Cryptosporidium parvum: Waterborn zoonotic parasite

Cryptosporidium parvum is predominately a parasite of neonate animals. Although exceptions occur, older animals generally develop poor infections, even when unexposed previously to this parasite.

One study has suggested that this may be a 57 kDa antigen found on ileal cells of neonates that binds a 47 kDa ligand at the apical end of sporozoites.

• Location in host

GIT  (gastrointestinal)  tract ,Within a closed compartment of the host cell plasmalemma, (parasitophorous vacuole)

• Transmission

 Infection is caused by ingestion of sporulated oocysts transmitted by the faecal-oral route. In healthy human hosts, the median infective dose is 132 oocysts.

• Genotypes

 Cryptosporidium “parvum”  exists as no less than two distinct species.

• Genotype 1 (or genotype H for human) is now termed Cryptosporidium hominis and is almost exclusively a parasite of humans (with a few minor exceptions).
• Genotype 2 (or genotype C for calf) is considered the traditional Cryptosporidium parvumand occurs in a wide range of animals, including humans. Rarely, both species can be found infecting the same person.

Life cycle

• Begins with ingestion of the sporulatedoocyst, the resistant stage found in the environment.Eachoocyst contains 4 infective stages termed sporozoites, which exit from a suture located along one side of the oocyst.
• The preferred site of infection is the ileum, and sporozoites penetrate individual epithelial cells in this region. Parasites reside on the lumenal surface of the cells, and they were once thought to occur extracellularly
• Multiple fission (=merogony; =schizogony) occurs, resulting in the formation of 8 merozoites within the meront. These meronts are termed Type I meronts and rupture open, releasing free merozoites. Once these merozoites penetrate new cells, they undergo merogony to form additional meronts. Type I merozoites are thought to be capable of recycling indefinitely and, thus, the potential exists for new Type I meronts to arise continuously.
• Type I merozoites are somehow triggered into forming a second type of meront, the Type II meront, which contains only 4 merozoites
• Some Type II merozoites enter cells, enlarge, and form macrogametes (=macrogametocyte). Others undergo multiple fission once inside cells, forming microgametocytes containing 16 non-flagellated microgametes.Microgametes rupture from the microgametocyte and penetrate macrogametes, thus forming a zygote.A resistant oocyst wall is then formed around the zygote (the only diploid stage in the life cycle), meiosis occurs, and 4 sporozoites are formed in the process. Formation of sporozoites is termed sporogony. These oocysts are passed in the feces and into the environment. Each haploid nucleus of the sporozoite contains 8 chromosomes

Autoinfective cycle

• Approximately 20% of the oocysts produced in the gut fail to form an oocyst wall and only a series of membranes surround the developing sporozoites. These “oocysts,” devoid of a wall, are sometimes termed “thin-walled oocysts.“. It is believed that the resulting sporozoites produced from thin-walled oocysts can excyst while still within the gut and infect new cells.
• Thus,  parvum appears to have two autoinfective cycles: the first by continuous recycling of Type Imeronts and the second through sporozoites rupturing from thin-walled oocysts.

Pathology

• Development of Cryptosporidiumoccurs more rapidly than many textbooks imply, and each generation can develop and mature in as little as 12-14 hours. Due to the rapidity of the life cycle, plus the autoinfective cycles, huge numbers of organisms can colonize the intestinal tract in several days.The ileum soon becomes crowded and secondary sites are often infected, such as the duodenum and large intestine.
• In immunosuppressed individuals, parasites can sometimes be found in the stomach, biliary and pancreatic ducts, and respiratory tract.

Clinical Signs

• Diarrhea, weight loss, and abdominal cramping are clinical signs of the disease and in immunosuppressed individuals electrolyte imbalance may occur.
• The prepatent period, which is the interval between infection and the first appearance of oocysts in the feces, is generally 4 days (3 days in heavy infections) in animals infected experimentally. However, in human outbreaks where lower numbers of oocysts are probably ingested, 4-6 days is probably typical.
• Patency, which is the length of time oocysts are shed in the feces, generally lasts 6-18 days (4-10 days of diarrhea) in immunocompetent individuals but may be prolonged in immunosuppressed patients.
• In some individuals, however, specifically young children, the elderly, and immunosuppressed patients, cryptosporidiosis became chronic and life-threatening.

Some individuals shed oocysts but appear asymptomatic

Risk Factor

• People who swim regularly in pools with insufficient sanitation (certain strains of Cryptosporidiumare chlorine-resistant)
• Parents of infected children
• People caring for other people with cryptosporidiosis
• Backpackers, hikers, and campers who drink unfiltered, untreated water
• Petting Farms and open farms with public access
• People, including swimmers, who swallow water from contaminated sources
• People handling infected cattle
• People exposed to human feces

Prevention

• Practice good hygiene
• Purify drinking water
• Limit swimming activity
• Avoid feacal exposure
• Handle new born and domestic animals with care
• Place the birds in cleand farms

Treatment

• Treatment of gastrointestinal infection in humans involves fluid rehydration, electrolyte replacement, and management of any pain.
• Nitazoxanide is the only drug approved for the treatment of cryptosporidiosis in immunocompetent hosts.
• Paromomycin may alleviate some of the diarrhoeal symptoms.
• Continuing antiretroviral drugs for HIV infection to boost the immune system may also control infection.

Control

• Because all Cryptosporidium infections are initiated though ingestion of environmentally resistentoocysts, control of this stage is the single most important factor in limiting the spread of the disease.
• Lengthy exposures to gaseous or aqueous solutions of ammonia, hydrogen peroxide, high concentrations of chlorine and related compounds, and short term exposure to ozone, significantly reduce numbers of viable parvumoocysts but only rarely result in 100% efficacy.
• Perhaps the single most effective and economical method of reducing the numbers of oocysts in the environment is simply dessication.

Authors: Sana Majeed *¹, Aisha Khatoon¹, Zain- Ul- Abidin²,Aneela Amin¹,Ashiq Ali¹,Fatima Yasin³.

¹ Department of Pathology, Faculty of Veterinary Science, University of Agriculture Faisalabad, Pakistan. ² Veterinary Research Institute, Lahore, Pakistan. ³Department of Parasitology Faculty of Veterinary Science, University of Agriculture Faisalabad, Pakistan.

* Corresponding Author Email: sanamajeed243@gmail.com