PEDIATRICS Vol. 108 No. 1 July 2001, p. e18

ELECTRONIC ARTICLE:
Invasive Serotype a Haemophilus influenzae Infections With a Virulence Genotype Resembling Haemophilus influenzae Type b: Emerging Pathogen in the Vaccine Era?

Received Nov 20, 2000; accepted Feb 10, 2001.

Elisabeth E. Adderson^{*, **}, Carrie L. Byington^*, LaShonda Spencer^*, , Amy Kimball^*, Musa Hindiyeh^§, , Karen Carroll^{, §,} , Susan Mottice^¶, E. Kent Korgenski^#, John C. Christenson^*, and Andrew T. Pavia^*,

From the Departments of ^* Pediatrics,  Medicine, and ^§ Pathology, University of Utah School of Medicine;  Associated Regional and University Pathologists; ^¶ Utah Department of Health, ^# Primary Children's Medical Center, Salt Lake City, Utah; and ^** St Jude Children's Research Center, Memphis Tennessee.

Objective.  Haemophilus influenzae type b causes severe disease in nonimmune infants and young children; other serotypes are uncommon pathogens and thought to have low virulence. Some have hypothesized that with the virtual elimination of H influenzae type b, other serotypes might acquire virulence traits and emerge as important pathogens of children. We describe the clinical, epidemiologic, and molecular biologic features of 5 cases of severe disease attributable to Haemophilus influenzae type a.

Methods.  After observing 4 cases of invasive disease caused by H influenzae type a, we reviewed microbiology records at 3 reference laboratories that perform all serotyping in Utah and surveillance databases. Strains of H influenzae type a and control strains were examined by Southern blotting with the use of the cap probe pUO38 and by pulsed-field gel electrophoresis. The putative virulence mutation, the IS1016-bexA deletion, was detected by polymerase chain reaction amplification and sequencing.

Results.  During a 10-month period, we observed 5 children with severe invasive disease caused by H influenzae type a. No isolates of H influenzae type a had been submitted to the reference laboratories between 1992 and 1998. The median age of patients was 12 months (range: 6-48 months). Four of 5 had meningitis and bacteremia; 1 had purpura fulminans. Three isolates, representing 1 of 2 pulsed-field gel electrophoresis patterns, contained the IS1016-bexA deletion and were associated with particularly severe disease.

Conclusions.  We describe an unusual cluster of severe disease caused by H influenzae type a that resembles the clinical and epidemiologic features of H influenzae type b disease. Our data support the hypothesis that the IS1016-bexA deletion may identify more virulent strains of H influenzae. Haemophilus influenzae, epidemiology, virulence, serotyping, pathogenicity. .

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