Mucosal Immune Responses of Mice Experimentally Infected with Pygidiopsis summa (Trematoda: Heterophyidae)

Mucosal immune responses against Pygidiopsis summa (Trematoda: Heterophyidae) infection were studied in ICR mice. Experimental groups consisted of group 1 (uninfected controls), group 2 (infection with 200 metacercariae), and group 3 (immunosuppression with Depo-Medrol and infection with 200 metacercariae). Worms were recovered in the small intestine at days 1, 3, 5, and 7 post-infection (PI). Intestinal intraepithelial lymphocytes (IEL), mast cells, and goblet cells were counted in intestinal tissue sections stained with Giemsa, astra-blue, and periodic acid-Schiff, respectively. Mucosal IgA levels were measured by ELISA. Expulsion of P. summa from the mouse intestine began to occur from days 3-5 PI which sustained until day 7 PI. The worm expulsion was positively correlated with proliferation of IEL, mast cells, goblet cells, and increase of IgA, although in the case of mast cells significant increase was seen only at day 7 PI. Immunosuppression suppressed all these immune effectors and inhibited worm reduction in the intestine until day 7 PI. The results suggested that various immune effectors which include IEL, goblet cells, mast cells, and IgA play roles in regulating the intestinal mucosal immunity of ICR mice against P. summa infection.

The eosinophils in parasitic infections

Local and peripheal eosinophilia is a common feature of many helminth infections that present large, non-phagocytable surfaces to the inmune system. The effect of the eosinophils on these organisms has been studied in the last 18 years using schistosoma mansoni, trichinella spiralis, and other helminths as models. The early infection causes a nonspecific inflammation rich in macrophages, lymphocytes and neutrophils that sets the stage for a subsequent inmune response. The predominant effector elements of the inmune response are anaphylactic antibodies, mast cells, and eosinophils. Mast cell products attract eosinophils and concentrate antibodies and complement-covered parasites by their Fc and/or C3c receptors and release oxygen radicals and/or preformed proteins on the helmith surface. The radicals alter molecules of the parasite and the proteins disrupt its tegument or cuticle. Occasionally, they may harm host cells. Eosinophils also phagocytize and harm extracellular trypanosoma cruzi and may play a role in the damage to the host heart tissue. The eosinophil response is regulated by eosinophilopoietic factors (interleukines [IL] 3 and 5, and granulocyte macrophage colony-stimulating factor) eosinophilotactic factors (C5a from complement, eosinophil chemotactic factor of anaphylaxis [ECF-A], histamine, platelet stimulating factor, and other ECFs from mast cells and basophils, and ECF from parasites), and eosinophiloactivating factors (IL-5 from Th2 lymphocytes, tumor necrosis factor from macrophages, antibodies, and complement components). Other phagocytic cells (macrophages and neutrophils) also exhibit important anti-helminthic activities

Schikhobalotrema solitaria sp. n. and S. acanthuri Yamaguti, 1970 (Haplosplanchnidae: Digenea) in Brazilian marine fishes

Schikhobalotrema solitaria sp. n. is described from Stephanolepis hispidus (Linnaeus, 1758), and is characterized by the relation between oral sucker and pharynx 1:1,1. This Relation in the other species ranges between 1:0.3-0.6. It is more similar to S. manteri Siddiqi & Cable, 1960 in the distribution of vitellaria, differing from it in the size of vitelline follicles, extension of uterus and in the size of the eggs. S. acanthuri Yamaguti, 1970 is referred for the first time in South America in Mugil liza Valenciennes, 1836 representing a new host record.

Failure of irradiated Echinostoma audyi and Hypoderaeum dingeri to sensitize Lymnaea rubiginosa snails.

Attempts to induce acquired resistance in Lymnaea rubiginosa snails against the echinostomes Echinostoma audyi and Hypoderaeum dingeri by means of irradiated miracidia were unsuccessful, although Lie and coworkers using similar methods had recently sensitized Biomphalaria glabrata against Echinostoma lindoense (1975a). In contrast to the B. glabrata-E. lindoense system, in Lymnaea rubiginosa the amebocytic response to irradiated parasites was slow: irradiated E. audyi sporocysts were encapsulated 15 to 28 days and H. dingeri sporocysts 20 to 27 days postexposure. No obvious enlargement of the amebocyte-producing organ was seen. No resistance was demonstrable to subsequent homologous challenge. Development of acquired resistance to a trematode infection in snails may be related to the speed with which the snails destroy the irradiated sporocysts.