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Human Rabies -- Texas

The first case of human rabies occurring in the United States since March 1983 was diagnosed July 27, 1984, in Houston, Texas. The patient, a 12-year-old Laotian refugee, had no known history of exposure to a rabid animal and had not traveled outside Texas since arriving in the United States in 1980.

The patient was in good health until July 11, when she complained of a headache. Over the next 4 days, she developed a sore throat, fever, fatigue, difficulty swallowing, and, finally, leg weakness. She was admitted to a community hospital in Houston on July 15. Initial evaluation disclosed a fever of 40 C (104 F), pharyngitis, retropharyngeal air, and a pneumomediastinum. The heart rate fluctuated between 100 beats/minute at rest to 280/minute when the patient was moved. She was treated for presumptive sepsis with antibiotics and corticosteroids. The following day, she was transferred to a university hospital because of the extreme lability of her heart rate and blood pressure. Provisional admitting diagnosis was Guillain-Barre syndrome. The patient was alert and oriented. There were no symptoms or signs except inability to swallow saliva and generalized weakness, more pronounced in the lower extemities; sensory examination was normal. Lumbar puncture revealed normal opening pressure, cell count, and protein. The patient was intubated because of profuse oral secretions, but rapidly became ventilator-dependent. On July 20, increased agitation was noted. Over the next 3 days, periods of decreased alertness and inability to follow commands developed. On July 24, her pupils became dilated and nonreactive to light. A brain biopsy was performed on July 27 after herpes simplex virus was recovered from a throat culture and a temporal focus of seizure activity developed on a repeat EEG. Histopathology revealed eosinophylic intracytoplasmic inclusions; electron microscopy revealed rhabdovirus, and the diagnosis of rabies was confirmed by fluorescent antibody testing. Experimental therapy with ribavirin was initiated. The patient died August 8, 27 days after onset of illness.

Sera and cerebrospinal fluid (CSF) were tested at CDC for rabies neutralizing antibodies using the rapid fluorescent focus inhibition test. On July 21, day 11 of illness, serum titer was lower than 1:5; on July 28, day 18, it had risen to 1:280. Appearance of neutralizing antibody in the serum may have been delayed because of the administration of corticosteroids early in the illness. CSF revealed a 1:11 titer on July 25. Rabies virus was isolated from a second brain biopsy obtained on July 31. Monoclonal antibody studies of the isolate have shown it to be a classic rabies virus, but it does not resemble two of the most common rabies virus substrains isolated in Texas from the Mexican free-tailed bat or from Texas skunks.

A total of 142 individuals (123 medical and paramedical personnel and 19 friends and family) with some degree of contact with the patient received postexposure prophylaxis. Reported by D Swanson, MD, R Feigin, MD, L Tanney, MD, M Feingold, MD, D Anderson, MD, C Baker, MD, L Jefferson, MD, V Knight, MD, J Laurent, MD, J Parke, MD, D Seavy, I Solis MD, Texas Children's Hospital, W Hill, MD, X Jones, R Wende, MD, Sam Houston Community Hospital, J Haughton, MD, J Baird, MPH, M Lugo-Faria, MD, G Reeve, PhD, M Wilson, MD, D Harrison, City of Houston Dept of Public Health, T Betz, MD, C Alexander, MD, Texas Dept of Health; Div of Viral Diseases, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: No more than five cases per year of human rabies have been reported in the United States since 1960. Despite its rarity, rabies should be considered in the differential diagnosis of progressive neurologic diseases, even in the absence of furious behavior, classic hydrophobia, or history of exposure.

In the present case, the pathogenesis of the retropharyngeal and mediastinal emphysema is unknown. The patient had many features of the less common paralytic form of rabies, in which hyperactivity is absent and paralysis dominates the clinical picture (1). The paralysis may ascend, as in the present case, mimicking Guillain-Barre syndrome. This presentation occurs in approximately 20% of human rabies cases, and appears more often after exposure to rabid bats and possibly after postexposure therapy with nerve-tissue vaccines available in some countries outside the United States.

The patient had no history of exposure to an animal known or suspected to be rabid before or after arrival in the United States. The possibility of acquisition outside the United States is remote. Although an exposure can be identified in most cases of rabies, no exposure has been identified in eight (19%) of the 43 cases occurring in the United States from 1960 through the present (2). Incubation periods of less than 1 year are found in 99% of cases; the longest well-documented incubation period was 701 days (3).

The large number of persons receiving postexposure prophylaxis because of contact with the patient demonstrates that tremendous costs may be incurred as a result of undiagnosed cases. The cost of a single postexposure regimen of five doses of human diploid cell rabies vaccine and 20 IU/kg of human rabies immune globulin is approximately $400 for the biologics alone. Postexposure therapy is indicated in certain circumstances after contact with a human rabies case. Although never reported, the theoretic possibility of human-to-human bite transmission exists, as does that of nonbite transmission by contamination of scratches, abrasions, or open wounds with potentially infectious material, such as saliva, urine, or brain tissue. Transmission between humans has only been documented in four persons who received corneal transplants from donors who died of undiagnosed rabies encephalitis. Once rabies is suspected, adherence to contact isolation procedures (4) can markedly reduce the need for postexposure therapy in health-care workers. Each potential exposure to human rabies should be carefully evaluated to minimize unnecessary rabies prophylaxis (5).

References

  1. Chopra JS, Banerjee AK, Murthy JMK, Pal SR. Paralytic rabies. A clinico-pathological study. Brain 1980;103:789-802.

  2. Anderson LJ, Nicholson KG, Tauxe RV, Winkler WG. Human rabies in the United States 1960-1979: epidemiology, diagnosis, and prevention. Ann Intern Med 1984;100:728-35.

  3. CDC. Human rabies death--West Virginia. MMWR 1965;14:195.

  4. Garner JS, Simmons BP. Guideline for isolation precautions in hospitals. Infect Control 1983;4:245-325.

  5. ACIP. Rabies prevention--United States, 1984. MMWR 1984;33:393-408.



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