Apicomplexa constitute one of the largest phyla of protozoa. Most Apicomple
xa, including those pathogenic to humans, are obligate intracellular parasi
tes. Their extracellular forms, which are highly polarized and elongated ce
lls, share two unique abilities: they glide on solid substrates without cha
nging their shape and reach an intracellular compartment without active par
ticipation from the host cell. There is now ample ultrastructural evidence
that these processes result from the backward movement of extracellular int
eractions along the anteroposterior axis of the parasite. Recent work in se
veral Apicomplexa, including genetic studies in the Plasmodium sporozoite,
has provided molecular support for this 'capping' model. It appears that th
e same machinery drives both gliding motility and host cell invasion. The c
ytoplasmic motor, a transmembrane bridge and surface ligands essential for
cell invasion are conserved among the main apicomplexan pathogens.