Mycobacterial diseases : tuberculosis & leprosy最新文献

{"title":"The World must Seriously Consider with Urgency the Use of Thioridazine in Combination with Conventional Antibiotics for Therapy of Extensively Drug Resistant Pulmonary Tuberculosis: Therapy Proven Effective in Argentina","authors":"L. Amaral","doi":"10.4172/2161-1068.1000E130","DOIUrl":"https://doi.org/10.4172/2161-1068.1000E130","url":null,"abstract":"Summary During the 1950's, the consensus among infection disease practitioners was that pulmonary tuberculosis, as a consequence of the e�怆ectveness of the two main anti-tuberculosis drugs, isoniazid (INH) and rifampicin (RIF), would soon be globally eradicated. However, as a consequence of civil unrest, wars, poverty and famine primarily in third world countries, the incidence of tuberculosis infections increased dramatically in these countries and what was once a curable infection, became frequently resistant to INH and RIF termed multi- drug resistance tuberculosis (MDR-TB) as a consequence of poor delivery of therapy, �ne�怆ectve therapy and patient non-compliance. By the late 1980's, the emergence of HIV/AIDS contributed further to the escalation of TB especially in Western countries and coupled to large numbers of migrants infected with Mycobacterium tuberculosis, the causative pathogen of pulmonary tuberculosis, that settled in the major cities of Western countries and later presented with active tuberculosis, the incidence of pulmonary TB reached critical levels, especially in New York City where the incidence quadrupled and more than half of the isolates of the infecting bacterium exhibited an MDR phenotype. It soon became clear MDR-TB was a dire threat to global health and because MDR-TB produces a high percentage of mortality, the need for e�怆ectve drugs was urgent. However, for a variety of reasons, the pharmaceutical industry did not respond, and the only anti-TB drugs that were available termed second-line of defence drugs, produced high incidence of morbidity, and for the most part, where support for therapy of TB is poor or non-existent, their e�怆ectve use was limited due to costs and MDR-TB patients were treated poorly and multi-drug resistance evolved to higher levels of resistance such as extensively drug resistant TB (XDR-TB), and in the last two years, especially in India, resistance progressed to the level where the infective organism was resistant to all known and available anti-TB drugs (TDR-TB). At the time of this writing, with the exception of one agent in combination with anti-TB drugs to which the infective bacterium was initially resistant, there are in e�怆ect no drugs that can e�怆ectvely treat XDR-TB and certainly TDR-TB. It is the purpose of this Editorial to present the proven potential of the old phenothiazine neuroleptic �䀆�ordzne (TZ) in combination with commonly available anti-TB drugs for the therapy of XDR and most likely TDR- TB. TZ has in vitro activity against all encountered Mtb regardless of its antibiotic resistance status (1-3). However, the activity takes place at concentrations of TZ that well exceed its toxic level in the human. Nevertheless, TZ induces the killing of phagocytosed MDR-Mtb and XDR-Mtb by non-killing macrophages at concentrations which are well within the limits of its toxic range in humans (4-6). �䀆ese latter studies were followed by a number of independent studies that demonstrated ","PeriodicalId":74235,"journal":{"name":"Mycobacterial diseases : tuberculosis & leprosy","volume":"28 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70587354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Review on Molecular Mechanism of First Line Antibiotic Resistance in Mycobacterium tuberculosis","authors":"Debasu Damtie, D. Woldeyohannes, Biniam Mathewos","doi":"10.4172/2161-1068.1000174","DOIUrl":"https://doi.org/10.4172/2161-1068.1000174","url":null,"abstract":"Tuberculosis (TB) is among the most common infectious diseases and frequent causes of death worldwide claiming many of lives annually. The problem of tuberculosis is hampered by the emergence of multi drug resistant(MDR) and extensively drug resistant (XDR) tuberculosis. Anti-tuberculosis drugs are a two-edged sword. While they destroy pathogenic Mycobacterium tuberculosis they also select for drug resistant bacteria against which those drugs are then ineffective. \u0000 In contrast to other bacteria, resistance of M. tuberculosis is exclusively associated with chromosomal mutations. Globally, the emergence of multidrug-resistant strains of M. tuberculosis is an increasing problem which adversely affects patient care and public health. The objective of this review is therefore to compile available literatures about the drug resistance mechanisms of M. tuberculosis which gives insight