Diagnostic Approach to a Patient with Suspected Central Nervous System Infection

Question 1: Where Is the Inflammation?

Microorganisms have a tropism to certain anatomic sites both in the CNS and outside. So anatomic localization helps identify the etiology or organism . S. pneumoniae and Neisseria meningitidis have tropism to the leptomeninges or pia-arachnoid layer. Herpes simplex virus-1 (HSV-1) has tropism to the medial temporal lobe, and West Nile virus has tropism to the basal ganglia. At a cellular level, poliovirus infects the anterior horn cells, and JC virus infects the oligodendrocytes, which produce myelin in the CNS. Anatomic localization can be done based on history, neurologic examination, imaging—especially with magnetic resonance imaging (MRI) of the CNS, and CSF analysis. A patient with meningitis can have headache, meningeal signs, leptomeningeal enhancement on a T1 post-contrast MRI of the brain, and increased white blood cells, with a low glucose on routine CSF analysis. The patient with HSV-1 encephalitis can present with amnesia and temporal lobe changes on brain MRI. Often clues to the diagnosis can be present at anatomic sites outside the CNS. Nocardia causes brain abscesses and lung nodules. Sarcoidosis causes basilar leptomeningeal meningitis, but a clue to the diagnosis could be bilateral hilar lymphadenopathy. Classifying the patient into the following anatomic syndromes is diagnostically useful, as that gives clues about the etiology or organism:

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  Meningitis: Leptomeningeal meningitis is inflammation of the pia–arachnoid layer, and pachymeningitis is inflammation of the dura.

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  Encephalitis or meningo-encephalitis: This is inflammation within the brain parenchyma with or without meningeal involvement.

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  Myelitis or myelo-radiculitis: This is inflammation of the spinal cord with or without involvement of the spinal nerve roots.

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  Space-occupying, ring-enhancing lesions in the brain on post-contrast CNS imaging.

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  Stroke or strokelike syndromes involving vascular territories of the brain ( Fig. 14.1 ).

  

Question 2: How Long Has It Been Going On?

Some microorganisms cause acute infections that progress over days, and some cause chronic infections that progress over weeks to months. Subacute infections, which are generally around 2 to 3 weeks in duration, could be either an acute infection that has lingered longer or a chronic infection that was diagnosed earlier. Virulent fast-growing bacteria like S. pneumoniae or N. meningitidis cause severe acute meningitis, but indolent slow-growing organisms like fungi and Mycobacterium tuberculosis cause chronic meningitis. A patient can also have recurrent acute CNS infections. This could be because of an immunodeficiency making one prone to a CNS infection multiple times. An example would be recurrent meningococcal infection with terminal complement deficiencies. Recurrent acute meningitis could also be from recurrent reactivation of a latent virus like HSV-2, which causes Molleret meningitis or benign recurrent lymphocytic meningitis.

Question 3: Is It Community Acquired or Health Care Acquired?

In the CNS, unlike other anatomic sites, hospital- or health care–acquired infections usually occur in the context of either neurotrauma or neurosurgery. The skull and the meninges are an effective barrier and defense against nosocomial pathogens entering the CNS. Only when the skull and dura are breached by trauma or surgery do hospital-acquired pathogens like Escherichia coli and Staphylococcus aureus find a portal of entry into the CNS. These organisms, unlike organisms that cause community-acquired bacterial meningitis like S. pneumoniae or N. meningitidis, lack the capacity to directly invade the CNS. It would be unusual to have a nosocomial pathogen causing CNS infection in a patient on the non-neurosurgical or non–critical care wards.