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Among HIV-infected patients with TB, extrapulmonary disease occurred in 40% of the patients, particularly in those with advanced immune suppression. Death during TB treatment was common, but the risk of death was reduced in patients who took co-trimoxazole, fluconazole, and antiretroviral therapy.
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Renal reflux was unilateral in the 23% of the patients, and bilateral in the remaining cases; 72% of the renal reflux were grade IV and 28% grade V. The renal injuries affected to male infants and reflux grade V. The renal injury was focal (27%), global (44%) and atrophic (29%). The 79% of the patients had conservative treatment, while 21% had surgical treatment. 100% infants with surgical treatment and 94.2% infants with conservative treatment were recovered (Test of Kaplan-Meier). The 27% of patients developed one or several urinary infections, but progression of old renal injuries or formation of new ones, were exceptional (3 cases): While the time the study lasted none of the patients developed chronic renal failure nor arterial hypertension.
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One hundred twenty-three patients with nonpulmonary infections due to Mycobacterium fortuitum or Mycobacterium chelonei were treated by wound debridement and with chemotherapy on the basis of in vitro susceptibilities of the organism. Of 76 patients with infections caused by M. fortuitum, 13 required no therapy or were adequately treated with surgery alone. Patients with active localized disease received single drug therapy (usually with a sulfonamide) for a mean period of 10.6 weeks for cellulitis and seven months for osteomyelitis. Patients with extensive disease received amikacin or amikacin plus cefoxitin (mean, four weeks) followed by a sulfonamide (mean, six months). The 47 patients with infections caused by M. chelonei received no therapy or were treated with surgery alone (6); with amikacin (10), erythromycin (6), doxycycline (3), or cefoxitin (1); or with amikacin plus cefoxitin followed by cefoxitin alone for a total of 10-12 weeks (20); or other multiple-drug regimens (1). Surgery was performed on 74 (60%) patients. Schlichter tests or serum drug levels were determined for 81 (66%) patients. Response to therapy was excellent; 68 (90%) infections with M. fortuitum and 34 (72%) with M. chelonei were successfully treated. Cultures became negative within six weeks of chemotherapy, except for sternal osteomyelitis, for which cultures were not negative until up to 14 weeks. Follow-up for a mean period of 12 months following therapy was possible in 80% of cases. Relapses were rare except in patients with disseminated disease, and drug resistance developed in only one patient. These studies demonstrate the value of routine susceptibility testing of these mycobacterial species and the benefit of chemotherapy on the basis of in vitro susceptibilities.
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Ninety-four hospitalized adult patients with reported sulfonamide allergies.
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Co-trimoxazole prophylaxis can reduce mortality from untreated HIV infection in Africa; whether benefits occur alongside combination antiretroviral therapy (ART) is unclear. We estimated the effect of prophylaxis after ART initiation in adults.
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Long-duration beta-lactam antibiotics are used for empirical treatment in female dogs with uncomplicated bacterial cystitis. However, women with bacterial cystitis are treated with short-duration potentiated sulfonamides because longer courses of beta-lactams result in lower cure and higher recurrence rates.
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Neither teicoplanin nor vancomycin at 2, 1 and 0.5 micrograms/ml consistently killed inocula of representative isolates of a multiple-drug-resistant (MDR) strain of Staphylococcus aureus in the presence of 65% (v/v) of fresh, defibrinated human blood, although both antibiotics sterilized tube contents in Mueller-Hinton broth (MHB). With added human blood, teicoplanin (1 microgram/ml) combined with rifampin (1 microgram/ml) was the most effective in vitro combination, followed by teicoplanin (1 microgram/ml) + amoxicillin (8 micrograms/ml) + clavulanate (3 micrograms/ml), ampicillin (8 micrograms/ml) + sulbactam (8 micrograms/ml), cefamandole (8 micrograms/ml), fosfomycin (4 micrograms/ml + 25 micrograms/ml glucose-6-phosphate), imipenem (8 micrograms/ml), netilmicin (4 micrograms/ml), trimethoprim + sulfamethoxazole (1/19 micrograms/ml) and vancomycin (1 microgram/ml), respectively. Conversely, teicoplanin (1 microgram/ml) combined with fusidic acid (0.5 micrograms/ml) and ofloxacin (4 micrograms/ml), respectively, proved ineffective with 65% (v/v) added human blood. In concurrent control tubes, however, all drug combinations were bactericidally active in MHB against the MDR strain of S. aureus.
