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To the best of our knowledge we are presenting the very first case of inadvertent intravascular administration of BCG and its successful treatment with anti-tuberculosis medications on a patient with superficial bladder cancer.
The use of the assay to rapidly diagnose MDR could guide simultaneous first- and second-line DST, and reduce the delay in administering appropriate regimens. Furthermore, detection of heteroresistance could prevent inaccurate "cured" treatment outcomes documented through smear microscopy and permit more sensitive detection of neonascent resistance.
Mutations M306I (n = 56), M306V (n = 18) and M306L (n = 3) in M. tuberculosis showed decreased susceptibility to ethambutol. The minimum inhibitory concentrations (MICs) in 73% (56/77) of embB306 mutants were at or just above the critical concentration (MICs, 5.0 to ≤12.5 µg/ml) of ethambutol reflecting borderline (or intermediate) resistance. Eight ethambutol-resistant isolates lacked embB mutations, probably due to mutational alterations elsewhere in the genome.
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We present a case of tuberculous peritonitis in the setting of alcoholic cirrhosis with ascites. A young American Indian male with alcoholic cirrhosis and ascites presented with low grade fever and weight loss. A diagnosis of tuberculous peritonitis was made by laparoscopic guided peritoneal biopsy. He was treated successfully with isoniazid and ethambutol for 24 months. The diagnosis of tuberculous peritonitis should be entertained in high risk populations such as American Indians, Asians, alcoholics, chronic ambulatory peritoneal dialysis patients and AIDS patients in the appropriate clinical setting. Definitive diagnosis can usually be made by laparoscopic guided peritoneal biopsy.
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Two patients who developed reversible renal failure during intermittent rifampicin therapy are described. Both had febrile reactions to rifampicin. The first was also found to have uraemia associated with swelling of the glomerular endothelial cells. The second developed tubular necrosis unassociated with haemolysis or shock. The pathogenesis of the renal lesion in these two patients, as revealed by light microscopy, immunofluorescence studies and electron microscopy, is discussed.
The pharmacodynamics of tuberculosis (TB) treatment should be further explored, to prevent emergence of resistance, treatment failure and relapse of infection. The diagnostic drug susceptibility tests guiding TB therapy investigate metabolically active Mycobacterium tuberculosis (Mtb) isolates under static conditions and as such are not informative with respect to the time-kill kinetics of anti-TB drugs and the emergence of resistance in metabolically lowly active or even dormant mycobacterial cells.
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We pursued the possibility that Mycobacterium kansasii might be an aetiological agent in Crohn's disease by carrying out a trial of treatment with antimycobacterial drugs. Twenty seven patients with Crohn's disease took part in a two year randomised double blind, crossover, controlled trial of rifampicin plus ethambutol against placebo. Fourteen patients completed the trial; four required an operation; five were withdrawn as poor compliers, and four because of adverse effects. There was no significant difference in response to the active drugs compared with placebo when expressed in terms of a Crohn's disease activity index or any clinical indicator of disease activity. There was no suggestion that any subgroup of patients - for example, different regions of bowel affected or previous operation - were favourably affected by the drugs. There was no consistent pattern of change in prednisolone requirements although eight patients on long term sulphasalazine had a significant reduction in their plasma sulphapyridine concentrations during the active treatment period. A significant reduction in total white blood count and an increase in plasma ALT were seen during active therapy. The results of the study do not suggest that rifampicin and ethambutol have a role to play in the treatment of Crohn's disease.
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The high resistance observed in isoniazid, which is a first-line drug, could result in an increase in multidrug resistance unless control programs are strengthened. Poverty should be addressed to reduce infection rates.
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The reliable supply of quality drugs in the form of fixed dose combination (FDC) is an essential part of tuberculosis treatment. The objective of this investigation was to evaluate whether the World Health Organization (WHO) simplified screening protocol for the bioequivalence assessment of rifampicin can be used for the evaluation of other components of FDC so as to ensure the bioavailability of all drugs at tissue site. These bioequivalence studies were conducted on 20 and 22 healthy male volunteers for evaluation of three and four drugs FDC formulations, respectively. Both studies were conducted as randomized, open, crossover trials and sampling schedule was upto 8h according to WHO recommended protocol for evaluation of rifampicin bioequivalence. The bioequivalence of isoniazid and pyrazinamide were estimated using AUC(0-8), AUC(0-alpha), and C(max). FDC formulation was considered bioequivalent to separate formulations for isoniazid and pyrazinamide if bioequivalence limit fall in between 0.80 and 1.25. Bioequivalence estimates of AUC(0-8) and AUC(0-alpha) for isoniazid and all the three pharmacokinetic measures of pyrazinamide were within the acceptable limits, whereas C(max) of isoniazid from four drugs FDC was outside the limit when evaluated by two-way ANOVA. After evaluation of isoniazid and pyrazinamide based on their pharmacokinetics, it was found that C(max) is being affected by limited sampling time points of WHO protocol. Further, AUC was a robust parameter unaffected by sampling schedule adopted. The WHO simplified protocol for assessment of rifampicin is also suitable for evaluating bioequivalence of isoniazid and pyrazinamide from FDC formulations. However, for comparison of rate of absorption by means of C(max), careful evaluation of concentration-time profile along with pharmacokinetics is necessary before final judgment.
