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Bacterial meningitis

Bacterial meningitis is a condition in which the layers lining the brain (the meninges) have become inflamed as a result of infection with bacteria. more...

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Symptoms and signs

The classic symptoms of bacterial meningitis are similar to those of other forms of meningitis, including fever, headache, light sensitivity (photophobia), and confusion. Because of the continuity of the meninges and the linings of the spinal cord, movements that place strain on the spinal cord can cause worsening pain. In particular, movement of the neck and stretching of the legs cause a worsening of symptoms.

Clinicians will often attempt to elicit objective evidence of these latter symptoms. Brudzinski's sign (a correlate of nuchal rugidity), is detected when the knees passively flex when the neck is brought forward in a patient lying supine. A similar phenomenon, Kernig's sign, refers to an inability to stretch the hamstrings of an affected patient lying supine. Both are likely reflex responses to attempts to place traction on inflamed dura.

Bacterial meningitis can seldom be distinguished from other forms of meningitis based on symptoms alone, and usually requires lumbar puncture for definitive diagnosis.


Meningitis is diagnosed when the cerebrospinal fluid, obtained via lumbar puncture, reveals the presence of an increased number of leukocytes. The condition is attributed to bacteria when their presence is detected via Gram stain or bacterial culture.


In most cases, the reason that the meninges have become infected is never determined. Occasionally, the infection is the result of direct bacterial invasion from infections of adjacent structures, such as the paranasal sinuses or the inner ear. The latter is seen more commonly in children with untreated otitis media, although it should be noted that the true incidence of this complication and the ability of antibiotics to prevent it is a matter of controversy. Finally, bacteria can reach the meninges via the bloodstream, in a phenomenon known as hematogenous spread. In this situation, the most common predisposing infection is bacterial endocarditis, an infection of the structures of the heart.


The most common organisms involved in bacterial meningitis include Neisseria meningitidis (or meningococcus), Streptococcus pneumoniae (G001), Haemophilus influenzae (G000), and Staphylococcus aureus (G003). Less common bacterial causes include Listeria monocytogenes, Staphylococcus and Escherichia coli. In developing countries, Mycobacterium tuberculosis is a common cause of bacterial meningitis. The less common organisms are particularly found in elderly or immunocompromised individuals.


The mainstay of treatment for bacterial meningitis is antibiotic therapy. Empiric therapy, directed at the most common organisms, is provided until a microbiologic diagnosis is made. The initiation of antibiotics in a patient suspected to have bacterial meningitis should not be delayed while a diagnosis is made, due to the high incidence of complications in untreated patients—including brain damage, hearing loss, and death.


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Issues in the management of bacterial meningitis
From American Family Physician, 10/1/97 by Allan R. Tunkel

The approach to the patient with acute bacterial meningitis depends on prompt recognition of the clinical syndrome and performance of a lumbar puncture to determine whether the cerebrospinal fluid values are consistent with the diagnosis. This article outlines the typical clinical features of and diagnostic approach to the patient with bacterial meningitis and discusses recommendations for antimicrobial and adjunctive therapies.

Clinical Features

More than 85 percent of patients with acute bacterial meningitis present with the classic triad of fever, headache and stiff neck.[1] The meningismus may be subtle, marked or accompanied by Kernig's and/or Brudzinski's signs (which occur in about 50 percent of adult patients). Other signs and/or symptoms include vomiting (35 percent of patients) seizures (30 percent of patients), and cranial nerve palsies and focal cerebral signs (10 to 20 percent of patients). Papilledema occurs in less than 1 percent of patients during the early phase of infection, and its presence should suggest an alternative diagnosis.

Some categories of patients may not present with many of these classic symptoms and/or signs. In neonates, clinical clues to the presence of meningitis include temperature instability (hypothermia or hyperthermia), listlessness, high-pitched crying, fretfulness, lethargy, refusal to eat, a weak sucking response, irritability, vomiting, diarrhea and respiratory distress.[2] Because neonates usually do not have meningismus, a change in the child's affect or state of alertness is one of the most important signs. A bulging fontanelle may occur late in the course of the disease in one third of neonates. Forty percent of neonates have seizures. In the elderly patient with bacterial meningitis, the presentation may be insidious, with lethargy or obtundation, no fever and variable signs of meningeal irritation.[3] Examination of cerebrospinal fluid in these patients is crucial in order to diagnose bacterial meningitis.

Diagnostic Evaluation

Examination of cerebrospinal fluid values following lumbar puncture is necessary to make a definitive diagnosis of bacterial meningitis; typical findings are shown in Table 1. In patients with typical cerebrospinal fluid findings of bacterial meningitis and a negative cerebrospinal fluid Gram stain, several other laboratory tests are available to assist in making an etiologic diagnosis.[4]

TABLE 1 Typical Cerebrospinal Fluid Values in Patients with Bacterial Meningitis

Duration of Therapy

The duration of antimicrobial therapy in patients with bacterial meningitis has traditionally been from 10 to 14 days for non-meningococcal isolates. However, several studies have documented that seven days of therapy is safe and effective for H. influenzae type b meningitis, although treatment durations must be individualized and some patients may require longer courses. Meningococcal meningitis can be treated for seven days with intravenous penicillin, although some authors have suggested that four days of therapy is adequate.

