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A 12 year old boy was admitted to hospital with fever, general malaise, cough and peripheral edema. The patient who have had rheumatic heart diseases-mitral insufficiency was found to be in congestive cardiac failure. In blood cultures Staphylococcus aureus and Alpha-hemolytic streptococcus grew. The regimens of Cephalothin-Gentamicin, Methicillin-Tobramicin, to which the organism were sensitive were given intravenously. On these therapy the patient continued to have fever. He was put on Trimethoprim-Sulfomethoxazole intramuscularly. He became afebril for the first time. After two weeks fever recurred. In spite of medical treatment, the infection persisted and the indication for surgery was considered. Mitral valve replacement with a Starr-Edwards prosthesis was carried out. Postoperatively, the patient was treated with TMP-SMZ. For the past 10 months the patient has remained afebril and without evidence of congestive heart failure.
Chronic granulomatous disease (CGD) is an inherited disease of the phagocyte NADPH oxidase system that causes defective production of toxic oxygen metabolites, leading to impaired bacterial and fungal killing, and recurrent life threatening infections; mostly by catalase producing organisms. Nocardiosis in CGD is well described, however actinomycosis is rare. We describe a patient of CGD with actinomycosis and nocardiosis coinfection. A 43-year-old male with history of recurrent discharging sinuses presented with fever, dyspnea and cough. He had multiple discharging sinuses over neck and anterior chest wall. There was only partial response to intravenous penicillin. Needle aspirate from chest wall showed co-infection with actinomyces and nocardia. His nitroblue tetrazolium (NBT) reduction test was negative. He was treated with penicillin, amikacin and trimethoprim-sulfamethoxazole and had good clinical and radiological response.
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Fifty-nine patients with active ocular toxoplasmosis were randomly assigned to 2 treatment groups: 29 were treated with pyrimethamine/sulfadiazine, and 30 patients received trimethoprim/sulfamethoxazole.
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For women with recurrent urinary tract infections (rUTI), the contribution of antibiotic use versus patient-related factors in determining the presence of antimicrobial resistance in faecal and urinary Escherichia coli, obtained from the same patient population, has not been assessed yet. Within the context of the 'Non-antibiotic prophylaxis for recurrent urinary tract infections' (NAPRUTI) study, the present study assessed determinants of antimicrobial resistance in E. coli isolated from urinary and faecal samples of women with rUTIs collected at baseline. Potential determinants of resistance were retrieved from self-administered questionnaires. From 434 asymptomatic women, 433 urinary and 424 faecal samples were obtained. E. coli was isolated from 146 (34%) urinary samples and from 336 (79%) faecal samples, and subsequently tested for antimicrobial susceptibility. Multivariable analysis showed trimethoprim/sulfamethoxazole (SXT) use three months prior to inclusion to be associated with urine E. coli resistance to amoxicillin (OR 3.6, 95% confidence interval: 1.3-9.9), amoxicillin-clavulanic acid (OR 4.4, 1.5-13.3), trimethoprim (OR 3.9, 1.4-10.5) and SXT (OR 3.2, 1.2-8.5), and with faecal E. coli resistance to trimethoprim (OR 2.0, 1.0-3.7). The number of UTIs in the preceding year was correlated with urine E. coli resistance to amoxicillin-clavulanic acid (OR 1.11, 1.01-1.22), trimethoprim (OR 1.13, 1.03-1.23) and SXT (OR 1.10, 1.01-1.19). Age was predictive for faecal E. coli resistance to amoxicillin (OR 1.02, 1.00-1.03), norfloxacin and ciprofloxacin (both OR 1.03, 1.01-1.06). In conclusion, in women with rUTI different determinants were found for urinary and faecal E. coli resistance. Previous antibiotic use and UTI history were associated with urine E. coli resistance and age was a predictor of faecal E. coli resistance. These associations could best be explained by cumulative antibiotic use.
Of 279 hospitalized HIV-infected children 128 (46%) were diagnosed with pneumonia and 26 (20%) of these had severe pneumonia. P. carinii was identified in 9 (35%) children with severe pneumonia. After June, 1996, the rate of severe pneumonia among all hospitalized children decreased from 16% from January through June, 1996, to 7% from July, 1996, through December, 1997 (P = 0.02). Cases of PCP decreased from 9 in 1996 to zero in 1997. The percentage of HIV-infected children receiving PCP prophylaxis at the time of admission increased from 53% before June, 1996, to 72% in late 1997 (P = 0.04). The overall percentage of patients with severe pneumonia receiving PCP prophylaxis at the time of admission was 34%. Breakthrough PCP occurred in 2 children with poor compliance. Patients with PCP were significantly younger than those without PCP (mean age, 10.6+/-10.6 vs. 29.8+/-28.3 months, P = 0.02).
All identified human studies dealing with bacteriuria or UTI in pregnancy were analyzed.
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Continued bacteriologic and clinical cure, such that alternative antimicrobial drugs were not required, among evaluable patients through the 4- to 11-day posttherapy visit, compared by treatment group.
Oral carbohydrate challenge test with 4000 kcal/d.
Early cotrimoxazole from 6 weeks of age in HIV-infected infants seemed to reduce probability of severe events but the study lacked statistical power to prove this. Even with systematic cotrimoxazole prophylaxis, infant morbidity and mortality remained high pointing towards a need for early pediatric HIV-diagnosis and antiretroviral treatment in Africa.
Sulfamethoxazole is the component of co-trimoxazole responsible for its efficacy against Pneumocystis carinii pneumonia, but this drug is associated with frequent adverse effects. Sulfamethoxypyridazine is significantly more effective than sulfamethoxazole against a murine model of P. carinii and might be a candidate for testing in infected patients.