Assessment of carriage of Haemophilus influenzae type a after a case of invasive disease.

TO THE EDITOR-We read with interest the paper by Kapogiannis et al. [1] describing 2 cases of severe invasive Haemophilus influenzae serotype a (Hia) disease. Non-type b H. influenzae is an uncommon cause of invasive disease; however, use of conjugate vaccine has resulted in a significant decrease in the incidence of H. influenzae type b (Hib) disease, and the relative importance of non-type b H. influenzae infections has increased. Enhanced awareness of non-type b H. influenzae disease is warranted, especially given the acquisition of virulence factors commonly associated with Hib by certain strains of non-type b H. influetizae [1-3]. We previously reported an outbreak of Hia disease in which 2 infants developed recurrent infections with Hia. Oropharyngeal swab cultures revealed Hia carriage in 5 (16%) of 31 close contacts of the 2 case patients [4]. On the basis of the absence of identification of secondary cases, there is no recommendation to provide chemoprophylaxis to close contacts of patients infected with non-type b H. influenzae; however, in this situation, rifampin chemoprophylaxis was prescribed to all close contacts of the 2 patients who developed reinfection, given that household transmission may have been occurring. We recently investigated another case of invasive Hia disease. The patient presented at age 6 months with a 1-day history of cough, fever, and decreased activity. Chest radiography revealed a right upper lobe infiltrate. Blood cultures grew H. influenzae that was 3-lactamase negative and was identified as serotype a by latex agglutination. The patient was treated with antimicrobials and returned to his baseline state of health. ELISAs of acuteand convalescent-phase serum samples found no detectable IgG antibodies to the Hia polysaccharide capsule. Oropharyngeal swab samples were collected from all close contacts of the patient and from members of 3 comparison families that had children of similar age to the case patient and who were residents of the same community but who were not close contacts. "Close contacts" were people residing with the case patient or nonresidents who spent -4 h with the index patient for at least 5 of the 7 days preceding the day of hospital admission of the index case [5]. Hia carriage was identified in 3 (43%) of 7 close contacts and in none of 20 comparison participants (exact P = .0 12). The treating clinician prescribed rifampin chemoprophylaxis to the 3 colonized individuals. We know of no cases of invasive Hia illness among contacts of persons with disease; however, the identification of carriage among contacts raises this concern. Additionally, because infants produce a weak or undetectable response to polysaccharide capsule, the possibility exists that they may develop recurrent invasive Hia disease as a result of transmission from close contacts. We suspect that this may have been the cause of recurrent illness among the cluster of cases we recently reported [4]. More studies are needed to help define the role, if any, of chemoprophylaxis among contacts of patients with non-type b H. influenzae. No populationbased prevalence study has been conducted to measure non-type b H. influenzae carriage; however, in Alaska, surveillance for encapsulated H. influenzae invasive disease is ongoing and we are continuing to assess carriage among close contacts and non-close contact members of the community. As Kapogiannis et al. [1] point out, it is important to monitor the incidence and serotype distribution of invasive encapsulated H. influenzae disease in infants and children; particular attention should be paid to the occurrence of recurrent invasive disease or of disease among contacts of case patients.