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Host Defense and Parasite Evasion
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
Trypanosoma evansi, the trypanosome responsible for the disease surra (also known as murina in South America) in domestic animals, on the other hand, makes use of a different strategy. By adhering to host erythrocytes, its surface antigens are effectively covered and consequently unavailable for immune recognition. This phenomenon has been described as an alternative to the antigenic variation observed in African trypanosomes. Another means of camouflage is for the parasite to simply adsorb host proteins to its surface. T. vaginalis employs this trick, but the real champions of appropriating host molecules are certainly the schistosomes. These trematodes, seemingly so vulnerable to immune surveillance in the circulatory system, avoid detection by disguising themselves with host blood-group antigens, clotting inhibitory factors, low-density lipoproteins and other molecules that adhere to their tegument. The ability of schistosomes to disguise themselves so effectively is considered to be a major hurdle in the development of an effective anti-schistosome vaccine, a topic we will return to in Chapter 9.
The Second Half of the Nineteenth Century
Published in Arturo Castiglioni, A History of Medicine, 2019
A number of trypanosomes have been found to be pathogenic. Though the earliest discovered (in the frog) and T. lewisi in the rat appear to be harmless, T. evansi (Griffith evans, 1880) was shown to be the cause of surra, a disease of ungulates. Sir David bruce (1855-1931) found that T. brucei (1894) caused the regularly fatal nagana, the animal disease transmitted by the tsetse fly (Glos-sina morsitans). In the equally fatal disease of man, T. gambiense (J. E. dutton, 1901) was found to be transmitted by another tsetse fly, Glossina palpalis. In addition to various other animal diseases, caused by T. equiperdum, T. theileri, and T. dimorphon,we should record the South American disease named (1909) for Carlos chagas (1879-1934), caused by T. cruzi and transmitted by biting insects of the family Reduviidas. Another group of parasitic diseases is represented by kala-azar, a tropical splenomegaly, caused by the flagellated body Leishmania donovani (1903). A cutaneous form —Aleppo or Delhi boil —is caused by L. tropica (J. H. wright, 1903). Still another group, Babesia (piroplasma), named after their Rumanian discoverer, V. babes (1854-1926), has been found to cause a number of relatively unimportant diseases of man and animals. Toxoplasma pyogenes was reported by A. Castellani (1914) as the cause of a grave human disease — toxoplasmosis.
Trypanosoma evansi
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2015
Eric S. Loker, Bruce V. Hofkin
Morphologically indistinguishable from Trypanosoma brucei, Trypanosoma evansi causes disease (called “surra” in Asia and “murrina” in South America) in many wild and domestic animals, including horses, camels, elephants, and dogs.
Mechanistic and biological characterisation of novel N 5-substituted paullones targeting the biosynthesis of trypanothione in Leishmania
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2020
Andrea Medeiros, Diego Benítez, Ricarda S. Korn, Vinicius C. Ferreira, Exequiel Barrera, Federico Carrión, Otto Pritsch, Sergio Pantano, Conrad Kunick, Camila I. de Oliveira, Oliver C. F. Orban, Marcelo A. Comini
The genus Trypanosoma and Leishmania encompasses parasitic protozoa that are the aetiological agents of several highly disabling and/or fatal diseases for humans and livestock (e.g. African sleeping sickness, Chagas’ disease, the different forms of leishmaniasis, Nagana and Surra disease). These parasites have a unusual thiol redox system that depends on the low molecular weight thiol trypanothione [N1,N8-bis(glutathionyl)spermidine, T(SH)2], which is absent in mammals1. From the pharmacological point of view, trypanosomatids present another attractive peculiarity; they lack genes for glutathione reductase and thioredoxin reductase2. Being devoid of backup pathways to maintain redox homeostasis, T(SH)2 is pivotal for parasite viability and virulence by providing reducing equivalents to cope with oxidative stress and sustain DNA synthesis and repair3. Indeed, most of the drugs used to treat trypanosomiasis and leishmaniasis are known to directly (e.g. efluornithine, antimonials, arsenates) or indirectly (e.g. benznidazole, nifurtimox and amphotericin) interfere with T(SH)2 metabolism4–7.