Fungal infections of the CNS occur rarely in healthy people. The presentation of fungal encephalitis is related to geographic area and a compromised immune system (Leedom & Underman, 2000). The common fungi found around the world that can infect the CNS include Cryptococcus neoformans, Histoplasma capsulatum,Aspergillus, and Candida albicans (Davis, 1999). Other fungi arefound only in certain regions: Coccidioides immitis, for example, is found in soil in central California, the southwest United States, northern Mexico, and areas of Argentina (Davis, 1999).
The fungal spores enter the body via inhalation. They initially infect the lungs, causing vague respiratory symptoms. In some cases, the fungi may enter the bloodstream, causing a fungemia. If the fungemia overcomes the person’s immune system, the fungus may spread to the CNS. The initial presentation is menin-gitis followed by encephalitis and brain abscesses. In addition to infecting the brain, the fungi may infect the spinal cord, produc-ing an abscess. The abscess will produce symptoms of spinal cord compression (Davis, 1999).
The common symptoms of fungal encephalitis include fever, malaise, headache, nuchal rigidity, lethargy, and mental status changes (Davis, 1999). C. neoformans is the most common fungus to infect the CNS. Symptoms of increased ICP related to hydrocephalus often occur (Go et al., 2000). Vascular changes are associated with C. immitis and Aspergillus (Leedom & Underman, 2000). Manifestations of vascular change may include arteritis or cerebral infarction.
CNS fungal infections present a diagnostic challenge because their presentations mimic other causes of encephalitis. The symp-toms develop over a 2-week period. Fungal infection may also be present in organs such as the lungs or kidney (Davis, 1999). The presence of a compromised immune system and a history of living. in or recently having traveled to a geographic area where specific fungi are found in the soil may suggest fungal encephalitis (Davis, 1999; Leedom & Underman, 2000). Laboratory evaluation of blood shows an elevated white cell count and anemia. In some cases, serologic tests may show fungal antibodies in serum (Davis, 1999). The CSF shows an elevated white cell count and protein levels. C. neoformans is readily identified in the CSF fungal cul-ture. The CSF culture is positive for other fungi in 50% of cases (Davis, 1999).
Neuroimaging is used to identify CNS changes related to fun-gal infection and will demonstrate fungal foci in organs initially invaded by the fungus. Although both MRI and CT scan are used in the workup for fungal encephalitis, MRI is more sensitive. The MRI may indicate lesions in the basal ganglia or thalamus, as well as hemorrhage, vascular complications, ischemia, aneurysm for-mation, or hydrocephalus (Go et al., 2000).
Medical management is directed at the causative fungus and the neurologic consequences of the infection. Seizures are controlled by standard antiseizure medications. Increased ICP is controlled by repeated lumbar punctures or shunting of CSF. In contrast to patients with cryptococcal meningitis, the use of repeated (once or twice daily) lumbar punctures in patients with fungal infec-tions has been an effective strategy to control increased ICP and has been associated with improved survival with fewer neurologic sequelae (Davis, 1999).
Antifungal agents are given for a specific period of time to cure the infection in patients with competent immune systems. Patients with compromised immune systems will receive anti-fungal therapy until the infection is controlled, after which they will receive a maintenance dose of the medication for an indefi-nite period of time.
Although the dose and duration of treatment depend on the causative fungi, amphotericin B (Abelcet, AmBisome, Amphocin, Amphotec, Fungizone, and Fungizone IV) is the standard anti-fungal agent used in treatment (Karch, 2002). Dosing must be high enough to penetrate the blood–brain barrier without causing renal toxicity.
Fluconazole (Diflucan) or flucytosine (5-FC, 5-fluorocytosine, Ancobon) may be administered in conjunction with ampho-tericin B. Both can be given orally and may be used as mainte-nance therapy. Potential side effects of fluconazole include nausea, abdominal pain, headache, dizziness, rash, reversible alopecia, and a transient increase in liver enzymes. When flucy-tosine is prescribed in conjunction with amphotericin B, bone marrow suppression may occur. Therefore, patients receiving these medications in combination should have leukocyte and platelet counts monitored twice a week (Davis, 1999).
If hydrocephalus develops and inflammation progresses, ICP will rise. Nursing assessment aimed at early identification of increased ICP is necessary to ensure early control and management. Patient comfort may be optimized by administering nonopioid analgesics, limiting environmental stimuli, and positioning. Administration of amphotericin B may cause fever, chills, and body aches. Giving diphenhydramine (Benadryl) and acetamin-ophen (Tylenol) approximately 30 minutes before giving am-photericin B may prevent these side effects. Renal toxicity due toamphotericin B is dose-limiting. Monitoring the serum creati-nine and blood urea nitrogen levels may alert the nurse to the de-velopment of renal insufficiency and the need to address the patient’s renal status.
Providing support will assist the patient and family to cope with the illness. Work-up of the patient for immunodeficiency diseases such as AIDS may put additional stress on the family. The nurse may need to mobilize community support systems for the patient and family.
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