understanding for the development of new therapeutic and diagnostic methods for the management of MDR and XDR tuberculosis infections. \u0000 Resistance to first line anti-TB drugs has been linked to mutations in at least 10 genes; katG, inhA, ahpC, kasA and ndh for INH resistance; rpoB for RIF resistance, embB for EMB resistance, pncA for PZA resistance and rpsL and rrs for STR resistance. The search for new anti-tuberculosis drugs shall consider new targets which are less susceptible for mutation.","PeriodicalId":74235,"journal":{"name":"Mycobacterial diseases : tuberculosis & leprosy","volume":"4 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2014-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2161-1068.1000174","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70581001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Abdominal Tuberculosis: a Benign Differential Diagnosis for Peritoneal Carcinosis: Report of a Case","authors":"D. Schweinfurth, R. Baier, S. Richter","doi":"10.4172/2161-1068.1000173","DOIUrl":"https://doi.org/10.4172/2161-1068.1000173","url":null,"abstract":"Tuberculosis remains a challenge in medicine despite availability of antibiotic treatments. Latent tuberculosis is found in a third of the world’s population. Abdominal tuberculosis is a rare condition in high-income countries, with peritoneal tuberculosis and splenic abscess occurring even less frequently, even in countries with higher prevalence of abdominal tuberculosis. We describe such an uncommon constellation of peritoneal tuberculosis and splenic abscess. Our case demonstrates the challenges in diagnosing abdominal tuberculosis, providing the caveat that tuberculosis should be kept in mind whenever unspecific findings occur in abdominal imaging or unusual surgical findings. In our case, thorough history-taking - including explicit questionings about tuberculosis exposition decades ago - provided the only lead pointing towards the correct interpretation of otherwise unspecific findings. In our case, tuberculosis as a differential diagnosis to peritoneal carcinosis was only implied after histopathological evaluation, followed by timely diagnostics for pulmonary involvement and potential infectiousness.","PeriodicalId":74235,"journal":{"name":"Mycobacterial diseases : tuberculosis & leprosy","volume":"4 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2014-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70580805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glycogenomics of Mycobacterium tuberculosis","authors":"A. Gupta, Amit Singh, Sarman Singh","doi":"10.4172/2161-1068.1000175","DOIUrl":"https://doi.org/10.4172/2161-1068.1000175","url":null,"abstract":"Glycogen is an important energy store of almost all living organisms. It is an alpha linked polymer comprised of thousands of glucose units. In bacteria it is usually synthesized when carbon ions are in excess in the growth medium and its synthesis helps for the survival of the bacteria under such nutritional conditions. Mycobacterium tuberculosis (M. tuberculosis), accumulates glycogen during the adverse condition such as reactive oxygen and nitrogen intermediates, low pH, nutrients and other vital element starvation for their survival in the host. Glycogen also plays a very important role in the pathogenesis of M. tuberculosis. The biosynthesis of glycogens is mediated by glycosyltransferases enzyme which can be divided into two families; glycogen transferase (GT) 3 and glycosyltransferases GT 5. Regulation of glycogen metabolism in bacteria involves a complex mechanism, involving several synthase enzymes such as glycogen synthase A (glgA), glycogen branching enzyme (glgB), and catalytic enzyme (glgC). Another enzyme known as glycogen phosphorylase (glgP), removes extra units of glucose from the non- reducing ends of the glycogen molecule. Several workers have recognized role of glycogen in Mycobacterial pathogenesis, in the recent years. Trehalose-dimycolate (TDM) and trehalose-monomycolate (TMM) present in the cell wall are indeed a precursor of mycolic acid of Mycobacteria, which plays an important role in its invasion and pathogenesis. This review focuses on various cycles and mechanisms involved in the glycogen synthesis in M. tuberculosis and its role in pathogenesis.","PeriodicalId":74235,"journal":{"name":"Mycobacterial diseases : tuberculosis & leprosy","volume":"4 1","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2014-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70581085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Brief review on Ecology and Evolution of Mycobacteria","authors":"K. Prasanthi, Murty Ds","doi":"10.4172/2161-1068.1000172","DOIUrl":"https://doi.org/10.4172/2161-1068.1000172","url":null,"abstract":"Tuberculosis