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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
Chopra JS, Banerjee AK, Murthy JMK, Pal SR. Paralytic rabies.
A
clinico-pathological study. Brain 1980;103:789-802.
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.
CDC. Human rabies death--West Virginia. MMWR 1965;14:195.
Garner JS, Simmons BP. Guideline for isolation precautions in
hospitals. Infect Control 1983;4:245-325.
ACIP. Rabies prevention--United States, 1984. MMWR
1984;33:393-408.
Disclaimer
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