Background: New Zealand is a developed country with high incidence of bacterial infections and postinfectious sequelae including rheumatic heart disease. We sought to describe the clinical and microbiology features of children with infective endocarditis (IE) between 1994 and 2012.
Methods: Retrospective review of patients <16 years identified from hospital records.
Results: In total 85 episodes occurred in 82 children and 68 (80%) were classified as Definite IE and 17 as Possible IE according to modified Duke criteria. From Pacific Island countries, 13 cases were referred. There were 72 children who originated in New Zealand, of whom 52% were either indigenous New Zealand Maori or Pacific migrants. The median age at diagnosis was 7 (0–15) years. Of the 85 cases, 51 (60%) had congenital heart disease 10 children with rheumatic heart disease developed IE. Of the 85 cases, 35 (41%) met our criteria for healthcare-associated IE. 39/85 underwent surgery for IE. As direct result of IE, 4 (4.7%) children died and 9% of survivors had neurologic sequelae. Attributable in-hospital mortality was 4.7%. Staphylococcus aureus was the most common organism, accounting for 26 episodes (30.6%). Other notable pathogens included Corynebacterium diphtheriae (10 cases, 11.8%) and Streptococcus pyogenes (7 cases, 8.2%). In 6 episodes, the microbiologic diagnosis was made by 16S ribosomal RNA testing of excised cardiac tissue.
Conclusions: Congenital heart disease was the major risk factor for IE; however, rheumatic heart disease is also an important risk factor in New Zealand, with implications for local endocarditis prophylaxis recommendations. In addition to a high burden of healthcare-associated and staphylococcal IE, pathogens such as C. diphtheriae and S. pyogenes occurred. 16S ribosomal RNA testing is a useful tool to determine the etiologic agent in culture-negative IE.
From the *Department of Pediatric Infectious Diseases, Starship Children’s Hospital, Auckland; †Department of Microbiology, Auckland District Health Board; ‡Department of Pediatric and Congenital Cardiac Services, Starship Children’s Hospital, Auckland; and §School of Population Child and Youth Health, University of Auckland, Auckland, New Zealand.
Accepted for publication October 14, 2013.
The authors have no funding or conflicts of interest to disclose
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Address for Correspondence: Rachel Webb, FRACP, Locum Pediatrician in Infectious Diseases, Starship Children’s Hospital, Auckland District Health Board, Private Bag 92024, Auckland, New Zealand. E-mail: firstname.lastname@example.org.