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Streptococcus pneumoniae is the most important respiratory tract pathogen in otitis, sinusitis, bronchitis, and community-acquired pneumonia. Over the past decades, there has been an increase in minimum inhibitory concentrations (MICs) to penicillin. Decreased susceptibility to penicillin is not the same as penicillin resistance. Decreased susceptibility to penicillin has occurred worldwide from dissemination of several resistant pneumococcal clones, and, to a lesser extent, from excessive use of ciprofloxacin, macrolides, and trimethoprim-sulfamethoxazole (TMP-SMX). Currently, penicillin resistance is defined by using a breakpoint of 2 microg/mL or more. Intermediately resistant strains (MIC 1-2 microg/mL) are also relatively sensitive depending on antibiotic concentration. Intermediate antibiotic susceptibility is concentration dependent. Antibiotic concentration at various body sites is determined by pharmacokinetic considerations. Except for very highly resistant strains, the treatment of penicillin-resistant S. pneumoniae causing bacteremia, sinusitis, otitis, bronchitis, or community-acquired pneumonia remains penicillin or any beta-lactam. Only in pneumococcal meningitis caused by penicillin-resistant pneumococci does the clinician have to use care in selecting an antipneumococcal antibiotic with adequate cerebrospinal fluid penetration and favorable kill ratios. Clinicians should be selective in antibiotic selection to minimize further decreases in penicillin susceptibility to S. pneumoniae. This is best achieved by using low-resistance potential antibiotics oral/intravenous mono-therapy at the full recommended dose. Therapeutic failure may occur in using lower doses at certain body sites. Macro-lides as monotherapy or as part of combination therapy should be minimized. Optimal therapy for non-central nervous system pneumococcal infection is with a respiratory quinolone (eg, levofloxacin, gatifloxacin, moxifloxacin), clindamycin, doxycycline, third-generation cephalosporins. For highly resistant pneumococci, levofloxacin, gatifloxacin, moxifloxacin, cefepime, meropenem, vancomycin, or linezolid may be used.
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From 1982 to 1988, 20 patients with pulmonary nocardiosis were diagnosed at the Department of Medicine, Chulalongkorn Hospital University. The infection was found to be common in immuno-compromised hosts particularly in patients who were suffering from lymphoreticular malignancy, systemic lupus erythematosus, nephrotic syndrome, pulmonary alveolar proteinosis and in patients who were receiving corticosteroids. The clinical manifestations were usually nonspecific. Diagnosis of pulmonary nocardiosis in cases who presented with a short duration of fever and productive cough was often delayed because they were considered to have acute bacterial pneumonia. The findings on chest roentgenogram were nonspecific as nonhomogeneous airspace infiltrates, cavitary lesions, nodule, or miliary infiltrates. The complete blood count frequently showed leukocytosis and neutrophilia. The diagnosis of nocardiosis was suspected if the staining of specimens obtained from the lesions showed typically weakly gram-positive and modified acid-fast branching filament organism and the diagnosis was confirmed by culture. The skin and the central nervous system were the most common hematogenous disseminations. Sulfamethoxazole and trimethoprim in combination were the drugs of choice. The treatment for a minimum of 6 months was appropriate in order to prevent relapse. Poor prognostic factors in nocardiosis were acute infection, Cushing's disease; and disseminated infection involving the central nervous system.
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An 82-year-old man with a recent history of depression became comatose following an overdose of escitalopram and oxazepam. He was admitted, ventilated for 7 days in the intensive care unit, and treated with piperacillin/tazobactam and cefepime for aspiration pneumonia. Following discharge to a medical ward, respiratory symptoms persisted and imaging confirmed pulmonary abscesses. Stenotrophomonas maltophilia was isolated from sputum and, on day 15, TMP/SMX 800 mg/160 mg 1 tablet every 12 hours was initiated. On day 35, the dose was increased to 800 mg/160 mg 2 tablets every 12 hours. By day 37, the patient was unsteady when attempting to stand. From day 40, he was noted to have features of HLGD with gait ignition failure, poor balance, and frequent falls. His other medications at this time were thiamine 100 mg daily, multivitamin 1 tablet daily, omeprazole 20 mg every 12 hours, and modified-release venlafaxine 150 mg daily. Investigation did not reveal any cause for his acute gait disturbance. TMP/SMX was stopped on day 48 and, by day 51, the patient's gait had returned to normal.
