Surprisingly, unlike most Apicomplexa, Cryptosporidium parvum appears to la
ck a plastid genome, Primers based upon the highly conserved plastid small-
or large-subunit rRNA (SSU/LSU rRNA) and the tUfA-tRNA(Phe) genes of other
members of the phylum Apicomplexa failed to amplify products from intracell
ular stages of C. parvum. whereas products were obtained from the plastid-c
ontaining apicomplexans Eimeria bovis and Toxoplasma gondii, as well as the
plants Allium stellatum and Spinacia oleracea. Dot-blot hybridization of s
porozoite genomic DNA (gDNA) supported these PCR results, A T, gondii plast
id-specific set of probes containing SSU/LSU rRNA and tufA-tRNA(Phe) genes
strongly hybridized to gDNA from a diverse group of plastid-containing orga
nisms including three Apicomplexa, two plants, and Euglena gracilis, but no
t to those without this organelle including C. parvum, three kinetoplastids
, the yeast Saccharomyces cerevisiae, mammals and the eubacterium Escherich
ia coli, Since the origin of the plastid in other apicomplexans is postulat
ed to be the result of a secondary symbiogenesis of either a red or a green
alga, the most parsimonious explanation for its absence in C. parvum is th
at it has been secondarily lost, If confirmed, this would indicate an alter
native evolutionary fate for this organelle in one member of the Apicomplex
a, It also suggests that unlike the situation with other diseases caused by
members of the Apicomplexa, drug development against cryptosporidiosis tar
geting a plastid genome or metabolic pathways associated with it may not be
useful.