The genus Cryptosporidium is a minute coccidian parasite of worldwide distribution that comprises a very large group of closely related obligate intracellular parasites. It was first observed in the gastric mucosal crypts of a laboratory mouse in 1907 by Tyzzer. It was recognized in 1976 as an important pathogen causing diarrhea in animals, and the first case of human infection was reported in 1976. It has also been reported to cause intractable diarrhea in AIDS patients, a leading cause of acute self-limiting diarrhea in previously healthy people, and chronic life-threatening diarrhea in immunocompromised individuals. Most Cryptosporidium species have a broad host range. Each species has been reported to infect humans on a regular basis. This includes Cryptosporidium parvum, Cryptosporidium hominis, Cryptosporidium meleagridis, Cryptosporidium felis, Cryptosporidium canis, Cryptosporidium muris, and lastly, Cryptosporidium pig and deer species. Most human infections are caused by Cryptosporidium parvum and Cryptosporidium hominis, which also affect animals like sheep, cattle, birds, rodents, and non-human primates. The parasite does not appear to be host-specific, and infection can spread from one host species to another. The parasite completes its life cycle, including sexual and asexual phases, in a single host (monoxenous). All cryptosporidiosis is transmitted through fecally contaminated food and water. Diagnosis can be made by microscopic identification of acid-fast-stained oocysts in a stool sample. It can also be diagnosed using stool antigen testing, polymerase chain reaction testing (PCR), or multiplex nucleic acid amplification testing (NAAT). Numerous experiments to treat Cryptosporidium using a wide variety of medications have been conducted. Spiramycin has been preliminary proven to be helpful. Treatment is also based on the features of the infected host. In immunologically healthy children, nitazoxanide with supportive care such as oral rehydration solution. There have been several clinical trials with rifamycins, azalides, and paromomycin. Prevention is through proper treatment of water supplies, handling known infected material by using gloves and wearing a gown, proper hand washing, and properly disinfecting potentially infected equipment.

Through this article, you’ll be able to answer the following questions:

• What are the diseases of Cryptosporidium parvum?
• What parasite is Cryptosporidium parvum?
• What is the most common cause of Cryptosporidium?
• Does metronidazole treat Cryptosporidium?
• What is the treatment for Cryptosporidium?
• How do you diagnose cryptosporidiosis?
• How is cryptosporidiosis transmitted?
• What is the infective stage of cryptosporidiosis?
• life cycle Cryptosporidium parvum

Classification of Cryptosporidium parvum

Morphology of Cryptosporidium parvum

Oocysts

• The oocysts are roundish in shape, measuring only 4-6µm.
• It is often confused with yeast cells.
• The mature oocyst consists of four small sporozoites, although they are not always visible.
• It has a thick, double-layered wall that protects the oocyst from environmental stresses. No spores are visible, but darkly stained granules may be present.

Schizonts and Gametocytes of Cryptosporidium parvum

• Other morphologic forms required to complete the Cryptosporidium life cycle include the schizonts, which contain four to eight merozoites, microgametocytes, and macrogametocytes.
• The average size of these morphological forms is 2 to 4µm.
• These morphological forms are not routinely seen in patient samples.

Life Cycle of Cryptosporidium parvum

• Infection begins when the host ingests thick-walled, sporulated oocysts, each of which contains four banana-shaped sporozoites.
• A minimum of 30 oocysts are necessary to initiate infection. An infected individual may release as many as a billion cysts during one infection.
• The sporozoites excyst when the oocyst enters the small intestine.
• A protein plug in the cyst wall blocks the escape route for sporozoites.
• Sporozoites attach to the surface of epithelial cells, most likely aided by numerous proteins secreted from their rhoptries and micronemes.
• After the sporozoite attaches to the cell surface, most likely mediated by thrombospondins and related adhesive proteins, microvilli in the area immediately adjacent to the parasite fuse and elongate, enveloping the parasite to create a unique intracellular environment.
• A specialized membrane structure develops at the interface between the parasite and the host cell.
• The parasite then induces alterations in the gene expression of the invaded host cell, eliciting the upregulation of osteoprotegerin, a TNF family member known to inhibit apoptosis.
• Such a strategy would favor the long-term survival of the parasite until it was able to complete its development to the next stage in its life cycle.
• The sporozoite differentiates into the type I meront, and division ensues, producing four haploid merozoites.
• The merozoites are released and attach to new epithelial cells, now differentiating into Type II meronts.
• Macrogamonts and microgamonts (pre-sex cells analogous to the gametocytes of plasmodia) are produced inside these new meronts.
• Following their release, microgamonts fuse with macrogamonts, forming thick-walled zygotes termed oocysts.
• This stage sporulates within the large intestine, and four haploid infectious sporozoites are produced.
• Oocysts can also be thin-walled. In this case, they sporulate and excyst within the same host, producing an autoinfection that may endure for months or years.
• Even in these cases, thick-walled oocysts are produced as well. Thick-walled oocysts pass out in feces and can infect another host.
• This type of oocyst is environmentally resistant and can remain viable for months to years in soil, given optimum moisture conditions.

