ISOSPORA SUIS PDF

The most commonly seen of all the Isospora species is Isospora suis in the pig. The eggs are subspherical, and the wall is colourless and thin. When sporulated each one contains two sporocyts each with four sporozoites. Life Cycle There are essentially three stages in the Isospora life cycle. The first is called sporogony and is the asexual stage of the parasite development.

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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.

Coccidiosis assumed greater importance with the introduction of confinement-rearing, continuous farrowing in warm buildings, and use of farrowing crates. Coccidiosis has re-emerged as a common cause of neonatal diarrhea, even in modern well-managed farms. 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. 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. Eimeria spp. Epidemiology 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. Pathogenesis 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 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. If adequate time has elapsed since initial infection, there may be oocysts in the feces. Diagnosis Diagnosis can be made most reliably by identifying the coccidia in histologic sections. 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. Coccidiosis can occur concurrently with other diseases so it may be necessary to eliminate them as additional causes of the diarrhea.

Control 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. Control is based on minimizing the dose of oocysts ingested. Scrupulous sanitation between groups of pigs is usually sufficient to prevent disease.

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Coccidiosis (Coccidia parasites)

Disease guide Background and history Coccidiosis is caused by small parasites called coccidia that live and multiply inside the host cells, mainly in the intestinal tract. There are three types, Eimeria, Isospora and Cryptosporidia. Disease is common and widespread in sucking piglets and occasionally in pigs up to 15 weeks of age. Diarrhoea is the main clinical sign.

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Coccidiosis

Transmissible gastroenteritis TGE Control and Prevention of Coccidiosis in Pigs A good level of hygiene in farrowing accommodation is necessary to minimize the spread of infection, and bedding should be destroyed and huts moved between litters. Disinfection can be used although available disinfectants are not particularly effective in combating I. Your veterinarian can provide advice on agents to combat the oocysts. Rodents also represent a potential means of spreading infection, and should be controlled Straw et al. Increased risk is associated with cross fostering piglets within 24 hours of birth Skampardonis et al. Treating Coccidiosis in Pigs Coccidial infection does not respond to antimicrobials Roberts and Walker, ; Taylor, or treatment via sows as they are not a major source of infection Straw et al.

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