This report emphasizes the desirability of clinicians and biologists working as a “team” in order that the significance of alimentary tract protozoa may be appreciated accurately in respect to clinical evidences of digestive dysfunction.
Attention is directed to the frequency with which protozoa may be demonstrated in the stools of patients who reside in the temperate zone. In the series studied (3780 patients), one or more species occurred in 7 per cent of patients who presented themselves for the elucidation and relief of digestive disorders.
In the temperate zone, food and water contamination by farm animals, flies, insects and by humans would seem to be an important means of spreading protozoal infestation. Particularly potent as disseminating sources are “truck farms” and hot-houses where fruits and vegetables are “forced” by manuring with the contaminated excreta of fowls and barnyard animals. Food and water fouling by protozoa furnish a public health problem, not as yet recognized by the health-boards of states and countries not tropically situated.
While it is recognized that the common “pathogenic” protozoa are endamoeba histolytica, lamblia and balantidium, there remains a reasonable probability that, in intestinal canals already the loci of open ulcerations (of systemic origin), such flagellate protozoa as trichomonas and chilomastix mesneli may aggravate such ulcers and intensify the clinical picture.
Several species of protozoa may simultaneously occur in vegetative or encysted form in one host. The finding of one species, particularly of a so-called “harmless” flagellate, does not justify the assumption that the digestive anomaly present is due to that organism: “hidden” foci of “pathogenic” protozoa may be agents contributing to the disorder or its maintenance. These organisms may be observed only after painstaking and persistent search. The gall-bladder, the vermiform appendix, colon haustra, diverticula or old, ragged or partly scarred ulcers serve as “foci of infestation” for such protozoa as endamoeba, lamblia or balantidium. Drainage of the biliary tract, metapylorically, by the aid of the duodenal tube, disclosed encysted or vegetative protozoa in 19 patients of this series.
Diarrhea, occurring in association with vegetative forms of protozoa, seems to be caused or aggravated by the protozoan, whether such organism be a “harmless” flagellate (trichomonas, chilomastix), one “pathogenic” (lamblia), an endamoeba or a cilium. Diarrhea was exhibited by 79 per cent of the series. The diarrhea, seemingly, is not alone due to low or absent gastric acid or to deficient pancreatic function. It is suggested that diarrhea represents a systemic, toxic manifestation dependent upon the absorption from the alimentary tract of poisonous amines, which amines appear as a result of food protein hydrolysis by protozoa or alimentary tract bacteria of the colon group. Some of the protein hydrolyzed, may be that of dead protozoa or bacteria, many stools exhibiting such in great excess.
Constipation occurred in nearly 5 per cent of patients; these patients were especially “toxic.” The toxicity of such patients suggests that diarrhea, so common in patients harboring protozoa, may be really a protective phenomenon; intestinal stasis admits of a greater degree of absorption of harmful chemical agents.
Abdominal pain or discomfort is common to the group; it may be severe or mild. When ulcerative lesions occur, severe pains may indicate threatened or actual perforation of the bowel (usually, terminal ileum or colon).
Anemia was observed in more than 70 per cent of the patients. It may be severe: the blood picture of 29 patients suggested or actually corresponded to that of hemolytic (“pernicious”) anemia. Such severe anemia occurred most frequently when the infesting protozoon was balantidium, lamblia or endamoeba. The absorption of toxic amines from the alimentary tract, as noted in instances of protozoiasis, may be the agent contributing to the appearance of “pernicious” anemia, when protozoa are absent, but when, within the alimentary tract, bacteria or yet unrecognized ferments split protein excess beyond the polypeptid stage. Especially, should such “toxic” agent be emphasized when protein cleavage occurs in the small gut and absorption of amines occurs from the jejunum.
Our study seems to lend evidence to the opinion that when vegetative protozoa are present and alimentary tract symptoms are associated, eosinophilia of varying degree commonly can be demonstrated.
Proctoscopic examination yields little, diagnostically, in early bowel infestations by protozoa. Even in advanced ulcerative lesions, proctoscopy reveals but a small segment of the possible damage. Diagnosis of protozoiasis should not await the appearance of lesions such as it is possible to locate by the proctoscope.
Roentgen evidence of the damage due to protozoa is of two types: (a) general, “toxic” (?) atony and (b) local evidences of ulceration, spasm, diverticula, stenosis or fibrosis. Colon lesions of similar form occur from other causes, e.g., tuberculosis, lues, systemically born acute or chronic infection or to dietetic imbalance. It would seem quite likely that some such type of lesion primarily produces the bowel ulcers and that protozoa are secondary invaders. From roentgen plates alone, frequently one cannot differentiate the lesions found in association with protozoa from lesions due to other causes.
Gastric and pancreatic secretory deficiency occurs commonly in patients whose stools harbor protozoa. Such faults may represent a “systemic toxic” action of protozoa, but evidence is not at hand which substantiates this view. The anemia associated with bleeding, ulcerative, protozoa-invaded bowel lesions may be a factor in causing diminished gastric and pancreatic secretion. Instances of protozoiasis where gastric and pancreatic secretion are within normal range are recorded. Low secretory efficiency of the gastric and the pancreatic glands is most commonly observed in infestation by the “pathogenic” protozoa.
“Occult” or gross blood in stools is evidence of open, ulcerative lesions; such lesions seem to be kept open and to progress most rapidly when lamblia, balantidium or endamoeba histolytica is the invader. It is not possible to exclude the “non-pathogenic” flagellates as agents which keep open certain colon or low ileum ulcers.
Stools containing vegetative forms of protozoa seem to exhibit a characteristic odor, due probably to their being alkaline and somewhat volatile from the presence of excess of ammonium, magnesium phosphate. Such crystals would appear to occur as and end step in protein cleavage and to putrefactive chemical processes. In these chemical changes, the action of protozoa may be combined with the effects of the large numbers of spirilla and colon-group bacilli so commonly present in the stools. The spirilla and bacilli may act as agents in preventing the healing of bowel ulcers.