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Professional Version

Coccidiosis of Pigs


Anthony Andrews

, BVetMed, PhD, DECBHM, DECSRHM, Anthony H. Andrews

Reviewed/Revised Aug 2022 | Modified Oct 2022

More than 9 species of Eimeria and one of Isospora infect pigs in North America. The problem is worldwide and is probably underreported. Isospora suis infects piglets and is found in up to 90% of herds, with 25% to >50% of litters affected. Eimeria spp very rarely infect neonates but are found in older pigs. Coccidiosis in pigs is best considered as one of two clinical entities dependent on age. One type is in neonatal piglets due to I suis and often intercurrent infections occur. Most Eimeria spp appear to be of low pathogenicity for neonates. The second type due to Eimeria spp occurs in older pigs, including gilts. It also infects wild boars. Both types occur in all types of production system worldwide and can have marked economic consequences.

Etiology of Coccidiosis of Pigs

The causative agent of coccidiosis in piglets is usually Isospora suis. Most Eimeria spp have low pathogenicity (causing approx 5% of infections) or do not occur in this age group.

Piglet neonates pick up infected sporulated oocysts from a contaminated environment. Initial invasion is of the cranial third of the jejunum. Isospora suis has 3 asexual and one sexual replication stages. Successive generations of meronts occur in the more distal parts of the small intestine, and they invade the cecum and colon. Third-generation meronts are produced in 4–6 days and oocysts first appear in the feces at about 5 days, continuing until day 8 or 9, with a second wave from day 11–14. Shed oocysts can become infective in 12–24 hours at 25º–35ºC. They are viable for >10 months.

Older pigs and weaned pigs are infected by various Eimeria spp, mainly in the small intestine, including E debliecki (often most common), E neodebliecki, E perminuta, E polita, E porci, E scabra, E spinosa, E suis, and E szechuanensis. Many Eimeria spp are localized in their distribution. Eimeria debliecki mainly infects the small intestine and later the colon to a lesser extent. The prepatent period is about 7 days. Eimeria neodebliecki affects the mid portion of the jejunum, with a prepatent period of approximately 6–8 days.

In piglets, infection starts in the cranial small intestine and progresses to the distal half of the small intestine as the various stages develop. Lesions of villous atrophy occur 5 days after infection and resolve 10–14 days after infection. Older pigs also have infection in the small intestine; the distribution and extent of damage varies with the species of Eimeria.

Epidemiology of Coccidiosis of Pigs

Isospora suis infection occurs in piglets in all systems from indoor intensive to outside extensive production. Piglets are mainly exposed to oocysts from others in contaminated farrowing and rearing accommodation. Disease is more severe when infection is contracted early in life. Thoroughly cleaned slatted floors decrease or prevent illness. Sows rarely shed I suis species, although infection may be introduced to a new herd by carrier sows. Postweaning infection is also from a contaminated environment. However, sows can carry Eimeria spp and transmit them to their offspring. Older pigs may be infected by the sows and with E scabra, illness can occur 4–8 weeks and later. Infection may enter a naïve herd from wild boars or new gilt introduction. Equally new gilts entering an infected herd may show clinical illness.

After exposure to I suis, immunity is strong. Pigs exposed to most of the Eimeria spp gain good immunity, but in adults it is often enhanced by low levels of infection. There may be a periparturient shedding of oocysts.

Clinical Findings of Coccidiosis of Pigs

In piglets, infection most commonly occurs from 5–15 days of age. Affected piglets develop diarrhea varying from creamy, pasty consistency or whitish feces to profuse watery yellowish diarrhea. Those infected are thinner than their counterparts of the same age and remain thin and hairy for several weeks. Severely affected piglets die, with mortality rates up to 20% in indoor and outdoor systems. After infection, reduced growth may continue.

In older pigs, infection is usually mild. Those ill develop diarrhea, which may be frothy, mucoid, or watery, with wasting. Clinical signs often start 9–12 days after infection. Some pigs continue to grow poorly.

Postmortem Lesions

In piglets, the small intestines are often flaccid, with contents varying from watery to a creamy liquid. Lesions consist of a thickening of the wall, with a necrotic lining confined to the jejunal and ileal wall. Often, the body is thin and dehydrated. Histologic examination shows large numbers of merozoites and male and female gametocytes in the intestinal wall. There is villous atrophy, blunting of villi, focal ulceration, increased mitotic activity in the crypt epithelium, and in severe cases, fibrinonecrotic enteritis with coccidial development stages in the epithelium.

In older pigs, there are local inflammatory lesions with lining slough in the jejunum and ileum. Histologically, villous atrophy is moderate and, at the villi tips, there is fibrinonecrotic material.

Diagnosis of Coccidiosis of Pigs

Often, clinical signs develop before oocysts are present in the feces. The age of the affected piglets and lack of response to antimicrobial treatment assist in diagnosis, as does the presence of oocytes in the feces. The oocysts are usually present in large numbers. Oocysts can be detected with saturated sodium chloride or glucose solution. Oocysts can be identified by their size, shape, and sporulation characteristics. If pigs die early without oocyst presence, staining of impression smears of the mucosa from jejunum and ileum can provide a rapid diagnosis.

Asexual stages of development occur. Histologic sections may be necessary. Fluorescent antibody testing and PCR assay may also be used. In older pigs, diagnosis is often slowly reached after lack of response to antibacterial agents, although management and previous farm history may assist.

