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Imported Human Rabies -- Australia, 1987

In November 1987, the illness of a 10-year-old Australian boy who had died of acute encephalitis 4 months earlier was confirmed as being rabies. This is the first laboratory-confirmed case of human or animal rabies ever reported from Australia.

The child had traveled with his mother to India, Pakistan, Nepal, Singapore, and Thailand between February and October of 1986, but no animal bites were reported during this period. He remained well until June 23, 1987, when headache developed, followed by fever, vomiting, and chills. During the next few days, he became anorexic, had a few episodes of delirium at night, and had pain in his right arm. Eight days after the onset of illness, incoordination and diplopia developed, along with a progressive weakness in his legs. When admitted to a local hospital, the patient had palsies of the sixth cranial nerve on the right side and of the seventh cranial nerve bilaterally. Analysis of a cerebrospinal fluid specimen showed normal cell counts and normal protein and glucose levels. A diagnosis of atypical Guillain-Barr*$$*Aae syndrome versus encephalitis was made, and on the 10th day of illness the patient was transferred to a regional medical center. At that time, he was unable to walk, and his reflexes were decreased on the right side. An electroencephalogram showed slow wave activity consistent with a diffuse encephalitis, and a computerized axial tomography scan was normal. A repeated lumbar puncture on the 12th day of illness showed 50 white blood cells/mm3, 18 red blood cells/mm3, elevated glucose, and normal protein levels. The patient was temporarily intubated because of irregular respiration. On the 14th day of illness, inappropriate antidiuretic hormone secretion, upper airway obstruction, and pneumonia developed, and the left lung collapsed. Seizures began 2 days later. The patient became comatose on the 19th day of illness, and he died 4 days later.

Hospital pathologists found eosinophilic intracytoplasmic inclusions, suggestive of Negri bodies, on fixed sections of brain tissue. A serum sample taken on the 21st day of illness had a rabies neutralizing antibody titer of 1,400 when analyzed at a reference laboratory 4 months later. No specimens were available for virus isolation.

In December, extensive interviews with relatives, friends, and other contacts of the patient revealed that the patient, an animal lover, had been injured by two animals in the 2 years before his death. He was severely scratched by a neighbor's dog 2 months before his onset of illness, but the dog remained healthy and did not have rabies antibodies when tested in December 1987. However, according to a travel companion, the patient was bitten on a finger by a wild monkey at a marketplace in northern India 16 months before the onset of illness. This incident was not reported to the boy's mother. A photograph of the patient feeding the monkeys at this marketplace was found in a school project he had prepared.

Rabies postexposure prophylaxis was recommended for nine health-care workers and four family members and friends who may have been exposed to the patient's saliva or nerve tissue during his illness. Reported by: K Dunn, BVSc, Commonwealth Dept of Primary Industries and Energy, Barton, Australian Capital Territory. J Faoagali, MBCHB, H Samartunga, MB, Royal Brisbane Hospital, Brisbane; P DeBuse, MB, D Fraser, MB, Royal Children's Hospital, Brisbane; R Stable, MBBS, B Patten, FRACP, D Martin, MBBS, Nambour General Hospital, Nambour; LL Laws, MVSc, Queensland Dept of Primary Industries, Moorooka; T St. George, PhD, Div of Tropical Animal Production, Commonwealth Scientific and Industrial Research Organization, Indooroopilly; RA Ramm, MB, RP Davison, MB, V Kelk, Queensland Dept of Health. Australian Animal Health Laboratory, Commonwealth Scientific and Industrial Research Organization, Geelong, Victoria. Australian Dept of Community Svcs and Health. Viral and Rickettsial Zoonoses Br, Div of Viral Diseases, Center for Infectious Diseases, CDC. Editorial Note: All available data indicate that this was an imported case of rabies. The only previous report of animal or human rabies in Australia is poorly documented, but, in 1867, a child and a dog from Tasmania had suspected rabies (1). Both animal and human rabies have been reported from all the countries in which the patient traveled except Singapore (2). (Nepal did not contribute to that survey.) The monkey bite in northern India 16 months before the onset of illness must be considered the probable exposure, but the patient might have received other unreported bites while traveling in Asia. If the patient was exposed in Asia, the incubation period would have been between 8 and 16 months. In one large study of human rabies, approximately 1% of cases had incubation periods of over 1 year (3). Cases of monkey-transmitted human rabies are rare; however, one extremely long incubation period (37.5 months) was reported (4).

In the Australian boy's case, paralysis dominated the clinical picture. The clinical picture and the prolonged course before the onset of coma are consistent with the paralytic form of rabies, which occurs in approximately 20% of cases (3).

Since Australia is considered a rabies-free country (2), animal rabies vaccination is not required and animals that bite people are not quarantined. If animal rabies should become endemic in Australia, an estimated 38,000 people per year might have to receive postexposure prophylaxis (5). In addition, millions of dollars would have to be spent on animal rabies vaccination and quarantine. Wild animals that might become reservoirs if rabies should be introduced into Australia include the dingo (a wild dog), red fox, feral cat, and bat. A limited serosurvey of bats in Queensland for rabies antibodies is in progress.

This report emphasizes the importance of rabies preexposure prophylaxis for travelers visiting rabies-endemic countries for more than 30 days (6), especially children who are likely to have unrecognized or unreported exposures. Preexposure prophylaxis can be administered intramuscularly or intradermally (7); however, the intradermal regimen should be completed at least 30 days before departure and should not be used if the person is taking chloroquine for malaria chemoprophylaxis. References

  1. Bisseru B. Rabies. London: William Heinemann Medical Books, 1972:18.

  2. World Health Organization. World survey of rabies XXII (for years 1984/85). Geneva: World Health Organization, Division of Communicable Diseases, 1987.

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

  4. Wilson JM, Hettiarachchi J, Wijesuriya LM. Presenting features and diagnosis of rabies. Lancet 1975;2:1139-40.

  5. Nixon J, Pearn J, McGarn F. Dog bite injuries to children: potential rabies threat to Australia. Med J Aust 1980;1:175-6.

  6. Centers for Disease Control. Health information for international travel 1987. Washington, DC: US Department of Health and Human Services, Public Health Service, 1987:108-12; DHHS publication no. (CDC)85-8280.

  7. Immunization Practices Advisory Committee. Rabies prevention: supplementary statement on the preexposure use of human diploid cell rabies vaccine by the intradermal route. MMWR 1986;35:767-8.

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