1054 PATHOGENIC PROTOZOA 



in America. He was followed by Musser and Stengel and, in 1891, 

 by Dock, and Councilman and Lafleur. The work of the last two 

 authors was especially complete and firmly established the entity of 

 this disease in America. In 1902 Jiirgens differentiated the pathogenic 

 amoeba from the harmless, and in 1903 the work of Schaudinn ap- 

 peared. This author, who was a zoologist by training, showed clearly 

 that there were two forms of parasitic amoebae and he followed out 

 most of the details in their life history, renaming them Entamoiba 

 histolytica and Entamozba coli. Schaudinn accepted the name for 

 the genus proposed by Casagrandi and Barbagallo (1895) but named 

 his pathogenic species histolytica and the non-pathogenic coli. These 

 names are still in use although the work of later investigators has 

 shown that many of his observations were erroneous. Our present 

 knowledge of this organism we owe to the work of Craig, Whitmore, 

 Walker, Sellards, Darling, Dobell and others. 



CLINICAL DYSENTERY 



Dysentery as a disease has been known from the earliest times 

 and references are found to it in Sanscrit and Egyptian literature 

 and in early Greek and Roman writings. Until recent years its 

 etiology was obscure, but we now recognize two separate forms, 

 bacillary and amoebic ; the former has already been described under 

 the dysentery bacilli. Amoebic dysentery is a distinct clinical entity, 

 and runs a course quite different from the bacillary form. It begins 

 gradually, and in some cases is chronic in character from the start. 

 Usually there is no rise in temperature nor any great change in 

 weight or health until the disease has existed some time. The bowel 

 movements become gradually more frequent and the fecal matter 

 is accompanied by larger and larger amounts of mucus and blood. 

 As the disease progresses and more and more of the colon is involved 

 the amount of blood and mucus increases until the stool contains 

 little else. The colicky pains increase in frequency and severity 

 and there is added tenesmus and finally nausea and vomiting. The 

 patient loses flesh and strength and when the stools increase to 

 twenty and thirty daily, becomes bed-ridden. The abdomen is con- 

 cave and tender on pressure, especially over the colon. The course 

 of the disease, if untreated, tends to progress with periods of remis- 

 sion, and spontaneous cure probably does not occur. Bacillary 



