Persons using assistive technology might not be able to fully access information in this file. For assistance, please send e-mail to: firstname.lastname@example.org. Type 508 Accommodation in the subject line of e-mail.
Rabies in the United States, 1981
Gregory L. Parham, D.V.M. Viral and Rickettsial Zoonoses Branch (Formerly Respiratory and Special Pathogens Branch)
Division of Viral Diseases Center for Infectious Diseases
Human rabies is a preventable disease that is nearly always fatal. The increasing reports of this disease in both domestic animals and wildlife underscore the importance of careful monitoring of the occurrence and spread of this disease (1-3t).
CDC has conducted surveillance of animal and human rabies since 1961. Case reports are submitted on a voluntary basis and therefore represent only a fraction of the true incidence of animal rabies in the United States.
Information in this report is based on reports collected by the health officers of the various states, territories, or other jurisdictions of the United States. A standardized form, the Monthly Report of Laboratory Confirmed Cases of Rabies, is used. Included are the county of origin, reporting month, number of animals examined, and species of animals examined. Specimens from animals suspected of having rabies are submitted for examination to a public health laboratory. Only those animals that are positive on examination using either the fluorescent rabies antibody (FRA) test or the mouse inoculation (MI) test are reported as actual cases of rabies.
In 1981, 7,211 laboratory-confirmed cases of animal rabies were reported in the United States and its territories (Guam, Puerto Rico, and the Virgin Islands of the United States), the largest number of cases since 1954, when 7,282 cases were reported.
Forty-eight states and Puerto Rico reported infected animals (Table 1). No cases were reported from the District of Columbia, Guam, Hawaii, Vermont, and the Virgin Islands. Seven kinds of animals accounted for 97% of the reported cases: skunks, 4,480 (62%); bats, 858 (12%); raccoons, 481 (7%); cattle, 465 (6%); cats, 285 (4%); dogs, 216 (3%); and foxes, 196 (3%). Of the reported animal cases, 6,127 (85%) occurred in wild animals and 1,084 (15%) in domestic animals. Approximately 95,000 animals were examined during 1981, and the rate of positivity was 8%.
Rabies in Wildlife. Seventy-three percent of all wildlife rabies cases reported for 1981 occurred in skunks. The 4,480 cases represent the most cases of skunk rabies ever recorded. Thirty-two states reported cases, mostly in the Central and Pacific regions of the United States. Minnesota reported rabies in pet skunks (4t). Bats continue to be the most widely distributed animal host for rabies. Forty-six states reported a total of 858 cases, the largest number of cases ever recorded. Thirteen states reported raccoon rabies. The total of 481 cases is the second largest number ever reported. Raccoon rabies has been endemic in the southeastern United States for several years and has now become well-established in Maryland, Virginia, and West Virginia (5t). Virginia reported 102 cases of raccoon rabies, second only to Georgia, which had 172 cases. In 1981, 196 cases of fox rabies were reported, 17 fewer than in 1980. Twenty-six states reported cases. New York reported 29 cases; Texas and Alaska reported 25 cases each.
Rabies in Domestic Animals. Thirty-one states and Puerto Rico reported rabies in domestic animals in 1981. Increases were recorded for all three major domestic animal hosts (dogs, cats, and cattle), and, for the first time ever, cases of rabies in cats outnumbered cases in dogs.
Rabies in Humans. Two cases of human rabies were reported for 1981 (6,7t). Both cases were unusual in that they had no clearly defined source of exposure. They are described in detail below.
