Class Kinetoplasta Phylum Euglenozoa: large and diverse group of protists including photosynthetic, heterotrophic, and parasitic species. Kinetoplasta are relatively basal species in the group. Euglenozoa Kinetoplastida Trypanosoma Cryptobia • Bodonids: free living or parasitic. – Ichthyobodo spp., Cryptobia spp. Blood pathogens of fish. • Trypanosomatids: parasitic in intestine of arthropods and/or in blood of vertebrates. – Human parasites: Trypanosoma gambiense, T. rhodesiense, T. cruzi; Leishmania spp. – Parasites of livestock: T. evansi, T. equinum, T. equiperdum. “African” Trypanosomes • Trypanosoma brucei, T. rhodesiense, T. gambiense. Sleeping sickness restricted to “fly belt” where vectors, Glossina spp. occur. Sleeping sickness • A wasting disease associated with successive waves of fevers. Parasite numbers in blood (parasitemia) increase dramatically during bouts. • Lymph nodes swell accompanied by pain, headache, weight loss, anemia, eventually death. • T. rhodesiense kills within months; T. gambiense is slower; invades CNS giving rise to sleeping sickness. VSG switching • One expression site active at a time. • Large archive of VSG genes throughout genome (some full genes, some pseudogenes). • Can switch from one full gene to another or produce mosaics of genes and pseudogenes. • Can switch active expression site. Epidemiology • Only certain species of Glossina transmit so distribution spotty through the fly belt. • Situation complicated by reservoir hosts which maintain the parasite even in the absence of man (T. rhodesiense > T. gambiense) Treatment and control • Key to control is surveillance of at-risk population and treatment: suramin or pentamidine (blood forms), melarsoprol (late stage, CNS); drugs have serious side effects which must be monitored. • Vectors control: remove scrub every year; control reservoirs, DDT Trypanosoma cruzi Vectors: Panstrongylus spp., Rhodnius spp., Triatoma spp. (Heteroptera; Reduviidae). Many potential reservoirs. Posterior station transmission. Parasites live in blood (trypomastigotes) and intracellularly (amastigotes) in vertebrate host. Pathogenesis-early • Small sore at bite site. Trypomastigotes enter cells, transform to amastigotes and divide producing a new crop of cells which are disseminated throughout body. Eventually host will destroy trypomastigates and other extracellular stages leaving pseudocysts in smooth and cardiac muscle. Cell Entry • parasite attaches to cell membrane and recruits lysosomes to the region. • Once in lysosome, acid environment stimulates parasite to produce a hole-making molecule that it uses to leave the lysosome. Pathogenesis-later • Variable: many cases resolve and present as symptomless throughout life of individuals; a few result in death during the acute phase; most often infections result in a chronic disease involving some level of cardiopathy. • Often autonomic ganglia are destroyed resulting in loss of tonus: megaoesophagus, megacolon Epidemiology • Enzootic • Separate strains infect humans and animals • Vector may inhabit houses and palms mixing sylvatic and domestic strains Treatment and Control • No cure exists and treatments affect only blood stream forms leaving pseudocysts intact. Treat cardiac symptoms. • Vector control cost effective: build houses less attractive to Triatomes and spray to kill insects. .