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CRECENT ADVANCES IN POLIOMYELITISThe Epidemiology of Poliomyelitis

By J. H. S. GEAR, B.Sc., D.P.H., D.T.M. and H.Rickettsial and Virus Diseases Laboratory, South African Institute of Medical Research, J7ohannesburg

Poliomyelitis is an age old disease, but it wasonly clearly recognized as a clinical entity in thefirst half of the last century. Until the middle oflast century it usually occurred in endemicsporadic form. Small outbreaks were recorded inSt. Helena, i834, in England, I834, and in theUnited States, I843. The first large. epidemicoccurred in Scandinavia in i868. In the I890'slarge epidemics began to appear in the NorthernUnited States. Since then, epidemics have re-curred at frequent intervals in these countries.More recently extensive epidemics have occurredin Australia and New Zealand. It is of consider-able significance that the countries most severelyaffected have the highest standards of living andof hygiene and sanitation. As other countrieshave attained comparable standards, they in turnhave suffered extensive epidemics.

Geographical, Racial and Age DistributionPrior to the recent war, poliomyelitis was

thoug'ht to be a rare disease in tropical and sub-tropical countries. However, the incidence ofparalytic cases does not necessarily reflect theincidence of infection. Indeed, it is now clearfrom observations made during the recent warthat poliomyelitis is a common infection in thetropics.

In the Middle East, Paul, Havens and vanRooyen (i944) noted that the incidence in Ameri-can soldiers was ten times what it was in Americansoldiers in the United States. Cases occurredamong local children in Egypt but severe para-.lytic infections, resembling those observed innewly-arrived Australian, New Zealand, Americanand European soldiers, could not be traced in theadult Egyptian civilians or soldiers. In Malta, theepidemic beginning late in i942 affected theMaltese children under five years old mostseverely. Of 6i persons over the age of 2o affectedonly four were Maltese, the remainder beingservicemen from the United Kingdom (Seddon,I943). In India McAlpine (I945) noted thestriking fact that the disease was five times morecommon in British officers than in other ranks.

In Japan Paul (I947)/noted that endemic polio-myelitis was common, but that large epidemics

did not seem to have been described there priorto 1938. He also notes that in Europe and theUnited States during the late nineteenth centurypoliomyelitis was regarded as being rather rareafter the age of 6, but that during the past genera-tion the age group attacked tends to be older thanit was before. He suggests the possibility that alarge amount of virus may persist in endemicareas such as Japan, and as a result the localpopulation is continually becoming immunizedvery extensively. Under these circumstances onlysmall children are left as the most susceptiblegroup and are thus in a position to contract thedisease.

In the South African epidemics of 1944-1945, itwas noted (Gear, 1946) that the Bantu were lessliable to paralytic poliomyelitis than Europeans.This difference in incidence seemed to be ofconsiderable epidemiological significance. It wassuggested that there may be inherent physio-logical differences in the susceptibility of the tworaces. Such variation has been noted in the relativesusceptibilities of the Negro and of the Europeanto malaria induced for therapeutic purposes.Diet may be concerned. It is known that dietinfluences the susceptibility of experimentalanimals to poliomyelitis. Thus mice fed on adiet deficient in thiamin are less susceptible toinfection with the Lansing strain of virus thanare normal mice. It may well be that the inade-quate staple maize diet of the African nativeaccounts for his relative resistance to poliomye-litis. However, the most likely explanationappears to be that, in their relatively insanitarysurroundings, people living under primitive con-ditions are regularly exposed to infection withendemic strains of the virus of poliomyelitis andso acquire an immunity not shared to the samedegree by the more hygienic European. It thusis to be expected that, in epidemics, the latter willsuffer more severely in all age groups exceptpossibly in the youngest.

It has not yet been shown that endemic strainsof poliomyelitis are more widespread amongstprimitive people than amongst those with higherstandards of living. There is evidence of this inthe serological immunity that has been demon-

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strated by a mouse protection test, using themouse-adapted Lansing strain of poliomyelitis todetect the presence or absence of antibodies inthe serum of individuals. Surveys-using thismouse protection test-have revealed that immu-nity to the Lansing strain is low in infants, butwith increasing age an increasing proportion ofindividuals show protection, until the majority ofadults are imnmune. It has also been shown incountries with a mixed population, that in allage groups except the youngest the percentage ofimmunes is higher in the indigenous natives thanin the European. It seems then that either thenative reacts earlier to the same exposure of virusor, alternatively and more likely, that he isexposed earlier and more regularly to the infec-tion. It is also evident from the surveys thatpoliomyelitis is indeed a world-wide disease, butthat infection is probably more widespread in therelatively backward countries in the tropics andsubtropics than elsewhere.

