709

and steepness of the Qs wave, from infarcts where therewas both clinical and histological evidence of some

muscle activity. Seeking another explanation, Prinzmetaland his associates recorded direct electrocardiogramsfrom parts of the ventricle which had been progressivelydamaged by burning or excision. When only subepi-cardial muscle was damaged R waves were still recorded,but when the outer third of the ventricular wall or the

deeper areas were involved R waves were replaced byQs waves. These observations suggested that the sub-endocardial muscle, probably because of its rapiddepolarisation, contributes nothing to the R wave in anepicardial lead, and that Qs leads can be produced bysubepicardial as well as by transmural infarction. Prinz-inetal and also Grant and Murray confirm the practicaldiagnostic importance of Qs waves and Q waves of 0-04sec. as signs of infarction, but seem to contradict eachother on the theoretical aspect. The difference may be

explained by the use of direct leads by Prinzmetal andof body-surface leads by Grant and Murray. This workhelps to explain some of the limitations of cardiographicdiagnosis.

1. See Lancet, 1946, ii, 871 ; Ibid, 1948, ii, 860 ; Ibid, 1949, i,1013 ; Ibid, 1952, i, 88.

2. Leifson, E., Carhart, S. R., Fulton, McD. J. Bact. 1955, 69, 73.3. Pijper, A. Nature, Lond. 1955, 175, 214.

THE GREAT SCHISMFOR some years microbiological circles have been

stirred by a debate, on the function of the bacterial

flagellum, between Prof. A. Pijper on the one side andalmost all the world on the other.! This heretic believesthat, far from being the organ of locomotion, the

flagellum is a trailing appendage of an automotive cell ;and his evidence is formidable. Oddly enough, throughoutthe argument little attention has been paid to thedetailed structure of flagella, apart from some picturesfrom the electron microscope which are more elegantthat informative. Now Leifson and his colleagues 2have shown that in stained preparations the flagellaof proteus have in the main two distinct and well-defined shapes. What they call " normal" is an openspiral (or zigzag) of two to three waves : " curly"is a tighter spiral (or zigzag) of four to six waves. Thetwo may be found on different flagella of the samebacterium, and there are two rarer types. Which typei. seen is influenced to some extent by the environmentin which the bacterium has grown. The wave-lengthsof each type of curve are remarkably constant for thesame species of bacterium. Almost simultaneouslyPijper has published a note on the same subject,based, as always, on observation of the living bacillusilluminated on the dark field by sunlight. He confirmshis original statement that as a general rule the bacteriumadvances by a spiral movement of its body with theflagellum sticking straight out behind, like an otter’srudder. (In the photographs this always seems a bitfuzzy.) Under circumstances which he has not yetdefined, this straight tail shortens and assumes a spiralshape which may have one of two wave-lengths, onetwice as long as the other. Initially the change is

reversible, but in the end the organ always finishes asa helix or splits into fine helicules. These may whirlabout for a short time and thereby give some erraticmovement to the bacterium (quite distinct in Pijper’sview from true motility), but their development isassociated with stiffening of the body and final immobility.A cautious view suggests that these two reports

describe the same phenomena modified by differencesin method. If the development of Pijper’s helicules isalways associated with death, or at any rate immobility,it is not surprising that they should be the structuresseen in stained preparations. He says that they mayappear to move to any part of the cell wall, which wouldexplain the lophotrichous and peritrichous arrangementsso loved by the systematists. What he does not mentionis whether these helicules retain the wave-length of thehelix from which they derive. Leifson has carefully

measured the wave-lengths of his two forms of curve,but does not call attention to what is clear from his

figures-that the wave-length of " normal" curves is

always about twice that of " curly." In comparingresults obtained by methods so different it would beunfair to ask for complete agreement, but it is a fairguess that Leifson’s flagella are Pijper’s helicules. Isthe fuzziness of Pijper’s rod-like flagellum due to its

being made up of a sheaf of flagellella And is this thebeginning of the end of the great schism ?

1. Magill, T. P. J. Immunol. 1955, 74, 1.2. Mon. Bull. Min Hlth Lab. Serv. 1955, 14, 34.

THE EVIL SPIRITS

MANY distinguished bacteriologists and immunologistshave talked optimistically of the problem of infectiousdiseases as virtually solved ; and in his presidentialaddress to the American Association of Immunologists,lDr. T. P. Magill has taken these people to task.

