Infection occurs by ingestion of sporocyst-containing oocysts: the sporocysts excyst in the small intestine and release their sporozoites, which invade the epithelial cells and initiate schizogony. Upon rupture of the schizonts, the merozoites are released, invade new epithelial cells, and continue the cycle of asexual multiplication. Trophozoites develop into schizonts which contain multiple merozoites. After a minimum of one week, the sexual stage begins with the development of male and female gametocytes. Fertilization results in the development of oocysts that are excreted in the stool. Cystoisospora belli infects both humans and animals. Diagnosis
Microscopic demonstration of the large typically shaped oocysts is the basis for diagnosis. Because the oocysts may be passed in small amounts and intermittently, repeated stool examinations and concentration procedures are recommended. If stool examinations are negative, examination of duodenal specimens by biopsy or string test (Enterotest) may be needed. The oocysts can be visualized on wet mounts by microscopy with bright-field, differential interference contrast (DIC), and epifluorescence. They can also be stained by modified acid-fast stain.Typical laboratory analyses include:
Microscopy
Morphologic comparison with other intestinal parasites
Bench aids for Cystoisospora

Prevention
Avoiding food or water that may be contaminated with stool can help prevent the infection of Cystoisospora (Isosporiasis). Good hand-washing, and personal-hygiene practices should be used as well. One should wash their hands with soap and warm water after using the toilet, changing diapers, and before handling food (CDC.gov). It is also important to teach children the importance of washing their hands, and how to properly wash their hands. Treatment
The treatment of choice is trimethoprim-sulfamethoxazole (Bactrim).
About 80% of lithium ingested appears to affect the proximal tubules by entering the collecting tubule cells through sodium channels, accumulating and interfering with the normal response to antidiuretic hormone in a mechanism that is not yet fully understood. High blood calcium causes natriuresis (increased sodium loss in the urine) and water diuresis, in part by its effect through the calcium-sensing receptor. Osmotic
Other causes of acquired nephrogenic diabetes insipidus include hypokalemia (low blood potassium), post-obstructive polyuria, sickle cell disease or trait, amyloidosis, Sjögren syndrome, renal cystic disease, Bartter syndrome, and various medications (amphotericin B, orlistat, ifosfamide, ofloxacin, cidofovir, vaptans).In addition to kidney and systemic disorders, nephrogenic diabetes insipidus can present itself as a side effect of some medications. The most common and well known of these medications is lithium, although there are many other medications that cause this effect with lesser frequency. Hereditary
This form of diabetes insipidus can also be hereditary due to defects in the following genes:

Diagnosis
Differential diagnosis includes nephrogenic diabetes insipidus, neurogenic/central diabetes insipidus and psychogenic polydipsia. They may be differentiated by using the water deprivation test. Recently, lab assays for antidiuretic hormone are available and can aid in diagnosis. If able to rehydrate properly, sodium concentration should be nearer to the maximum of the normal range.