Genetic and phenotypic analysis of the ESKAPE pathogens Acinetobacter baumannii and Klebsiella pneumoniae
Although many bacteria remain susceptible to antibiotics, a group of microbes has arisen that plague hospitals due to their ability to evade the effects of antibiotics: Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species. These have been dubbed the ESKAPE pathogens and they are responsible for the majority of infections in US hospitals. The therapeutic options for infections caused by these bacteria are limited, and thus the study and understanding of their various mechanisms of resistance is critical. Acinetobacter and Klebsiella species are particularly distinguishing themselves due to pan-resistant phenotypes that produce carbapenemases capable of inactivating carbapenems—drugs of last resort for multi-drug resistant infections. Extended study on these two species could be revelatory—they parallel each other in many ways, and understanding the mechanisms of antibiotic resistance acquisition in each would offer a model for understanding future pathogens that might emerge; these mechanisms also provide a target for novel therapeutics to combat otherwise unmanageable infections. Since biofilm formation is intimately tied with both novel gene acquisition and antibiotic resistance, it lends itself as an obvious target for novel therapies to either restore sensitivity to antibiotics, or prevent the development of new resistances. We treated MDR strains of Acinetobacter baumannii with methyl-α-D-glucopyranoside (MDG), a non-metabolizable glucose analog, and observed the effects on biofilm formation. We additionally sequenced the genomes of five clinical isolates of Klebsiella pneumoniae, and analyzed the genomic basis for their observed antibiotic resistant phenotypes. Elucidation of the processes that drive biofilm formation can provide targets that will aid in the amelioration of infections caused by biofilm growth.