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prophylactic factor, and it would be interesting to hearother views on this point.

Finally, I would submit that the fact that the conditionoccurs in 50% of the adult population in Europe does notprevent it from being a disorder: it simply indicates thatit is a common one.

Broadgreen Hospital,Thomas Drive,

Liverpool L14 3LB. PATRICK TURNER.

VIRUS-ASSOCIATED GASTROENTERITIS INCHILDREN

SIR,-Further to the communication of Appleton andHiggins,l I report here the finding of virus particles 26 nmin diameter (fig. 1) in the faeces of a 2-year-old childadmitted to hospital with acute gastroenteritis.

Fsces samples were taken from 30 children, aged from1 month to 2 years, who had mild diarrhoea and vomiting.20% suspensions were prepared in buffered saline and theclarified extract was examined by immune electron micro-scopy. Of the 30 samples 6 contained rotaviruses, 1 con-tained the 16 nm particles singly and in clumps, and in theremainder no virus was found. In no specimen was thereany evidence of aggregation of virus particles. In addition,in the sample containing the 26 nm agent adenovirus par-

1. Appleton, H., Higgins, P. G. Lancet, 1975, i, 1297.

Fig. 1-Electron micrograph of faecal extract showing 26 nmparticles x 86,000.

Fig. 2-Electron micrograph of faecal extract showing 26 nmparticles together with single adenovirus particle x 55,000.

ticles were also present (fig. 2); neither agent could bepropagated in cell-culture.

It is as yet unclear whether the adenovirus or the smallparticles were -responsible for the symptoms. The size ofthe latter rules out the possibility of its being adeno-satellitevirus, and in size it bears a clear relationship to the 27 nmparticle of the Norwalk agent 2; closer examination of someof the particles showed a distinct hexagonal outline,suggesting icosahedral symmetry. However, no sub-structure could be distinguished.

It is also possible that certain types of virus-mediatedgastroenteritis may be the result of a multiple infectionwith two or more agents. Further studies are in progressand will be reDorted.Department of Biology,

The Polytechnic,Sunderland. A. P. WYN-JONES.

ELECTROLYTE DISTURBANCES INBEER DRINKERS

SiR,--We were interested in the " hypo-osmolaritysyndrome " of beer drinkers described by Dr Hilden andDr Svendsen (Aug. 9, p. 245). We wish to report a similarbut biochemically more extreme case.A 60-year-old unemployed Latvian was admitted after several

episodes of collapse and sweating. He was grossly confused andvolunteered no specific complaints. From his wife’s story it wasestimated that he habitually drank 10-15 pints of beer daily,chiefly ’Guinness’ (approximate electrolyte content: sodium 0-8

SERUM AND URINE ELECTROLYTES

Na and K mmoi/1; creatinine and urea mg/dl; osmolarity mosmol/kg.* After saline infusion.

mol/pint, potassium 18 mol/pint). He had also had episodes ofpsychiatric disturbance in the past and had been treated in apsychiatric hospital. His present illness had been continuingfor two or three days and had kept him confined to bed at home,without access to alcohol. On admission he was taking bendro-fluazide 5 mg daily, but up to the time of his present illness (i.e.,two or three days before admission) he had been taking digoxinand propranolol as well. On admission, he was found to have asharp postural drop in blood-pressure (120/70 mm Hg lying,unrecordable when erect), but no other abnormal physical signs,apart from his confusion. At that time he had gross hypo-natraemia and hypo-osmolarity (see accompanying table). He wastreated by restriction of fluid intake and by intravenous infusionof2mol/1 saline. This produced a dramatic response in biochemistryand blood-pressure (170/90 lying, 160/90 standing). His mentalstate also improved greatly. One month later the biochemicalfindings were normal.At no time throughout this illness was there any bio-

chemical or clinical evidence of liver disease. As this manhad been confined to bed for two days without access toalcohol immediately before admission to hospital, it isunlikely that alcohol in the serum was producing a " pseudo-hyponatraemia ". It therefore seems likely that, as withthose cases described by Dr Hilden and Dr Svendsen,- the2. Kapikian, A. Z., Wyatt, R. G., Dolin, R., Thornhill, T. S., Kalica,

A. R., Chanock, R. M. J. Virol. 1972, 10, 1075.

560

cause of this man’s abnormal biochemistry and confusionwas a chronic inadequate intake of both sodium and food.In contrast to their series, this patient showed signs ofsevere extracellular volume depletion, in that he hadsevere postural hypotension.

City Hospital,Hucknall Road,

Nottingham NG5 1PB.

D. C. BANKSB. R. F. LECKY.

UNSAFE ANÆSTHETIC SUPPLY SYSTEMS

SIR,-No person concerned with the supply of anxstheticgases can remain complacent under the present arrange-ments. The essential problem is the failure to adopt asystem of supply which is inherently " failsafe ", andnotably the use of identical pipes to supply different gases.

All systems of flexible supply-pipes are potentiallyfallible so long as oxygen and nitrous oxide are fed throughidentical pipes. The only safe answer is to supplyanxsthetic gases through pipes of differing size and colour,which cannot be physically interchanged. This system isused in Sweden. My commendation of it to the HealthDepartment was met by the comment that only antistaticpiping can be used in theatres, and coloured piping is notnecessarily antistatic. I would suggest that, since theantistatic requirement presumably applies to the possibilityof a static charge being transmitted from the anaestheticmachine to earth, it would be satisfactory for one

pipe to be black antistatic rubber and another pipe to beplastic of an entirely different colour, as in the Swedishsystem.

