Coccidiosis in goats is a complex, multifactorial problem. Disease depends on the various stresses to which the individual is subjected, the environment, the extent of contamination, and exposure to infection. In many countries, it is the most common cause of diarrhea in indoor goat kids >4 weeks old.
Goats develop some (not total) immunity to coccidiosis, with a need to achieve a balance between sufficient oocyst exposure to allow immunity without causing clinical disease. Wild goats rarely suffer from coccidiosis because they are browsers and feed over large areas. The nomadic existence of farmed goats in some countries means kids are exposed to small numbers of oocysts mainly produced by the adults or older goats. This allows a protective immunity to be built up and to be maintained without illness. However, when on a farm, especially when used for indoor goat milk production, young goats with high coccidial exposure may develop clinical signs.
Etiology of Coccidiosis of Goats
Coccidiosis in goats occurs worldwide. Seventeen species have been identified, including E alijevi, E aspheronica, E arloingi, E caprina, E caprovina, E christenseni, E gilruthi (formerly Globidium gilruthi), E hirciee, E jolchijevi, and E ninakohlyakimovae (most pathogenic). Often, several species infect the goat kid at the same time. Except possibly for E gilruthi, all the goat Eimeria spp are considered host specific and do not transfer from goats to sheep. In outdoor rearing, there can be concurrent coccidial and helminth infections.
Little is know about the pathogenicity of each Eimeria spp, although five can cause disease: E arloingi (small intestine), E christenseni (small intestine), E ninakohlyakimovae (small and large intestine), E caprina (small and large intestine), and E hirci (unknown location). Generally, those infecting the lower part of the gut are most harmful. Those Eimeria spp considered nonpathogenic invade the small and large intestine (E alijevi) or an unknown location (E aspheronicae, E caprovina, and E jolchijevi).
The life cycle is direct. Oocysts are produced in 2–4 weeks (the prepatent period), depending on species. The infective sporocyst stage is reached in 1–2 days under optimal conditions but may take several weeks in cold weather. The thick shell allows many oocysts to overwinter. The most pathogenic stages are the gamonts. The ingestion of a single oocyst can result in 1–2 million oocysts after a month. The life cycle of E gilruthi is uncertain.
Each Eimeria sp infects cells in preferential sites in either the small or large intestine. Those damaging the crypt cells of the large intestine tend to be most harmful to the host because cell replacement is slow and no compensatory effects can occur from other parts of the gut. In some cases, there is decreased water absorption and severe hemorrhage where the large intestinal mucosa is denuded. Reduced fluid retention can lead to hypokalemia, hyponatremia, and hypophosphatemia. The pathogenesis of E gilruthi is unknown, although it occurs in the abomasum.
Epidemiology of Coccidiosis of Goats
Almost all goat kids become infected with coccidian oocysts. Adult animals can be infected, although they are resistant to clinical disease. Small numbers of ingested oocysts complete their life cycle throughout adult life.
When clinical disease occurs in kids, it is often because of the periparturient rise in oocyst excretion in pregnant does, probably compounded by residual infection in the environment and exacerbated by multiplication through successive groups of kids. Usually, clinical signs occur in 1- to 2-month-old kids when large numbers of oocysts are ingested over a short period. This occurs particularly in kids reared indoors in inadequately or irregularly cleaned pens, or where they are kept in overcrowded conditions or when varying age groups are penned together. These poor conditions are more likely to occur in milking herds where kidding occurs year round. In goats kept at pasture, coccidiosis can still occur in the kids. If the grass is short, as when the weather is dry or the ground is overstocked, then the kids are exposed to large numbers of oocysts. Poorly drained feeding, resting, or watering areas can become heavily contaminated with oocysts. Permanent pastures can contain overwintered oocysts.
Immunity requires about a month of continual exposure to the oocysts to develop. Further exposure to the oocysts enhances immunity, and a few oocysts are shed.
Clinical Findings of Coccidiosis of Goats
Most clinical cases occur between 5–8 weeks of age. Most goat kids have inapparent infection. In subacute or acute infections, the usual signs are poor fecal pellet formation (pasty feces), decreased appetite, stary coat, and decreased weight gain. More severe acute cases show diarrhea with or without blood presence, possible tenesmus, dullness, anorexia, and weight loss. Severe problems lead to rapid onset of diarrhea, often with blood, tenesmus, signs of abdominal pain, lethargy, weakness, recumbency, and death. In chronic infections, there is increased time to puberty, increased time to finish, decreased weight gain, and decreased feed intake. There have been several reports of liver failure in milking goats due to hepatobiliary coccidiosis.
Postmortem Lesions
Lesions occur in the alimentary tract; often, they are not obvious. Most animals that do not die of coccidiosis only show thickening of the small or large intestinal wall at postmortem examination. Severely affected goats that die may be in poor body condition and may be dehydrated, with inflammation, hemorrhage, and thickening of the upper and lower large intestine with denuded mucosa. Pinpoint white spots due to giant meronts may be seen by eye in the small intestine. Eimeria arloingi causes polyp formation and mucosal hyperplasia in the small intestine. Mucosal scrapings show large numbers of the stages of the parasitic life cycle, especially gamonts and oocysts. Histologically, villous epithelium is sloughed, and inflammatory cells are in the lamina propria and submucosa. Eimeria gilruthi produces abomasitis, with edema, hemorrhages, and raised nodules of the abomasal mucosa. Histologically, the nodules consist of the organisms surrounded by an area of necrosis.
