Pathophysiology in fish trypanosomiasis: The interaction between Trypanosoma carassii and goldfish erythropoietic system during the course of infection

• Author / Creator

  McAllister, Mark

• Trypanosoma carassii is a hemoflagellate parasite that infects a variety of cyprinid fish. The primary pathophysiology of T. carassii infections in fish is the onset of a prolonged anemia, characterized by significant decreases in the number of circulating red blood cells during peak parasitemia. Erythropoiesis is the physiological process which produces new red blood cells and is an essential component in recovery from infection. Previous work in mammalian model systems has suggested that parasite-mediated changes to the immune and erythropoietic systems play a significant role in host anemia. However, the mechanism(s) by which T. carassii induces anemia during the course of infection remain to be elucidated.
  The gene expression profile of critical erythropoiesis regulators was measured during the course of infection with T. carassii, as well as in fish made anemic using phenylhydrazine. Significant upregulation of pro-erythropoietic genes was observed in chemically induced anemia, but not during peak parasitemia. Furthermore, the expression of proinflammatory cytokines was markedly different between chemically and parasitically induced anemia.
  A recombinant goldfish erythropoietin (rgEPO) was shown to promote erythroid colony formation in vitro. EPO is the main regulator of erythropoiesis and was shown to be downregulated during the early and acute stages of infection. To examine whether the modulation of key erythropoietic factors was responsible for the observed anemia, I administered rgEPO in vivo during the early and acute stages of the infection. The administration of rgEPO in vivo reduced the severity of anemia but did not restore erythrocyte numbers in infected fish. Proinflammatory cytokines were upregulated during T. carassii infection, specifically tumor necrosis factor-alpha (TNF) and interferon-gamma (IFN). To examine whether these cytokines influence erythropoiesis, progenitor cells were incubated with recombinant goldfish IFN and TNF. Addition of both of these cytokines was shown to suppress the development of erythroid progenitor cells in vitro.
  My masters research examined the host-parasite interaction between goldfish and T. carassii, specifically focusing on the interplay between anemia, erythropoiesis, and inflammation. The results of my thesis research suggest that host proinflammatory responses, combined with direct red blood cell damage induced by T. carassii, are involved in the onset and maintenance of anemia during infection.

• Subjects / Keywords

  • Trypanosoma
  • Erythropoiesis
  • Goldfish
  • Anemia
  • Pathophysiology

• Graduation date

  Fall 2019

• Type of Item

  Thesis

• Degree

  Master of Science

• DOI

  https://doi.org/10.7939/r3-bqpy-v179

• License

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