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To evaluate the effect of total bowel decontamination (TD) and selective bowel decontamination (SD) in a non-protective environment clinical and laboratory data of children treated for acute leukaemia between 1983 and 1991 were analysed retrospectively. From 1983 until 1989 34 patients [18 acute non-lymphoblastic leukaemia (ANLL) patients, 16 acute lymphoblastic leukaemia (ALL) patients] received TD and 31 patients (8 ANLL patients, 23 ALL patients) received SD from 1987 until 1991. TD consisted of colistin sulphate, neomycin, cephaloridine and amphotericin B orally as well as Orabase and sterilized food, while the patients were nursed in a single room. SD consisted of oral colistin sulphate, neomycin and amphotericin B. Those patients with ANLL were nursed in a single room; patients with ALL were nursed in a single room during remission induction therapy only. All patients except those with ANLL receiving TD received Pneumocystis carinii pneumonia prophylaxis with cotrimoxazole. Because the two groups were heterogeneous for diagnosis and chemotherapy the occurrence of fever (central body temperature at least 38.5 degrees C) and major infections (septicaemia of infections of the deep tissues or organs) were registered during periods of neutropenia (neutrophilic granulocytes < or = 500/mm3 for at least 8 days). Patients on TD had 55 periods of neutropenia, patients on SD 80. Patients on TD had 89.1 periods of fever/100 periods of neutropenia whereas patients on SD had 56.3. Also patients on TD had 27.3 major infections/100 periods of neutropenia whereas patients on SD had 11.3. Major infections predominantly consisted of septicaemia caused by gram-positive bacteria. We conclude that, in this study, TD in a non-protective environment does not offer better protection against major infections that SD in patients with ALL or ANLL.
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The aim of this study was to determine the penetration of trimethoprim, sulphamethoxazole and its main metabolite--N4-acetylsulphamethoxazole into cantharidin-induced skin blister fluid following administration of a single oral combination dose of 320 mg trimethoprim and 1600 mg sulphamethoxazole. Moreover, penetration of the two drugs into skin blister fluid was compared with penetration into the theoretical peripheral compartment calculated on the basis of plasma levels found. The material consisted of 12 male patients with bacterial skin diseases, treated at the Department of Dermatology and Venerology, Pomeranian Academy of Medicine in Szczecin. The age of the patients was 19-64 years (mean 42 +/- 14), weight 61-112 kg (mean 77 +/- 15), height 166-196 cm (mean 175 +/- 8). Prior to enrollment, normal function of gastrointestinal tract, liver and kidneys, and absence of allergy to the drugs studied was ascertained. The susceptibility of pathogens of cotrimoxazole (trimethoprim + sulphamethoxazole) was confirmed with bacteriological tests. Skin blisters were induced by applying 0.25% cantharidin ointment. Drug concentrations in plasma and skin blister fluid were measured with high-performance liquid chromatography. Peak concentrations of trimethoprim in plasma and skin blister fluid were 8.5 +/- 1.1 mumol/L after 3 +/- 1 h and 5.6 +/- 0.8 mumol/L after 7 +/- 2 h, respectively. The differences between both compartments as to parameters measured were statistically significant. In the theoretical peripheral compartment, peak concentration was 5.8 +/- 2.2 mumol/L after 9 +/- 6 h. Half-times of trimethoprim in plasma and skin blister fluid were 11.1 +/- 4.5 h and 12.3 +/- 4.9 h, respectively, and did not differ significantly. The degree of drug penetration into blister fluid defined as the ratio of area under concentration-time curves for blister fluid and plasma was 0.94 +/- 0.23. The differences between pharmacokinetic parameters of trimethoprim in skin blister fluid and theoretical peripheral compartment were not