Neisseria meningitidis: Antigenic Structure, Pathogenesis, Pathology and Clinical Findings, Diagnostic Laboratory Tests, Immunity, Treatment Flashcards
(9 cards)
Neisseria meningitidis: antigenic structure
Neisseria meningitidis is a gram-negative diplococcus with a polysaccharide capsule that defines its serogroups (A, B, C, Y, W-135). The capsule is antiphagocytic and essential for virulence. It also has outer membrane proteins (porins), pili for attachment, lipooligosaccharide (LOS) that acts as endotoxin, and IgA protease that cleaves IgA on mucosal surfaces.
Neisseria meningitidis: pathogenesis
N. meningitidis colonizes the nasopharynx, then enters the bloodstream. It crosses the blood-brain barrier to infect the meninges. Its capsule resists phagocytosis. LOS endotoxin causes severe inflammation, vascular damage, increased permeability, and shock. Petechiae and purpura are due to small vessel thrombosis. Disseminated intravascular coagulation (DIC) and Waterhouse-Friderichsen syndrome (adrenal hemorrhage) can occur.
Neisseria meningitidis: pathology and clinical findings
Meningococcal meningitis: sudden onset of fever, headache, stiff neck, photophobia, vomiting, and altered mental status. Meningococcemia: petechial rash, purpura, hypotension, DIC, and possible shock. Waterhouse-Friderichsen syndrome: bilateral adrenal hemorrhage, hypotension, and death. Complications: hearing loss, neurologic deficits.
Neisseria meningitidis: diagnostic tests
Diagnosis includes gram stain of CSF (shows gram-negative diplococci inside neutrophils), culture on chocolate agar or Thayer-Martin medium, and PCR of CSF or blood. Latex agglutination detects capsular polysaccharide. Blood cultures often positive. Rapid diagnosis critical due to rapid progression.
Neisseria meningitidis: immunity
Immunity depends on antibodies against the capsule. Complement (especially C5–C9) is important for killing. Deficiency in terminal complement increases risk. Natural immunity increases with age due to exposure. Vaccines stimulate protective antibodies, but type B capsule is poorly immunogenic due to similarity to human neural tissue.
Neisseria meningitidis: treatment
Empiric treatment: intravenous ceftriaxone or penicillin G. Rifampin, ciprofloxacin, or ceftriaxone used for prophylaxis of close contacts. Resistance is rare but monitored. Rapid treatment reduces mortality.
Neisseria meningitidis: epidemiology
Carried asymptomatically in nasopharynx, especially in adolescents. Spread by respiratory droplets. Most common in crowded settings (e.g., dorms, military). Highest risk in infants, teens, and complement-deficient individuals. Outbreaks often involve serogroups A, B, C, Y, or W-135 depending on region.
Neisseria meningitidis: prevention and control
Vaccines are available: quadrivalent vaccine (A, C, Y, W-135) and serogroup B vaccine. Recommended for adolescents, high-risk groups, and during outbreaks. Chemoprophylaxis (rifampin, ciprofloxacin, ceftriaxone) for close contacts. Isolation of patients prevents transmission.
Moraxella catarrhalis
Moraxella catarrhalis is a gram-negative diplococcus, oxidase-positive, and part of the normal upper respiratory flora. It causes otitis media, sinusitis, and bronchitis, especially in children and patients with COPD. It produces beta-lactamase, so resistant to penicillin. Treated with amoxicillin-clavulanate, second/third-gen cephalosporins, or macrolides.