Since the end of the war serious epidemics haveoccurred in many countries. In some, epidemicswere experienced for the first time. There isreason to believe that some of these epidemicsfollowed the introduction of invasive strains ofvirus by servicemen and others returning fromthe Middle East and other theatres of war. Follow-ing the outbreaks in the Middle East in 194I, Maltawas affected in 1942, South Africa in I944,Mauritius and St. Helena in I945, NorthernRhodesia in I946, France in 1946, and Germany in1947. Great Britain suffered her first extensiveepidemic in 1947.

Seasonal DistributionIn England the summer of I947 was unusually

early, warm and prolonged. It may be that therewas a causal relationship between the warmweather and the prevalence of poliomyelitis. In-deed, it has often been suggested that epidemics ofpoliomyelitis can be correlated with-rainfall andtemperature, but no definite conclusion can yet bedrawn as to which meteorological factors areconcerned and how they act. There is no doubthowever that in the temperate zone, althoughwinter outbreaks have been described (Leake,1947, Ward and Sabin, I944), poliomyelitis isessentially a disease of the warm weather months.In the United States cases first occur in the south,then with the summer, poliomyelitis advancesnorthwards to involve the Northern States, whereit almost always reaches its peak incidence at theend of August or in the beginning of September.Several hypotheses have been advanced to explainhis peculiar seasonal prevalence.It is argued by Aycock (1948) that most infective

diseases have a characteristic seasonal pattern, and

he suggests that seasonal physiological changes inthe host are responsible for increased suscepti-bility to poliomyelitis during the warm weather.It has been suggested that loss of chloride insweating may increase the liability to infectionwith the virus (Rinehart, I944).The peculiar summer prevalence has led other

investigators to suspect environmental factors inthe spread of poliomyelitis. Before discussingthese it will be appropriate to describe what isknown of the virus responsible for this disease.

The VirusObviously it is essential to our understanding

of the epidemiology of poliomyelitis that thenumber of strains of virus should be accuratelyknown. Burnet and Keogh (1938) first suggestedthe existence of more than one, type of polio-myelitis virus when they showed that a strainisolated in the Victoria epidemic of 1937 was im-munologically distinct from the Rockefeller In-stitute strain. Hitherto further investigation hasbeen delayed by lack of a sufficient number ofmonkeys for the necessary tests. Now a beginninghas been made on the studv. Of about ten strainsisolated in different epidemics in different yearsand in different parts of the United States,Morgan (1948) by her technique of intramuscularvaccination followed by intracerebral challengehas shown that they fall into two or three groupsonly. One of these is the Lansing- type. Theoriginal Lansing strain was isolated from a fatalcase of infantile paralysis occurring near Linsingin Michigan. Armstrong passaged this strain frommonkeys to cotton rats, then to white mice. It hasnow been passaged many times in a large numberof laboratories. Except for one relatively avirulentvariant produced by Theiler, it is still highlyvirulent for monkeys when inoculated intra-cerebrally.

All the human strains of poliomyelitis, such asYSK and M.E.F.I., which it has been possible totransmit to rodents, have been found to be of theLansing type. Although as already noted irmmu-nity to the Lansing virus is widespread, it seemsthat this type of virus is not often responsible forepidemics.

So far it has not been possible to transmit thenon-Lansing type human poliomyelitis virus toany animals except primates. It has not yet beendetermined clearly how many different strains ofvirus are included in the non-Lansing group, butof those tested all fall into one, or at most, twotypes (Morgan 1948).At the recent International Poliomyelitis Con-

ference in New York, it was agreed that the termpoliomyelitis virus should be restricted to thoseviruses conforming to the original description of

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this agent. It is identified by the characteristicexperimental disease in the monkey, by thecharacter and distribution of the histologicallesions in the spinal cord and brain of infectedprimates, by its host range, and by its immuno-logical properties. These poliomyelitis virusescan be classified into two groups:

(a) Lansing type virus transmissible to monkeysand alho to certain rodents including cottonrats and white mice.

(b) Non-Lansing type viruses transmissible toprimates but not to any other experimentalanimal.

It was agreed that Theiler's virus, which causesa disease in mice clinically and pathologicallysimilar to human poliomyelitis, should be knownby the name he originally proposed, namely thevirus of spontaneous mouse encephalomyelitis.

