Pathogenic bacteria undergo a multitude of interactions with host immune cells to establish an infection and cause disease. One of these interaction axes involves the formyl peptide receptors (FPRs) used by innate immune cells to detect and kill invading bacteria. Despite the importance of these receptors in driving early immune responses to pathogens, few resources exist to study these receptors in vivo. Here, we generate Fpr2-/-, Fpr3-/-, Fpr1/3-/-, and Fpr1/2/3-/- mice to aid in the study of combinational effects of FPRs during bacterial infection. Using these new tools, we find that Fpr1-/-, Fpr2-/-, and Fpr3-/- mice have a delayed time-to-death during lethal challenge with Yersinia pestis. These survival phenotypes could not be solely attributed to altered chemotaxis or bacterial effector translocation by the type III secretion system. Additionally, we find that Fpr1, but not Fpr2 or Fpr3, is activated by N-terminally-formylated peptides secreted by Y. pestis. Together, these experiments reveal a convoluted interaction between formyl peptide receptors and plague-causing Yersinia.