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Pneumococcal Serotypes Causing Acute Otitis Media Among Children in Barcelona (1992–2011): Emergence of the Multiresistant Clone ST320 of Serotype 19A

Gene, Amadeu MD*; Amo, Eva del Msc*; Iñigo, Melania PhD*; Monsonis, Manuel BSc*; Pallares, Roman MD; Muñoz-Almagro, Carmen MD*

The Pediatric Infectious Disease Journal: April 2013 - Volume 32 - Issue 4 - p e128–e133
doi: 10.1097/INF.0b013e31827c54dc
Original Studies

Background: There is scarce information about changes in serotypes and clonal types of Streptococcus pneumoniae causing acute otitis media (AOM) in recent years, particularly in European countries.

Methods: Pneumococcal serotypes and clones from S. pneumoniae strains isolated from children with AOM who were attended at Hospital Sant Joan de Déu, Barcelona (1992 to 2011), were studied. Heptavalent pneumococcal conjugate vaccine (PCV7) was introduced in June 2001. We defined 3 periods: prevaccine period 1992 to 2001, early vaccine period 2002 to 2006 and late vaccine period 2007 to 2011.

Results: There were 376 pneumococcal strains causing AOM, and 373 (99.2%) of them were serotyped. AOM caused by PCV7 serotypes declined significantly: 161 of 245 (65.7%) episodes in 1992 to 2001 versus 22 of 67 (32.8%) in 2002 to 2006 versus 8 of 61 (13.1%) in 2007 to 2011 P < 0.001. In the last period (2007 to 2011), the potential serotype coverage for the PCV10 was 16.4% and for the PCV13 was 68.9% (P < 0.001). Serotype 19A increased from 5.7% in 1992 to 2001 to 42.6% in 2007 to 2011 (P < 0.001). Among strains with penicillin minimal inhibitory concentration ≥0.12 μg/mL (n = 241), serotype 19A rose from 2.3% in the first period to 57.9 % in the last period (P < 0.001). The clonal-type ST320 was initially detected in 2005, and in the period 2007 to 2011, the ST320 was found in 72.7% of nonsusceptible serotype 19A isolates.

Conclusions: Among children with AOM, a rapid expansion of the multiresistant clone ST320 expressing serotype 19A has been observed in Barcelona. The implementation of PCV13, which includes this serotype, may decrease the prevalence of AOM and reduce antimicrobial resistance.

From the *Department of Molecular Microbiology, Hospital Universitari Sant Joan de Deu, Esplugues; and Infectious Diseases Service and Clinical Research Unit, Idibell, Ciberes, Bellvitge Hospital and University of Barcelona, Barcelona, Spain.

Accepted for publication November 2, 2012.

Conceived and designed the experiments: A.G., R.P. and C.M.-A. Performed the experiments: E.d.A., M.I. and M.M. Analyzed the data: R.P. and C.M.-A. Wrote the article: A.G., R.P. and C.M.-A. Revised the article: all authors.

This work was supported by Agència de Gestió d’Ajuts Universitaris i de Recerca [SGR00136] and Instituto de Salud Carlos III, Ministry of Heath, Madrid, Spain [PI10/02058]. E.d.A. has received funding from Instituto de Salud Carlos III. The authors have no other funding or conflicts of interest to disclose.

Address for correspondence: Carmen Muñoz-Almagro, MD, PhD, Molecular Microbiology Department, University Hospital Sant Joan de Deu, P° Sant Joan de Déu, 208950 Esplugues, Barcelona, Spain. E-mail:

© 2013 Lippincott Williams & Wilkins, Inc.