Drug resistance among acid-fast bacilli

Kato‐Maeda, Midori; Sifuentes–Osornio, José; Babadilla-del-Valle, M; Gm, Ruiz-Palacios; Ponce-de-Leon, Antonio Carlos

doi:10.1016/s0140-6736(05)77019-7

Cited by 11 publications

(5 citation statements)

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“…The development of embB306 mutations may predispose M. tuberculosis to the development of resistance to multiple antibiotics and may increase the ability of these multiple-drug-resistant isolates to be transmitted between subjects. (7,16,24). The samples from Spain consisted of all isolates collected at the General Penitentiary Hospital Microbiology Laboratory from a longitudinal study of tuberculosis performed between January 1993 and June 1994 (11 (55,56) that were submitted to the mycobacteriology research laboratory at Central Arkansas Veterans Healthcare System for genotype analysis.…”

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confidence: 99%

Role of embB Codon 306 Mutations in Mycobacterium tuberculosis Revisited: a Novel Association with Broad Drug Resistance and IS 6110 Clustering Rather than Ethambutol Resistance

Hazbón

Bobadilla-del-Valle

Guerrero

et al. 2005

Antimicrob Agents Chemother

103

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Mutations at position 306 of embB (embB306) have been proposed as a marker for ethambutol resistance in Mycobacterium tuberculosis; however, recent reports of embB306 mutations in ethambutol-susceptible isolates caused us to question the biological role of this mutation. We tested 1,020 clinical M. tuberculosis isolates with different drug susceptibility patterns and of different geographical origins for associations between embB306 mutations, drug resistance patterns, and major genetic group. One hundred isolates (10%) contained a mutation in embB306; however, only 55 of these mutants were ethambutol resistant. Mutations in embB306 could not be uniquely associated with any particular type of drug resistance and were found in all three major genetic groups. A striking association was observed between these mutations and resistance to any drug (P < 0.001), and the association between embB306 mutations and resistance to increasing numbers of drugs was highly significant (P < 0.001 for trend). We examined the association between embB306 mutations and IS6110 clustering (as a proxy for transmission) among all drug-resistant isolates. Mutations in embB306 were significantly associated with clustering by univariate analysis (odds ratio, 2.44; P ‫؍‬ 0.004). In a multivariate model that also included mutations in katG315, katG463, gyrA95, and kasA269, only mutations in embB306 (odds ratio, 2.14; P ‫؍‬ 0.008) and katG315 (odds ratio, 1.99; P ‫؍‬ 0.015) were found to be independently associated with clustering. In conclusion, embB306 mutations do not cause classical ethambutol resistance but may predispose M. tuberculosis isolates to the development of resistance to increasing numbers of antibiotics and may increase the ability of drug-resistant isolates to be transmitted between subjects.The antibiotic ethambutol (EMB) appears to inhibit the growth of both Mycobacterium tuberculosis and Mycobacterium smegmatis by blocking the synthesis of arabinogalactan. Arabinogalactan biosynthesis is dependent on the activity of the embABC gene cluster, which encodes the arabinotransferases that mediate the polymerization of arabinose into arabinan. Several lines of evidence suggest that EMB exerts its toxic effect on mycobacteria by inhibiting the embABC-encoded proteins (26,27,34,35,46), and mutations in embABC also appear to play a key role in the development of EMB resistance in both M. tuberculosis and M. smegmatis (34). Associations between EMB resistance and mutations in embA, embB, and embC have been reported in clinical strains of M. tuberculosis (41), and mutations in codon 306 of the embB gene (embB306) in M. tuberculosis are seen in approximately 50% of all EMB-* Corresponding author. Mailing address:

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confidence: 99%

Role of embB Codon 306 Mutations in Mycobacterium tuberculosis Revisited: a Novel Association with Broad Drug Resistance and IS 6110 Clustering Rather than Ethambutol Resistance

Hazbón

Bobadilla-del-Valle

Guerrero

et al. 2005

Antimicrob Agents Chemother

103

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“…The Australian samples included isolates from patients originating throughout Asia (Afghanistan, China, Hong Kong, India, Indonesia, Korea, Laos, Pakistan, Philippines, and Vietnam). The Arkansas, Orizaba, and Huauchinango isolates were obtained as part of community-based studies (10,15,38). The Uganda isolates were obtained from an urban medical center in Kampala; however, virtually all of these samples originated from patients who were indigenous to the local area.…”