It was also agreed that the MM virus and themurine SK virus should not be included in thepoliomyelitis virus group as their origin is indoubt.The MM strain has been used for work on many

aspects of virus. Unlike the true human polio-myelitis viruses, it has been cultured in fertileeggs (Enright & Schultz, I947). It has beenisolated in highly purified form (Gollan, I948).Vaccines have been prepared (Gard, I947) andit has been used for chemotherapeutic experimentsto test a large number of drugs (Bieter, i948).While all this work is of great value in the field ofgeneral virus research, it cannot be applied to thevirus of poliomyelitis.

Recently it has been shown that the MM virusand the virus of encephalomyocarditis isolatedfrom a champanzee in Florida are immunolo-gically similar (Warren, I948), and that both areimmunologically related to the Mengo virusrecently described by Dick et al. (1948). TheMengo virus was isolated from a naturally para-lysed monkey, from mosquitoes, and from amongoose caught in the compound of the YellowFever Research Institute, Entebbe, Uganda.That this virus can also infect man was clear whenDick himself contracted the infection, whethernaturally or through laboratory exposure is notknown. He suffered from fever, associated withintense headache, nerve deafness and weakness ofthe trapezius.

It thus appears that a new group of viruses hasbeen uncovered. As one member of this group,the Mengo virus, was isolated in Uganda; as thetwo others, the MM and the encephalomyo-carditis virus, were isolated in the United States;and as it has been shown that the sera of somesoldiers who suffered an acute illness in thePacific theatre of war neutralize the virus ofencephalomyocarditis, it appears that this group

of viruses has a wide distribution in the world.How often they cause disease in man, and whetherthis disease in man often simulates poliomyelitis,has not yet been determined.

Spread of InfectionThe method of spread of the virus of polio-

myelitis remains a vexed question. In consideringthis problem it is relevant to note where the virusis found during an epidemic. It obviously ispresent in the patient, from whom it can bereadily isolated from the throat for 4-5 days priorto the onset of symptoms, and for 3-4 daysafterwards. Apart from this limited period, thevirus has only rarely been detected in the throat.On the other hand, it can be readily isolated fromthe faeces of a larger proportion of cases and for alonger time, regularly for three weeks and occa-sionally for even as long as I2 weeks (Horstmannet al., 1944).The virus has occasionally been isolated from

the throats (Howe and Bodian I947) and hasrepeatedly been isolated from the faeces ofapparently healthy contacts of cases. It canbe regularly isolated from the group in intimateassociation with the patient, such as the familycontacts. This group may remain infected for aslong as two months after the occurrence of thefirst, and maybe the only, paralytic case. Thehigh incidence of infection among householdcontacts has been emphasized by a number ofinvestigators, in contrast to the relatively lowerincidence among .extra-household contacts andthe still lower incidence among non-contacts inthe same neighbourhood. This indicates thatthere is no widespread infection in the neighbour-hood caused by some factor in the environmentcommon to all. It suggests that a source of infec-tion exists in the household. It seems mostprobable that this source of infection is one of theinfected members of the household. This sug-gests that infection takes place by contact. Infec-tion of contacts may take place from virus in thesecretion of the throat and from virus excretedin the faeces. That the virus from the throat maybe responsible for contact transmission is seen inthe agreement between the infectious period of acase as determined by epidemiological study andthe period during which the virus may berecovered from the throat (Gordon, et al., 1948).

Observations of Aycock and Kessell (I943)indicated an infectious period extending fromfour days before to five days after onset of symp-toms. If faecal virus were responsible for trans-mission during contact, the period of infectious-ness of a case would begin earlier and last longerthan has been found to be the case.

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However, the acceptance of the respiratorydroplet transmission hypothesis leaves unex-plained the remarkable seasonal incidence ofpoliomyelitis. Although winter epidemics havebeen described, epidemics in temperate climatesoccur almost without exception in the summerand autumn months of the year, the time whenknown alimentary infective diseases such astyphoid and dysentery are commonest, and thetime of year when insects and other arthropodsare prevalent. It is relevant then to question whereelse, besides patients and contacts, may the virusbe found.The virus has been isolated from the sewage of

