Coccidiosis in Cattle

Epidemiology: Infections with a single species of coccidium are rare in nature; mixed infections are the rule. Eimeria zurnii and E. bovis are the most pathogenic species, but E. auburnensis and the other species may contribute to the total disease picture, and some of them may cause marked signs by them-selves if they are present in large enough numbers.

Bovine coccidiosis is primarily a disease of young animals. It ordinarily occurs in calves 3 weeks to 6 months old. Older calves and even adult animals may be affected under conditions of gross contamination, but they are usually symptomless carriers.

Calves become infected by ingesting oocysts along with their feed or water. The severity of the disease depends upon the number of oocysts they receive. If they get only a few, there are no symptoms, and repeated infections produce immunity without disease. If they get more, the disease may be mild and immunity may also develop. It they get a large number, severe disease and even death may result.

Crowding and lack of sanitation greatly increase the disease hazard. Successive passage of coccidia from one animal to another often builds up infection to a pathogenic level, since in each passage the recipient receives more oocysts than in the previous one. This is the reason for the common observation that calves placed in a lot where others are already present may suffer more from coccidiosis than those which were there first. This successive passage from a carrier to a symptomless "multiplier" to a sub-clinical case to a fatal case was described by Boughton (1945) as typical of the transmission of bovine coccidiosis. In addition, it is likely that recycling by repeated infections of a single individual may also play an important part.

Coccidia of cattle

A little-understood type of bovine coccidiosis is winter coccidiosis. This occurs when it is so cold that oocyst sporulation should be minimal if it occurs at all. Presumably there is enough heat in the bedding to permit sporulation. Another explanation which has been advanced is that the stress of winter conditions exacerbates a latent infection. This explanation is not easy to validate, however, in view of the self-limiting nature of coccidial infections.

Davis, Herlich and Bowman (1959, 1959a, 1960, 1960a) found that concurrent infections of cattle with the nematodes, Trichostrongylus colubriformis or Cooperia punctata, exacerbated the effects of coccidia in calves, but that Ostertagia ostertagi and Strongyloides papillosus had no such effect.

Diagnosis

Bovine coccidiosis can be diagnosed from a combination of history, signs, gross lesions at necropsy and microscopic examination of scrapings of the intestinal mucosa and of feces. Diarrhea or dysentery accompanied by anemia, weakness, emaciation and inappetance are suggestive of coccidiosis in calves. Secondary pneumonia is often present. The lesions found at necropsy have already been described.

Microscopic examination is necessary to determine whether the lesions are due to coccidia or to some other agent. However, diagnoses will often be missed if one relies only on finding oocysts in the feces. There may be none there at all in the acute stage of zurnii coccidiosis. Similarly, the mere presence of oocysts in the feces is not proof that coccidiosis is present; it may be coccidiasis. To be sure of a diagnosis, scrapings should be made from the affected intestinal mucosa and examined under the microscope. It is not enough to look for oocysts, however, but schizonts, merozoites and young gametes should be recognized.

Treatment

A number of investigators (Boughton, 1943; Boughton and Davis, 1943; Davis and Bowman; 1952, 1954; Hammond et al., 1956; Senger et al., 1959) have found that the sulfonamides have some value against bovine coccidiosis.

Other types of compounds which are used in avian coccidiosis are unsatisfactory. For example, Hammond et al. (1957) found that nicarbazin was effective in preventing experimental coccidiosis due to E. bovis in calves only at doses which were toxic to the animals. Gardner and Wittorff (1955) found that 0.1 to 0.3% furacin in the ration was toxic to dairy calves, causing nervous signs and reducing or preventing weight gains. Even 0.01% of the drug had some toxic effect. It injures the myelin sheaths and causes cerebral damage.

Gasparini, Roncalli and Ruffini (1958) claimed that drenching with 4 g per 100 kg ammonium sulfate plus 2 ml lactic acid in a liter of milk twice a day for 4 consecutive days cured coccidiosis due to E. zurnii in 2 herds of cattle in Italy. They believed that the ammonium sulfate worked by releasing ammonia, and added the lactic acid to prevent release from taking place in the stomach. However, their work was improperly controlled, and the efficacy of this compound remains to be determined.

Sulfamethazine and sulfamerazine appear to be better than sulfaquinoxaline or other sulfonamides. They are only partially effective, however. They do not prevent the diarrhea, but they do reduce the severity of the disease. Thus, Davis and Bowman (1954) found that sulfamethazine reduced the severity of experimental infections with E. zurnii or mixed species in calves and that treated calves gained slightly more weight than the controls. Drug treatment was started before infection, and no immunity to subsequent exposures was produced. Hammond et al. (1956) found that sulfamerazine or sulfaquinoxaline, given to calves at the rate of 0.143 g per kg body weight for 2 days and 0.072 g per kg for 2 more days, decreased the severity of coccidiosis due to E. bovis if they were administered between 13 and 17 days after experimental infection. They were not effective earlier or later than this. The drugs presumably act on the merozoites after their release from the schizonts. Senger et al. (1959) found that a mixture of equal parts sulfamerazine and sulfamethazine given by mouth at the rate of 213, 143 and 70 mg per kg body weight 13, 14 and 15 days, respectively, after inoculation reduced the severity of the disease and did not interfere with the development of immunity.

Hammond et al. (1959) found that a single treatment with 0.215 g per kg sulfamethazine or sulfabromomethazine 13 days after experimental inoculation with E. bovis effectively controlled coccidiosis. Administration of either compound on alternate days at the rate of 0.0215 g per kg for as short a period as 10 to 18 days after inoculation also effectively controlled coccidiosis, while in 1 experiment treatment at this rate 12 and 14 days after inoculation suppressed the disease. This treatment did not interfere with the development of immunity.

Since the sulfonamides are generally only partially effective, preventive measures are more important than curative ones.

Prevention

Sanitation and isolation are effective in preventing coccidiosis. Beef calves should be dropped and kept on clean, well drained pastures. Overstocking and crowding should be avoided. Feed and water containers should be high enough to prevent fecal contamination. Feed lots should be kept dry and should be cleaned as often as possible. Concrete or small gravel are preferable to dirt.

Dairy calves should be isolated within 24 hours after birth and kept separately. Individual box stalls which are cleaned daily may be used. Slat-bottom pens are also effective and require less cleaning. Allen and Duffee (1958) described a simple, raised, wooden home-made stall with a 4 by 2-1/2 foot slatted floor in which dairy calves can be raised separately for the first 3 months. Davis (1949) and Davis and Bowman (1952) described a 5 x 10 x 3 foot outdoor portable pen which can be moved to a fresh site once a week and thus eliminates the need for cleaning. It is made primarily of net wire and 1 x 4 lumber, with a removable roof and siding at one end. The pens should not be returned to the same ground for a year.

These methods will not eliminate all coccidia, but they will prevent the calves from picking up enough oocysts to harm them. In addition, they will greatly reduce lice, helminth parasites, pneumonia, white scours and other diseases.

The unsporulated oocysts of E. zurnii are killed by sunlight in 4 hours or by drying at 25% relative humidity or below in several days. They are not harmed by freezing at -7 to -8° C for as long as 2 months, and half of them survive as long as 5 months; at -30° C, however, only 5% survive 1 day. The oocysts are killed by 10-6 M mercuric chloride, 0.05 M phenol, 0.25 M formaldehyde, 1.25% sodium hypochlorite, or 0.5% cresol (Marquardt, Senger and Seghetti, 1960).