SIGNIFICANCE OF PHENOMENON 377 



Experimental evidence of Roskam (1934), Ledingham (1914) 

 and Bedson (1921, 1922) sho\\s that reduction in the number of 

 platelets cannot be held solely responsible for the disease. Roskam 

 foinid that in animals in Avhich the platelet coinit had been re- 

 duced by the intraxenous injection of gelatin, the fjleeding time 

 was only slightly prolonged. In addition to the destruction of 

 platelets, there exists a factor of greater importance in the pro- 

 duction of the disease, namely, damage to the capillary endo 

 thelium. This assimiption is stipported by Bedson and Leding- 

 ham's histological studies on experimental pmpura (produced by 

 injection of antiplatelet serinn) xvhich demonstrates sxvelling of 

 the vascular endotheliinu. 



Roskam, Kretz, and Tempka (qtioted by Landau and 

 Hejman) , and more recently. Landau and Hejman (1934) and 

 others reported clinical cases in Avhich it xvas shown that purpina 

 is independent of the number of platelets. There are also "latent" 

 stages of the disease in xvhich no hemcjrrhages are observed in 

 spite of prolonged bleeding time (sixty mintues) and complete 

 al^sence of blood platelets. As pointed out by Morawitz, Bedson, 

 and Roskam, it is possible that thrombocytopenia and vascidar 

 damage coexist since the same poisons show an affinity for both 

 the blood vessels and blood platelets ontogenetically related. 



Pratt (1927) states that the probability still remains that \ irtises 

 or bacterial toxins may be invohed in the etiology of the malady. 

 There is suggestixe evidence that at least some of the conditions, 

 especially the actite form of thrombocytopenia, bear a close re- 

 semblance to acute infectiotis diseases. In many instances a history 

 of a preceding actite infectious disease or a sudden and stormy on- 

 set may be obtained. 



In symptomatic thrombocytopenic pinpiua the manifestations 

 are the same as in the essential thrombocytopenia. The disease 

 may occiu' as a complication of a large group of infectious dis- 

 eases, i.e., sepsis, typhoid fever, meningitis, diphtheria, scarlet 

 fever, measles, smallpox, syphilis, and malaria. The symptomatic 

 thrombocytopenia is considered by most atithors to be the result 

 of a toxic influence tipon the bone marroxv and blood vessels. 

 Pratt notes that the leucopenia resulting from injiny to myeloid 

 tissue presents an important differential diagnostic feature. 



In connection with the problems discussed in this monograph 

 it is of special interest that in typhoid fever, xvhere the etiological 

 agents are capable of producing actixe principles of the phenome- 



