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  • 7/30/2019 Tropical Immersion Foot2

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    TROPICAL IMMERSION FOOT

    SIR,-Have Dr Allen and Mr Taplin (Nov. 24, p. 1185)considered the possibility that cercariae from avian ormammalian species of blood-flukes may play some part in

    the condition under discussion ? Schistosomal cercarial

    dermatitis is often extremely itchy-not a feature described

    by Allen and Taplin in their subjects-but the pattern of

    reactivitycould be altered

    by prolongedimmersion. It

    would be interesting to know if the Vietnam patientsdeveloped blood eosinophilia or other evidence of possibletrematode infestation.

    P.O. Box 1907,

    Bulawayo,Rhodesia. J. CHARLES SHEE.

    INTRAVENOUS FEEDING

    SIR,-Iwas sorry to learn that Mr Wright (Dec. 8,p. 1335) has had such difficulties with insulin and glucoseand that he warns against its use in seriously ill andcachectic patients. This was the very group for whichwe introduced it and in which we found striking bio-chemical and clinical improvement. I can only supposethat he is not using it in the same way or that he is givingsomething else, such as excessive water, to produceundesirable effects. If, of course, one allows the blood-

    sugar to rise to the very high levels that are seen in hyper-osmolar diabetic coma, and then brings the blood-sugardown fast with insulin, precisely the sort of disequilibriumsyndrome which he describes is produced. The hypo-phosphataemia of which he writes and which was alsomentioned in your editorial (Nov. 24, p. 1179) is well-

    recognised. I do not think anyone familiar with intravenous

    feeding techniques would now fail to add phosphate unlessthe regimen also included a phosphate-containing prepara-

    tion, such as Intralipid or Aminosol .I find Mr Wrights theoretical discussion puzzling.

    Firstly, he cites cellular overhydration in his patientswithout producing evidence for it and then he suggeststhat raising the blood-sugar or giving insulin are responsiblefor this. If the free glucose within the cell rises con-

    comitantly with the plasma-glucose then the changes inextracellular and intracellular osmolality will cancel eachother out and no water will pass into the cell. Apart fromthe

    "

    disequilibrium syndrome ", which is easy enough to

    avoid, I cannot see how insulin could make the matter

    worse-certainly not by causing glucose to pass against aconcentration gradient as Mr Wright suggests. Indeed,since insulin enhances phosphorylation in most tissues andcauses synthesis of large molecules from small, it should

    have the effect of lowering intracellular osmolality. Flear 4

    has produced good evidence that changes in cellular

    hydration do occur after injury and that these are relatedto alterations of membrane permeability and to changes inthe concentration of intermediary metabolites other than

    glucose. Evidence has also been produced that insulin

    may, in fact, improve this situation.22

    There are many factors, as well as insulin, involved inthe glucose intolerance after injury. In view of thevariable insulin resistance after injury I am not surprisedthat your correspondent found a lack of correlation between

    glucose utilisation and plasma-insulin levels.

    General Hospital,Nottingham NG1 6HA. S. P. ALLISON.

    1. Hinton, P., Allison, S. P., Littlejohn, S., Lloyd, J. Lancet, 1971, i,767.

    2. Hinton, P., Allison, S. P., Littlejohn, S., Lloyd, J. ibid. 1973, ii,218.

    3. Allison, S. P. in Parenteral Nutrition (edited by A. W. Wilkinson).Edinburgh, 1972.

    4. Flear, C. T. G. J. clin. Path. 1970, 23, suppl. 4, 16.

    PSITTACOSIS

    SiR,-Dr McKendrick and his colleaguespublishedthe C.F.T. serum titres which we obtained using a psittacosisgroup antigen commonly employed in this country.Though a 4-fold rise in antibody was demonstrated in5 out of 6 patients the titres were so low that we mighthave missed the laboratory diagnosis if we had not beenaware beforehand of the firm clinical and epidemiologicaldiagnosis. The antigen was used at the recommended

    strength, but was slightly anti-compleraentary and couldnot be used satisfactorily at higher concentration. Laterwe prepared an ether-extracted psittacosis group antigen,which was not anti-complementary, and performed chess-board titrations on the serum samples from the outbreak.It became apparent that the first antigen we had used hadbeen at suboptimal strength for the detection of antibodyin early convalescent serum. The titres we obtained

    using the ether-extracted antigen were as follows:

    The second serum specimens gave titres about 16-fold

    higher with the ether-extracted antigen than with the

    suboptimal antigen originally used.

    School of Pathology,Middlesex Hospital Medical School,

    London W1P 7LD.

    D. S. DANE

    J. R. PATTISON.

    VACCINATION AGAINST

    CYTOMEGALOVIRUS ?

    SIR,-Professor Elek and Professor Stem (Jan. 5, p. 1) ad-vocate the eventual vaccination of all adolescent girls with alive tissue-culture-adapted strain of cytomegalovirus. It is

    surprising to find the possible cancer hazard of such a

    procedure dismissed so lightly, since it is now clear that

    many members of the herpesvirus group are oncogenic.Mareks disease of the domestic fowl,2 renal adenocarci-noma of the frog,3 lymphocytic leukxmia of the guineapig

    4

    are all naturally occurring malignancies associated with

    herpesviruses. Experimentally herpesviruses saimiriandateles6 cause lymphomas and leukxmia in primates. Epstein-Barr virus transforms human lymphocytes in culture andthere is a close association between this virus and both

    African

    lymphomaand

    nasopharyngealcarcinoma.8

    Seroepidemiological studies show a correlation between

    herpesvirus simplex type 2 and carcinoma of the cervix,and, in one case at least, a fragment of viral D.N.A. hasbeen found covalently linked to cell D.N.A.10 An associationbetween herpesvirus simplex type 1 and carcinoma of the

    lip has also been claimed. 11 Both of these latter viruses

    1. McKendrick, G. D. W., Davies, J., Dutta, T. Lancet, 1973, ii, 1255.2. Churchill, A. E., Biggs, P. M. Nature, 1967, 215, 528.3. Granoff, A. in Oncogenesis and Herpesviruses; p. 171. Lyons, 1972.4. Hsiung, G. D., Kaplow, L. S. J. Virol. 1969, 3, 355.5. Melendez, L. V., Daniel, M. D., Hunt, R. D., Frazer, C. E. O.,

    Garcia, F. G., King, N. W., Williamson, M. E. J. natn. CancerInst. 1970, 44, 1175.

    6. Melendez, L. V., Hunt, R. D., Daniel, M. D., Frazer, C. E. O.,Barahona, H. H., Garcia, F. G., King, N. W. in Oncogenesis and

    Herpesviruses; p. 451, Lyons1972.

    7. Zur Hausen, H., Diehl, V., Wolf, H., Schulte-Holthausen H.,Schneider, U. Nature New Biology, 1972, 237, 189.

    8. Wolf, H., Zur Hausen, H., Becker, V. ibid. 1973, 244, 245.9. Rawls, W. E., Iwamoto, K., Adam, E., Melnick, J. L., Green, G. H.

    Lancet, 1970, ii, 1142.

    10. Roizman, B., Frenkel, N. Cancer Res. 1973, 33, 1402.11. Wyburn-Mason, R. Br. med. J. 1957, ii, 615.