The oocysts, which inhabit water sources, are known for their toughness and can be found in a wide range of water conditions from clean drinking water to contaminated waste water and to saltwater (Castro-Hermida et al., 2010).Oocysts generally remain viable in a temperature range of 4-22˚C. Oocysts can, however, remain viable for up to 12 weeks when kept at 25˚C.At warmer temperatures, they tend to degrade more rapidly as their protective proteins become denatured.When inside of the human body, the life stages are subject to mildly acidic pH levels and warm temperatures of the small intestine and colon.Oocysts are found to grow in the ileocecal adenocarcinoma cell line.Sporozoites attach the epithelial tissue and are enveloped by the intestinal microvilli, making them intracellular, but unexposed to the cell cytoplasm(Carey et al., 2004).
In general, Cryptosporidium species are identified by their hosts, however there are exceptions.Cryptosporidium hominis and Cryptosporidium parvum are responsible for more than 90% of Cryptosporidium infection in humans (Xiao & Feng, 2008).However, while C. hominis is usually found exclusively in humans, C. parvum is zoonotic, and is known to infect 152 species of mammals, most commonly cows (Carey et al., 2004).
Because it is morphologically indistinguishable from C. parvum, C. hominis was once considered to be of the same species. Recent molecular advancements have proven otherwise. The Cryptosproidium hominis species has eight chromosomes containing 9.16 million bases.The genome of C. parvum is made up of 9.11 million bases.Exons make up 6.29 million bases in C. hominis and 6.8 million bases in C. parvum, producing 3,994 and 3,952 genes respectively.Both species possess 45 tRNA genes and 6 5S RNA genes (Xu et al., 2004).
There is currently no vaccine or curative treatment for Cryptosporidiosis.Treatment is based largely on keeping the patient comfortable and hydrated.Because of this fact, prevention of infection is the only truly effective management of the parasite (Carey et al., 2004).
Due to its usual transmission to humans via water, management of Cryptosporidium hominis is focused on inactivating oocysts through chemical, mechanical, and temperature treatment of water sources.Coagulation/flocculation involves treating water samples with coagulant pretreatment and flocculation to produce clumps of colloids and agglomerates to be filtered out more easily.Conventional filters are inefficient for removal of oocysts due to their small size, but reverse-osmosis filters and micro- and ultrafiltration serve to efficiently remove oocysts from the water system (Suunotel et al., 2006).Temperature changes have also proven to be effective in inactivation.Freezing at -72ºC for 1 minute or 10-20 minutes at -45ºC can inactivate oocysts (Carey et al., 2004).
Chemical treatments have shown variable results.While chlorine is generally ineffective, ozone has proven to be moderately effective due to its release of free radicals that damage the parasite’s DNA (Carey et al., 2004).
Proper hygiene is also necessary to prevent transfer by contaminated food.Thorough produce and hand washing before and after handling potentially contaminated food is a strong defense against infection.
The oocyst measures 4.4-4.5μm in length and 4.4-5.9μm in width.It is remarkably similar to its sister species, Cryptosporidium parvum, that also measures the same.Thick-walled oocysts infect other hosts.Thin-walled oocysts serve to re-infect the same host, releasing more infective sporozoites.Nutrient uptake is due to a feeder organelle that attaches to the host cell cytoplasm.Invasive life stages have special secretory organelles that produce proteins to aid in infection of the cell (Carey et al., 2004).
Presence of Cryptosporidium hominis has been recorded throughout the world (Morgan-Ryan, et al., 2002).Outbreaks have been reported in many different areas, including the United States, England, Japan and other countries worldwide(Xiao & Feng, 2008).While, traditionally, C. parvum has been the primary cause of infection in Europe, C. hominis has seen a significant increase, putting its infection numbers above C. parvum.Cryptosporidium hominis infection is, however, more prevalent in areas such as South America, Australia, and Africa (Chako et al., 2010).Highest incidence occurs in developing countries where poor hygiene practices occur (Putignani & Menichella, 2010).
An endoparasite, Cryptosporidium hominis’ major hosts are humans and monkeys (Caccio et al., 2005).Natural infection has also been recorded in a lamb and a dugong (Carey et al., 2004).It was even found present in number of calves in the UK, USA, Australia, and India, though these associations are extremely rare (Xiao & Feng, 2008).For study purposes, neonatal pigs are often artificially infected, as mice and dogs are immune to the parasite.
Cryptosporidium hominis experiences life stages typical of a coccidian including sexual and asexual stages.Oocysts are found in water sources as well as fecal-contaminated foods.When ingested by the primary definitive host of C. hominis – humans – the oocyst is transported to the gut.The oocyst possesses a parsitophorous vacuole that protects its developing sporozoites, of which each oocyst contains four, from the host immune system.When exposed to trypsin and sodium taurochlorate, the sporozoites emerge from the oocyst and begin to take root in the gut epithelium. After development into trophozoites, they feed on epithelial tissue before undergoing merogony. Merozoites are produced through two different stages of merogony.Type I produces merozoites that reinfect the cell and undergo asexual reproduction.Type II produces merozoites that are released to infect neighboring cells and reproduce sexually. Upon becoming established in new cells, they further develop into micro- or macrogametocytes.Proteins released by these invasive life stages allow them easier entrance into a cell.When macrogametocytes are fertilized, they develop into zygotes which later progress to form an oocyst that is excreted in the feces.(Carey et al., 2004)(Suunotel, et al., 2006).The entire life cycle of C. hominis takes place within 72 hours (Morgan-Ryan, et al., 2002).
