In helminthic infections, humans may serve as the definitive host to the sexually mature adult worms (eg, Taenia saginata) or as the intermediate host to the larval stages (eg, Echinococcus granulosus). Occasionally, they serve as both the definitive and the inter-mediate host to the same worm (eg, Trichinella spiralis, Taenia solium). Unlike protozoan parasites, most adult helminths are incapable of increasing their numbers within their de-finitive host. As a result, the severity of clinical illness is related to the total number of worms acquired by the host over time. Most small worm loads are, in fact, asymptomatic and may not require therapy. Many worms are long-lived, however, and repeated infec-tions can result in very high worm loads with subsequent disability. The pathogenesis of both protozoan and helminthic disease is highly variable. The fish tapeworm Diphyl-lobothrium latum competes with the host for nutrients. The protozoan Giardia lamblia and the helminth Strongyloides stercoralis interfere with the absorption of food across the intestinal mucosa. Hookworm infections cause loss of iron, an essential mineral. Other helminths, such as Clonorchis sinensis and Schistosoma haematobium, compromise the function of important organs by obstruction, secondary bacterial infection, and induction of carcinomatous changes. Occasionally, as in the case of echinococcosis, disease results from pressure and displacement of normal tissue by the slow growth of the parasitic cyst. In malaria, the primary pathogenic mechanism appears to be the invasion and subsequent alteration or destruction of human erythrocytes. Similarly, many helminthic larvae are ca-pable of tissue invasion and destruction. Entamoeba histolytica can destroy host cells without actual cellular invasion. Finally, immunologic mechanisms are responsible for tis-sue damage and clinical manifestations in many diseases. Allergic or anaphylactic reac-tions play a major role in the cutaneous reactions to invading hookworm, strongyloides, and schistosome larvae (ground itch, swimmers’ itch) and in the fever, rash, and lym-phadenopathy that accompany the therapeutic destruction of onchocercal microfilariae (Mazzotti reaction). Transient pneumonias induced by the pulmonary migration of As-caris and other nematode larvae (Loeffler’s syndrome), nocturnal paroxysms of asthma insome patients with filariasis (tropical pulmonary eosinophilia), and the shock, asthma, and urticaria that follow rupture of a hydatid cyst are all immunologically mediated. He-molysis in malaria and cardiac damage in Chagas’ disease are thought, at least in part, to reflect antibody-mediated cytotoxicity. Immune complex diseases are seen in schistosomi-asis (Katayama syndrome) and malaria (nephrosis). The granulomatous reaction to schis-tosomal eggs, the muscle damage in trichinosis, and the entire clinicopathologic spectrum of the leishmanial infections appear to be caused by cell-mediated immune responses.
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