Josemir Sander detailed the relationship between epilepsy, the most common serious neurological condition worldwide, and a number of parasites. Epilepsy is a symptom complex, so diagnosis relies on clinical history rather than a specific test. Incidence is higher in developing countries than in the industrialized world, and appears to be higher in rural areas than in urban areas. Furthermore, endemic infections may be responsible for the increased incidence in low-income countries.

Maureen Durkin discussed ostensibly preventable or controllable infections that are important causes of childhood cognitive disability, paralysis, epilepsy, blindness, and deafness in developing countries. These infections include congenital disorders, such as syphilis, rubella, and cytomegalovirus, as well as infections occurring during infancy and childhood, such as malaria, meningitis, Japanese viral encephalitis, measles, poliomyelitis, and trachoma.

Eduardo Gotuzzo described clinical experience with HTLV-1, a retrovirus that causes adult T-cell leukemia and is endemic in much of Latin America.The virus produces 3 different clinical patterns: cancer, autoimmune disease, and immunosuppression disease. In developing countries, 80 percent of lymphomas are non-Hodgkins lymphoma, and 10 pecent of the non-Hodgkins lymphomas seen by the Peruvian national cancer center are associated with HTLV-1. A second clinical presentation is tropical dysplastic paraparesia (TSP). The third clinical pattern associated with the infection is immunosuppression.

Sanaa Kamal described chronic hepatitis C infection with and without schistosomiasis. Patients typically present in their thirties or forties with gastrointestinal bleeding, usually massive, and compromised liver function and status. These patients progress rapidly to end stage disease, usually dying in their forties. Coinfected individuals have significantly higher fibrosis levels and are unable to achieve spontaneous viral clearance.

Altaf Lal described interactions between the human immunodeficiency virus (HIV) and malaria to illustrate how different pathogens interact with each other and how they modulate the disease process. Infant mortality is higher in babies born to mothers who are infected with placental malaria and HIV-1, and these infants have lower levels of acquired passive immunity. Concurrent infections also promote pathogen diversity. The interactions, however, are extremely complex. For example, acute measles suppresses HIV replication significantly.



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