Cryptosporidium hominis is well known to cause the illness, Cryptosporidiosis, in humans.It is often acquired through contact with infected water sources where the oocysts can persist for long periods of time in ambient temperatures.Inside the human small intestine, C. hominis colonizes the epithelium, leaching nutrients from the cellsand leading to diarrhea, cramping, dehydration, anemia, and various systemic symptoms, such as joint and eye pain.Cryptosproidium hominis is also transmitted in fecal-contaminated foods.A particular outbreak of Cryptosporidiosis in Copenhagen was related to two contaminated food sources at buffet; carrots and red peppers (Putignani & Menichella, 2010).
A 2007 study done in Colorado, New Mexico, Iowa, and Idaho to determine cases of Cryptosporidiosis among 57 sufferers determined that 51 of the cases were caused by five subtypes of C. hominis, while only 5 victims suffered from infection by C. parvum. The final patient was found to be infected by the horse genotype of Cryptosporidium (Xiao et al., 2009).
Since it was first reported in 1976, human Cryptosporidiosis has been reported in 95 countries (Morgan-Ryan, et al., 2002).Cryptosporidiosis caused by C. hominis is more prevalent in North and South America, while C. parvum is responsible for more cases in Europe (Caccio et al., 2005).
Cryptosporidium hominis, along with Cryptosporidium parvum, is among the medically important Cryptosporidium species.[1] It is an obligate parasite of humans that can colonize the gastrointestinal tract resulting in the gastroenteritis and diarrhea characteristic of cryptosporidiosis. Unlike C. parvum, which has a rather broad host range, C. hominis is almost exclusively a parasite of humans. As a result, C. hominis has a low zoonotic potential compared to C. parvum. It is spread through the fecal-oral route usually by drinking water contaminated with oocyst laden feces.[2] There are many exposure risks that people can encounter in affected areas of the world. Cryptosporidium infections are large contributors of child death and illness in heavily affected areas, yet low importance has been placed on both identifying the species and finding more treatment options outside of nitazoxanide for children and AIDS patients.[3]
Cryptosporidium hominis shares many similar characteristics with C. parvum including identical oocyst morphology and life-cycle. The different cryptosporidium species share nearly identical morphological features, so differentiation is only seen at the molecular level.[4] As a result, C. hominis is most easily differentiated from C. parvum through genetic analysis via time-intensive PCR-restriction fragment length polymorphism or gene sequencing.[5]
The life cycle of Cryptosporidium hominis is similar to that of others of the genus with infective sporozoites from ingested oocysts invading gut epithelium. From there, they undergo merogony and generate merozoites, which escape and can reinvade additional cells and form a secondary meront. The secondary meront then releases secondary merozoites which reinvade and undergo gametogony forming micro and macrogametocytes. The gametocytes can then fuse, forming a zygote, which starts the cycle again.
Though symptoms in most immunocompetent persons will resolve without treatment, nitazoxanide has been approved for treatment of diarrhea resulting from cryptosporidiosis. The effectiveness of nitazoxanide in immunocompromised patients, however, is uncertain and current treatments revolve around boosting the host immune system to aid in symptom resolution.[6] Current avenues for treatment include scanning the Cryptosporidium hominis genome for possible targets for vaccine development.[7]
Cryptosporidium hominis, along with Cryptosporidium parvum, is among the medically important Cryptosporidium species. It is an obligate parasite of humans that can colonize the gastrointestinal tract resulting in the gastroenteritis and diarrhea characteristic of cryptosporidiosis. Unlike C. parvum, which has a rather broad host range, C. hominis is almost exclusively a parasite of humans. As a result, C. hominis has a low zoonotic potential compared to C. parvum. It is spread through the fecal-oral route usually by drinking water contaminated with oocyst laden feces. There are many exposure risks that people can encounter in affected areas of the world. Cryptosporidium infections are large contributors of child death and illness in heavily affected areas, yet low importance has been placed on both identifying the species and finding more treatment options outside of nitazoxanide for children and AIDS patients.
Cryptosporidium hominis, bersama dengan Cryptosporidium parvum, adalah spesies Cryptosporidium yang penting dalam dunia medis.[1] Spesies ini merupakan parasit obligat manusia yang dapat berkoloni di saluran pencernaan dan usus yang menyebabkan gastroenteritis dan diare.
Cryptosporidium hominis, bersama dengan Cryptosporidium parvum, adalah spesies Cryptosporidium yang penting dalam dunia medis. Spesies ini merupakan parasit obligat manusia yang dapat berkoloni di saluran pencernaan dan usus yang menyebabkan gastroenteritis dan diare.