H influenzae type b was the leading cause of invasive bacterial disease among children in the United States prior to licensing of Haemophilus b conjugate vaccines. Based on its active surveillance areas, the Centers for Disease Control and Prevention (CDC) now estimate that H influenzae type b disease in children under the age of 5 years has been reduced by 95%. ³ Before effective vaccines were introduced,it was estimated that one in 200 children developed invasive H influenzae type b disease by the age of 5 years. In children less than 5 years of age, the mortality rate for invasive H influenzae type b disease ranged between 3% and 6%. ³ In more than 60% of these children, meningitis was the clinical syndrome and permanent sequelae ranging from mild hearing loss to mental retardation affecting 20% to 30% of all survivors. ³ Ninety-five percent of the cases of invasive H influenzae disease among children <5 years of age were caused by organisms with the type b polysaccharide capsule. Approximately two-thirds of all cases of invasive H influenzae type b disease affected infants and children <15 months of age, a group for which a vaccine was not available until late 1990. ^4,5

Incidence rates of invasive H influenzae type b disease have been shown to be increased in certain high-risk groups, such as native Americans (both American Indians and Eskimos), blacks, individuals of lower socioeconomic status, and patients with asplenia, sickle cell disease, Hodgkin's disease, and antibody deficiency syndromes. ^5,6 Studies also have suggested that the risk of acquiring primary invasive H influenzaetype b disease for children under 5 years of age appears to be greater for those who attend day care facilities. ^7,8,9,10

The potential for person to person transmission of the organism among susceptible individuals has been recognized. Studies of secondary spread of disease in household contacts of index patients have shown a substantially increased risk among exposed household contacts under 4 years of age. ¹¹ Adults can be colonized with H influenzae type b from children infected with the organism. ¹²

The response to ActHIB^® is typical of a T-dependent immune response to antigen. The prominent isotype of anticapsular PRP antibody induced by ActHIB^® is IgG. ¹³ A substantial booster response has been demonstrated in children 12 months of age or older who previously received two or three doses. Bactericidal activity against H influenzae type b is demonstrated in serum after immunization and statistically correlates with the anti-PRP antibody response induced by ActHIB^{® 14}

Antibody to H influenzae capsular polysaccharide (anti-PRP) titers of >1.0 µg/mL following vaccination with unconjugated PRP vaccine correlated with long-term protection against invasive H influenzae type b disease in children older than 24 months of age. ¹⁵ Although the relevance of this threshold to clinical protection after immunization with conjugate vaccines is not known, particularly in light of the induced, immunologic memory, this level continues to be considered as indicative of long-term protection. ⁴ The immunogenicity and safety of ActHIB^® has been demonstrated in the United States and worldwide. ActHIB^® induced, on average anti- PRP levels >1.0 µg/mL in 90% of infants after the primary series and in more than 98% of infants after a booster dose. ¹⁴

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