are tiny (2–6 μm), obligate intracellular
parasites related to other coccidian protozoan, including Toxoplasma,
Cyclospora, Isospora, Plasmodium, Eimeria, and Sarcocystis.Cryptosporidium species
primarily infect the gastrointestinal tract of a variety of vertebrate
hosts, including humans.1 Host range is largely
a function of species, as a given species of parasite most efficiently
maintains infection within a few species of hosts.
Over 20 species of Cryptosporidium have been
described, but there is some debate as to the exact number of species.2 Two
species, C hominis and C parvum, account
for nearly all of the disease caused by Cryptosporidium species
in humans and are the species of public health significance. C
parvum was formerly divided into two genotypes (genotypes
I and II), but current classification separates genotype I into
a separate species known as C hominis.3 This
distinction is important, as humans are essentially the only known
reservoir of C hominis, and the species is more
efficient at causing disease in humans. Furthermore, studies that
distinguish between the two species in cohorts of infected patients
generally find a higher prevalence of C hominis; however,
the exact prevalence of either species depends on the principal
mode of spread (human-to-human vs. zoonotic), sanitation, and living
Cryptosporidium completes its life cycle within
a single host1,11(Fig. 345-1).
Infection occurs after ingesting the sporulated, thick-walled oocysts.
Excystation occurs in the small intestine after exposure to bile
salts and pancreatic enzymes, releasing four sporozoites. These sporozoites
penetrate a surface epithelial cell in the intestinal mucosa and
form an intracellular parasitophorous vacuole. They then differentiate
into uninuclear trophozoites, which undergo asexual replication (merogony)
to form type I meronts. The type I meront can then autoinfect other
surface epithelial cells or differentiate into a type II meront. The
type II meront then undergoes gametogomy, producing
both microgametocytes and macrogametocytes. These gametocytes fertilize
to produce oocysts. The life cycle is complete when the oocysts
undergo sporogomy, resulting in infectious sporozoites within the
oocysts. Approximately 80% of the oocysts produced in this
fashion are environmentally resistant, thick-walled cysts that are
excreted in the feces. The remaining 20% are thin-walled
cysts that undergo another autoinfective stage. The autoinfectious
stages are important features in the parasite’s life cycle
and accounts for persistent and occasionally severe disease, even
when a low inoculum of cysts are ingested.
Cryptosporidium life cycle. The infectious
sporulated oocyst is ingested by a susceptible host. Exposure to
digestive enzymes and bile salts releases four motile sporozoites
that immediately attach and invade adjacent epithelial cells. The
sporozoites develop in a parasitophorous vacuole that is intracellular
but extracytoplasmic; there, they form trophozoites that differentiate through
nuclear division into schizonts. Type I schizonts contain 6 to 8
nuclei that mature into 6 to 8 merozoites, which then infect neighboring
cells and continue the asexual ...
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