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    fluoresced at lower titres. Pathogenicity of isolates showingpositivity by the preceding tests was demonstrated by intra-nasal instillation into weaned, white Swiss mice. Mortality of80-100% ensued in 4-7 days routinely. Confirmation of thecause of death was obtained by direct observation of amoebain the harvested brain tissues and by prolific growth of the re-covered organisms in Changs medium which is selective forpathogenic Ncegleria.

    These studies which resulted in the first isolation of patho-genic Ncegleria in Florida from thermally polluted and fresh-water lakes appear to indicate that thermal pollution of watersin Florida plays a minor role in the maintenance of pathogenicNaegleria in nature. Freshwater lakes from which isolates wereobtained have been used for water sports by thousands of peo-ple each year and only seven fatalities due to pathogenicNcegleria infections have been recorded, the first being in1962. We suggest that other factors, probably host related,play a much greater role in the development of primaryamoebic meningo-encephalitis in man than does the mere pre-sence of the organisms in the water.

    this research was sponsored in part by grants R-803511 andR-804375 from the Environmental Protection Agency and in part bythe State of Florida, Department of Health and Rehabilitative Ser-vices. T7 ",, V_"h-Office of Laboratory Services,Department of Health and Rehabilitative Services,Tampa, Florida 33614, U.S.A.


    U.S. Environmental Protection Agency,Epidemiology Branch,Field Studies Division,Health Effects Research Laboratory,Cincinnati, Ohio 45268. S. L. CHANG


    SIR,-Dr Jackson and his colleagues4 rightly condemn thepractice of starting antihypertensive therapy after only onemeasurement of blood-pressure. They are also justified in criti-cising the choice of therapy in the six cases they report. Therepeated reference to "symptomless" hypertension, however,may be misleading. Surely it is now generally accepted that thereasons for lowering the blood-pressure in hypertensive pa-tients have little to do with symptoms. One could also disputethe proposition that treatment of hypertension in the over-six-ties is not worthwhile because it fails to reduce mortality.6 Themain benefit of antihypertensive therapy is prevention ofstroke. 7

    While debate will continue about the meaning of words suchas "elderly" and "hypertension", the prospect of disablinghemiparesis in the final years of life should be considered byany physician in deciding whether or not to treat the elderlyhypertensive. ,

    Department of Internal Medicine,University of Cincinnati Medical Center,Cincinnati, Ohio 45267, U.S.A. MARTIN FAIRMAN

    SIR,-Dr Jackson and his colleagues4 rightly make the pointthat antihypertensive treatment in the elderly may be simplymeddlesome medicine. However, they do not clearly enoughmake the point that elderly patients may be especially sensitiveto antihypertensive drugs, at least at the beginning of treat-ment, although this is mentioned in the discussion.

    3. Butt, C. G. New Engl. Med. 1966, 274, 1476.4. Jackson, G., Piercianowoki, T. A., Mahon, W., Condon, J. Lancet, 1976, ii,

    1317.5. Pickering, G. W., Hypertension Causes, Consequences and Management.

    Edinburgh, 1974.6. Fry, J. Lancet, 1974, ii, 431.7. Hamilton, M., Harpur, J., Beevers, D. G., Fairman, M. J., Postgrad. med.

    J. 1973,49,905.

    If beta-receptor blocking agents are used in the elderlybecause of ischaemic heart-disease it is important to start witha small dose because otherwise severe postural hypotensionmay occur, as I learnt to my cost when starting treatment ofan elderly general practitioner who was also a personal friend.

    Whittington Hospital,London N19 5NF E. MONTUSCHI


    SIR,-Severe hypotension and collapse may follow the useof prazosin.1 Since prazosin is thought to work by directrelaxation of arterial smooth muscle severe cardiovascularside-effects would not be expected; such side-effects are notcommonly associated with the clinical use of direct vasodilat-ing agents such as hydrallazine or diazoxide. While using anin-vitro technique to study human arterial responses, we haveobserved effects of prazosin which may explain some of its side-effects.

    Spiral strips of operative specimens of uterine, splenic andileocolic arteries ("visceral arteries") and post-mortem speci-mens of palmar digital arteries ("peripheral arteries") weresuspended at 37C and the force developed at increasing con-centrations of noradrenaline was measured. Prazosin in thera-

    peutic concentrations4 had different effects on the dose-res-ponse curves to noradrenaline in the arteries of the twovascular beds studied (see figure).

    1. Gabriel, R. G., Meek, D., Ghosh, B. D. Lancet, 1975, i, 1095.2. Bendall, M. J., Baloch, K. H., Wilson, P. R. Br. med. J. 1975, ii, 727.3. Constantine, J. W. in Prazosin (edited by D. W. K. Cotton); p. 16. Amster-

    dam, 1974. 4. Wood, A. J. J. clin. exp. Physiol. Pharmac. 1975, 2, 446.

    Noradrenaline dose-response curves.

    The curves were calculated as a percentage of the standard contrac-ture produced by 80 mmol/1 potassium chloride obtained in six isolatedvisceral arteries (A) and five isolated "peripheral arteries" (B) (seetext). The curves were obtained in the absence of prazosin (1-) orin the presence of prazosin 40 nmol/1 (0-0) or 80 nmoVl (ABL BEach point represents the mean of the responses:i:s.E.M..