Like Dubos, whose latest book is reviewed on p.704, hedraws attention to our anthropomorphic attitude of mind.He points out that the peaceful bacterium, trying to findfood and shelter in man, is termed an aggressor, whereasit is just as reasonable to call man the aggressor ; andthat many of the manifestations of disease arise onlywhen man tries to exorcise these supposedly evil spirits.This viewpoint has virtues, not the least of which is itsrecognition that the aim of preventive medicine shouldbe less to eliminate an infection than to attempt to cometo terms with it. Attempts at elimination may have beenless strikingly successful than the decline in mortality-rates suggests. It is galling to have to admit that therates for tuberculosis, diphtheria, measles, and pneu-monia began to fall long before modern preventivemeasures could have taken effect. A factor that is often

neglected in calculations on trends of an infectious diseaseis its natural history or ecology. There are many examplesof diseases which have ravaged populations until in thecourse of time they have lost their malignant character.Such a change may be due to any of several causes.Huge numbers of susceptible people may havedied, leaving a resistant core ; and in the microbial

population it is the less virulent organisms whose survivalis favoured, since the organisms which kill their hosthave entered a blind alley. The recent myxomatosisepizootics in Australia and in this country have shownsuch processes. There are likewise examples of diseasesregaining their former severity.

Magill’s lecture will have failed in its purpose if it

encourages any ideas of nihilism : public-health measures,immunisation, and antitoxin therapy are indispensable.The lesson to be lea,rnt is that infectious diseases are farfrom conquered and that present methods of controllingthem are far from perfect. In our pride at how muchknowledge of bacteriology and immunology has beengained, we must beware of becoming too complacentabout the evil spirits.

FOOD-POISONINGTHE Public Health Laboratory Service has published

another of its valuable annual reports on food-poisoningin England and Wales. This report, on the year 1953,2contains an immense amount of data, much of which isgiven in tables ; and it lacks the dramatic impact of thesame facts described in narrative form. In 1953 therewere 5277 incidents-an increase of 1758 over the

previous year. These incidents consisted of outbreaks,family outbreaks, and sporadic cases. The increase isreflected in all the causes listed-namely staphylococci,Clostridium welchii, undiscovered, and particularlysalmonella. Better reporting must be taken into account,but by the most optimistic estimate there has been nodecrease in food-poisoning. The authors of this reportbelieve that at least 4000 cases were not notified-whichis a very high proportion.As in previous years meat dishes, particularly processed

or made-up meat dishes, were the most important vehicle ;

710

but ham and boiled bacon were particularly importantas vehicles of staphylococcal food-poisoning. Milkcaused 12 outbreaks, of which 7 were associated withfresh milk, 4 with dried milk, and 1 with cannedmilk. 3 of the fresh-milk outbreaks were caused bySalmonella typhimurium ; 1 of these was due to infec-tion of pasteurised milk during bottling, and another tounpasteurised tuberculin-tested milk. 2 of the fresh-milk outbreaks were due to Staphylococcus aureus,

originating from infected cows. Several outbreaks wereassociated with sweetmeats ; and one of these, knownto have affected two people, was associated with vanillaslices : " S. enteritidis var. danysz was isolated from thepatients and from mice in the bakery concerned. The

bakery had been baited with S. enteritidis var. danyszto clear it of vermin a month earlier."The types of salmonella followed the same pattern as

in previous years. About 76% of cases were due toS. typhimurium (aertrycke) with S. thompson, S. enteritidisvar. jena, and S. bovis morbificans next in order but

accounting for only 7% of cases ; the forty-six exogenoustypes accounted for 9% of cases. Cl. welchii food-poison-ing was associated with meat dishes in every instance,except possibly 1 where the vehicle was not recorded.

Fifty-one deaths were recorded. This report showsthat food-poisoning gives rise to a considerable amountof sickness with consequential loss of working-time.Much of this could be avoided bv the education andcoöperation of the food-handler. We hope that the newFood Hygiene Advisory Council will accept as one of itsfirst duties the education of the housewife, shopkeeper,restaurateur, and other food-handlers.

1. Chiari, H. Beitr. Path. Anat. 1899, 26, 1.2. Cited by Budd, G. In Diseases of the Liver. Philadelphia, 1946.3. Palmer, E. D. Ann. intern. Med. 1954, 41, 266.

