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Human Rabies -- West Virginia, 1994

On October 15, 1994, a 41-year-old male resident of Wirt County, West Virginia, died from rabies. This report summarizes the clinical course, epidemiologic investigation, and probable exposure history of this case.

On October 4, the man was examined at a local hospital with a 1-day history of shaking, speech difficulties, unwillingness to bring liquids to his mouth, vomiting, and severe anxiety. During examination, he had good long-term recall but a short attention span and became extremely agitated when anyone approached him for examination. A white blood cell count (WBC) was 13,600/mm superscript 3 (normal: 5000-10,000/mm superscript 3), and urinalysis indicated greater than 80 mg/dL ketones (normal: absent), 100 mg/dL protein (normal: absent), trace blood (normal: absent), and carboxy acid tetrahydrocannabinol of 79 ng/mL (normal: absent). Preliminary diagnosis was acute psychotic reaction associated with use of ethanol or marijuana or ingestion of other drugs. The man declined further examination and treatment and left the same day without being admitted.

On the evening of October 4, the man was examined at a regional hospital with extreme agitation and muscle tremors; he was admitted to the intensive-care unit for apparent encephalopathy. Findings on admission included an oral temperature of 101.1 F (38.3 C) and pulse of 64 beats per minute. Laboratory test results included a WBC of 18,100/mm superscript 3, creatinine phosphokinase of 1912 IU (normal: 5-50 IU), and a lactic dehydrogenase of 1000 U/L (normal: less than 300 U/L). Following evaluation, the preliminary differential diagnoses included rabies, tetanus, viral encephalitis, acute hemorrhagic encephalitis, and drug toxicities or withdrawal. Efforts to control spastic movements included treatment with valium, librium, ativan, phenobarbital, and morphine. Because of frequent expectoration of frothy saliva from the mouth, he was placed in isolation. On October 6, he was paralyzed with pavulon/tracrium to control extreme agitation and spastic muscle activity, mechanically ventilated, treated with acyclovir for possible viral infection, and then transferred to a tertiary-care facility.

On October 6 and 7, serial computerized tomographies of the brain revealed low attenuation in the left temporal lobe suggestive of inflammation or neoplasm. On October 6 and 10, cerebrospinal fluid specimens were obtained, but findings were nonspecific. Serologic tests were negative for eastern equine, western equine, St. Louis, and California group arboviral encephalitides. A serum sample and nuchal biopsy specimen obtained on October 7 and a brain biopsy specimen (left temporal lobe) obtained on October 10 were tested for rabies. On October 12, the West Virginia Bureau of Public Health Laboratory diagnosed rabies by both fluorescent antibody stain and demonstration of Negri bodies in the brain tissue, and treatment with paralytic/sedative drugs was terminated; the patient died on October 15.

Subsequent confirmatory analysis at CDC included detection of rabies neutralizing antibody in serum and the detection of rabies antigen by direct fluorescent antibody staining of the nuchal biopsy specimen. The specific viral RNA was identified as a variant associated with the silver-haired bat (Lasionycteris noctivagans).

Interviews with friends and family members on October 15 indicated that, in late June or early July 1994, the decedent and two acquaintances had shot a bat from the front porch of his house and that the decedent had examined the head of the bat by opening its mouth and feeling the teeth. Descriptions of the bat were consistent with the red bat (Lasiurus borealis).

Postexposure rabies immunoprophylaxis was administered to 48 persons (15 medical technicians, 12 registered nurses, four physicians, two licensed practical nurses {LPNs}, one LPN student, one physician assistant, one housekeeper, one secretary, and 11 family members and friends). Reported by: MS Hardman, MA Ballesca, MD, DM Senseng, MD, Roane General Hospital, Spencer; S Spencer, SD Hanna, MD, BM Louden, MD, MA Morehead, MD, P Anderson, St. Joseph's Hospital, Parkersburg; B McTaggart, A Khan, MD, AA Marfin, MD, PJ Marks, MD, E Sang, MD, MA Fisher, MD, RW Farr, MD, Robert C. Byrd Health Sciences Center of West Virginia Univ, Morgantown; J Merrill, Mid-Ohio Valley Health Dept, Elizabeth; C Slemp, MD, F Lambert, Jr, DrPH, D Dodd, L Haddy, MS, State Epidemiologist, West Virginia Dept of Health and Human Resources. Viral and Rickettsial Zoonoses Br, Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: This report describes the 21st case of human rabies reported in the United States since 1980 and the first from West Virginia since 1979. Of the 21 cases, 11 are presumed to have been acquired inside the United States, and nine have been attributed to bat-associated virus. As a result of exposure to these 21 human rabies cases, at least 880 persons have received postexposure rabies immunoprophylaxis at an estimated direct cost of $900,000 (1).

Although a specific exposure to rabies was not elicited before this patient's death, a presumptive diagnosis of rabies had been considered early during hospitalization. As a consequence, the initiation of strict isolation practices reduced the number of persons exposed and, therefore, eliminated the need for postexposure prophylaxis for health-care workers involved with the patient's transfer to and care at the tertiary-care facility. This case emphasizes that prompt collection and analysis of antemortem specimens in suspected cases of human rabies may expedite diagnosis and minimize unnecessary exposures and treatments.

Bat rabies is enzootic in the United States, and cases have been reported from all 48 contiguous states. Although distinct variants of rabies virus have been confirmed in red bats, this case is the first in which the silver-haired bat variant has been potentially linked with red bats. Because the natural history of rabies virus circulation among bats is not completely understood, mammalogists should collaborate with local health departments in the taxonomic identification of bats submitted for rabies diagnosis. In addition, CDC requests that brain tissue from rabid silver-haired and red bats be forwarded from state diagnostic laboratories to CDC's Viral and Rickettsial Zoonoses Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, telephone (404) 639-1050.

Exposure to potentially rabid animals (e.g., downed bats and other wild animals) should be avoided. However, postexposure prophylaxis is recommended for all persons bitten by such animals and for nonbite exposures involving contamination of lesions or mucous membranes with potentially infectious materials such as saliva (2). Because some bat bites may be less severe -- and therefore more difficult to recognize -- than bites inflicted by larger mammalian carnivores, rabies postexposure treatment should be considered for any physical contact with bats when bite or mucous membrane contact cannot be excluded (3). Because reduction of bat populations is neither feasible nor desirable as a means of controlling rabies in bats, rabies-prevention programs should emphasize the exclusion of bats from human dwellings to minimize direct contact with humans and companion animals.


  1. Fishbein DB, Robinson LE. Rabies. N Engl J Med 1993;329:1632-8.

  2. ACIP. Rabies prevention -- United States, 1991: recommendations of the Immunization Practices Advisory Committee (ACIP). MMWR 1991;40(no. RR-3).

  3. CDC. Human rabies -- California, 1994. MMWR 1994;43:455-7.

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