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358 BRITISH MEDICAL JOURNAL 13 FEBRUARY 1971 respiratory paralysis requiring assisted respiration. of the lower reaches of the river. It was again observed as an In this series of cases the cranial nerves were unusually epidemic of several hundred cases among people living in Br Med J: first published as 10.1136/bmj.1.5745.358 on 13 February 1971. Downloaded from severely affected, with ophthalmoplegia, facial diplegia, and small groups along the middle reaches of the river between weakness of bulbar muscles. Occasionally lesions of nerve Garissa and Garsen. Both episodes were associated with roots seemed to be restricted and unilateral, giving pain, heavy floods so that the people, their domestic animals, and weakness, and wasting in the muscles of the shoulder girdle probably also wild species had to take refugeon "islands" in the on one side, as is well recognized to 6ccur in so-called neuralgic flood. Mansonia mosquitoes were breeding extensively amyotrophy. In two cases severe loss of position and joint in the flood waters. Despite contact between the sense was noted in both hands, and there was also evidence of affected population and the surrounding nomads no spread spinal cord disease, but there was nothing to indicate from to the latter was reported, nor did the disease spread to un- their previous history that these patients were suffering from affected people in the hospital to which cases were admitted. multiple sclerosis. In a single fatal case there was clinical and Clinically there was fever lasting three or four days, some- pathological evidence of severe lesions of both roots and times associated with severe headache, backache, and marked spinal cord, and the pathological changes were those of a prostration. Patients had one or at most two vesicular lesions demyelinating radiculomyelitis with some inflammatory cell which resembled pocks but regressed without pustulation. infiltration. Two patients suffered an encephalopathy with Lesions occurred on the upper arm, face, neck, or trunk but headache and confusion, leading to transient coma or semi- never on the hands or lower limbs. coma and producing subsequently a prolonged amnesia for the The virus isolated from the lesions was shown to be the period of the illness. The cerebrospinal fluid was abnormal cause of the disease, because when inotulated into a human in both cases, as was the electroencephalogram. volunteer (previously repeatedly vaccinated against smallpox) The author was clearly impressed with the apparent or into rhesus or vervet monkeys it reproduced the character- response to corticotrophin by patients in all groups. Certainly istic lesion, from which virus was re-isolated. That the virus the rapid improvement which followed its administration in was a pox virus was confirmed by the characteristic histology many ofthe patients suggested that this remedy was influencing of the lesions, the demonstration of elementary bodies and the course of the disease. This response also gives some (by electron microscopy) vaccinia-like particles in them, and, support to the concept that these complications are due to most conclusive, that the virus could reactivate heat-inactivated an autoimmune demyelinating process. On the other hand, vaccinia virus. Antiserum raised against the virus in a monkey spontaneous improvement in transverse myelitis and in the gave a specific gel-precipitation reaction with extracts from Guillain-Barre syndrome does occur. In the treatment of the lesions in the naturally infected patients. The human this syndrome, in particular, neurological opinion is sharply volunteer had regional lymphadenitis but no systemic illness, divided at the moment between those who believe that perhaps because the virus had been laboratory-passaged. corticotrophin should be given and those who believe that it The unusual features of tanapox virus are that it caused should not. Majority opinion still appears to favour the view lesions (and probably grows) only in human and monkey cell that corticotrophin should be given as early as possible in the cultures, not in chick embryos, chick embryo cell cultures, course of such illnesses, and Dr. Wells's experience would rabbit or bovine embryo cells. It caused no disease in baby suggest that it should certainly be given to patients suffering mice, guinea pigs, rabbits, a calf, lamb, pig, or goat. No http://www.bmj.com/ from these rare but increasingly well-recognized complications serological relationship could be detected with the vaccinia- of influenza and influenza-like illnesses. variola group of pox viruses (which includes monkey pox), with molluscum with a 1 British Medical Journal, 1970, 1, 248. contagiosum, range of domestic 2 Brain, W. R., and Walton, J. N., Brain's Diseases of the Nervous System, animal pox viruses, or with fowlpox virus. However, it 7th edn. London, Oxford University Press, 1969. 