Toxoplasma gondii, an intracellular pathogen capable of infecting virtually any nucleated cell, is the causative agent of toxoplasmosis. The immunocompromised and unborn fetuses are at risk of developing complications from disseminated toxoplasmosis. In order to propagate its infection, T. gondii must traverse biological barriers and invade new host cells; and as such, motility is critical for virulence. Motility is also important for invasion and egress, and Ca2+ influx enhances both steps. During intracellular growth, T. gondii resides within a specialized intracellular vacuole that is reported to function as a sieve to permit for the exchange of small molecules; thus, the surrounding milieu of intracellular parasites is likely in equilibrium with the host cytoplasm. Calcium signaling, governed by fluctuations in cytosolic calcium ion (Ca2+) concentration, regulates a plethora of cellular responses and is utilized universally across life. Previous studies in Toxoplasma have shown that cytosolic Ca2+ signals are deciphered to modulate key lytic cycle processes including gliding motility and conoid (apical organelle used for secretion of proteins) extrusion. Yet, the questions of “how” and “when” cytosolic Ca2+ oscillations are decoded into the repetitive rounds of activation/deactivation of the Ca2+ effectors/binding proteins needed for glideosome (molecular machinery used for motility) activation remain unknown. The use of Genetically Encoded Calcium Indicators (GECI’s) has revolutionized the field of Ca2+ signaling and provides a direct means to investigate Ca2+ dynamics. GCaMP’s, a common GECI, are single-wavelength fluorescent sensors whose intensity is proportional to Ca2+ concentrations. Here, I present work investigating how intracellular parasites are exposed to the same fluxes of host cytosolic ionic composition that occur during a host cell signaling event. I present work highlighting the construction and implementation of an in-house custom- made algorithm that links Ca2+ signaling patterns to motility patterns. We employ pharmacology to selectively release or inhibit Ca2+ influx from the extracellular environment or Intracellular Calcium Stores (ICS) and identify how the corresponding Ca2+ oscillation patterns are decoded into types of motility. Our work expands our knowledge of the host-pathogen interaction of T. gondii and provides novel, innovate methodologies to study the signaling events that govern progression through the lytic cycle.