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Enterobacter bugandensis, a newly discovered enterobacterial bacteria in nosocomial infections.

By Fernando Gómez Acebo Ruíz. Microbiology group 03. 2nd year of Biotechnology grade.




As many other species of its genus E. bugandensis (EB-247) is a highly virulent Gram-negative bacterium responsible for nosocomial infections, particularly neonate infections that can lead to sepsis, lower respiratory tract infections, skin and soft-tissue infections, urinary tract infections or death. Due to the environment they thrive, these bacteria are naturally resistant to many types of antibiotics, and although they represent a serious problem in the medical world their pathogenicity mechanism is not well understood.

In an article recently published in Scientific reports, Pati et.al. provide insight in EB-247 behavior, pathogenicity and response to antibiotics. A detailed analysis of EB-247’s genome revealed genes that codified for capsules, efflux pumps and the colicin E2 toxin. It also encodes genes for iron metabolism, biofilm formation, and a resistance plasmid; all of which are related with pathogenicity. The bacteria have been found to be resistant to tetracyclin, ciprofloxacin, ampicillin and many other third line antibiotics.


The researchers assessed the virulence of EB-247 through a comparative study using wax moth larvae injected with various pathogenic bacteria; the group inoculated with EB-247 had a 77% survival rate, while the S. Typhimurium and E. coli had 87% and 100% respectively. Posterior studies in mice shoed that the bacteria affect mainly intraperitoneal and cecum areas, and causes a high production of cytokines, observed in the animal serum. High production of cytokines is associated with septic shock. Furthermore EB-247 showed growth in high concentrations of human serum.


However, possible bacteria inhibition strategies have been proposed by the researchers, mainly targeted at different stages of iron metabolism, which the bacteria scavenge from ferritin. As many other bacteria, EB-247 uses siderophores to reduce the non-soluble Fe3+ ion into the metabolizable Fe2+.


The lasso peptide MccJ25 (microcin J25), produce by some species of the bacteria Escherichia coli, can be used to inhibit bacterial replication. MccJ25 inhibits the iron siderophore receptor FhuA and further inhibits bacterial growth by blocking the NTP uptake channel of the bacterial RNA polymerase. Still, EB-247 high pathogenicity and resistance encourage further research in order to combat this emerging danger.




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