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Pediatric Cases From Colombia Caused by a Panton-Valentine Leukocidin-Positive Community-Acquired Methicillin-Resistant Staphylococcus aureus ST8-SCCmecIVc Clone

Alvarez-Olmos, Martha Isabel MD, MPH; Enríquez, Sandra P. MD; Pérez-Roth, Eduardo PhD; Méndez-Alvarez, Sebastián PhD; Escobar, Javier MSc; Vanegas, Natasha PhD; Moreno, Jaime MSc

The Pediatric Infectious Disease Journal: October 2009 - Volume 28 - Issue 10 - p 935
doi: 10.1097/INF.0b013e3181b2102b
Letters to the Editors
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Departamento de Pediatría; División de Infectología Pediátrica; Fundación Cardioinfantil IC; Universidad del Rosario; Bogotá, Colombia (Alvarez-Olmos, Enríquez)

Laboratorio de Biología Molecular; Instituto de Investigación; Hospital Universitario “Nuestra Señora de la Candelaria”; Tenerife, España, Spain (Pérez-Roth, Méndez-Alvarez)

Instituto de Genética Molecular Bacteriana; Universidad El Bosque; Bogotá, Colombia (Escobar, Vanegas)

Grupo de Microbiología; Instituto Nacional de Salud; Bogotá, Colombia (Moreno)

Departamento de Microbiología; Universidad de La Laguna; Tenerife, España, Spain (Méndez-Alvarez)

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To the Editor:

Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) infection is on the increase throughout the world. Panton-Valentine Leukocidin-positive (PVL) S. aureus strain dissemination in the community represents a public health concern about severe complications in children. Infections for CA-MRSA ST8, clonally related with USA300, have recently appeared in Colombia.1

We are reporting the first pediatric CA-MRSA infection cases that occurred in Bogotá between June 2004 and May 2006.2 The first case concerned a previously healthy 14-year-old boy who developed severe sepsis with multiorgan failure, infectious endocarditis of the tricuspid valve, and septic pulmonary embolism associated with deep vein thrombosis, bilateral pyomyositis, and osteomyelitis of the lower extremities; he recovered after prolonged medical and surgical treatment. The second case involved a 9-month-old male with congenital Toxoplasma infection who developed respiratory failure associated with pneumonia and cervical cellulitis and responded to antimicrobial therapy. The third case concerned a 16-year-old boy from Bogotá with a history of recurrent furuncles associated with spontaneous drainage in his lower extremities during the previous 3 months. He was admitted because of an acute onset of progressive inflammatory local signs in the left inguinal area that limited his walking; he responded to medical and surgical treatment.

The 3 isolates recovered from patients were confirmed as MRSA, the presence of nuc and mecA genes having been detected by polymerase chain reaction. The minimal inhibitory concentrations (MICs) were determined by using the agar diffusion test, according to Clinical and Laboratory Standards Institute.3 The oxacillin MICs for the 3 isolates were 32, 4, and 8 μg/mL, respectively. The third MRSA exhibited the MLSB constitutive phenotype in double-disk diffusion assay (D test), with erythromycin (>64 μg/mL MIC) and clindamycin resistance (32 μg/mL MIC). The 3 isolates were positive for the PVL genes (lukF-PV and lukS-PV) and harbored SCCmec type IVc. The 3 MRSA isolates SmaI macrorestriction profiles revealed 3 unique patterns clustering above 87% similarity into 1 pulsed-field gel electrophoresis type by computer analysis. The 3 strains were ascribed to ST8 by multilocus sequence typing belonging to the same sequence type as USA300, a common pulsed-field gel electrophoresis type in the United States with a similarity higher than 75%.

These 3 isolates were not epidemiologically related. The clinical spectrum of the cases ranged from mild to severe infection. All cases showed some degree of skin, deep soft tissue, or bone compromise, as has been frequently described in children, and similar to the first report of adult cases from Columbia.4 Molecular typing identified these 3 isolates as belonging to the ST8-MRSA-IVc clone; they carried the PVL genes often associated with CA isolates.

A retrospective report has suggested that CA-MRSA strains have been circulating in Colombia since 2001; they may have been ignored, along with their significant public health implications.5 Awareness about what is happening in our country will help us to evaluate the current state of our epidemiology regarding CA-MRSA infection and to develop strategies of infection control, following the lead of several other countries.

Martha Isabel Alvarez-Olmos, MD, MPH

Sandra P. Enríquez, MD

Departamento de Pediatría

División de Infectología Pediátrica

Fundación Cardioinfantil IC

Universidad del Rosario

Bogotá, Colombia

Eduardo Pérez-Roth, PhD

Sebastián Méndez-Alvarez, PhD

Laboratorio de Biología Molecular

Instituto de Investigación

Hospital Universitario “Nuestra Señora de la Candelaria”

Tenerife, España, Spain

Javier Escobar, MSc

Natasha Vanegas, PhD

Instituto de Genética Molecular Bacteriana

Universidad El Bosque

Bogotá, Colombia

Jaime Moreno, MSc

Grupo de Microbiología

Instituto Nacional de Salud

Bogotá, Colombia

Sebastián Méndez-Alvarez, PhD

Departamento de Microbiología

Universidad de La Laguna

Tenerife, España, Spain

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REFERENCES

1.Arias CA, Rincón S, Chowdhury S, et al. MRSA USA300 clone and VRFE a US-Colombian connection? N Engl J Med. 2008;359:2177–2179.
2.Garner JS, Jarvis WR, Emori TG, et al. CDC definitions for nosocomial infections, 1988. Am J Infect Control. 1988;16:128–140.
3.Clinical Laboratory Standards Institute. Performance Standards for Antimicrobial Susceptibility Testing: Fifteenth Informational Supplement, M100-S14. Wayne, PA: Clinical Laboratory Standards Institute; 2008.
4.Alvarez CA, Barrientes OJ, Leal AL, et al. Community-associated methicillin-resistant Staphylococcus aureus, Colombia. Emerg Infect Dis. 2006;12:2000–2001.
5.Buitrago G, Castillo JS, Leal AL, et al. Methicillin-resistant Staphylococcus aureus - community acquired phenotype spread in hospitals in Bogotá, Colombia. Clin Microbiol Infect. 2008;14:S411–S411.
© 2009 Lippincott Williams & Wilkins, Inc.