Dirofilaria immitis, canine heartworm, is a filarial nematode that may have genetic features that favor the development of drug resistance, including rapid rates of mutation, large population sizes, and high levels of gene flow. This parasite is currently treated with macrocyclic lactone anthelminthics, and while it has not yet shown evidence for evolving resistance to these chemotherapeutic compounds, resistance has evolved in related filarial nematodes infecting ruminants and humans. Heartworm samples from domestic dogs and coyotes were obtained via donations from veterinarians and researchers across the United States. I isolated and characterized 11 microsatellite loci for canine heartworm. Using the observed distribution of alleles, I determined the amount of genetic variability and quantified the partitioning of genetic variance. In conjunction with microsatellite data, specific mitochondrial (cox1) and Wolbachia (wsp and ftsZ) loci were used to genotype a subset of host taxa. Results indicate a lack of mitochondrial diversity and maximum likelihood trees show no discernable geographic patterning on a continental scale. This is not unexpected in a Wolbachia-infected organism like D. immitis as this bacterium has been shown to purge mitochondrial diversity in numerous model systems. After establishing baseline genetic parameters, a model of population dynamics was created to answer questions about the potential spread of drug resistance alleles. In the absence of selection, gene flow between subpopulations drives the dispersal of drug resistance alleles. Fixation time is directly proportional to selection pressure. When resistance alleles arise in a source population they spread more rapidly than if they arise in a sequestered population.