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Background  Malaria is transmitted when an infected mosquito delivers  Plasmodium  sporozoites into a vertebrate host. There are many species of  Plasmodium  and, in general, the infection is host-specific. For example , Plasmodium gallinaceum  is an avian parasite, while  Plasmodium berghei  infects mice. These two parasites have been extensively used as experimental models of malaria transmission . Plasmodium falciparum  and  Plasmodium vivax  are the most important agents of human malaria, a life-threatening disease of global importance. To complete their life cycle,  Plasmodium  parasites must traverse the mosquito midgut and form an oocyst that will divide continuously. Mature oocysts release thousands of sporozoites into the mosquito haemolymph that must reach the salivary gland to infect a new vertebrate host. The current understanding of the biology of oocyst formation and sporozoite release is mostly based on experimental infections with  P.  berghei , and the conclusions are generalized to other  Plasmodium  species that infect humans without further morphological analyses.    Results  Here, it is described the microanatomy of sporozoite escape from oocysts of four  Plasmodium  species: the two laboratory models,  P. gallinaceum  and  P. berghei , and the two main species that cause malaria in humans,  P.  viv ax and  P. falciparum . It was found that sporozoites have species-specific mechanisms of escape from the oocyst. The two model species of  Plasmodium  had a common mechanism, in which the oocyst wall breaks down before sporozoites emerge. In contrast,  P. vivax  and  P. falciparum  sporozoites show a dynamic escape mechanism from the oocyst via polarized propulsion.    Conclusions  This study demonstrated that  Plasmodium  species do not share a common mechanism of sporozoite escape, as previously thought, but show complex and species-specific mechanisms. In addition, the knowledge of this phenomenon in human  Plasmodium  can facilitate transmission-blocking studies and not those ones only based on the murine and avian models.

Species-specific escape of Plasmodium sporozoites from oocysts of avian, rodent, and human malarial parasites