cities and towns during an epidemic. In a sewageworks, the virus was found in the settled sewageand the humus tank effluent, but not in the sand-filtered effluent (Gear, 1946). Virus has not yetbeen found in the sewage in inter-epidemic years,which include non-epidemic summer months. Asits presence in sewage reflects the degree of in-fection of a community, it follows that infectionof the community is widespread during anepidemic. It also indicates that in the winter andin non-epidemic summers, virus is not presentin sufficient amount to be demonstrable by theinoculation of small amounts of sewage intomonkeys. This does not mean there may not be afew infections in the community. It does excludewidespread infection.As the virus has been demonstrated in the

humus tank effluent, it is possible that watersupplies may become contaminated from thissource. However, there was no evidence in therecent epidemics to suggest that infection wascommonly waterborne. There are only a fewauthentic examples of milkborne cases. The vastmajority of cases are obviously not infected frommilk.The summer incidence naturally raises the

question as to whether poliomyelitis may not bean arthropod-borne disease. The virus has beenisolated from flies on a number of occasions,since Paul and Trask first demonstrated itspresence in flies in I940. There is still controversyas to whether the presence of virus in flies is ofmajor importance in the epidemiology of thedisease, or whether it is an incidental findingwhen the virus is prevalent in the community.Some argue that as the virus is present in thefaeces and in the sewage during an epidemic, it isnot surprising that virus is found in batches offlies, but these authorities, mostly epidemio-logists, deny that flies play a major role in thespread of poliomyelitis (Anderson, I947). How-ever, the suspicion that flies may have some rolein the spread of poliomyelitis is strengthened byrecent observations by Melnick and Penner (I947).

They observed that after feeding infected humanstools to the blowfly Phormia regina, virus couldbe detected in their excreta for 2-3 weeks. Incontrast, biologically inert carmine and Theiler'svirus were detected in gradually decreasing quan-tities for 3-5 days only. It has not yet been provedthat the virus multiplies in the fly, but thesefindings certainly suggest that there may be abiological relationship between flies and the virus.Their further reports should be awaited withinterest.The seasonal incidence of poliomyelitis and the

deciduous fruit season correspond in almost allcountries of the world, but as yet no direct relation-ship between eating fruit and infection with thevirus has been demonstrated.To summarize then, it appears that the only

clear evidence is of spread from human to human.There are so many clear instances that there isgeneral agreement that this is a common methodof spread. It is not clear whether the spread takesplace via respiratory droplets or via hand tomouth contamination. From the public healthpoint of view, perhaps, it is not important as longas it is recognized that infection takes place fromhuman to human. There is also general agreementthat this may not be the only method of spread.Indeed, it seems probable that poliomyelitis maybe spread both as a respiratory droplet infectionand as an alimentary infective disease.

Laboratory InfectionsVirus diseases are notorious for causing labora-

tory infections. Poliomyelitis was once regardedas an exception, but this is no longer the case. Anumber of cases in which the infection wasprobably acquired in the laboratory are onrecord (Sabin and Ward, 1941 ; Gear, 1946;Wenner and Paul, I947). All laboratory tech-nicians concerned were working with strainsrecently isolated from human - sources. Twocases ended fatally. It should be stressed thatsuch work is not without danger. Cases amongstnurses and doctors attending cases, although notnumerous, are not as infrequent as commonlysupposed.

Natural laboratory infections of primates arealso on record. Howe and Bodian (I944) describeda case of natural infection of a chimpanzee.Recently Bodian (1948) has described a naturalinfection of a rhesus monkey fed on desoxy-pyridoxine.

PathogenesisHowever poliomyelitis is spread, there is no

doubt that of those infected only a minoritydevelop symptoms and still fewer develop paralysis.Various estimates have been made as to the pro-

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portion of silent and recognizable infections.Laboratory studies suggest that for every iopersons infected only one will have symptoms.The immunity surveys in which it has been shownthat 8o-ioo per cent. of adults are immune to theLansing strain suggest that the proportion ofsilent infections must be much highel and maybe of the order of i,ooo to i.The question as to why the unlucky few develop

paralysis is obviously a very important one. Ithas long been suspected that undue fatigue andviolent exercise predispose a person to a paralyticattack. Ritchie Russell (I947) recently investi-gated the role of exercise in his series of cases andfound that- all the severely paralysed cases hadundergone severe exertion within a probablysignificant period before the onset of his illness.The role of tonsillectomy is still in dispute.

Although the chances of being infected when theoperation is performed are slight, if a person orchild should be harbouring the virus at the timeof operation or should become infected so-onafterwards, there seems to be no doubt that he ismuch more liable to a bulbar form of the diseasethan a person who has not recently undergone theoperation of tonsillectomy. Carious teeth andbreaches of the mucous membrane are suspectedportals of entry of the virus, but no conclusiveincrimination of their role has been forthcoming.Nevertheless, they should continue to be suspect.In times of epidemic therefore it is wise to avoidoperations on the oro-nasal mucous membraneand to avoid excessive or exhausting exercise.

