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Epidemiologic Notes and Reports Human Rabies -- Texas, Arkansas, and Georgia, 1991

From August through October 1991, three persons, one each in Texas, Arkansas, and Georgia, died from rabies. Including these three cases, 16 cases of human rabies have been reported to CDC from 1980 through 1991; seven of these are believed to have been acquired in the United States (1). This report summarizes epidemiologic and clinical information regarding the three recent cases.

Patient 1. During August 7-9, a woman from Starr County, Texas, had increasing nervousness, shortness of breath, and difficulty swallowing. On August 9, she was admitted to a local hospital with a diagnosis of panic disorder. During the first 3 hospital days, her temperature fluctuated from 97 F (36 C) to 106 F (41 C). On August 12, rabies was first considered in the differential diagnosis because of aerophobia, hydrophobia, agitation, and incoherence alternating with periods of coherence; a skin biopsy and saliva, serum, and cerebrospinal fluid (CSF) specimens were obtained from the patient. An ascending paresis developed, and on August 16 she was transferred to another hospital for a computerized axial tomographic scan of the head; only an old infarct in the left cerebellum was found. After the scan, she had a respiratory arrest that progressed to cardiac arrest; she was resuscitated but did not regain consciousness and died on August 20.

The serum and CSF specimens obtained on August 12 were negative for rabies antibody; in addition, the skin biopsy from the nape of the neck, tested at CDC, was negative for rabies by the direct immunofluorescent antibody (DFA) test. However, on August 17, rabies virus was detected in cell culture of the saliva specimen at CDC. Monoclonal antibody typing showed the rabies virus isolate to be identical to the virus strain found in dogs in Mexico and along the border of Mexico and Texas. A second skin biopsy from the nape of the neck, obtained on August 19, was positive by DFA.

The woman had no known exposure to rabies. She was a native of Texas and had resided all her life in Starr County, where rabies is endemic in dogs and coyotes. She occasionally visited relatives in northern Mexico but had last been there more than 1 year before onset of illness. She had a history of a dog bite at 9 years of age but had no other known animal bites.

As a result of possible exposure to this patient, 43 persons received postexposure prophylaxis. At the first hospital, 30 members of the staff who provided care for the patient--before isolation precautions were instituted on August 12--were treated because of concern about possible exposure to saliva. At the second hospital, postexposure treatment was given to seven persons who assisted in the resuscitation that followed the patient's respiratory arrest and who were unaware of the suspected diagnosis. All six members of the patient's household also received rabies prophylaxis.

Patient 2. On August 17, a man from Clark County, Arkansas, had onset of a sore throat and headache. On August 19, he visited his doctor because of difficulty swallowing and sore throat. On examination, his temperature was 99 F (37 C); he appeared agitated and tremulous and had pharyngitis. He was treated parenterally and orally with antibiotics and sent home. That evening, family members found him pacing and spitting frequently; he appeared anxious and fearful, and his facial muscles were twitching. He was taken to the local emergency room and later was transferred to a tertiary-care hospital, where he complained of headache, generalized itching, difficulty swallowing, and a gagging sensation; he was alert and oriented but tremulous, agitated, and photophobic. Differential diagnosis included drug overdose, viral encephalitis, and tetanus; although rabies was considered, he had no history of animal bites.

On August 20, he required intubation because of frequent vomiting and obtundation. He developed rhabdomyolysis, and his temperature was intermittently as high as 106 F (41 C). On August 23, he had a cardiac arrest and was resuscitated but thereafter had no sign of brain stem function. He died on August 25.

Postmortem samples of brain tissue were positive for rabies by DFA testing at the Arkansas Department of Health, and monoclonal antibody typing at CDC suggested a rabies variant commonly found in the silver-haired bat (Lasionycteris noctivagans).

