Cystoisospora, a parasite.
Isospora comes from the genus of Eimeriidae family,
say that three times fast, and is a coccidian parasite which is probably easier to look at than to describe.
The picture in front of you is the classic image of a coccidian parasite sort of encysted in a firm outer shell or wall.
The isospora go through classic developmental stages
which we’ll discuss shortly each of which has a possible contribution to the clinical pathogenesis
so the schizonts, gamonts, oocysts.
Transmission as you're seeing with most parasites is via fecal-oral spread of the oocysts
from the contaminated water. Incubation after ingesting an oocyte is approximately one week
and the typical human pathogen which we are most concerned about is Isospora belli.
Let's look now then at the mechanism of the pathogenesis and as for the other water
associated parasites, there is a first an ingestion stage, a processing stage through the gut
and then an eventual departure from the gut of recreated oocysts
which can either infect others or certainly contaminate a water supply.
However the primary infection, the first sign of inflammation occurs
when the oocysts are ingested and break down into the first stage
which attaches to the brush border of the small intestinal mucosa.
Let’s look at that a little bit more closely. Having ingested the oocyte it sort of excysts itself
and releases sporozoites which attach to the brush border of the intestinal epithelium
as you can see in this slide.
The sporozoites are then inserted into the cytoplasma of the cell
where they undergo asexual replication to create merozoites.
After the merozoites are created, they rupture through their host cell
which is the first sign of inflammation and a triggering of the human immune response.
This allows for malabsorption, petechial hemorrhages, and sort of a chronic scarring
of those affected cells leading to villous atrophy and crypt hypertrophy.
Next is the sexual reproduction stage and so the merozoites reenter another host cell
so this is an autoinfection stage infection reoccurring within the lumen of the gut
and then goes through sexual maturation to then create a gamont
and then to release a fully formed cyst into the stool.
Again, a rupture, a lysis of the host cell occurs leading potentially
to even further inflammation and all the results as we just talked about after the asexual stage.
So, how this looks clinically then, is the patient will develop non-bloody diarrhea.
Non-bloody because it's usually the intestinal epithelial cells not the vasculature
which are being ruptured in this case, however, because this will affect the actual intestinal wall,
there may be abdominal pain related to that.
Certainly there will be fever associated with this ongoing repetitive, re or autoinoculation stages of inflammation.
Then, the malabsorption is probably the more prominent part of the Isospora belli infection.
Malabsorption because these cells are unable to retain or absorb water and other nutrients.
So patients may become severely dehydrated,
they certainly can also have associated weight loss and for patients
who chronically infected such as infants or immunosuppressed patients -
they have a malabsorptive syndrome and may have failure to thrive or failure to gain weight
as the presenting symptom.
Diagnosis is by demonstrating the oocysts in stool,
and again as you saw on the very first image it’s a characteristic coccidian appearance of the oocyst.
Treatment then especially for those who are immunocompromised or very young,
is with a sulfonamide especially trimethoprim/sulfamethoxazole.
Isospora, and Isospora belli are the classic pathogen in this case
and they're a very typical sort of sexual and asexual maturation cycle as seen in the coccidian parasites.
Remember them well, you’ll see this pattern repeat in other typical and similar parasites.