There is little evidence to suggest that bacterialinfections of the intestine play any part in increas-ing liability to the paralytic form of the disease.How poliomyelitis invades the central nervous

system is a question of considerable practical andtheoretical interest. It is now clear that it does notinvade the central nervous system via the olfactorynerves and bulb. This route is commonly takenin monkeys infected by intranasal instillation ofthe virus. These monkeys show lesions of theolfactory bulb, but such lesions are rarely found innaturally occurring fatal human cases.

Titrations of different tissues of such fatalhuman cases have shown that in addition to thecentral nervous system, the virus is present in thepharyngeal mucosa, in the jejunal wall, and in thefaecal contents but not the wall of the large in-testine. On occasion the virus has been isolatedfrom the mesenteric lymph glands, and in onefatal laboratory infection following contaminationof a cut hand, in the corresponding axillary lymphglands. Careful studies of the pathology in fatalhuman cases and in experimental animals indicatethat the virus gains entrance to the central nervoussystem via the axones of nerves. The nerves

supplying the throat are especially implicated.Recent work by Faber et al. (1948) on monkeyshas indicated that virus is much more likely toinfect the central nervous system following aninfection of the throat than one of the smallintestine.

PathologyRecent work by Bodian (1948) has shown that

only certain parts of the central nervous systemare affected by the pathological lesions of polio-myelitis. These include the anterior horn cells ofthe spinal cord and brain stem, the thalamus andthe motor area of the brain; The other areas ofthe brain, brain stem and,thalamus are spared.This complete picture is often of value in decidingwhether a case is poliomyelitis or not.

Regarding the cytopathology, he notes that thechanges occurring in the basophilic Nissl sub-stance of the cytoplasm appear to be valid in-dicators of the functional state of the neurone.

ImmunityThe immunity following an attack of poliomye-

litis appears to be of long duration. It is not yetknown whether repeated subclinical infections arenecessary to inaintain the state of immunity.Considering the age distribution of cases, thisseems unlikely. Although not unknown, secondattacks of paralytic poliomyelitis are rare.

Intensive efforts are naturally being made todevelop a prophylactic vaccine. A relativelyavirulent strain of the Lansing virus has beendeveloped (Theiler, 1948) but for obvious reasonsthis has not been given a human trial. Experi-mentally, vaccines containing inactive virus havebeen made which have conferred protection onthe monkeys inoculated, so that they resist in-fection when challenged with a fully virulentstrain. Methods of producing these killed vaccineson a large scale have not yet been evolved.

Prevention of Spread.The general precautions usually adopted for

dealing with an epidemic of poliomyelitis includethe isolation of cases, the closing of schools andswimming baths, and the prohibition of childrenfrom attending public gatherings and places ofentertainment. To be effective, the isolationwould have to include the whole of each affectedfamily and the period should be extended fromthree to eight weeks. Such stringent isolation isusually impracticable, for other reasons un-desirable and often unavailing.

Indeed, experience has shown that all themeasures enforced to prevent the spread ofpoliomyelitis have little effect. It could hardly beotherwise in a disease in which only a small

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proportion of those infected show symptoms ofinfection and are recognized. To quote Molner(1948). 'The only significant statement which aperson can make as far as prophylaxis of polio-myelitis is concerned is that up to this timenothing has been found to be effective, and theonly encouraging statement which can be madeis that clinical and research efforts are ever expand-ing in the hope of finding some effective ways andmeans through which preventive measures maybe exercised.'

BIBLIOGRAPHYANDERSON, G. W. (1947), Lancet, 67, 10-13.AYCOCK, W. L. (1948), Personal communication.AYCOCK, W. L., and KESSEL, J. F. (I943), Am. J. med. Sci.,

205, 454-465.BIETER, R. N. (1948), 'Experimental Chemotherapy of Polio-

myelitis,' Proceedings First Intemational Poliomyelitis Con-ference.

BODIAN, D. (1948), Am. j. Hyg., 48, 87.BODIAN, D. (1948), Bull. Johns Hopkins Hospital, 83, I.BURNET, F. M., and KEOGH, E. V. (1938), Med. J7. Australia,

2, I30.DICK, G. W. A., BEST, A. M., HADDOW, A. J., and

SMITHBURN, K. C. (1948), Lancet, 2, 286-289.ENRIGHT, J. B., and SCHULTZ, E. W. (1947), Proc. Soc. exp.

