Wildlife rabies has been enzootic in France since 1968; however, 13 of the 14 human cases in France were imported, and one was in a person infected through a corneal transplant (1). On May 9, 1992, a 3-year-old boy who resided in Algeria died from rabies encephalitis in Paris. This report summarizes the investigation of this case by the Pasteur Institute.

On March 17, 1992, the boy was chased by a dog in his village in Algeria, fell, and sustained a wound on his forehead. Witnesses confirmed that the boy's wound resulted when he fell on a stone and that he was not bitten or licked by the dog. No rabies treatment was started. The boy remained well until April 15, when he complained of headache. He was hospitalized in Algeria on April 19 with agitation, hyperthermia, aerophobia, and hydrophobia. On April 23, he was transferred from Algeria to an intensive-care unit at a hospital in Paris with suspicion of viral encephalitis of unknown origin. Tests for rabies antibody in serum and cerebrospinal fluid (CSF) on April 24 were negative, and other etiologies (e.g., diphtheria and organophosphate poisoning) were considered. On April 30 he became comatose and was placed under respiratory monitoring; he received external cardiac pacing after atrioventricular dissociation. Daily electroencephalographic monitoring showed decreasing brain activity. He developed diabetes insipidus on May 8 and died on May 9, 25 days after onset of symptoms and 17 days in the intensive-care unit.

A second serum sample obtained on May 5 was positive for rabies antibody by enzyme-linked immunosorbent assay and rapid fluorescent focus inhibition test. Testing using daily controls indicated rising antibody titers until death on May 9. Neck-skin biopsies and corneal smears performed on May 5 and May 9 were negative by fluorescent antibody test (FAT). CSF samples obtained on April 24 and April 27 and on May 5 and May 9 were negative for rabies antigen detection by rapid rabies enzyme immunodiagnosis (RREID) test and for rabies virus isolation on neuroblastoma cells; however, the CSF sample obtained on May 9 was positive for rabies antibody. Saliva samples were obtained daily from May 5 through May 9; the samples of May 7 and May 9 were positive by RREID on cell sediment. Complete autopsy was not authorized by the family, but a postmortem retro-orbital brain sample confirmed rabies diagnosis by FAT, isolation on neuroblastoma cells, RREID, and mouse inoculation test. Mouse inoculation tests with saliva and CSF remained negative.

Postexposure rabies prophylaxis was administered to 143 hospital staff and family members in Paris who had been exposed to the patient during nursing and hospital care before diagnosis and who had handled saliva and body samples. Family members and exposed hospital staff in Algeria were informed of the diagnosis. Exact data about the number of persons given rabies postexposure prophylaxis in Algeria are not available.

Investigations in the boy's hometown revealed that the dog that chased him in March did not remain healthy, as reported to the family, but died (or was killed) shortly after the incident and may have been implicated in another rabies fatality of a child at the end of April 1992.

Reported by: P Sureau, MD, M Herzog, MD, H Bourhy, DVM, Rabies Unit, Pasteur Institute; M Cloup, MD, P Hubert, MD, S Couderc, MD, Pediatric Intensive Care Unit, Sick Children's Hospital, Paris. Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: Although rabies is enzootic among wildlife species, human rabies is rarely acquired in France. Human and animal rabies have been reported in countries of northern Africa in which most cases imported into France were acquired. In every case, the vector animal was a dog. Worldwide, dogs are responsible for more than 90% of human cases (2). In the case described in this report, no dog bite was documented; consequently, because a definite exposure was not established, post- exposure prophylaxis was not given to the boy. However, the putative short incubation period (29 days) is consistent with an exposure to the upper body (3). 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. The possible contact with the dog was the probable exposure, but the boy might have received other unreported bites or exposure to rabies virus.

The early manifestations of rabies are usually nonspecific and can be difficult to differentiate from other encephalitic diseases. Rabies progresses to one of two distinct presentations: the most common furious form, characterized by hydrophobia, aerophobia, or episodic agitation and anxiety; or the least common paralytic form. Rabies should be considered in any patient with rapidly progressive encephalitis of unknown etiology, particularly in patients who have lived in an area with enzootic canine rabies (4).

Rabies postexposure prophylaxis is recommended for all persons bitten or scratched by animals that may be rabid. Rabies rarely results from exposures other than bites, scratches, contact with mucous membranes, or contact with an open wound with saliva or other potentially infectious rabies material from a person or animal with rabies. When a bite or mucous-membrane exposure cannot be excluded, postexposure treatment should be given to persons who have had physical contact with rabid animals. Treatment should be initiated as soon as possible after bites or scratches by known or suspected rabid animals.

Postexposure prophylaxis is recommended for persons who report a possible infectious exposure (e.g., bite, scratch, open wound, or mucous-membrane con- tamination with saliva or other infectious material) to a human with rabies. However, exposure to a human with rabies has not been implicated as a means of rabies transmission except following cornea transplantation from donors who died from rabies. Casual contact with a person with rabies (i.e., touching the patient) or contact with noninfectious fluid or tissue (e.g., blood, urine, or feces) does not constitute an exposure and is not an indication for prophylaxis (5). In this report, the number of hospital employees and family members (143) given postexposure prophylaxis was unusually high; however, the delay in definite diagnosis was considered to have resulted in increased exposure to the child.

References

1. CDC. Human-to-human transmission of rabies via a corneal transplant -- France. MMWR 1980;29:25-6.

2. World Health Organization. World survey of rabies XXV (for year 1989). Geneva: World Health Organization, Division of Communicable Diseases, Veterinary Public Health Unit, 1992; publication no. WHO/Rabies/92.203.

3. Fekadu M. Rabies in Ethiopia. Am J Epidemiol 1982;115:266-73.

4. CDC. Health information for international travel, 1991. Atlanta: US Department of Health and Human Services, Public Health Service, 1991:113-6; DHHS publication no. (CDC)91-8280.

5. Anderson LJ, Winkler WG, Vernon AA, Helmick CG, Roberts MR. Prophylaxis for persons in contact with patients who have rabies. N Engl J Med 1980;320:967-8.

Disclaimer   All MMWR HTML documents published before January 1993 are electronic conversions from ASCII text into HTML. This conversion may have resulted in character translation or format errors in the HTML version. Users should not rely on this HTML document, but are referred to the original MMWR paper copy for the official text, figures, and tables. An original paper copy of this issue can be obtained from the Superintendent of Documents, U.S. Government Printing Office (GPO), Washington, DC 20402-9371; telephone: (202) 512-1800. Contact GPO for current prices.

Page converted: 08/05/98

HOME  |  ABOUT MMWR  |  MMWR SEARCH  |  DOWNLOADS  |  RSS |  CONTACT POLICY  |  DISCLAIMER  |  ACCESSIBILITY

Morbidity and Mortality Weekly Report Centers for Disease Control and Prevention 1600 Clifton Rd, MailStop E-90, Atlanta, GA 30333, U.S.A Department of Health and Human Services

This page last reviewed 5/2/01