azithromycin may present as a drug-induced aseptic meningitis. Leukocytosis in the CSF with
a polymorphonuclear predominance is typical with drug-induced meningitis, and the clinical
clue to the presence of drug-induced meningitis is the presence of eosinophils in the CSF. In
drug-induced meningitis, the CSF also contains increased protein, but the CSF glucose is rarely
decreased. Red blood corpuscles (RBCs) or an increased CSF lactic acid level are not features of
drug-induced meningitis. Treatment is discontinuation of the offending agent (1,5,16,17).
Serum Sickness
Serum sickness is a systemic reaction to the injection of, or serum-derived antitoxin
derivatives. Since such toxins are not used much anymore, serum sickness is now most
commonly associated with the use of certain medications, includingb-lactam antibiotics,
sulfonamides, and streptomycin among the antimicrobials. Non-antimicrobials associated with
serum sickness include hydralazine, alpha methyldopa, propanolol, procainamide, quinidine,
phenylbutazone, naproxen catapril, and hydantoin. Symptoms typically begin about two
weeks after the initiation of drug therapy and are characterized by fever, arthralgias/arthritis,
and immune complex mediated renal insufficiency. Urticaria, abdominal pain, or lymphaden-
opathy may or may not be present. Neurologic abnormalities are part of the systemic picture
and include a mild meningoencephalitis, which occurs early in the first few days with serum
sickness. Ten percent of patients may have papilledema, seizures, circulatory ataxia, transverse
myelitis, or cranial nerve palsies. The clues to serum sickness systemically are an increased
sedimentation rate, a decreased serum complement, microscopic hematuria/RBC casts, and
hypergammaglobulinemia. The CSF typically shows a mild lymphocytic pleocytosis, protein is
usually normal but may be slightly elevated as is the CSF glucose. The cause of the patient’s
fever and meningeal symptoms may be related to serum sickness if the clinician appreciates
the association of the CNS findings and extra-CNS manifestations of serum sickness.
Treatment is with corticosteroids (1–5).
Collagen Vascular Diseases
SLE often presents with CNS manifestations ranging from meningitis to cerebritis, and
encephalitis. The most frequent CNS manifestation of SLE is aseptic meningitis, which needs to
be differentiated from ABM. CNS manifestations of SLE usually occur in patients who have
established multisystem manifestations of SLE. CNS SLE is usually present as part of a flare of
SLE. SLE flare may be manifested by fever, an increase in the signs/symptoms of SLE
manifested in previous flares. Laboratory tests suggesting flare include new or more severe
leukopenia, thrombocytopenia, increased erythrocyte sedimentation rate (ESR), polyclonal
gammopathy, proteinuria/microscopic hematuria. The CSF in patients with SLE includes a
lymphocytic predominance (usually <100 WBCs/mm^3 ). Polymorphonuclear neutrophils
(PMNs) may predominate early in SLE and aseptic meningitis. The RBCs are not present in
the CSF with SLE, aseptic meningitis, and the CSF lactic acid level is also normal. The
definitive test for diagnosing CNS SLE is to demonstrate a decreased C 4 level in the CSF.
Unfortunately, patients with a flare of CNS lupus are predisposed to bacterial meningitis/viral
encephalitis. CCU clinicians must be careful to be sure that the patient with an SLE flare with
CNS manifestations does not have a superimposed ABM or acute viral encephalitis (1,8,19–24).
Granulomatous angiitis of the CNS is an uncommon cause of aseptic meningitis. The
fever and encephalopathy are the most common manifestations of granulomatous angiitis of
the CNS, but the focal abnormalities, including seizures and cranial nerve palsies, may mimic
bacterial meningitis. Systemic laboratory tests are unhelpful. The ESR is usually elevated. The
CSF profile includes a lymphocytic predominance (usually<200 cells/mm^3 ), a low CSF
glucose may occur, RBCs are rarely present. Such findings are also compatible with the
diagnosis of HSV meningoencephalitis, or aseptic meningitis. The diagnosis of granulomatous
angiitis of the CNS is made by head CT/MRI imaging demonstrating vasculitic lesions in the
CSF (19,20).
Behc ̧et’s disease is multisystem disorder of unknown etiology characterized by oral
aphthous ulcers, genital ulcers, eye findings, and neurological manifestations in up to one
quarter of patients. CNS presentation of Behc ̧et’s may be the presenting finding in about 5% of
Meningitis and Its Mimics in Critical Care 137