Chapter 151.

Zoonotic encephalitis is most often an arboviral infection transmitted hematologically by an arthropod vector and animal host. Often the vector is a mosquito or tick and the animal host is a small animal or bird. The one exception is rabies (see Chap. 147), which follows peripheral nerve tracts after inoculation from an infected animal's bite. Additionally, encephalitis may be seen in the nonviral zoonotic infections of Bartonella henselae, Brucella canis, borreliosis, Coxiella burnetii, Ehrlichia spp., listeriosis, leptospirosis, Lyme disease, RMSF, psittacosis, and toxoplasmosis.^9,29,30

The clinical presentation is a prodromal illness with malaise, myalgia, fever, and occasionally parotitis. This prodromal phase advances to a sudden decline in mental status associated with headache and fever. However, there are no specific signs and symptoms that determine the exact etiology and causative organism of encephalitis. The CSF is often abnormal, showing a slightly elevated opening pressure, normal to slightly elevated protein concentration, normal glucose levels, and predominance of lymphocytes. The electroencephalogram is abnormal with diffuse bilateral slowing interrupted by occasional spike activity. CSF viral cultures are frequently sterile, and the infectious agent is rarely isolated from the CSF.^29–32 ELISA of serum can be used to detect most arboviral infections causing encephalitis. Computed axial tomography is often negative with no evidence of focal findings or abnormalities. Magnetic resonance imaging often does reveal evidence of encephalitis by the imaging of cerebral swelling. If the CT scan were negative, following up with an MRI scan would be the prudent course of investigation. Treatment is supportive and directed toward decreasing elevated intracranial pressure.

West Nile Virus Encephalitis

The West Nile virus was first isolated in the West Nile District of Uganda in 1937, and since then was commonly found in vertebrates in Africa, Eastern Europe, West Asia, and the Middle East.³³ It is a member of the Japanese encephalitis serocomplex of the Flaviviridae family of viruses.³⁴ In 1999 it was detected in the western hemisphere.

The mode of transmission involves mosquitoes, primarily of the Culex species, that feed on infected birds, which serve as the natural reservoir for the virus. Over 110 species of birds have been identified as being infected by the West Nile virus in the United States. Most of these birds are crows, ravens, and jays.³⁴

Infected mosquitoes transmit the virus to humans and other animals when taking a blood meal.

There is an incubation period of 3 to 15 days after an infected bite. About 20 percent of those bitten develop fever and a flu-like illness, "West Nile fever." The classic presentation for West Nile fever is that of a mild dengue-like illness of sudden onset with fever, lymphadenopathy, headache, abdominal pain, vomiting, rash, conjunctivitis, eye pain, and anorexia. Duration is typically 3 to 6 days.³⁴

Meningoencephalitis occurs in approximately 1 in 150 patients that become infected and is more common than meningitis. Risk factors for the development of meningoencephalitis are immunocompromised host (HIV, TB, or malaria), or advanced age. Complaints of weakness out of proportion to physical examination findings are common and myoclonus is nearly a universal finding. Interestingly, complete flaccid paralysis may occur and can be confused with Guillain-Barré syndrome. Other neurologic findings include parkinsonian-like signs, ataxia, extrapyramidal signs, cranial nerve abnormalities, myelitis, optic neuritis, and seizures. Treatment for West Nile virus is supportive.³⁴

Laboratory findings for West Nile virus infection are limited to a total leukocyte count that is either normal or slightly elevated. Hyponatremia has been occasionally associated with patients with encephalitis. Cerebrospinal fluid demonstrates mostly lymphocytes, protein elevation, and a normal glucose. Computed tomography of the brain shows no evidence of acute disease, though with progressive meningoencephalitis cerebral edema may be noted.

Diagnosis is made by identifying West Nile virus (WNV)-specific IgM antibody in serum or CSF specimens. IgM-specific antibody is an acute-phase identifier that can persist in serum for up to 12 months postinfection. IgG WNV-specific antibody is found in the convalescent phase in both serum and CSF. As of this writing, PCR testing is still in an experimental stage.³⁴

Methods to reduce the exposure risk for West Nile virus include use of mosquito repellents, clothing with long sleeves and long pants, and avoiding the outdoors during dawn and dusk. The insect repellent recommended is DEET (N,N-diethyl-m-toluamide and related compounds). Personal insect repellents should not be used on infants under 6 months of age. Use of mesh covers on strollers is recommended for this age group, along with protective clothing.³⁴

Zoonotic Meningitis