Abstract

Previously it was shown that application of probiotics stopped the acquisition of vancomycin-resistant Enterococcus faecium (VRE) by patients in an early rehabilitation ward. Once the application of probiotics ended, we examined whether acquisition of VRE reoccurred. Furthermore, we examined whether probiotics altered prevalence of vancomycin-susceptible E. faecium (VSE) and Gram-negative bacteria, which produce extended spectrum beta-lactamase (ESBL). Although probiotic application ceased in April 2018, VRE-colonized patients rarely presented on that ward until 2019. Probiotic treatment also resulted in a decreased number of patients with VSE and ESBL. While decreased incidence of VRE occurred immediately, decreased VSE and ESBL numbers occurred months later. A probiotic-mediated decrease of VSE and ESBL incidence cannot be explained when assuming bacterial transmission exclusively as a linear cause and effect event. The decrease is better understood by considering bacterial transmissions to be stochastic events, which depend on various driving forces similar to an electric current. We hypothesize that VRE, VSE and ESBL uptake by patients and by staff members mutually reinforced each other, leading staff members to form a bacterial reservoir, similar to a condenser that stores electrical energy. Probiotic treatment then inhibited regeneration of that store, resulting in a breakdown of the driving force.

Highlights

  • Antibiotic resistance is a global burden complicating treatment of bacterial infections

  • We examined the effect of probiotics on the acquisition of vancomycin-susceptible E. faecium and Gram-negative bacteria producing extended spectrum beta-lactamase (ESBL)

  • The application of two probiotics to patients on early rehabilitation ward of the Ingolstadt Hospital (ERWIN) who were being treated with antibiotics inhibited the spread of vancomycin-resistant E. faecium (VRE)

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Summary

Introduction

Antibiotic resistance is a global burden complicating treatment of bacterial infections. It is estimated that by 2050, up to 300 million premature deaths may be attributable to infections with multi-resistant bacteria [1]. An increasing number of Gram-negative bacteria, mainly enterobacteriaceae, are able to produce enzymes that destroy penicillin and cephalosporin antibiotics. Bacteria producing enzymes that inactivate third generation cephalosporin antibiotics are referred to as extended spectrum beta-lactamase (ESBL) producers if the genes encoding these enzymes are located on plasmids, which facilitate transmission to other bacteria. Apart from multi-resistant Gram-negative bacteria, vancomycin-resistant Enterococcus faecium (VRE) was indexed by the World Health Organization. Res. Public Health 2020, 17, 6100; doi:10.3390/ijerph17176100 www.mdpi.com/journal/ijerph

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