Protists are single-celled eukaryotes that reside in vastly different ecological niches, have complex life cycles and diverse phylogenetic origins. Many are parasitic and of significant global health relevance. The capacity of protists to rapidly adapt to major changes in their environment is critical to their survival. In most instances, they undertake these adaptations without cell division and must massively reconfigure their transcriptional and expressional behaviours. Among parasitic protists, these changes are essential for establishing infection and must occur within a few minutes of invasion, such that they appear pre-programmed. Pre-programming (‘cell-fating’) has been explored heavily in eukaryotic cells, including in developmental biology and stem cell differentiation. Post-transcriptional regulation (PTR), particularly mediated through translational repression, a phenomenon through which transcripts are held in stasis for later translation, is a key regulator of cell fate. PTR mechanisms, including in cell-fating, metabolism and other key functions, are heavily effected through a suite of RNA-binding proteins (RBPs). These have been shown, particularly in Plasmodium ('malaria parasite'), to have importance during it's initial infection. Noting this, RBPs are poorly characterized in most parasitic protists, beyond the behavior of a small number of RBPs in Plasmodium and Toxoplasma. We have bioinformatically mined and curated the ‘RBPome’ of 8 major parasitic protists – including three major diarrhoeal parasites, Cryptosporidium parvum, Giardia duodenalis, Entamoeba histolytica, the primary two human malaria parasites,Plasmodium falciparumand Plasmodium vivax, the causative agent of African sleeping sickness, Trypanosoma brucei, the sexually transmittedTrichomonas vaginalis, andToxoplasma gondii. We have employed a multi-omics approach to explore behaviour of these RBPs over each parasite life-cycle and with respect to major ecological transitions during cyst formation and infection. This analysis found the global down-regulation of RBPs for most species at each major ecological change and specific up-regulation of a small suite of conserved RBPs. We explore the role of these up-regulated RBPs in translational repression and discuss their potential in setting the fate of infective cells as an essential and conserved mechanism under-pinning parasitic protozoan infection biology.