Nature abhors vacuum, but public health is loving it: the sustained decrease in the rate of invasive Haemophilus influenzae disease.

Received 1 December 2004; accepted 2 December 2004; electronically published 18 February 2005. Reprints or correspondence: Dr. Jay C. Butler, 4055 Tudor Centre Dr., Anchorage, AK 99508 (JButler@cdc.gov). Clinical Infectious Diseases 2005; 40:831–3 This article is in the public domain, and no copyright is claimed. 1058-4838/2005/4006-0009 Prevention of invasive Haemophilus influenzae type b (Hib) infection through immunization is one of the great public health successes of the late 20th century. Hib conjugate vaccines have consistently led to a 90% decrease in the incidence of invasive disease in all settings where they have been incorporated into routine infant immunization schedules [1]. Although economic constraints have limited the use of the vaccines primarily to industrialized nations, Hib vaccines prevent ∼21,000 cases of Hib meningitis and ∼38,000 cases of invasive Hib disease in the world annually [2]. In industrialized countries, certain populations at greater risk of invasive Hib disease, such as American Indians and Alaska Natives, have particularly benefited from immunization [3]. The remarkable effectiveness of Hib conjugate vaccines has raised hopes that Hib disease can be eliminated in the United States and has fueled enthusiasm for introducing routine Hib vaccination into developing countries [1, 4]. As invasive Hib disease has become less common in areas where conjugate vaccines are routinely used, the proportion of invasive H. influenzae infections caused by serotypes a and c–f, as well as unencapsulated strains, have increased. Although clinicians and public health officials can celebrate the remarkable decrease in the number of invasive H. influenzae infections, 3 important questions must be addressed: Are non–type b H. influenzae infections becoming more common? What is the appropriate public health response to cases of invasive infection with non– type b H. influenzae? And what are the major gaps in our knowledge regarding non–type b H. influenzae? The first question is not a new one. Before licensure and routine use of Hib vaccines, concerns were raised that the incidence of infection due to non–type b H. influenzae might increase if these organisms filled the microbiological niche vacated by Hib. Hib is transmitted via respiratory droplets from the oropharynx of persons colonized with the organism. Given that non–type b H. influenzae can occupy the same anatomic site as Hib and can have nutritional requirements similar to those of Hib, replacement colonization and disease are biologically plausible. In the case of another encapsulated bacterial pathogen, Streptococcus pneumoniae, persons immunized with conjugate vaccine are more likely to be colonized with nonvaccine serotypes and are more likely to have otitis media caused by these strains [5, 6]. However, during the first few years after the introduction of Hib conjugate vaccines, no significant changes in non– type b H. influenzae colonization or disease were detected, despite decreases in the rates of Hib pharyngeal acquisition and invasive disease [7, 8]. Concerns about immediate replacement of Hib disease by invasive infections caused by non–type b H. influenzae have not been borne out. The report by Millar et al. [9] in this issue of Clinical Infectious Diseases provides a longer-term perspective on the risk of replacement disease, with data on the epidemiology of invasive H. influenzae type a (Hia) disease among Navajo and White Mountain Apache children in the American Southwest during the period of 1988–2003. Hib vaccine coverage has been 190% among these children during the most recent 12 years of surveillance, and rates of invasive Hia disease have increased minimally, if at all. One limitation of the data is the short period of surveillance before widespread use of Hib conjugate vaccines. No cases of Hia infection were detected during the first 3 years of surveillance. If these 3 years represent a baseline that extends back many years before the beginning of surveillance in 1988, the