Section: Bacterial Isolatesmentioning

confidence: 99%

Global Phylogeny ofMycobacterium tuberculosisBased on Single Nucleotide Polymorphism (SNP) Analysis: Insights into Tuberculosis Evolution, Phylogenetic Accuracy of Other DNA Fingerprinting Systems, and Recommendations for a Minimal Standard SNP Set

et al. 2006

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We analyzed a global collection of Mycobacterium tuberculosis strains using 212 single nucleotide polymorphism (SNP) markers. SNP nucleotide diversity was high (average across all SNPs, 0.19), and 96% of the SNP locus pairs were in complete linkage disequilibrium. Cluster analyses identified six deeply branching, phylogenetically distinct SNP cluster groups (SCGs) and five subgroups. The SCGs were strongly associated with the geographical origin of the M. tuberculosis samples and the birthplace of the human hosts. The most ancestral cluster (SCG-1) predominated in patients from the Indian subcontinent, while SCG-1 and another ancestral cluster (SCG-2) predominated in patients from East Asia, suggesting that M. tuberculosis first arose in the Indian subcontinent and spread worldwide through East Asia. Restricted SCG diversity and the prevalence of less ancestral SCGs in indigenous populations in Uganda and Mexico suggested a more recent introduction of M. tuberculosis into these regions. The East African Indian and Beijing spoligotypes were concordant with SCG-1 and SCG-2, respectively; X and Central Asian spoligotypes were also associated with one SCG or subgroup combination. Other clades had less consistent associations with SCGs. Mycobacterial interspersed repetitive unit (MIRU) analysis provided less robust phylogenetic information, and only 6 of the 12 MIRU microsatellite loci were highly differentiated between SCGs as measured by G ST . Finally, an algorithm was devised to identify two minimal sets of either 45 or 6 SNPs that could be used in future investigations to enable global collaborations for studies on evolution, strain differentiation, and biological differences of M. tuberculosis.Compared to many bacterial species, Mycobacterium tuberculosis harbors relatively little genetic diversity (21, 34, 37); however, there is increasing evidence that the interstrain variation that exists is biologically significant. Clinical M. tuberculosis isolates have variable gene expression profiles (25) and have different numbers of genes deleted from their chromosome (32). In animal models, M. tuberculosis appears to engender a range of immune responses and variable degrees of virulence depending on the infecting strain (5,7,47,55). In human infections, molecular epidemiological studies have suggested that certain M. tuberculosis types, identified by DNA fingerprinting, can be especially prone to drug resistance acquisition (17, 59, 65) or to global dissemination (3, 9, 27, 40, 66,

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“…A more alarming aspect of tuberculosis is the emergence of multidrug-resistant strains of M. tuberculosis (MDRTB) that is a widespread phenomenon (Snider & Roper 1992, Frieden et al 1993, Iseman 1993, Kato-Maeda et al 1999. The common finding has been a high rate of primary resistance to isoniazid (INH) and to the combination of isoniazid and rifampin (RIF) (Garcia-Garcia 2000) and a high rate of resistant (17.2%) to all the four commonly used antimycobacterial agents for treatment and prophylaxis of TB, including RIF (Granich et al 2000, Singh & Kaur 2004.…”

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Detection of rifampin resistance patterns in Mycobacterium tuberculosis strains isolated in Iran by polymerase chain reaction-single-strand conformation polymorphism and direct sequencing methods

Isfahani¹,

Tavakoli²,

Salehi³

et al. 2006

Mem. Inst. Oswaldo Cruz

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Drug resistance among acid-fast bacilli

Cited by 11 publications

References 1 publication

Role of embB Codon 306 Mutations in Mycobacterium tuberculosis Revisited: a Novel Association with Broad Drug Resistance and IS 6110 Clustering Rather than Ethambutol Resistance

Role of embB Codon 306 Mutations in Mycobacterium tuberculosis Revisited: a Novel Association with Broad Drug Resistance and IS 6110 Clustering Rather than Ethambutol Resistance

Global Phylogeny ofMycobacterium tuberculosisBased on Single Nucleotide Polymorphism (SNP) Analysis: Insights into Tuberculosis Evolution, Phylogenetic Accuracy of Other DNA Fingerprinting Systems, and Recommendations for a Minimal Standard SNP Set

Detection of rifampin resistance patterns in Mycobacterium tuberculosis strains isolated in Iran by polymerase chain reaction-single-strand conformation polymorphism and direct sequencing methods

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