Extended-spectrum β-lactamase (ESBL), AmpC β-lactamase, and carbapenemase-producing bacteria greatly threaten human health. Resistance rates in Enterobacterales vary across regions. ESBL rates range from 2% in the USA to 70% in India, AmpC rates from 30% in India and carbapenemase rates from <1% in Europe to a staggering 65% in India. In Sri Lanka, ESBL rates are as high as 50%, AmpC β-lactamase rates are around 19%, and carbapenemase producers comprise 9%-11% of clinical isolates. The predominant ESBL types locally are CTX-M and SHV, for AmpC, CMY and DHA, and for carbapenemases, OXA-48-like, and NDM. Porin mutations contributing to β-lactam resistance include premature stop codons in ompF in Escherichia coli and the Iaa134-135GD insertion mutation in ompK36 in Klebsiella pneumoniae. The spread of β-lactamase resistance occurs through clonal expansion and horizontal gene transfer mediated by mobile genetic elements. Some well-known resistant clones reported from Sri Lanka are K. pneumoniae ST14, ST147 and ST340 and E. coli ST131. The ColKP3 plasmid with ISEcp1, which promotes rapid dissemination of carbapenem resistance, and a cluster of aac (6c)-Ib-cr, blaOXA-1, and catB3 genes associated with an IS26 composite transposon have been identified. Standard methods for detecting β-lactamase production in Enterobacterales have limitations. Multiple β-lactamases and other resistance mechanisms have resulted in false test results in Sri Lankan isolates. Despite the cost, molecular methods have shown promising results. Some important data from Sri Lanka is available in the literature. However, there remains much to investigate.
Perera et al. (Wed,) studied this question.