eMedicine Specialties > Infectious Diseases > CNS Infections
Western Equine Encephalitis: Treatment & Medication
Updated: Oct 31, 2007
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Medical Care
Focus initial medical care on a prompt diagnosis with differentiation from other potentially treatable causes of the patient's symptoms. Because the disease mimics other encephalitides and meningitis or meningoencephalitis, implement prompt drug therapy. The physician should probably begin with triple antibiotic therapy for generalized bacterial coverage and begin acyclovir (10 mg/kg) to empirically treat herpes simplex virus.
- Like all alphaviruses, western equine encephalitis (WEE) has no specific treatment. Management remains focused primarily on supportive and preventive measures. Treatment also varies based on the stage of the disease. In the early stages of the viral prodrome, diagnosis is essential. Prophylactic use of steroids, ribavirin, or anticonvulsants in this early viremic stage has not been studied.
- Once the patient is comatose, perform obvious measures (eg, respiratory maintenance with ventilator support). Ideally, maintain early awareness regarding whether the patient will require transfer to an appropriate level of care (eg, a critical care unit). In addition, appropriately maintain the patient's nutritional status.
- If the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is present, treat accordingly (see Syndrome of Inappropriate Antidiuretic Hormone Secretion).
- Pharmacologic therapy consists primarily of antipyretics, analgesics, and anticonvulsants.
- Although no current medical therapies are available for WEE, recent research has revealed some possibilities.
- Viral envelope proteins are capable of being functionally expressed in culture and in the future may lead to a subunit vaccine for WEE.
- An antibody with appropriate specificity attenuates the intracellular processes necessary for viral replication in animal models.
- Cytotoxic T cells play an important part in the recovery from CNS lesions in mice.
- Nucleoside analogs (eg, ribavirin) have in vitro activity, but no clinical application is yet apparent.
- Additionally, a repertoire of mouse monoclonal antibodies (MAbs) against WEE currently exists; these are currently not in clinical practice and may eventually become a form of immunodetection or immunotherapy.
- Whether these therapies can be productive in humans remains to be elucidated.
Surgical Care
Surgical treatments for this disease are not available, except for appropriate neurologic procedures directed at a large CNS bleed or the consequences of markedly elevated CNS pressure. Rarely, brain biopsy may be performed.
Consultations
Consultations are primarily obtained for supportive measures.
- Consultation with an infectious disease specialist is particularly relevant if the physician is unable to determine the etiology of the encephalitis or meningoencephalitis. The most important contribution is likely to be the ability to rapidly ascertain a potentially reversible cause of the patient's symptoms.
- Similar to the reasons for obtaining a consultation with an infectious disease specialist, neurologists may provide early insightful information and aid in the diagnostics (eg, EEG) and treatment of complications.
- If a general practitioner treats the patient, a critical care consultant is valuable to coordinate ICU care.
- Consult a neurosurgeon only if needed for treatment of complications.
Diet
Undertake appropriate nutritional measures based on the patient's mental status.
Medication
The drugs currently used consist of agents capable of ameliorating neurologic complications. Antipyretics are used as needed. Additionally, suitable analgesics and amnestics are appropriate once the patient is intubated. Antibiotics are of no value in this situation and may predispose the patients to superinfections. Once the physician determines that the patient does not have a bacterial infection, antibiotics are discontinued. Initiate anticonvulsants either when a seizure has occurred or is probable, particularly in the pediatric population, in whom prevalence is high. Corticosteroids are administered early and serve multiple functions. They decrease inflammation, decrease cerebral edema, and correct any adrenocortical insufficiency.
Anticonvulsant agents
These agents prevent seizure recurrence and terminate clinical and electrical seizure activity.
Phenytoin (Dilantin)
May act in motor cortex, where it may inhibit spread of seizure activity. Activity of brain stem centers responsible for tonic phase of grand mal seizures may also be inhibited.
Individualize the dose. Administer a larger dose before retiring if dose cannot be divided equally. Rate of infusion must not exceed 50 mg/min to avoid hypotension and arrhythmia.
Adult
Loading dose: 15-20 mg/kg PO/IV once or as divided doses, followed by 100-150 mg per dose at 30-min intervals
Initial dose: 100 mg (125 mg susp) PO/IV tid
Maintenance dose: 300-400 mg/d PO/IV divided tid or qd/bid if using ER; increase to 600 mg/d (625 mg/d susp) may be necessary; not to exceed 1500 mg/24h
Pediatric
Loading dose: 15-20 mg/kg PO/IV once or as divided doses
Initial dose: 5 mg/kg/d PO/IV divided bid/tid
Maintenance dose: 4-8 mg/kg PO/IV divided bid/tid
>6 years: May require minimum adult dose (300 mg/d); not to exceed 300 mg/d
Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, phenylbutazone, succinimide, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim, and valproic acid may increase phenytoin toxicity; effects may decrease when taken concurrently with barbiturates, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, and sucralfate; may decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, quinidine, theophylline, methadone, metyrapone, mexiletine, oral contraceptives, and valproic acid
Documented hypersensitivity; sinoatrial block; second- and third-degree AV block; sinus bradycardia; Adams-Stokes syndrome
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Perform blood counts and urinalyses when therapy is begun and at monthly intervals for several months thereafter to monitor for blood dyscrasias; discontinue use if a skin rash appears and do not resume use if rash is exfoliative, bullous, or purpuric; rapid IV infusion may result in death from cardiac arrest marked by QRS widening; caution in acute intermittent porphyria and diabetes (may elevate blood sugars); discontinue use if hepatic dysfunction occurs
Diazepam (Valium)
Depresses all levels of CNS (eg, limbic, reticular formation), possibly by increasing activity of GABA. Alternatively, lorazepam can be used when indicated.
