Parasites produce damage to man by 1) Consumption of nutrients 2) Destruction of tissues 3) Traumatic lesions 4) Toxic action 5) Immunoallergic reactions. Humans react against parasitic attack with their natural and acquired defences. Age, race, sex, genetic endowment and nutritional status are some of the factors which influence natural immunity. Acquired cellular immunity is responsible for the state of premunition which avoids superinfection in some parasitoses. The development of an infection or of the clinical disease in an individual will depend on the interaction between the aggressive factors of the parasite and the defensive capacities of the host. In the great majority of cases an equilibrium will result: in other words, an infection. When there is a great load of parasites with great pathogenicity affecting a susceptible host, a disease will develop which can eventually result in death. Treatment should be administered on the basis of clinical, epidemiological or prophylactic considerations. In amebiasis the virulence of the races is the main parasitic factor. The difference between virulent races is quantitative and not qualitative and can be demonstrated by phagocytosis of red blood cells, “toxin” production and by inoculation into the liver of newborn hamsters. The cytotoxin has at least two components: collagenase and amebapore. The nutritional status, intestinal lumenal pH and redox potential, secretory IgA and mucus and plasma complement are some of the host factors which influence the pathogenicity of amebae. Curative treatment is indicated on intestinal or extraintestinal invasive amebiasis. Prophylactic treatment should be administered to infected food handlers and infected persons in developed countries. In toxoplasmosis, curative treatment is indicated in patients with clinical manifestations of acquired or congenital infection, in acute, sub-acute or chronic, reactivated periods. The clinical symptomatology must be correlated with serological testing which indicates “activity”. In some acquired lymph node toxoplasmosis, without general compromise, asthenia, adynamia or fever, treatment is not needed because of its good prognosis. Chronic inactivated cases, or sequelae do not require treatment. Prophylactic treatment is indicated: in: 1) Pregnant women with seroconversion to avoid congenital infection. 2) In apparently healthy children with asymptomatic congenital infection, to avoid late ocular lesions. 3) In individuals who receive immunosupressive therapy and have serological evidence of toxoplasmosis activity. In the larva migrans syndrome, treatment is indicated in patients with symptomatology oreosinophilia. The therapy may produce remission of the clinical picture or of the eosinophilia.