is one of the grand old diseases and among the top burdened diseases of the world. Most Mycobacteria are environmental saprophytes except Mycobacterium tuberculosis and Mycobacterium leprae, which are obligate pathogens. However, several studies indicate that the selection of the pathogens in an ever changing environment do occur by a variety of deletion mutations over time. Mycobacterium tuberculosis might have originated from an environmental ancestor. Some studies even predict that some of the environmental saprophytic mycobacteria may become pathogens in near future because of the selection pressure of the environment. In this context, this article briefly outlines the ecology and evolution of the Mycobacteria.","PeriodicalId":74235,"journal":{"name":"Mycobacterial diseases : tuberculosis & leprosy","volume":"4 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2014-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70580855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diagnosis and Management of Tuberculosis in Candidates for Tumor Necrosis Factor Alpha Antagonists: An Experts Survey","authors":"K. Birkenkamp, M. Lauzardo, B. Mangura, M. Brito, D. Griffith, B. Seaworth, P. Escalante","doi":"10.4172/2161-1068.1000171","DOIUrl":"https://doi.org/10.4172/2161-1068.1000171","url":null,"abstract":"Background: There are some controversies regarding the management of latent tuberculosis infection and tuberculosis in patients with rheumatologic indications for biologic therapy. \u0000Objectives: To describe current expert opinions and preferences regarding the evaluation and management of latent tuberculosis infection and tuberculosis in candidates and recipients of tumor-necrosis factor-alpha blocking therapy. \u0000Methods: A questionnaire addressing preferences related to management and treatment of latent tuberculosis infection and active tuberculosis in tumor-necrosis factor-alpha blocking candidates was distributed to tuberculosis and rheumatology experts across the United States between August 18, 2009, and June 21, 2010. Survey responses were formulated as a 5-point Likert scale (strongly disagree to strongly agree), or as a priority rank order list (1 to 6 or 7), and data were analyzed for percent agreement and median rankings. \u0000Measurements and main results: The tuberculin skin test and interferon-gamma release assays for latent tuberculosis infection screening were highly accepted among tuberculosis and rheumatology experts. Most participants supported the use of daily isoniazid for 9 months for latent tuberculosis infection therapy, but responses were mixed regarding timing to initiation of tumor-necrosis factor-alpha blocking therapy. Most tuberculosis experts supported standard anti-tuberculosis therapy for treatment of tuberculosis, but preferences varied among rheumatologists. In contrast, most rheumatologists believed tumor-necrosis factor-alpha blocking therapy should be stopped in individuals with active tuberculosis, while opinions varied among tuberculosis experts. \u0000Conclusions: Agreement among experts was common regarding preferences for diagnosis and management of latent tuberculosis infection and tuberculosis under hypothetical but likely common clinical scenarios, but some differences exist.","PeriodicalId":74235,"journal":{"name":"Mycobacterial diseases : tuberculosis & leprosy","volume":"12 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2014-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70580835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Male Genital Tuberculosis","authors":"Tarık Yonguç, I. Bozkurt","doi":"10.4172/2161-1068.1000169","DOIUrl":"https://doi.org/10.4172/2161-1068.1000169","url":null,"abstract":"Genitourinary system is the most common extrapulmonary site after lymph node involvement affected by tuberculosis (TB). TB can affect whole male genital organs; epididymis, testis, prostate, seminal vesicle, vas deferens, scrotal skin, bulbourethral glands and penis. Although male genital TB (MGTB) is reported rarely in the literature, most of the cases are overlooked. It is not always very easy to diagnose MGTB because there is no pathognomonic sign. Sometimes, it can be difficult to differentiate TB orchitis from testicular cancer. If laboratory and radiological findings are not enough for diagnosis then biopsy and surgical procedures such as epididymo-orchiectomy may be required.","PeriodicalId":74235,"journal":{"name":"Mycobacterial diseases : tuberculosis & leprosy","volume":"4 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2014-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70580592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pigments and