Successful Treatment of Pulmonary<i>Mycobacterium xenopi</i>Infection in a Natural Killer Cell–Deficient Patient with Clarithromycin, Rifabutin, and Sparfloxacin

Schmitt, H. J.; Riehl, J; Adam, Gerhard; Sieberth, Heinz–Günter; Haase, G.

doi:10.1086/520140

Cited by 20 publications

(12 citation statements)

References 54 publications

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“…This MIC is higher than those previously published (5,7). The MICs of other antimicrobials against strain Elb 3441 are as follows: RIF, 0.5 g/ml; INH, 0.5 g/ml; EMB, 16 g/ml; AMK, 4 g/ml; OFX, 2 g/ml; LVX, 1 g/ml; CIP, 2 g/ml; SPX, 0.25 g/ml; GMX, 4 g/ml; and MXX, 0.25 g/ml.…”

contrasting

confidence: 64%

Efficacies of Clarithromycin Regimens against Mycobacterium xenopi in Mice

Lounis

Truffot-Pernot

Bentoucha

et al. 2001

Antimicrob Agents Chemother

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Mice were infected intravenously with 3.5 ؋ 10 7 CFU of Mycobacterium xenopi and treated with various clarithromycin-containing regimens or left untreated for 4 weeks. All nine of the clarithromycin-containing regimens reduced the CFU counts to the levels below the pretreatment values, indicating that these regimens had a bactericidal effect on M. xenopi in mice. The rifampin-isoniazid-ethambutol regimen was significantly less bactericidal than clarithromycin alone or clarithromycin-containing combined regimens.

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contrasting

confidence: 64%

Efficacies of Clarithromycin Regimens against Mycobacterium xenopi in Mice

Lounis

Truffot-Pernot

Bentoucha

et al. 2001

Antimicrob Agents Chemother

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“…However, synergy between clarithromycin and rifabutin against M. avium has been demonstrated in vitro [20], since when both drugs are administered simultaneously, the rifabutin concentration increases between 4 and 37-fold [21]. This could explain the therapeutic usefulness of rifabutin against M. xenopi [22] and in nontuberculous mycobacterial lymphadenitis [23]. Our data also explain the failure of prophylaxis with rifabutin, when used as monotherapy, in the prevention of M. celatum infections [24].…”

Section: Discussionmentioning

confidence: 65%

Mutant prevention concentration: a new tool for choosing treatment in nontuberculous mycobacterial infections

Rodrı́guez

Cebrián

López

et al. 2004

International Journal of Antimicrobial Agents

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“…Like other protein synthesis inhibitors that affect the large subunit, they can also prevent the formation of the 50S particle in growing cells (8). Natural macrolides, such as erythromycin, are not effective against mycobacteria, but semisynthetic derivatives, such as clarithromycin and azithromycin, have stronger antimycobacterial activities and are widely used to treat infections caused by some nontuberculous mycobacteria (NTM) (13,46,55). However, these semisynthetic macrolides are not effective for the treatment of tuberculosis because of the natural resistance of M. tuberculosis (41,50).…”

mentioning

confidence: 99%

Molecular Basis of Intrinsic Macrolide Resistance in the Mycobacterium tuberculosis Complex

Buriánková

Doucet‐Populaire

Dorson

et al. 2004

Antimicrob Agents Chemother

137

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The intrinsic resistance of the Mycobacterium tuberculosis complex (MTC) to most antibiotics, including macrolides, is generally attributed to the low permeability of the mycobacterial cell wall. However, nontuberculous mycobacteria (NTM) are much more sensitive to macrolides than members of the MTC. A search for macrolide resistance determinants within the genome of M. tuberculosis revealed the presence of a sequence encoding a putative rRNA methyltransferase. The deduced protein is similar to Erm methyltransferases, which confer macrolide-lincosamide-streptogramin (MLS) resistance by methylation of 23S rRNA, and was named ErmMT. The corresponding gene, ermMT (erm37), is present in all members of the MTC but is absent in NTM species. Part of ermMT is deleted in some vaccine strains of Mycobacterium bovis BCG, such as the Pasteur strain, which lack the RD2 region. The Pasteur strain was susceptible to MLS antibiotics, whereas MTC species harboring the RD2 region were resistant to them. The expression of ermMT in the macrolide-sensitive Mycobacterium smegmatis and BCG Pasteur conferred MLS resistance. The resistance patterns and ribosomal affinity for erythromycin of Mycobacterium host strains expressing ermMT, srmA (monomethyltransferase from Streptomyces ambofaciens), and ermE (dimethyltransferase from Saccharopolyspora erythraea) were compared, and the ones conferred by ErmMT were similar to those conferred by SrmA, corresponding to the MLS type I phenotype. These results suggest that ermMT plays a major role in the intrinsic macrolide resistance of members of the MTC and could be the first example of a gene conferring resistance by target modification in mycobacteria.The Mycobacterium genus comprises more than 70 species, including the major human pathogens responsible for tuberculosis (Mycobacterium tuberculosis, Mycobacterium africanum, and Mycobacterium bovis) and leprosy (Mycobacterium leprae). This genus also includes soil saprophytes and water microorganisms, some of which (e.g., those belonging to the Mycobacterium avium complex) can cause opportunistic infections, especially in immunocompromised patients. Mycobacteria are intrinsically resistant to most commonly used antibiotics and chemotherapeutic agents. Due to its specific structure and composition, the mycobacterial cell wall is an effective permeability barrier, considered to be a major factor in promoting this natural resistance (25). Only a few drugs are active against mycobacteria, and the emergence of multidrug-resistant M. tuberculosis strains is becoming a major problem worldwide (16).Macrolides inhibit protein synthesis in a wide range of bacteria by binding to the large ribosomal subunit (18,23). Like other protein synthesis inhibitors that affect the large subunit, they can also prevent the formation of the 50S particle in growing cells (8). Natural macrolides, such as erythromycin, are not effective against mycobacteria, but semisynthetic derivatives, such as clarithromycin and azithromycin, have stronger antimycobacterial activities a...

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Successful Treatment of PulmonaryMycobacterium xenopiInfection in a Natural Killer Cell–Deficient Patient with Clarithromycin, Rifabutin, and Sparfloxacin

Cited by 20 publications

References 54 publications

Efficacies of Clarithromycin Regimens against Mycobacterium xenopi in Mice

Efficacies of Clarithromycin Regimens against Mycobacterium xenopi in Mice

Mutant prevention concentration: a new tool for choosing treatment in nontuberculous mycobacterial infections

Molecular Basis of Intrinsic Macrolide Resistance in the Mycobacterium tuberculosis Complex

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