September 8, 1916] 



SCIENCE 



353 



tine of the most susceptible part of the popu- 

 lation — that is to say, of the children. ISTo 

 more effectual way of dealing with the situa- 

 tion is known. 



The disease is one that has been studied with 

 great success during the last few years in 

 America, more particularly by Flexner and 

 his pupils, to whom we owe many of the re- 

 cent discoveries made as to its etiology and the 

 way in which it may be communicated from 

 one person to another. The great advances 

 made in this regard during the last five or six 

 years may perhaps be shown by a brief history 

 of the disease. It was first isolated as a dis- 

 tinct entity from the mixed mass of paralyses 

 affecting children by von Heine in 1840, re- 

 ceiving the name " spinal paralysis of chil- 

 dren " ; naturally there could be no exact 

 knowledge of its pathological anatomy at this 

 early date. Two or three decades later Pre- 

 vost and Vulpian, Charcot and Joffroy and 

 others described accurately the microscopical 

 lesions that could be found in the spinal cords 

 of patients dying of the disease. In 1890 

 Medin, taught by the study of a Swedish epi- 

 demic of infantile paralysis, extended our 

 knowledge of its various clinical types, par- 

 ticularly in the symptomatology of their initial 

 stages. Further advances were made by 

 Wickman in 1905 and the succeeding years, 

 particularly so far as the epidemiology of the 

 disease is concerned. Many other physicians 

 and pathologists could be mentioned as having 

 cleared up various obscure points in connec- 

 tion with infantile paralysis, or, as it is some- 

 times termed, Heine-Medin's disease, or the 

 Heine-Medin-Wickman disease; its bacterial 

 cause was looked for with great persistence, 

 and between the years 1898 and 1907 was 

 identified by a number of observers, quite 

 wrongly, with various cocci cultivated from 

 the cerebro-spinal fluid of patients who had or 

 had died of the disease. Fuller experience, 

 however, proved that errors had been made 

 here, and in 1911 Eomer summed the matter 

 up correctly when he said that the true bac- 

 terial cause of the disease was still unknown. 

 Both cultural experiments and experiments on 

 animals had failed to reveal it. Yet the sea- 

 sonal and epidemic incidence of infantile 



paralysis and the inflammatory character of 

 the lesions observed in it post mortem made it 

 certain that some living and transmissible 

 virus was the cause of the disease. 



So far as its transmissibility was concerned, 

 Landsteiner and Popper have shown that cer- 

 tain apes — hamadryads and macaques — could 

 be infected with a disease indistinguishable 

 from infantile paralysis, as we see it in chil- 

 dren, by inoculation with an emulsion of the 

 spinal cord of patients dying of the disease. 

 The virus was found to be a filter-passer, and 

 to survive preservation in glycerine for many 

 months. In 1912 Kling, of Stockholm, suc- 

 ceeded in recovering the virus from washings 

 from the mouth, nose, trachea and small in- 

 testine of fatal cases of infantile paralysis. 

 But the actual microbe causing the disease re- 

 mained unknown until 1913, when it was iso- 

 lated, grown on artificial media, and carefully 

 described by Flexner and ISToguchi. The suc- 

 cess of these investigators where so many 

 others had failed is to be attributed to their 

 discovery of a suitable culture medium. 

 Growths were made anajrobically under a layer 

 of paraffin, in a solid agar medium containing 

 sterile unfiltered ascitic fluid, or brain extract 

 and sterile rabbit kidney. Minute colonies of 

 the virus were obtained, composed of globular 

 or globoid bodies averaging in young cultures 

 0.15 to 0.30 M in size, arranged singly or in 

 short chains or masses. Third generation cul- 

 tures from human tissues, and cultures in the 

 fifth generation from the tissues of experi- 

 mentally infected monkeys, were found to pro- 

 duce typical acute anterior poliomyelitis in ex- 

 perimental animals. 



At the present time, therefore, we are in 

 the possession of a good deal of positive knowl- 

 edge with regard to the pathogenesis and epi- 

 demiology of infantile paralysis. The virus 

 producing the disease has been isolated, culti- 

 vated and employed for the transmission of 

 the disease to experimental animals in in- 

 vestigations that have proved invaluable and 

 indispensable for the increase of our knowl- 

 edge of its spread among human beings. The 

 virus has been found in the naso-pharynx of 

 human carriers of the disorder, who though 

 they have never apparently suffered from it 



