Chapter 136. Meningococcal Infections (Part 7)

ComplicationsPatients with meningococcal meningitis may develop cranial nerve palsies, cortical venous thrombophlebitis, and cerebral edema. Children may develop subdural effusions. Permanent sequelae can include mental retardation, deafness, and hemiparesis. The major long-term morbidity of fulminant meningococcemia is the loss of skin, limbs, or digits that results from ischemic necrosis and infarction.Diagnosis Few clinical clues help the physician distinguish the patient with early meningococcal disease from patients with other acute systemic infections. ...
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Chapter 136. Meningococcal Infections (Part 7) Chapter 136. Meningococcal Infections (Part 7) Complications Patients with meningococcal meningitis may develop cranial nerve palsies,cortical venous thrombophlebitis, and cerebral edema. Children may developsubdural effusions. Permanent sequelae can include mental retardation, deafness,and hemiparesis. The major long-term morbidity of fulminant meningococcemia isthe loss of skin, limbs, or digits that results from ischemic necrosis and infarction. Diagnosis Few clinical clues help the physician distinguish the patient with earlymeningococcal disease from patients with other acute systemic infections. Themost useful clinical finding is the petechial or purpuric rash (see Fig. 52-5), but itmust be differentiated from the petechial lesions seen with gonococcemia (see Fig.137-2), Rocky Mountain spotted fever (see Fig. 167-1), hypersensitivity vasculitis(see Fig. 52-4), endemic typhus, and some viral infections. In one case series, one-half of the adults with meningococcal bacteremia had neither meningitis nor arash. The definitive diagnosis is established by recovering N. meningitidis, itsantigens, or its DNA from normally sterile body fluids (e.g., blood, CSF, orsynovial fluid) or from skin lesions. Meningococci grow best on Mueller-Hintonor chocolate blood agar at 35˚C in an atmosphere that contains 5–10% CO2.Specimens should be plated without delay. N. meningitidis bacteria are oxidase-positive, gram-negative diplococci that typically utilize maltose and glucose. A Grams stain of CSF reveals intra- or extracellular organisms in ~85% ofpatients with meningococcal meningitis. The latex agglutination test formeningococcal polysaccharides in the CSF is less sensitive. PCR amplification ofDNA in buffy coat or CSF samples is more sensitive than either of these tests; likethe latex agglutination test, PCR is unaffected by prior antibiotic therapy, asneither method requires viable organisms. Throat or nasopharyngeal specimens should be cultured on Thayer-Martinmedium, which suppresses the competing oral flora. Throat or nasopharyngealcultures are recommended only for research or epidemiologic purposes, since apositive result merely confirms the carrier state and does not establish theexistence of systemic disease. Meningococcal Infections: Treatment (Table 136-1) A third-generation cephalosporin, such as cefotaxime orceftriaxone, is preferred for initial therapy. One of these cephalosporins incombination with other agents may cover other bacteria (such as Streptococcuspneumoniae and Haemophilus influenzae) that can cause the same syndromes(Chap. 376). Penicillin G remains an acceptable alternative for confirmed invasivemeningococcal disease in most countries. However, the prevalence ofmeningococci with reduced susceptibility to penicillin has been increasing, andhigh-level penicillin resistance has been reported. Other options includemeropenem. In the patient who is allergic to β-lactam drugs, chloramphenicol is asuitable alternative; chloramphenicol-resistant meningococci have been reportedfrom Vietnam and France. The newer fluoroquinolones gatifloxacin,moxifloxacin, and gemifloxacin have excellent in vitro activity against N.meningitidis, with measurable central nervous system (CNS) penetration, andappear promising in animal models. Patients with meningococcal meningitisshould be given antimicrobial therapy for at least 5 days. While glucocorticoidtherapy for meningitis in adults is controversial, many experts administerdexamethasone, beginning if possible before antibiotic therapy is initiated; theschedule is 10 mg IV given 15–20 min before the first antibiotic dose and thenevery 6 h for 4 days. The data regarding steroid use to diminish CNS inflammationare strongest for H. influenzae and S. pneumoniae meningitis, especially inchildren. Table 136-1 Antibiotic Treatment, Chemoprophylaxis, andVaccinations for Invasive Meningococcal Disease Antibiotic Treatmenta 1. Ceftriaxone 2 g IV q12h (100 mg/kg per day) or cefotaxime 2 g IV q4h 2. For penicillin-sensitive N. meningitidis: Penicillin G 18–24 million unitsper day in divided doses q4h (250,000 units/kg per day) 3. Chloramphenicol 75–100 mg/kg per day in divided doses q6h 4. Meropenem 1.0 g (children, 40 mg) IV q8h 5. In an outbreak setting in developing countries: Long-actingchloramphenicol in oil suspension (Tifomycin), single dose Adults: 3.0 g (6 mL) Children 1–15 years old: 100 mg/kg Children Rifampin (oral)Adults: 600 mg bid for 2 daysChildren ≥1 month old: 10 mg/kg bid for 2 daysChildren Vaccinationc A, C, Y, W-135 vaccine (Memomune, Aventis Pasteur) or A, C vaccine Single 0.5-mL subcutaneous injection New C; A, C; and A, C, Y, W-135 meningococcal conjugate vaccinesd a Patients with meningococcal meningitis should receive antimicrobialtherapy for at least 5 days. b Use is recommended for close contacts of cases or if ceftriaxone is notused for primary treatment. c At present, use is generally limited to the control of epidemics and toindividuals with increased risk of meningococcal disease. Vaccine efficacy wanesafter 3–5 years, and vaccine is not effective in recipients