ABSTRACT
The fitness cost associated with the evolution of resistance to rifampin in Mycobacterium tuberculosis may be different in clinical isolates compared to in vitro-generated mutants. An atypical Beijing strain (attenuated phenotype) demonstrated the ability to spread despite acquiring resistance to rifampin. Transmission was linked to human immunodeficiency virus coinfection (P = 0.029), raising concern for the spread of drug resistance in vulnerable populations.
Subject(s)
Antibiotics, Antitubercular/pharmacology , HIV Infections/complications , Mycobacterium tuberculosis/drug effects , Rifampin/pharmacology , Tuberculosis, Multidrug-Resistant/complications , Tuberculosis, Multidrug-Resistant/transmission , Codon/genetics , Drug Resistance, Bacterial , Genotype , HIV Infections/epidemiology , HIV Infections/virology , HIV-1 , Humans , Microbial Sensitivity Tests , Mutation , Mycobacterium tuberculosis/classification , Mycobacterium tuberculosis/genetics , Polymorphism, Single Nucleotide , Prevalence , South Africa/epidemiology , Tuberculosis, Multidrug-Resistant/epidemiology , Tuberculosis, Multidrug-Resistant/microbiologyABSTRACT
During October 2005, four children in a school in Cape Town were identified with multidrug-resistant tuberculosis (MDR-TB). Genetic analysis confirmed that these isolates belonged to a single cluster (Beijing cluster 220) and that all harboured a -15 inhA(C-T) promoter mutation demonstrating transmission. Genetic analysis of isolates cultured from patients from the Boland-Overberg-South Cape-Karoo and Cape Town regions showed that 28% (58/209) of patients infected with a Beijing strain had the cluster 220 genotypes and that all harboured the same -15 inhA(C-T) promoter mutation. The presence of these transmissible MDR-TB strains may pose a threat to the community, and rigorous infection control measures are needed to ensure the safety of those exposed.