Life Cycle of Cryptosporidium parvum

Cellular and Molecular Pathogenesis of Cryptosporidium parvum

• The lack of response to a wide range of medications is one of the most frustrating and perplexing characteristics of Cryptosporidium parvum. The reason for this is the impermeability of the altered microvillus-derived membrane complex surrounding the parasite to many chemotherapeutic agents.
• The pathogenesis of Cryptosporidium parvum and its secretory diarrhea are still being fully understood, but this is changing as the genome is now completely sequenced.
• Now that more than 25 potential virulence-causing factors have been identified, researchers are examining how each of these factors specifically contributes to damage and diarrhea.
• Excystation, adhesion and locomotion, invasion, intracellular multiplication and survival, and host cell damage all appear to be mediated by specific virulence factors.
• Hemolysins, proteases, and phospholipases are a few examples of the elements that might directly harm host cells.
• Proinflammatory cytokines like IL-8 may also be involved, in addition to microbial virulence factors.
• Individuals with healthy immune systems develop protection against the initial infection.
• Although the exact mechanisms causing the parasite to be removed from the gastrointestinal tract have not yet been identified, at least two classes of antibodies, IgA and IgG, as well as several cellular-based immune mechanisms, are thought to play important roles.
• The number of oocysts needed to cause infection in healthy human volunteers who had already developed anti-C. parvum IgG levels (exposed, immune) was higher, and these volunteers showed fewer symptoms than their non-exposed (non-immune) counterparts.
• Additionally, it has been noted that patients with recurrent infections in areas where Cryptosporidium parvum is endemic exhibit milder symptoms.
• Although AIDS patients may produce an antibody response that can be detected in their intestinal and serum secretions, this does not help them get rid of the infection.
• Many HIV-positive children who later developed AIDS are dying from this opportunistic infection in underdeveloped tropical areas.

Clinical Disease (Signs, symptoms, causes)

• As was previously mentioned, an infection is typically brought on by consuming contaminated water, coming into contact with an infected person or animal, eating tainted food, or, in rare cases, inhaling an aerosol.
• In immunocompetent people, disease can range from an infection with symptoms to mild or severe watery diarrhea.
• The acute stage of the infection is frequently characterized by upper abdominal cramps, anorexia, nausea, weight loss, and vomiting.
• It doesn’t seem that exposure intensity and disease severity are related.
• A second infecting dose of oocysts may be asymptomatic in people who have already developed clinical disease and recovered from it, or they may only experience mild, temporary diarrhea.
• In an immunocompetent host, cryptosporidiosis is self-limited and lasts for 2 weeks, though it can last longer in some people.
• In some people, diarrhea can be severe, resulting in several liters of diarrhea per day or even persistent diarrhea that affects growth and nutrition.
• Because the diarrhea lasts longer and there is typically some weight loss, children are the group that is most severely affected.
• Sadly, thanks to the development of molecular testing, it is now known that one of the top four causes of diarrhea in children under the age of five is cryptosporidiosis.
• Those receiving cancer chemotherapy experience even worse side effects, including prolonged, potentially fatal diarrhea and significant weight loss.
• In patients with AIDS, cryptosporidiosis is a chronic condition that can last for months or even years. During this time, patients can lose more than three liters of fluid per day and are in grave danger of passing away; the case fatality rate can be as high as
• Associated conditions like malnutrition or super infection with other pathogens are frequently the cause of death.
• Acalculous biliary disease can be brought on by an extraintestinal infection in the bile duct.

