Stenotrophomonas maltophilia is an aerobic gram-negative multidrug-resistant bacterium widely distributed in natural and clinical environments. This opportunistic pathogen is associated with various infectious diseases, mostly respiratory, urinary tract, bloodstream infections [1]. Catheter insertion, severe traumatic injuries, burns and other factors can increase the risk of infections caused by S. maltophilia [2]. S. maltophilia is characterized by innate resistance to various classes of antibiotics, such as β-lactams, aminoglycosides, macrolides, chloramphenicol, tetracyclines, therefore infections caused by this bacterium are difficult to treat. Despite the wide spectrum of infections caused by S. maltophilia there is still little known about its other virulence factors. The ability to form biofilms, pili, adhesins, flagella, as well as various enzymes are mostly suggested virulence factors of S. maltophilia [3].
The aim of this study was to compare the prevalence of antibiotic resistance and virulence factors encoding genes in clinical and natural isolates of S. maltophilia. Antibiotic resistance and virulence factors encoding genes detection was performed on a total of 75 S. maltophilia isolates, consisting of 42 environmental and 33 clinical isolates from Lithuania. All clinical isolates were isolated from patients, environmental isolates were isolated from different sources such as soil, water bodies, fish gut.
Detection of the antibiotic resistance genes showed that genes providing resistance to β-lactams (blaL1 and blaL2) and aminoglycosides (phT, aph(3')-IIc and aph(6)) were commonly detected in both environmental and clinical S. maltophilia isolates. The qnr gene conferring resistance to quinolone class antibiotics was detected in majority clinical, but only two environmental isolates. The higher prevalence of resistance genes in clinical isolates can be related to the intensive use of antibiotics in clinical settings. The hly gene encoding hemolysin was found in almost all clinical and nearly half of the natural isolates. The protease encoding stmpr2 gene was detected in almost all isolates, whereas the protease encoding stmpr1 gene was more abundant in clinical isolates.