Acute Meningitis

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The presentation is dramatic with clinical manifestations developing over only a few hours to days. High fever, headache, photophobia, stiff neck, and altered mental state are the typical presenting symptoms. Headache and vomiting due to raised intracranial pressure may be a presenting manifestation in young children. Infants, immune suppressed individuals, and the elderly may not develop neck stiffness and hence may lack the cardinal signs of meningeal irritation. Most often other clinical signs or specific predisposing conditions may be absent. However, if present, they may offer important diagnostic clues.

Etiology

The leading causes of acute meningitis are viruses and bacteria. The most dreaded of all is meningoccal meningitis. The presence of purpura or petechial rash on the trunk, lower extremities, mucous membranes including conjunctiva but absence in the nail beds is highly suggestive but not diagnostic of meningococcemia. Children with fulminant meningococcal septicemia may develop the Waterhouse-Friderichsen syndrome characterized by cardiovascular collapse associated with hypoadrenalism and disseminated intravascular coagulation.

The leading cause of acute bacterial meningitis is H. influenza in children; however, the incidence seems to be decreasing following the introduction of an effective vaccine. It is frequently associated with epiglotitis or otitis media. The most common cause of bacterial meningitis in adults is Streptococcus pneumoniae. Medical conditions commonly associated with pneumococcal meningitis include pneumonia, otitis media, head

From: Management of Antimicrobials in Infectious Diseases Edited by: A. G. Mainous III and C. Pomeroy © Humana Press Inc., Totowa, NJ

trauma associated with CSF leaks, and alcoholism. Pneumococci are also the most common cause of meningitis in children with sickle-cell anemia and other aspleenic states.

Listeria monoctyogenes is an important cause of neonatal meningitis and transmitted via the maternal genital tract. Diabetics, renal transplant patients, alcoholics, the elderly, and sometimes normal individuals may also develop Listeria meningitis by ingesting contaminated food. Listeria typically causes a rhombencephalitis affecting predominately the post-fossa structures. Patients with neutropenia are at particular risk for meningitis due to Pseudomonas aeruginosa and other enterobacteria. Because of their inability to mount an inflammatory response, these patients may have minimal meningeal response.

The most common cause of viral meningitis are enteroviruses followed by arboviruses. Establishing the exact viral etiology is of academic and epidemiological interest because no specific treatment is currently available for these viruses. The only exception is human immunodeficiency virus (HIV) infection which may present with an aseptic meningitis at the time of seroconversion.

Noninfectious causes of acute meningitis include systemic lupus erythematosus, rare reactions to nonsteroidal antiinflammatory drugs, and diseases of uncertain etiology such as Mollaret's meningitis (herpes virus-2 implicated in some cases) (1) and Behcet's syndrome. Additionally, Subarachnoid-hemorrhage and pituitary apoplexy may present as acute meningitis.

Laboratory Diagnosis

In a patient with suspected meningitis, there exists an urgency to establish the diagnosis by a CSF evaluation because it has been clearly shown that delay in treatment is the most critical factor in determining morbidity and mortality with bacterial meningitis. However, it has become common practice to obtain a computed to mography (CT) or magnetic resonance imaging (MRI) scan prior to performing a lumbar puncture even in the absence of focal neurological signs. Such a practice may be justified in situations where neuroimaging can be obtained immediately, the patient does not appear seriously ill, or if there is uncertainty about the neurological findings. However, in the absence of focal neurological signs and/or papilledema, a lumbar puncture can be safely performed without first obtaining a CT or MRI scan. Following the lumbar puncture, antimicrobial therapy should be started promptly pending results. Because antibiotics take about 24 h to sterilize the cerebrospinal fluid (CSF), lumbar puncture can be done after starting antibiotics within the same day.

In general viral meningitis causes a lymphocytosis in the CSF with a normal protein and glucose, while bacterial meningitis causes an elevation of the polymorphonuclear cells and protein but a decrease in glucose in the CSF. The presence of hemorrhage in the CSF may suggest HSV-1 meningoencephalitis. Exceptions to these CSF patterns include hypoglycorrhachia with some viruses and polymorphonuclear pleocytosis early in the course of viral meningitis.

Treatment of Bacterial Meningitis

Empirical Therapy of Community Acquired Bacterial Meningitis

The most common organism in nonneonates is Streptococcus pneumoniae. However, increasing strains are resistant to penicillin and some are resistant to third-generation cephalosporins. Cephalosporin-resistant strains are usually a problem in children and not

Table 1

Antimicrobial Therapy of CNS Bacterial Infections Based on Pathogen

Organism

Antibiotic

Comments

Streptococcus pneumoniae Sensitive to penicillin Relatively resistant to penicillin Resistant to penicilün

Neisseria meningitidis Gram-negative bacilli

(except P. aeruginosa) Pseudomanas aeruginosa

Listeria monocytogenes

Staphylococci Methicillin-resistant staphylococcus Streptoccocus agalactiae Haemophilus influenzae

Enterobacteriaceae

Penicillin G

Ceftriaxone or cefotaxime Vancomycin plus cefotaxime or ceftriaxone + intraventricular vancomycin Penicillin G or ampicillin Ceftriaxone or cefotraxime

Ceftazidime

Ampicillin

Nafcillin Vancomycin

Ampicillin or penicillin Cefotaxime or ceftriaxone

Cefotaxime or ceftriaxone

May add aminoglycoside in first week of treatment.

Cephalosporins are in active.

May add rifampicin.

Increasingly strains are resistant to ampicillin or chloramphenicol or both.

adults (2). Hence for relatively penicillin-resistant strains (minimal inhibitory concentration 0.1 to 1.0 ^g/mL) a third-generation cephalosporin (cefotaxime or ceftriaxone) is the drug of choice. For highly penicillin-resistant strains or cephalosporin-resistant strains (minimal inhibitory concentration >2.0 ^g/mL), vancomycin with or without rifampicin is the antibiotic of choice. See table 1 for recommended drug therapy for other organisms. Patients with neutropenia and meningitis should be treated with a third-generation cephalosporin (ceftazidime for Pseudomonas) and vancomycin (3).

Adjunctive Steroid Therapy

The inflammatory process, although essential to control the infection, can also be detrimental to the host due to the release of neurotoxic cytokines. Several studies have confirmed the benefit of concomitant use of dexamethasone therapy in children (2 mo of age). The American Academy of Pediatrics recommends 0.6 mg/g/d in four divided dosages given intravenously for the first 4 d of antibiotic therapy. Current recommendation is to start the first dose of steroids 20 min before initiation of antibiotic therapy. The most serious side effect of dexamethasone therapy is gastrointestinal bleeding. For this reason, concomitant intravenous H2 antagonist is recommended. The greatest benefit of steroid therapy has been in the prevention of sensorineural hearing loss due to H. influenzae meningitis in children (reviewed in ref. 4).

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