Human Rabies -- California, 1994

In January 1994, a 44-year-old California man died from a bat-associated strain of rabies; he had had no known animal bite or other rabies exposure. Rabies was not clinically suspected nor confirmed until 1 month after his death. This report summarizes the case investigation.

On January 1, the man was evaluated at a local hospital emergency department for right-arm pain of 3 days' duration. He reported that 1 week earlier, he had had transient diarrhea; 3 weeks earlier, he had had a sore throat, fever, chills, and malaise for 5 days. The patient was a licensed acupuncturist and regularly treated himself with acupuncture for chronic right-elbow pain. He denied recent international travel or being bitten by an animal. On physical examination, cervical disk disease was presumptively diagnosed, and he was treated symptomatically and released.

On January 4, the man returned to the hospital with tingling and numbness in his right arm; treatment with oral prednisone was initiated. Weakness and pain in the arm progressed, and on January 7, a magnetic resonance imaging scan of the spine demonstrated findings consistent with cervical myelitis. The patient was admitted to the hospital with a diagnosis of postviral transverse myelitis; therapy included intravenous steroids and immunoglobulin. He complained about tingling and muscle twitches of the right side of his trunk and face and mild shortness of breath when drinking liquids. On physical examination, the man had decreased or absent reflexes; decreased sensation of the right side of his face, arm, and trunk; decreased muscle tone and strength in his right arm; and Horner syndrome of his right eye. His total white blood cell count was normal (8300 cells/mm superscript 3) with 79% segmented neutrophils. Examination of cerebrospinal fluid revealed a normal glucose level, elevated protein (98 mg/dL), and 5 white blood cells/mm superscript 3 (67% lymphocytes and 33% monocytes).

On January 8, the patient became anxious and developed hypertension, tachycardia, and tachypnea; his oral temperature was 103.6 F (39.8 C). On January 9, he had respiratory failure and was intubated. On January 13, his rectal temperature dropped to 96.0 F (35.6 C), and an electric blanket was used to maintain his body temperature. Therapy was initiated with acyclovir and ganciclovir for possible herpes simplex or cytomegalovirus encephalitis.

On January 14, nerve conduction studies revealed diffuse motor-neuron axonal loss. On January 15, the patient was unresponsive to sound and pain stimuli and had no spontaneous movements. Electroencephalograms on January 15 and 18 demonstrated diffuse slowing and alpha rhythm consistent with encephalopathy. On January 18, brain stem reflexes could not be elicited; ventilatory support was withdrawn, and the patient died. An autopsy was performed on January 19.

On February 18, Negri bodies were noted in formalin-fixed brain specimens. On February 24, rabies was confirmed by fluorescent antibody testing of frozen brain tissue at both the county and state health departments. Monoclonal antibody testing and nucleotide sequence analysis of viral nucleic acid conducted at CDC implicated a strain of rabies associated with the silver-haired bat (Lasionycteris noctivagans).

Family members reported that the patient had cared for a sick stray kitten for several days during the spring of 1993. He had no known history of being bitten or scratched. The kitten had been taken to an animal shelter, and its final disposition was unknown. In 1991, the patient had visited caves in Utah but had no known contact with bats. His only travel outside the United States was to Mexico in 1976 and the Virgin Islands in 1992. He frequently camped outdoors without using a tent; he last camped outdoors during September 1993.

As a result of reported close contact with the patient and/or his secretions, rabies postexposure prophylaxis was administered to one family member and 25 health-care workers beginning on February 25.

Reported by: R Phelps, MD, DE Collins, MD, JA Kram, MD, P Stoll, J Wrobel, Summit Medical Center; R Davis, MD, K Aldape, MD, Univ of California-San Francisco Medical Center; D Henton, Univ of Southern California, Los Angeles; CL Smith, MD, B Benjamin, MD, L Frank, A Chandler, E Pontiflet, Alameda County Health Dept, Oakland; M Giles, S Fannin, MD, Los Angeles County Health Dept, Los Angeles; M Brashear, J Rosenberg, MD, R Emmons, MD, RJ Jackson, MD, GW Rutherford, III, MD, State Epidemiologist, California Dept of Health Svcs. Viral and Rickettsial Zoonoses Br, Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: Since 1980, 19 human rabies cases have been reported in the United States. Of these, eight were acquired outside the United States from exposure to domestic animals. The case in this report is the third fatal human rabies case since 1985 that was diagnosed approximately 1 month postmortem. Antemortem diagnosis of rabies is often difficult because of nonspecific clinical presentation during the prodromal phase and the infrequent occurrence of human rabies in the United States.

Rabies should be considered in the differential diagnosis of any rapidly progressive encephalitic disease of suspected viral etiology, even in the absence of a definitive history of animal bite or other exposure. In addition to rapidly progressive encephalitis, manifestations suggestive of rabies in the case described in this report included paresis and paresthesia, areflexia, hydrophobia, anisocoria, and related autonomic dysfunction. Early diagnosis of rabies alters neither the patient's treatment course nor prognosis. However, the advantages of early rabies diagnosis include early initiation of infection-control measures to prevent exposure of caregivers to rabies virus-containing body fluids not included under universal precautions (1) and identification of potential candidates for postexposure prophylaxis (2).

This California case is the eighth since 1980 in which a strain of rabies associated with bats was implicated. A definite exposure through a bat's bite was identified in only one of the eight cases; contact with a bat was associated with two additional cases in which animal bites were not detected; in five, no history of exposure to bats was known. Bat-associated strains of rabies can be transmitted to humans either directly through a bat's bite or indirectly through the bite of an animal previously infected by a bat.

Bat rabies is enzootic in the contiguous United States; 647 rabies-positive bats were reported from 46 states during 1992 (3). The silver-haired bat (L. noctivagans) -- the rabies virus variant identified in this case and in five other cases since 1980 -- is widely distributed from Alaska to the southern United States during fall and spring but is uncommon throughout its range. These bats usually roost in rock crevices and under loose tree bark (4); however, during fall and spring migration, they use a variety of temporary shelters (e.g., wood piles and open outbuildings) but only rarely use closed structures (e.g., attics). Although L. noctivagans is infrequently submitted for rabies diagnosis, this species is an important source of domestically acquired human rabies. Of approximately 25,000 bats submitted for rabies diagnosis and identified to species in 15 states during 1956-1992, 796 (3%) were L. noctivagans; of these, 41 (5%) were rabid.

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. Bats perform important ecologic functions that preclude population reduction as a rabies-control strategy. Because domestic animals may serve as indirect links in the transmission of enzootic wildlife rabies to humans, all dogs and cats should have a current rabies vaccination (5).

References

1. CDC. Update: universal precautions for prevention of transmission of human immunodeficiency virus, hepatitis B virus, and other bloodborne pathogens in health-care settings. MMWR 1988;37:377-82,387-8.

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

3. Krebs JW, Strine TW, Childs JE. Rabies surveillance in the United States during 1992. J Am Vet Med Assoc 1993;203:1718-31.

4. Hall ER. The mammals of North America. New York: John Wiley & Sons, 1981.

5. National Association of State Public Health Veterinarians, Inc. Compendium of animal rabies control, 1994. J Am Vet Med Assoc 1994;204:173-6.

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