Coccidiosis is a disease of the largeand small intestines caused by pro-tozoa. The coccidia are very host

specific parasites; cattle coccidia affect onlycattle, and coccidia from goats, sheep,dogs or cats will not cause disease incattle. The major damage that occursfrom this organism is the damage tothe gut cells as the parasite repro-duces. Multipli-cation occurs sorapidly, that the final release ofoocysts (eggs) into the manurerepresents over 23 milliontimes the number of eggs theanimal originally swallowed.The eggs are resistant to envi-ronmental stress and thus aredifficult to completely removefrom the environment. They arefrequent contaminants of feedand water, and once ingested byother cattle, the life cycle startsagain in a new host.

The life cycle of coccidia is complicated.After being passed in the manure, and ex-posed to the environment for 2-3 days, eachoocyst will develop 8 sporozoites. Once ingestedby a susceptible victim, the oocyst ruptures re-leasing the sporozoites. These then penetrate thelining cells of the small intestines and begin a pe-riod of multiplication that destroys intestinal cellsas asexual reproduction occurs. This multiplica-tion results in the release of millions of mero-zoites to invade the large intestine. It is there thatthe final stage of sexual reproduction occurswhere male and female parasites unite to producethe oocyst and the fertile “egg” appears (micro-scopic) in the manure. The clinical signs of coc-cidiosis generally occur because of this last largeintestinal stage, resulting in bloody diarrhea,straining and the passage of clumps of necroticintestinal lining. However, because damage canalso occur in the small intestine if sufficient in-testinal lining cells are destroyed, diarrhea, un-thriftiness and poor doing cattle can be a resulteven before oocysts are found in the stool.

It is estimated that as few as 50,000 oocysts in-gested by a young susceptible calf can result insevere disease. While this sounds like a ridicu-lously large number, bear in mind that theseoocysts are microscopic and cannot be seen bythe naked eye. Fifty thousand would occupyonly a tiny amount of space. Furthermore, theeggs are very resistant to environmental condi-tions such as heat and cold, and thus remain in-fective for long periods. Contamination of feed

Coccidiosisby Pat White, DVM

or water can increase the likelihood of infection.The severity of the disease is directly related tothe number of oocysts ingested. In light infec-tions, the damage to the gut is minimal, and be-cause the intestinal epithelial cells replacethemselves at such a rapid rate, any damage isquickly repaired. However, in the case of heavyinfections, about 2 weeks after the eggs are con-sumed, most of the cells at the base of the intes-tinal glands are filled with merozoites (asexuallyreproduced life stages) and gametocytes (lifestage with both male and female counterparts inthe large intestine that finally result in the pro-duction of the oocyst). When all those cells dieand rupture because of their infestation, damageis severe, there is loss of blood, fluid, elec-trolytes and proteins. Dead intestinal cells aresloughed and also passed out in the diarrhea.

Immunologically naïve animals consumeoocysts from manure contaminated pasture,feed, water or bedding and also by groomingcontaminated hair coats of their pasture mates.Most animals infected with coccidia do notshow signs of disease. This is due to a normallylow dose exposure and subsequent immunity tothat particular coccidian species. These animalswill appear healthy but feed efficiency may be

reduced and lower weight gains could be seen.Subclinical disease is the most common syn-drome in growing cattle. Calves may appear un-

thrifty with manure stained backsides.Clinical disease is also a condition usuallyof the immature animal due to lack ofacquired immunity, compounded byany number of stressful events, in-cluding weather changes, over-crowding, long travel, filthysurroundings or other concurrentillnesses such as shipping fever.Calves are most susceptible be-tween 3 weeks and 6 months ofage and most clinically sick an-imals will be less than 12months old. Weaning with con-solidation of calves into closequarters is the perfect place to ex-pect an outbreak.

In mild cases, animals may be asymp-tomatic, or may have only watery diar-

rhea, with little or no blood and exhibit arough hair coat. Severely affected animals

may have severe, watery diarrhea with generalemaciation and weakness that may cause the calfto defecate without rising, thus soiling itshindquarters. Straining with defecation is usuallyevident and rapid dehydration, weight loss andanorexia (not eating) may also occur in suchcases. In these severe cases, diarrhea may containblood, mucous and stringymasses of tissue due tothe presence of the epithelium of the intestines.Severe infections are not common but unfortu-nately, death can be a result.

Certain species of the many coccidia that affectcattle are more likely to cause severe disease.Eimeria zuernii, E bovis and E. auburnensis arethe main culprits in cattle. Other species may bepresent but are far less likely to be pathogenic.Susceptibility to infection varies. Some animalsare naturally immune. Most others will developimmunity with exposure; however, this is just tothe species causing illness and exposure to anew variety can induce disease. Many animalswill carry the parasites and coexist reasonablywell with the parasite until severe periods ofstress. Older cattle may break with coccidiosiswhen brought to a new herd and exposed to anovel strain for that individual.