significant. Peak concentrations of sulphamethoxazole in plasma and skin blister fluid were 295 +/- 47 mumol/L after 3 +/- 1 h and 182 +/- 46 mumol/L after 8 +/- 2 h, respectively. The differences between both compartments as to parameters measured were statistically significant. In the theoretical peripheral compartment, peak concentration was 239 +/- 58 mumol/L after 7 +/- 4 h. Half-times of sulphamethoxazole in skin blister fluid and plasma were 9.7 +/- 3.3 h and 10.0 +/- 1.1 h, respectively and did not differ significantly. The drug penetrated into blister fluid to a high extent, although less than trimethoprim, the degree of penetration being 0.82 +/- 0.21. The majority of pharmacokinetic parameters in blister fluid and theoretical peripheral compartment did not differ significantly except for time to peak concentration. Peak concentration of N4-acetylsulphamethoxazole, the main metabolite of sulphamethoxazole, was significantly lower in blister fluid than plasma and took longer to achieve. The half-time of the metabolite was significantly longer in blister fluid than in plasma, whereas the ratio of area under concentration-time curves in these two biological fluids of 0.86 +/- 0.18 was similar to that of the parent drug. The results show that both trimethoprim and sulphamethoxazole administered together penetrate from plasma into skin blister fluid to a great extent and achieve concentrations exceeding the MIC for susceptible pathogens. This finding confirms the usefulness of this treatment in bacterial skin diseases. The cantharidin-induced skin blister is a useful technique to determine the penetration into skin of a drug and its metabolite and to evaluate pharmacokinetic parameters. In some cases, this test cannot be replaced with theoretical calculations based on drug concentrations in blood.
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Physicians admitted a 45-day old boy to King Khalid University Hospital in Riyadh, Saudi Arabia who had had a fever (39.8 degrees Celsius) for 2 days. He was irritable and did not feed very well at the breast. He was a healthy full term infant. The physicians could not identify an infection in the infant. 2 weeks before the infant became ill, the mother had a fever, progressive malaise, and right hip pain for 5 days. Based on a positive Brucella serology, her physician treated her with tetracycline and streptomycin. She exclusively breastfed the infant during the illness. Neither the mother nor the infant had any contact with farm animals, but a friend did give the mother raw goat milk 2 weeks postpartum. 79% of the white blood cell count contained lymphocytes. They believed he had bacterial sepsis so they treated him with intravenous ampicillin and cloxacillin. His temperature peaked daily between 38-39 degrees Celsius for the 1st 3 days. After hearing of the mother's illness with brucellosis and since the blood, urine, and cerebrospinal fluid cultures were negative for common bacterial pathogens, the physicians then administered oral trimethoprim-sulphamethoxazole and rifampicin for 6 weeks. His condition improved quickly and by day 7 the fever had subsided. 2 weeks after admission, his Brucella agglutination titer was 1:160 and his blood culture grew Brucella melitensis. At the same time, they measured the mother's blood and breast milk titers which were both positive (1:320 and 1:640 respectively). They could not isolate B. melitensis in either her blood or breast milk, however. Perhaps the antibiotics wiped out the organisms. 1 year after admission, the boy was fine. Seroconversion occurred within 2 weeks which may mean that he acquired brucellosis recently and postnatally. The physicians believed that the only route of transmission was breast milk.
Data were analyzed from 4825 persons aged > or =13 years with HIV infection enrolled from 4 outpatient facilities from 1990 to 1998. The association between P aeruginosa infection and demographic, risk behavior, and clinical factors was assessed.
