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Corynebacterium glutamicum belongs to the mycolic acid-containing actinomycetes, which also include Mycobacterium, Nocardia, and Rhodococcus. The cells of this group possess a cell wall with a thick outer layer composed primarily of mycolic acid, which functions as a permeability barrier. To investigate the mechanism of mycolic acid-containing layer (mycolate layer) formation, we have developed a fluorescence microscopic technique detecting the mycolate layer in situ. The staining specificity of fluorescence-labeled phospholipid analogs was determined by simultaneous staining with the hydrophobic fluorescent dye Nile Red and peptidoglycan-staining fluorescence-conjugated vancomycin. We found that fluorescence-labeled phospholipid analogs preferentially stain the mycolate layer. Using this technique, we observed the effect of the anti-mycobacterial drug ethambutol on C. glutamicum mycolate-layer formation. Ethambutol interfered specifically with mycolate-layer formation on the division planes and cell poles, while the side-wall mycolate layer was not severely affected. This indicates that mycolate-layer formation occurs mainly on division planes and cell poles in C. glutamicum, where the peptidoglycan layer is actively synthesized.
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Gynaecomastia due to anti-tubercular chemotherapy is a rare side effect. Isoniazid causing breast tissue enlargement has been very rarely reported. We report a 60-year old, male patient of Pulmonary Tuberculosis who was started on antituberculous treatment (ATT) with rifampicin (R), isoniazid (H), ethambutol (E) and pyrazinamide (Z) together for initial two months and R, H & E thereon. After five months of initiation of treatment, while receiving RHE, he developed painful bilateral gynaecomastia. Isoniazid was stopped and patient was continued on R & E till completion of the treatment up to nine months. After stopping isoniazid, his breast swelling subsided to some extent and became non-tender. Follow up, at six months, after stopping the course of treatment, patient was asymptomatic except for slight bilateral non-tender breast enlargement.
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The accomplishment of the principles for the prevention of a germ resistance and the development of new principles of treatment and highly effective antituberculotics has led to the fact that nowadays actually each case of tuberculosis may be treated and cured purely internally. This progress in the individual treatment were achieved by recommendations of therapy which are actualized from time to time. The modern treatment consists of a daily application of three effective antituberculotics for two to three months, fellowed by an intermittent application twice a week. The duration of the initial intensive period and the whole time of therapy is determined by the clinical and social state before the beginning and by the combination of drugs. INH, rifampizine, streptomycin and ethambutol form the components of the therapy combinations which at present are to be used no longer than twelve months. The redetection of the special microbiological qualities of the pyrazineamide and their importance for the prevention of relapses introduces the last phase of the development of the therapy of tuberculosis. By its means it is possible to shorten the duration of the treatment to 9 months and less and thus to increase the acceptability and cooperation, to decrease the toxicity and costs.
The overall prevalence of DR TB was 86 (6.6%) with an increase from 23 (5.6%) patients pre-2010 to 63 (7%) post-2010 (P = 0.40). Nine (10.4%) patients were diagnosed on the basis of contact with a parent with DR TB. Overall fluoroquinolone resistance increased from 9 (39.1%) pre-2010 to 59 (93.7%) post-2010 (P = 0.0001): moxifloxacin resistance increased from 2 (8.7%) to 29 (46%) (P = 0.0018) and ofloxacin resistance increased from 7 (30.4%) to 30 (47.6%) (P = 0.14). Ethionamide resistance also increased from 6 (26.1%) to 31 (49.2%) (P = 0.04), aminoglycoside resistance was one (4.3%) pre-2010 and 12 (19%) post-2010 (P = 0.17) and resistance remained virtually the same for both amikacin [0 pre-2010 and 6 (9.5%) after 2010] and kanamycin [one (4.3%) pre- and 6 (9.5%) post-2010]. Of the first-line drugs, resistance remained the same for isoniazid [23 (100%) to 61 (96.8%)], rifampicin [22 (95.7%) to 51 (80.9%),P = 0.17], pyrazinamide [15 (65.2%) to 35 (55.6%), P = 0.47], ethambutol [14 (60.9%) to 38 (60.3%), P = 1.00] and streptomycin [19 (82.6%) to 50 (79.4%), P = 1.00]. Resistance to PAS remained unchanged [2 (8.7%) to 5 (7.9%), P = 1.00].
We report a rare case in a female infant (age, 3.5 months) with primary immunodeficiency (IFN-γ/IL-12 pathway defect) who presented with suppurative lymphadenitis after Mycobacterium bovis BCG vaccination. The strain of M. bovis BCG identified was found to be resistant to isoniazid and rifampin. The patient was treated with a special pharmacological regimen involving isoniazid (in a limited, strategic manner), ethambutol, streptomycin, and IFN-γ, after which there was complete resolution of the lesions.
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This is a one-year laboratory-based study. Specimens from suspected new TB patients sent to the TB laboratory of the Department of Medical Microbiology, University College Hospital Ibadan, Nigeria from May 1, 2005 to April 27, 2006 were processed and analyzed. The specimens were stained with Ziehl-Neelsen (Z-N) reagents and cultured on Lowenstein-Jensen medium, incubated at 37 degrees C for 6-8 weeks. Isolates were confirmed as MDR-TB by Z-N reactions and biochemical methods. Drug susceptibility to streptomycin, ethambutol, rifampicin and isoniazid was done using Bactec 460 TB radiometric method.
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We described enlargement of intrathoracic diffuse large B-cell lymphoma (DLBCL) during treatment of pulmonary tuberculosis in a 78-year-old man. The patient had previously undergone treatment for pulmonary tuberculosis about 50 years ago and showed disease recurrence in 2010. Although after tuberculosis treatment with the standard chemotherapy regimen of isoniazid, rifampicin, ethambutol, and pyrazinamide, we observed a clear resolution of the main X-ray shadows, a nodular shadow in the right upper lung field was observed to have increased in size. After evaluation by transbronchial biopsy of the upper right lung lobe, we diagnosed DLBCL with subepithelial infiltration of an airway. This is a rare case of coexistence of active pulmonary tuberculosis and intrathoracic DLBCL.
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The role of the serine/threonine kinase PknH in the physiology and virulence of Mycobacterium tuberculosis was assessed by the construction of a pknH deletion mutant. Deletion of the pknH gene did not affect sensitivity to the antimycobacterial drug ethambutol, although it was previously thought to be involved in regulating expression of emb genes encoding arabinosyl transferases, the targets of ethambutol. Nevertheless, transcription analyses revealed that genes associated with mycobacterial cell wall component synthesis, such as emb and ini operons, are downstream substrates of the PknH signaling cascade. In vitro survival studies revealed that a mutant with a deletion of the pknH gene displayed increased resistance to acidified nitrite stress, suggesting that nitric oxide is one of the potential environmental triggers for PknH activation. The effect of pknH deletion on mycobacterial virulence was investigated in BALB/c mice. In this model, the DeltapknH mutant was found to survive and replicate to a higher bacillary load in mouse organs than its parental strain and the pknH-complemented strain. In contrast, another closely related kinase mutant, the DeltapknE mutant, obtained from the same parental strain, was not affected in its virulence phenotype. Infection of THP-1 cells or in vitro growth studies in 7H9 medium did not reveal a significant in vitro growth advantage phenotype for the DeltapknH mutant. In conclusion, we propose that the serine/threonine kinase PknH plays a role in regulating bacillary load in mouse organs to facilitate adaptation to the host environment, possibly by enabling a regulated chronic infection by M. tuberculosis.
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Two large cities in the Philippines.