[6] On January 8, 2025, a group of scientists from the Cryptosporidiosis Therapeutics Advocacy Group (CTAG) released an article in the newsletter Global Health NOW advocating for Cryptosporidiosis to be raised to the status of Neglected Tropical Disease (NTD) by the World Health Organization (WHO).
[11][12] In immunocompetent individuals, cryptosporidiosis is primarily localized to the distal small intestine and sometimes the respiratory tract as well.
[2][9] In immunocompromised persons, cryptosporidiosis may disseminate to other organs, including the hepatobiliary system, pancreas, upper gastrointestinal tract, and urinary bladder;[2][9] pancreatic and biliary infection can involve acalculous cholecystitis, sclerosing cholangitis, papillary stenosis, or pancreatitis.
Other apicomplexan pathogens include the malaria parasite Plasmodium, and Toxoplasma, the causative agent of toxoplasmosis.
[2][14] The pattern of Cryptosporidium life cycle fits well with that of other intestinal homogeneous coccidian genera of the suborder Eimeriina: macro- and microgamonts develop independently; a microgamont gives rise to numerous male gametes; and oocysts serving for parasites' spreading in the environment.
Electron microscopic studies made from the 1970s have shown the intracellular, although extracytoplasmic localization of Cryptosporidium species.
Other potential sources include insufficiently treated water supplies, contaminated food, or exposure to feces.
[3] The high resistance of Cryptosporidium oocysts to disinfectants such as chlorine bleach enables them to survive for long periods and still remain infective.
[20] The following groups have an elevated risk of being exposed to Cryptosporidium:[3] Cases of cryptosporidiosis can occur even in cities that have a properly de-contaminated water supply.
[25] 20% of oocysts have thin walls and so can reinfect the host by rupturing and releasing sporozoites that start the process over again.
[24] Part of the small intestine can be stained with hematoxylin and eosin (H & E), which will show oocysts attached to the epithelial cells.
Real-time monitoring technology is now able to detect Cryptosporidium with online systems, unlike the spot and batch testing methods used in the past.
[37][38] In the US the law requires doctors and labs to report cases of cryptosporidiosis to local or state health departments.
They should wait until at least two weeks after diarrhea stops before entering public water sources, since oocysts can still be shed for a while.
[1] The US CDC notes the recommendation of many public health departments to soak contaminated surfaces for 20 minutes with a 3% hydrogen peroxide[clarification needed] (99% kill rate) and then rinse them thoroughly, with the caveat that no disinfectant is guaranteed to be completely effective against Cryptosporidium.
[40] Symptomatic treatment primarily involves fluid rehydration, electrolyte replacement (sodium, potassium, bicarbonate, and glucose), and antimotility agents (e.g., loperamide).
Immunocompetent individuals with cryptosporidiosis typically experience a short (i.e., duration of less than 2 weeks) self-limiting course of diarrhea that may require symptomatic treatment and ends with spontaneous recovery; in some circumstances, antiparasitic medication may be required (e.g., recurrent, severe, or persistent symptoms);[11] however reinfection frequently occurs.
[41] In immunocompromised individuals, such as AIDS patients, cryptosporidiosis resolves slowly or not at all, and frequently causes a particularly severe and persistent form of watery diarrhea coupled with a greatly decreased ability to absorb key nutrients through the intestinal tract.
As a result, infected individuals may experience severe dehydration, electrolyte imbalances, malnutrition, wasting, and potentially death.
[44] The best treatment approach is to improve the immune status in immunodeficient individuals using highly active antiretroviral therapy that includes an HIV protease inhibitor along with continued use of antiparasitic medication.
[41] A Cochrane Collaboration review recommended that nitazoxanide be considered for use in treatment despite its reduced effectiveness in immunocompromised individuals.
For example, synthetic isoflavone derivates have been shown to fight off Cryptosporidium parvum both in vitro and in animal studies.
[28][48] In Eastern Europe cryptosporidiosis in humans and animals is common, but there are considerable gaps in surveillance and a lack of comparable methods which limit the understanding of the disease and detection of outbreaks.
[49][50] Roughly 30% of adults in the United States are seropositive for cryptosporidiosis, meaning that they contracted the infection at some point in their lives.
Human Cryptosporidium parvum infections are particularly prevalent and often fatal in infants in developing countries and to immunocompromised people, such as AIDS patients.
There is no commercially available effective vaccine against Cryptosporidium parvum, although passive immunization utilizing different zoite surface (glyco)proteins has shown promise.
Developmental stages of the life cycle of the parasite might act as possible targets for vaccine development.
The organism is detected in 65–97% of the surface-water supply in the United States and is resistant to most disinfectants used for the treatment of drinking water.
Antibodies in the serum of humans and animals infected with Cryptosporidium parvum react with several antigens, one of which is a 15 kDaTooltip kilodalton protein (CP15) located on the surface of the organism.
This protein is a good candidate for use as a molecular vaccine because previous studies have shown that a monoclonal antibody to CP15 confers passive immunity to mice.