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Human Rabies -- Oregon, 1989

On February 7, 1989, rabies was identified as the cause of death in an 18-year-old Mexican man who had died 4 days earlier of acute encephalitis in Oregon. He had no known exposure to the disease. This was the first case of human rabies in the United States since 1987 and the first in Oregon since 1978.

The patient was well until January 17, 1989, when he developed fever, nausea, vomiting, dyspnea, and cough. On January 22, he was treated at a local emergency room for bronchitis. On January 24, he went to another clinic with complaints of chills, myalgias, and sore throat and was diagnosed as having a viral upper respiratory illness. He was admitted to a Portland, Oregon, hospital on January 26 with fever, chills, and localized periumbilical pain suggesting acute appendicitis; during the next 2 days, the pain continued. Although his fever persisted, serial peripheral white cell counts remained normal. Ultrasound and two computerized axial tomography (CAT) scans of his abdomen were normal.

On January 28, the patient developed vertigo and subsequent acute obtundation. CAT scan of his head was normal; however, examination of the cerebrospinal fluid (CSF) revealed a mild pleocytosis with 9 white blood cells/mm3 (8% segmented polymorphonuclear cells, 78% lymphocytes, 10% macrophages, and 4% monocytes) and 10 red blood cells/mm3. The CSF glucose level was 81 mg/dL, and protein was 39 mg/dL. Tests on spinal fluid, blood, urine, sputum, and stool were negative for bacterial, fungal, viral, and mycobacterial pathogens. An electroencephalogram revealed mild to moderate slowing of electrical activity and did not suggest herpes encephalitis. On January 30, he had areflexia of all his deep tendons and asymmetrical palsies of cranial nerves VII and XII; that day, the patient had a cardiopulmonary arrest. He died February 3.

Although the possibility of rabies had been considered during hospitalization, specific diagnostic tests were not obtained until after the patient died. Direct fluorescent antibody staining of brain tissue collected at autopsy and submitted to the Oregon Public Health Laboratory was positive for rabies virus. Monoclonal antibody testing by CDC determined the antigenic pattern of the virus was the one found in areas of Latin America with enzootic canine rabies and in areas of California with enzootic skunk rabies.

During the 72 hours after diagnosis, extensive interviews were conducted with the patient's co-workers in Oregon, including two who originally traveled with him from Michoacan, Mexico. In March 1988, 11 months before onset of symptoms, the patient and his companions had driven by car from Michoacan through California to Oregon. Except for two trips to Washington in September and December of 1988, the patient had remained in northern Oregon, where he worked as an agricultural laborer. Interviews failed to identify a possible source of rabies exposure. Mexican health officials conducted an investigation in the patient's home area but found no additional information on possible exposures to rabies. Postexposure rabies prophylaxis was recommended for seven of his co-workers and two hospital workers who reported nonbite exposures to the patient's saliva. Reported by: M Loveless, MD, T Schacker, MD, Oregon Health Sciences University, Portland; H Osterud, MD, Washington County Health Dept, Hillsboro; R Sokolow, MBA, M Skeels, PhD, Oregon State Public Health Laboratory; L Williams, DVM, D Fleming, MD, LR Foster, MD, State Epidemiologist, Office of Health Status Monitoring, Oregon Dept of Human Resources. Div of Field Svcs, Epidemiology Program Office; Viral and Rickettsial Zoonoses Br, Div of Viral and Rickettsial Diseases, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: As human rabies has decreased in the United States, the proportion of rabies patients with no known exposures to rabid animals has increased. Between 1960 and 1979, a source of infection was not identified in 16% (6/38) of U.S. rabies cases (1). Since 1980, the proportion has increased to 60% (6/10); none of the three most recent patients reported exposure (2-7). Of the 38 human cases during 1960-1979, rabies was diagnosed before death in 30 (79%) (1), in contrast to only 40% of the five most recent cases (3-6). Rabies is often not considered in the differential diagnosis in persons with no known recent exposure to animals. It was unlikely that this patient's infection was acquired in Oregon for the following reasons. First, antigenic typing of the rabies virus, which can help determine the geographic source of infection (8,9), suggested that infection had occurred in areas of Latin America with enzootic dog rabies or areas of California with enzootic skunk rabies. Although the patient might have been bitten by a skunk during his 2-day trip through California, his traveling companions were unaware of such an event. Second, Oregon surveillance data since 1984 show that none of 33 skunks tested were positive for rabies. Based on this information and on the absence of reported indigenous skunk rabies in Oregon since 1966, Mexico was considered the most likely source of exposure. Regardless of whether the patient was exposed in Mexico or California, the incubation period would have exceeded 10 months.

