Vol. 39 No. 5 (2022): OCTUBRE
Original Article

Invasive diseases due to Streptococcus pyogenes in the pediatric population. Clinical-molecular characterization 2014-2020

Alejandra Vomero
Universidad de la Republica Uruguay
Bio
Gabriela Garcia Gabarrot
Ministerio de Salud Pública, Uruguay
Bio
Liliana Cedres
Universidad de la República, Montevideo Uruguay
Bio
Ines Mota
Hospital Pediátrico-Complejo Hospitalario Pereira Rossell, Montevideo, Uruguay
Bio
Gabriela Algorta
Universidad de la Republica Uruguay
Bio
Catalina Pirez
Universidad de la Republica Uruguay
Bio

Published 2022-11-27

How to Cite

1.
Vomero A, Garcia Gabarrot G, Cedres L, Mota I, Algorta G, Pirez C. Invasive diseases due to Streptococcus pyogenes in the pediatric population. Clinical-molecular characterization 2014-2020. Rev. Chilena. Infectol. [Internet]. 2022 Nov. 27 [cited 2026 Jun. 2];39(5). Available from: https://revinf.cl/index.php/revinf/article/view/1512

Abstract

Background: Streptococcus pyogenes (EGA) is an agent of invasive disease (ID); its high morbidity and mortality requires epidemiological surveillance. Aim: To describe the clinical and epidemiological characteristics of children hospitalized with ID due to GAS in a reference center in Uruguay from January 1-2014 to December 31-2020, including a study of virulence factors. Methods: Descriptive and retrospective. Case definition: Isolation of GAS in sterile sites. Variables: epidemiological, clinical, laboratory, treatment and evolution. Strains were typified by sequencing of the emm gene. Chromosomal profiles were obtained by digestion of the DNA with the Smal enzyme. Presence of SpeB, SpeA and SpeC genes and susceptibility to antibiotics were performed. Results: Admissions rate: 3.98/10,000. 22 patients were included; osteoarticular infection (n=11), pleuropulmonary infection (n=6), non-cutaneous abscess (n=4) and blood isolation (n=1). Mean age: 44 months; 8 cases were severe, their mean age was lower (16 months). All pneumonia cases were severe and one patient died. Twelve strains were sequenced: 5 emm1 (4 emm1.29 and 1 emm1) and 1 of each: emm6.4, emm81, emm12, emm28, emm22, emm87, emm11. All were SpeB+. Toxin profiles: SpeA+SpeC-Ssa-(5), SpeA-SpeC+Ssa-(4) SpeA-SpeC-Ssa-(2) and SpeA-SpeC+Ssa+(2). Conclusions: This study allows to give continuity to a previous study. Greater typing of GAS was achieved, which may contribute to its molecular clinical knowledge. There was no record of patients diagnosed with TSS or necrotizing fascitis, unlike the previous series.