The diagnostics and treatment of tropical diseases

by E. R. Stitt

In 4 cases fed with material from acute dysenteric stools or from amoebae-containing pus from liver abscess, and containing motile amoebae, there was no resulting dysentery, the 4 cases of experimental dysentery resulting from feeding of material from normal stools of carriers.

As regards the cases which became parasitized, but did not develop dysentery, it is suggested that the amoebae live as commensals in the intestine of the host and only penetrate the intestinal mucosa and become tissue parasites when there occurs depression of the natural resistance of the host or as the result of some lesion of the intestine. That the pathogenic amoebae are more than harmless commensals, however, is shown by the fact that they alone, and not the nonpathogenic Entamoeba coli, are capable of penetrating a possibly damaged intestinal mucosa.

Epidemiology.—The chief factor in the spread of amoebic dysentery would seem to be the encysted amoebae in the stools of convalescents, or symptomless carriers, rather than the motile amoebae in dysenteric stools. When such carrier has to do with the preparation of food, he becomes a particular source of danger.

This probably explains the endemic rather than the epidemic characteristics of the spread of amoebic dysentery because, if the innumerable vegetative amoebae in dysenteric stools were equally operative with the more sparsely eliminated cysts, there would be epidemics of amoebic dysentery similar to those of bacillary dysentery. The old idea that water, fruit or vegetables, from which one can isolate amoebae on culture, are sources of infection must be abandoned, as such cultural amoebae are known to have no pathogenic relation to man.

Vegetative amoebae undergo disintegration in a short time after the stool is passed, so that they are probably rarely concerned in amoebic infections but the resisting cysts may be washed from a dried stool into a water supply or even be transported in dust to lodge on unprotected foodstuffs.

Flies may possibly act as transmitting agents. As bearing on the probable importance of such flies as Musca domestica and Fannia canalicularis in transmitting amoebic infections may be noted the findings of Wenyon that the faeces of such flies, as well as Lucilia and Calliphora, after feeding on cyst-containing human faeces, teem with such cysts. In a dissection of 1027 house flies caught in Mesopotamia Buxton found ova of parasites of man in 4.09%. The percentage of infection with E. histolytica cysts was O.3%.

Pathology

Wenyon thinks that the pathogenic amoebae work their way into the tubular glands of the intestines and multiply and subsequently, either by pressure of their pseudopodia or through the disintegrating action of some toxic substance elaborated by them, they force their way into the underlying submucosa. In this location they produce a gelatinous, oedematous necrosis, which shows a marked absence of polymorphonuclears, but a proliferation of connective tissue cells. The process is regenerative rather than inflammatory.

Small hemispherical elevations of the overlying mucosa mark the location of the deeper-lying necrotic process. With the multiplication of the amoebae and the extension of the necrotic process in the submucosa we have thrombi formed in the terminals of the portal vein and possibly in those of the mesenteric arteries, which in the former case may result in emboli being swept up the portal vein to lodge in the liver and form a starting point for a similar necrosing process there or, as the result of interference with the blood supply of the overlying mucosa, cause this to undergo necrosis and be cast off as a slough, leaving an oval or irregular ulcer with deeply undermined edges and a floor formed by the muscular coat. The ulcers may be no larger than a pin’s head or they may be 1 or 2 inches in diameter or by coalescence be still larger. The gelatinous necrosis in the submucosa always extends beyond the limits of the necrosis of the mucosa, thus explaining the undermining. At times the muscular coats of the intestines are involved thus leading to a slough which involves all coats except the serous one. Bacterial infection, with coagulation necrosis of the mucosa overlying the amoebic process, is also responsible for some of the tissue destruction.