Page images
PDF
EPUB

Human Rabies - Continued

examination revealed no focal neurological abnormalities. A psychiatric disorder was also considered because he had priapism and expressed great concern about recent pubertal changes.

Lumbar punctures, performed on November 30 and December 2, revealed no WBCs and normal protein levels (15 mg/dL on November 30 and 40 mg/dL on December 2). A computerized tomographic (CAT) scan of the head was normal; an electroencephalogram showed moderate diffuse slow wave activity. On December 2, he experienced episodes of hyperthermia (temperature as high as 41.7 °C [107.1 °F]), hypotension (blood pressure 54mm Hg systolic), hypoventilation (arterial blood, pCO2 55 mm Hg, pO2 78 mm Hg), bradycardia (heart rate, 40/min), and increased oral secretions (>1 liter/day). He became comatose, was intubated, and was transferred to a university hospital with a diagnosis of metabolic encephalopathy.

At the time of transfer, the patient had no corneal reflexes, but his doll's eye and gag reflexes were intact. The patient was examined for arthropod or other bite marks, but none were found. A lumbar puncture on December 3 revealed 52 mg/dL of protein (normal, 15-50) and 4 WBC/mm3 (21% polymorphonuclear leukocytes, 44% lymphocytes, 35% monocytes). Magnetic resonance imaging and CAT scans of the head revealed watershed infarcts. On December 8, a lumbar puncture showed a pleocytosis of 25 WBC/mm3 (21% polymorphonuclear cells, 40% lymphocytes, 39% monocytes) and protein of 53 mg/dL. His CPK, which had risen to 10,000 IU/mL, decreased to 600 IU/mL after treatment with diuretics and fluids. His peripheral WBC count ranged between 22,700/mm3 and 12,700/mm3. Despite vigorous supportive measures, the patient's condition deteriorated. He died on December 15, 19 days after onset of illness, with a diagnosis of encephalitis of unknown etiology.

On December 18, brain tissue was tested and found positive for rabies by fluorescent rabies antibody staining. Negri bodies were found subsequently, and rabies virus was isolated from brain tissue. The virus was typed by monoclonal antibodies (1,2). Its reactivity with a panel of monoclonal antibodies to rabies virus nucleocapsid and glycoprotein antigens distinguished it from variants associated with the disease in insectivorous bats in the United States but was identical to that of the virus from the skunk rabies enzootic in northern California.

Serum specimens collected on November 28 and December 9 were negative for rabies-neutralizing antibody, but a postmortem specimen collected on December 16 had a titer of 65,536 by the rapid fluorescent focus inhibition test. No antibodies were detected in cerebrospinal fluid (CSF) samples collected on November 30, December 2, and December 8. Rabies virus could not be isolated from the latter specimen.

Because of possible contact with the patient and his copious secretions, 12 family members and 75 of 177 health-care workers received rabies postexposure prophylaxis, at a cost of $39,000 for the immune globulin and vaccinations. A questionnaire, designed to identify staff who had been exposed,* was administered to hospital, medical examiner, and transport staff. Twenty-five staff members reported exposures to patient's saliva and received rabies postexposure prophylaxis. Rabies postexposure prophylaxis was also administered to a number of other staff members whose exposure status was uncertain. None of three medical examiner's staff received vaccinations because isolation procedures (use of gowns, gloves, masks, and goggles) were followed during the autopsy.

'Defined as contamination of an open wound or mucous membrane with saliva, other ratory tract secretions, brain tissue, or CSF.

[blocks in formation]

Reported by: B Bartlow, MD, T Crooks, MD, A Duckett, RN, St. Luke's Hospital; D Dempsey, MD, J Conte, MD, B Bouvier, RN, UCSF Medical Center; F Taylor, MD, J Wilbur, PhD, San Francisco Dept of Public Health; B Stephens, MD, San Francisco Medical Examiner/Coroner; RW Emmons, MD, PhD, DG Constantine, DVM, SB Werner, MD, RR Roberto, MD, California Dept of Health Svcs. Epidemiology Program Office, Div of Field Svcs; Viral and Rickettsial Zoonoses Br, Div of Viral Diseases, Center for Infectious Diseases, CDC.

Editorial Note: The source of this child's exposure to rabies remains unknown. Including this case, nine cases of human rabies have been diagnosed in the United States since 1980. Three of the patients had been exposed to dogs in rabies-endemic countries outside the United States. The other six patients, including the one whose case is reported here, had no definite history of exposure to rabies (3-7). Three of these six cases were diagnosed post-mortem.

