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and vitamins A and D. There is perhaps little hopethat calcium given orally will reach the lens. Sup-ported by Tsuji’s investigations 7 on the reactionsof isolated lens protein, Burdon-Cooper believes thatpotassium restrains the denaturation of these proteins ;it may be administered as iodide drops but moreusually ionisation is employed, the eye being coveredwith a pad soaked in potassium iodide and exposedto a current of 2-5 ma. Repeated treatments aresaid to clarify the lens, but it does not seem to haveoccurred to anyone to treat bilateral cataract usingthe other eye as a control. Fischer’s investigation 8of the penetration of salts into the eye should befollowed up. The remedies in the second group havelittle to commend them. Sodium iodide dropshave been used on the ground that cataract may beassociated with a thyroxic deficiency, and Danielsclaims that a definite amount of iodine can berecovered from a lens extracted from an eye whichhas been treated with iodine baths. The thirdmethod, injection of lens proteins, finds more favourin America than in this country, and the reasonsgiven for using them are in dispute.Apart from these remedies, many of which are

open to criticism, it is usual to attend to the generalwell-being of the patient by the removal of septicfoci and by administration of such substances as

calcium and vitamin C. The fact that the poorerclasses are more prone to cataract suggests that anample and varied diet may be of value in prevention.Lacking more definite information we must hopethat the organised research now going on in manycountries will lead to the identification of some sub-stance specially important to the nutrition of the lens.

THEORIES OF THE SPREAD OF POLIOMYELITIS

FORTUNATELY in this country poliomyelitis rarelyassumes what might be termed epidemic pro-portions. Happily the small outbreak in Essex to whichwe referred last week does not seem to be spreading,only 2 or 3 further cases having been reported.Every summer sporadic cases are notified and theirappearance reminds us of our relative ignorance ofthe epidemiology of this disease and our inabilityto control its manifestations. It has been generallyaccepted that poliomyelitis is one of those diseaseswhich is spread by means of infective droplets andthat the virus reaching the nasopharynx of a

susceptible individual passes inwards to the olfactorybulb via the olfactory hairs, its spread thence to thecord being axonal. The evidence in support of thisconception is of such weight that it cannot be lightlydisregarded, but during the last year or two it hasbeen questioned. Those who find the droplet theoryof the spread of poliomyelitis unconvincing point totwo of its epidemiological features: the frequentinability to establish evidence of direct or indirectcontact between cases occurring in an epidemicand the seasonal incidence of the disease. Dr.Lumsden, medical director of the United StatesPublic Health Service, has recently drawn attentionto these discrepancies. 9 It does not however seemdifficult to trace the lines of spread of poliomyelitisin a virulent epidemic, such as the last Melbourneone. There evidence of spread by personal contactwas readily established, so much so that at leasta few new cases had already been isolated beforesigns of infection developed. It is in epidemics of aless virulent type, in which the percentage of silentinfections is high, that the chain of personal contact

7 Tsuji, T., Biochem. J. 1932, 15, 33.8 Fischer, F. P., Arch. f. Augenheilk. 1934, 108, 527.

9 See Lancet, 1938, 1, 1402.

ceases to be apparent, just as it does in cerebro-spinal meningitis.The second objection to the theory of the droplet

spread of poliomyelitis-its seasonal incidence-is a ’much more serious one. All those diseases likemeasles, influenza, and the common cold which arespread by infective droplets have a winter seasonalincidence, whereas poliomyelitis usually occurs inthe later half of the summer. Why this should beit is difficult, if not impossible, to say at present.It is worth nothing however that we really do notknow whether infection with the virus of polio-myelitis is more widespread in winter than summer.We know only that clinical cases of the disease occurmore commonly in the summer and this might be dueto some particular state of the host rather than towidespread infection.

There is indeed much still to learn about polio-myelitis. J. D. Trask, A. J. Vignec, and J. R. Paul 10at Yale have been re-examining the evidence thatthe virus of poliomyelitis can be demonstrated in thestools. They suspended the whole stool in 120 c.cm.of water, allowed it to sediment, and treated thesupernatant fluid with ether in the refrigerator for24 hours to kill bacteria. They then inoculated

monkeys intraperitoneally with 30 c.cm. of thisetherised extract. The fact that the monkeydeveloped the typical clinical picture of poliomyelitisand its spinal cord the characteristic histologicalchanges showed that the virus was present in thespecimen, but successful passage to a second monkeywas deemed necessary before the results were regardedas positive. By this means the Yale workers haveisolated poliomyelitis virus from one out of eightpatients, the positive results being obtained in anatypical case in an infant, aged 18 months,on the 2nd, 14th, and 25th days of disease. Theyalso draw attention to the stability of the virusin the stools-positive results were obtained withmaterial which had been stored for weeks-and theysuggest that a high degree of pollution of sewagemight occur during an epidemic. Even if itdoes it is difficult to see what part fsecal excre-

tion of virus is going to play in the spread of the disease.This would imply infection by the alimentary routeand the bulk of the experimental evidence on thispoint hardly supports such a possibility.

SEDORMID AND PURPURA

A LARGE number of therapeutic substances mayin exceptional circumstances produce different typesof blood dyscrasia. Thus gold salts and sulphanil-amide derivatives may cause severe anaemia or

agranulocytosis; benzene may cause anaemia or

thrombocytopenia ; while amidopyrine is oftena factor in agranulocytosis. Sedormid appears tobe unique in affecting only the thrombocytes andnever the red or white cells. In our present issueDr. T. Joekes describes a further case of thrombo-

cytopenia and purpura appearing suddenly in a

man who had taken sedormid over a long period withno ill effect. He has traced 37 similar recordedcases, to which might be added 4 more recentlydiscussed by V ogl.l1 Usually the patients recoverwhen the sedormid is discontinued, and sometimesfurther attacks follow minute doses of the suspecteddrug, thus proving its setiological significance. Themode of action of sedormid is as little understoodas that of any other chemical that affects haemopoietictissue. Joekes states that on sternal marrow puncturethe megakaryocytes were seen to be considerably

10 J. Amer. med. Ass. July 2nd, 1938, p. 6.11 Vogl, A., Wien. Arch. inn. Med. 1938, 32, 273.