Trypanosoma cruzi

toxoplasma gondii

Chagas disease, also known as American trypanosomiasis, is caused by infection with the protozoan parasite Trypanosoma cruzi. The organism T cruzi and infection in humans were first described in 1909 by the Brazilian physician Carlos R. J. Chagas.[1]T cruzi is found mostly in blood-sucking triatomine insects (kissing bugs) and small mammals in a sylvatic cycle that is enzootic from the southern and southwestern United States to central Argentina and Chile. T cruzi infection in humans occurs in a spotty distribution throughout the range of the sylvatic cycle. New cases of vector-borne T cruzi infection usually occur in persons who live in primitive houses in an area where the sylvatic cycle is active. The living quarters are invaded by infected triatomines, which become domiciliary. Infected insects take blood meals from humans and their domestic animals and deposit parasite-laden feces. The parasites are then transmitted via contact with breaks in the skin, mucosal surfaces, or the conjunctivas. Transmission can also occur congenitally or via blood transfusion or organ transplantation. T cruzi infection is life-long. A minority of persons with long-standing T cruziinfection develop the serious cardiac and gastrointestinal problems that characterize chronic symptomatic Chagas disease. The parasite T cruzi is a member of the family Trypanosomatidae in the order Kinetoplastida and belongs to a special section called Stercoraria. The infective forms of T cruzi are contained in the feces of the insect vectors and gain entry into its mammalian hosts through contamination. This mechanism of transmission contrasts with that of the two subspecies of African trypanosomes that cause human disease, Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense, which are transmitted via the saliva of their vectors, and with the mechanism by which the nonpathogenic trypanosome found in the Americas, Trypanosoma rangeli, is transmitted to its mammalian hosts. Vectors of T cruzi Triatomines, which transmit T cruzi, belong to the family Reduviidae in the order Hemiptera. Reduviidae has 22 subfamilies, including the Triatominae. Although the vectors of T cruzi are occasionally referred to as reduviids, this term is not appropriate since the vast majority of the species in the family Reduviidae are phytophagous or insectivorous and do not transmit the parasite. All triatomine species are able to transmit T cruzi to humans, but only a handful become domiciliary to any great extent and are important as T cruzivectors. Many more triatomine species

are involved in the widespread sylvatic cycles. Triatomines have 5 nymphal stages (instars), all of which can harbor and transmit T cruzi. The three vector species most important in the transmission of T cruzi to humans include Triatoma infestans, Rhodnius prolixus, and Triatoma dimidiata. Historically, T infestans has been by far the most important, as it has been the primary vector in the subAmazonian endemic regions. Since the early 1990s, many Chagas disease control programs have focused on eliminating domiciliary T infestans. These efforts have been successful in Uruguay, Chile, and, most recently, Brazil, all of which have been declared transmission-free by the Pan American Health Organization. Major progress has also been made in Argentina and Bolivia. R prolixus is typically found in Central America and in the Andean nations. The range of T dimidiata is similar but also extends far into Mexico. Other domiciliary species occupy more restricted areas and play less-important roles in the transmission of T cruzi to humans. The sylvatic species can also colonize human dwellings and thus present a potential risk for transmission.

The modes of transmission of T cruzi to humans Historically, most transmissions of T cruzi to humans have resulted from the contamination of vulnerable surfaces (eg, breaks in the skin, mucosae, and the conjunctivas) with the feces of infected vectors Pathophysiology An inflammatory lesion caused by T cruzi that may appear at the site of entry in patients with acute Chagas disease is called a chagoma. Histologic changes may include interstitial edema, lymphocytic infiltration, and reactive hyperplasia of adjacent lymph nodes due to intracellular parasitism of muscle and other subcutaneous tissues. When parasitized host cells rupture, trypomastigotes are released and can often be detected by microscopic examination of anticoagulated blood. As the infection spreads systemically, muscles, including the myocardium, and various other tissues become parasitized. Acute myocarditis, consisting of patchy areas of necrosis and infected cells, may develop. The pseudocysts occasionally seen in sections of infected tissues are intracellular aggregates of amastigotes. The patent parasitemias of the acute illness may be accompanied by lymphocytosis, and transaminase levels may be elevated. The cerebrospinal fluid may contain parasites. Some people can be infected and never develop symptoms. For those who do, Chagas disease has three stages, each with different symptoms. Acute infection -- A few people (about 1% of cases) have symptoms soon after infection. The most recognized acute symptom is swelling of the eye on one side of the face, usually at the bite wound or where feces were rubbed into the eye. Other symptoms are tiredness, fever, enlarged liver or spleen, swollen lymph glands, and sometimes a rash, loss of appetite, diarrhea, and vomiting. Infants and very young children can get an oftenfatal swelling of the brain. Indeterminate stage: During the indeterminate stage, about 8 to 10 weeks after infection, infected persons have no symptoms. Chronic infection: Some people develop serious, irreversible damage to the heart or intestinal tract that appears 10 to 20 years after infection. Heart-related problems include an enlarged heart, altered heart rate or rhythm, heart failure, or cardiac arrest.

Enlargement of parts of the digestive tract can result in severe constipation or problems with swallowing.

Toxoplasmosis is a zoonotic infection in humans caused by the protozoal intracellular parasite Toxoplasma gondii. Cats are the primary hosts, while humans and other mammals serve as intermediate hosts. Infection with T gondii is common among humans, and it is estimated that one third of the world's population has been exposed. However, most infections are subclinical, and disease typically only becomes apparent in congenitally acquired infection and in patients with significant immunodeficiency such as in acquired immunodeficiency syndrome (AIDS). Toxoplasma infection is generally acquired via eating undercooked or raw meat infected with tissue cysts, via ingestion of food or water contaminated with infected cat feces, or congenitally from mother to fetus Pathophysiology Life cycle of Toxoplasma gondii The life cycle of T gondii involves several forms. The oocyte is produced in the feline intestine and produces sporozoites. Sporozoites mature outside of the cat to become tachyzoites, which infect a wide variety of tissues, producing an inflammatory response and a wide array of symptoms. Tachyzoites eventually form tissue cysts in which bradyzoites develop and replicate. In most immunocompetent hosts, bradyzoites are confined to the tissue cysts in which they are slowly replicating; however, in the setting of immune compromise bradyzoites can become tachyzoites, and thus spread infection again to different tissues. Humans enter the life cycle of T gondii by ingesting meat infected with tissue cysts, or ingesting materials contaminated with infectious oocysts. T gondiimay also be acquired transplacentally or via transplantation of infected organs or blood transfusions.[

Most primary infections produce no symptoms. The time between exposure to the parasite and symptom development is 1 - 2 weeks. The disease can affect the brain, lung, heart, eyes, or liver. Symptoms in persons with otherwise healthy immune systems: Enlarged lymph nodes in the head and neck Headache Mild illness with fever, similar to mononucleosis Muscle pain Sore throat

Symptoms in immunosuppressed persons: Confusion Fever Headache Retinal inflammation that causes blurred vision Seizures

Chagas disease and Taxoplasmosis

Ivan S Tangliben BSN-2 Submitted to: Dr. Marc Collao