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Primary HIV infection can occur in 40-90% of individuals recently infected with HIV. Variable symptoms usually suggestive of a flu-like illness as well as high-level HIV viraemia and steep decline in CD4 cell count are often noted. We report a case of a previously healthy homosexual man who presented with symptoms suspicious of primary HIV infection as well as non-productive cough associated with chest CT finding of diffuse ground glass appearance in lungs. Recent HIV seroconversion was confirmed. Diagnosis of Pneumocystis jirovecii pneumonia was made on transbronchial lung biopsy. The symptoms improved rapidly after initiation of treatment with trimethoprim-sulfamethoxazole. It is important to recognise that although Pneumocystis pneumonia is generally seen in the setting of AIDS, it can occasionally also occur during primary HIV infection.
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A 45-year-old man living on a hobby farm was admitted to hospital for investigation of lung lesions, weight loss and low grade fevers. P. pseudomallei was cultured from material from an aspiration biopsy of a mediastinal mass.
A retrospective investigation was done in an SCI rehabilitation center. The microbiologic culture results of urine and ejaculate or prostatic fluid samples were collected from 34 men with SCI presenting with recurrent urinary tract infections and bacterial prostatitis. Furthermore, patient characteristics, bladder diary details, and the administered antibiotic treatment were collected.
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It has been studied in a series of 30 children affected of brucellosis, the most important epidemiologic, clinical and biologic characteristics. It has been emphasized the good response to the combined treatment of tetracycline and streptomycin.
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Pneumocystis carinii pneumonia is a life-threatening complication of diseases and therapies associated with immunosuppression. Approximately 80 percent of patients with acquired immunodeficiency syndrome will develop pneumocystis pneumonia. Diagnosis is important, because effective therapy is available. In most cases, diagnosis can be made by sputum analysis. Bronchoalveolar lavage will yield a diagnosis in 85 to 90 percent of patients with pneumocystis pneumonia, and is used when sputum induction and analysis is unproductive, unavailable or negative. Transbronchial biopsy and, rarely, open lung biopsy will yield the etiology of pneumonia in the remaining patients. Pentamidine or trimethoprim-sulfamethoxazole is the treatment of choice. Toxicity often occurs, including hypoglycemia, nephrotoxicity, neutropenia and rash. Corticosteroids are helpful in moderate to severe disease. Mortality for the first episode of P. carinii pneumonia averages 20 percent. Prophylaxis effectively prevents and reduces the incidence of future episodes.
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Burkholderia pseudomallei is a saprophytic Gram-negative bacterium responsible for the tropical infectious disease melioidosis. Melioidosis is endemic to northern Australia and Southeast Asia. In this study, 234 isolates of B. pseudomallei obtained from the first positive clinical specimen from 234 consecutive patients diagnosed with melioidosis between October 2009 and September 2012 were reviewed. All isolates were susceptible to meropenem and ceftazidime. In total, 226 isolates (96.6%) were susceptible to doxycycline and 232 (99.1%) were susceptible to trimethoprim/sulfamethoxazole (TMP/SMX; co-trimoxazole). Primary resistance of B. pseudomallei to ceftazidime and/or meropenem is exceedingly rare and clinicians can be confident in the current treatment guidelines for melioidosis. Whether the very low rates of TMP/SMX resistance seen in Australia reflect the global situation requires further studies using Etest, especially to clarify the rate of resistance in Thailand.
Shigellosis is a common cause of morbidity, especially in the very young and old, in developing countries. The disease is treated with antibiotics. Surveillance of antimicrobial resistance trends is essential owing to the global emergence of antimicrobial resistance.
Mycetoma is a chronic granulomatous disease caused by bacteria or true fungi. It affects the skin the underlying tissue and sometimes subjacent bones and organs. The diagnosis of the disease is confirmed by the microscopic identification and by isolating the infecting agent. Actinomycetoma are treated with trimethoprim-sulfamethoxazole and/or diamino-diphenyl-sulfona (DDS). In patients resistant to these treatments adding amikacin cures about 95% of the resistant cases. In true fungi mycetoma, amphotericin B, ketoconazole, itraconazole, and in some cases these combined with surgery is the treatment of choice.
