Introduction

Attacks of clinical coccidiosis in cattle are marked by diarrhea, loss of blood, dehydration and anorexia. Even these signs are not always dramatically presented. Blood may or may not be evident in the feces. The disease results in a decline in general health, a failing appetite and eventually a loss of condition. The precise mechanism of development of these signs and the details and degree of recovery from coccidial infections are incompletely understood. It is certain that the physiologic and cellular pathologic changes which occur in infected animals significantly affect their ability to throw off the disease and return to normal. Such changes can also be expected to affect the ability of the animals with clinical coccidiosis to resist other diseases. The altered intestinal function has been shown to markedly affect nutrient and water intake from the gut of chickens with coccidiosis which can be expected to have a similar effect in cattle with this disease. It is not surprising to note that blood components such as hemoglobin, serum globulin, glucose and phosphorus, and other characteristics, are significantly altered in cattle with coccidiosis. Although little is known about the long-term effects of coccidiosis in cattle, loss of condition, reduced gains and mortality are of vital importance to dairy and beef producers.

The organisms which cause coccidiosis are tiny one-celled protozoa, chiefly of the genus Eimeria. Coccidia are very host specific—that is, coccidia which affect cattle do not affect birds, and vice versa. Another way in which coccidia differ from most other parasites is that often several species of coccidia occur in a single species of host. Twenty-one species have been described as occurring in cattle, 10 in sheep, 10 in rabbits and nine in poultry.

Although 15 to 21 species of coccidia have been described as occurring in cattle, only two species, Eimeria bovis and E. zurnii, are known regularly to cause coccidiosis accompanied by bloody diarrhea. Low-level infection with one or several species of coccidia is present in 100% of cattle, with no apparent damage to the host. Examinations for coccidia are made by collecting fecal samples and mixing with a concentrated sugar solution to cause the coccidia to float to the surface where they can be recovered for microscopic examination. Such an examination will permit a trained observer to identify the species of coccidia involved. This, along with other clinical signs, will enable assessment of the impact of the infection on the health of the animal.

The Parasites

Coccidia have a complex life cycle with several stages simultaneously occurring in separate host cells. Click here to see an interactive diagrammatic representation of the life cycle of E. bovis. It should be noted that the stage found in the feces is the oocyst. The oocyst, which has a protective wall resistant to physical, chemical and bacterial action, is discharged from the animal in the feces. With favorable environmental conditions of temperature and moisture, the oocyst goes through a maturation process called sporulation, which makes it infective to cattle. When the sporulated oocyst is ingested by the host, the sporozoites within it excyst and penetrate cells of the intestinal wall. They grow and develop into schizonts. Schizonts undergo a multiple dividing process that results in the formation of numerous new individuals called merozoites. After the schizont matures, the merozoites are released by the rupture of the host cell and they invade new cells and repeat the process.

For E. bovis, the second-generation merozoites enter new host cells and undergo sexual production, culminating in the formation of oocysts. All of the life cycle stages within the host are completed in a minimum of about 18 days with the peak in numbers of oocysts discharged occurring about 19 to 22 days after initiation of infection. The sexual stages are more numerous than the asexual stages—and they do more damage to their host cells. The signs of coccidiosis usually occur at the same time oocysts are passed in the feces.

E. zurnii, another pathogenic species of cattle coccidia, has been found to produce schizonts in both the small and large intestine between two and 19 days after infection. Sexual stages have also been observed at both sites. Oocysts may be discharged as early as Day 19. All of the stages are found in the epithelial cells.

E. auburnensis is unusual in that the schizont is deeply imbedded and the sexual stages characteristically parasitize cells of mesodermal origin. The microgametocytes are unusually large—so large that they can be observed without the aid of a microscope. The stages of the life cycle within the host are completed in about 18 days. Like E. bovis, E. ellipsoidalis develops in the small intestine, but all the known stages occur in the epithelial cells lining the crypts. The stages of the life cycle within the host are relatively short, requiring only about 10 days. In severe infections, E. ellipsoidalis can produce a nonbloody diarrhea which generally lasts only a few days. E. alabamensis also develops within the intestine but is distinctive in that the parasites lie within the nucleus of the host cell. It is not generally pathogenic, except in unusually heavy infections.

Distribution of Bovine Coccidia

Bovine coccidiosis occurs within cattle worldwide and at all times of the year. In the United States, these representative studies show how widespread coccidiosis is and how many cattle are infected in various locations:

Wisconsin

In one study, oocysts of E. bovis were found¹ in 40.7% of 2,492 fecal samples from cattle of all ages. They were relatively more numerous in samples from cattle over four and one-half months old than in samples from younger calves. Oocysts of E. zurnii were found in 42.2% of the same fecal samples as checked for E. bovis.

A second study² involving a spring survey of dairy cattle between one week and 18 months of age found coccidia in all 71 counties sampled—in fact, only 16.5% of the individual samples were negative for oocysts.

Iowa

Coccidia were found³ in 86 of 510 fecal specimens of adult cows (16.9%) and in 27 of 83 specimens from calves (32.6%).

Illinois

Coccidia were found⁴ in 85% of the fecal specimens from 795 beef calves from 35 farms. The percentage of cattle coccidia found were E. bovis, 52%; E. zurnii, 37%; E. auburnensis, 46%; E. ellipsoidalis, 40%; E. canadensis, 35%; E. alabamensis, 17%; E. cylindrica, 12%; E. subspherica, 8%; E. wyomingensis, 6%; E. brasiliensis, 4%; Isospora spp., 2%; and E. bukidnonensis, 1%.

