Staphylococcus epidermidis in feedings and feces of preterm neonates

Abstract

Staphylococcus epidermidis has emerged as the leading agent causing neonatal late-onset sepsis in preterm neonates; although the severity of the episodes caused by this species is often underestimated, it might exert relevant short- and long-term detrimental effects on neonatal outcomes. In this context, the objective of this study was to characterize a collection of S. epidermidis strains obtained from meconium and feces of preterm infants, and to assess the potential role of the enteral feeding tubes as potential reservoirs for this microorganism. A total of 26 preterm infants were enrolled in the study. Meconium and fecal samples were collected weekly during their first month of life (n = 92). Feeding samples were collected after their pass through the enteral feeding tubes (n = 84). S. epidermidis was present in the fecal samples of all the infants in, at least, one sampling time at concentrations ranging from 6.5 to 7.8 log10 CFU/g. Initially, 344 isolates were obtained and pulsed-field gel electrophoresis (PFGE) profiling allowed the reduction of the collection to 101 strains. Among them, multilocus sequence typing (MLST) profiling showed the presence of 32 different sequence types (ST). Globally, most of the STs to hospital-adapted high-risk clones and belonged to clonal complexes (CC) associated to the hospital environment, such as CC2. The virulence gene most commonly detected among the strains was altE. High resistance rates to macrolides and aminoglycosides were detected and 64% of the strains harboured the mecA gene, which was codified in SCCmec types. Our results indicates the existence of a complex and genetically diverse S. epidermidis population in the NICU environment. A better knowledge of S. epidermidis strains may help to devise strategies to avoid their conversion from symbiont to pathobiont microorganisms in the NICUs.

Fig 1. ST clones colonizing infants and the food samples used to feed them (after their pass through the enteral feeding tubes) during the first month of life.

Sequence types (ST) clones associated with hospital environment are represented in black and those belonging to community in grey. Clones recently described are represented in grey with the clone number in black.

Fig 2. MLST genetic diversity using minimum spanning tree algorithm.

Each circle represents a different MLST clone; size depends on the number of isolates in the group. Clone number is indicated above circle; Circles are colored depending on the frequency of the clone in the analyzed samples: black represent frequency in feces, light grey in MOM, dark grey in donor milk and white in formula milk samples. Clones considered to be of high risk are highlighted in bold. Genetically related sequence types (STs) are connected by grey lines.

Fig 3. Profiles of antibiotic susceptibility and virulence factors in the different ST clones.

At least one different sequence types (ST) per infant is represented in each line. Results are represented in function of frequency. Black squares means 100% of the isolates were resistant to an antibiotic or present a virulence determinant, while black and grey striped boxes means 75–99%, grey squares 50–74%, grey and white striped squares 25–49% and white boxes 0–24%. Black bars in the left side of the figure represent the percentage of virulence genes present in each ST while the grey bars on the right side of the figure shows the percentage of antibiotic resistances per ST. OXA: Oxacillin; GM: Gentamicin; TOB: Tobramycin; LVX: Levofloxacin; ERY: Erythromycin; CLI: Clindamycin; LNZ: Linezolid; DAP: Daptomycin; TEIC: Teicoplanin; VAN: Vancomycin; TGC: Tigecycline; FOS: Fosfomycin; FUS: Fusidic Acid; MUP: Mupirocin; RIF: Rifampicin; SXT: Trimethoprim-sulphamethoxazole.