Neisseria & Moraxella
A killer of young adults, a master of disguise and an ear-infection cousin
Identification
Shared features. Neisseria and Moraxella are gram-negative, oxidase-positive diplococci that pair like kidney beans. Neisseria grow on chocolate agar; Thayer-Martin agar (chocolate base with vancomycin, colistin, nystatin and trimethoprim) suppresses normal flora so they can be recovered from throat, genital or rectal specimens.
| Feature | N. meningitidis | N. gonorrhoeae | M. catarrhalis |
|---|---|---|---|
| Sugars fermented | Glucose and maltose | Glucose only | Neither |
| Capsule and vaccine | Polysaccharide capsule; MenACWY and MenB vaccines | No capsule; no vaccine | No vaccine |
| Spread | Respiratory droplets | Sexual contact; vaginal delivery | Upper-airway colonizer |
| Main diseases | Meningitis, meningococcemia | Urethritis, cervicitis, PID, DGI, ophthalmia neonatorum | Otitis media, sinusitis, COPD exacerbations |
| Treatment | Ceftriaxone or penicillin G | Ceftriaxone ± doxycycline | Amoxicillin-clavulanate, cephalosporin or macrolide |
Meningococcal disease
Carriage and spread. N. meningitidis colonizes the nasopharynx of healthy carriers and spreads by respiratory droplets, so crowding in college dormitories and military barracks favors outbreaks. Serogroups B, C and Y cause most US disease; serogroup A historically drove epidemics across the sub-Saharan meningitis belt.
Virulence. The polysaccharide capsule resists phagocytosis. Lipooligosaccharide (LOS), shed in large amounts in outer-membrane blebs, is the endotoxin behind the cytokine storm, and IgA protease and pili aid colonization.
Clinical syndromes. Meningitis brings fever, headache and neck stiffness. Meningococcemia starts with fever and petechiae that can coalesce into purpura fulminans with DIC, skin necrosis and limb loss. Bilateral adrenal hemorrhage (Waterhouse-Friderichsen syndrome) causes acute adrenal insufficiency and refractory shock. Patients deteriorate within hours, so antibiotics must not wait for imaging or lumbar puncture.
Terminal complement deficiency (C5–C9) and C5 inhibitors such as eculizumab (used for PNH and atypical HUS) remove the membrane attack complex that lyses Neisseria, causing recurrent or overwhelming meningococcal disease and disseminated gonococcal infection. Screen with CH50, and vaccinate before starting eculizumab.
Treating and preventing meningococcal disease
- Treat the patientceftriaxone immediately; penicillin G once susceptibility is known; droplet precautions for the first 24 hours of therapy
- Protect close contactshousehold and daycare contacts and anyone exposed to oral secretions receive rifampin, ciprofloxacin or single-dose IM ceftriaxone, the choice in pregnancy
- VaccinateMenACWY conjugate at 11–12 years with a booster at 16; protein-based MenB vaccines for high-risk groups and outbreaks
High-risk groups. Asplenia, complement deficiency or complement-inhibitor therapy, HIV, military recruits, travelers to the meningitis belt, microbiologists and first-year students in residence halls. The serogroup B capsule is polysialic acid resembling human neural cell adhesion molecule, so it is poorly immunogenic; MenB vaccines target surface proteins such as factor H-binding protein.
Gonococcal disease
Immune evasion. Pili attach to urethral and cervical epithelium and undergo antigenic variation (pilin gene recombination) and phase variation (switching on and off), as do Opa proteins. With no capsule and an ever-changing surface, reinfection is common and no vaccine exists.
- Men: purulent urethritis with dysuria.
- Women: often silent cervicitis that ascends to PID (salpingitis, tubo-ovarian abscess, infertility, ectopic pregnancy) or Fitz-Hugh-Curtis perihepatitis with RUQ pain and violin-string adhesions.
- Other mucosa: pharyngitis and proctitis.
- Disseminated infection: tenosynovitis, a few painless extremity pustules and migratory polyarthralgia, or a purulent monoarthritis, usually of the knee; a classic cause of septic arthritis in sexually active young adults.
- Neonates: hyperpurulent ophthalmia neonatorum 2–5 days after vaginal delivery, which can perforate the cornea.
Diagnosis and treatment. NAAT of urine or site-specific swabs is the test of choice; in symptomatic men, gram-negative diplococci inside neutrophils on a urethral Gram stain are diagnostic, and culture allows susceptibility testing. Uncomplicated infection is treated with one IM dose of ceftriaxone, adding 7 days of doxycycline when chlamydia has not been excluded; partners are treated and patients retested at about 3 months. Resistance has made fluoroquinolones obsolete.
Erythromycin 0.5% ophthalmic ointment at birth prevents gonococcal ophthalmia; established disease needs systemic ceftriaxone. Chemical irritation from prophylactic agents appears on the first day, whereas chlamydial conjunctivitis appears later (days 5–14) and is not reliably prevented by the ointment.
Moraxella catarrhalis
Airway pathogen. This gram-negative, oxidase-positive diplococcus colonizes the upper airway. It is the third common cause of otitis media and sinusitis in children, after S. pneumoniae and nontypeable H. influenzae, and triggers COPD exacerbations in adults. Nearly all strains produce β-lactamase, so amoxicillin alone fails; amoxicillin-clavulanate, a cephalosporin or a macrolide is used. On agar, its colonies slide intact across the plate like a hockey puck.