2
1314 cholesterol or artheromatous emboli could be a cause of ulcer, but no clear clinical picture has emerged which could imply a direct link between emboli and ulceration.’ 0 Other investigators have suggested that certain vascular structures were associated with a tendency to peptic ulceration. These formations, described by their appear- ances as microcherries, glomeruli, and venous lakes, were found more often in the lips of patients with ulcers than in those of individuals without ulcers.ll The same workers later noted that the presence of these structures in the lips could be correlated with alterations in the blood-vessels of the stomach and duodenum.12 On p. 1300 this week Mr. Cox and his colleagues record their investigation of gastric fibrinolysis and suggest that intrafibrinolytic activity is increased in ulcer patients and could be an important factor in the initiation of haemorrhage and ulceration, a situation which would be rather the reverse of that envisaged by Virchow. Blood was taken at operation from vessels draining the stomach and from a peripheral vein in 13 patients with evidence of duodenal ulceration (combined with gastric ulceration in 2), and from a control group of 13 patients undergoing abdominal surgery for other conditions, such as gallstones. Free plasmin was not detected in any specimen of peripheral-vein blood nor in 6 samples of gastric arterial blood. Appreciable fibrinolytic activity was, however, found in gastric-vein blood from 11 of the 13 ulcer patients, but in only 5 of the control group. In addition plasminogen activator was detected in the mucosa obtained at pyloroplasty in 3 of the ulcer patients. The suggestion is that more emphasis should perhaps be placed on the role of fibrinolysis in gastric ulceration and haemorrhage. Certainly these promising initial find- ings must be explored further : the importance of fibrinolysis in relation to haemorrhage might, for instance, be investi- gated by comparing fibrinolytic activity in gastric-vein blood obtained from ulcer patients with and without bleeding. VIRUS GROWTH AND VIRULENCE FROM the host’s point of view the most important property of a virus is its virulence-its ability to produce disease or death in the organism it attacks-and the new issue of the British Medical Bulletin, 13 devoted to medical virology, considers, in particular, how viruses multiply and produce disease. Virulence is not synonymous with virus multiplication, for some viruses multiply well without producing any disease in the host, whereas others may form toxins which are damaging or even lethal when injected, without further multiplication of the virus. Some strains of a virus may give rise to no overt disease, whereas others may be fatal. A direct study of virulence in viruses affecting man is clearly difficult, but the New- castle-disease virus 14 which infects fowls is much more amenable to laboratory study. A large number of strains of this virus have been isolated from outbreaks in different parts of the world, and some of these have been studied in great detail. Antigenic differences appear to be unrelated to virulence, but there is an association between the speed 10. Taylor, N. S.. Gueft, D., Lebowich, R. J. Gastroenterology, 1964, 47, 97. 11. Gius, J. A., Boyle, D. E., Castle, D. D., Congdon, R. H. J. Am. med. Ass. 1963, 183, 725. 12. Gius, J. A. Boyle, D. E., Congdon, R. H. Boyd, W. C. Archs Surg., Chicago, 1965, 91, 221. 13. Br. med. Bull. 1967, 23, no. 2. 14. Waterson, A. P., Pennington, T. H., Allan, W. H. ibid. p. 138. of virus growth and virulence of different strains. Virulence in the Newcastle-disease virus implies the ability to damage cells of the brain and spinal cord, but some of the less virulent strains can multiply within the brain and may in fact attain higher levels of infectivity than the virulent strains. The important difference seems to be that the virulent strains multiply rapidly and soon overwhelm the host defences, whereas the less virulent strains multiply more slowly and do not produce irre- versible damage to the host. The differences, in bio- chemical terms, between these two situations are not yet known, but a comparison of the chemical changes induced in host cells by defective and delayed myxovirus infections 15 is a promising line of investigation. If the chemical basis of virus replication can be determined, it may be possible to redirect the metabolism of normally susceptible cells so that they yield defective or abortive infections, with consequent benefit to the host. GERMICIDAL ACTION OF SEA WATER BACTERIA survive for a shorter time in sea water than in fresh water whether this comes from a stream or from the tap. " Synthetic " sea water-i.e., compounded in the laboratory to the same chemical composition-and sea water which has been boiled or filtered or stored in the laboratory are also less bactericidal than fresh sea water. All this has been known for a long time, but the reasons are still unknown.16 A favourite explanation has been the biological action of protozoa or other animalcules, but there seems to be no proof of this. If the problem were of more importance to the public health it might be pursued with greater vigour. The beaches of the civilised world (and perhaps of other parts too) show a varying degree of contamination by sewage, but unless this is excessive (which can usually be judged by the naked eye) not much harm results.17 Whether an enteric bacterium lives there for 2 days or 6 does not matter. Enteric viruses enter the sea by the same route as bacteria, and it has been argued with more emotion than conviction that some cases of poliomyelitis are due to this source. The evidence for this is weak. There is no doubt, however, that poliovirus can survive in sea water for several days and in fresh water for at least twice as long. It is one of the viruses most useful for experimental pur- poses. The technical methods for recovery and counting are well established, and it withstands the hazards of the laboratory better than most. Some recent work from Lebanon on the fate of this virus in sea water is of interest. Surface sea water collected without debris inactivated 103 T.C.D.5o poliovirus per ml. in 6-9 days.18 The same water boiled or stored at room temperature was less viricidal, but passage through a Seitz filter did not affect the inactivation-rate. The effect must have been due to some substance in solution rather than any particulate matter alive or dead. The main chemical constituents of sea water tested individually had little effect; but when combined into a " synthetic " sea water they inactivated low concentrations of poliovirus, though not so quickly as the natural sea water. With higher concentrations of virus they were less successful. Boiling the synthetic sea water did not change its viricidal properties. It seemed from 15. Fraser, K. B. ibid. p. 178. 16. Greenberg, A. E. Publ. Hlth Rep., Wash. 1956, 71, 77. 17. Report, J. Hyg., Camb. 1959, 57, 435. 18. Matossian, A. M., Garabedian, G. A. Am. J. Epidem. 1967, 85, 1.