In patients with bacterial meningitis caused by enteric gram-negative bacilli, treatment should be continued for three weeks because of the high rate of relapse in patients treated with shorter courses of therapy. S. pneumoniae meningitis should be treated for 10 to 14 days. Antimicrobial therapy lasting from 14 to 21 days is recommended for meningitis caused by L. monocytogenes, Staphylococcus aureus and S. agalactiae. However, it is important to note that these treatment durations are based more on tradition than on rigidly standardized clinical trials.[1] Table 4 summarizes current recommendations for the duration of antibiotic treatment.

[22.] Wenger JD, Hightower AW, Facklam RR, Gaventa S, Broome CV. Bacterial meningitis in the United States, 1986: report of a multistate surveillance study. J Infect Dis 1990;162:1316-23.

[23.] Lebel MH, Hoyt MJ, McCracken GH Jr. Comparative efficacy of ceftriaxone and cefuroxime for treatment of bacterial meningitis. J Pediatr 1989; 114:1049-54.

[24.] Schaad UB, Suter S, Gianella-Borradori A, Pfenninger J, Auckenthaler R, Bernath O, et al. A comparison of ceftriaxone and cefuroxime for the treatment of bacterial meningitis in children. N Engl J Med 1990,322:141-7.

[25.] Fong IW, Tomkins KB. Review of Pseudomonas aeruginosa meningitis with special emphasis on treatment with ceftazidime. Rev Infect Dis 1985;7:604-12.

[26.] Rodriguez WJ, Khan WN, Cocchetto DM, Feris J, Puig JR, Akram S. Treatment of Pseudomonas meningitis with ceftazidime with or without concurrent therapy Pediatr Infect Dis J 1990;9:83-7.

[27.] Tunkel AR, Scheld WM. Treatment of bacterial meningitis. In: Hooper DC, Wolfson JS, eds. Quinolone ant/microbial agents. Washington, D.C.: American Society for Microbiology, 1993:481-95.

[28.] Cherubin CE, Appleman MD, Heseltine PN, Khayr W, Stratton CW. Epidemiological spectrum and current treatment of listeriosis. Rev Infect Dis 1991;13:1108-14.

[29.] Richards SJ, Lambert CM, Scott AC. Recurrent Listeria monocytogenes meningitis treated with intraventricular vancomycin [Letter]. J Antimicrob Chemother 1992,29:351-3.

[30.] Quagliarello V, Scheld WM. Bacterial meningitis: pathogenesis, pathophysiology, and progress. N Engl J Med 1992,327:864-72.

[31.] Tunkel AR, Scheld WM. Pathogenesis and pathophysiology of bacterial meningitis. Clin Microbiol Rev 1993,6:118-36.

[32.] Odio CM, Faingezicht I, Paris M, Nassar M, Baltodano A, Rogers J, et al. The beneficial effects of early dexamethasone administration in infants and children with bacterial meningitis. N Engl J Med 1991;324:1525-31.

[33.] Schaad UB, Lips U, Gnehm HE, Blumberg A, Heinzer I, Wedgwood J. Dexamethasone therapy for bacterial meningitis in children. Lancet 1993;342:457-61.

[34.] Paris MM, Hickey SM, Uscher MI, Shelton S, Olsen KD, McCracken GH Jr. Effect of dexamethasone on therapy of experimental penicillin and cephalosporin-resistant pneumococcal meningitis. Antimicrob Agents Chemother 1994;38:1320-4.

[35.] Lyons MK, Meyer FB. Cerebrospinal fluid physiology and the management of increased intracranial pressure. Mayo Clin Proc 1990;65:684-707.

[36.] Ashwal S, Perkin RM, Thompson JR, Schneider S, Tomasi LG. Bacterial meningitis in children: current concepts of neurologic management. Curr Prob Pediatr 1994;24:267-84.

ALLAN R. TUNKEL, M.D., PH.D. is associate professor of medicine and associate chair for education at Allegheny University of the Health Sciences, MCP * Hahnemann School of Medicine, Philadelphia, and director of the internal medicine residency program at Allegheny University Hospitals, Philadelphia. Dr. Tunkel graduated from the UMDNJ--New Jersey Medical School, Newark, where he also received his Ph.D. He completed an internship and residency in internal medicine at the Medical College of Pennsylvania Hospital, Philadelphia. Dr. Tunkel also completed a fellowship in infectious diseases at the University of Virginia Health Sciences Center, Charlottesville.

W. MICHAEL SCHELD, M.D. is professor of medicine and neurosurgery, associate chair for residency programs and director of the internal medicine residency training program at the University of Virginia School of Medicine, Charlottesville. He received his medical degree from Cornell University Medical College, New York City and completed an internship, residency and fellowship in infectious diseases at the University of Virginia Health Sciences Center.

Address correspondence to Allan R. Tunkel, M.D., Ph.D. Department of Internal Medicine, Allegheny University Hospitals, MCP, 3300 Henry Ave., Philadephia, PA 19129.

Dr. Tunkel is a member of the speaker's bureaus for Pfizer Inc. and Roche Pharmaceuticals.

COPYRIGHT 1997 American Academy of Family Physicians
COPYRIGHT 2004 Gale Group

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