[Schistosoma mansoni. Correlation between parasite burden and endoscopic and histopathological humoral changes].
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Pathological and hemodynamic investigations were performed in 5 canadian patients who had been infected by Schistosoma mansoni four months before in Martinique. Mononuclear cell infiltration of portal tracts was disclosed in all 5 patients; it was associated with eosinophilic infiltration in 3, hepatocellular necrosis in 3, granulomas in 2 and fibrosis in 2. Presinusoidal portal hypertension was demonstrated in 4 out of the 5 patients. These observations suggest that histological changes are constant at this stage after infestation by S. mansoni and could be responsible for the early development of portal hypertension which is classically a late feature of the disease.
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Comparative oral glucose tolerance test performed in 30 patients with hepato-intestinal schistosomiasis and 30 controls, showed that the mean value of glycemia in the former group was superior. However, none of these patients show a diabetic G.T.T. curve.
The authors expose their conclusions after controlling 181 young soldiers affected by schistosomiasis in an epidemic having occured in Tchad en 1973-74, none of them having been later on submitted to parasitic infection: --relative value of classical diagnosis criteria (50 p. 100); --reliability of immunologic symptoms; -- frequency, importance and precocity of specific granulomatous hepatic changes, detected by laparoscopie and biopsy (87,2 p. 100 of the cases). The value of niridazole is confirmed but continuance of granulomatosis after clinical recovery is not an exceptionnal possibility five years after the treatment, then raising diagnostic and immunologic problems.
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Clinical manifestations of chronic, uncomplicated and severe, complicated disseminated strongyloidosis of a patient infected with Strongyloides stercoralis are shown. Cutaneous, gastrointestinal, hepatobiliary, pulmonary, rheumatic, neurological, psychiatric symptoms, as well as those of genitourinary, and cardiovascular systems and other clinical manifestations are discussed.
HL 707, Liroldine, a novel synthetic compound, was found effective against both extraintestinal and intestinal amoebiasis in animal models. Its activity against hepatic infection in golden hamsters is comparable with that of different derivatives of nitroimidazoles used for human treatment. Against intestinal amoebiasis in Wistar rats, the activity was superior to nitroimidazoles and chloroquine. Paramomycin was comparable and diloxanide furoate was marginally superior. The comparative in vitro and in vivo studies with standard marketed drugs and Liroldine indicate an excellent profile of the compound against experimental amoebiasis. LD50 of Liroldine determined in mice is 910 mg/kg x 1, po and 940 mg/kg x 1 ip).
Hemostasis was studied in 18 patients with the hepato-intestinal form of Schistosomiasis mansoni and in 23 with the hepato-splenic form. Both groups are compared referring to alterations found. The relations between plasmatic coagulation factors and hepatocytic function tests are studied. In 6 patients the explorations were repeated after administration of hycanthone. In the patients with the hepato-splenic form, the presence of chronic consumptive coagulophathy was found. The coagulopathy disappeared either by treatment with heparine or by splenectomy. This observation points out the importance of splenomegaly in the development of chronic consumptive coagulopathy, and may be an important factor in indicating splenectomy in a patient with portal hypertension due to Schistosomiasis mansoni.
The liver seems to be very attractive for many parasites which may either inhabit the organ or pass through during their normal development or may be carried to the liver leading to destruction there. Malaria parasites have a short developmental stage in the hepatocytes, but they do not damage the organ. For the leishmanias (Leishmania donovani complex) are the Kupffer cells are the target cells causing visceral leishmaniasis or kala azar. Nematodes of the ascarid group have a special affinity for the liver. The larvae of the human Ascaris have to pass through the parenchyma once during their developmental cycle, the larvae of animal ascarids on the contrary migrate within the liver for longer periods of time. Eggs of the schistosomes are carried via the portal system into the liver and trapped there in the tissue. An inflammatory granuloma develops around them. If the egg load is high, fibrosis of the liver may finally develop leading to portal hypertension. While small liver flukes (Clonorchis, Opisthorchis) living in the bile ducts do little harm to the liver in most cases, the larger liver fluke Fasciola hepatica destroys liver tissue during an early migratory phase of several weeks duration. Larval cestodes of the genus Echinococcus are usually found in the liver as closed cysts growing by expansion (E. granulosus) or as more solid structures growing by infiltration and destruction (E. multilocularis). Destruction results also if ameba (Entamoeba histolytica) invade the liver. Large areas of necrosis, liver abcesses are formed.
High yields of ova of Schistosoma mansoni were obtained from the livers and intestines of infected mice by digestion of the homogenized tissue with the proteolytic enzyme pinguinain.
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