Bovine Coccidiosis

Bovine Coccidiosis: Etiology, Life Cycle, Pathogenesis, Clinical Signs, Diagnosis & Treatment

Bovine coccidiosis is an important protozoan disease of cattle caused by several species of Eimeria, particularly Eimeria bovis and Eimeria zuernii. The disease primarily affects young calves and is characterized by enteritis, diarrhea, dehydration, poor weight gain, and, in severe cases, dysentery and death. Transmission occurs through ingestion of sporulated oocysts contaminating feed, water, or the environment. Overcrowding, poor sanitation, and intensive management practices increase the risk of infection. This article covers the etiology, life cycle, pathogenesis, clinical signs, diagnosis, treatment, and control of bovine coccidiosis, along with the morphology and biological characteristics of the major pathogenic Eimeria species.

Bovine coccidiosis is primarily a disease of young animals. Calves between 3 weeks and 6 months of age are commonly affected, although older calves and adult animals may also be affected; however, they are usually symptomless carriers. Factors such as overcrowding and poor sanitation greatly increase the incidence of the disease.

Severe outbreaks of coccidiosis occur on farms with large numbers of calves, especially under intensive rearing systems. There are 13 species of Eimeria affecting cattle, of which E. zuernii and E. bovis are the most important and pathogenic species.

Etiology

Bovine coccidiosis is caused by protozoan parasites of the genus Eimeria. More than 13 Eimeria species infect cattle, but Eimeria bovis and Eimeria zuernii are the most pathogenic and are responsible for the majority of clinical cases in calves.

Eimeria zuernii (Winter Coccidiosis)

Among the Eimeria species infecting cattle, Eimeria zuernii and Eimeria bovis are the two most pathogenic species and are responsible for most clinical cases of bovine coccidiosis.

• Location: Small intestine and large intestine (cecum, colon, and rectum)
• Disease: “Winter Coccidiosis” in calves

Morphology of Oocyst

• Oocysts are subspherical, subovoid, ovoid, or sometimes ellipsoidal, measuring 12–29 × 10–21 µm.
• The oocyst wall is smooth, colorless, and consists of a single layer.
• No micropyle.
• No residuum.
• A polar granule may be present or absent.
• The sporocysts are ovoid with a tiny Stieda body.
• The sporozoites are elongate.
• Sporulation time: 2–10 days.

Life Cycle

The life cycle of E. zuernii is similar to the general life cycle pattern of Eimeria spp., but the prepatent period is 15–17 days.

In this species, the development of different stages occurs at different locations, as follows:

• The first-generation schizonts develop in the lamina propria of the lower ileum within 14–16 days.
• The second-generation schizonts are found in the cecum and proximal colon.
• Macrogamonts and microgamonts are found in the epithelial cells of the small and large intestines after 16 days of infection.
• Prepatent period: 15–17 days.

Pathogenesis and Clinical Signs

E. zuernii is the most pathogenic Eimeria species affecting cattle. The disease may occur in either an acute or chronic form. The acute form is characterized by hemorrhagic diarrhea with marked tenesmus. In severe cases, frank blood may be present in the feces. Consequently, the hindquarters of affected animals may appear as though they have been smeared with red paint. Affected animals become anemic, weak, and emaciated, and may exhibit straining and coughing simultaneously. This may result in diarrheic feces being expelled up to 2–3 meters.

In severe infections, death may occur as early as seven days after the onset of clinical signs. If the calf survives for 7–10 days after the onset of infection, recovery usually follows. E. zuernii may also cause a chronic form of the disease, characterized by diarrhea with little or no blood in the feces. Affected animals become dehydrated, emaciated, weak, and listless, with drooping ears and sunken eyes.

Postmortem Lesions

• Generalized catarrhal enteritis involving both the small and large intestines.
• The cecum and colon are filled with semifluid hemorrhagic material or even frank blood containing fibrinous clots.
• The intestinal epithelium is eroded, leaving large denuded areas infiltrated with lymphocytes and leukocytes.
• Diffuse hemorrhage is observed in acute cases, whereas petechial hemorrhages are seen in the chronic form.

Immunity

Recovered animals develop resistance to reinfection, although the immunity is not complete.

Eimeria bovis

Eimeria bovis affects the small intestine during schizogony and the terminal ileum, cecum, and colon during gametogony.

Oocyst Morphology

• Ovoid in shape with a blunt, narrow end.
• The oocyst wall is smooth and consists of two layers.
• Micropyle inconspicuous.
• No residuum or polar granule.
• The sporocyst is ellipsoidal with an inconspicuous Stieda body and residuum.
• Sporozoites have clear globules at each end.
• Sporulation time: 2–3 days.

Life Cycle

The life cycle of E. bovis is similar to the general life cycle pattern of Eimeria spp., but the prepatent period is 16–21 days.

The development of different stages is as follows:

The first-generation schizonts develop in the endothelial cells of the lacteals within the villi of the posterior small intestine. They mature 14–18 days after infection, measure approximately 207 × 435 µm, and produce 5,000–17,000 merozoites.

These merozoites are visible to the naked eye as whitish bodies. The second-generation schizonts are found in the epithelial cells of the cecum and colon, measure approximately 10 × 9 µm, and produce 30–36 merozoites. The sexual stages occur only in the cecum and colon. The prepatent period is 16–21 days.

Pathogenesis and Clinical Signs

E. bovis is the second most pathogenic Eimeria species affecting cattle, after E. zuernii. It causes severe disease characterized by bloody diarrhea (dysentery) with marked tenesmus, a rise in body temperature approximately 18 days after infection, and death in severe cases.

Severe pathological changes occur in the cecum, colon, and terminal ileum due to the development of gamonts in these locations. Initially, the intestinal mucosa becomes congested, edematous, thickened, and shows petechial or diffuse hemorrhages. In addition, the intestinal lumen contains a large amount of blood.

At a later stage, the intestinal mucosa becomes destroyed and sloughs off, following which a patchy or continuous membrane forms over the affected surface.

Diagnosis

• History
• Clinical signs
• Gross lesions at necropsy
• Microscopic examination of intestinal scrapings for developmental stages
• Fecal examination; however, in acute infections, oocysts may not be detected.

Differential Diagnosis

Bovine coccidiosis should be differentiated from intestinal anthrax.

Treatment

• Amprolium: 20–25 mg/kg in feed for 4–5 days.
• Lincomycin HCl: 1 g/calf in drinking water for 21 days.
• Sulfonamides: 150 mg/kg orally.
• Monensin: 16.5 g/ton of feed for 3–31 days.
• Lasalocid: 3 mg/kg body weight in feed.

Control

• Maintain a high standard of sanitation on the farm.
• Treat infected animals promptly.
• Avoid overcrowding, and keep calves separated from adult animals.
• Keep the floor dry at all times.
• Burn contaminated bedding materials.
• Dispose of manure regularly.
• Keep feeders and waterers elevated to prevent contamination of feed and water with feces.