Cells of Haemophilus influenzae—the major human pathogen of this genus—are pleomorphic, ranging from coccobacilli to long, slender filaments. H. influenzae may produce a capsule (six capsular types have been distinguished) or may be unencapsulated (Figure 1). The capsule is an important virulence factor. Serious, invasive H. influenzae disease is associated particularly with capsular type b (Hib), which is composed of polyribose phosphate. Hib is especially important as a pathogen of young children, although it can cause disease in individuals of all age groups. Nontypeable (unencapsulated) strains may also cause serious disease and are a significant cause of pneumonia among older adults and individuals with chronic lung disease.

Fig1. Haemophilus influenzae (electron micrograph) showing thick capsules.

A. Epidemiology

 H. influenzae is a normal component of the upper respiratory tract flora in humans and may also colonize the conjunctiva and genital tract. Humans are the only natural hosts, and colonization begins shortly after birth, with unencapsulated strains and Hib being carried most frequently. H. influenzae illnesses are usually sporadic in occurrence.

 B. Pathogenesis

 H. influenzae is transmitted by respiratory droplets. Immunoglobulin A (IgA) protease produced by the organism degrades secretory IgA, facilitating colonization of the upper respiratory tract mucosa. From this site, H. influenzae can enter the bloodstream and disseminate to distant sites. Diseases caused by H. influenzae, therefore, fall into two categories (Figure 2). First, disorders such as otitis media, sinusitis, epiglottitis, and bronchopneumonia result from contiguous spread of the organism from its site of colonization in the respiratory tract. Second, disorders such as meningitis, septic arthritis, and cellulitis result from invasion of the bloodstream, followed by localization of H. influenzae in these and other areas of the body.

Fig2. Infections caused by Haemophilus influenzae.

 C. Clinical significance

 H. influenzae has been a leading cause of bacterial meningitis, primarily in infants and very young children, frequently in conjunction with an episode of otitis media. A vaccine against H. influenzae type b, administered to infants, has dramatically decreased the frequency of such infections (Figure 3). Clinically, H. influenzae meningitis is indistinguishable from other purulent meningitides and may be gradual in onset or fulminant (sudden onset with great severity). Mortality from meningitis is high in untreated patients, but appropriate therapy reduces mortality to about 5 percent. Survivors may be left with permanent neurologic sequelae, especially deafness.

Fig3. Incidence of Haemophilus influenzae type b meningitis in a pediatric population in the United States. PRP = polyribose phosphate.

D. Laboratory identification

A definitive diagnosis generally requires identification of the organ ism (for example, by culture on chocolate agar). H. influenzae is fastidious and requires supplementation with hemin, factor X, and nicotinamide adenine dinucleotide (NAD+), factor V. H. influenzae can be cultured on chocolate agar (lysed blood cells provide these growth factors) but cannot be grown on blood or MacConkey agar. Isolation from normally sterile sites and fluids, such as blood, cerebrospinal fluid (CSF), and synovial fluid, is significant, whereas isolation from pharyngeal cultures is inconclusive. Rapid diagnosis is crucial because of the potentially fulminant course of type b infections. In cases of meningitis, Gram staining of CSF commonly reveals pleomorphic, gram-negative coccobacilli (Figure 4). Type b capsule may be identified directly in CSF, either by the capsular swelling (quellung) reaction or by immunofluorescent staining . Capsular antigen may be detected in CSF or other body fluids using immunologic tests, such as latex agglutination, countercurrent immunoelectrophoresis, ELISA, and radio immunoassay.

Fig4. Summary of Haemophilus disease. 1  Indicates first-line drugs; 2 indicates alternative drugs. NAD = nicotinamide adenine dinucleotide.

E. Treatment

When invasive H. influenzae is suspected, a suitable antibiotic (for example, a third-generation cephalosporin, such as ceftriaxone or cefotaxime) should be started as soon as appropriate specimens have been taken for culture (see Figure 4). Antibiotic sensitivity testing is necessary because of emergence of strains resistant to antibiotics commonly used to treat H. influenzae (for example, strains with β-lactamase-mediated ampicillin resistance). Sinusitis, otitis media, and other upper respiratory tract infections are treated with trimethoprim-sulfamethoxazole or ampicillin plus clavulanate.

F. Prevention

Active immunization against Hib is effective in preventing invasive disease and also reduces respiratory carriage of Hib (see Figure 3). The current vaccine, generally given to children younger than age 2 years, consists of Hib polyribose phosphate (PRP) capsular carbohydrate conjugated to a carrier protein . Rifampin is given prophylactically to individuals in close contact with a patient infected with H. influenzae ––particularly those patients with invasive disease (for example, H. influenzae meningitis).

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