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Human Rabies -- Texas, 1990

On June 5, 1990, a 22-year-old man died of rabies encephalitis in Hidalgo County, Texas, along the Mexican border. This was the fourth case of human rabies known to be acquired in the United States since 1980 and the first case in Texas since 1985. This report summarizes the case investigation.

On April 13, the man was bitten on the right index finger by a bat while at a tavern in Mercedes, Texas. The patient did not obtain medical care for the bite; he remained well until May 30, when he complained of right hand weakness. On June 1, he complained of right arm numbness and dysesthesias. On June 2, he exhibited several episodes of staring and unresponsiveness lasting 10-15 seconds. He consulted a physician in Mexico, who prescribed an unknown medication. That evening he presented to a hospital emergency room in Texas complaining of right hand pain. Based on a history of a puncture wound with a catfish fin earlier in the week, he was treated with ceftriaxone and tetanus toxoid.

On June 3, when he returned to the emergency room complaining of "spasms," he was hyperventilating and had a white blood cell (WBC) count of 11,100 per mm3. Although he was discharged after reporting some improvement, he subsequently had intermittent episodes of rigidity, breath holding, hallucinations, and difficulty in swallowing; eventually he refused liquids. That evening he was admitted to the intensive-care unit of another hospital in Texas with a preliminary diagnosis of either encephalitis or tetanus. Manifestations included frequent spasms of the face, mouth, and neck; stuttering speech; hyperventilation; and temperature of 100.1 F (37.8 C). The WBC count was 17,100 per mm3 with a granulocytosis. He was sedated and observed.

On the morning of June 4, the patient was confused, disoriented, and areflexic. Although his neck was supple, muscle tonus was increased in his upper extremities. Analysis of cerebrospinal fluid (CSF) indicated slightly elevated protein (51 mg divided by L; normal: 15-45 mg divided by L); slightly elevated glucose; and 3 red blood cells and 1 WBC per dL. An electroencephalogram showed abnormal slow and alpha activity without focal abnormality. Because the patient had uncontrolled oral secretions, he was intubated. His temperature rose to 107 F (41.7 C), and he had marked diaphoresis. Later on June 4, the patient's supervisor from work reported the man's history of a bat bite to hospital authorities. CSF, serum, and skin biopsy (taken from the nape of the neck) samples were forwarded to CDC for rabies testing; all of these samples were negative. The patient became comatose and died on June 5. Postmortem samples of brain tissue were positive for rabies by the direct immunofluorescence antibody test. Monoclonal antibody typing suggested that the rabies variant was the Mexican free-tailed bat (Tadarida braziliensis mexicana) strain.

Although the period of rabies virus infectivity before onset of clinical symptoms (i.e., preclinical secretion of rabies virus) is probably only a few days, for the purpose of contact investigation for this case, public health authorities considered the 2 weeks before onset of the patient's symptoms to be the period of infectivity. Consequently, postexposure prophylaxis was initiated for 67 of 100 possibly exposed contacts among family, friends, coworkers, and medical personnel.

The patient had worked as a phlebotomist for a blood bank and had donated blood on May 22 before onset of symptoms. His platelets had been transfused before he became ill, but the remainder of his blood products were destroyed. Although rabies virus was not isolated from the patient's blood and he was probably not infectious when he donated, the platelet recipient received rabies immunoprophylaxis. Reported by: J Martin, MD; P Brattin, Valley Baptist Medical Center, Harlington; H Acevedo, McAllen; M Kelly, MD, Bur of Disease Control and Epidemiology, S Neill, PhD, Texas Dept of Health. Viral and Rickettsial Zoonoses Br, Div of Viral and Rickettsial Diseases, CDC.

Editorial Note

Editorial Note: The primary types of animal exposures leading to human rabies in the United States have changed since 1950 (1), when most cases were acquired from domestic animals. From 1980 through 1990, 13 cases of human rabies in the United States were reported to CDC; four (30.8%) were acquired domestically.

Bat rabies occurs everywhere in the continental United States: during 1989, each of the 48 contiguous states and the District of Columbia reported infected bats. From 1980 through 1990, the number of reported infected bats peaked in 1984 with 1038. In 1989, California and Texas reported the highest number of infected bats (117 and 72, respectively). Rabies is enzootic in the Mexican free-tailed bat, the most important vector of rabies in the southwestern states; rabies isolation rates vary from 0.5% in apparently normal bats to greater than 50% in clinically affected bats (2). In the southeastern and mid-Atlantic states, rabies is most prevalent in the migratory red bat.

Based on monoclonal antibody analysis and exposure history, three of the four cases of human rabies acquired within the United States from 1980 through 1990 resulted from exposure to bats. In general, postexposure prophylaxis should be initiated for persons exposed to vampire, frugivorous, and insectivorous bats; it may be discontinued if the bat is tested and found negative for rabies. In 1980 and 1981, 10% of persons who received rabies prophylaxis had been bitten by bats (3).

In addition to rabies virus, other causes of viral encephalitis in humans in the United States include herpes simplex, St. Louis encephalitis, eastern equine encephalitis, Venezuelan equine encephalitis, and La Crosse viruses (4-6). The most common clinical manifestation of viral encephalitis is acute onset of febrile illness with headache, fever, disorientation, behavioral and speech changes, and other neurologic signs. As this report indicates, diagnosis of central nervous system infections is difficult. Although definite exposure histories are sometimes absent, a history of an animal bite and a rapidly progressive encephalitis should prompt health-care providers to consider rabies in the differential diagnosis.

Human rabies can be prevented by avoiding contact with rabid animals. Most terrestrial mammals are susceptible to rabies virus infection. Contact should be avoided with all wild and domestic animals exhibiting atypical behavior. Family dogs and cats should be vaccinated against rabies. If human exposures do occur, immediate cleansing of the bite wound with soap and water is recommended. When possible, the biting animal should be captured and submitted for testing for rabies. Medical care should also be sought to assess the need for tetanus vaccination, general wound care, and rabies prophylaxis.


  1. CDC. Rabies surveillance, United States, 1988. MMWR 1989;38(no. SS-1).

  2. Constantine DG, Tierkel ES, Klecker MD, Hawkins DM. Rabies in New Mexico cavern bats. Public Health Rep 1968;83:303.

  3. Hughes SS. The virus: a history of the concepts. New York: Science History Publications, 1977.

  4. Whitely RJ. Viral encephalitis. N Engl J Med 1990;232:242-50.

  5. Luby JP. St. Louis encephalitis. Epidemiol Rev 1979;1:55-73.

  6. Shope RE. Epidemiology: mechanisms of cause, distribution, and transmission of viral disease. In: Fields BN, Knipe DM, Chanock RM, Melnick JL, Roizman B, Shope RE, eds. Virology. New York: Raven Press, 1985:145-51.

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