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Clinical, bacteriologic, epidemiologic and hospital infection-control observations related to an inter-hospital outbreak of methicillin-resistant Staphylococcus aureus are described. The outbreak involved 66 patients at the University of Oregon Health Sciences Center (UOHSC) and its closely affiliated VA hospital, the Portland VA Medical Center (PVAMC). No environmental source of infection was identified; person-to-person transmission was most likely responsible for its spread. Surveillance cultures demonstrated nasal colonization in house staff and nursing personnel at both hospitals. Inter-hospital transfer of infection was, in all likelihood, achieved via nasal carriage by a single physician. Case-control analysis indicated a significantly increased risk (p less than 0.05) of acquisition of infection related to age, number of days hospitalized, severity of underlying disease and number of invasive procedures. Prior antibiotic receipt was a significant risk factor when analyzed by univariate analysis (p less than 0.01), but, in contrast to previous studies, this was not a significant risk factor (p greater than 0.05) when related variables were controlled by multivariate analysis. Prevention of spread of infection by routine infection control measures was less effective at PVAMC than at UOHSC. Patients at PVAMC were significantly older and had longer durations of hospitalization (p less than 0.05). Antimicrobial therapy of colonized patients and personnel appeared to assist in the control of the outbreak at PVAMC. Antimicrobial therapy with topical bacitracin and oral rifampin, alone or in combination with oral trimethoprim-sulfamethoxazole, was effective in eliminating colonization with methicillin-resistant S. aureus.
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A 53-year-old woman with a history of liver abscesses and Crohn disease presented with Burkholderia cepacia pneumonia and required a right middle lobe resection. Nitroblue tetrazolium test results confirmed the diagnosis of CGD, and Western blot analysis revealed the absence of the 47-phagocyte oxidase protein. Levels of Crohn-associated specific antibodies to Saccharomyces cerevisiae and Escherichia coli outer membrane porin C were elevated.
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Actinomycosis is a chronic suppurative granulomatous disease caused by the filamentous bacteria, Actinomyces israelii, which was once thought to be a fungus. It is a Gram-positive, aerobic or microaerophillic, non acid-fast hyphal organism which fragments into coccoid or bacillary forms and, unlike the fungus, does not form conidia. Accessory breast tissue usually occurs along the milk lines, frequently in the axilla and rarely in the thighs. Actinomycosis of the breast is very uncommon and we report the case of a multiparous woman who had a painful lump in the axilla which, on histopathologic examination, showed actinomycosis within the accessory breast tissue.
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This study aims to compare resistance rates of urinary E. coli from otherwise healthy women with uncomplicated UTI and pyelonephritis in the ED to rates in our ED antibiogram.
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Fourteen isolates (12.9%) were PRP by the E-test; nine of these (8.3%) were intermediately resistant and five (4.6%) were highly resistant. All strains were sensitive to rifampin and vancomycin. Increased frequency of resistance to oral and parenteral cephalosporins and carbapenems was found among PRP; for most of these antibiotics, resistance exceeded 40% of the PRP. In addition, 20% of the PRP were resistant to macrolides and all penicillin-susceptible and PRP were resistant to a combination of trimethoprim and sulfamethoxazole.
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Electronic databases including Pubmed, Central and EMBASE were searched without limits to language from 1980 to April 2010. Conference database searches were performed, experts were contacted and bibliographies were handsearched.
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The presence of Tropheryma whippelii was demonstrated in the PAS-negative mesenteric granulomatous lymph nodes of a patient affected by Whipple disease. Ultrastructurally a few bacteria, enclosed by a membrane characteristic of Tropheryma whippelii, were found in the extracellular spaces and remnants of bacteria were found in the phagocytic vacuoles of macrophages. The scarce number of bacilli, probably due to the fact that the disease was at an initial phase, could explain the absence of PAS positivity. This case confirms the role of the electron microscopy in the diagnosis of Whipple disease, especially for extra-intestinal lesions and at the initial phase of the disease, when the characteristic PAS-positive macrophages can be absent.
