Drug-resistant TB may bring epidemic

Nature (Impact Factor: 41.46). 05/1992; 356(6369):473. DOI: 10.1038/356473a0
Source: PubMed


Research opportunities are opening up for the long-neglected study of mycobacterium tuberculosis, a disease of poverty that is once again on the rise. TB is back.

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    • "Our incapacity to eradicate this disease is in part due to the specific cell envelope of mycobacteria which plays an important role in pathogenesis and confers resistance to antibiotic and bactericidal treatments (Daffe and Draper, 1998). The situation is exacerbated by the emergence of multi drug-resistant (Culliton, 1992) and extensively drug-resistant (Raviglione and Smith, 2007) tuberculosis. A prerequisite for effective control of the disease is a better understanding of the host–pathogen interactions and their contribution to pathogenesis. "
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    ABSTRACT: Infection of the zebrafish with Mycobacterium marinum is regarded as a well-established experimental model to study the pathogenicity of Mycobacterium tuberculosis. Herein, a M. marinum transposon mutant library was screened for attenuated M. marinum phenotypes using a Dictyostelium discoideum assay. In one attenuated mutant, the transposon was located within tesA, encoding a putative type II thioesterase. Thin-layer chromatography analyses indicated that the tesA::Tn mutant failed to produce two major cell wall-associated lipids. Mass spectrometry and nuclear magnetic resonance clearly established the nature of missing lipids as phthioglycol diphthioceranates and phenolic glycolipids, respectively, indicating that TesA is required for the synthesis of both lipids. When injected into the zebrafish embryo bloodstream, the mutant was found to be highly attenuated, thus validating the performance and relevance of the Dictyostelium screen. Consistent with these in vivo findings, tesA::Tn exhibited increased permeability defects in vitro, which may explain its failure to survive in host macrophages. Unexpectedly, virulence was retained when bacteria were injected into the notochord. Histological and ultrastructural studies of the infected notochord revealed the presence of actively proliferating mycobacteria, leading to larval death. This work presents for the first time the notochord as a compartment highly susceptible to mycobacterial infection.
    Molecular Microbiology 04/2011; 80(4):919 - 934. DOI:10.1111/j.1365-2958.2011.07618.x · 4.42 Impact Factor
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    ABSTRACT: This work deals with channel-tunnel dependent multidrug efflux pumps and type I secretion systems, more concrete with the improved classification of the adaptor protein family, the characterization of the TolC-homologue protein HI1462 of Haemophilus influenzae, and the molecular characterization of the interaction between TolC and AcrA of Escherichia coli. Diese Arbeit beschäftigt sich mit Channel-Tunnel-abhängigen Multidrug Efflux Pumpen und Typ I Sekretionssystemen, genauer gesagt mit der verbesserten Klassifikation der Familie der Adapter-Proteine, der Charakterisierung des TolC-homologen Proteins HI1462 aus Haemophilus influenzae, und der molekularen Charakterisierung der Interaktion zwischen TolC und AcrA aus Escherichia coli.
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