Production of icaADBC-encoded polysaccharide intercellular adhesin and therapeutic failure in pediatric patients with staphylococcal device-related infections

Bernardo Diemond-Hernández,Guadalupe Miranda-Novales,Fortino Solórzano-Santos,Leoncio Peregrino-Bejarano,Blanca Leaños-Miranda

doi:10.1186/1471-2334-10-68

Abstract

BackgroundBiofilm production has been established as a virulence factor which allows Staphylococcus to adhere and persist in medical devices. The objective was to determine whether therapeutic failure in patients infected with Staphylococcus spp. is linked to biofilm production, the presence of the ica operon, and the bacterial insertion sequence element IS256.MethodsStaphylococcus spp. isolates from patients with device-related infections were collected. Therapeutic failure with proper antimicrobial treatment was registered. Biofilm phenotype was determined by Congo red test agar and Christensen assay. Presence of the ica operon genes A-D and IS256 was detected by PCR. Differences were compared through x2.Results100 isolates from staphylococcal infections episodes were included: 40 sepsis/bacteremia, 32 ependymitis, and 28 peritonitis. 73.77% of CoNS and 79.5% of S. aureus isolates harbored the icaD gene, 29% of all isolates IS256-A+ IS256-D genes, icaA and icaB genes were only found in CoNS (27.8% and 21.3% respectively). Therapeutic failure occurred in 95.4.% of patients with a positive IS256-A+ IS256-D S. epidermidis isolate, RR 5.49 (CI 95% 2.24-13.44 p ≤ 0.0001), and 85.76% in CoNS isolates, RR 2.57 (CI 95% 0.97-6.80, p = 0.05). Although none S. aureus was positive for IS256-A + IS256-D, therapeutic failure was observed in 35.8%.ConclusionsThe presence of icaA/D genes along with the sequence element IS256 was associated with therapeutic failure in most CoNS infections, even though its absence in S. aureus isolates does not ensure therapeutic success.

Highlights

Biofilm production has been established as a virulence factor which allows Staphylococcus to adhere and persist in medical devices
S. epidermidis was isolated in 45 episodes, S. aureus in 39 and diverse coagulase negative Staphylococcus (CoNS)non-epidermidis in 16 (S. hominis, S. haemolyticus, S. lugdunensis, S. auricularis, S. warnerii and S. sciurii). 33% of the isolates were oxacillin-resistant, 31% were resistant to amikacin, 26% to norfloxacin and 0% to vancomycin
IcaADBC genes and the bacterial insertion sequence IS256 were detected in most of the strains, except for two strains of S. auricularis, one S. warnerii and one S. sciurii. 73.77% of CoNS and 79.5% of S. aureus isolates harbored the icaD gene; icaA, icaB and icaC genes were present in 27.8%, 21.3% and 9.8% of CoNS isolates (Table 2, figure 1)

Summary

Introduction

Biofilm production has been established as a virulence factor which allows Staphylococcus to adhere and persist in medical devices. The objective was to determine whether therapeutic failure in patients infected with Staphylococcus spp. is linked to biofilm production, the presence of the ica operon, and the bacterial insertion sequence element IS256. PIA is composed of a beta-1,6-N-acetylglucosamine polymer synthesized by an enzyme codified by the ica operon found on the bacterial chromosome, that includes a regulating element of four genes (A, B, C, and D), and a transposable element, IS256 [11]. It is known that the A gene codifies the N-acetylglucosamyl transferase enzyme responsible for synthesizing PIA. This enzyme is not very active in vitro, but co-expression of the D gene increases the activity. IcaB is the deacetylase responsible for the deacetylation of mature PIA and the transmembrane protein IcaC seems to be involved in externalization and elongation of the growing polysaccharide [9,12]

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