More Merck Manual

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I posted too fast - here is the rest of my post

http://www.merck.com/pubs/mmanual/section13/chapter158/158h.htm

Systemic Candidiasis

http://www.merck.com/pubs/mmanual/section14/chapter176/176d.htm

Subacute And Chronic Meningitis

Etiology

Subacute and chronic meningitis may develop with fungal infections, TB, Lyme

disease, AIDS, syphilis, or noninfectious disorders, such as sarcoidosis,

Behçet's syndrome, and neoplasms--eg, leukemia, lymphomas, melanomas,

metastatic carcinoma to the brain, and gliomas (particularly glioblastoma,

ependymoma, and medulloblastoma). Subacute meningitis may result from

chemical reactions to certain intrathecal injections. Chronic meningitis

must be distinguished from acute meningitis or encephalitis, in which

recovery is protracted, and from recurrent meningitis (eg, due to

craniopharyngioma leakage or trauma).

Immunosuppressive drugs and the AIDS epidemic have increased the incidence

of CNS fungal infections, both of the meninges and of brain tissue.

Cryptococcus sp is the most common cause in those with AIDS, Hodgkin's

disease, or lymphosarcoma and in those using high-dose corticosteroids long

term. Coccidioides, Mucor, Candida, Actinomyces, Histoplasma, and

Aspergillus sp are less common (see Ch. 158).

Neoplastic meningitis with diffuse leptomeningeal involvement is a

continuing problem in acute lymphoblastic leukemia, especially for children

being treated with antileukemic drugs, which do not cross the blood-brain

barrier. Rarely, the first sign of malignant disease is a subacute meningeal

inflammation.

Symptoms, Signs, and Diagnosis

Manifestations are similar to those in acute meningitis but evolve more

slowly--over weeks rather than days. Fever may be minimal. In neoplastic

meningitis, headache, dementia, backache, and cranial and peripheral nerve

palsies are common. Chronic communicating hydrocephalus may be a

complication. The course may be progressive and fatal within a few weeks or

months.

Because cerebral symptoms evolve slowly, differential diagnosis includes

structural lesions (eg, brain tumors, abscesses, subdural effusions). Active

TB elsewhere in the body or a known malignancy suggests the etiology, but

CSF must be examined to establish a diagnosis unless contraindicated. CSF

cell count is generally < 1000/µL with lymphocytic predominance; glucose is

frequently low, and protein may be high (see Table 165-3). In neoplastic

meningitis, CSF findings include lymphocytic pleocytosis, low glucose,

slightly elevated protein, and, frequently, elevated pressure. In syphilis,

CSF findings resemble those in other subacute meningitides, except glucose

is usually normal; CSF and blood VDRL (Venereal Disease Research

Laboratories) test and STS results are usually positive.

Microscopic examination or culture of CSF is needed to identify malignant

cells or a causative organism. Because most infections must be treated for a

long time with highly specific drugs, identification of the organism is

essential before therapy is begun. Fungi can be identified in centrifuged

sediment; TB, by acid-fast or immunofluorescent staining. Identification of

tumor cells, TB, and some fungi (eg, aspergilli) depends on the volume of

CSF examined or cultured. As much as 30 to 50 cc of CSF (from serial lumbar

punctures) may be required.

Treatment

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