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Faced with intense levels of chloroquine (CQ) resistance in Plasmodium falciparum malaria, Rwanda replaced CQ with amodiaquine (AQ)+sulfadoxine-pyrimethamine (SP) in 2001, and subsequently with artemether-lumefantrine (AL) in 2006, as first-line treatments for uncomplicated malaria. Following years of discontinuation of CQ use, re-emergence of CQ-susceptible parasites has been reported in countries including Malawi, Kenya and Tanzania. In contrast, high levels of SP resistant mutant parasites continue to be reported even in countries of presumed reduced SP drug selection pressure. The prevalence and distributions of genetic polymorphisms linked with CQ and SP resistance at two sites of different malaria transmission intensities are described here to better understand drug-related genomic adaptations over time and exposure to varying drug pressures in Rwanda. Using filter paper blood isolates collected from P. falciparum infected patients, DNA was extracted and a nested PCR performed to identify resistance-mediating polymorphisms in the pfcrt, pfmdr1, pfdhps and pfdhfr genes. Amplicons from a total of 399 genotyped samples were analysed by ligase detection reaction fluorescent microsphere assay. CQ susceptible pfcrt 76K and pfmdr1 86N wild-type parasites were found in about 50% and 81% of isolates, respectively. Concurrently, SP susceptible pfdhps double (437G-540E), pfdhfr triple (108N-51I-59R), quintuple pfdhps 437G-540E/pfdhfr 51I-59R-108N and sextuple haplotypes were found in about 84%, 85%, 74% and 18% of isolates, respectively. High-level SP resistance associated pfdhfr 164L and pfdhps 581G mutant prevalences were noted to decline. Mutations pfcrt 76T, pfdhfr 59R and pfdhfr 164L were found differentially distributed between the two study sites with the pfdhfr 164L mutants found only at Ruhuha site, eastern Rwanda. Overall, sustained intense levels of SP resistance mutations and a recovery of CQ susceptible parasites were found in this study following 7 years and 14 years of drug withdrawal from use, respectively. Most likely, the sustained high prevalence of resistant parasites is due to the use of DHFR/DHPS inhibitors like trimethoprim-sulfamethoxazole (TS) for the treatment of and prophylaxis against bacterial infections among HIV infected individuals as well as the continued use of IPTp-SP within the East and Central African regions for malaria prevention among pregnant women. With regard to CQ, the slow recovery of CQ susceptible parasites may have been caused partly by the continued use of CQ and/or CQ mimicking antimalarial drugs like AQ in spite of policies to withdraw it from Rwanda and the neighbouring countries of Uganda and Tanzania. Continued surveillance of P. falciparum CQ and SP associated polymorphisms is recommended for guiding future rational drug policy-making and mitigation of future risk of anti-malaria drug resistance development.
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Ontario data submitted to the Canadian Bacterial Surveillance Network (CBSN) between January 1, 1998 and June 30, 2002 were analyzed for rates of resistance in various pathogen-antibiotic combinations. The effect of the LU policy on the level and rate of change of antibiotic resistance was estimated using time series models.
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Of 2898 children investigated 103 cases of invasive pneumococcal disease (70 definite and 33 probable) were identified, suggesting that the incidence of this infection in the study community is at least 554/100,000/year in children younger than 1 year of age and 240/100,000/year in those younger than 5 years, rates many times higher than those found in industrialized societies. The mean age of presentation was 15 months; more boys than girls were affected. Cases of pneumonia were encountered 8 times more frequently than those of meningitis. Antibiotic resistance was rarely found and cases of pneumonia, but not meningitis, responded well to treatment. Case-fatality rates in children with pneumonia and meningitis were 1 and 55%, respectively. The most prevalent pneumococcal serotypes were types 6, 14, 19, 1 and 5.
In a randomized, crossover, multiple dose study, ten healthy volunteers received the recommended dosages of cotrimoxazole (80 mg trimethoprim and 400 mg sulfamethoxazole) and co-tri-famole (80 mg trimethoprim and 400 mg sulfamoxole) for five days each. Urinary levels of trimethoprim and each sulfonamide were measured daily for five days. The urinary ratios of trimethoprim and sulfonamide for both formulations were consistently lower than those considered optimal for synergy. Concentration of trimethoprim in the urine from both preparations was found to be greatly in excess of the MIC for trimethoprim-sensitive urinary pathogens (approximately 2 microgram/ml). The sulfonamide levels achieved were not consistently in excess of their MIC (approximately 200 microgram/ml) for either preparation.
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No significant difference in the incidence of clinically significant GO was observed between the CiA and Tcr groups up to 90 days of immunosuppressive therapy.