1.The histopathological lesions produced in bisexual infections with Schistosoma mansoni in experimentally infected mice, hamsters, rats, guinea pigs and rabbits have been described, and have been compared with those produced by S. japonicum and S. haematobium.
2.In hosts in which the worms mature with greatest rapidity and attain the largest size, fertile eggs are deposited in, or are carried to, the smallest blood vessels. The most typical lesions are those seen in the liver. They are circumscribed, are more or less acute at first, develop into a characteristic pseudotubercle and finally result in a scar. The intensity of the pathology depends upon the number of eggs deposited.
3.In hosts in which the worms mature slowly and remain relatively small, egg deposition is delayed and most of the eggs may be unfertilized and appear as collapsed shells, producing little or no acute reaction or ultimate scarring of the tissue.
4.The eggs of S. japonicum usually produce more severe lesions than those of S. mansoni or S. haematobium, partly because they are often deposited in large groups, and partly because each fertilized egg seems to exert a more acute toxic effect on the surrounding tissue.
5.Living worms in terminal vessels do not apparently stimulate a tissue reaction, but dead worms stimulate thrombosis of the vessel and an intense perivascular reaction which leads to disappearance of the worm, scar formation and often recanalization of the vessel. Dead worms are found more frequently in unsuitable hosts.
6.In the liver periportal infiltration of leucocytes, described previously in unisexual infections, is also found in bisexual infections. It is more acute and extensive in early infections than later and is more frequent and intense in S. mansoni than in S. japonicum and S. haematobium infections. It does not appear to contribute significantly to ultimate fibrosis of the liver and is interpreted as an allergic reaction to the worms inhabiting the portal-mesenteric veins.
7.Areas of red-staining “coagulative necrosis” of liver parenchyma, previously described in unisexual infections, are also sometimes found in bisexual infections regardless of the duration of the infection. They may represent infarcts caused by occlusion of a portal venule or hepatic arteriole.
8.In the animals studied there was no visible evidence that the mere presence of living worms in the portal-mesenteric veins contributed significantly to the development of cirrhosis of the liver.
9.In the mucosa and submucosa of the intestine fertile eggs often do not stimulate much tissue reaction, but in the muscularis and serosa the egg lesions are similar to those in the liver.
10.In the urinary bladder lesions produced by eggs of S. japonicum and S. haematobium are similar to those in the intestine.
11.Eggs and adult worms of all three species were found in the lungs in some animals of each species employed in these experiments. This was probably the result mainly of migration of worms from the portal-mesenteric veins through anastomoses into the pelvic systemic veins or into the vena cava in the upper abdomen. Enlargement of these anastomoses, caused by obstruction to the portal circulation in the liver, probably facilitates passage of both worms and eggs through the anastomoses.
12.Lesions produced in the lungs by eggs were similar to those produced in the liver by the same species of egg. Worms were found mostly in arterioles but occasionally in alveolar cavities. Living worms caused little or no tissue reaction, but dead worms produced thrombosis of vessels and intense perivascular cellular reaction and ultimate scarring. In some late infections with S. japonicum in rabbits the lung pathology was intense, with fibrinous pleural adhesions and fluid in the pleural cavities.
13.In the spleen, areas of focal necrosis were found in some of the mice with early S. mansoni infections, and increase of fibrous tissue was seen in some late infections. Extensive fibrosis and thickening of the capsule were present in some late infections with S. japonicum. Egg lesions were sometimes found in the spleen.
14.From the histological observations in this study it is concluded that most of the pathology in the species of animals employed is produced by fertilized eggs and dead worms, forming localized lesions which, if numerous enough, lead to extensive scarring. If the infection becomes inactive or is terminated, and if the scars are not too extensive they may entirely disappear, and normal structure and function of the tissues may be restored. The early periportal cellular infiltration in the liver is interpreted as an allergic phenomenon resulting from the presence of worms in the portal-mesenteric veins. It decreases as the infection continues, and does not appear to contribute significantly to ultimate cirrhosis of the liver.