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Chapter: Medical Microbiology: An Introduction to Infectious Diseases: Introduction to Pathogenic Parasites: Pathogenesis and Chemotherapy of Parasitic Diseases

Parasites: Immunity

The large size, complex structure, varied metabolic activity, and synthetic prowess of most parasites provide their human host with an intense antigenic challenge.



The large size, complex structure, varied metabolic activity, and synthetic prowess of most parasites provide their human host with an intense antigenic challenge. Generally, the resulting immunologic response is vigorous, but its role in modulating the parasitic invasion differs significantly from that in viral and bacterial infections. It is apparent from the chronic course and frequent recurrences typical of many parasitic diseases that acquired resistance is often absent. When present, it is generally incomplete, serving to moderate the intensity of the infection and its associated clinical manifestations rather than to destroy or expel the causative pathogen. In fact, clinical recovery and resistance to reinfection in some parasitoses require the persistence of viable organisms at low concentration within the body of the host (premunition). Complete sterilizing immunity with prolonged resistance to reinfection is exceptional.


This pusillanimous response does not result from any dearth of immunologic mechanisms available to the host. All those generally exercised against the more primitive microorganisms, including antibodies, cytotoxic T lymphocytes, activated macrophages, natural killer cells, antibody-dependent cell-mediated toxicity, lymphokines, and complement activation, have been shown to play a part in moderating parasitic infection. In worm infections, some of these mechanisms find unique implementation. On invasion of tissue, helminths stimulate the production of IgE, the Fc portion of which binds to mast cells and basophils. Interaction of the antibody with parasitic antigen triggers the release of histamine and other mediators from the attached cells. These may injure the worm directly

or, by increasing vascular permeability and stimulating the release of chemotactic factors, may lead to the accumulation of other cells and IgG antibodies capable of initiating antibody-dependent, cell-mediated destruction of the parasite. The specific killer cell involved is often the eosinophil. These cells attach by their Fc receptor site to IgG antibody- coated parasites and degranulate, releasing a major basic protein that is directly toxic to the worm.


The techniques by which parasites have been shown to evade the consequences of the host’s specific acquired immunity are numerous. Included among them are seclusion within immunologically protected areas of the body, continual alteration of surface antigens, and active suppression of the host’s effector mechanisms. A number of protozoa are shielded from humoral defenses by virtue of their intracellular location. Some have even found ways to avoid or survive the normally lethal environment of the phagolysosome of the macrophage. T. cruzi, for example, lyses the phagosomal membrane, providing escape into the cytoplasm, whereas Toxoplasma gondii inhibits fusion of the phagosome with lysosomes. Leishmania species, capable of neither of these feats, are resistant to the action of lysosomal enzymes and survive in the phagolysosomes.


Toxoplasma, cestode larvae, and Trichinella spiralis armor themselves against immunologic attack by encysting within the tissue of the host. The gut lumen is, perhaps,the largest immunologic sanctuary within the body, because, unless the integrity of the in-testinal mucosa is breached by injury or inflammation, this barrier protects lumen-dwelling parasites from most of the effective humoral and cellular immune mechanisms of the host, allowing almost unfettered growth and multiplication.

Most immune effector mechanisms are directed against the surface antigens of the par-asite, and alteration of these antigens may blunt the immunologic attack. Many parasites undergo developmental changes within their hosts that are generally accompanied by alter-ations in surface antigens. Immune responses directed at an early developmental stage may be totally ineffective against a later stage of the same parasite. Such stage-specific immu-nity has been demonstrated in malaria, schistosomiasis, and trichinosis, accounting for the seeming paradox of parasite survival in a host resistant to reinfection with the same strain of organism. Even more intriguing is the ability of some parasites to vary the antigenic characteristics of a single developmental stage. The trypanosomes that cause African sleeping sickness circulate in the bloodstream coated with a thick layer of glycoprotein. The development of humoral antibody to this coating results in the elimination of the para-site from the blood. This is followed by successive waves of parasitemia, each associated with a new glycoprotein antigen on the parasite against which the previously produced an-tibody is ineffective. The parasite is capable of producing more than 100 glycoprotein vari-ants, each encoded by a different structural gene. The expression of individual genes from this large genetic repertoire is controlled by the sequential transfer of a duplicate copy of each gene to an area of the parasite responsible for gene expression.

Several protozoan and helminthic pathogens are thought to be capable of neutralizing antibody-mediated attack by shedding and, later, regenerating specific surface antigens. Adult schistosomes, in addition, may immunologically hide from the host by masking themselves with host blood group antigens and immunoglobulins.

A number of parasites can destroy or inactivate immunologic mediators. Tapeworm larvae produce anticomplementary chemicals, and T. cruzi splits the Fc component of attached antibodies, rendering it incapable of activating complement. Several protozoa, most notably T. brucei, the etiologic agent of African sleeping sickness, induce polyclonal B-cell activation leading to the production of nonspecific immunoglobulins and eventual exhaustion of the antibody-producing capacity of the host. This and other protozoa can produce nonspecific suppression of both cellular and humoral effector mechanisms, enhancing the host’s susceptibility also to a variety of unrelated secondary infections. Patients with disseminated leishmaniasis display a specific inability to mount a cellular immune response to parasitic antigens in the absence of evidence of generalized immuno-suppression.

Finally, the thick, tough cuticle of many adult helminths renders them impervious to immune effector mechanisms designed to deal with the less robust microbes.


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