The works presented in this thesis aimed to investigate clinical, in vitro, and molecular processes on host-pathogen interactions within the filarial nematode Brugia malayi. The hypothesis of the first study was whether we would observe early clinical indicators of B. malayi infection in the cat distinguishing between those that would become microfilaremic (mf+) versus amicrofilaremic (mf-). Though there was no significant difference between mf+ and mf- cats, there were 2 animals that presented with a delayed phenotype that differed from these two groups. Dogs were also infected with B. malayi L3 to determine whether they could be experimental hosts for this parasite, along with measuring inter- and intraspecies differences with the cats. Dogs became infected, though mf was transient. Dogs that were mf- had elevated lymphocytes, implicating lymphocyte clearance of these parasites. Between cats and dogs, eosinophilia was elevated in the cats, but not dogs, suggesting these granulocytes may play a protective role for the parasite in a primary infection. The aim of the second study was to determine whether the addition of heavy metal ions would facilitate development, molting, and survival in an in vitro culture assay. The hypothesis was zinc and iron ions will aid B. malayi L3 molting and survival, thereby facilitating development into the L4 stage while copper ions will hinder development. Copper ions were found to kill B. malayi L3 in culture, zinc encouraged development, but not survival, and iron facilitated survival but did not develop. The final study aimed at identifying parasite-derived miRNAs found in infected feline plasma. We hypothesized that we could identify host immunity gene transcripts targeted by B. malayi secreted miRNAs. Nine gene targets were identified that targeted potential immune processes, suggesting that miRNAs secreted by B. malayi may affect the immune response of the host.