Cryptosporidium

Morphology

• Cryptosporidium has unique distinction among coccidia , having the smallest oocyst.
• Oocyst have smooth colorless bilayered oocyst wall having ultra structurally faint suture like line.
• Each sporulated oocyst contains four sporozoites lying parallel to one another.
• Oocyst are ovoid or spheroidal, measuring 5×4.5 µm in size.

Note: Invagination: Process of being turned inside out or folded back on itself to form cavity or pouch.

Mode of transmission

• Ingestion of thick-walled oocyst
• Inhalation of oocyst
• Mechanical vectors, arthropods and through fomites

Lifecycle

• Lifecycle is complicated and fascinating
• Infection acquires through ingestion of oocyst contaminating food and drinking water or through inhalation.
• Reach either intestine or respiratory tract of host
• After excystation, they don not invade intestinal wall, instead they stop between layers of cell wall and begin to multiply. Sporozoites forms deep notches gradually invaginating it in glove-like fashion.
• Parasite is enveloped by double unit membrane of host cell entirely enclosing parasite within parasitophorous envelope.
• They undergo schizogony with division of nucleolus of trophozoite resulting two types of schizonts- type I and type II. Type I appears first and contain 6-8 nuclei developing to merozoites.
• Resultant merozoites may develop into another type I schizont or may give rise to type II schizont which possess only four merozoites.
• Some of these merozoites invade new host cells and develop into either type I or type II schizonts while majority of them initiate sexual multiplication.
• Fusion of microgametes with macrogametes results in zygote formation. Each zygote changes to oocyst and initiates sporulation.
• Two types of oocysts are distinguished as thin-walled and thick-walled. Thin-walled oocyst doesn’t leave hosts intestine and initiate new developmental cycle. This mode of infection is called ‘auto-infection’, which is unique among all types of coccidia. Thick-walled oocyst pass out in faeces of the host.
• In case of healthy immune system, body eventually fights off the parasite, intestine heals and symptoms subside. In case of immune compromised host, infection is virtually endless.

Pathogenesis/ Clinical signs

• Calves with cryptosporidiosis usually have mild to moderate diarrhea, that persist for several days. Feces are yellow or pale, watery and contain mucus.
• Abdominal discomfort
• Marked weight loss and emaciation
• Apathy, anorexia and dehydration
• PM lesions include : Mild to moderate villus atrophy, degeneration and sloughing off of enterocytes, crypt hypertrophy and in respiratory form, there may be excessive swollen mucosa and infiltration of inflammatory cells.

Diagnosis

• Detection of oocyst in faeces pf infected animals using Ziehl-Neelsen stain, fecal flotation techniques , ELISA, fluorescent-labelled Ab, immunochromatographic test and PCR.

Treatment and control

• No known treatment against cryptosporidiosis. Deco quinate, Sulphaquinoxaline and halofuginone lactate have been shown therapeutic effect.
• Affected calves should be supported with fluids and electrolytes both orally and parenterally, until recovery.
• Disease is difficult to control. Calves should be born in clean environment and adequate amounts of colostrum should be fed at an early stage.
• Calves should be kept separate without contact fed at least 2 weeks of life with strict hygiene at breeding.
• Diarrhoeic calves should be isolated from healthy calves during course of diarrhea and ensure that no mechanical transmission takes place.