The Emergence of Pneumococcus Type 19A as the Major Cause of Mastoiditis in Children
Abstract & Commentary
By Dean L. Winslow, MD, FACP, FIDSA, Chief, Division of AIDS Medicine, Santa Clara Valley Medical Center; Clinical Professor, Stanford University, School of Medicine, Section Editor, HIV, is Associate Editor for Infectious Disease Alert.
Synopsis: Forty-one pneumococcal mastoiditis cases were identified and 19A (n = 19) was the most common serotype. The prevalence of serotype 19A as a cause of mastoiditis increased dramatically over the time period and was correlated with the introduction of the 7-valent pneumococcal conjugate vaccine (PCV7). Mastoiditis due to pneumococcus type 19A were more likely to present with subperiosteal abscess and require surgical intervention, and isolates were more likely to demonstrate antimicrobial resistance than non-type 19A isolates.
Source: Ongkasuwan J, et al. Pneumococcal mastoiditis in children and the emergence of multidrug-resistant serotype 19A isolates. Pediatrics. 2008;122:34-39.
Since 1993, clinical isolates of s. pneumoniae from normally sterile sites, including middle ear cultures, have been prospectively obtained from the Texas Children's Hospital clinical microbiology laboratory, and stored frozen. A retrospective chart review was performed for all patients in the database diagnosed with pneumococcal mastoiditis between 1995 and 2007. Data on immunization with PCV7 was included in the review. Isolates were serotyped by the capsular swelling method, and susceptibility testing was performed by both Bauer-Kirby and microbroth dilution methods. In addition, isolates were examined by pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST).
Both the total number of mastoiditis cases and the proportion due to S pneumoniae type 19A increased dramatically since 2003. In 2006 and 2007, all 15 cases of pneumococcal mastoiditis cases were due to type 19A. Statistical analysis revealed significant differences between cases due to type 19A and non-19A cases, including the presence of sub-periosteal abscess in all 19 cases of type 19A mastoiditis and in only 3/22 non-19A cases. Mastoidectomy was required in 17 of the type 19A cases and in only 10 of the non-19A cases. PFGE genotyping of the 19A isolates revealed that eight of the 19 isolates were indistinguishable, six appeared to be closely related, and five were considered to be unrelated. The identical and closely related isolates (clones A1-6) had penicillin MIC's ≥ 2 ug/mL, whereas the unrelated isolates had values between 0.1 and 0.5 ug/mL. Similarly, the ceftriaxone MIC for all clone A isolates was 1 ug/mL, whereas only one of the unrelated isolates had a ceftriaxone MIC of 1 ug/mL and four isolates had MICs of ≤ 0.25 ug/mL. Resistance to erythromycin was present in all clone A isolates and in none of the unrelated isolates. Clindamycin resistance was present in 13/14 clone A isolates and in none of the unrelated isolates.
Prior to 2000, serotype 19F was the predominant pneumococcal serotype isolated from middle ear fluid in pediatric patients with otitis media and mastoiditis. In the prevaccine era, children with serotype 19F isolates were half as likely as serotype 19A isolates to present with subperiosteal abscess and to require surgical intervention. Since the introduction of PCV7, the non-vaccine S. pneumoniae serotype 19A has emerged as the dominant serotype recovered from children at Texas Children's Hospital. It is likely that a similar phenomenon has, or will, occur in other communities where PCV7 is administered to a high proportion of young infants. While PCV7 is an effective vaccine that has been shown to significantly reduce the morbidity and mortality of invasive pneumococcal disease due to vaccine serotypes, the emergence of serotype 19A as a major cause of mastoiditis is an important clinical observation. Physicians should be aware of the often more aggressive clinical course and presence of antimicrobial resistance in mastoiditis due to type 19A isolates.