Biol. and Med., 66, 541-544.FABER, H. K., SILVERBERG, R., DONG, L., and LUZ, L.

(1948), 'Entry and Excretion of Poliomyelitis Virus,' Proceed-ings First International Poliomyelitis Conference.

GARD, S., and LINDHOLM, 0. (I947), Acta med. Scandinav.,129, 184-192.

GEAR, J. H. S. ('946), 'Poliomyelitis in Southern Africa,' Proc.Congress S. Afr. med. Ass.

GOLLAN, F. (1948), ' Purification of the MM PoliomyelitisVirus,' Proceedings First International Poliomyelitis Con-ference.

GORDON, F. B., SCHABEL, F. M., CASEY, A. E., and FISH-BEIN, W. L. (1948), J. infect. Dhs., 82, 294.

HORSTMAN, D. M., WARD, R., and MELNICK, J. L. (1944),J. Amer. med. Ass., 126, io6I.

HOWE, H. A., and BODIAN, D. (I947), Amer. J. Hyg., 45, 219.HOWE, H. A., and BODIAN, D. (i944), J. exp. Med., 80, 383.LEAKE, J. P., BOLTEN, J., and SMITH, H. F. (I9I7), Pubi.

Health Rep. Wash., 32, 199S-2015.McALPINE, D. (I94S), Lancet, 2, 130.MELNICK, J. L., and PENNER, L. R. (1947), Proc. Soc. exp.

Biol. and Med., 65, 342-346.MORGAN, I. (1948), ' Mechanisms of Immunity in Poliomyelitis,

Proceedings First International Poliomyelitis Conference.MOLNER, J. G. (1948), New Orleans Med. and.Surg. J., Ioo,

408-413.PAUL, J. R., HAVENS, W. P., and vAN ROOYEN, C. C. (I944),

' Poliomyelitis iin British and American Troops in the MiddleEast.'

PAUL, J. R. (I947), Amer. J. Hyg., 45, 206.RINEHART, J. F. ':944), J. ment. and nerv. Dis., 99, 822.RUSSELL, R. (I94;j), Brit. med. J., 2, 1023.SABIN, A. B., and X'VARD, R. (1941), Science, 94, II3.SEDDON, H. J. (2943), Lancet, 2, S49.THEILER, M. (I 148), Personal communication.WARD, R., and SA:111N, A. B. (1944), Yale J. Biol. and Med., x6,

45'.

WARREN, J., Perr-nal communication.WENNER, H. A., at l PAUL, J. R. (1947), Amer. J. med. Sci., 213,

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EDITORIAL-(Continued from page 2)

writing in the closing years of last century,described the epidemic nature of the disease. Suchwas the influence of these two that it becameknown as the Heine-Medin disease.

In I909 Landsteiner and Popper successfullytransferred the disease to rhesus monkeys byintraperitoneal injection from a fatal human case.Intracerebral injection was soon found to beequally effective, whilst filtration through thefinest porcelain filter failed to prevent the passageof the causative agent. In 1913 Flexner andNoguchi described the globoid bodies which wereonly shown to be incidental in the disease aftermuch study in 1936. Rosenow persisted in hisstreptococcal theory. Experimental work wasgreatly handicapped by the necessity for usingmonkeys. Much enthusiasm was therefore shownwhen Armstrong in 1939 succeeded in trans-ferring the Lansing strain of the virus to the cottonrat and thence to white mice. This and a numberof other strains have been isolated from casesoccurring in different parts of the world and havebeen,shown to have different characteristics.

More recently the virus has been obtained infairly pure form by ultra-centrifugation. It hasbeen cultured with difficulty, the greatest successbeing obtained on media containing living nervoustissues using tissue culture methods, emphasizingthe neurotropic property of the virus. By electronmicroscopy it has been shown to be filamentousin nature and to have a particle size from IO-250.It is thought to contain nucleoprotein but itschemical analysis is still far from complete.The need for research into the cause and method

of spread of this scourge has been recognized in theUnited States in the National Foundation forInfantile Paralysis (see page i8). Inspired by thedynamic personality of President Roosevelt andgenerously supported by public subscription, thisfoundation has instigated and financed anenormous amount of research in all branches ofthe subject. Not least of its benefactions is thepublication of a monthly summary of worldliterature on the subject. We pray that the laboursof these and other workers will be rewarded.

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