For this patient, specific diagnostic tests for rabies might have been delayed because the initial clinical presentation suggested respiratory and gastrointestinal infection. Although respiratory tract infection is the most common diagnosis initially considered in patients with rabies, it was present in less than 20% of cases in one review (1).

Although only six cases of human-to-human rabies transmission--all in cornea transplant patients--have been well documented (10-14), there is a theoretical risk of human-to-human transmission (10,15) by bites or direct saliva contact to mucous membranes or broken skin. This risk, although low, was of sufficient concern that postexposure prophylaxis was recommended for nine persons in the Oregon case.

For this episode, only a small proportion of health-care workers and other persons received postexposure prophylaxis. In contrast, for the 10 U.S. cases from 1977 to 1979, an average of 49 contacts per patient were treated (1). An average of 92 contacts per case for four recent U.S. human rabies cases received prophylaxis (3,4,6,7). However, hospitals are moving toward the implementation of universal precautions (16); this practice may help explain why so few health-care workers in Oregon needed prophylaxis.


1.Anderson LJ, Nicholson KG, Tauxe RV, Winkler WG. Human rabies in the United States, 1960 to 1979: epidemiology, diagnosis, and prevention. Ann Intern Med 1984;100:728-35. 2.CDC. Rabies surveillance, United States, 1987. MMWR 1988;37(suppl SS-4). 3.CDC. Human rabies--California, 1987. MMWR 1988;37:305-8. 4.CDC. Human rabies diagnosed 2 months postmortem--Texas. MMWR 1985;34:700,705-7. 5.CDC. Human rabies--Pennsylvania. MMWR 1984;33:633-5. 6.CDC. Human rabies--Texas. MMWR 1984;33:469-70. 7.CDC. Human rabies--Michigan. MMWR 1983;32:159-60. 8.Smith JS, Reid-Sanden FL, Roumillat LF, et al. Demonstration of antigenic variation among rabies virus isolates by using monoclonal antibodies to nucleocapsid proteins. J Clin Microbiol 1986;24:573-80. 9.Rupprecht CE, Glickman LT, Spencer PA, Wiktor TJ. Epidemiology of rabies virus variants: differentiation using monoclonal antibodies and discriminant analysis. Am J Epidemiol 1987;126:298-309. 10.Helmick CG, Tauxe RV, Vernon AA. Is there a risk to contacts of patients with rabies? Rev Infect Dis 1987;9:511-8. 11.Houff SA, Burton RC, Wilson RW, et al. Human-to-human transmission of rabies virus by corneal transplant. N Engl J Med 1979;300:603-4. 12.CDC. Human-to-human transmission of rabies via a corneal transplant--France. MMWR 1980;29:25-6. 13.CDC. Human-to-human transmission of rabies via corneal transplant--Thailand. MMWR 1981;30:473-4. 14.Gode GR, Bhide NK. Two rabies deaths after corneal grafts from one donor (Letter). Lancet 1988;2:791. 15.Warrell DA, Warrell MJ. Human rabies and its prevention: an overview. Rev Infect Dis 1988; 10(suppl 4):S726-31. 16.CDC. Recommendations for prevention of HIV transmission in health-care settings. MMWR 1987;36(suppl 2S).

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