Intermittent three-times-weekly antibiotic therapy is recommended for the initial treatment of patients with noncavitary nodular bronchiectatic Mycobacterium avium complex lung disease. Although some experts recommend switching from intermittent to daily therapy for patients whose sputum has persistent positive cultures after intermittent therapy, the clinical efficacy of these modifications is unknown. Of 20 patients whose sputum had persistent positive cultures after 12 months of intermittent antibiotic therapy, specimens from 6 patients (30%) achieved a negative culture after a change to daily therapy.
Treatment of chronic bacterial infections, such as tuberculosis (TB), requires a remarkably long course of therapy, despite the availability of drugs that are rapidly bacteriocidal in vitro. This observation has long been attributed to the presence of bacterial populations in the host that are "drug-tolerant" because of their slow replication and low rate of metabolism. However, both the physiologic state of these hypothetical drug-tolerant populations and the bacterial pathways that regulate growth and metabolism in vivo remain obscure. Here we demonstrate that diverse growth-limiting stresses trigger a common signal transduction pathway in Mycobacterium tuberculosis that leads to the induction of triglyceride synthesis. This pathway plays a causal role in reducing growth and antibiotic efficacy by redirecting cellular carbon fluxes away from the tricarboxylic acid cycle. Mutants in which this metabolic switch is disrupted are unable to arrest their growth in response to stress and remain sensitive to antibiotics during infection. Thus, this regulatory pathway contributes to antibiotic tolerance in vivo, and its modulation may represent a novel strategy for accelerating TB treatment.
The chief complaint in 70% of patients was intractable cough, particularly in those with tracheal tuberculosis. The predominant radiological features were patchy bi-apical infiltrates of variable intensity without cavitation; for six patients, however, plain radiographs revealed no abnormalities. The ulcerous lesions could be classified into three stages: active, healing and scarring. Furthermore, we divided scarring stage into two subtypes, polypoid and non-polypoid. Most of the patients were treated with isoniazid, rifampin, and streptomycin (SM) or ethambutol. Approximately one-third of the patients, not randomly selected, were treated with aerosolized SM and corticosteroids in addition to conventional oral therapy.
One hundred and thirty-seven newly diagnosed TB patients (26 (19%) being HIV positive) from all age groups were recruited into the study. Each specimen was cultured using BACTEC MGIT960, followed by inoculation and growth on Lowenstein-Jensen (LJ) medium. Primary identification was carried out using an immunochromatographic technique (Capilia TB-Neo), and further confirmed by genotyping. Drug susceptibility testing (DST) was carried out by the agar proportion method.
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The Mycobacterium avium complex is the most common cause of nontuberculous mycobacterial lung disease worldwide; yet, an optimal treatment regimen for M. avium complex infection has not been established. Clarithromycin is accepted as the cornerstone drug for treatment of M. avium lung disease; however, good model systems, especially animal models, are needed to evaluate the most effective companion drugs. We performed a series of experiments to evaluate and use different mouse models (comparing BALB/c, C57BL/6, nude, and beige mice) of M. avium infection and to assess the anti-M. avium activity of single and combination drug regimens, in vitro, ex vivo, and in mice. In vitro, clarithromycin and moxifloxacin were most active against M. avium, and no antagonism was observed between these two drugs. Nude mice were more susceptible to M. avium infection than the other mouse strains tested, but the impact of treatment was most clearly seen in M. avium-infected BALB/c mice. The combination of clarithromycin-ethambutol-rifampin was more effective in all infected mice than moxifloxacin-ethambutol-rifampin; the addition of moxifloxacin to the clarithromycin-containing regimen did not increase treatment efficacy. Clarithromycin-containing regimens are the most effective for M. avium infection; substitution of moxifloxacin for clarithromycin had a negative impact on treatment efficacy.