Pathogenesis","authors":"B. Saviola","doi":"10.4172/2161-1068.1000168","DOIUrl":"https://doi.org/10.4172/2161-1068.1000168","url":null,"abstract":"In recent years pigments have been identified in human nutrition to have a positive effect on human health and reduction to oxidative stress exposure. In the media it has become common wisdom that colourful food is naturally better to consume for humans and animals. Now recently it has been shown that pigments aid microbial species as well, and conversely these microbial pigments may result in more morbidity and mortality for the human host infected by these colourful microbes. Similar pigments that are available for consumption in food are also present in many bacterial species. Presumably these pigments aid the bacteria in their survival in the environment and within a human or animal host. Importantly, interference with the production of certain microbial pigments results in some bacterial strains that are more susceptible to environmental stressors and the host immune system. These studies seem to indicate a role of pigments for in vivo survival by microbial species.","PeriodicalId":74235,"journal":{"name":"Mycobacterial diseases : tuberculosis & leprosy","volume":"153 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2014-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2161-1068.1000168","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70580462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of Family System Characteristics on Adherence to Directly Observed Treatment, Short-Course (Dots) in Pulmonary Tuberculosis-ACohort Study","authors":"Ulises Rosado-Quiab, R. Cedillo-Rivera, David Alej, ro Cabrera-Gaytan, Alfredo Vargas-Valerio","doi":"10.4172/2161-1068.1000166","DOIUrl":"https://doi.org/10.4172/2161-1068.1000166","url":null,"abstract":"Objective: To evaluate the association of the characteristics of the family system in adherence observed treatment short in patients with pulmonary tuberculosis in three cities of the south-southeast of Mexico. \u0000Material and methods: Cases of pulmonary tuberculosis were studied, who started treatment at first-level units. The follow-up was 6 months or until the patient lost his grip, emigrated to another city, died, or decided not to continue the study. Intrafamilial relationships were assessed, family functioning (FACES III) and social network (DUKE UNC-11); adherence was assessed with test-Greene Morinsky. We calculated incidence of non-adherence and relative risk factors studied. Variables with significant differences in the bivariate analysis were subjected to the proportional hazards model of Cox. \u0000Results: Two hundred and thirty four patients were included; the total track joined 36,937 days, with a median of 175 days. Patients with dysfunctional family have RR=8.95 (95% CI=4.51-17.76, p<0.001) compared with those with functional family, and patients with non-functional network showed RR=2.22 (95% CI=1.13-4.35, p 0.002) compared with those with functional social network. In the Cox regression model adjusted for education, statistical significance was maintained for family functionality. Family functioning influences the cohorts studied in treatment adherence","PeriodicalId":74235,"journal":{"name":"Mycobacterial diseases : tuberculosis & leprosy","volume":"4 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2014-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70580340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protection Vs. Pathology in Tuberculosis: How Our Growing Understanding of the Molecular Regulators of Cell Recruitment Could Lead to New Therapies","authors":"J. Harding, M. Sandor, J. Hardling","doi":"10.4172/2161-1068.1000167","DOIUrl":"https://doi.org/10.4172/2161-1068.1000167","url":null,"abstract":"The granuloma is the hallmark pathological structure in patients infected with Mycobacterium tuberculosis (Mtb). It is a collection of mostly innate and adaptive immune cells organized around Mtb bacilli with a defined spatial arrangement and cellular composition [1-3]. Infection with Mtb begins after a few inhaled bacilli are phagocytosed by lung-resident macrophages. Infected macrophages release of TNFα, which initiates a cytokine storm and supports the release of other pro-inflammatory cytokines and chemokines like Il-1β, IL-6, Il-12, CCL2, and, CCL5, to name a few [4]. Eventually, dendritic cells from the granuloma transport bacterial antigen to the lymph node and activate Mtb-specific CD4 and CD8 T-cells, which then migrate to the granuloma and enhance macrophage anti-microbial activity with the release of IFNγ [5-8].","PeriodicalId":74235,"journal":{"name":"Mycobacterial diseases : tuberculosis & leprosy","volume":"2014 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70580253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}