Diagnosis of Coccidiosis of Goats
History (an outbreak of diarrhea in goat kids >4 weeks old)
Suboptimal environmental conditions conducive to coccidial presence
Clinical signs
Diagnosis is based on history, age of kids, clinical signs (severe diarrhea), fecal examination, and postmortem findings.
Fecal samples should be taken from several goats with and without clinical signs. On fecal flotation (saturated salt or sucrose solution), the feces usually show high oocyst counts, but speciation to show the presence of a pathogenic species should be done. Coccidial oocyst count importance can be complicated by animal selection, timing of sampling, presence of nonpathogenic Eimeria spp, and lack of agreement on interpretation of important oocyst counts. Speciation is recommended to ensure that the Eimeria spp present are pathogenic. Impression smears show stages of coccidial development. If necessary, histologic examination can help confirm infection.
Differential diagnoses are similar to those for coccidiosis in lambs. If clinical signs are in kids from approximately 1 month of age and older, most problems can be differentiated by examination of fecal samples. Salmonellosis and other bacterial infections can be determined by means of bacteriologic culture. Coronavirus and rotavirus can be shown by ELISA. Cryptosporidia can be detected by oocyst examination or ELISA. Helminths are indicated by presence of eggs in feces of outdoor kids. Otherwise, digestive and nutritional problems can be determined from the history and feed examination. Management problems can be determined from history and observation.
Treatment of Coccidiosis of Goats
All severely affected kids should be removed to a hospital pen or to a different pasture. If possible, others in the group should be moved to uncontaminated or less contaminated areas. Indoor kids should receive generous clean bedding frequently, with feed and water troughs raised to prevent contamination. Outside, any feed and watering areas should be sited on well-drained land and fecal contamination prevented. Stocking density should be decreased.
In most countries, few or no treatments are licensed for goats, although products licensed for cattle and sheep are often available. Water and feed intake is usually decreased in ill kids, so it is best to treat by drenching rather than rely on including any medicine in the drinking water or feed. It may be necessary to use electrolyte and nutritional solutions to feed ill kids.
Diclazuril (1 mg/kg, PO, once) and toltrazuril (20 mg/kg, PO, once) have been used successfully; doses may need to be repeated. A metabolite of toltrazuril, ponazuril (10 mg/kg, PO, once) reduced oocyst counts when used experimentally in goat kids. Currently, it is not licensed in goats but is indicated for equine protozoal myeloencephalitis.
Decoquinate (1 mg/kg, PO, every 24 hours for 28 days) can be used as a treatment and is licensed in some countries for sheep. Individual dosing may be necessary.
Sulfadimethoxine (55 mg/kg, PO or in the drinking water, for first day, then 27.5 mg/kg for 3 days) can be helpful in the early stages of acute infection, but in the US and some other countries it is an extralabel use. The extralabel sulfadimidine (sulfamethazine) dosage that is effective in treating coccidia in goats is 100 mg/kg, PO, every 24 hours for 7 days. Potentiated sulfonamides have been used by injection or orally.
Use of amprolium oral solution (50 mg/kg, PO, every 24 hours for 5 days) has been reported. It is not labeled for goats in the US. It is thought that where it is used on some goats farms, resistance has developed. It may be advisable to provide thiamine (vitamin B1) after amprolium use.
Control and Prevention of Coccidiosis of Goats
Management control of coccidiosis is a delicate balance between ensuring that kids are exposed to infection and so acquire immunity, and preventing them from developing clinical disease. Management plays a key role in prevention by ensuring all areas used by goats, and especially kids, are thoroughly cleaned and disinfected after each period of occupation, ensuring all pens are not overcrowded, and keeping kids in small groups of the same age and maintaining them as that group. An all-in/all-out rearing system is ideal. Feed and water troughs should be raised off the ground to prevent fecal contamination. When kids are kept on grass, they must not be overcrowded, with feed and need water points sited in well-drained areas. Shelters must be kept clean and have dry, well-bedded floors. The grass in paddocks should be kept long so that kids develop immunity through low-level exposure.
In kids, decoquinate (0.5 mg/kg) may be fed in problem herds for about 1–2 months commencing before the risk period. If used, it is important to ensure sufficient feed intake by all the kids or otherwise increase the in-feed inclusion rate. It is approved by US FDA for prevention in nonlactating goats.
Diclazuril and toltrazuril can also be used for prevention at similar dosages to treatment. In some countries, toltrazuril is licensed for goats.
Treatment with sulfadimidine (sulfamethazine) reduces environmental contamination with oocysts.
In nonlactating goats, adding monensin to the feed at 18 g/ton is preventive. It is approved by the FDA for confined goats but not licensed in some other countries. If used, it must be mixed correctly to prevent toxicity. Lasalocid acid is also used but it is not approved by the FDA in goats, although it can be used for confined sheep.
Drenching or adding amprolium to drinking water is used to treat goats at weaning although it is not approved by the FDA for the species.
Natural products such as Lespedeza cuneata in feed pellets have decreased fecal signs and oocyst counts in kids.