Adult
5-15 mg IV q5min, repeat prn; not to exceed 30 mg in 8 h
Pediatric
0.05-0.3 mg/kg/dose IV/IM over 2-3 min q15-30min; repeat in 2-4 h prn; not to exceed 10 mg
Increases toxicity of benzodiazepines in CNS with coadministration of phenothiazines, barbiturates, alcohols, and MAOIs
Documented hypersensitivity; narrow-angle glaucoma
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity)
Corticosteroids
These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.
Dexamethasone (Decadron, Baldex, AK-Dex)
Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.
Adult
16 mg PO/IV, followed by 4-10 mg PO/IV q6h
Pediatric
0.08-0.3 mg/kg/d or 2.5-10 mg/m2/d PO/IV divided q6-12h
Effects decrease with coadministration of barbiturates, phenytoin, and rifampin; dexamethasone decreases effect of salicylates and vaccines used for immunization
Documented hypersensitivity; active bacterial or fungal infection
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Increases risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering drug; abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications of glucocorticoid use
Methylprednisolone (Solu-Medrol, Medrol, Depo-Medrol)
Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.
Adult
3 mg/kg IV over 15 min, followed in 45 min with 5.4 mg/kg/h IV
Pediatric
0.5-1.7 mg/kg/d or 5-25 mg/m2/d PO/IV/IM divided q6-12h
Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics
Documented hypersensitivity; viral, fungal, or tubercular skin infections
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use
Antiviral agents
These agents consist of acyclovir or valacyclovir and are often used as empiric treatments for possible herpes simplex encephalitis.
Acyclovir (Zovirax)
This is a herpes virus–specific antiviral used for peripheral and systemic manifestations of acute viral illness.
Adult
5-10 mg/kg IV q8h; PO not recommended
Pediatric
Administer as in adults
Concomitant use of probenecid or zidovudine prolongs half-life and increases CNS toxicity of acyclovir
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in renal failure or when using nephrotoxic drugs
More on Western Equine Encephalitis |
| Overview: Western Equine Encephalitis |
| Differential Diagnoses & Workup: Western Equine Encephalitis |
 Treatment & Medication: Western Equine Encephalitis |
| Follow-up: Western Equine Encephalitis |
| References |
| « Previous Page | Next Page » |
References
Netolitzky DJ, Schmaltz FL, Parker MD. Complete genomic RNA sequence of western equine encephalitis virus and expression of the structural genes. J Gen Virol. Jan 2000;81 Pt 1:151-9. [Medline].
Bianchi TI, Aviles G, Monath TP. Western equine encephalomyelitis: virulence markers and their epidemiologic significance. Am J Trop Med Hyg. Sep 1993;49(3):322-8. [Medline].
Sellers RF, Maarouf AR. Weather factors in the prediction of western equine encephalitis epidemics in Manitoba. Epidemiol Infect. Oct 1993;111(2):373-90. [Medline].
Johnson AJ, Martin DA, Karabatsos N. Detection of anti-arboviral immunoglobulin G by using a monoclonal antibody-based capture enzyme-linked immunosorbent assay. J Clin Microbiol. May 2000;38(5):1827-31. [Medline].
Chiles RE, Reisen WK. A new enzyme immunoassay to detect antibodies to arboviruses in the blood of wild birds. J Vector Ecol. Dec 1998;23(2):123-35. [Medline].
Gahlinger PM, Reeves WC, Milby MM. Air conditioning and television as protective factors in arboviral encephalitis risk. Am J Trop Med Hyg. May 1986;35(3):601-10. [Medline].
Elgart ML. Medical pearl: permethrin can prevent arthropod bites and stings. J Am Acad Dermatol. Aug 2004;51(2):289. [Medline].
Adams RD, Victor M, Ropper AH. Encephalitis. In: Principles of Neurology. 6th ed. New York, NY: McGraw-Hill; 1997:749-55.
Bennet JC, Plum F. Other arthropod-borne infections. In: Cecil Textbook of Medicine. 20th ed. Philadelphia, Pa: WB Saunders; 1996:1810-14.
