JAC Advance Access originally published online on October 15, 2007
Journal of Antimicrobial Chemotherapy 2007 60(6):1405-1406; doi:10.1093/jac/dkm387
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Correspondence |
erm(A)-mediated macrolide resistance and ability to invade human respiratory cells in a Streptococcus dysgalactiae subspecies equisimilis pharyngeal isolate
1 Institute of Microbiology and Biomedical Sciences, Polytechnic University of Marche Medical School, Via Tronto 10/A, 60123 Ancona, Italy 2 Institute of Maternal-Infantile Sciences, Polytechnic University of Marche, Via Corridoni 11, 60100 Ancona, Italy
* Corresponding author. Tel: +39-071-220-6296; Fax: +39-071-220-6293; E-mail: b.facinelli{at}univpm.it
Keywords: group C streptococci , erythromycin-resistant , A549 cells , cell invasion
Streptococcus dysgalactiae subspecies equisimilis [S. dysgalactiae subsp. equisimilis: ß-haemolytic, large-colony-forming streptococci belonging either to group C (GCS) or G (GGS)] is increasingly recognized as a human pathogen.1 It can cause mild and serious infections such as pharyngitis, infections of skin and soft tissues, neonatal infections, bacteraemia and invasive diseases that are traditionally associated with Streptococcus pyogenes [group A streptococci (GAS)].2
A ß-haemolytic streptococcus was isolated from the throat swab of a 14-year-old boy with pharyngotonsillitis not resolved by a 5 day erythromycin treatment. The throat isolate was identified as GCS S. dysgalactiae subsp. equisimilis using the standard rapid antigen extraction method, agglutination techniques and a rapid ID 32 STREP kit (bioMérieux, Marcy-l’Étoile, France). The strain, designated SdyIMR, was tested for antibiotic susceptibility according to the CLSI guidelines (Document M100-S16, 2006) and was found to be resistant to erythromycin (MIC, 2 mg/L). The triple disc test (erythromycin plus clindamycin and josamycin) assigned the strain to the iMLS-C phenotype.3 PCR experiments, using primers internal to GAS resistance genes,3 revealed the presence of erm(A), which has rarely been reported in GCS S. dysgalactiae subsp. equisimilis.4 emm typing (http://www.cdc.gov/ncidod/biotech/strep/protocol_emm-type.htm) assigned SdyIMR to stC839.0, previously described in GCS endotracheal, pharyngeal and blood isolates collected in the USA, Brazil, India and Australia and also found in GGS isolates (http://www.cdc.gov/ncidod/biotech/strep/types_emm103-124.htm).2
The ability of SdyIMR to invade human respiratory cells (A549 cells, ATCC CCL 185) was evaluated in a standard antibiotic protection assay and compared with that of two previously characterized cell-invasive pharyngeal GAS isolates, high-invasive SP1090 [iMLS-B/erm(A)] and low-invasive SP1161 [iMLS-C/erm(A)], carrying the internalization-associated prtF1 gene.3,5 Invasion efficiency of SdyIMR was lower than that of SP1090 but similar to that of SP1161 (Figure 1), demonstrating an ability to invade A549 cells. Intracellular SdyIMR was culturable from cells 48 h after infection, suggesting that it is able to survive intracellularly, as previously demonstrated for GAS.5 The presence of the fnb gene, coding for Fn-binding protein FnB,6 was demonstrated in SdyIMR by PCR. As in GAS, multiple cocci were consistently found inside cells by microscopy and DNA sequences internal to fnb, and erm(A) continued to be amplified by PCR in infected cells until day 20 (both data not shown).
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To our knowledge, this is the first report of a GCS S. dysgalactiae subsp. equisimilis isolate combining macrolide resistance and ability to enter human respiratory cells. As previously suggested for GAS, such a combination of resistance and virulence traits may confer an increased ability to propagate and spread, enabling escape from penicillin and other ß-lactams (confined to the extracellular fluid) because of intracellular location and from macrolides (active in intracellular compartments) because of resistance.3
This work was supported in part by a grant from the Italian Ministry of Education, University and Research.
None to declare.
References
1 Oster HR, Bisno AL. Group C and group G streptococcal infections: epidemiologic and clinical aspects. In: Gram-positive Pathogens—Fischetti VA, Novick RP, Ferretti JJ, et al, eds. (2000) Washington, DC: ASM Press. 184–90.
2 Davies MR, McMillan DJ, Beiko RG, et al. Virulence profiling of Streptococcus dysgalactiae subspecies equisimilis isolated from infected humans reveals 2 distinct genetic lineages that do not segregate with their phenotypes or propensity to cause diseases. Clin Infect Dis (2007) 44:1442–54.[CrossRef][Web of Science][Medline]
3 Facinelli B, Spinaci C, Magi G, et al. Association between erythromycin resistance and ability to enter human respiratory cells in group A streptococci. Lancet (2001) 358:30–3.[CrossRef][Web of Science][Medline]
4
Lopardo HA, Vidal P, Sparo M, et al. Six-month multicenter study on invasive infections due to Streptococcus pyogenes and Streptococcus dysgalactiae subsp. equisimilis in Argentina. J Clin Microbiol (2005) 43:802–7.
5 Spinaci C, Magi G, Varaldo PE, et al. Persistence of erythromycin-resistant group A streptococci in cultured respiratory cells. Pediatr Infect Dis J (2006) 25:880–3.[CrossRef][Web of Science][Medline]
6 Lindgren PE, McGavin MJ, Signas C, et al. Two different genes coding for fibronectin-binding proteins from Streptococcus dysgalactiae. Eur J Biochem (1993) 214:819–27.[Web of Science][Medline]
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