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general practitioner might come back into his own, witha heavy responsibility for health education and advice.Top among the Butterfield priorities was the right

attitude of mind for those working in the medical-careservices: better understanding of the total situation andthe details of their work. Experiments in the integrationand financing of the various branches of the N.H.S. on anarea basis were urgently needed; and operational researchwas particularly necessary to improve communication.If medical-care services were to get their deserts inmodern society, we should have to find other ways ofbringing influence to bear than " the word in the ear ofsick but powerful politicians ". Politics being now ayounger man’s game, that sort of influence might be along time coming. Far better to lobby for the notionthat the Minister of Health, as head of such a largecorporation, should certainly have full cabinet rank.

Perhaps that was the highest priority of all, for all the restcould flow from it.

HAND, FOOT, AND MOUTH DISEASE

A NEW disease is always of interest, especially when itis known by an unusually straightforward name (albeit onewhich might lead to confusion with a topical animal con-dition). The outbreak of

" febrile illness with pharyngeallesions and exanthem " in 60 cases in Toronto in 1957 I

was almost certainly the same illness as that which Alsopand his colleagues 2 labelled " hand, foot, and mouthdisease ". In November, 1963, Crow et a1.3 drew attentionto the condition, and in the ensuing six months over 100cases, from all parts of Britain, were reported in the corre-spondence columns of the British Medical,7ournal; and inthe summer of 1964 there was a massive outbreak, mainlyamong schoolchildren, in Cardiff.4 4The eruption presents most often as a few scattered

vesicles on the sides of the hands and feet and around the

tips of fingers and toes and, in younger children, as

maculopapular lesions of the buttocks and, occasionally,elsewhere. Regression is generally spontaneous, within aweek or so. Mouth lesions begin as bright-red macules2-8 mm. in diameter, soon becoming painful shallowulcers resembling aphthse. Systemic upset is generallytrivial, though transient pyrexia is sometimes noted. Evansand Waddington 4 reported gastrointestinal upset a fewdays before the onset of the rash, but this prodromalsymptom is not a consistent finding.

Virological examination of fxces and vesicle fluid hasestablished that enteroviruses of the Coxsackie group Aare responsible. In the Cardiff outbreak the total numberof clinical infections was difficult to assess, but in oneschool 123 out of 374 children and 6 out of 11 teachersbecame ill: Coxsackie A16 was isolated from 23/67 fxcalspecimens and 12/18 vesicles. Miller and Tindall,5 des-cribing a small series in the U.S.A., found fxcal CoxsackieA16 in 7 out of 11 cases: of the 4 negative cases, 1 hadCoxsackie A5, 1 had Coxsackie B5, and 2 had echovirus 9.Altogether, B5 was isolated in 2 cases and echovirus 9in 6. Coxsackie A10 has also been implicated.

Fortunately, the illness is short-lived and is of com-

paratively minor importance in relation to the total time1. Robinson, C. R., Doane, F. W., Rhodes, A. J. Can. med. Ass. J. 1958,

79, 615.2. Alsop, J., Flewett, T. H., Foster, J. R. Br. med. J. 1960, ii, 1708.3. Crow, K. D., Warin, R., Wilkinson, D. S. ibid. 1963, ii, 1267.4. Evans, H. D., Waddington, E. Br. J. Derm. 1967, 79, 309.5. Miller, G. D., Tindall, J. P. J. Am. med. Ass. 1968, 203, 827.

a child might be off school. However, Evans and Wad-dington 4 saw one unusual case-a woman aged eighty-four in whom hand, foot, and mouth disease persisted fora year and then recurred over a further eighteen-monthperiod.

IMMUNOLOGY AND CANCER

AT a University of Dundee symposium on May 31Prof. George Klein divided the evolution of cancer

immunology into three phases: the optimistic phase from1903, when much valueless work was performed onoutbred animals; the pessimistic phase from 1929, whenthe feeling was that no tangible evidence for immunityin cancer had been demonstrated; and finally the realisticphase, dating from the development of inbred mousestrains, the demonstration of histocompatibility antigens,and the definition of an antigenic basis for the host’sresponse to its tumour.

Discussing the in-vitro and in-vivo methods of detect-ing tumour-specific antigens, Professor Klein preferredimmunofluorescent tests, rather than some widelyaccepted cytotoxic assays, because they were more

sensitive and totally lacking in any threshold effect. Therewas no correlation between immunosensitivity of a

particular tumour in vitro and its sensitivity in vivo.Professor Klein reviewed his own work demonstratingtransplantation resistance to methylcholanthrene-inducedsarcomas in the autochthonous host. The increasedincidence of tumours induced by polyoma virus in

neonatally thymectomised mice and of Maloney-virustumours in mice treated with antilymphocytic serumreflected immunological influences in the developmentand growth of tumours in their original host. From thetherapeutic point of view, he speculated that such tumoursmight prove sensitive to specific vaccination or non-

specific reticuloendothelial stimulation by s,.c.G. In those

vertically transmitted R.N.A.-virus tumours where resis-tance in the primary host could not be demonstrated, hesuggested that their development might be prevented ifimmunological tolerance to the virus could be broken ortransmission of the virus prevented.The application of immunofluorescent techniques to

demonstrate isoantibody to Burkitt’s lymphoma hadshown that the antibody in convalescent serum was

apparently non-specific in in-vitro tests. 13 of 16 tumour

biopsy specimens from different patients showed signi-ficant staining with sera from a patient whose tumourregressed in 1963. The chance finding that serum frompatients with infectious mononucleosis reacted withBurkitt’s lymphoma cells just as well as with sera frompatients in whom the tumour had regressed has led tothe conclusion that EBB virus may be an importantaetiological factor in Burkitt’s lymphoma. This virus mayinduce both diseases or it may permit another passengervirus to bring about neoplastic change. In so far as the

geographical distribution of this tumour corresponds tothat of malaria in Africa, EBB virus may act as a co-factorwith malarial parasites in inducing Burkitt’s lymphoma.

Describing the demonstration of T antigen in adeno-virus-transformed mouse cells, Dr. H. G. Pereira remarkedthat this specific antigen was apparently coded by theviral genome and was produced in transformed cells at

an early stage of virus multiplication but was not sub-sequently incorporated into virus particles. The complexadenovirus structure contained 252 protein subunits, and