Commentary
Article Outline
[Ann Emerg Med. 2009;54:85.]
Historically, emergency physicians were well acquainted with invasive disease caused by Hib. Today, most physicians in training will finish residency never having seen a child present with complications caused by Hib. Since 1990, a conjugate Hib vaccine has decreased the annual incidence of invasive disease to near nondetectable levels.1 However, the above report describes an unusually high frequency of cases identified in 2008 in Minnesota, mainly among underimmunized children.2
H influenzae is a Gram-negative coccobacillus originally identified in 1889 in a patient who died from an influenza-like illness. Indeed, the bacterial pathogen was believed to cause the flu until a viral origin was identified in 1933. Although there are many strains of H influenzae, the most basic subdivisions categorize the bacteria as either encapsulated (Hi serotypes a to f), or unencapsulated (nontypable) H influenzae. The most pathogenic serogroup, Hib, has a capsule of type b polyribosylribitol polysaccharide. The type b capsule is important for the virulence of the organism (enabling bacterial evasion of phagocytosis and propagation of complement-mediated cell lysis) and in development of host immunity after vaccination. Maternal antibodies provide protection for the neonate until 2 months of age. Thereafter, because of an immature immune system, the normal infant or toddler remains vulnerable to many common encapsulated bacteria, including Hib, until 5 years of age. Thus, Hib infection is rare before 2 months of age and after 5 years. Nontypable H influenzae is still a common cause of respiratory tract infections in adults and children, unaffected by Hib vaccination.
The epidemiology of illness from Hib has changed dramatically since the broad implementation of Hib vaccination in 1990. In the prevaccination era, Hib was the most common cause of bacterial meningitis in early childhood in the United States. The median age of persons with bacterial meningitis in the United States in 1986 was 15 months. By 1995, the median age had increased to 25 years.3 Unfortunately, the disease is still common in countries that do not routinely immunize. It is estimated that 118 million children around the world are not currently immunized, and approximately 400,000 deaths per year occur worldwide from Hib.4, 5
The Minnesota cases described above remind us that children in the United States may still be susceptible to Hib because of parents who decline immunizations and because of vaccine shortages. Children who are too young to complete the primary series and those who are undervaccinated remain at higher risk. Rates of infection are notably higher in American Indian and Alaskan natives. A few reported cases were among children who had completed a primary vaccination series, indicating that, although the vaccine is highly efficacious, failure does occasionally occur.1 Most cases of invasive Hib infection manifest as meningitis or pneumonia. Less commonly, epiglottitis, periorbital and facial cellulitis, osteoarticular infection, or isolated bacteremia can develop.5
The diagnostic evaluation for febrile children, particularly those between the ages of 6 months and 36 months, has changed with the widespread use of conjugate Hib and pneumococcal vaccinations.6 Data from the prevaccination era showed that the risk of meningitis for untreated H influenzae bacteremia was 26%, compared with Streptococcus pneumoniae, which had a risk of only 6%.7 Emergency physicians should have a higher level of suspicion for invasive Hib disease in undervaccinated children and consider a more liberal use of diagnostic testing (including blood cultures) and empiric antibiotics. A third-generation cephalosporin such as ceftriaxone remains the drug of choice for invasive Hib infections. Oral agents such as amoxicillin/clavulanate can be used for less serious infections.
Emergency physicians should remain vigilant for the possibility of invasive Hib disease in susceptible children, including meningitis, pneumonia, and epiglottitis. Because vaccination is central to preventing the well-described complications of invasive HiB infection, all parents should be encouraged to complete immunizations for their children.
References
- . Progress toward elimination of Haemophilus influenzae type b invasive disease among infants and children—United States, 1998-2000. MMWR Morb Mortal Wkly Rep. 2002;51:234–237
- . Invasive Haemophilus influenzae type b disease in five young children—Minnesota, 2008. MMWR Morb Mortal Wkly Rep. 2009;58:58–60
- Bacterial meningitis in the United States in 1995. N Engl J Med. 1997;337:970–976
- . Worldwide Haemophilus influenzae type b disease at the beginning of the 21st century: global analysis of the disease burden 25 years after the use of the polysaccharide vaccine and a decade after the advent of conjugates. Clin Microbiol Rev. 2000;13:302–317
- . WHO position paper on Haemophilus influenzae type b conjugate vaccines. Wkly Epidemiol Rec. 2006;81:445–452
- . Management of fever without source in infants and children. Ann Emerg Med. 2000;36:602–614
- Practice guidelines for the management of infants and children with fever without source 0-36 months of page. Pediatrics. 1993;92:1–12
Section editors: David A. Talan, MD; Gregory J. Moran, MD; Robert Pinner, MD
PII: S0196-0644(09)00530-7
doi:10.1016/j.annemergmed.2009.05.020
© 2009 Published by Elsevier Inc.