Diagnosis is made from a combination of historyof illness and sanitation for the herd, clinicalsigns, gross lesions found at autopsy, and micro-scopic evaluation of intestinal scraping from thedead animals or microscopic evaluation of the

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manure. Diarrhea may precede the heavy dis-charge of oocysts by several days and diarrheamay continue after the discharge of oocysts, thusfinding evidence of coccidia in the manure maybe difficult. Differential diagnoses include sal-monellosis, Bovine Viral Diarrhea, malnutritionpoisons or other intestinal parasites. If coccidio-sis is believed to be responsible for cattle deaths,a complete autopsy should be performed to con-firm the diagnosis, and stool samples should beexamined immediately after diarrhea first ap-pears in sick calves.

Animals can die from coccidiosis; either directlyor from secondary diseases. While many sickanimals will recover, permanent damage to thegut may occur resulting in poor weight gain oreven stunting.

So called “nervous coccidiosis” is associatedwith heavy coccidia infestations. It is theorizedthat the coccidia produce a soluble protein exo-toxin that is encephalotoxic. Signs include mus-cle tremors, convulsions, nystagmus (eyesmoving back and forth or up and down in arapid, rhythmic manner) and other central nerv-ous system symptoms. Mortality is very high, inthe 80-90% range.

Clinical coccidiosis, that is, an animal showingsigns of disease, must be treated as soon as pos-sible. In an outbreak, the clinically affected an-imals should be isolated and given individualtreatment, both specific for the coccidia and sup-portive as necessary. Mass medication is indi-cated for those animals in the same grouping.Nervous coccidiosis requires extensive support-ive care that may be hard to economically justifyfor a condition with such a poor prognosis. It isbest to treat each sick animal individually butthese same treatments can be used in a herd sit-uation. Sulfa drugs such as sulfadimethoxine(Albon), sulfamethazine or the vitamin B1 ana-log amprolium (Corid) are the mainstay of treat-ment for clinical coccidiosis. All can be used asa drench or as a water additive. Most sick calveswill still continue to drink water but if there is

any question of the calf’s ability or desire todrink from a communal water supply, that ani-mal should be dosed individually by bodyweight and the medication administered as adrench directly into the animal’s mouth.Animalsthat refuse to drink and or eat will require addi-tional symptomatic treatment such as IV fluids.The rest of the exposed animals should betreated with the addition of these medications inthe drinking water. Medicated water should bemixed up once per day. Generally treatment foracute coccidiosis continues for 5-6 days and allcalves in a group of animals should be treatedeven if some are asymptomatic. Sulfas have theadvantage of providing antibacterial effects forsecondary infections that may be associated withcoccidiosis, such as pneumonia or bacterial en-teritis (gut infection). Amprolium replaces vita-min B1 (thiamine) in the coccidia, interferingwith its life cycle. High doses for prolonged pe-riods beyond those recommended can result inthiamine deficiency in treated animals. Like-wise, high doses of thiamine to the animalsunder treatment can interfere with the efficacyof the drug. Secondary conditions such as dehy-dration, bacterial pneumonia may require spe-cific treatment.

There are several products available to preventcoccidiosis in a group of cattle, before any ofthem show signs. These medications must beused for 28 days at a minimum, to ensure thatthey have a chance to act on the part of the lifecycle for which they are effective. Amproliumcan be used as a preventative at half the dosagerequired for treatment. Other useful drugs in-clude the ionophore antibiotics lasalocid (Bo-vatec) and monensin (Rumensin) and thecoccidiostat decoquinate (Deccox). These are alleffective preventatives, given well before signsof disease appear, but with the exception of am-prolium at the higher dose, none are effectivetreatments for clinical disease. These productswill do no good in animals already showing signsof coccidiosis. The ionophore antibiotics lasa-locid and monensin have the advantage of beingvery good growth promotants. However, they

are usually mixed with grain and they have oneimportant disadvantage; they are both poison-ous to dogs and horses and can be fatal if in-gested by the wrong species. If these productsare used, extreme care should be taken to ensurethat horses and dogs have no access to the premixor any grain containing them. If you have horsesor dogs, decoquinate or amprolium are safer op-tions.

Using preventatives may have an unwanted sideeffect in that withdrawal from them has been re-ported to result in fatal coccidiosis in some ani-mals, presumably because the drug suppressedthe development of immunity with subsequentfatal reexposure. Anecdotally, some animals fedionophores for the purpose of increased gain andreduction of bloat from “hot” rations have donevery poorly when put out to pasture, presumablyfor the same reason. When these products areused in feedlot situations, slaughter is the end re-sult and re-exposure is a non-issue. In the caseof replacement animals, care should be takenwhen they are first weaned from the prod-ucts. They should be pastured in clean areas, withminimal previous contamination so that their firstintroduction to the parasite is at low num-bers. This will allow for immunity to develop.Animals should be closely observed for evidenceof acute disease and treated accordingly.

Coccidiosis is difficult to control with absoluteprecision. Overcrowding should be avoided, par-ticularly until animals have a chance to developimmunity to the protozoa in their environment.Calving areas should be well drained and kept asdry as possible. Feeders and waterers should behigh enough to avoid heavy fecal contamination.The population density of animals must be kept toa minimum. Facilities allowing no access to pas-ture must be routinely cleaned on a daily basis tolimit infective oocysts in the environment. Keep-ing this parasite at bay requires an ongoing com-bination of good husbandry practices, amplespace for animal housing and careful use of indi-cated chemotherapeutics.