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Chapter 136. Meningococcal Infections (Part 7)

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Chapter 136. Meningococcal Infections (Part 7)

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Complications Patients 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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  1. Chapter 136. Meningococcal Infections (Part 7) Complications Patients 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. The most useful clinical finding is the petechial or purpuric rash (see Fig. 52-5), but it must 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-
  2. half of the adults with meningococcal bacteremia had neither meningitis nor a rash. The definitive diagnosis is established by recovering N. meningitidis, its antigens, or its DNA from normally sterile body fluids (e.g., blood, CSF, or synovial fluid) or from skin lesions. Meningococci grow best on Mueller-Hinton or 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 Gram's stain of CSF reveals intra- or extracellular organisms in ~85% of patients with meningococcal meningitis. The latex agglutination test for meningococcal polysaccharides in the CSF is less sensitive. PCR amplification of DNA in buffy coat or CSF samples is more sensitive than either of these tests; like the latex agglutination test, PCR is unaffected by prior antibiotic therapy, as neither method requires viable organisms. Throat or nasopharyngeal specimens should be cultured on Thayer-Martin medium, which suppresses the competing oral flora. Throat or nasopharyngeal cultures are recommended only for research or epidemiologic purposes, since a positive result merely confirms the carrier state and does not establish the existence of systemic disease. Meningococcal Infections: Treatment
  3. (Table 136-1) A third-generation cephalosporin, such as cefotaxime or ceftriaxone, is preferred for initial therapy. One of these cephalosporins in combination with other agents may cover other bacteria (such as Streptococcus pneumoniae and Haemophilus influenzae) that can cause the same syndromes (Chap. 376). Penicillin G remains an acceptable alternative for confirmed invasive meningococcal disease in most countries. However, the prevalence of meningococci with reduced susceptibility to penicillin has been increasing, and high-level penicillin resistance has been reported. Other options include meropenem. In the patient who is allergic to β-lactam drugs, chloramphenicol is a suitable alternative; chloramphenicol-resistant meningococci have been reported from 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, and appear promising in animal models. Patients with meningococcal meningitis should be given antimicrobial therapy for at least 5 days. While glucocorticoid therapy for meningitis in adults is controversial, many experts administer dexamethasone, beginning if possible before antibiotic therapy is initiated; the schedule is 10 mg IV given 15–20 min before the first antibiotic dose and then every 6 h for 4 days. The data regarding steroid use to diminish CNS inflammation are strongest for H. influenzae and S. pneumoniae meningitis, especially in children.
  4. Table 136-1 Antibiotic Treatment, Chemoprophylaxis, and Vaccinations 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 units per 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-acting chloramphenicol in oil suspension (Tifomycin), single dose Adults: 3.0 g (6 mL) Children 1–15 years old: 100 mg/kg Children
  5. Rifampin (oral) Adults: 600 mg bid for 2 days Children ≥1 month old: 10 mg/kg bid for 2 days Children
  6. 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 antimicrobial therapy for at least 5 days. b Use is recommended for close contacts of cases or if ceftriaxone is not used for primary treatment. c At present, use is generally limited to the control of epidemics and to individuals with increased risk of meningococcal disease. Vaccine efficacy wanes after 3–5 years, and vaccine is not effective in recipients
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