Diagnosis of Cryptosporidium parvum

• Diagnosis can be made by identifying acid-fast-stained oocysts in a stool microscopic examination. By flotation in a sugar solution, oocysts can be isolated from stool and stained using acid-fast methods. By cold Ziehl-Neelsen technique, the internal structures appear acid fast
• With Jenner-Giemsa stain, the oocysts in faeces smears appear as blue spherical bodies containing a few eosinophilic granules.
• Fluorescent staining with auramine phenol has been reported to be a useful technique.
• Definitive identification can be made by indirect immunofluorescence using specific antibody. In acute diarrhoea, the oocysts are abundant, but when they are scanty, concentration by the formol-either technique may be employed.
• Stool antigen testing (ELISA): monoclonal antibody antigen tests have high sensitivity, are simple to perform, and can be used on both feces and tissue specimens.
• Multiplex nucleic acid amplification testing (NAAT) or directed polymerase chain reaction (PCR). In outbreaks and epidemiological investigations, PCR testing is highly sensitive and can identify specific genotypes.

Treatment

• No specific treatment is available. The disease spontaneously cures in people with normal immune responses.
• Cryptosporidiosis treatment is based on characteristics of the infected host.
• Based on studies demonstrating early clinical improvement, earlier resolution of diarrhea, and improved elimination of oocyst shedding in immunologically healthy children, nitazoxanide is the drug of choice.
• HIV-1-infected patients should be started on highly active antiretroviral therapy (HAART) to rebuild their immune systems.
• All patients should receive supportive care, including oral rehydration when possible and intravenous therapy if necessary.
• Several clinical trials with rifamycins, azalides, and paromomycin have shown no clear benefit, demonstrating the difficulty of treating acute or established disease.

Prevention and Control

• Proper water treatment
• Handling known infected material with gloves and a gown (when appropriate)
• Proper hand washing and disinfecting potentially infected equipment with full-strength commercial bleach or 5% to 10% household ammonia are critical to Cryptosporidium prevention and control.
• Additionally, enteric precautions should be observed when working with known infected individuals.

Conclusion

In conclusion, Cryptosporidium parvum is a parasitic protozoan that can cause severe gastrointestinal illness in humans. It is transmitted through the ingestion of contaminated water or food, and can also be spread through direct contact with infected individuals or animals. Therefore, it is important to practice good hygiene and ensure the safety of water sources and food supplies to prevent the spread of Cryptosporidium parvum infections.

Additionally, individuals with weakened immune systems, such as those with HIV/AIDS or undergoing chemotherapy, are particularly vulnerable to severe complications from Cryptosporidium parvum infections. These individuals should take extra precautions to avoid exposure, such as filtering their water and thoroughly cooking their food. By following these preventative measures, we can greatly reduce the incidence of Cryptosporidium parvum infections and protect the health of ourselves and others. In addition to individuals with weakened immune systems, young children and the elderly are also at a higher risk of developing severe complications from Cryptosporidium parvum infections. It is crucial for caregivers and healthcare providers to be aware of this vulnerability and take necessary precautions. Proper hygiene practices, such as frequent handwashing and disinfecting surfaces, can also help prevent the spread of this parasite. By prioritizing these preventative measures, we can collectively work towards minimizing the impact of Cryptosporidium parvum infections on public health.

References

• Laberge, I.; Griffiths, M. W., Prevalence, detection and control of Cryptosporidium parvum in food. International journal of food microbiology 1996, 32 (1-2), 1-26.
• Katsumata, T.; Hosea, D.; Ranuh, I. G.; Uga, S.; Yanagi, T.; Kohno, S., Short report: possible Cryptosporidium muris infection in humans. The American journal of tropical medicine and hygiene 2000, 62 (1), 70-2
• Burgner, D.; Pikos, N.; Eagles, G.; McCarthy, A.; Stevens, M., Epidemiology of Cryptosporidium parvum in symptomatic paediatric oncology patients. Journal of paediatrics and child health 1999, 35 (3), 300-2.
• Rossignol, J. F.; Ayoub, A.; Ayers, M. S., Treatment of diarrhea caused by Cryptosporidium parvum: a prospective randomized, double-blind, placebo-controlled study of Nitazoxanide. J Infect Dis 2001, 184 (1), 103-6.
• Tate, K. W.; Pereira, M. D. G. C.; Atwill, E. R., Efficacy of vegetated buffer strips for retaining Cryptosporidium parvum. Journal of environmental quality 2004, 33 (6), 2243-51
• Parasitology for Medical and Clinical Laboratory Professionals by Ridley, John W. Ridley (z-lib.org).pdf
• Textbook of Medical Parasitology © 2007, CK Jayaram Paniker