Coccidiosis is a usually acute invasion and destruction of intestinal mucosa by protozoa of the genera Eimeria or Isospora. Clinical signs include diarrhea, fever, inappetence, weight loss, emaciation, and in extreme cases, death. However, many infections are subclinical. Coccidiosis is an economically important disease of cattle, sheep, goats, pigs, poultry (see Coccidiosis), and also rabbits, in which the liver as well as the intestine can be affected (see Coccidiosis). In dogs, cats, and horses, coccidiosis is less often diagnosed but can result in clinical illness. Other genera, of both hosts and protozoa, can be involved (see Cryptosporidiosis, see Sarcocystosis, and see Toxoplasmosis).
Etiology and Epidemiology
Eimeria and Isospora typically require only one host in which to complete their life cycles. Some species of Isospora have facultative intermediate (paratenic or transfer) hosts and a new genus name, Cystoisospora, has been proposed for these species of Isospora. Coccidia are host-specific, and there is no cross-immunity between species of coccidia.
Coccidiosis is seen universally, most commonly in young animals housed or confined in small areas contaminated with oocysts. Coccidia are opportunistic pathogens; if pathogenic, their virulence may be influenced by various stressors. Therefore, clinical coccidiosis is most prevalent under conditions of poor nutrition, poor sanitation, or overcrowding, or after the stresses of weaning, shipping, sudden changes of feed, or severe weather.
In general, for most species of farm animals, the infection rate is high and rate of clinical disease is low (5–10%), although up to 80% of animals in a high-risk group may show clinical signs. Most animals acquire Eimeria or Isospora infections of varying severity when between 1 mo and 1 yr old. Older animals usually are resistant to clinical disease but may have sporadic inapparent infections. Clinically healthy, mature animals can be sources of infection to young, susceptible animals.
Infection results from ingestion of infective oocysts. Oocysts enter the environment in the feces of an infected host, but oocysts of Eimeria and Isospora are unsporulated and therefore not infective when passed in the feces. Under favorable conditions of oxygen, humidity, and temperature, oocysts sporulate and become infective in several days. During sporulation, the amorphous protoplasm develops into small bodies (sporozoites) within secondary cysts (sporocysts) in the oocyst. In Eimeria spp, the sporulated oocyst has 4 sporocysts, each containing 2 sporozoites; in Isospora spp, the sporulated oocyst has 2 sporocysts, each containing 4 sporozoites.
When the sporulated oocyst is ingested by a susceptible animal, the sporozoites escape from the oocyst, invade the intestinal mucosa or epithelial cells in other locations, and develop intracellularly into multinucleate schizonts (also called meronts). Each nucleus develops into an infective body called a merozoite; merozoites enter new cells and repeat the process. After a variable number of asexual generations, merozoites develop into either macrogametocytes (females) or microgametocytes (males). These produce a single macrogamete or a number of microgametes in a host cell. After being fertilized by a microgamete, the macrogamete develops into an oocyst. The oocysts have resistant walls and are discharged unsporulated in the feces. Oocysts do not survive well at temperatures below ∼30°C or above 40°C; within this temperature range, oocysts may survive ≥1 yr.
Of the numerous species of Eimeria or Isospora that can infect a particular host, not all are pathogenic. Concurrent infections with 2 or more species, some of which may not normally be considered pathogenic, also influence clinical disease. Within pathogenic species, strains may vary in virulence.
Clinical signs of coccidiosis are due to destruction of the intestinal epithelium and, frequently, the underlying connective tissue of the mucosa. This may be accompanied by hemorrhage into the lumen of the intestine, catarrhal inflammation, and diarrhea. Signs may include discharge of blood or tissue, tenesmus, and dehydration. Serum protein and electrolyte concentrations (typically hyponatremia) may be appreciably altered, but changes in Hgb or PCV are seen only in severely affected animals.
Oocysts can be identified in feces by salt or sugar flotation methods. Finding appreciable numbers of oocysts of pathogenic species in the feces is diagnostic (>100,000 oocysts/g of feces in severe outbreaks), but because diarrhea may precede the heavy output of oocysts by 1–2 days and may continue after the oocyst discharge has returned to low levels, it is not always possible to find oocysts in a single fecal sample; multiple fecal examinations of one animal or single fecal examinations of animals housed in the same environment may be required. The number of oocysts present in feces is influenced by the genetically determined reproductive potential of the species, the number of infective oocysts ingested, stage of the infection, age and immune status of the animal, prior exposure, consistency of the fecal sample (free water content), and method of examination. Therefore, the results of fecal examinations must be related to clinical signs and intestinal lesions (gross and microscopic). Furthermore, the species must be determined to be pathogenic in that host. The finding of numerous oocysts of a nonpathogenic species concurrent with diarrhea does not constitute a diagnosis of clinical coccidiosis.
The life cycles of Eimeria and Isospora are self-limiting and end spontaneously within a few weeks unless reinfection occurs. Prompt medication may slow or inhibit development of stages resulting from reinfection and, thus, can shorten the length of illness, reduce discharge of oocysts, alleviate hemorrhage and diarrhea, and lessen the likelihood of secondary infections and death. Sick animals should be isolated and treated individually whenever possible to ensure delivery of therapeutic drug levels and to prevent exposure of other animals. However, the efficacy of treatment for clinical coccidiosis has not been demonstrated for any drug, although it is widely accepted that treatment is effective against reinfection and should therefore facilitate recovery.
Most coccidiostats have a depressant effect on the early, first-stage schizonts and are therefore more appropriately used for control instead of treatment. Soluble sulfonamides are commonly administered orally to calves with clinical coccidiosis and are perceived to be more effective than intestinal sulfonamide formulations (boluses). Amprolium is also administered orally to calves, sheep, and goats with clinical coccidiosis. Preventive treatment of healthy exposed animals as a safeguard against additional morbidity is an important consideration when treating individual animals with clinical signs.
Prevention is based on limiting the intake of sporulated oocysts by young animals so that an infection is established to induce immunity but not clinical signs. Good feeding practices and good management, including sanitation, contribute to this goal. Neonates should receive colostrum. Young susceptible animals should be kept in clean and dry quarters. Feeding and watering devices should be clean and must be protected from fecal contamination; this usually means feed is placed in troughs above the ground and positioned so that it is difficult for fecal contamination of feed to occur. Stresses (eg, weaning, sudden changes in feed, and shipping) should be minimized.
Preventive administration of coccidiostats is recommended when animals under various management regimens can be predictably expected to develop coccidiosis. In virtually all cases, Eimeria spp are implicated. Decoquinate and ionophorous antibiotics are widely used for this purpose in young ruminants. Continuous low-level feeding of decoquinate, lasalocid, monensin, or amprolium during the first month of feedlot confinement has been reported to have preventive value. Ionophorous antibiotics and amprolium have been reported to be effective in goat kids, as have sulfonamides and amprolium in pigs.
Last full review/revision March 2012 by Peter D. Constable, BVSc (Hons), MS, PhD, DACVIM