AMERICAN TRYPANOSOMIASIS(CHAGAS’ DISEASE )
American trypanosomiasis is a disease produced by T. cruzi and transmitted by true bugs of the family Reduviidae. Clinically, the infection presents as an acute febrile illness in children and a chronic heart or gastrointestinal malady in adults.
Chagas’ disease affects 16 to 18 million people in a geographic area extending from Central America to southern Argentina, producing death in 50,000 annually. Within these areas, it is the leading cause of heart disease, accounting for one fourth of all deaths in the 25- to 44-year age group. Transmission occurs primarily in rural settings where the reduviid can find harborage in animal burrows and in the cracked walls and thatch of poorly constructed buildings. This large (3-cm), winged insect leaves its hiding place at night to feed on its sleeping hosts. Its predilection to bite near the eyes or lips have earned this pest the nick-names of “kissing bug” and “assassin bug.” Most new infections in these areas occur in chil-dren. Infection can also be acquired in utero, and, less frequently, through breastfeeding.
In addition to humans, a number of wild and domestic animals, including rats, cats, dogs, opossums, and armadillos, serve as reservoirs. The close association of many of these hosts with human dwellings tends to amplify the incidence of disease in humans and the difficulty involved in its control.
Organ transplantation and transfusion-related infections are rapidly increasing prob-lems in urban settings within endemic areas. Recrudescence of the latent infection is in-creasingly seen in immunosuppressed individuals, including patients with HIV infections. More effective blood bank screening provides hope that transmission of this disease will be substantially curtailed in the near future.
An estimated 50,000 infected Latin American immigrants are currently living in the United States. Because T. cruzi has been found in both vertebrate and invertebrate hosts in the southwestern United States, there is a possibility of sustained transmission of this organ-ism within this country. Although serologic evidence suggests that the acquisition of human infection in this area is not uncommon, clinically apparent autochthonous cases have been rare. The majority of these acquired the infection through blood – blood transfusions.
Multiplication of the parasite at the portal of entry stimulates the accumulation of neu-trophils, lymphocytes, and tissue fluid, resulting in the formation of a local chancre or chagoma. The subsequent dissemination of the organism with invasion of tissue cells pro-duces a febrile illness that may persist for 1 to 3 months and result in widespread organ damage. Any nucleated host cell may be involved but those of mesenchymal origin, espe-cially the heart, skeletal muscle, smooth muscle, and glial nerve cells, are particularly susceptible. Cell entry is facilitated by binding to host cell fibronectin; a 60-kd T. cruzi surface protein (penetrin) appears to promote adhesion. Following penetration, the trypo-mastigote escapes the phagolysosome via the production of a pore-forming protein, trans-forms to the amastigote form, and multiplies freely within the cytoplasm to produce a pseudocyst, a greatly enlarged and distorted host cell containing masses of organisms. With the rupture of the pseudocyst, many of the released parasites disintegrate, eliciting an intense inflammatory reaction with destruction of surrounding tissue. The development of an antibody-dependent, cell-mediated immune response leads to the eventual destruc-tion of the T. cruzi parasites and the termination of the acute phase of illness.
Parasitic antigens released during this acute phase may bind to the surface of tissue cells, rendering them susceptible to destruction by the host’s immune response. It has been suggested by some that this results in the production of antibodies that cross-react with host tissue, initiating a sustained autoimmune inflammatory reaction in the absence of systemic manifestation of illness. In the heart, this reaction leads to changes in coro-nary microvasculature, loss of muscle tissue, interstitial fibrosis, degenerative changes in the myocardial conduction system, and loss of intracardiac ganglia. In the digestive tract, loss of both ganglionic nerve cells and smooth muscle results in dilatation and loss of peristaltic movement, particularly of the esophagus and colon.
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