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Coccidiosis of Cattle

By Peter D. Constable, BVSc (Hons), MS, PhD, DACVIM, College of Veterinary Medicine, University of Illinois

Twelve Eimeria spp have been identified in the feces of cattle worldwide, but only three (E zuernii, E bovis, and E auburnensis) are most often associated with clinical disease. The other Eimeria spp have been shown experimentally to be mildly or moderately pathogenic but are not considered important pathogens.

Coccidiosis is commonly a disease of young cattle (1–2 mo to 1 yr) and usually is sporadic during the wet seasons of the year. “Summer coccidiosis” and “winter coccidiosis” in range cattle probably result from severe weather stress and crowding around a limited water source, which concentrates the hosts and parasites within a restricted area. Although particularly severe epidemics have been reported in feedlot cattle during extremely cold weather, cattle confined to feedlots are susceptible to coccidiosis throughout the year. Outbreaks usually occur within the first month of confinement. Cows may contribute to environmental contamination of E bovis oocysts through a periparturient increase in fecal oocyst counts. Time to onset of diarrhea after infection is 16–23 days for E bovis and E zuernii and 3–4 days for E alabamensis; clinical disease due to coccidiosis does not typically occur in the first 3 wk of life. Coccidiosis is therefore not considered part of the neonatal diarrhea complex in calves.

The most typical syndrome of coccidiosis is chronic or subclinical disease in groups of growing animals. Calves may appear unthrifty and have fecal-stained perineal areas. In light infections, cattle appear healthy and oocysts are present in normally formed feces, but feed efficiency is reduced. The most characteristic sign of clinical coccidiosis is watery feces, with little or no blood, and animals show only slight discomfort for a few days. Severe infections are rare. Severely affected cattle develop thin, bloody diarrhea that may continue for >1 wk, or thin feces with streaks or clots of blood, shreds of epithelium, and mucus. They may develop a fever; become anorectic, depressed, and dehydrated; and lose weight. Tenesmus is common because the most severe enteritis is confined to the large intestine, although pathogenic coccidia of cattle can damage the mucosa of the lower small intestine, cecum, and colon. During the acute period, some calves die; others die later from secondary complications (eg, pneumonia). Calves that survive severe illness can lose significant weight that is not quickly regained or can remain permanently stunted. Calves with concurrent enteric infections (eg, Giardia) may be more severely affected than calves with coccidia infections alone. In addition, management factors, such as weather, housing, feeding practices, and how animals are grouped, are important in determining the expression of clinical coccidiosis in cattle.

Nervous signs (eg, muscular tremors, hyperesthesia, clonic-tonic convulsions with ventroflexion of the head and neck, nystagmus) and a high mortality rate (80%–90%) are seen in some calves with acute clinical coccidiosis. Outbreaks of this “nervous form” are seen most commonly during, or after, severely cold weather in midwinter in Canada and the northern USA; there are no reports of the “nervous form” outside this geographic location. Affected calves may die <24 hr after the onset of dysentery and nervous signs, or they may live for several days, commonly in a laterally recumbent position with a mild degree of opisthotonos. Nervous signs have not been reported in experimental clinical coccidiosis in calves, which suggests that the nervous signs may be unrelated to the dysentery or, indeed, even to coccidiosis.

Diagnosis of coccidiosis is by finding oocysts on fecal flotation or direct smear or by the McMaster technique. Quantitative oocyst counts on individual rectal samples from at least five calves in a pen are helpful to confirm coccidiosis as a cause of clinical disease. Differential diagnoses include salmonellosis, bovine viral diarrhea, malnutrition, toxins, or other intestinal parasites.

Coccidiosis is a self-limiting disease, and spontaneous recovery without specific treatment is common when the multiplication stage of the coccidia has passed.

Drugs that can be used for therapy of clinically affected animals include sulfaquinoxaline (6 mg/lb/day for 3–5 days) and amprolium (10 mg/kg/day for 5 days). Sulfaquinoxaline is particularly useful for weaned calves that develop bloody diarrhea after arrival at a feedlot. For prevention, amprolium (5 mg/kg/day for 21 days), decoquinate (22.7 mg/45 kg/day for 28 days) and lasalocid (1 mg/kg/day to a maximum of 360 mg/head/day), or monensin (100–360 mg/head/day) can be used. The major benefits of coccidiostats are through improved feed efficiency and rate of gain.

In an outbreak, clinically affected animals should be isolated and given supportive oral and parenteral fluid therapy as necessary. The population density of the affected pens should be reduced. All feed and water supplies should be high enough off the ground to avoid fecal contamination. Mass medication of the feed and water supplies may be indicated in an attempt to prevent new cases and to minimize the effects of an epidemic. Cattle with coccidiosis and nervous signs should be brought indoors, kept well-bedded and warm, and given fluid therapy orally and parenterally. However, the case fatality rate of calves with coccidiosis and nervous signs is high despite intensive supportive therapy. Parenteral sulfonamide therapy may be indicated to control development of secondary bacterial enteritis or pneumonia, which may be seen in calves with coccidiosis during very cold weather. Corticosteroids are contraindicated, because they increase shedding of oocysts and have induced clinical disease in subclinically infected calves.

Coccidiosis has been difficult to control reliably. Overcrowding of animals should be avoided while they develop an immunity to the coccidial species in the environment. Calving grounds should be well drained and kept as dry as possible. All measures that minimize fecal contamination of hair coats and fleece should be practiced regularly. Feed and water troughs should be high enough to avoid heavy fecal contamination. Control of coccidiosis in feeder calves brought into a crowded feedlot depends on management of population density, presence of appropriate feed bunks, or use of chemotherapeutics, to control the numbers of oocysts ingested by the animals while effective immunity develops.

Coccidiostats are used to control naturally occurring coccidiosis. The ideal coccidiostat suppresses the full development of the life cycle of the coccidia, allows immunity to develop, and does not interfere with production performance. Sulfonamides in the feed at 25–35 mg/kg for ≥15 days are effective to control coccidiosis in calves. Monensin is an effective coccidiostat and growth promotant in calves. Postweaning coccidiosis in beef calves has been controlled using monensin administered via intraluminal continuous-release devices. Lasalocid is related to monensin and is also an effective coccidiostat for ruminants. Mixing lasalocid in the milk replacer of calves beginning at 2–4 days of age is an effective way to control coccidiosis. Lasalocid is also effective as a coccidiostat when fed free-choice in salt at a level of 0.75% of the total salt mixture. A level of 1 mg/kg is the most effective and rapid and is recommended when outbreaks of coccidiosis are imminent. Decoquinate in the feed at 0.5–1 mg/kg suppressed oocyst production in experimentally induced coccidiosis of calves. Decoquinate is most effective in preventing coccidial infections when fed continually in dry feed at 0.5 mg/kg. Monensin, lasalocid, and decoquinate at the manufacturer’s recommended levels are equally effective. Toltrazuril administered at 15 mg/kg as a single oral dose, 14 days after animals are moved into group housing, effectively prevents diarrhea due to coccidiosis. Diclazuril (5 mg/kg) is being investigated as an oral anticoccidial in calves.

Control of infection should include changes in management factors that contribute to development of clinical disease. Inadequate housing and ventilation should be corrected, feeding practices adopted that avoid fecal contamination of feed, calves grouped by size, and an “all-in/all-out” method of calf movement from pen to pen adopted.