The man was a native of Arkansas and had never traveled outside the southwestern region of the state. He had lived in a previously abandoned, rural house. A friend reported that one night in early July a bat had landed on the man's mouth; the patient killed and disposed of it. Although the friend had detected no bites or scratches on the man's face, other friends and co-workers whom the patient had told about the incident recalled bites on his thumb or scratches on his chest.

A total of 99 persons identified as having possible exposures to the patient--from 2 weeks before onset of his symptoms through the time of his death--received postexposure prophylaxis. Of these persons, 32 were community contacts, which included one sex partner, eight family members, 14 health-care personnel who had been near the patient's saliva and vomitus, and nine friends and co-workers who had had recent contact with the patient's saliva through shared utensils. The other contacts included a mortician and 66 (44%) of the 150 hospital staff involved in care of this patient and concerned about their contact with his saliva or vomitus.

Patient 3. On October 2, a woman from Walker County, Georgia, (on the Tennessee-Georgia border) developed sore throat, headache, and fever. She was treated at a local emergency room with parenteral antibiotics and discharged. On October 4, she developed additional symptoms including difficult and painful swallowing, agitation, and a fever of 104 F (40 C). She was admitted to a local hospital; later that day she was transferred to a referral hospital, where rabies and other viral encephalitides were considered in the differential diagnosis. Her condition continued to deteriorate, with progressive obtundation; on October 8, she died of cardiac arrest. Rabies was diagnosed postmortem by demonstration of Negri bodies in brain tissue and confirmed by DFA at the Tennessee State Department of Health Laboratory and at CDC. Monoclonal antibody typing at CDC suggested the involvement of the same rabies variant as that isolated from patient 2.

The patient had moved to Walker Country, Georgia, from Hamilton County, Tennessee, 8 months before her illness. Extensive interviews with the patient's family and friends in Georgia and Tennessee did not reveal any known animal exposure. She had never traveled outside the United States and had not engaged in outdoor activities. Reported by: R Gonzales, MD, M Ramirez, MD, Rio Grande Hospital, Starr County; M Jelinek, MD, C Milan, MSN, Mission Hospital, Hidalgo County; M Kelley, MD, DM Simpson, MD, State Epidemiologist, Texas Dept of Health. T Brinkley, MD, G Taylor, MD, Baptist Medical Center; A Harris, Clark County Sheriff's Office, Arkadelphia; D Saugey, National Park Svc, Hot Springs; M Edelmann, JP Lofgren, D Berry, T McChesney, MD, State Epidemiologist, Arkansas Dept of Health. DL Dean, DO, District 1-1 Div of Public Health, Walker County; JD Smith, JA Wilber, MD, State Epidemiologist, Div of Public Health, Georgia Dept of Human Resources. P Alexander, MD, Univ of Tennessee College of Medicine; M Kosanovich, MD, SS Hawkins, MD, J Grant, Erlanger Medical Center, Chattanooga; VA Boaz, MD, HW Roddy, MSEH, T Burke, D Needham, S Goforth, RJ Jerardi, MSHP, Chattanooga-Hamilton County Health Dept; S Allom, Cleveland Community Hospital; E Waters, Bradley County Health Dept; JM BeVille, MD, RH Hutcheson, MD, State Epidemiologist, Tennessee Dept of Health and Environment. Div of Field Epidemiology, Epidemiology Program Office; Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: Although rabies is enzootic among many species of wild animals, human rabies is rarely acquired in the United States. The last reported case in the United States occurred in June 1990 in Texas (2), in a county adjacent to that in which patient 1 resided. The last reported cases of human rabies in Arkansas and Georgia occurred in 1956 and 1960, respectively.

A definite bite by an animal was not established as a clear exposure for any of the three patients in this report. A bite by a proven or presumed rabid animal was identified in all 15 of the cases reported in the 1960s and in 18 (78%) of the 23 reported in the 1970s, but only four (40%) of the 10 reported in the 1980s. Because many patients with rabies have died or are severely ill at the time rabies is diagnosed, it is sometimes not possible to determine an exposure. In some cases, however, failure to establish a clear exposure may reflect the possibility that exposure occurred many years before onset of symptoms (3). Patient 1 may have been exposed when she was bitten as a child, but it is more likely she incurred a recent unreported or unrecognized exposure associated with the rabies epizootic ongoing since 1987 among dogs and coyotes in her county of residence (1). Canine rabies is a long-standing problem along the U.S.-Mexican border, although human rabies of canine origin acquired in the United States has not been documented since 1979 (4).

