Gain in resistance but loss in virulence in a hospital-associated pathogen

A study led by Dr. Jordi Vila, ISGlobal researcher and director of the Antibiotic Resistance Initiative, shows that the loss of lipopolysaccharide (LPS) is involved in the acquisition of colistin resistance in Acinetobacter nosocomialis while decreasing its virulent capacity. 

The Acinetobacter group includes A. pittii, A. baumannii y A. nosocomialis and is the cause of an increasing number of hospital-associated infections. Worryingly, A. baumanii has demonstrated the ability to acquire resistance to all antibiotics presently on the market. To date, most strains are still susceptible to colistin, an antibiotic to which its close relative A. nosocomialis has shown a high level of resistance. 

In the present study, the authors compared gene and protein expression in colistin-susceptible or –resistant strains of A. nosocomialis, selected in vitro, in order to identify the mechanisms underlying colistin resistance. They found that, similar to what has been reported for A. baumanii, the acquisition of colistin resistance is associated with the loss in the synthesis of LPS, an external membrane component of all Gram-negative bacteria, due to mutations in the lpxD gene.  Importantly, using an infection model in the worm C. elegans, they found that colistin-resistant strains were less virulent. 

Acinetobacter bacteria can cause pneumonias and blood infections in critically ill patients. It is estimated that, in the USA alone, the Acinetobacter group is responsible for 12,000 infections every year, almost half of which are multidrug resistant.  

Reference:

Vila-Farrés X, Ferrer-Navarro M, Callarisa AE, Martí S, Espinal P, Gupta S, Rolain JM, Giralt E, Vila J. Loss of LPS is involved in the virulence and resistance to colistin of colistin-resistant Acinetobacter nosocomialis mutants selected in vitro. J Antimicrob Chemother. 2015 Aug 25.