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Published on: February 23, 2014
Pediatric mastoiditis in the pneumococcal conjugate vaccine era: symptom duration guides empiric antimicrobial
Mark G Roddy1, Scott S Glazier, Dewesh Agrawal
1Division of Emergency Medicine, Children's National Medical Center, Washington, DC 20010, USA.
Insights
The heptavalent pneumococcal conjugate vaccine (PCV) did not change the rate of Streptococcus pneumoniae causing pediatric mastoiditis. Empiric ceftriaxone therapy is insufficient post-PCV due to increased resistance.
Area of Science:
- Pediatric infectious diseases
- Microbiology
- Vaccinology
Background:
- The microbiology of acute otitis media has shifted during the heptavalent pneumococcal conjugate vaccine (PCV) era.
- This study hypothesizes that pediatric mastoiditis may exhibit similar etiological changes.
Purpose of the Study:
- To compare the etiology of pediatric mastoiditis before and after the introduction of the PCV.
- To guide empiric antimicrobial therapy in pediatric emergency departments.
Main Methods:
- A retrospective chart review was conducted for patients diagnosed with mastoiditis between January 1995 and April 2005.
- Etiological agents were identified through culture results.
Main Results:
- Streptococcus pneumoniae remained a common cause of mastoiditis, with no significant change in its proportion post-PCV.
- A notable increase in ceftriaxone non-susceptibility was observed in post-PCV Streptococcus pneumoniae isolates (30% vs. 7%).
- Pseudomonas aeruginosa was significantly more prevalent in chronic mastoiditis compared to acute mastoiditis.
Conclusions:
- The introduction of PCV has not altered the incidence of Streptococcus pneumoniae-related pediatric mastoiditis.
- Current empiric antimicrobial therapy, relying solely on ceftriaxone, is inadequate for treating mastoiditis in the post-PCV era due to emerging resistance patterns.
Background:
The microbiology of acute otitis media has changed in the heptavalent pneumococcal conjugate vaccine (PCV) era. We hypothesize similar changes with pediatric mastoiditis.
Objectives:
To compare the etiology of mastoiditis in the pre-PCV (January 1995-December 2000) and post-PCV (January 2001- April 2005) eras to guide empiric antimicrobial therapy in the pediatric emergency department.
Methods:
Retrospective chart review of all patients admitted with a diagnosis of mastoiditis from January 1995 to April 2005.
Results:
: One hundred twenty-two charts were reviewed, 68 pre-PCV and 54 post-PCV. Etiological agents were determined by culture results in 60 patients. The most common bacterial isolates were Streptococcus pneumoniae (24), Pseudomonas aeruginosa (12), Staphylococcus aureus (12), Streptococcus pyogenes (8), and Haemophilus influenzae (2). There was no reduction in mastoiditis due to S. pneumoniae from the pre-PCV to the post-PCV eras (odds ratio [OR], 0.9; 95% confidence interval [CI], 0.4-2.1; P = 0.77). Ceftriaxone nonsusceptibility was seen in 30% of post-PCV S. pneumoniae isolates compared with 7% of pre-PCV isolates. Acute mastoiditis was diagnosed in 93 patients, and chronic mastoiditis (defined as >or=3 wk of symptoms) was diagnosed in 29 patients. Streptococcus pneumoniae was more likely to be implicated in acute versus chronic mastoiditis (OR, 9.2; 95% CI, 1.2-52.2; P = 0.01). Pseudomonas aeruginosa was more frequently implicated in chronic versus acute mastoiditis (OR, 16.4; 95% CI, 2.1-75.8; P = 0.0003).
Conclusions:
There was no difference in the proportion of pediatric mastoiditis cases caused by S. pneumoniae in the pre-PCV versus post-PCV eras. Empiric antimicrobial therapy with ceftriaxone alone is not sufficient in the post-PCV era.
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