582

Ebola infections was the rapid onset of cachexia and dehydration, exacerbated by anorexia and dysphagia due to an ulcerative enanthem. Chest pain accompanied by a dry cough was common in Sudanese patients. As with Marburg infections there is evidence that Ebola virus can persist in the body for at least two months after the initial attack. Despite the similarity of the clinical picture and the morphological appearance of Marburg and Ebola viruses, immunity to Marburg does not seem to confer immunity to Ebola. This was dramatically demonstrated in Zaire where a patient was treated with Marburg immune plasma with no beneficial effect. Each outbreak of Marburg or Ebola infection has produced disease in attendant nursing and medical personnel. This effect was so drastic in Sudan and Zaire that two hospitals were brought to a complete standstill. In Maridi Hospital, Sudan, 76 hospital staff became ill and 41 of them died. Transmission was due to direct contact with sick patients and particularly through contact with patients’ blood. Unfortunately, at the height of the outbreak, supplies of protective clothing including gowns, gloves, and face masks were insufficient and staff were not conversant with barrier-nursing techniques. A consignment of African green monkeys (Cercopithecus cethiops) imported from Uganda introduced Marburg virus to Germany in 1967 and led to the misleading and inappropriate term, green monkey disease. It is now

generally accepted

that

monkeys

are not

the natural

reservoir of this virus. Extensive epidemiological investigations after the South African outbreak failed to detect a natural reservoir of infection and no reservoir of Ebola virus has yet been uncovered.

AMYOTROPHIC LATERAL SCLEROSIS THE aetiology of amyotrophic lateral sclerosis (A.L.S.) is unknown, but one possibility is that the condition may be the result of infection by a virus. Research trends have been reviewed at a symposium.1 Pathologically, A.L.S. is characterised by degenerative changes in the anterior-horn cells of the spinal cord and pyramidal cells in the cerebral cortex and by absence of the inflammatory response that accompanies most viral infections. The recognition that the spongiform encephalopathies of mankuru and Jacob-Creutzfeld disease, are clearly transmissible infections although they too are characterised by a lack of inflammatory cells has somewhat strengthened the argument that A.L.s may be another slow-virus infection. Epidemiologists have revealed foci of strikingly increased prevalence in Guam, in the Kii peninsula of Japan, and in New Guinea ;3 these could be interpreted as evidence of an infectious origin of A.L.S., but more probably these three forms are distinct from the classic disease. Associations have been reported between antecedent poliomyelitis and tick-borne encephalitis and the development of A.L.S., but in neither case is the evidence compelling. In Hamburg, 70% of a group of 18 A.L.S. patients were said to have antibodies 1.

Lateral Sclerosis. Edited by J. M. ANDREWS, R. T. JOHNSON, and M. A. B. BRAZIER. New York and London: Academic Press. 1976. Pp.

Amyotrophic

298. $17; £12.05. C., Gibbs, C. J. in The Nervous System. (edited by D. B. Towers), Vol. 1, The Clinical Neurosciences; p. 113. New York, 1975. Johnson, R. T. in Amyotrophic Lateral Sclerosis. (edited by J. M. Andrews, R. T. Johnson, and M. A. B. Brazier); p. 173. New York, 1976.

2. Gajdusek, D.

3.

against tick-bone encephalitis virus, but the world-wide distribution of A.L.S. cannot be explained on this basis.* Intensive efforts to demonstrate a virus by culturing brain and other tissues from A.L.S. patients have been

unrewarding.5S Two separate studies on animals could be interpreted providing support for the notion that the origin of A.L.s. is infectious. Theiler’s virus, a murine picornavirus, has long been known to ice a paralytic disease in mice not unlike poliomyelitis in man.6 A chronic myelopathy in mice caused by a variant of Theiler’s virus resembles A.L.S. in that the inflammatory response is considerably less than that in the acute form of Theiler’s infection,7but there are still some important differences between the animal model and A.L.S. in man. In a separate study on wild mice trapped in California, a chronic lower-motor-neuron disease was identified which is transmissible to laboratory mice and is due to infection with a murine type-C oncornavirus or retrovirus. Type-C viruses are ubiquitous in mice and are known to cause lymphomas and other tumours; the paralytic disease is a newly recognised manifestation of type-C virus infection. Virus particles have been demonstrated by electron microscopy in neurons of wild-caught mice, and the paralytic disease seems to be a direct effect of virus acting upon neuronslO and not, as in lymphocytic choriomeningitis virus infection in mice, an inas

direct effect resulting from an immunological reaction. The absence of inflammatory cells in affected mice is striking, and this has added credence to the idea that A.L.s. could be caused by a similar mechanism. Evidence to support this new concept is now being sought by electron microscopy, by serological examination for evidence of surface antigens of murine type-C viruses, and by biochemical examination for evidence of R.N.A.instructed D.N.A. polymerase (reverse transcriptase) in patients with A.L.S. In a preliminary study, no reverse transcriptase was demonstrable in normal or diseased human brains from the U.S.A., but some activity was present in brains from Guam, both from normal subjects and from patients with A.L.s. and Parkinson’s disease." Such studies are clearly important and should be extended, with careful and critical evaluation of any clues. The discovery of the neurological manifestations of murine type-C virus infection was an unexpected finding in the course of a study directed towards revealing spontaneously occurring cancer in wild populations of mice. The presence of neurotropic retroviruses in other species besides the mouse and the sheep (visna virus) is to be expected. Whether or not these viruses will prove to be important in neurological disorders of man remains to be seen. 4. 5.

Muller, W. K., Hilgenstock, F. J. Neurol. 1975, 211, 11. Cremer, N. E., Oshiro, L. S., Norris, F. H., Lennette, E. H. Archs Neurol. 1973, 29, 331. 6. Theiler, M. J. exp. Med. 1937, 65, 705. 7. Lipton, H. L. Infect. Immun. 1975, 11, 1147. 8. Lipton, H. L., Dal Canto, M. C. in Amyotrophic Lateral Sclerosis, (edited by J. M. Andrews, R. T. Johnson, and M. A. B. Brazier); p. 263. New York, 1976. 9. Gardner, M. B., Henderson, B. E., Officer, J. E., Rongey, R. W., Parker, J. C., Oliver, C., Estes, J. D., Huebner, R. J. J. natn. Cancer Inst. 1973. 51, 1243. 10. Gardner, M. B., Rasheed, S., Klemont, V., Rongey, R. W., Brown, J. C., Dworsky, R., Henderson, B. E. in Amyotrophic Lateral Sclerosis, (edited by J. M. Andrews, R. T. Johnson, and M. A. B. Brazier); p. 217. New York, 1976. 11. Viola, M. V. ibid. p. 235.

Amyotrophic lateral sclerosis.

582 Ebola infections was the rapid onset of cachexia and dehydration, exacerbated by anorexia and dysphagia due to an ulcerative enanthem. Chest pain...
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