Hib

Haemophilus influenzae type b (Hib) is distinguished from nontypeable H. influenzae strains by its polysaccharide capsule composed of polyribosylribitol phosphate (PRP), which is the primary virulence factor allowing evasion of phagocytosis and complement-mediated lysis. Before vaccine introduction, Hib was the leading cause of bacterial meningitis in children aged 6 months to 5 years, and also caused epiglottitis (presenting with drooling, tripod positioning, and 'thumbprint sign' on lateral neck X-ray), septic arthritis, cellulitis, pneumonia, and bacteremia. Risk is highest in unvaccinated children and those with asplenia (splenectomy or sickle cell disease), since the spleen is critical for clearing encapsulated organisms via opsonization.

The Hib conjugate vaccine links the PRP capsular polysaccharide to a protein carrier (e.g., diphtheria toxoid, tetanus toxoid, or meningococcal outer membrane protein), converting a T-independent antigen into a T-dependent one. This allows for immune memory and effective response in infants, whose immune systems respond poorly to polysaccharide antigens alone. The vaccine is part of the routine childhood immunization schedule, typically given at 2, 4, 6, and 12-15 months.

Diagnosis involves Gram stain (small gram-negative coccobacilli), culture on chocolate agar requiring factors V (NAD) and X (hematin), and latex agglutination or PCR for capsular antigen detection. Treatment for invasive disease is typically a third-generation cephalosporin (ceftriaxone or cefotaxime) due to increasing beta-lactamase-mediated ampicillin resistance. Rifampin prophylaxis is given to close contacts of patients with invasive Hib disease to eradicate nasopharyngeal carriage.

Key board-relevant points: encapsulated organism requiring opsonization for clearance, classic cause of epiglottitis and meningitis in unvaccinated children, growth requires factors V and X on chocolate agar, and the conjugate vaccine mechanism exemplifies converting T-independent to T-dependent antigen response.