Abstract
A better understanding of the mechanisms underpinning the growth of mycobacteria could help identify targets for new antibiotics.
Highlights
The rise of antimicrobial resistance has significantly reduced the options available for treating tuberculosis (TB) and other diseases caused by bacteria, threatening to plunge humanity back into the pre-antibiotic era
As the bacterial cell wall has formed the basis of successful antibiotic therapy for decades, the search for new TB drugs has led to renewed interest in the mycobacterial cell wall as a drug target (Alderwick et al, 2015)
Mycobacteria, a genus that includes the bacteria that cause leprosy and Buruli ulcer, have a complex cell wall that consists of an outer capsule-like layer, anchored by long-chain fatty acids known as mycolic acids, and two polymers (Kieser and Rubin, 2014)
Summary
The rise of antimicrobial resistance has significantly reduced the options available for treating tuberculosis (TB) and other diseases caused by bacteria, threatening to plunge humanity back into the pre-antibiotic era. Mycobacteria, a genus that includes the bacteria that cause leprosy and Buruli ulcer, have a complex cell wall that consists of an outer capsule-like layer, anchored by long-chain fatty acids known as mycolic acids, and two polymers (Kieser and Rubin, 2014). Current tuberculosis drugs that target the cell wall affect the synthesis of the mycolic acids and the arabinogalactan layer, but none are directed at peptidoglycan.
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