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The incidence of hematologic abnormalities was evaluated in 120 children with otitis media treated respectively with cotrimoxazole (trimethoprim-sulfamethoxazole) (group 1), cotrimoxazole plus folinic acid (group 2) and amoxicillin (group 3) in therapeutic doses for ten days. Only eosinophilia (an absolute count greater than or equal to 0.5 X 10(9)/l) (group 1 = 10%, 2 = 5%, 3 = 7.5%) and neutropenia (polymorphonuclear neutrophilic leucocyte count less than or equal to 1.5 X 10(9)/l) (group 1 = 35%, 2 = 17.5%, 3 = 13.3%) were noted. Early neutropenia (evident on the 5th day of therapy) occurred in all the treatment groups, thus it is not related to cotrimoxazole administration and in most cases neutrophil count reversed to normal in few days without drug discontinuation. Late neutropenia (evident after 10 days of treatment) appeared only in cotrimoxazole treated children (p less than 0.05). No superimposed bacterial infection was demonstrated in any case. Late neutropenia seems to be strictly related to the sequential blockage of folinic acid metabolism and can be prevented by the concomitant administration of folinic acid.
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Thymidine-auxotrophic small colony variants (SCVs) of Staphylococcus aureus are frequently isolated from the chronically infected airways of patients suffering from cystic fibrosis. To date, little is known regarding the molecular mechanisms leading to the formation of this special phenotype, but the auxotrophism for thymidine suggests that impaired thymidine metabolism might play a major role. Sequence analysis of the thymidylate synthase-encoding thyA gene of six clinical thymidine-auxotrophic S. aureus SCVs revealed that all isolates had mutations within thyA. In five isolates the function of the thymidylate synthase was definitely impaired: three of them showed a truncation of the thyA coding sequence by nonsense or frame-shift mutations, in one further isolate the active site of the enzyme was affected by an internal 12-bp deletion, and another isolate had a 173-bp deletion spanning the 5'-terminal region of thyA and the preceding DNA sequence. The sixth isolate showed two amino acid substitutions within the thyA gene product. To confirm the importance of impaired thymidylate synthase synthesis or activity for the formation of the thymidine-auxotrophic SCV phenotype, we constructed a thyA knock-out mutant of a wild-type S. aureus strain. This mutant showed all characteristics of clinical SCVs, such as slow growth, decreased pigment production, reduced hemolytic activity, auxotrophism for thymidine, resistance to trimethoprim/sulfamethoxazol, and reduced plasma coagulase activity. Complementation of the thyA knock-out mutant with intact thyA in trans nearly restored the normal phenotype. In conclusion, these data confirm at the molecular level that impaired thymidylate synthase function is causative for the formation of the thymidine-auxotrophic SCV phenotype in S. aureus.
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We conducted a randomized, double-blind, placebo-controlled clinical trial at Mulago Hospital, a large hospital that serves the urban and semiurban populations of Kampala, Uganda. One hundred eighty-one HIV-infected children were enrolled at 6 mo and randomized to receive vitamin A supplementation, 60 mg retinol equivalent, or placebo every 3 mo from ages 15 to 36 mo. Morbidity was assessed through a 7-d morbidity history every 3 mo, and vital events were measured. Children received daily trimethoprim-sulfamethoxazole prophylactic therapy.
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The patients were divided into three groups, each consisting of 17 patients: group 1: a single-dose of piperacillin / tazobactam 4.5 g i. v., group 2: ciprofloxacin 500 mg or cotrimoxazol 960 mg i. v. / p. o. and group 3: varying administration and duration of different kinds of antibiotics as control group. The basic characteristics of the patients such as age, body-mass-index, risk factors, diseases, former surgeries and medication were similar between all three groups. Also there were no significant differences in intraoperative parameters such as operation time, blood loss and other postoperative complications.
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As the case presented here illustrates, nocardiosis, like other infections in which cell-mediated immunity plays a large defensive role, can relapse after apparent cure and occasionally at times remote from the original infection. Although relapse in patients with transplants has been cited as a reason for continued prophylaxis, only a few of these cases are adequately documented. This case supports the advice of those authors who give suppressive antibiotic therapy for the duration of immunosuppression in transplant recipients recovering from infections due to Nocardia sp. Alternatively, many transplant centers are routinely using TMP/SMX chemoprophylaxis in all solid organ transplantations to prevent opportunistic infections with Pneumocystis and Listeria sp. Primary prophylaxis has also been associated with a decreased incidence of nocardial infections.