CDC. Arboviral disease--United States, 1994. MMWR Morb Mortal Wkly Rep. Sep 8 1995;44(35):641-4. [Medline].
Davis NL, Brown KW, Johnston RE. A viral vaccine vector that expresses foreign genes in lymph nodes and protects against mucosal challenge. J Virol. Jun 1996;70(6):3781-7. [Medline].
Deresiewicz RL, Thaler SJ, Hsu L. Clinical and neuroradiographic manifestations of eastern equine encephalitis. N Engl J Med. Jun 26 1997;336(26):1867-74. [Medline].
Francki RIB, Faquet CM, Knudson DI. Classification and nomenclature of viruses. Arch Virol. 1991;2:223.
Fulhorst CF, Hardy JL, Eldridge BF. Natural vertical transmission of western equine encephalomyelitis virus in mosquitoes. Science. Feb 4 1994;263(5147):676-8. [Medline].
Gleiser RM, Urrutia J, Gorla DE. Effects of crowding on populations of Aedes albifasciatus larvae under laboratory conditions. Entomologia Experimentalis et Aplicata. May 2000;95(2):135-140.
Gorbach SL, Bartlett JG, Blacklow NR. Other arthropod-borne viruses. In: Infectious Diseases. Vol 2. Philadelphia, Pa: WB Saunders; 1998:1411-14.
Gutierrez KM, Prober CG. Encephalitis. Identifying the specific cause is key to effective management. Postgrad Med. Mar 1998;103(3):123-5, 129-30, 140-3. [Medline].
Hahn CS, Lustig S, Strauss EG. Western equine encephalitis virus is a recombinant virus. Proc Natl Acad Sci U S A. Aug 1988;85(16):5997-6001. [Medline].
Huang C, Chatterjee NK, Grady LJ. Diagnosis of viral infections of the central nervous system. N Engl J Med. Feb 11 1999;340(6):483-4. [Medline].
Johnson RT. The pathogenesis of acute viral encephalitis and postinfectious encephalomyelitis. J Infect Dis. Mar 1987;155(3):359-64. [Medline].
Kramer LD, Fallah HM. Genetic variation among isolates of western equine encephalomyelitis virus from California. Am J Trop Med Hyg. Apr 1999;60(4):708-13. [Medline].
Long MC, Nagata LP, Ludwig GV. Construction and characterization of monoclonal antibodies against western equine encephalitis virus. Hybridoma. Apr 2000;19(2):121-7. [Medline].
Mandell GL. Alphaviruses causing encephalitis. In: Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 5th ed. Philadelphia, Pa: Churchill-Livingstone; 2000.
Nasci RS, Gottfried KL, Burkhalter KL, et al. Sensitivity of the VecTest antigen assay for eastern equine encephalitis and western equine encephalitis viruses. J Am Mosq Control Assoc. Dec 2003;19(4):440-4. [Medline].
Obrecht RE, Patrick PD. Neuropsychological sequelae of adolescent infectious diseases. Adolesc Med. Oct 2002;13(3):663-81. [Medline].
Reisen WK, Chiles RE. Prevalence of antibodies to western equine encephalomyelitis and St. Louis encephalitis viruses in residents of California exposed to sporadic and consistent enzootic transmission. Am J Trop Med Hyg. Nov 1997;57(5):526-9. [Medline].
Reisen WK, Meyer RP, Presser SB. Effect of temperature on the transmission of western equine encephalomyelitis and St. Louis encephalitis viruses by Culex tarsalis (Diptera: Culicidae). J Med Entomol. Jan 1993;30(1):151-60. [Medline].
Roos KL. Encephalitis. Neurol Clin. Nov 1999;17(4):813-33. [Medline].
Sokolova TM, Selivanova TK, Lebedev AIu. Sindbis viruses of various geographic origin and differentiation of them from Western equine encephalomyelitis viruses using the polymerase chain reaction. Vopr Virusol. May-Jun 1996;41(3):117-22. [Medline].
Tsai TF. Arboviral infections in the United States. Infect Dis Clin North Am. Mar 1991;5(1):73-102. [Medline].
Weaver SC, Kang W, Shirako Y. Recombinational history and molecular evolution of western equine encephalomyelitis complex alphaviruses. J Virol. Jan 1997;71(1):613-23. [Medline].
Weaver SC, Lorenz LH, Scott TW. Pathologic changes in the midgut of Culex tarsalis following infection with Western equine encephalomyelitis virus. Am J Trop Med Hyg. Nov 1992;47(5):691-701. [Medline].
Further Reading
Keywords
western equine encephalitis, WEE, inflammation of the brain parenchyma, meninges, herpes simplex virus, arbovirus, Culex tarsalis, C tarsalis, Aedes species, eastern equine encephalitis, EEE, Venezuelan equine encephalitis, VEE, Sindbis virus, neurotropic alphavirus, diffuse CNS involvement, meningitis, meningoencephalitis, St. Louis encephalitis, Aedes albifasciatus, A albifasciatus, encephalitides