A 27-year-old male who worked as a day laborer had been in relatively good health until June 21, 1981, when he visited an emergency room in Oklahoma City complaining of sore throat and pain in his right ear. He was given penicillin V tablets and pain medication for acute pharyngitis. In the period June 22-24, he was seen on four separate occasions by different physicians for increasing throat pain and difficulty in swallowing, and on one occasion for numbness of his left arm. He was treated with penicillin, antihistamines, and parenteral steroids. Increasing dysphagia led to his hospitalization on June 25. At that time he was diagnosed as having possible aspiration pneumonia and was noted to be agitated and confused. Soon after admission he had a respiratory arrest and was intubated. Neurologic examination revealed the patient to be comatose with depressed extraocular movements, left pupillary diameter larger than the right, diffuse left-sided spasticity, decreased corneal reflexes, poor caloric responses, and poor doll's-eye reflex. The initial neurologic diagnosis was a possible brain abscess or subdural empyema. A computerized tomography scan showed no mass lesions; lumbar puncture revealed a protein level of 85 mg/dL, a glucose level of 158 mg/dL, 6 lymphocytes/mmðcp6å3ðcp9,11å, and 16 red blood cells/mmðcp6å3ðcp9,11å. The patient was treated with multiple antibiotics and given respiratory support. By June 30, he was in deep coma with no brain-stem reflexes. He died 4 days later.
Family and friends were unable to recall any specific exposure the patient might have had to rabid animals or animal bites. Review of emergency-room logs in the Oklahoma City area did not show that the patient had recently sought medical attention for an animal bite. The patient lived with his father, a friend, and a pet dog in Oklahoma City. Rabies vaccination history for the dog was questionable, but the animal remained healthy. The patient had spent March, April, and May camping near Corsicana, Texas. On returning to Oklahoma City on June 1, he did not mention having been bitten by an animal while in Texas. This is another in the increasing number of rabies cases with no identified source of exposure.
The other patient was a 40-year-old U.S. citizen living in Empalme, Sonora, Mexico, who was bitten on the right hand by his dog on June 22, 1981. The animal was immediately killed, and the head was shipped to the Hermosillo Health Laboratory, Hermosillo, Mexico, for rabies examination. Brain material examined histologically with Sellers stain revealed no evidence of Negri bodies diagnostic of rabies. Because of the laboratory report and a history of recent rabies vaccination of the dog, this person was not given rabies postexposure prophylaxis.
The patient remained well until August 19, 58 days after the bite, when he developed paresthesias and numbness of his right hand near the site of the bite. During the next several days, he complained of fever, malaise, and aching in his right arm. By August 24, 6 days after onset of symptoms, the patient was having spasms of the throat, especially when drinking water. A local physician discussed the possibility of rabies, but the patient discounted the diagnosis. Increasing agitation and insomnia ensued, and hydrophobia became so severe that he elected not to shower because of the resulting painful throat spasms. On August 26, the patient traveled to Tucson, Arizona, where he was admitted to the University of Arizona Health Sciences Center with the diagnosis of probable rabies.
In the first 24 hours after admission, the patient was lucid and able to give a coherent medical history. On examination, however, he was agitated, with marked pharyngeal and neck muscle spasms when water was wiped on his forehead or when a stream of air was directed at his face. Right-arm weakness and right deltoid fasciculations were observed initially, and the illness progressed to flaccid paralysis of all limbs within 72 hours.
Immediately after he was admitted to the hospital, a neck biopsy was done, and the diagnosis of rabies was confirmed by direct fluorescent antibody testing of the tissue at CDC. The patient was given a single dose each of human diploid cell rabies vaccine and of human rabies immune globulin (HRIG). A lumbar puncture revealed an opening pressure of 270 ml Hðcp6å2ðcp9,11åO, a protein level of 26 mg/dL, a glucose level of 82 mg/dL, and no cells. Urinalysis showed a specific gravity of 1.033 and was otherwise normal. Hematologic examination revealed a white blood count of 14,200 with 81% polymorphonuclear leukocytes, two band cell forms, 12 lymphocytes, and five monocytes. Multiple specimens were obtained for virus isolation from nasopharyngeal, rectal, throat, and conjunctival swabs, whole blood, tracheal aspirates, urine and urine sediment, and cerebrospinal fluid (CSF).
An interferon treatment protocol was begun on the tenth day of illness. Human leukocyte interferon was given twice a day intramuscularly and once a day intraventricularly through an Omaya reservoir connected by a cannula to the right lateral ventricle of his brain.