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In the late 1960s, the combination of trimethoprim and sulphamethoxazole (co-trimoxazole) was introduced into clinical practice and used to treat many infectious diseases, such as urinary tract infections, respiratory infections, sexually transmitted diseases, Gram-negative sepsis, enteric infections and typhoid fever. Subsequently, co-trimoxazole was reported to be effective against numerous bacterial, fungal and protozoal pathogens, including Nocardia, Listeria monocytogenes, Brucella, Stenotrophomonas maltophilia, Burkholderia, Coxiella burnetii, Tropheryma whipplei, atypical mycobacteria, and Pneumocystis jirovecii. Among protozoal infections, in addition to toxoplasmosis, co-trimoxazole has been used to treat susceptible Plasmodium falciparum, Cyclospora and Isospora infections. Several retrospective and prospective studies have demonstrated good clinical outcome with co-trimoxazole in treating invasive methicillin-resistant Staphylococcus aureus infections. We summarize herein the accumulated evidence in the literature on the new, 'unconventional' clinical use of co-trimoxazole during the last three decades. In the era of widespread antibiotic resistance and shortage of new antibiotic options, large-scale, well-designed studies are needed to explore the tremendous potential concealed in this well-established drug.
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In 9 studies with a total of 4050 patients, use of transesophageal echocardiography was associated with higher rates of a diagnosis of endocarditis (14%-28%) compared with transthoracic echocardiography (2%-15%). In 4 studies, clinical or transthoracic echocardiography findings did not predict subsequent transesophageal echocardiography findings of endocarditis. Five studies identified clinical or transthoracic echocardiography characteristics associated with low risk of endocarditis (negative predictive values from 93% to 100%). Characteristics associated with a low risk of endocarditis include absence of a permanent intracardiac device, sterile follow-up blood cultures within 4 days after the initial set, no hemodialysis dependence, nosocomial acquisition of S. aureus bacteremia, absence of secondary foci of infection, and no clinical signs of infective endocarditis. Of 81 studies of antibiotic therapy for MRSA bacteremia, only 1 high-quality trial was identified. In that study of 246 patients with S. aureus bacteremia, daptomycin was not inferior to vancomycin or an antistaphylococcal penicillin, each in combination with low-dose, short-course gentamicin (clinical success rate, 44.2% [53/120] vs 41.7% [48/115]; absolute difference, 2.4% [95% CI, -10.2% to 15.1%]).
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In contrast to prior experience in this setting, three of four Shigella flexneri strains recently isolated from patients in Northeastern Brazil with acute inflammatory diarrhea were found to be resistant to sulfamethoxazole, trimethoprim and the combination in vitro. We performed mating studies to determine if the resistance was transferable, and then isolated and characterized plasmid DNA from the resistant Shigella isolates, other resistant Enterobacteriaceae isolated simultaneously from the stools of these individuals, and transconjugant strains. Each of the resistant Shigella strains contained a large plasmid. These plasmids were of different molecular weights ranging from 30 to 50 Mdal in size. Two of these plasmids were transferred with sulfamethoxazole-trimethoprim resistance to E. coli K-12 recipient strains. These findings of transferable resistance to sulfamethoxazole-trimethoprim associated with plasmids in Shigella and in other Enterobacteriaceae raises concerns about the potential limitations of this widely used antimicrobial combination.
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The recommended treatment of Pneumocystis jirovecii pneumonia (PCP) is high-dose trimethoprim-sulfamethoxazole (TMP-SMX) in an equivalent of TMP 15-20 mg/kg/day and SMX 75-100 mg/kg/day for 2 or 3 weeks. High rates of adverse events are reported with this dose, which raises the question if lower doses are possible.
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The mean GO score was significantly lower (p=0.014) in the Tcr group (6.4%) compared with the CiA group (17.9%) after 90 days of immunosuppressive therapy. At 90 days post-transplant, clinically significant GO was observed in four patients of the CiA group and in two of the Tcr group. This difference was not statistically significant (0.66).
