The pathogenesis of both protozoan and helminthic disease is highly variable. Many factors contribute to this variability and included among them may be factors such as parasite size, induced injury, reproductive potential, nutritional requirements (including metabolites or toxins produced), niche selection (often influenced by individual life cycles and migration patterns through the host), and last, but not the least, immunologic consequences of infection.
Parasite size may or may not be a predictor of pathogenesis. Many of the parasitic Protozoa, including those that cause malaria (Plasmodium), African sleeping sickness (Trypanosoma brucei subspecies), Chagas disease (Trypanosoma cruzi), and leishmaniasis (Leishmania), are among the most pathogenic. The giant cestode, Diphyllobothrium latum, can reach sizes exceeding 10 m, yet produces a pernicious anemia due to vitamin B12 competition with the host in less than 1% of the infected individuals. Ascaris lumbricoides, which can grow up to a foot in length can cause severe intestinal blockage if enough worms are present. The larval hydatid cyst of the tapeworm Echinococcus granulosus can achieve considerable size if given long enough to grow and can put tremendous pressure on organs it may be found within.
Parasite-induced injury frequently results from parasite invasion of host tissues. Hookworms, Strongyloides and Trichuris, repeatedly probe the intestinal or colon lining, promoting and inducing extensive, immunologically mediated inflammatory responses. In these cases, worm burden determines the extent of the pathogenesis. The egg laying of schistosome parasites determines the pathology of this infection as many eggs get trapped in tissues in their attempt to leave the host. The result is extensive inflammation and eventual fibrosis of affected tissues.
The reproductive potential of parasites varies considerably. Protozoa generally have very short generational times. In large part, this is due to the asexual nature of their reproduction for much of their life cycles. Rates vary from several hours (African trypanosomes) to several days (malaria). This can place tremendous pressure on host resources with attendant consequences. Helminthes, however, are usually incapable of reproducing within their definitive hosts, so overall worm burden becomes a greater determinant of pathogenesis. This, in turn, will depend on how many eggs, or larvae, initiated the infection. An exception is encountered in Trichinella, in which fertile females residing within the intestinal lining give birth to larvae that migrate to the musculature.
Nutritional requirements among parasites vary tremendously, although most tend to be facultative anaerobes. All Trypanosoma spp. metabolize carbohydrates from their host, but the metabolites are fermentation-like end products of pyruvate that can affect endothelial linings within the host. Malaria parasites of the genus Plasmodium ultimately have rather synchronous infections and produce byproducts of metabolism, including insoluble hemozoin, which when released from infected cells trigger a rise in proinflammatory cytokines that cause fever and impair the functioning of macrophages. Hookworms, because of their voracious appetite and wasteful digestive methods, deplete the iron ...