Lewisham Hospital,London SE13 6LH. J. M. CUNDY.

STRAINING, SITTING, AND SQUATTINGAT STOOL

SIR,--Dr Trowell (Sept. 6, p. 456) says that little isknown of the bulk-forming properties of different forms ofdietary bulk. This is not the case. It has been shown byWilliams and Olmstedt 1 that in normal individuals,when there is an increased dietary intake of cellulose,hemicellulose, or lignin, there is a variable effect on stoolweight. They also produce a table of ability of variousplant sources to’increase stool weight; cotton-seed wholeshave the least effect, then in increasing efficacy cellulose,alfalfa, leaf meal, wheat, bran, canned peas, corn-germmeal, sugar-beet pulp, cabbage, carrots, and finally agar-agar. There is a twenty-fold difference in capacity to bindwater between cotton-seed wholes and agar-agar.

In considering dietary sources of fibre the amount offibre taken with a vegetable will vary. Turnip and celerycontain 4% dry material whereas bran contains 85% drymaterial. Fibre obtained from wheat bran holds five timesits own weight of water, yet fibre from carrot and turnipwill hold between 27 and 30 times its own weight in water.Thus, if an allowance is made for the fibre content of theoriginal raw plant and the water-holding capacity of thedried material, 100 g of bran, despite its very modestwater-holding capacity, will have a superior overall hydro-philic property (450 g water per fibre in 100 g raw material),mango 320 g water per 100 g raw material, carrot 220 gwater; apple (180 g water) and brussel sprout have potenthydrophilic properties that can be utilised in increasingstool weight. 2Our studies with unprocessed bran showed increased

stool weight in normal subjects and patients with diver-

1. Williams, R. D., Olmstedt, W. H. J. Nutr. 1936, 11, 433.2. McConnell, A. A., Eastwood, M. A., Mitchell, W. D. J. Sci. Fd

Agric. 1974, 25, 1457.

ticular disease. Bran appears to modify fsecal flow patternsby acting as a vehicle for molecular or gel water in normalpeople 3 and as a vehicle for interstitial water in diverticulardisease.4 This source of fibre enhanced colonic filling andreduced the intraluminal pressure to various stimuli in thedistal colon in patients with diverticular disease. Thereduction in pressure is more evident with coarse bran.s

Therefore we agree with your editorial (July 5, p. 18)that a bulkier stool may be a more readily passed stool.

Wolfson Gastrointestinal Laboratories,Western General Hospital,Edinburgh EH4 2XU.

MARTIN EASTWOODW. D. MITCHELLA. N. SMITH.

STOOL WEIGHTS IN NORTH INDIANS

SIR,-Several articles and letters in your journal haveshown an interest in stool weights in different communities.Small stool weights and prolonged transit-times in theEuropeans and Americans seem to be related to the lowfibre content of their diets and are being considered as acause of several diseases of the Western world, such asappendicitis, ischaemic heart-disease, diverticular diseaseof the colon, carcinoma of the colon, &c. 6,7 Since manyof these diseases are relatively uncommon in India andthe food eaten here much less refined, we studied the stoolweights of healthy Indians in the human-nutrition unit ofour hospital. 24-hour stool weights of 550 individuals

STOOL WEIGHTS IN NORMAL NORTH INDIANS (g. PER 24 HOURS)

were measured by averaging 3 days’ stool collection,starting at least 3 days after being on the hospital diet,which was very similar to their usual diet. The hospitaldiet contained 10-12 g. of crude fibre, 40 g. of fat, 360 g.of carbohydrates, and 60 g. of protein per day, totallingan energy intake of about 2000 Cal. per day. The mean andrange of stool weights of these subjects are shown in thetable. Only 168 subjects had stool weights of 200 g. or less,which is the upper limit in most Western communities.*The rest had much higher stool weights, 41 of them700 g. or more. Teenage boarding-school pupils in theU.K. passed on average 110 g. of stool per day, and Englishadults on a typical European diet passed 104 g. per day.’It is of interest to note that the dietary fibre intake of oursubjects was 10-12 g. per day, compared with 5 g. per dayin the Western diet.9 The stool weights in our subjects are,on the other hand, comparable to those of 275 g. in ruralschoolchildren and 470 g. in adult villagers in Africa.’The crude-fibre intake in these rural Africans averages ashigh as 248 g. per day.10Between these two extremes of stool weights-i.e., in

’those on Westernised diet and those on full fibre diet as inAfrica and India-there are several communities occupyingintermediate positions. 7 The general pattern of stool

3. Findlay, J. M., Smith, A. N., Mitchell, W. D., Anderson, A. J. B.,Eastwood, M. A. Lancet, 1974, i, 146.

4. Findlay, J. M., Mitchell, W. D., Eastwood, M. A., Anderson, A. J. B.Smith, A. N. Gut, 1974, 15, 207.

5. Kirwan, W. O., Smith, A. N., McConnell, A. A., Mitchell, W. D.,Eastwood, M. A. Br. med. J. 1974, ii, 187.

6. Painter, N. S. Proc. R. Soc. Med. 1970, 63, suppl. p. 144.7. Burkitt, D. P., Walker, A. R. P., Painter, N. S. Lancet, 1972, ii, 1408.8. Steigman, F. Am. J. dig. Dis. 1942, 19, 423.9. Antar, M. A., Ohlson, M. A., Hodges, R. E. Am. J. clin. Nutr.

1964, 14, 169.10. Lubbe, A. M. S. Afr. med. J. 1971, 45, 1289.