Abstract
The airborne pathogen Mycobacterium tuberculosis is responsible for a present major public health problem worsened by the emergence of drug resistance. M. tuberculosis has acquired and developed streptomycin (STR) resistance mechanisms that have been maintained and transmitted in the population over the last decades. Indeed, STR resistant mutations are frequently identified across the main M. tuberculosis lineages that cause tuberculosis outbreaks worldwide. The spread of STR resistance is likely related to the low impact of the most frequent underlying mutations on the fitness of the bacteria. The withdrawal of STR from the first-line treatment of tuberculosis potentially lowered the importance of studying STR resistance. However, the prevalence of STR resistance remains very high, could be underestimated by current genotypic methods, and was found in outbreaks of multi-drug (MDR) and extensively drug (XDR) strains in different geographic regions. Therefore, the contribution of STR resistance to the problem of tuberculosis drug resistance should not be neglected. Here, we review the impact of STR resistance and detail well-known and novel candidate STR resistance mechanisms, genes, and mutations. In addition, we aim to provide insights into the possible role of STR resistance in the development of multi-drug resistant tuberculosis.
Highlights
Tuberculosis (TB) is an airborne transmissible infectious disease caused by the bacteria Mycobacterium tuberculosis
The mechanisms that allowed for STR resistant bacteria to continue transmitting in the population, possibly since the first M. tuberculosis STR resistant strains emerged decades ago, remain elusive
M. tuberculosis might have evolved different mechanisms that promoted the fixation of STR resistance even without strong selective pressure
Summary
Tuberculosis (TB) is an airborne transmissible infectious disease caused by the bacteria Mycobacterium tuberculosis. Category II treatment is not recommended, and STR has limited clinical application due to the high incidence of resistant strains It is still in use in some cases as a substitute for amikacin against MDR-TB in the longer regimens or as an affordable alternative for low resource settings [10,13,18]. One variant in gid, Leu16Arg, was incorrectly described in the past as a resistant conferring mutation before different studies found that it was present both in STR susceptible and resistant clinical isolates from the M. tuberculosis LAM sub-lineage of lineage 4. It is likely that the different levels of STR resistance depend on the location of the mutation on rpsL, rrs, or gid genes, on the genomic context of the isolate, and possibly other factors
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