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A disease characterized by diarrhea in suckling and recently weaned pigs. The disease is usually caused by Isospora suis but occasionally by other Eimeria spp.


“Neonatal” coccidiosis caused by Isospora suis usually occurs in confinement-raised, one to three week old, nursing piglets and is less frequent and severe in older recently weaned piglets. Coccidiosis occurs in all countries where confinement rearing and continuous farrowing are practiced.

Although several coccidia of the genus Eimeria commonly infect one to three month old swine, clinical disease rarely occurs. Disease only occurs when previously unexposed pigs are placed in highly contaminated environments including unsanitary nurseries or grow/finish facilities.

Historical information

Although Isospora suis infection was identified as a cause of enteritis in 1934, it was not identified as a serious problem for swine raisers until the mid-1970s. Coccidiosis assumed greater importance with the introduction of confinement-rearing, continuous farrowing in warm buildings, and use of farrowing crates. These innovations facilitated rapid completion of the life cycle of I. suis in high numbers. Coccidiosis has re-emerged as a common cause of neonatal diarrhea, even in modern well-managed farms.


Isospora suis is the usual cause of coccidiosis in very young, confinement-raised pigs. Oocysts become infective in about 12 hours at temperatures of 68-97˚F. This is within the range maintained in many confinement farrowing facilities. After ingestion of sporulated oocysts, patency in neonatal pigs can occur in as little as five days.

Isospora suis goes through the usual stages of sporogeny, excystation, and endogenous development with multiplication in intestinal epithelium as is reported in other species. Development usually occurs in epithelium of the small intestine, especially in the jejunum and ileum, less often in the duodenum, cecum and colon. Development usually occurs in the cells on distal portions of intestinal villi; in severe infections it may occur in cryptal epithelium. Fully sporulated oocysts of I. suis have two sporocysts; each of these has four sporozoites. Eimeria spp. are quite similar but have a longer (18 day) life cycle and a higher affinity for the large intestine and distal small intestine.


Coccidia are initially introduced into farrowing facilities by carrier sows. Oocysts produced by dams or more likely, their parasitized piglets, survive in farrowing rooms and crates and become a major source of infection for subsequent litters. Once infected, piglets magnify the numbers of oocysts and heavily contaminate the environment. As a result of this buildup of oocysts, piglets are able to ingest high numbers of oocysts, a requisite for producing clinical disease. Inadequate sanitary practices between farrowing groups undoubtedly facilitate this buildup.

In a warm, moist environment, oocysts in feces-contaminated farrowing rooms and crates soon become infective. They are ingested when piglets first nurse or when they ingest feed, water or feces in the farrowing crate. The sporozoites within oocysts mature and are released to penetrate enterocytes. Many enterocytes are destroyed by the developing coccidia. Released oocysts are passed in the feces.


The development of coccidia in enterocytes results in desquamation of enterocytes, especially those on the distal tips of villi. The severity of lesions is related to the number of oocysts ingested. Bacteria in the intestine, including Clostridium, may contribute to overall severity of the lesions. When many coccidia are ingested, lesions are severe. In serious infections, the erosion of villous epithelium results in loss of fluid and failure of surviving epithelium to absorb nutrients and fluids. This leads to diarrhea, dehydration, and loss of electrolytes, perhaps death.

Since regeneration of villous epithelium occurs more slowly in neonates, they are more severely affected. If piglets ingest only small numbers of oocysts, they survive and are immune unless stressful environmental or secondary infections intervene.

Clinical signs

Signs can occur as early as five days after birth but are more commonly seen in piglets from one to three weeks old. Signs include yellow to clear, pasty to watery diarrhea, dehydration, rough hair coat and failure to gain weight. The clinical disease within a litter can appear in two waves; the first wave (four to six days) representing infection and subsequent contamination of the farrowing crate environment by a few affected pigs, the second wave appearing four to eight days later after the rest of the litter becomes infected. Piglets usually continue to nurse but may vomit milk. Morbidity is high but mortality is variable, often moderate. Producers often report neonatal diarrhea that resembles colibacillosis but that fails to respond to antibiotic therapy. Fecal blood is not a feature of porcine coccidiosis.


Lesions are usually restricted to the intestinal tract, especially the lower jejunum and ileum. Lesions vary in severity, depending on the number of oocysts ingested. In mild infections, the intestine tends to be turgid. Mild fibrinous enteritis may be visible in short segments of the lower small intestine. In severe infections, there may be extensive fibrinonecrotic enteritis. Occasionally the duodenum, cecum or colon are affected.

Microscopically, there is necrosis and, later, atrophy and fusion of some mucosal villi, hyperplasia of cryptal epithelium and elongation of mucosal crypts. Shortened villi may be covered by cuboidal or flattened epithelial cells. Various stages of Isospora suis are apparent in parasitized cells. If adequate time has elapsed since initial infection, there may be oocysts in the feces.


Diagnosis can be made most reliably by identifying the coccidia in histologic sections. The presence of paired type-1 merozoites are considered diagnostic for I. suis. Several areas of infected mucosa should be examined in order to maximize sensitivity of the histological examination as distribution of microscopic lesions and merozoites is unpredictable.

Diagnosis by fecal examinations may be possible but is thought to be less sensitive than examination of affected small intestinal tissue. It is best attempted on piglets that have been sick two to three days so that oocysts have had time to develop. Feces collected at earlier or later stages of the disease may contain few or no oocysts. In fecal samples, either “hazy bodies” between the oocyst wall and the sporont, or oocysts in the 2-cell stage, are diagnostic for I. suis.

Coccidiosis can occur concurrently with other diseases so it may be necessary to eliminate them as additional causes of the diarrhea. These include rotaviral infection, colibacillosis, transmissible gastroenteritis, parasitism by Strongyloides ransomi, and infection withClostridium perfringens type A or C.


A vigorous, effective sanitation program, along with careful cleaning and disinfection of farrowing crates between farrowings is essential. Strong bleach or ammonium compounds can be used for disinfection after thorough cleaning of the crates. Between farrowings, steam cleaning of the entire farrowing facility may be necessary. Sealing all surfaces with paint or a water seal may be preferable to break the cycle of infection. Wooden and concrete surfaces are particularly difficult to clean effectively on affected farms. Installation of perforated metal or plastic flooring in the crates will be beneficial in the control of coccidiosis and other neonatal enteric diseases.

On farms known to be affected by coccidiosis, routine treatment of all piglets with toltrazuril* early-on will minimize the incidence and severity of coccidiosis. There is no proven, widely accepted anticoccidial or drug for use in dams that is effective at controlling the disease in neonates.

Most cases of coccidiosis associated with Eimeria spp. are the result of the introduction of naïve pigs into a heavily contaminated environment. Control is based on minimizing the dose of oocysts ingested. Scrupulous sanitation between groups of pigs is usually sufficient to prevent disease.

* There is no FDA-approved toltrazuril product in the United States. Therefore, toltrazuril is illegal to use in food animals in the United States in any form. These drugs may be approved for food animal use in other countries. However, drugs approved in other jurisdictions may not be legally imported and used in food animals in the United States, regardless of their labels in other countries.  For more information on the status of the use of potential medications for coccidia control for U.S. veterinarians, please consult the American Association of Swine Veterinarian Website at