GERMICIDAL ACTION OF SEA WATER

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Page 1: GERMICIDAL ACTION OF SEA WATER

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cholesterol or artheromatous emboli could be a cause ofulcer, but no clear clinical picture has emerged whichcould imply a direct link between emboli and ulceration.’ 0

Other investigators have suggested that certain vascularstructures were associated with a tendency to pepticulceration. These formations, described by their appear-ances as microcherries, glomeruli, and venous lakes, werefound more often in the lips of patients with ulcers than inthose of individuals without ulcers.ll The same workerslater noted that the presence of these structures in the lipscould be correlated with alterations in the blood-vesselsof the stomach and duodenum.12On p. 1300 this week Mr. Cox and his colleagues

record their investigation of gastric fibrinolysis and suggestthat intrafibrinolytic activity is increased in ulcer patientsand could be an important factor in the initiation of

haemorrhage and ulceration, a situation which would berather the reverse of that envisaged by Virchow. Bloodwas taken at operation from vessels draining the stomachand from a peripheral vein in 13 patients with evidence ofduodenal ulceration (combined with gastric ulceration in2), and from a control group of 13 patients undergoingabdominal surgery for other conditions, such as gallstones.Free plasmin was not detected in any specimen of

peripheral-vein blood nor in 6 samples of gastric arterialblood. Appreciable fibrinolytic activity was, however,found in gastric-vein blood from 11 of the 13 ulcer

patients, but in only 5 of the control group. In addition

plasminogen activator was detected in the mucosa obtainedat pyloroplasty in 3 of the ulcer patients.The suggestion is that more emphasis should perhaps

be placed on the role of fibrinolysis in gastric ulcerationand haemorrhage. Certainly these promising initial find-ings must be explored further : the importance of fibrinolysisin relation to haemorrhage might, for instance, be investi-gated by comparing fibrinolytic activity in gastric-veinblood obtained from ulcer patients with and withoutbleeding.

VIRUS GROWTH AND VIRULENCE

FROM the host’s point of view the most importantproperty of a virus is its virulence-its ability to producedisease or death in the organism it attacks-and the newissue of the British Medical Bulletin, 13 devoted to medicalvirology, considers, in particular, how viruses multiplyand produce disease. Virulence is not synonymous withvirus multiplication, for some viruses multiply wellwithout producing any disease in the host, whereas othersmay form toxins which are damaging or even lethal wheninjected, without further multiplication of the virus.Some strains of a virus may give rise to no overt disease,whereas others may be fatal. A direct study of virulence inviruses affecting man is clearly difficult, but the New-castle-disease virus 14 which infects fowls is much moreamenable to laboratory study. A large number of strains ofthis virus have been isolated from outbreaks in different

parts of the world, and some of these have been studied ingreat detail. Antigenic differences appear to be unrelatedto virulence, but there is an association between the speed10. Taylor, N. S.. Gueft, D., Lebowich, R. J. Gastroenterology, 1964, 47, 97.11. Gius, J. A., Boyle, D. E., Castle, D. D., Congdon, R. H. J. Am. med.