These six patients ranged from 5 to 27 years of age; four were 13 years of age or younger. Rabies virus could be isolated and typed by monoclonal antibodies from specimens from four of the patients. In two of the cases, the rabies variants were similar to those found in rabid insectivorous bats (4,6). Retrospective interviews with the family of one of these patients revealed that the patient was probably bitten by a bat 7 months before the onset of illness (4). Outside the United States, some cases involving patients with no reported exposure have been attributed to exposure to bats (8,9). The etiology of other cases cannot be determined (10). Cases of rabies involving persons with no known exposure have long puzzled investigators (10,11) and, with the decline in indigenous human rabies in the United States, now make up a larger proportion of the total.

In the current case and a previous one (5), the rabies variant was similar to that found in rabid terrestrial animals in the state where the patient lived, a finding that suggests that contact with rabid bats was not responsible for the disease. Although the patients' families and friends were interviewed in depth and could recall no possible exposures, the patients themselves could not be thoroughly questioned. It is possible that, as children, they might not have understood the danger of contact with some animals or might not have reported superficial exposures. Both cases involved children who had emigrated from rabies-endemic areas several years earlier,* a fact that raises the possibility of exposure in their country of origin. However, human rabies cases with incubation periods of a year or more are extremely rare (12). Unfortunately, monoclonal antibody typing cannot distinguish among the isolates from these two patients, variants found in some terrestrial wildlife epizootics (skunks in California and foxes in Texas [5]), and those found in dog rabies enzootic areas of Asia.

As in other cases of rabies, many of the early features of this patient's illness (fever, chills, back pain) were nonspecific and suggestive of many common infections (12,13). Although priapism has been previously reported as a presenting manifestation of rabies (14), its presence in a 13-year-old boy wary of recent pubertal changes and without signs or laboratory results compatible with more common causes of priapism (sickle cell anemia, chronic granulocytic leukemia, and spinal cord injury) presented a difficult diagnostic challenge. Other aspects of his illness, including abdominal pain, opisthotonic posturing, lability of temperature, pulse, and respiratory rate, have been more commonly noted in rabies cases (12). Although the normal CSF on two occasions may have further obscured the diagnosis, the cerebrospinal *Seven years earlier for the patient whose illness is reported here and 4 years earlier for the other patient (5).

Human Rabies - Continued

fluid is frequently normal during the first week of illness and sometimes remains normal even later in the course of the disease (13).

Because human rabies is rare in developed countries, the diagnosis is especially difficult without an exposure history. The disease should be considered in the differential diagnosis of any person with rapidly progressive, unexplained encephalitis, even when no history of exposure to a rabid animal is given. Persons caring for such patients should avoid exposure to saliva and other potentially infectious materials.

References

1. Smith JS, Reid-Sanden FL, Roumillat LF, et al. Demonstration of antigenic variation among rabies virus isolates by using monoclonal antibodies to nucleocapsid proteins. J Clin Microbiol 1986;24:573-80.

2. Rupprecht CE, Glickman LT, Spencer PA, Wiktor TJ. Epidemiology of rabies virus variants: differentiation using monoclonal antibodies and discriminant analysis. Am J Epidemiol 1987;126:298–309.

3. Centers for Disease Control. Human rabies-Oklahoma. MMWR 1981;30:343-4, 349.

4. Centers for Disease Control. Human rabies-Michigan. MMWR 1983;32:159-60.

5. Centers for Disease Control. Human rabies-Texas. MMWR 1984;33:469–70.

6. Centers for Disease Control. Human rabies-Pennsylvania. MMWR 1984;33:633-5.

7. Centers for Disease Control. Human rabies diagnosed 2 months postmortem—Texas. MMWR 1985;34:700, 705-7.

8. Hurst EW, Pawan JL. An outbreak of rabies in Trinidad: without history of bites, and with the symptoms of acute ascending myelitis. Lancet 1931;2:622-8.

9. Lumio J, Hillbom M, Roine R, et al. Human rabies of bat origin in Europe. Lancet 1986;1:378. 10. Nikolić M. Tollwuttodesfälle bei Menschen ohne Verletzungen oder Kontakt mit einem tollwüttigen oder an Tollwut verdächtigen Tiere. Arch Hyg Bakteriol 1952;136:80-4.