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Overall, 308 visits were screened, and 217 were included. Of these, 78.3% were CA-UTI, and 21.7% were HA-UTI. Females comprised 88.5% of all patients. E coli was the most common pathogen overall and in both subgroups. E coli resistance to levofloxacin was 13.5% overall, 9.2% for CA-UTI, and 38.5% for HA-UTI compared with 27% on the hospital antibiogram. E coli resistance to sulfamethoxazole/trimethoprim was 26.9% overall, 25.2% for CA-UTI, and 34.6% for HA-UTI vs 26% on the antibiogram.
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We conducted a randomized prospective multicenter study to compare the safety and efficacy of once daily oral cefixime (8 mg/kg) to twice daily oral trimethoprim/sulfamethoxazole (TMP/SMX) (8/40 mg/kg/day) for the treatment of acute urinary tract infection in children ages 6 months to 13 years. Seventy-six patients (38 in each group) were studied. Thirty-seven percent were younger than 3 years of age. Escherichia coli was the most common isolate in both groups (85%). Eighty-five percent of all Gram-negative organisms were susceptible to TMP/SMX and all were susceptible to cefixime. Seventy-two percent of all patients were febrile at the time of diagnosis. Both groups were treated for 7 to 10 days. Peripheral white blood cell counts, erythrocyte sedimentation rate, body temperature and urinalysis returned to normal at the same rate in both groups. No failures were observed and relapse occurred in 3 cases within the 4 weeks after treatment (2 in the cefixime group and one in the TMP/SMX group). Side effects were observed in 14% of the cefixime group and 16% of the TMP/SMX group and were all mild enough not to necessitate discontinuation of therapy. We conclude that the efficacy and safety of cefixime administered once daily compared favorably with TMP/SMX administered twice daily for acute uncomplicated urinary tract infection.
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In Malawi, high case fatality rates in patients with tuberculosis, who were also co-infected with HIV, and high early death rates in people living with HIV during the initiation of antiretroviral treatment (ART) adversely impacted on treatment outcomes for the national tuberculosis and ART programmes respectively. This article i) discusses the operational research that was conducted in the country on cotrimoxazole preventive therapy, ii) outlines the steps that were taken to translate these findings into national policy and practice, iii) shows how the implementation of cotrimoxazole preventive therapy for both TB patients and HIV-infected patients starting ART was associated with reduced death rates, and iv) highlights lessons that can be learnt for other settings and interventions.
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Overall, 1117 children were included, of whom 89 % were ART-treated and 67 % received cotrimoxazole. Overall, there were 51 malaria events occurring in 48 children: 28 confirmed and 23 probable; 94 % were uncomplicated malaria. The overall IR of malaria (confirmed and probable) was 18.3/100 CY (95 % CI: 13.3-23.4), varying from 4.2/100 CY (95 % CI: 1.1-7.3) in children on ART and cotrimoxazole to 57.3/100 CY (95 % CI: 7.1-107.6) for those receiving no treatment at all. In univariate analysis, age < 5 years was significantly associated with a 2-fold IR of malaria compared to age >10 years (incidence rate ratio [IRR] = 2.18, 95 % CI: 1.04-4.58). Adjusted for severe immunodeficiency, cotrimoxazole reduced significantly the IR of first malarial episode (adjusted IRR [aIRR] = 0.13, 95 % CI: 0.02-0.69 and aIRR = 0.05, 95 % CI:0.02-0.18 in those off and on ART respectively). Severe immunodeficiency increased significantly the malaria IR (aIRR = 4.03, 95 % CI: 1.55-10.47). When considering the IR of confirmed malaria only, this varied from 2.4/100 CY (95 % CI: 0.0-4.8) in children on ART and cotrimoxazole to 34.4/100 CY (95 % CI: 0.0-73.3) for those receiving no treatment at all. In adjusted analyses, the IR of malaria in children on both cotrimoxazole and ART was significantly reduced (aIRR = 0.05, 95 % CI: 0.01-0.24) compared to those receiving no treatment at all.