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Bacterial infections 

Bacterial infections

Bacterial infections

Diederik van de Beek

, Jeremy Farrar

, and Guy Thwaites

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date: 28 March 2017

Bacterial meningitis occurs in a number of clinical situations, including spontaneous (the most important category), post-traumatic, and device-associated (relating to cerebrospinal fluid shunts and drains). Each of these is associated with a particular pattern of infecting organisms, clinical presentation and outcome, but overall there is high morbidity and mortality.


(1) Adult spontaneous community-acquired meningitis—80 to 85% of cases are caused by Neisseria meningitidis or Streptococcus pneumoniae in most countries, with Listeria monocytogenes, aerobic Gram-negative bacilli (e.g. Escherichia coli), Haemophilus influenzae and Staphylococcus aureus causing most of the others. Streptococcus suis serotype 2 is an important cause in Asia. (2) Post-traumatic meningitis—most hospital-acquired infections are caused by aerobic Gram-negative bacilli; S. pneumoniae causes most community acquired disease. (3) Device-associated meningitis—most infections are nosocomial and caused by coagulase-negative staphylococci or Staph. aureus.

Patients with recurrent meningitis frequently have an underlying anatomical or immunological defect (particularly hypogammaglobulinaemia or complement deficiencies). In some parts of the world, HIV infection has altered the pattern of aetiological agents (and presentation and outcome of meningitis), with Mycobacterium tuberculosis increasingly common.

Clinical features

(1) Community-acquired meningitis—the classic triad of fever, nuchal rigidity, and altered mental status is present in just under 50% of patients. Other manifestations include rashes (particularly with meningococcal disease), seizures and focal neurological signs. Clinical tests of ‘meningeal irritation’ (e.g. Kernig’s sign, Brudzinski’s signs, and nuchal rigidity) are unreliable. Tuberculous, cryptococcal, and other fungal meningitides usually develop more slowly than pyogenic bacterial disease. (2) Post-traumatic bacterial meningitis—often indistinguishable clinically from spontaneous meningitis. (3) Device-associated meningitis—usual presentation is insidious, with features of shunt blockage such as headache, vomiting, fever, and a decreasing level of consciousness.

Investigation and treatment

Speed is of the essence—the first step in the management of acute bacterial meningitis is to obtain blood cultures and start antimicrobial therapy and (when indicated) adjunctive dexamethasone, along with providing any necessary supportive care. In the United Kingdom, family doctors are advised to give parenteral antibiotics before transferring the patient to hospital if meningococcal meningitis is suspected.

Lumbar puncture—this is the diagnostic procedure of choice if the diagnosis of bacterial meningitis cannot be ruled out, and can be safely performed without a preceding cranial CT scan to detect brain shift and evidence of herniation provided that the patient does not have any of the following: (1) signs suggesting a space-occupying lesions—papilloedema or focal neurological signs, excluding cranial nerve palsy, (2) new-onset seizure, (3) moderate-to-severe impairment of consciousness, or (4) an immunocompromised state.

The cerebrospinal fluid—the opening pressure is usually raised. Frank turbidity instantly suggests the diagnosis of pyogenic meningitis. On microscopic examination the white blood cell count is typically over 1000 cells/μ‎l, and over 100 cells/µl in over 90% of cases, with neutrophils usually predominant, and organisms may be seen after Gram or acridine orange staining. Elevated protein and depressed glucose concentrations aid in distinction from viral meningitis. Culture of organisms has a sensitivity of about 80% in untreated cases, but this is much reduced in those who have been partially treated, when lumbar puncture results must be interpreted with particular care when attempting to differentiate viral, tuberculous, and bacterial disease. Rapid bacterial antigen tests and tests based on the polymerase chain reaction (PCR) for bacterial DNA are increasingly used.

Antimicrobial therapy—the choice of initial treatment is based on knowledge of which bacteria most commonly cause the disease, based on age and/or clinical circumstances, and on local antimicrobial susceptibility patterns. Adults with community-acquired disease would typically receive initial treatment with (1) vancomycin, with (2) ceftriaxone or cefotaxime, with (if age >50 years, alcoholism, or altered immune status) (3) ampicillin, which would then be modified based on cerebrospinal fluid culture results and in vitro susceptibility testing.

Dexamethasone—this appears to be beneficial in HIV-negative adults with confirmed bacterial meningitis, but there is no evidence for a beneficial effect in those who are HIV-positive and not on antiretroviral drugs.

Complications—these include meningoencephalitis, systemic compromise, stroke, and raised intracranial pressure. Various adjunctive therapies have been described to improve outcome in such patients, including anti-inflammatory agents, anticoagulants, and strategies to reduce intracranial pressure, but there are few randomized clinical studies with which to judge whether they are effective.


The incidence of bacterial meningitis can be reduced by (1) vaccination—this is available against H. influenzae type b, pneumococcal and meningococcal disease; (2) chemoprophylaxis—given to close adult contacts of meningococcal disease (and children of <4 years exposed to H. influenzae type b).

Acknowledgement: The authors and editors acknowledge the inclusion of material from the chapter by D A Warrell, J J Farrar, and D W M Crook in the 4th edition of the Oxford Textbook of Medicine.

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