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To estimate the impact of cotrimoxazole prophylaxis on the survival of human immunodeficiency virus (HIV)-positive tuberculosis (TB) patients.
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One hundred fifty-one men with genital ulcer disease were assigned randomly to treatment with one of five oral antimicrobial regimens: (1) sulfadimidine (1 g four times daily for seven days); (2) tetracycline (500 mg four times daily for seven days); (3) trimethoprim-sulfamethoxazole (TMP-SMZ; 160 mg of TMP and 800 mg of SMZ twice daily for seven days); (4) doxycycline (300 mg as a single dose); or (5) TMP-sulfametrole (640 mg of TMP and 3,200 mg of sulfametrole once as a single dose). Haemophilus ducreyi was isolated from 81 (54%) of the men, and 35 strains were available for testing of antimicrobial susceptibility. The TMP-SMZ and TMP-sulfametrole regimens were more effective than sulfadimidine, tetracycline, or single-dose doxycycline in curing ulcers. Only one of 35 strains tested was susceptible to tetracycline (less than or equal to 8 mg/liter), and only ten of 35 strains were susceptible to doxycycline (less than or equal to 4 mg/liter), whereas all were susceptible to trimethoprim (less than or equal to 2 mg/liter). The correlation between in vitro susceptibility and bacteriologic response to the antimicrobial agents requires further investigation. In particular, sulfonamide resistance did not always identify failure to respond to sulfadimidine.
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The effect of cotrimoxazole (CTX) on plasma levels of 6-mercaptopurine (6-MP) was studied in the rat. Animals receiving CTX in conjunction with 6-MP were found to have a marked but non-significant decrease in the area under the plasma time curve as compared with animals receiving 6-MP alone. It is suggested that the bioavailability and thereby, the antileukaemic effect) during maintenance therapy of ALL of 6-MP may be decreased by the co-administration of CTX.
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Co-trimoxazole is a sulfonamide-containing antibiotic that is effective in the treatment of several infections and for prophylaxis of Pneumocystis jiroveci pneumonia. This drug has been reported as a common culprit drug for the Stevens-Johnson syndrome (SJS) and for toxic epidermal necrolysis (TEN). Human leukocyte antigens (HLAs) play a key role in the immunopathogenesis of severe cutaneous reactions induced by several drugs. This study investigated the association between the HLA class I and HLA-DRB1 polymorphisms and co-trimoxazole-induced SJS/TEN in a Thai population.
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During the 80-week study period, 162 women were treated for a vulvar abscess. Methicillin-resistant S aureus was isolated from 85 of 133 (64%) cultured vulvar abscesses. No presenting signs or symptoms were more common among patients with MRSA abscesses. Women with an MRSA vulvar abscess were not more likely to require inpatient admission or experience treatment complications. Inpatient treatment occurred in 64 of 162 (40%) patients and was predicted by medical comorbidities: diabetes (45.3%, odds ratio [OR] 2.29, 95% confidence interval [CI] 1.12-4.72), hypertension (34.4%, OR 2.33, 95% CI 1.06-5.13), initial serum glucose greater than 200 (37.5%, OR 3.32, 95% CI 1.48-7.51), and signs of worse infection, ie, larger abscesses (mean 5.2 cm) (P<.001) and elevated white blood cell count of at least 12,000/mm3 (45.3%, OR 3.04, 95% CI 1.44-6.43).
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This case report, for the first time, documents acute porphyria attack as a result of a sequential combination of 3 common medications. This is the first case report of the concomitant presence of both acute porphyria and Arnold Chiari malformation, 2 genetic disorders with unclear association.
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Forty-nine E. coli, K. pneumoniae, K. oxytoca and E. cloacae ESBL-producing isolates were studied. In antimicrobial susceptibility analyses, many of the isolates exhibited resistance to aminoglycosides, fluoroquinolones and trimethoprim-sulfamethoxazole. Gene amplification analysis and sequencing revealed that 75.5% (n=37) of the isolates harbored blaCTX-M-15 and 38.7% (n=19) harbored blaSHV-12. The non-ESBLs resistance genes detected were blaTEM-1, blaOXA-1, aac(6')-Ib,aac(6')-Ib-cr, tetA, sul-1, sul-2, qnrA, qnrB and catB-3. We found dfrA and aadA gene cassettes in the class 1 integron variable regions of the isolates, and the combination of dfrA17-aadA5 to be the most prevalent. All blaCTX-M-15 positive isolates also contained the ISEcp1 insertion element. Conjugation and transformation experiments indicated that 70.3% of the antibiotic resistance genes resided on plasmids. Through a PCR based replicon typing method, plasmids carrying the blaSHV-12 or blaCTX-M-15 genes were assigned to either the IncFII replicon type or, rarely, to the HI2 replicon type. All isolates were subtyped by the rep-PCR and ERIC-PCR methods.Phylogenetic grouping and virulence genotyping of the E. coli isolates revealed that most of them belonged to group A1. One isolate assigned to group B2 harbored blaCTX-M-15 and five virulence genes (traT, fyuA, iutA, iha and sfa) and was related to the O25b-ST131 clone.
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A 46-year-old woman developed concurrent CMV and Pneumocystis carinii pneumonia (PCP) 140 days after autologous peripheral blood stem cell transplantation (APBSCT) for AML. She was seropositive for CMV before undergoing APBSCT and had required prednisone for immune thrombocytopenia and allergic dermatitis for 9 weeks prior to the onset of pneumonia. She had also been receiving PCP prophylaxis with pentamidine aerosol every month for 3 months before developing symptoms. The pneumonia was complicated by severe hypoxia, requiring ventilator support and pneumothorax requiring chest tube thoracostomy. She recovered following treatment with trimethoprim-sulfamethoxazole (TMP-SMX), prednisone, gancyclovir and intravenous immunoglobulin. Although the overall incidence of severe CMV disease is low after APBSCT, preventive measures such as surveillance culture and secondary prophylaxis with gancyclovir may be warranted in patients whose cellular immune response is further compromised by corticosteroid use or other factors.
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It is postulated that the unstable hydroxylamine metabolite of sulphamethoxazole is responsible for the adverse reactions to co-trimoxazole and in HIV infection systemic glutathione deficiency leads to a reduced capacity to counteract the hydroxylamine toxicity. This hypothesis has been investigated by studying the metabolism of sulphamethoxazole and assessing glutathione status in HIV infection in order to explore the modification of treatment. It is concluded that the toxicity of plasma sulphamethoxazole hydroxylamine is counteracted by normal glutathione concentrations as is the case in HIV-seropositive patients, but that increased oxidation within certain cells in HIV infected individuals may possibly give rise to increased concentrations of reactive intermediates of sulphamethoxazole. Sulphametrole and sulphamethoxazole have similar half-lives but are metabolized differently: in vivo no oxidised metabolites of sulphametrole could be detected. In a retrospective study the rate of adverse reactions to trimethoprim-sulphametrole appeared to be in the lower range of those reported for trimethoprim-sulphamethoxazole indicating that the combination of trimethoprim-sulphametrole may be more favourable. The ratio of trimethoprim:sulphonamide is 1:5, but in-vitro studies with Toxoplasma gondii indicate that because of the synergic effect of both agents the dose of sulphonamide is possibly unnecessarily high.