Montana

One or more of nine Eimeria species were identified in 64.9% of the cattle examined.⁵

It has been suggested that these numbers will only increase. While this suggestion is not yet validated by data, increased concentration of animals can be expected to favor increased incidence of coccidial infection.

Losses from Bovine Coccidiosis

Coccidiosis is one of the five most economically important intestinal diseases in the cattle industry. Recent estimates place the annual cost of coccidiosis at one hundred million dollars. Because of the insidious nature of coccidiosis, much of the damage from the disease has already occurred by the time signs and symptoms are discernible. The expense of animals that die from coccidiosis, or secondary infections that gain a foothold because of the disease, can easily be estimated. However, the major loss from coccidiosis probably comes as the result of poor rate gains from subclinically infected animals.

Animals severely affected by coccidiosis lose weight and do not regain it during the normal growing period.⁶ Studies show that “yearling” cattle that had been severely affected by coccidiosis when two months old were 95 lbs. (43.2 kg) lighter than uninfected controls at the end of an 11-month experimental period. These animals required four to eight weeks to make up the weight loss as a result of the infection. Following recovery, the animals gained at about the same rate as the control group but would have required an additional 40 days or more of feeding to attain the same end weight.

The cost of therapy after a clinical outbreak of cattle coccidiosis occurs is considerably higher than the cost of early treatment of infection to prevent the disease.⁷ At least a portion of this higher cost is a result of the need for special handling of the animals for veterinary service and the need for medication for secondary diseases such as pneumonia. Furthermore, later treatment may not be as effective, since the sexual stages of the life cycle of coccidia are generally not as sensitive to coccidiostats as the earlier asexual stages. Therefore, a strategic plan of preventive treatment based on previous history of the disease in a particular environment, and other management considerations, could offer the best way to reduce losses due to cattle coccidiosis.

Development of Immunity

Since most severe cases of coccidiosis occur in calves, it can be inferred that some form of immunity is acquired as a result of exposure to the disease. In fact, a study proved that cattle infected with E. bovis do develop resistance to reinfection, persisting from three months to one year or longer.⁸ Resistance to reinfection with E. zurnii and E. ellipsoidalis have also been reported but not quantitated. By contrast, infections of E. alabamensis have been shown to elicit little immunity.

In studies on the nature of immunity to bovine coccidia, one report⁹ indicates that the firstgeneration schizonts and/or merozoites occurring in the small intestine, as well as the second-generation schizonts, merozoites and gametocytes occurring in the large intestine, are affected by the immune reaction. The effects on the stages of the life cycle in the large intestine were observed to be of greater importance than the effects on the stages in the small intestine. It was also observed that the immune reaction affects the numbers but not the timing of the various life cycle stages. Oocysts of E. bovis retained in the mucosa for several weeks acted as a continuing source of antigenic stimulations in immune animals. This report also found that invasion of the intestinal mucosa by first-generation merozoites of E. bovis was inhibited in immune calves. Although studies¹⁰ have been able to demonstrate the presence in calves of antibodies against E. bovis merozoites and oocysts two weeks after infection, the importance of these antibodies has not been clearly established. The rapid turnover rate of the epithelial cells lining the intestinal wall and the fact that these are the host cells for the coccidia suggest that the source of the refractory activity resides outside these cells. The exact nature of the resistance to reinfection remains to be determined.

The Need for Parasite Control

The following are some of the ways in which coccidia damage their host:

1. By damaging the host’s intestinal tissues, which results in reduced absorption capacity.

2. By causing blood and tissue loss for which there is an obvious cost of replacement.

3. By damaging intestinal epithelium, and allowing other kinds of pathogenic organisms and toxins to enter.

4. By inducing immunosuppression, coccidial infection reduces the ability of the host animal to resist other infections.

Modern confinement operations concentrate both the host and parasite populations. These high-density operations are ideal for survival and reproduction of coccidia and other parasites, leading to clinical infections.

As a result of this increased parasite load, and the economic pressures for feed efficiency in production animals, producers can no longer afford to let clinical and subclinical coccidiosis go uncontrolled.

References

1. Boughton DC. Bovine coccidiosis: from carrier to clinical case. North Am Vet 1945:147.

2. Hasche MR, Todd AC. Prevalence of bovine coccidia in Wisconsin. JAVMA 1959;May 15:449.

3. Zimmerman WJ, Hubbard ED. Gastrointestinal parasitism in Iowa cattle. JAVMA 1961;139:555.

4. Szanto J, Mohan LVP, Levine ND. Prevalence of coccidia and gastrointestinal nematodes in beef cattle in Illinois and their relation to shipping fever. JAVMA 1964;144:741.

5. Jacobson RH, Worley DE. Incidence and distribution of helminth parasites and coccidia in Montana cattle. Am J Vet Res 1969;30(7):1113.

6. Fitzgerald PR, Mansfield ME. Effects of bovine coccidiosis on certain blood components, feed consumption, and body weight changes of calves. Am J Vet Res 1972;33(7):1391-1397(Ref3).

7. Fitzgerald PR. The economics of bovine coccidiosis. Feedstuffs 1972;Sept 4:28.

8. Senger CM, Hammond DM, Thorne JL, Johnson AE, Wells M. Resistance of calves to reinfection with Eimeria bovis. J Protozool 1959;6:51-58.

9. Hammond DM, Anderson FL, Miner ML. The site of the immune reaction against Eimeria bovis in calves. J Parasitol 1963;41:414-424.

10. Anderson FL, Lowder LJ, Hammond DM, Carter PB. Antibody production in experimental Eimeria bovis infections in calves. Exper Parasitol 1965;16:23-35.