Ass. 1963, 183, 725.12. Gius, J. A. Boyle, D. E., Congdon, R. H. Boyd, W. C. Archs Surg.,

Chicago, 1965, 91, 221.13. Br. med. Bull. 1967, 23, no. 2.14. Waterson, A. P., Pennington, T. H., Allan, W. H. ibid. p. 138.

of virus growth and virulence of different strains.Virulence in the Newcastle-disease virus implies the

ability to damage cells of the brain and spinal cord, butsome of the less virulent strains can multiply within thebrain and may in fact attain higher levels of infectivitythan the virulent strains. The important difference seemsto be that the virulent strains multiply rapidly and soonoverwhelm the host defences, whereas the less virulentstrains multiply more slowly and do not produce irre-versible damage to the host. The differences, in bio-chemical terms, between these two situations are not yetknown, but a comparison of the chemical changes inducedin host cells by defective and delayed myxovirus infections 15is a promising line of investigation. If the chemical basisof virus replication can be determined, it may be possibleto redirect the metabolism of normally susceptible cells sothat they yield defective or abortive infections, with

consequent benefit to the host.

GERMICIDAL ACTION OF SEA WATER

BACTERIA survive for a shorter time in sea water than infresh water whether this comes from a stream or from the

tap. " Synthetic " sea water-i.e., compounded in the

laboratory to the same chemical composition-and seawater which has been boiled or filtered or stored in the

laboratory are also less bactericidal than fresh sea water.All this has been known for a long time, but the reasonsare still unknown.16 A favourite explanation has been thebiological action of protozoa or other animalcules, butthere seems to be no proof of this. If the problem were ofmore importance to the public health it might be pursuedwith greater vigour. The beaches of the civilised world(and perhaps of other parts too) show a varying degree ofcontamination by sewage, but unless this is excessive

(which can usually be judged by the naked eye) not muchharm results.17 Whether an enteric bacterium lives therefor 2 days or 6 does not matter.

Enteric viruses enter the sea by the same route as

bacteria, and it has been argued with more emotion thanconviction that some cases of poliomyelitis are due to thissource. The evidence for this is weak. There is no doubt,however, that poliovirus can survive in sea water forseveral days and in fresh water for at least twice as long.It is one of the viruses most useful for experimental pur-poses. The technical methods for recovery and countingare well established, and it withstands the hazards of thelaboratory better than most. Some recent work fromLebanon on the fate of this virus in sea water is of interest.Surface sea water collected without debris inactivated103 T.C.D.5o poliovirus per ml. in 6-9 days.18 The samewater boiled or stored at room temperature was less

viricidal, but passage through a Seitz filter did not affectthe inactivation-rate. The effect must have been due tosome substance in solution rather than any particulatematter alive or dead. The main chemical constituents ofsea water tested individually had little effect; but whencombined into a " synthetic " sea water they inactivatedlow concentrations of poliovirus, though not so quickly asthe natural sea water. With higher concentrations of virusthey were less successful. Boiling the synthetic sea waterdid not change its viricidal properties. It seemed from

15. Fraser, K. B. ibid. p. 178.16. Greenberg, A. E. Publ. Hlth Rep., Wash. 1956, 71, 77.17. Report, J. Hyg., Camb. 1959, 57, 435.18. Matossian, A. M., Garabedian, G. A. Am. J. Epidem. 1967, 85, 1.

Page 2: GERMICIDAL ACTION OF SEA WATER

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these experiments that the inactivating properties ofnatural sea water depend on two factors: a combination ofthe salts in solution; and an unknown heat-labile sub-stance which, because it will pass a Seitz filter, must alsobe in solution. The technical difficulties of further pro-gress are considerable. Search for an unknown factor bychemical methods is an unrewarding sport. Sea water isnot a uniform substance, and comparative work with waterfrom different sites might give a useful hint: equally, it

might teach us nothing.For obvious reasons we know very little about the sea

as an environment, and it is time that we learned more.Unlike the sybarites of today, our grandparents bathedbecause it was " healthy ". They might have acceptedthis work on the viricidal action of sea water as confirmingtheir beliefs, but they probably meant no more than coldand beastly.

DETECTION OF EARLY ARTERIOSCLEROSIS

ARTERIOSCLEROSIS is difficult to diagnose during life.

Diagnosis post mortem is comparatively easy, but for

necropsy data to be useful they must cover a high pro-portion of all deaths in a demographically defined area,including deaths in the home. We have previouslydescribed 1 a study sponsored by the World Health

Organisation and begun in January, 1963, in which

specimens of the aorta and coronary arteries were

obtained from some 13,500 necropsies. But postmortemevidence, though very helpful, cannot fully replace thatderived from live patients, and various methods havebeen suggested for such investigations. Arteriographyis clearly impracticable in large population studies.

