Dissertations, Theses, and Capstone Projects

Date of Degree

2-2025

Document Type

Dissertation

Degree Name

Ph.D.

Program

Biology

Advisor

Susan Perkins

Committee Members

Jayne Raper

Weigang Qiu

Kirk Deitsch

Brandon Ogbunu

Subject Categories

Biology | Ecology and Evolutionary Biology | Immunology of Infectious Disease | Parasitology

Keywords

Plasmodium, Malaria, Hemoglobin Digestion, Host Cell Invasion, Host Immune Response, Anole Lizards

Abstract

Malaria is historically one of the most severe parasitic human diseases and is still responsible for over half a million deaths annually. Plasmodium species, the causative agents of malaria, are often characterized by two hallmark features of their asexual stages: the invasion of vertebrate red blood cells and the presence of hemozoin pigment as a byproduct of host hemoglobin digestion. Despite their evolutionary relatedness to mammalian Plasmodium, wildlife malaria parasites are understudied, leaving their vast genetic diversity to be explored. Lizard-infective malaria parasites, for example, include over 100 species of Plasmodium and present a diverse array of phenotypes, some of which diverge from these classically defined malarial traits.

Plasmodium floridense, Plasmodium azurophilum, and Plasmodium leucocytica infect anole lizards throughout the Caribbean islands, including the endemic Anolis sabanus lizard on Saba Island. Like other Plasmodium species, P. floridense infects red blood cells and produces hemozoin. Plasmodium azurophilum also infects red blood cells, however, its sister species, P. leucocytica, infects white blood cells. This is atypical for Plasmodium parasites and represents an expansion into a new cellular niche. Two of these three Anolis-infecting parasites (P. azurophilum and P. leucocytica) also do not produce hemozoin and have seemingly evolved alternative mechanisms of hemoglobin digestion for nutrient acquisition. All three species exist as chronic infections and do not appear to harm their Saban anole host—a vast difference from their mammalian relatives. These traits (new cellular niches, lack of hemoglobin digestion, low virulence) likely evolved to decrease interspecific competition during multi-infections.

In my dissertation, I used transcriptomics to investigate the genetic basis behind these unique phenotypes in this lizard-malaria system. I characterized the host transcriptomic response to all three parasites and found no evidence of transcriptomic differences in infected versus uninfected hosts. This is the first transcriptomic evidence for the previously described low virulence phenotypes in this lizard-malaria system. I also analyzed the expression of known genes in key mammalian Plasmodium pathways (hemoglobin digestion and blood cell invasion) and found evidence for the conservation of many of these genes in all three lizard malaria species. Relative to mammalian Plasmodium genes, however, I show evidence of changes in selective pressures along the lizard malarial genes. As there is currently no whole genome sequence for any lizard-infective Plasmodium species, this is the first comparative genetic analysis across these pathways in mammalian and lizard Plasmodium.

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