On March 15, 1995, a 4-year-old girl who resided in Lewis County, Washington, died from rabies. This report summarizes the clinical course, epidemiologic investigation, and probable exposure history of the case.

On March 8, the child was transported to a local hospital after a 2-day history of drowsiness, listlessness, abdominal pain, anorexia, sore throat, and pain on the left side of her neck. During examination in the emergency department, she had nasal congestion and drooling. Rhinitis and bilateral conjunctivitis were diagnosed; antibiotics and symptomatic treatment were prescribed, and she was discharged.

On the morning of March 9, she was transported to the same hospital because of an axillary temperature of 104.0 F (40.0 C) and behavioral changes. In addition, she had had hallucinations, difficulty standing, and insomnia and refused to drink fluids. On examination in the emergency department, findings included an axillary temperature of 101.2 F (38.4 C), pulse of 210 per minute, respiratory rate of 32 per minute, an enlarged reactive right pupil, and tremors. Laboratory test results included a white blood cell count of 20,800/mm3 (normal: 5000-10,000 mm3), blood urea nitrogen of 45 mg/dL (normal: 0-25 mg/dL), and sodium level of 151 mmol/L (normal: 135-145 mmol/L). Preliminary diagnoses included dehydration and possible drug intoxication, and intravenous fluids were administered. Screening of urine for drugs was negative, and computerized axial tomography of the brain was within normal limits.

Later on the morning of March 9, her temperature increased, and she had a seizure. Cerebrospinal fluid findings were nonspecific. She was intubated for hypoventilation. In the emergency department and during air transport to the intensive-care unit of a regional hospital, she became bradycardic and required cardiopulmonary resuscitation. On arrival at the regional hospital, preliminary differential diagnoses included sepsis, viral encephalitis, and drug toxicity; ceftriaxone and acyclovir were administered. She became comatose, and an electroencephalogram (EEG) obtained on March 10 revealed generalized sharp and slow wave discharges. On March 13, an EEG revealed moderate to severe generalized slowing of cerebral activity. Based on information from family members about the child's possible exposure to a bat, diagnostic testing for rabies was initiated. A nuchal skin biopsy obtained on March 13 was positive for rabies by direct fluorescent antibody (DFA) testing at CDC on March 14.

On March 15, the child died. On autopsy, gross examination revealed massive cerebral edema with uncal herniation and intracytoplasmic inclusions in the brain and spinal cord. At the Washington State Department of Health Public Health Laboratories a specimen of brain tissue obtained at autopsy also was positive by DFA, and rabies virus was isolated by mouse inoculation. Analysis at CDC also included viral isolation from sputum obtained on March 14 and a positive DFA and nucleotide sequence analysis result from brain tissue obtained at autopsy.

During the child's hospitalization, family members reported that, on February 18, a bat had been found in her bedroom. Family members had examined the child but found no evidence of a bite. The bat was removed from the house, destroyed, and buried in the yard. On March 14, the local health department exhumed the bat. Despite trauma, decomposition, and partial consumption of the specimen by maggots, the bat brain was positive for rabies by DFA and nucleotide sequence analysis. Presumptive identification of the bat at CDC was either Myotis californicus or M. ciliolabrum. In addition, based on nucleotide sequence analysis, the rabies virus from the decedent and the bat were identical and was identified as a variant associated with small Myotis bats in the western United States.

Based on possible percutaneous or mucous membrane exposure to tears or saliva from the patient, postexposure rabies immunoprophylaxis was administered to 72 persons: six registered nurses, six respiratory therapists, one laboratory technician, one diagnostic imaging technician, two physicians, six family members, and 50 children and adults who were contacts in a day care center.

Reported by: A Paves, MD, P Gill, J Mckenzie, MN, Providence Hospital, Centralia; R Renbarger, RS, T Bell, MD, Lewis County Health Dept, Chehalis; A Movius, MD, H Baden, MD, PP O'Rourke, MD, A Melvin, MD, S Kuhl, MD, S Johnson, MD, J Bradshaw, MD, K Goodrich, L Spath, D Krous-Riggert, MPH, J Smith, MN, Children's Hospital and Medical Center, Seattle; M Goldoft, MD, J Kobayashi, MD, S LaCroix, MS, B Wieman, P Stehr-Green, DrPH, State Epidemiologist, Washington State Dept of Health. Viral and Rickettsial Zoonoses Br, Div of Viral and Rickettsial Disease, National Center for Infectious Diseases, Div of Field Epidemiology, Epidemiology Program Office, CDC.

Editorial Note

Editorial Note: The rabies case described in this report was the first to be documented in a human in the United States during 1995 and is consistent with a major epidemiologic pattern: since the 1950s, bats increasingly have been implicated as wildlife reservoirs for variants of rabies virus transmitted to humans. Variants of rabies virus associated with bats have been identified from 12 of the 25 cases of human rabies diagnosed in the United States since 1980. However, a clear history of animal bite exposure was documented for only six of these 25 cases. This finding suggests that even apparently limited contact with bats or other animals infected with a bat variant of rabies virus may be associated with transmission.

The inability of health-care providers to elicit information from patients about potential exposures to bats may reflect circumstances that hinder recall or the limited injury inflicted by a bat bite. For example, the family members of the child described in this report had not witnessed contact between the child and the bat, and she denied a bite or any other contact on the night of the incident; however, both the epidemiologic findings and molecular data indicated that infection resulted from contact with the bat.

The case in Washington and reports of similar cases (1,2), underscore that, in situations in which a bat is physically present and the person(s) cannot exclude the possibility of a bite, postexposure treatment should be considered unless prompt testing of the bat has ruled out rabies infection. This recommendation should be used in conjunction with guidelines of the Advisory Committee on Immunization Practices (3) to maximize a health-care provider's ability to respond to situations in which accurate exposure histories cannot be obtained and to ensure that inappropriate postexposure treatments are minimized.

References

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

2. CDC. Human rabies -- New York, 1993. MMWR 1993;42:799,805-6.

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

   
   

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