11. Held JR, Tierkel ES, Steele JH. Rabies in man and animals in the United States, 1946-65. Public Health Rep 1967;82:1009-18.

12. Hattwick MAW. Human rabies. Public Health Rev 1974;3:229–74.

13. Anderson LJ, Nicholson KG, Tauxe RV, Winkler WG. Human rabies in the United States, 1960 to 1979: epidemiology, diagnosis, and prevention. Ann Intern Med 1984;100:728-35. 14. Bhandari M, Kumar S. Penile hyperexcitability as the presenting symptom of rabies. Br J Urol 1986;58:224.

[blocks in formation]
[ocr errors][merged small][merged small][merged small][merged small][merged small][merged small][merged small]

7 May 1988

C. 2

May 27, 1988 / Vol. 37 / No. 20

309 Serum 2,3,7,8-Tetrachlorodibenzo-p-
dioxin Levels in Air Force Health Study
Participants - Preliminary Report
312 Cave-Associated Histoplasmosis -
Costa Rica

313 State- and Sex-Specific Premature
Mortality Due to Ischemic Heart
Disease 1985

[graphic]

Serum 2,3,7,8-Tetrachlorodibenzo-p-dioxin Levels in
Air Force Health Study Participants

[ocr errors]

Preliminary Report

In 1978, the United States Air Force responded to a congressional mandate to initiate an epidemiologic study of the possible health effects of exposure to herbicides and their 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) contaminants in Air Force veterans who served in the Ranch Hand defoliation operation during the Vietnam conflict. Accordingly, the Air Force conducted a nonconcurrent prospective study, the Air Force Health Study, of all 1,267 members of the Ranch Hand unit and a series of matched controls (1).

The controls were selected from the Air Force veterans who served in air cargo units stationed in Southeast Asia (but not in Vietnam) during the same period as the Ranch Hand unit and were individually matched to the Ranch Hand personnel by date of birth, rank (officer, enlisted), and occupation. Investigators assumed that the controls had not been exposed to herbicides or TCDD during the war. Both groups were given physical examinations in 1982 (2), 1985 (3), and 1987-1988. They will be examined again in 1992, 1997, and, finally, during the concluding year, 2002.

Recently, CDC scientists developed a method for measuring TCDD in human serum (4). This lipid-based measurement, which is highly correlated with paired measurements of TCDD in adipose tissue (r= 0.98) (5), has been applied to U.S. Army veterans (6) as well as to participants in the phase of the Air Force Health Study reported here.

This phase of the Air Force study focused on measuring serum TCDD levels in 150 Ranch Hand veterans and 50 controls. All participants were enlisted men; the Ranch Hand veterans had been either herbicide loaders or herbicide specialists in Vietnam. Serum samples from all 200 participants were collected at four Red Cross Centers (Atlanta, Cleveland, Los Angeles, and Tulsa) according to a standardized protocol. One hundred forty-seven of the specimens obtained from Ranch Hand personnel and 49 of those from controls yielded serum TCDD levels that met the quality control criteria (4).

The demographic and health characteristics of Ranch Hand personnel and controls were similar (Table 1); however, their serum TCDD levels differed markedly (Figure 1). The mean serum level of the 147 Ranch Hand personnel was 49 parts per trillion (ppt) (median, 26 ppt); 62% had TCDD levels above 20 ppt, which is considered the upper limit for U.S. residents without known TCDD exposure (7). The mean serum

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES/PUBLIC HEALTH SERVICE

[merged small][ocr errors][merged small]

TABLE 1. Selected characteristics of 200 Air Force Health Study participants, by group, 1987

[blocks in formation]

*Controls were based outside of Vietnam and had tours of 2 to 3 years.

*From questionnaire.

*Defined as the equivalent of smoking one pack of cigarettes per day for 1 year.

"Defined as the equivalent of drinking 1.5 ounces of an 80-proof alcoholic beverage per day for 1 year.

FIGURE 1. Serum TCDD* levels of Ranch Hand and control veterans participating in the TCDD-measurement phase of the Air Force Health Study, 1987

[merged small][subsumed][subsumed][merged small][ocr errors][subsumed][subsumed][subsumed][subsumed][subsumed][merged small][merged small][merged small][merged small][merged small][subsumed][ocr errors][subsumed][subsumed][merged small][merged small][merged small][merged small][graphic][merged small][merged small][merged small]
« PreviousContinue »