CHIARI’S SYNDROME

THE clinical picture that results from occlusion of thehepatic veins is generally called after Chiari, who gavethe first clear account of its pathogenesis 1 ; the disorderhad first been reported by Lambron 2 some fifty yearsearlier. From the number of published cases-115 by1952-this syndrome might seem very rare ; but this

figure may be misleading, for Palmer 3 has reported 7cases verified by necropsy and 4 presumptive cases allseen within a period of thirty-two months. These caseswere found at a large tumour clinic : one of the com-monest causes of the syndrome is encroachment bymetastatic tumours on the hepatic veins ; but sincethis is a late complication of malignant neoplastic diseaseit probably develops usually after the patient’s dischargefrom hospital.The clinical features of the syndrome depend largely

on the rate at which the hepatic veins are occluded. Inacute cases nausea, vomiting, and severe pain in theright hypochondrium due to rapid enlargement of theliver as a result of congestion may be quickly followed bydeath from hypotensive shock. Less acute cases are

characterised by severe and rapidly accumulating ascitesand signs of portal hypertension with a developingcollateral circulation. Signs of hepatic failure are usuallypronounced, and death results from hepatic coma.

Simultaneously developing oedema of the legs indicatesinvolvement of the inferior vena cava in the occlusiveprocess. Chronic cases closely resemble hepatic cirrhosis,which may indeed develop as a result of the chronic liverinjury due to the greatly impaired intrahepatic circu-lation. Function tests invariably indicate severe

parenchymal damage : bromsulphalein excretion ismuch reduced, the serum albumin-globulin ratio isreversed, and the flocculation test is almost invariablypositive. Patients rarely survive complete occlusionfor more ’than a few months. Ruptured cesophagealvarices, portal or mesenteric thrombosis, or inter-

current infection lead to death in the few who do notdie of hepatic coma.

’

Neoplastic involvement of the hepatic veins probablyaccounts for the majority of cases of Chiari’s syndrome,but occlusion of these veins or their ostia undoubtedlyarises as a complication of many other conditions.Palmer usefully classines these under the followingheadings : congenital, mechanical, haematological, diffuseand local liver disease, acquired vascular disease, anddisease of neighbouring organs. He lists some 42 con-ditions as likely to be responsible for hepatic venousocclusion, of which 27 are known each to have accountedfor one or more instances. In patients severely ill with,for example, leukaemia, cirrhosis, or local suppuration inchest or abdomen the syndrome may easily be overlooked,and even at necropsy the thrombosed hepatic veins areeasily missed if not specifically sought; and this mayexplain why published cases are so few.

1. Scott, J. C. J. Bone Jt Surg. 1955, 37B, 107.2. Selye, II. The Physiology and Pathology of Exposure to Stress.

Montreal, 1950.

STRESS FACTOR IN THE DISC SYNDROMEWE may be on the threshold of important discoveries

relating to the physiology and pathology of the inter-vertebral disc. There is now evidence that the inter-vertebral disc is a hydraulic unit with a mechanismgenerating an internal tension suited to the load imposedon it. The nucleus pulposus, exposed to isotonic saline,can generate considerable pressures (100-200 mm. Hg)when resistance is offered to its swelling; and it isconceivable that an acute attack of lumbago might bedue to disturbance of the mechanism controlling theaccess of fluid to the nucleus pulposus, with resultingtension-a possible parallel with the mechanism ofacute glaucoma. These speculations suggest possibleexplanations of the lumbago which follows exposureto cold and wet where there is no evidence of trauma.Scott 1 has described experimental evidence that

swelling of the nucleus pulposus can be produced underthe conditions of the " stress reaction " or " generaladaptation syndrome." 2 The work reported by Scottwas done on voles by D. H. Chitty, who exposed animalsto strangers for about two hours a day for three or fourdays and then compared the size of the nucleus pulposusof each disc with that in control animals. Statisticalanalysis showed that the difference between experi-mental and control animals was highly significantIn support of the thesis that raised disc tension may bethe basis of acute lumbago in man, Scott reproducesradiographs showing excessive hollowing of the opposingsurfaces of vertebral bodies which enclose discs of rathermore spherical shape than is commonly seen. But manysurgeons will regard this as a normal variation, commonlypresent without acute back pain; and in any case

one would suppose it impossible for a vertebral body toadapt itself to a swollen disc in the three or four weeksduring which the raised pressures of the acute tensionepisode are presumed to be present.We must here distinguish the difference in psychological

states between patients with acute disc episodes andpatients with chronic low-back pain. Commonly, womenwho are depressed and unhappy subconsciously allowthemselves to be disabled by pain of a degree which otherwomen tolerate more or less easily. Those who toleratetheir discomfort do not tend to consult doctors; inother words, patients coming to hospital because of chronicbackache are a self-selected group. On the other hand,in the case of really violent episodes of acute disc painalmost every patient seeks medical advice. The experi-mental evidence of a " stress factor " relates essentiallyto acute disc episodes ; but, though most surgeons wouldagree on the association of chronic backache with psycho-logical disturbances, many will deny that this associationis common in cases of acute disc lesions.