A total of 40 rats were divided into four groups: A normal group, hyperuricemia group, benzbromarone group (9 mg/kg) and total saponins from rhizoma dioscoreae nipponese (TDN) group (40 mg/kg). Adenine (100 mg/kg) and ethambutol (250 mg/kg) were used to induce hyperuricemic rats. Immunohistochemical and Western blotting methods were used to detect the mRNA and proteins expressions of rat organic anion transporter1 (rOAT1), rat organic anion transporter3 (rOAT3) and rat urate transporter1 (rURAT1) in the kidneys of different groups.
Ethambutol is frequently used in the treatment of tuberculosis, and, although optic neuropathies have been reported with the use of ethambutol, this adverse side effect has been considered to be rare and generally reversible with discontinuation of the medication. However, we recently saw two patients with renal tuberculosis treated with ethambutol in whom visual loss from toxic optic neuropathies was severe and irreversible despite careful ophthalmological monitoring and prompt discontinuation of the agent at the first sign of impaired visual function. While ethambutol treatment is most commonly instituted for pulmonary tuberculosis, it is interesting to note that both of these patients had renal tuberculosis. Since ethambutol is actively excreted via the renal system, compromise of renal function such as due to renal tuberculosis may lead to serum concentration elevations of ethambutol sufficient to produce optic neuropathy.
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To evaluate the mycobacterium efficacy of linezolid to Mycobacterium tuberculosis bacilli and Non-tuberculous mycobacteria (NTM) in vitro, and to analyze the interaction between linezolid and other anti-TB drugs in vitro.
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Participants were monitored for absolute change in lesion diameter and decrease in granuloma burden, if present, on completion of therapy.
We treated a 35-year-old woman who had AIDS with neurologic involvement caused by Mycobacterium tuberculosis. She developed a yellow-white chorioretinal infiltrate with indistinct borders and mild vitreitis in the right eye, probably caused by this pathogen.
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[3H]-uridine was incorporated by Mycobacterium bovis BCG with increasing intensity as the incubation period was increased. Rifampicin and isoniazid inhibited incorporation of the label rapidly. Similar inhibition was seen with M. tuberculosis H37Rv and several clinical isolates of M. tuberculosis both in axenic medium and inside macrophages. Ofloxacin and ciprofloxacin were both inhibitory but clofazimine was not. The combination of rifampicin with either isoniazid or ethambutol produced enhanced killing, but the combination of ethambutol and isoniazid was not synergic. Mycobacterium avium-intracellulare isolates from AIDS patients were less susceptible to rifampicin and were unaffected by isoniazid, ethambutol, clofazimine, ofloxacin and ciprofloxacin. The results obtained by inhibition of [3H]-uridine incorporation by intracellular mycobacteria correlated with conventional in-vitro MICs and was reproducible and rapid; a definitive result was obtainable within seven days.
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Both lactate dehydrogenase (339 U/l) and C-reactive protein (112 mg/l) were elevated; the platelet count was low (73000/microliters). Cerebrospinal fluid was unremarkable, as was computed tomography of the skull. But magnetic resonance imaging revealed multiple spotty lesions with low contrast-medium uptake throughout the brain, pointing to a disseminated bacterial or mycotic infection. 3 days later the chest-ray showed small nodular soft shadows in the lungs, and lung functions had decreased. Mycobacteria were found in the urine and liver biopsy showed granulomatous hepatitis, establishing the diagnosis of miliary tuberculosis in the presence of silicosis.
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A 65-year-old woman, treated with prednisolone (5 mg daily) for rheumatoid arthritis, visited our hospital because of right chest pain. Chest CT showed small nodular shadows in the right lung accompanied with right pleural effusion. A pulmonary Mycobacterium gordonae infection was diagnosed, since M. gordonae was identified twice from her sputum. She was treated with rifampicin, ethambutol and streptomycin for two months, and then streptomycin was replaced with clarithromycin. Three months after the initial treatment, M. gordonae was eradicated from her sputum. Pleural puncture revealed bloody, exudative, lymphocytotic pleural effusion, but no malignant cells were identified. Although pathological diagnosis by thoracoscopic pleural biopsy could not be performed, it is likely that the pleural effusion was associated with the pulmonary M. gordonae infection in the present case.
Bronchogenic cysts are lesions of congenital origin derived from the primitive foregut and are the most common primary cysts of the mediastinum. They are most frequently unilocular and contain clear fluid. Respiratory distress is the most common presentation in pediatric patients, manifested by recurring episodes of cough, stridor, wheezing and retractions.