with fluoroquinolones has recently been reported. We undertook to study the antibiotic susceptibility pattern and the incidence of quinolone resistance in 36 consecutive isolates of Neisseria gonorrhoeae from April to November 2000. METHOD: Antibiotic susceptibility testing was performed by the Kirby Bauer disc diffusion technique and minimum inhibitory concentration (MIC) of ciprofloxacin was determined by the agar dilution method. Penicillinase producing N. gonorrhoeae (PPNG) were identified by using the nitrocefin disc method. RESULTS: Thirty six strains of N. gonorrhoeae obtained from 44 consecutive male patients (81.9%) were studied. By the disc diffusion method, only 3 (8.3%) of these isolates were found to be sensitive to ciprofloxacin. All isolates were sensitive to ceftriaxone while 23 (63.9%) were sensitive to tetracycline and 12 (33.3%) to penicillin. Four (11.1%) of the N. gonorrhoeae isolates were PPNG. Twenty seven (75%) isolates were found to be resistant to ciprofloxacin by MIC determination. INTERPRETATION & CONCLUSION: Incidence of ciprofloxacin resistance amongst N. gonorrhoeae isolates is on the rise in New Delhi. Periodic monitoring of antimicrobial susceptibility pattern of N. gonorrhoeae to antimicrobials other than quinolones is essential to prevent treatment failure in patients with gonorrhoea.

Anti-Infective Agents↗

Native aortic valve tissue systemic embolization complicating bacterial endocarditis.

Systemic embolic events are known complications of bacterial endocarditis. Embolization of prosthetic valves has previously been reported in the literature. We report a case of embolization of native aortic valve tissue to the popliteal artery as the presenting event in a patient with subacute bacterial endocarditis. To our knowledge, this rare complication has not been previously reported.

Adult↗

Initial characterization of the complement activating compounds in extracts of smokeless tobacco.

Aqueous extracts of smokeless tobacco (ST) have been shown to be potent activators of complement. However, the mechanisms by which smokeless tobacco activates complement are not well understood. This study was undertaken to identify the complement activating compounds in ST extracts. The approximate molecular size of the activating agent(s) in smokeless tobacco was determined by dialyzing aqueous extracts of loose leaf chewing tobacco (1S1), dry snuff (1S2), and moist snuff (1S3). Following dialysis (total dilution effect of 1:10(9)), using a membrane with a molecular weight retention limit of 12-14 kDa, all extracts retained full capacity to activate serum complement as determined by a hemolytic assay. Fractionation of the extracts by gel filtration chromatography revealed that the complement activating agents in ST were high molecular weight compounds that eluted between 400 kDa and the void volume (1500 kDa) of a Sephacryl S300 column. The high molecular weight complement-activating peak was isolated and found to be a more potent complement activator than the unfractionated extract. The chemical nature of the complement activating compounds was determined by subjecting the extracts to boiling for 30 min, an organic extraction with chloroform/methanol 2:1, or treatment with a DNAse/RNAse enzyme cocktail. None of these treatments destroyed the capacity of ST extracts to activate complement, suggesting that the activating agents may be carbohydrate-like. Finally, an extraction protocol designed to remove polyphenols significantly diminished the complement activating capacity of the ST extracts. These results clearly demonstrate that the complement activating substances in smokeless tobacco extracts may be large (>400 kDa) polyphenol-containing compounds (i.e. tannins). Identification of this agent(s) will be important for distinguishing the mechanism of smokeless tobacco-induced complement activation.

Complement Activation↗

Encephalopathy in a patient with Addison disease.

Patients with adrenal insufficiency manifest a myriad of metabolic disorders which can inflict neurologic damage. Here we present an unusual clinical presentation and distinctive imaging features in a patient with Addison disease.

Addison Disease↗

Smokeless tobacco extracts activate complement in vitro: a potential pathogenic mechanism for initiating inflammation of the oral mucosa.

The use of smokeless tobacco has been linked to an increased incidence of inflammation of the buccal and gingival mucosa. However, the mechanisms by which smokeless tobacco initiates inflammation are not well understood. The complement cascade is a ubiquitous source of proinflammatory molecules and can be activated rapidly by a wide variety of agents. Therefore, the effect of smokeless tobacco on complement was investigated as a potential pathogenic mechanism for triggering inflammation of the oral mucosa. Aqueous extracts of loose leaf chewing tobacco (1S1), dry snuff (1S2), and moist snuff (1S3), added to normal human serum, depleted complement hemolytic activity in a dose-dependent manner. Experiments utilizing sera deficient in one specific complement component indicated that the smokeless tobacco-induced depletion of hemolytic activity was due largely to consumption of C3. Furthermore, assays designed to test the activity of the alternative pathway of complement clearly showed that all three extracts depleted the hemolytic activity of this pathway. Finally, all three smokeless tobacco extracts activated the alternative pathway since significantly elevated levels of the cleavage fragments iC3b and Bb were detected in extract-treated serum. High quantities of the classical pathway cleavage fragment C4d also were detected in serum treated with moist snuff (1S3). The results clearly demonstrate that smokeless tobacco extracts activate the alternative pathway and also suggest some measure of classical pathway activation. Activation of complement by smokeless tobacco may be a mechanism for initiating inflammation of the oral mucosa.

Complement Activation↗