202 RESEARCH IN PROTOZOOLOGY 



(1928) also has referred to his early work with it. For the most 

 part, however, the exudate either was ignored or erroneous inter- 

 pretation of the appearances were made. A study of the papers of 

 Thomson and Thomson (1916) and of Bartlett (1917) will show 

 to what extent misconception and misinterpretation have gone and 

 will save the student from similar errors, especially after he has 

 compared the descriptions of these authors with those of Bahr 

 and Willmore (1917-18) and Willmore and Shearman (1918). 

 Other publications that should be consulted are those of Ander- 

 son (1921), Woodcock (1920), and Haughwout (1924a and b), 

 and Haughwout and Callender (1925). There is not space to go 

 into details here, but the subject is adequately covered in the 

 papers I have named. The principle may be broadly stated in a 

 single sentence : 



The cellular exudate from the bowel is a replica of the histo- 

 pathology of the condition. 



Dysentery of bacterial origin is an acute inflammatory, toxic 

 process. The bowel wall, accordingly, undergoes the reactions char- 

 acteristic of acute, toxic inflammation and the exudate derived 

 from it naturally shows the same characters. Therefore, we know 

 we are dealing with an organism that produces inflammation and 

 toxic necrosis. 



On the other hand, we find that the mode of attack on the 

 bowel wall by Entamoeba histolytica and Balantidinm coli is of 

 an entirely different nature. Here, destruction of tissue by the 

 parasites occurs only in their immediate neighborhood. It is a 

 non-toxic proteolysis by enzymes elaborated by the parasites, and 

 is not, in any sense, an inflammatory process. Any inflammatory 

 reaction in such cases always is attributable to secondarily in- 

 vading bacteria. 



Thus are laid down the basic criteria for our inquiries into the 

 differential diagnosis of dysenteries and diarrheas. The reactions 

 of cellular structures to invasion by pathogenic bacteria are sharply 

 expressed. The reactions of identical structures to the attacks of 

 pathogenic protozoa are strikingly different and, in the cases of 

 Entamoeba histolytica and Balantidium coli our knowledge is suf- 

 ficient to give us a basis for comparison. 



This would seem to open the way for easy sailing, but, unfor- 

 tunately, the course is far from clear. Much remains to be learned, 

 and much confronts us that must be disproved and then unlearned. 



