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IgE level in parasitic diseases before and after specific therapy.

Fifty patients (3-12 years old) with parasitic infestation vz: E. histolytica, Oxyuris, H. nana, Ascaris and mixed infection were compared to ten healthy age and sex matched normal school children. They were subjected to stool and urine analysis total and differential white count, serum protein and serum IgE estimation before and after the specific treatment. The absolute eosinophilic count was high during infestation in all groups and significantly decreased after treatment (P less than 0.01). The serum IgE showed a significant increase during infestation in all groups. It decreased significantly after treatment in Entamoeba histolytica, Hymenolepis nana, and Ascaris groups (P less than 0.025). It decreased but with insignificant difference in Oxyuris and mixed infection groups probably due to the ease of reinfection and the need for longer duration of therapy. It was concluded that both serum IgE elevation and eosinophilia are important hallmarks of intestinal parasitic infections and the absolute eosinophilic count could be earlier indicator for responsiveness to treatment.

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[Parasitic diseases of the liver].

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.

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Immune responses in parasitic diseases. Part B: mechanisms.

A number of host defenses provide variable resistance against parasites. From the biological point of view, invading parasites must not eliminate the susceptible host population; therefore, antiparasite immunity plays an essential role in limiting the invasion and proliferation of parasites. Several differences exist between immune responses to parasites and immune responses to other microorganisms. Effector mechanisms include T lymphocyte-mediated inflammatory granuloma formation and encapsulation involving the deposition of fibrous tissue. In some instances, passive immunity can be transferred by serum antibodies. Antibodies may act via complement fixation, granulocyte adhesion, opsonization, inhibition of invasion, or mast cell degranulation. Of the nonspecific factors, macrophage activation, natural killer cells, and serum factors other than antibodies are critical in the battle against parasites. The net result of these immune responses may be antiparasitic, proparasitic, of no consequence to either host or parasite, or harmful to the host.

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