Coccidiosis

Introduction: Coccidiosis in cattle is caused by a protozoal parasite, mainly Eimeria spp., and is a disease of management in production operations. This disease is especially a problem in confinement/housing operations where infective oocysts of the parasite can accumulate. It is common in young animals at particular times of the year which may reflect the stress of weaning, decreased antibody levels, or the stress of crowded conditions. While most infections are self limiting, the loss of production time in a lamb or calf crop can be devastating economically, thus control measures are warranted. The infection rate is high, but the rate of clinical disease is low, although outbreaks can occur.

An Eimeria oocyst that has not yet sporulated.

Pathophysiology: Oocysts shed in the feces of adults or infected cohorts are ingested by naive animals early in life. The severity of the disease depends on the number of oocysts ingested. In most cases, the infection involves low numbers of parasites, and damage to the gut is minimal. However, if a large enough infective dose is consumed, clinical disease can be very severe. The prepatent period (the time from ingestion of oocyst to production of oocysts in the feces) for Eimeria is 21 days, therefore this is not a disease of newborn calves.

In order to understand how this parasite causes its damage, it is important to understand its complex life cycle.

Sporulated oocysts are ingested and pass through all stages of their life cycle in the alimentary mucosa. Different species localize in different parts of the intestine.

Once ingested, the sporulated oocysts release sporozoites into the gastrointestinal tract. (Click here for a movie of a sporozoite exiting the oocyst)

These sporozoites enter into the enterocytes, undergo asexual reproduction forming clusters of merozoites called schizonts. (Follow this link to see a histopathology slide of schizonts).

The schizonts rupture to release the merozoites back into the lumen of the gut. This release causes destruction of intestinal cells. It is this destruction of the enterocytes by the merozoites which is responsible for the clinical signs associated with this disease.

The merozoites mature and enter into other intestinal cells to propagate asexually. Asexual reproduction is self-limiting and ceases after several generations.

Eventually, these merozoites will form macro- and microgametocytes and reproduce sexually. The result of the sexual stage of reproduction is production of oocysts which are shed into the feces.

The oocysts complete development and become infective (sporulate) outside the host's body.

The life cycle of Eimeria spp. is the same as the life cycle for Cryptosporidium parvum. Click here for a diagram illustrating this life cycle (the diagram is the bottom choice on the page).

A high infective dose of oocysts can lead to severe destruction of the intestinal mucosa, causing a malabsorptive diarrhea. The diarrhea is characterized by fibrin casts, mucus, and blood. Less severe cases may only be clinically evident by mild diarrhea and decreased average daily gain. The chronic cases may be complicated by low immune response and secondary infections with the bovine respiratory disease complex.

Questions For Your Consideration...

Based on your understanding of the life cycle, is it possible that an animal could exhibit signs of clinical coccidiosis and not be shedding oocysts in its feces?

Based on your understanding of the disease, could an animal be infected and shedding oocysts without exhibiting clinical signs?

How would you confirm that the clinical signs were caused by coccidiosis?

Signalment: Calves, kids, and lambs greater than 21days of age.

Young dairy calves

A young goat kid

A newborn lamb

Clinical Signs: Clinical signs of coccidiosis include dehydration, decreased appetite, +/- mild fever, unthrifty appearance, profuse diarrhea with mucous, blood, fibrin casts, and diptheritic membranes. Large bowel diarrhea signs include tenesmus which can lead to rectal prolapse. In kids and lambs there is a chronic syndrome characterized by animals that are "poor doers." In severe cases, scarring of the epithelium may lead to chronic malabsorptive diarrhea.

Clinical Pathology: Eimeria may be positively identified on fecal flotation, however positive identification depends on the stage of the life cycle the parasite is exhibiting. If the animal has just become infected, it is possible that the animal will show clinical signs, but will not yet be shedding oocysts. Also, a baseline level of shedding should be expected in most herds, thus positive identification of oocysts should be interpreted carefully. Low numbers of oocysts present on fecal floatation may indicate subclinical infection, while high oocyst findings are most commonly reported in animals with significant clinical signs. If a CBC is performed, anemia or hemoconcentration due to dehydration may be seen.

Gross Pathology: Hemorrhagic enteritis and acute to chronic inflammatory bowel disease is noted on necropsy. The severity of the lesions will depend on the number of organisms ingested.

	Coccidiosis: Multiple nodules in the small intestine due to Eimeria spp. schizonts. Bristol BioMedical Image Archive, University of Bristol
	Rectum: haemorrhagic proctitis due to Eimeria zuernii (coccidiosis). Bristol BioMedical Image Archive, University of Bristol
	Coccidiosis: Small intestine of a goat. Bristol BioMedical Image Archive, University of Bristol

Histopathology: Villous blunting is common and organisms will be evident in H & E stained preparations of the large intestine. In heavy infections, the destruction of enterocytes and resulting inflammation can be extensive.

Diagnosis: The common methods used to diagnose coccidiosis include fecal floatation and fecal smear.