Usually many fecal oocysts are present. Speciation involves using potassium dichromate to sporulate the oocysts and can assist in determining control.

Postmortem findings assist in diagnosis. Impression smears of affected areas show coccidial development stages. Histologic examination of the caudal small intestine shows lesions plus asexual and sexual stages of the life cycle.

In piglets, fecal samples can be used to differentiate the most likely diagnoses at this age. They include Clostridium perfringens type A enterotoxemia Clostridium perfringens Type A Enteritis in Pigs Disease associated with type A strains of Clostridium perfringens is a milder condition than disease associated with C perfringens type C. Diagnosis is challenging, because C... read more , Clostridium perfringens type C enterotoxemia Clostridium perfringens Type C Enteritis in Pigs Infection of the small intestine by type C strains of Clostridium perfringens causes a highly fatal, necrohemorrhagic enteritis. It most commonly affects piglets 1–5 days old; however... read more <i >Clostridium perfringens</i> Type C Enteritis in Pigs toxin, enteric colibacillosis Enteric Colibacillosis in Pigs Enteric colibacillosis is a common disease of nursing and weanling pigs caused by colonization of the small intestine by enterotoxigenic strains of Escherichia coli (ETEC). Colonization... read more Enteric Colibacillosis in Pigs , rotavirus Rotaviral Enteritis in Pigs Rotaviral enteritis is a common disease of the small intestine of pigs. Pigs of all ages are susceptible to infection; however, diarrheal disease usually occurs in nursing piglets and weaned... read more , transmissible gastroenteritis (TGE), and cryptosporidia Cryptosporidiosis in Animals Cryptosporidiosis is a highly prevalent gastrointestinal parasitic disease caused by protozoan species of the genus Cryptosporidium that infect a wide range of animals, including people... read more Cryptosporidiosis in Animals . Starvation and crushing can be determined at postmortem examination.

Treatment of Coccidiosis of Pigs

All farrowing pens and areas should be thoroughly cleaned and indoor accommodation disinfected with effective disinfectants. Outdoor areas should be well drained and regularly relocated. Orally administered electrolyte solutions are helpful and probably need to be administered individually.

In piglets, those clinically affected and the others in the same litter or group should receive anticoccidial treatment.

Sulfonamides can be used. Sulfamethazine (sulfadimidine) in drinking water may be used but usually needs to be administered individually. Sulfaquinoxaline can be effective. Trimethoprim sulfonamide by injection or orally can be useful.

Treatment of individual clinically affected pigs with amprolium is administered at 10–25 mg/kg, PO, for 4–5 days, and to the rest of the group at 10 kg 25% premixed per ton of feed to decrease oocyst shedding.

Toltrazuril (20 mg/kg, PO, once) may assist in infected animals. In older pigs, it is important to determine causes and mitigate against them (decreasing overcrowding, removing pigs from contaminated areas, etc).

Monensin at 100 g/ton feed can be used with variable results.

Prevention and Control of Coccidiosis of Pigs

It is essential that all farrowing areas and accommodation is thoroughly cleaned, disinfected, and ideally, steam cleaned. Some ammonia-based disinfectants kill the oocysts but can only be used in areas vacated by animals. Areas should be dry, and ideally, fallow periods should be observed before further occupation. The cleaned pen should remain empty for as long as possible. Outdoor systems should have any accommodation and equipment cleaned and disinfected, and the ground areas should be well drained and frequently relocated.

Control of coccidiosis in newborn piglets infected with I suis is difficult and unreliable. The use of coccidiostats in the feed of the sow for several days or a few weeks before and after farrowing is recommended and is used in the field, but results are variable. Feeding coccidiostats to neonatal pigs from birth to weaning is reported, but it is difficult to ensure sufficient intake.

Monensin (100 g/ton of sow feed) is used from before farrowing until weaning; however, usage has been shown experimentally to be ineffective for prevention of coccidiosis in piglets.

Sulfadimidine (100 g/ton of feed) can be administered to sows from entering farrowing quarters until weaning.

Toltrazuril (20 mg/kg, PO, once) is licensed in some countries for coccidiosis prevention in 3–5 day old piglets and is shown to decrease oocyst excretion, incidence of diarrhea, and weight gain impairment in piglets with experimentally induced coccidiosis. Diclazuril (5 mg/kg, PO, once) is being investigated as an anticoccidial treatment in piglets.

Experimentally, a vaccine containing I suis sporozoite attachment protein is used apparently successfully, but nothing is available commercially.

For older pigs, thorough cleaning and, if allowed, use of fumigation with methyl bromide or ammonia at a final concentration of 2%, kills oocysts. Steam cleaning, raising the temperature to 65ºC for at least 15 minutes, or flame guns also kill oocysts. Commercially available ammonium chloride and sodium hydroxide product is used to kill oocysts.

Sulfadimidine can be added to the feed (100 g/ton) and should be administered to sows from entering the farrowing accommodation until weaning.

Using amprolium at the treatment rate has variable results. Feeding as a 25% premix at 10 kg/ton of feed is suggested.

Feeding monensin at the treatment rate has produced mixed results. Feeding at 100 g/ton of sow feed for 7–10 days before farrowing and for 2 weeks after arrowing might decrease oocyst shedding for pigs after weaning.

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