Abstract
β-lactams, the most widely used class of antibiotics, are well-tolerated, and their molecular mechanisms of action against many bacteria are well-documented. Mycobacterium abscessus (Mab) is a highly drug-resistant rapidly-growing nontuberculous mycobacteria (NTM). Only in recent years have we started to gain insight into the unique relationship between β-lactams and their targets in Mab. In this mini-review, we summarize recent findings that have begun to unravel the molecular basis for overall efficacy of β-lactams against Mab and discuss emerging evidence that indicates that we have yet to harness the full potential of this antibiotic class to treat Mab infections.
Highlights
Mycobacterium abscessus (Mab) was first discovered in 1953 (Moore and Frerichs, 1953), it was only recently that genomic sequencing differentiated the Mab complex into three subspecies: M. abscessus sensu stricto, M. abscessus subsp. bolletii, and M. abscessus subsp. massiliense (Adekambi et al, 2004, 2006; Viana-Niero et al, 2008)
In recent years have we started to gain insight into the unique relationship between β-lactams and their targets in Mab. In this mini-review, we summarize recent findings that have begun to unravel the molecular basis for overall efficacy of β-lactams against Mab and discuss emerging evidence that indicates that we have yet to harness the full potential of this antibiotic class to treat Mab infections
We identified thirty-five studies with documented minimum inhibitory concentration (MIC) ranges of β-lactams against clinical isolates of Mab globally (Table 1)
Summary
Mycobacterium abscessus (Mab) was first discovered in 1953 (Moore and Frerichs, 1953), it was only recently that genomic sequencing differentiated the Mab complex into three subspecies: M. abscessus sensu stricto, M. abscessus subsp. bolletii, and M. abscessus subsp. massiliense (Adekambi et al, 2004, 2006; Viana-Niero et al, 2008). Massiliense (Adekambi et al, 2004, 2006; Viana-Niero et al, 2008) These subspecies exhibit differential susceptibilities to certain antibiotics and differential clinical outcomes. Mab can cause pulmonary disease in addition to skin and soft tissue infections, lymphadenitis, and disseminated disease. The cure rate for Mab lung disease is only 30–50% (Jarand et al, 2011), with a recent review reporting sputum culture conversion rates as low as 25% with antibiotic treatment alone (Diel et al, 2017). Poor treatment outcomes of Mab infection have been ascribed to both innate and acquired drug resistance. Current treatment regimens are suboptimal, as they require several months of intravenous multidrug therapy with potentially cytotoxic antibiotics and produce poor outcomes (Wallace et al, 1985; Floto et al, 2016). We will briefly summarize Mab treatment recommendations, discuss unique molecular targets of β-lactams in Mab, and highlight emerging insights into how β-lactams may be leveraged to treat individuals infected with Mab
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