Mutations in atpG2 may confer resistance to gentamicin in Listeria monocytogenes


 Introduction Listeriosis, a foodborne infection caused by 
 
 Listeria monocytogenes
 
 , could lead to febrile listerial gastroenteritis and a more invasive form which is often associated with a high mortality and hospitalisation rate. Gentamicin, used as an adjunct therapy with ampicillin, remains the treatment of choice for this life-threatening and invasive infection.
 
 Gap statement Nevertheless, there is little data on gentamicin resistance determinants in 
 
 L. monocytogenes
 
 .
 
 Aim In this study, we selected and characterised B2b, a gentamicin-resistant mutant derived from 
 
 L. monocytogenes
 
 ATCC 19115 to determine the target(s) of resistance in 
 
 L. monocytogenes
 
 after exposure to gentamicin.
 
 Methodology Whole-genome sequencing was carried out to identify the mutation site(s) and possible mechanism(s) of resistance. The mutant was characterised using antimicrobial susceptibility testing and PCR. For biological verifications, complementation and allelic exchange mutagenesis were carried out.
 
 Results We found that the gentamicin resistance in B2b was caused by a 10 bp deletion in atpG2 which encodes a gamma subunit of the ATP synthase in 
 
 L. monocytogenes
 
 . Using atpG2 PCR, various other mutations were identified in other gentamicin resistant mutants derived from ATCC 19115. In addition, the mutation from B2b, when introduced into 
 
 L. ivanovii
 
 , also caused gentamicin resistance in this 
 
 Listeria
 
 species.
 
 Conclusion Hence, atpG2 mutations appear to be important determinants of gentamicin resistance not only in 
 
 L. monocytogenes
 
 but possibly also in other 
 
 Listeria
 
 species.