Studies on heterologous resistance between schistosomiasis mansoni and fascioliasis.

S. mansoni and F. gigantica GSTs were purified from adult worm homogenates by affinity chromatography. Assessment of both SmGST and FgGST as candidate vaccines was done by comparing vaccinated mice groups challenged with S. mansoni cercariae with control ones in terms of worm load, tissue egg number viability and maturity, and the survival rate of the animals. SmGST 5 ug vaccination generally appeared to confer best protection against homologous challenge followed by FgGST 5 ug while vaccination with both antigens using low doses (2 ug) appeared to have no specific role in decreasing worm load but had significant effects on egg production.

Transmission of circulating schistosomal antigens from infected mothers to their newborns.

Two previous reports have appeared in the literature regarding tansplacental transfer of Schistosoma mansoni antigens which raised the question of its reality. In a previous study the senior author, and others (1992 & 1997) detected circulating antigens of S. mansoni and S. haematobium in infected patients, using monoclonal antibodies 128C3, with a very high sensitivity using ELISA. This work tried to answer the question of antigen transfer possibility using a high sensitive assay in 50 mothers and their newborns at birth and 1, 3, and 6 months after delivery. The assay used in the present work could detect circulating S. mansoni antigens in 45 infected mothers (90%) with active S. mansoni infection. A significant direct increase in mean antigen levels was found with the intensity of infection evaluated by egg counting (p < 0.01). The clinical stage of the diseased mothers was apparently unrelated to the ELISA test values as no significant relations were observed. Positive antigen levels were detected in 33 newborns (66%) of the 45 positive antigen mothers, then the percentage positivity was directly decreased with the advancement of age as only 5 infants (10%) had positive antigen levels compared to 0% at 6 months of age. A positive correlation between newborn serum antigen concentration and concentration of antigen in sera of their mothers was obtained. This work answers some of the questions concerning the ability of the used monoclonal to detect antigens in newborns and the possibility of antigen transfer through the placenta alone or incorporated in immune complexes forms. This work clarifies the time of antigen disappearance from the circulation.

Visceral and cutaneous leishmaniasis comparative ultrastructure of host-parasite interactions.

The comparative ultrastructure of host-parasite interactions is described for the first time in patients with visceral (VL) and cutaneous (CL) leishmaniasis. In patients with VL, the parasite invades the bone marrow (BM) macrophages (Mcs) and neutrophils, while in patients with CL, the parasite invades the dermal fibroblasts in addition to Mcs. The skin Mcs seem to have more lethal effects on the parasite than the BM Mcs; this is possibly due to the presence of numerous melanosomes with acid phosphatase activity in the Mcs digestive vacuole. In patients with high level of VL parasitaemia, the parasite may induce the BM reticulocytes to phagocytose both the parasite and mature erythrocytes, i.e. lost recognition. In patients with low level of VLparasitaemia, the parasite may induce the BM Mcs to be haemophagocytic, i.e. temporarily mimick malignant histiocytosis until the course of treatment. In early stages of CL infection, the cellular infiltrate consists of the monocyte-macrophage system, plasma cells, lymphocytes and fibroblasts; while in the late stages, two types of epithelioid cells (ECs) are added to the infiltrate and are involved in the formation of tuberculous granulomas. Type I ECs thought to produce a granuloma factor, while type II ECs possibly precedes healing by fibrosis. However, the severity of host-parasite interactions seems to depend mainly on species of the parasite, the degree of parasitaemia, the type of infected tissue(s), and the variation of host tissue reaction against the parasite from one patient to another.

Studies on the effect of acute doses of indomethacin (prostaglandins inhibitor) during induced liver failure.

Fifty four male mice were divided into 3 main groups. Control group (6 mice), Schistosoma mansoni infected group (24 mice) and carbon tetrachloride (CC14) treated group (24 mice). The last two groups were further subdivided into (4) subgroups (6 mice/each). One of them served as a control while the other 3 subgroups received (0.75, 1.25 & 2.5 mg/100g B.W.) of indomethacin respectively. CC14 treated mice were severely live 2 damaged than those infected by S. mansoni. Indomethacin made the liver functions deteriorate. Schistosomiasis did not affect kidney functions while urea & creatinine were elevated in CC14 treated group. Indomethacin led to more elevation of both. Histological studies of liver treated by CC14 revealed portal venous congestion, granular cytoplasm and cellular infiltration while schistosomiasis produced the classic granulomatous reaction. Indomethacin treatment led to distortion of hepatic cell arrangement as well as marked cellular infiltration and congestion. On the other hand, kidney treated with CC14 showed cellular infiltration around glomeruli, indomethacin caused marked congestion and cellular infiltration. Schistosoma infection did not produce any histological changes. All recorded changes could be attributed to the toxic effect of indomethacin, inhibition of prostaglandins and weakness of the immunological cells of the liver.

Comparison of the hepatoprotective effects of immune cells and serum in Schistosoma mansoni-infected immunosuppressed mice.

Immunosuppressed mice with heavy Schistosoma mansoni infections suffer from a severe hepatotoxicity reaction soon after the onset of infection patency, and this may be directly consequent upon the failure of the hosts to mount adequate granulomatous responses to embolized parasite eggs. Immune serum or immune peripheral lymphocytes from normal S. mansoni-infected immunologically intact donor mice were transferred to homologously-infected syngeneic T-cell deprived recipients to test the respective capacities of the transferred humoral or cellular immune effector elements to prevent hepatocellular damage and to reconstitute granuloma formation. Transferred immune serum was very effective in preventing liver cell damage, but did not significantly reconstitute the capacity to form granulomas in the recipients. In contrast, mice receiving immune spleen and mesenteric lymph node cells had their capacity to form granulomas around liver-bound eggs reconstituted, but lymphoid cell transfer was less effective in protecting against hepatocyte damage than serum transfer. Protection of host tissues may therefore not be the main role of the T-cell mediated S. mansoni egg granuloma.

Bilharzial arthropathy of the temporomandibular joint.

Bilharzial was experimentally induced in Swiss albino mice in order to study the histopathological changes in the TMJ in case of Bilharzial infection. The bony components of the joint showed massive chronic inflammatory cell infiltration. The articular disk (meniscus) showed thickening and hyperplastic changes with narrowing of the joint space. The articulating surfaces showed erosions and irregularity. It was concluded that Bilharziasis can cause arthropathy of the temporomandibular joint (TMJ).

Does the immunopathology induced by schistosome eggs potentiate parasite survival?

Infection with schistosomes is accompanied by inflammatory lesions resembling delayed hypersensitivity reactions, that are induced by eggs in host tissues. Here Michael Doenhoff and his colleagues demonstrate that T-cell-deprived mice excrete much fewer eggs than do intact control animals. From the results of serum and cell transfer experiments, they conclude that immune processes assist egg expulsion and thus contribute to the parasite's success.