Morphology and Cultural Characteristics
Haemophilus influenzae belongs to the family Pasteurellaceae. These are small, non-motile, Gram-negative bacteria lacking spores, but possessing pili. Pleomorphism is characteristic: smears may reveal spherical, ovoid, and rod-shaped forms, as well as short filaments. The most crucial, though variable, structural element is the capsule.
Functionally, they are facultative anaerobes. Their key metabolic feature is the inability to synthesize respiratory enzymes. They require preformed blood factors for growth:
- Factor X (protoporphyrin IX / hemin) — required for the synthesis of respiratory chain enzymes.
- Factor V (NAD or NADP) — a cofactor for redox reactions.
Growth is poor on plain blood agar because NADases in intact erythrocytes destroy Factor V. The medium of choice is chocolate agar. During its preparation, blood agar is heated to 80 °C, which causes hemolysis (releasing Factors X and V) and inactivates the enzymes that destroy them. The satellite phenomenon is also characteristic: H. influenzae grows abundantly around colonies of Staphylococcus aureus, which secrete NAD into the medium and lyse erythrocytes.
Antigens and Virulence Factors
The bacterium possesses a somatic O-antigen and a capsular polysaccharide K-antigen. Based on the capsule, 6 serotypes (a–f) are distinguished. The most clinically significant is type b (Hib), whose capsule consists of polyribosylribitol phosphate (PRP).
Main virulence factors:
- Capsule — the leading factor. It exhibits anti-complement activity, protects against phagocytosis, and helps the bacterium survive and invade tissues.
- Endotoxin (lipooligosaccharide) — increases the permeability of tissue barriers (including the blood-brain barrier) and paralyzes the cilia of the respiratory epithelium.
- IgA protease — inactivates mucosal protective antibodies.
- Pili — provide adhesion to the epithelium. Interestingly, unencapsulated strains possess greater adhesiveness, allowing them to colonize the portal of entry and cause localized inflammation.
Epidemiology and Pathogenesis
Haemophilus influenzae is a strict anthroponosis. The source of infection is a sick person or a carrier (unencapsulated strains are more commonly carried). The transmission route is airborne.
Incidence is strictly tied to age-related immunology. Up to 3–6 months, infants are protected by maternal IgG. Afterwards, their levels decline, while the child's own antibody production against the T-independent capsular antigen is physiologically immature in children under 2 years of age. A peak of severe infections occurs during this period.
Clinical variants of infection:
- Unencapsulated strains: Cause sinusitis, otitis media, bronchitis, and pneumonia (frequently in the elderly, smokers, and immunocompromised individuals).
- Encapsulated strains (Hib): Cause invasive systemic disease via hematogenous dissemination. These include purulent meningitis (with risks of vision loss, deafness, and hydrocephalus) and acute bacterial epiglottitis (fulminant laryngeal edema with risk of asphyxia). The mortality rate of severe untreated forms reaches 90%.
Diagnosis and Treatment
In cases of meningitis, a presumptive diagnosis can be made via cerebrospinal fluid microscopy. For rapid detection of capsular antigen, PCR, DFA, and latex agglutination are used. The gold standard is bacteriological culture: inoculation onto chocolate agar with confirmation of X and V factor dependence.
For invasive systemic forms, empirical therapy is initiated immediately with third-generation cephalosporins (e.g., ceftriaxone). Approximately 25% of strains produce $\beta$-lactamases, so beta-lactamase inhibitor combinations (e.g., amoxicillin + clavulanate) are used for localized forms.
Prevention: Conjugate vaccines are used (where the PRP capsular antigen is linked to a carrier protein, such as diphtheria toxoid). This converts the antigen into a T-dependent one, successfully inducing a robust immune response in infants from an early age.