3Greenfield, J. G., Journal of Pathology and Bacteriology, 1930, 33, 453. showed an antigenic relationship to yabapox virus' and was 4 Kapila, C. C., Kaul, S., Kapur, S. C., Kalayanam, T. S., and Banerjee, found to be similar or identical to a "yaba-like" pox virus2 D., British MedicalJournal, 1958, 2, 1311. Dunbar, J. M., Jamieson, W. M., Langlands, J. H. M., and Smith, G. H., which has caused epidemics in at least three primate colonies on 27 September 2021 by guest. Protected copyright. British Medical journal, 1958, 1, 913. in the United States. The lesions in the monkeys were similar 6 Flewett, T. H., and Hoult, J. G., Lancet, 1958, 2, 11. 7 McConkey, B., and Daws, R. A., Lancet, 1958, 2, 15. to those of tanapox and there were no deaths. Nine people handling the monkeys developed lesions on the hand or fore- arm (usually at sites of injury) ranging in diameter from 1 to 2-5 cm. Some of them had severe lymphangitis, adenitis, and a systemic illness with temperatures over 102°F (38_9°C).3 Tanapox This "yaba-like" virus is thought to be a latent infection of vervet monkeys or sooty mangabeys, but the outbreaks Tanapox is a newly described disease of exceptional interest. occurred in macaques.2 A report on it by Professors A. W. Downie and G. S. Nelson The relationship of tanapox virus to yaba virus is of interest. and their colleagues appears at page 363 of the B.M.J. this The latter was isolated in Nigeria from laboratory rhesus week. Not only is it caused by a pox virus with unusual monkeys' with an outbreak of tumours. It has been shown to characteristics, but the virus is related to a virus known to be cause similar benign tumours in man.4 It would be useful to oncogenic in man. The disease is probably a zoonosis, and it know what tanapox virus would do in an immunosuppressed has occurred in an area where agricultural development and a monkey. large increase in human population is foreseen. The Tana The evidence suggests that tanapox is an infection of wild River basin (whence the name) in Kenya is a large, mainly primates transmitted to man mechanically on the contami- arid plain with a small, mostly nomadic population, but plans nated mouth-parts of blood-sucking insects-on the Tana exist for it to become one of the major areas of irrigated River probably by the flood-enhanced population of Mansonia agriculture in Africa. mosquitoes. Myxomatosis (another pox virus) is similarly The disease was first seen in September 1957 as a small transmitted among rabbits-by mosquitoes in Australia but outbreak ht a mission school in the swamp-forest flood plain probably mainly by fleas in Britain. In the same way tanapox BRITISH MEDICAL JOURNAL 13 FEBRUARY 1971 359 could probably be transmitted by many kinds of blood- sucking insect in many parts of the world. An unanswered Corticotrophin Immunoassay Br Med J: first published as 10.1136/bmj.1.5745.358 on 13 February 1971. Downloaded from question is whether viraemia occurs either in monkeys or in Human corticotrophin (ACTH) is a polypeptide comprising man or whether the insects can become infected when probing some 39 amino-acid residues.' The first 24 and the last six the lesions. Viraemia levels (if any) should be studied and of these residues are common to many animal species. Like transmission experiments made with blood-sucking insects. all single-chain polypeptides, ACTH has one end with an The rather sluggish antibody response observed suggests that amino group (the N terminal end) and another with a carboxyl viraemia may not occur or be slight and transient. If trans- group (the C terminal end). By a series of chemical dissections mission depends on the occasional mosquito probing a rare of the molecule, H. Imura and colleagues2 showed that lesion, then transmission is probably very slow except when corticotrophin activity resided in the N terminal amino-acids there are exceptionally high insect populations-for example, 1-24, and that by themselves the C terminal residues 25-39 in flood conditions. Transmission among wild primates may were without such activity. depend on ectoparasites such as fleas. It is possible to raise in the rabbit antibodies against The disease in man was mild and discovered only incident- different parts of the human ACTH molecule-against ally during surveys for filariasis and schistosomiasis. It could residues 1-24 (N terminal ACTH), 25-39 (C terminal go unnoticed in many underdoctored areas and so may be ACTH), and residues 11-24.3 In this issue of the B.M.J. more widespread than is at present recognized. If it is a Dr. G. M. Besser and his colleagues (page 374) describe how zoonosis, its incidence would be sporadicand it should be they have used two of these tools to study the plasma levels of sought elsewhere in Africa. It may occur among tourists on ACTH found in patients with different forms of adreno- safari and must certainly be watched for among people who cortical insufficiency and have studied the mechanisms which handle monkeys for laboratories.
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