Clonal Diversity, Biofilm Formation, and Antimicrobial Resistance among Stenotrophomonas maltophilia Strains from Cystic Fibrosis and Non-Cystic Fibrosis Patients.

Arianna Pompilio,Giovanni Di Bonaventura,Vincenzo Savini,Giovanni Gherardi,Ersilia Fiscarelli

doi:10.3390/antibiotics9010015

Abstract

The intrinsic antibiotic resistance of Stenotrophomonas maltophilia, along with its ability to form biofilm both on abiotic surfaces and host tissues, dramatically affects the efficacy of the antibiotic therapy. In this work, 85 S. maltophilia strains isolated in several hospital of central Italy and from several clinical settings were evaluated for their genetic relatedness (by pulsed-field gel electrophoresis, PFGE), biofilm formation (by microtiter plate assay), and planktonic antibiotic resistance (by Kirby–Bauer disk diffusion technique). The S. maltophilia population showed a high genetic heterogeneity: 64 different PFGE types were identified, equally distributed in cystic fibrosis (CF) and non-CF strains, and some consisted of multiple strains. Most of the strains (88.2%) were able to form biofilm, although non-CF strains were significantly more efficient than CF strains. CF strains produced lower biofilm amounts than non-CF strains, both those from respiratory tracts and blood. Non-CF PFGE types 3 and 27 consisted of strong-producers only. Cotrimoxazole and levofloxacin were the most effective antibiotics, being active respectively against 81.2% and 72.9% of strains. CF strains were significantly more resistant to piperacillin/tazobactam compared to non-CF strains (90% versus 53.3%), regardless of sample type. Among respiratory strains, cotrimoxazole was more active against non-CF than CF strains (susceptibility rates: 86.7% versus 75%). The multidrug resistant phenotype was significantly more prevalent in CF than non-CF strains (90% versus 66.7%). Overall, the multidrug-resistance level was negatively associated with efficiency in biofilm formation. Our results showed, for the first time, that in S. maltophilia both classical planktonic drug resistance and the ability of biofilm formation might favor its dissemination in the hospital setting. Biofilm formation might in fact act as a survival mechanism for susceptible bacteria, suggesting that clinical isolates should be routinely assayed for biofilm formation in diagnostic laboratories.

Highlights

Among the “emerging” pathogens recognized in the recent years, Stenotrophomonas maltophilia plays a significant role in colonization and infection in hospital, and less often, community settings.This opportunistic pathogen has, been implicated in a variety of nosocomial infections, especially in intensive care unit patients, life-threatening diseases in immunocompromised patients with hematological malignancies and cancers, and respiratory tract infections in patients with chronic lung diseases [1,2].S. maltophilia commonly causes pneumonia, bacteremia, sepsis, and wound infections, and less commonly, urinary tract infections, endocarditis, soft tissue infections, meningitis, osteochondritis, peritonitis, and ophthalmic infections [1,2]
The selection for persister cells occurs under conditions that include hostile host environments, a damage response being caused by sublethal concentrations of antibiotics, and bacterial biofilms [25]
In agreement with earlier works [20,21,42], overall, our findings suggest that, in S. maltophilia, susceptible bacteria may use biofilm formation in this regard, probably because the biofilm-mediated resistance might be less expensive in terms of energy requirements than chromosomal resistance mechanisms

Summary

Introduction

S. maltophilia commonly causes pneumonia, bacteremia, sepsis, and wound infections, and less commonly, urinary tract infections, endocarditis, soft tissue infections, meningitis, osteochondritis, peritonitis, and ophthalmic infections [1,2]. Pseudomonas aeruginosa is the most prevalent pathogen in cystic fibrosis (CF) patients, S. maltophilia is being increasingly isolated from CF airways, due to its ability to evade many antipseudomonal antibiotics [3,4,5,6]. In this clinical setting, the microorganism can account for perseverant colonization and chronic infection, the clinical relevance in these patients is yet unclear

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