Oscillometry (by visual means or by recording) can revealpressure gradients in the limb and was used by Widmerand his colleagues 2 to determine the prevalence of

peripheral arteriosclerosis in 6400 working people ofvarious ages. They found arteriosclerosis in about 1 %of their population, including some subjects who wereunaware of having the disease. But their study probablyleft many cases undected; for, as Fiddian et a1.3 haveshown, not only is the lumen already severely restrictedwhen a pressure gradient is noted, but extensive diseasein the periphery may cancel out the gradient.Techniques have also been developed on the basis of

radioisotope uptake or disappearance from the limb,but all are complex and therefore unsuitable for fieldsurveys. Flow measurement can be done by plethys-mography,4 indicator dilution techniques,5 or flow-meter.All these techniques are quite intricate, and diagno-sis is certain only when arterial obstruction is alreadysevere. Possibilities of recording changes in conductivityof tissues in relation to pulsatile flow have not yet beenfully evaluated. 6 pulse tracings registered from oscillo-meters are, in general, overdamped and do not lendthemselves to detailed analysis.Cooper and his colleagues now propose a promising

method for the early recognition of peripheral arterio-1. See Lancet, 1966, i, 139.2. Widmer, L. K., Greensher, A., Kannel, W. B. Circulation, 1964, 30,

836.3. Fiddian, R. V., Byar, D., Edwards, E. A. Archs Surg., Chicago, 1964,

88, 83.4. Siggaard-Andersen, J. Acta chir. scand. 1965, 130, 190.5. Hobbs, J. T., Edwards, E. A. Ann. Surg. 1963, 158, 159.6. Polzer, K., Schuhfried, F., Heeger, H. Br. Heart. J. 1960, 22, 140.7. Cooper, D., Hill, L. T., Jr., Edwards, A. J. Am. med. Ass. 1967 199, 449.

sclerosis, based on changes in the externally recordedpulses of the lower extremities. The method seems

capable of detecting narrowing of the arterial lumenbefore a pressure gradient develops. The test is simpleand can be performed by a technician, with no cum-bersome preparation of the patient. Thus, it is suitablefor the investigation of large populations, and it may beparticularly useful for aetiological and epidemiologicalstudies. The method depends on two measurements,which can be defined numerically, in external pulserecording and which may thus be used for comparison.These are the rate of ascent (the systolic slope) and theintegrated pulse amplitude or deflection. Both measure-ments show a considerable overlap between normal andarteriosclerotic subjects when pulses are recorded at

rest, but good differentiation is achieved during reactivehyperaemia. In the arteriosclerotic limb normal augmen-tation of the pulse during reactive hypertmia is pre-sumably absent owing to a lowering of arterial pressurein the limb and to stiffening and lack of compliance ofthe arterial walls. In early arteriosclerosis stiffening ofthe arterial wall would presumably be the only cause.Apart from atherosclerosis, which blocks the lumen,there are other forms of arteriosclerosis, such as

Monckeberg’s sclerosis or the sclerosis of ageing, whichare common and in which loss of elasticity would pro-bably also produce a positive result. Conditions otherthan arteriosclerosis may also give rise to small-volumepulses, which may or may not be augmented by reactivehyperxmia, including heart conditions, such as aorticstenosis, or any low-output state. Further news of themethod as applied in field trials will be awaited with

great interest.

THE BASIC SCIENCES IN LAGOS

MEDICAL schools everywhere, and especially in Africa,are plagued by a shortage of preclinical teachers. Overthe past four years the Commonwealth Fund of New

York, in association with the University of Rochester, hassent six such teachers to the University of Lagos MedicalSchool. In addition, five faculty members have gone fromLagos to Rochester on research grants from the Fund.Under a new scheme financed by the Fund, six promisingstudents will be given predoctoral fellowships for twoyears in the basic and paraclinical medical sciences-oneyear to be spent in Lagos and one in Rochester. On

completion of the fellowship the student will sit an

examination for a B.sc. (honours) or M.sc. degree in theUniversity of Lagos. The grant from the Fund-1:700for the year in Lagos, and El 300 for the year in Rochester-is meant to compensate the student for the two-yeardelay in his qualifying as a doctor. In return, he mustbind himself to teach for at least two years in Lagos orelsewhere in Nigeria or West Africa after graduation. TheUniversity of Lagos is considering the establishment of aninstitute of basic medical sciences during the next quin-quennium (1968-73). Towards the end of that periodthe first batch of graduates trained to teach in the basicor paraclinical medical sciences should be comingforward.The Commonwealth Fund grants should go some way

towards easing the situation in West Africa. Ultimatelythe Lagos school may be able to help schools in other partsof Africa.