Infectious complications in pediatric cochlear implants.

OBJECTIVES: Infectious complications may cause significant delay in cochlear implant device initiation and programming and be a source of additional morbidity. We reviewed our experience with infectious complications in the pediatric age group to determine specific sources that may not be seen in adults. STUDY DESIGN: A retrospective analysis from a single implant center. METHODS: Cases of pediatric cochlear implants were reviewed for data on infectious complications. Complications were identified as "major" or "minor," "early" or "delayed." Information was gathered regarding any comorbid, chronic health condition. Data related to the causative organism(s) were collected. RESULTS: Two hundred sixty-eight cases of pediatric implants were reviewed. Twenty-two cases were identified (an infection rate of 8.2%), all classified as "major." The majority, 12, were classified as "delayed" complications. Twenty-one cases required explantation with 14 successfully reimplanted. Five cases (in 4 patients) or 23% were associated with a specific chronic pediatric condition including two children with tracheostomies. Among implanted children who had chronic health conditions, 42% developed implant-related infections. Among otherwise healthy implanted children, only 6.6% developed implant-related infections. Resistant bacterial infections were not identified. CONCLUSIONS: Health conditions in the pediatric age group were associated with 23% of our complications, a risk factor not previously identified in the literature. These children, demonstrating seven times the infection rate of healthy children, should be carefully observed postoperatively. Overall, cochlear implantation in children continues to be associated with a low risk of infectious complications.

Airway hyperresponsiveness, late allergic response, and eosinophilia are reversed with mycobacterial antigens in ovalbumin-presensitized mice.

Pretreatment with mycobacterial Ags has been shown to be effective in preventing allergic airway inflammation from occurring in a mouse model. Because most asthmatics are treated after the development of asthma, it is crucial to determine whether mycobacterial Ags can reverse established allergic airway inflammation in the presensitized state. Our hypothesis, based upon our previous findings, is that mycobacteria treatment in presensitized mice will suppress the allergic airway inflammation with associated clinical correlates of established asthma, with the noted exception of factors associated with the early allergic response (EAR). BALB/c mice sensitized and challenged with OVA were evaluated for pulmonary functions during both the EAR and late allergic response, and airway hyperresponsiveness to methacholine. Following this, sensitized mice were randomized and treated with placebo or a single dose (1 x 10(5) CFUs) of bacillus Calmette-Guérin (BCG) or Mycobacterium vaccae via nasal or peritoneal injection. One week later, the mice were rechallenged with OVA and methacholine, followed by bronchoalveolar lavage (BAL) and tissue collection. Mice treated with intranasal BCG were most significantly protected from the late allergic response (p < 0.02), airway hypersensitivity (p < 0.001) and hyperreactivity (p < 0.05) to methacholine, BAL (p < 0.05) and peribronchial (p < 0.01) eosinophilia, and BAL fluid IL-5 levels (p < 0.01) as compared with vehicle-treated, sensitized controls. Intranasal M. vaccae treatment was less effective, suppressing airway hypersensitivity (p < 0.01) and BAL eosinophilia (p < 0.05). No changes were observed in the EAR, BAL fluid IL-4 levels, or serum total and Ag-specific IgE. These data suggest that mycobacterial Ags (BCG>>M. vaccae) are effective in attenuating allergic airway inflammation and associated changes in pulmonary functions in an allergen-presensitized state.