Bat rabies is endemic in most states (1,5,6), and bats have accounted for five of the seven indigenously acquired human rabies cases reported since 1980 (2,7,8). Although patient 2 had close contact with a bat, no bite was identified, and the patient did not seek postexposure treatment. Patient 3 had no known exposure to rabies but was infected with the same strain as patient 2, suggesting possible exposure to a silver-haired bat.

The earliest manifestations of rabies are commonly nonspecific constitutional complaints. The disease then progresses to one of two distinct presentations: the more common furious form (characterized by hydrophobia, aerophobia, or episodic agitation and anxiety) or the less common paralytic form. Rabies should be considered in any patient with a rapidly progressive encephalitis of unknown etiology (9), particularly in patients who have lived in an area with endemic canine rabies or who have had an exposure or other close contact with a recognized reservoir of the disease. One hallmark of rabies is its rapid progression to death; no survivors have been reported since 1977.

Rabies postexposure prophylaxis is recommended for all persons bitten or scratched by wild or domestic animals that may be carrying the disease. Exposures other than bites or scratches rarely result in infection. However, postexposure treatment is recommended for persons who report having an open wound or mucous membrane contaminated with saliva or other potentially infectious material (e.g., brain tissue) from a rabid animal. Since the size of bites by bats may be small in comparison to those inflicted by terrestrial animals (6), it may be prudent to consider postexposure treatment for physical contact with bats when a bite or mucous membrane exposure cannot be excluded. Treatment should always be initiated as soon as possible after bites or scratches by known or suspected rabid animals occur.

Postexposure prophylaxis also is recommended for persons who report a possibly infectious exposure (e.g., bite, scratch, or open wound or mucous membrane contaminated with saliva or other infectious material) to a human with rabies. However, exposure to a human with rabies has never been implicated as a means of rabies transmission except following cornea transplantation from donors who died of unsuspected rabies encephalitis (10). Casual contact with an infected patient (e.g., touching the patient) or contact with noninfectious fluids or tissues (e.g., blood, urine, or feces) does not alone constitute an exposure and is not an indication for prophylaxis (10).

References

  1. Reid-Sanden FL, Dobbins JG, Smith JS, Fishbein DB. Rabies surveillance in the United States during 1989. J Am Vet Med Assoc 1990;197:1571-83.

  2. CDC. Human rabies--Texas, 1990. MMWR 1991;40:132-3. 3. Smith JS, Fishbein DB, Rupprecht CE, Clark K. Unexplained rabies in three immigrants in the United States: a virologic investigation. N Engl J Med 1991;324:205-11.

  3. Glosser JW, Hutchinson LR, Rich AB, Huffaker RH, Parker RL. Rabies in El Paso, Texas, before and after institution of a new rabies control program. J Am Vet Med Assoc 1970; 157:820-5.

  4. McChesney TC, Spatz H, Edelman M. Bat rabies in Arkansas. Journal of the Arkansas Medical Society 1983;80:181-5.

  5. Constantine DG. Bat rabies in the southwestern United States. Public Health Rep 1967;82:867-88.

  6. CDC. Human rabies--Pennsylvania. MMWR 1984;33:633-5.

  7. CDC. Human rabies--Michigan. MMWR 1983;32:159-60.

  8. Whitley RJ. Viral encephalitis. N Engl J Med 1990;323:242-50.

  9. Helmick CG, Tauxe RV, Vernon AA. Is there a risk to contacts of patients with rabies? Rev Infect Dis 1987;9:511-8.



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