Despite intensive support, his course was complicated by bilateral bronchopneumonia, acute renal failure, hypotension, autonomic instability, and seizures. He died suddenly of respiratory and vascular collapse on September 11.
Serum and CSF collected daily for the entire period of hospitalization remained negative for rabies antibody by rapid fluorescent inhibition tests done at CDC. Isolation of rabies virus was confirmed by mouse inoculation from a throat swab and tracheal aspirate on the eleventh day of illness and from another tracheal aspirate on the fifteenth day of illness. No virus was isolated from daily CSF samples. Direct fluorescent antibody staining of frozen postmortem tissue was positive for rabies antigen from kidney parenchyma, bladder nerve tissue, skin of the neck, skin from the bite site, occipital nerve, pharynx, choroid plexis, sural nerve, dorsal root ganglion, stellate ganglion, right radial nerve, cervical spinal cord, hippocampus, and pons.
Questioning of the patient and his family revealed no known positive rabies exposure other than the dog bite. The patient also owned three other dogs. The male dog that had bitten him had been unusually aggressive for 3 or 4 days before the bite incident. It was assumed this behavior resulted from contact with another of the dogs, a female in estrus. Several weeks after the bite incident, the female died of a paralytic disease and was buried without being examined. Within the previous year, all four of the patient's dogs had been vaccinated for rabies with inactivated suckling mouse brain vaccine.
This is another case of rabies with no proven source of exposure, although there is suggestive evidence that the dog bite he received on June 28 is the likely source of infection. If this is so, then the vaccine given the dog failed to protect it, and the negative laboratory report on the dog was erroneous. This case is also interesting as it represents the first rabies patient in the United States treated extensively with interferon, unfortunately without impeding progression of the disease. Discussion
Animal rabies continues its upward trend of recent years (1-3t). While all cases reported here are laboratory confirmed, there are undoubtedly thousands of cases (mostly in wildlife) that are not examined. Rabies in wild animals kept as pets continues to be a problem in some areas. CDC recommends that wild and exotic animals not be kept as pets and that animal rabies vaccines only be used for those species of animals for which they are approved (8t).
Human diploid cell strain rabies vaccine (HDCV) was licensed in June 1980 (9t). Experience with this vaccine has been excellent, and it has replaced duck embryo rabies vaccine (DEV) as the treatment of choice for both preexposure and postexposure rabies prophylaxis (10t). Serologic testing is no longer required for persons who received the recommended preexposure or postexposure treatment regimens of HDCV (11t).
ReferencesCDC. Rabies--United States, 1980. MMWR 1981;30:147. CDC. Rabies surveillance report--Annual Summary, 1979. Atlanta: CDC, October 1981. CDC. Rabies surveillance report--Annual Summary, 1978. Atlanta: CDC, May 1981. CDC. Rabies in a pet skunk--Minnesota. MMWR 1981;30:47-8. CDC. Rabies in raccoons--Virginia. MMWR 1981;30:353-5. CDC. Human rabies--Oklahoma. MMWR 1981;30:343-9. CDC. Human rabies acquired outside the United States from a dog bite. MMWR 1981;30:537-40. CDC. Compendium of animal rabies vaccines--1981. MMWR 1981;30:161-4. CDC. Rabies prevention. MMWR 1980;29:265-80. CDC. Discontinuation of duck embryo rabies vaccine. MMWR 1981;30:407-8. CDC. Supplementary statement on rabies vaccine and serologic testing. MMWR 1981;30:535-6.
Disclaimer All MMWR HTML documents published before January 1993 are electronic conversions from ASCII text into HTML. This conversion may have resulted in character translation or format errors in the HTML version. Users should not rely on this HTML document, but are referred to the original MMWR paper copy for the official text, figures, and tables. An original paper copy of this issue can be obtained from the Superintendent of Documents, U.S. Government Printing Office (GPO), Washington, DC 20402-9371; telephone: (202) 512-1800. Contact GPO for current prices.**Questions or messages regarding errors in formatting should be addressed to email@example.com.
Page converted: 08/05/98
This page last reviewed 5/2/01