![]() |
Fact Sheet No. 10:
|
![]() |
By John Maas, DVM, MS
|
||
Coccidiosis causes significant economic losses in cattle. Although most cattle are exposed to coccidia and infected, most of the infections are self-limiting and mild or asymptomatic. The parasites that cause this condition are members of the species Eimeria, and the most important of this species for causing disease in cattle are Eimeria bovis and Eimeria zuernii.
The life cycle of these parasites is complex. Single cell oocysts are passed in the feces of cattle, are resistant to disinfectants, and can remain in the environment (particularly moist, shady areas) for long periods of time and maintain their infectivity. The oocysts sporulate and these sporulated oocysts are ingested by the host and the sporozoites are released in the intestine. Sporozoites enter the intestinal cells, form trophozoites, which in turn divide into many merozoites. These merozoites penetrate additional intestinal epithelial cells and form more meronts. Eventually, macrogametes and microgametes are formed which combine to produce the next generation of oocysts. When the oocysts are mature, they rupture the host cell and are released into the lumen of the intestine and pass out in the feces. The reproduction of these organisms is phenomenal as illustrated by the following:
1 oocyst X 8 sporozoites
X 120,000 first generation merozoites
X 30 second generation merozoites
X 80% macrogametocytes
= 23,040,000 oocysts
The potential damage to the intestinal cells is obvious. It is estimated that as few as 50,000 infective oocysts ingested by a young susceptible calf can cause severe disease. The replication of the coccidia within the host's intestinal cells and the subsequent rupture of the cells is responsible for the disease and the clinical signs that develop.
The severity of the disease is directly related to the dose of infective oocysts that are ingested. The more oocysts ingested, the more severe the subsequent disease. With light infections, the damage to the gut cells is minimal and because the cells in the gastrointestinal tract are replaced rapidly the damage is quickly repaired. In the case of heavy infections, about two weeks after the oocysts are ingested, most of the epithelial cells at the base of the intestinal glands are occupied by meronts or gametocytes. As these cells rupture, damage is severe and there is loss of blood into the feces. Also, fluid, electrolytes, and blood proteins (albumin) are lost.
Most animals infected with coccidia do not show signs of illness. This is due to the normally low dose and after a course of infection the animal is immune to that particular Eimeria species. However, this does not mean they are immune to all Eimeria species. Therefore, coccidiosis is primarily a disease of the young where there is crowding, stress, and/or nonimmune animals. Older cows certainly act as a reservoir and shed oocysts into the environment. Stress such as shipping, weaning, dietary changes, steroid therapy, and other problems can precipitate an outbreak of coccidiosis. Older cattle immune to their own endemic species of coccidia can become infected and/or ill when moved to a new herd and exposed to a different species.
The clinical signs of coccidiosis can include the following:
Many cattle are affected and experience weight loss or decreased weight gains without showing obvious illness and these cattle account for the majority of the economic losses. Your veterinarian can diagnose coccidiosis on the basis of clinical signs, fecal oocysts examinations, and post mortem examination of dead animals (if that occurs).
Once an accurate diagnosis is made there are a number of drugs useful in treatment or prevention. Some of the drugs that can be used for treatment include:
Some of these drugs and dosages may require a veterinarian's prescription and extended withdrawal time, be sure to check with your veterinarian before treating animals.
Drugs can be very useful in helping to prevent coccidiosis and some of these are listed below:
Both lasalocid and monensin are polyether ionophores which are used to increase feed efficiency and weight gains; however, they also have effectiveness to prevent (not treat) coccidiosis. Monensin has a lower threshold for toxicity and cattle must be gradually introduced to it in their diet to prevent diarrhea, feed refusal, or toxicity.
Drugs useful for treatment are not necessarily useful for prevention and vice versa. Drugs administered in feed or water may not be consumed by sick animals, so the owner must be aware of this in treating ill cattle.
In a clinical research trial conducted at the Sierra Foothill Research and Extension Center in 1995 looked at the effect of prevention of coccidiosis on weanling cattle. Calves were preconditioned to a feed supplement prior to weaning. The supplement did not contain any drugs prior to weaning. At weaning, the calves were split into 3 groups randomly. The groups continued to receive their supplement base which then contained
The animals were closely monitored for signs of clinical disease, fecal oocyst counts, and weight gains. The cattle were maintained on the treatments for only 28 days. At the end of the treatment period, the cattle with access to the two anti-coccidial compounds gained 0.5 pounds per day more than the control group. These cattle were not heavily parasitized and can best be characterized as mildly to moderately infected with coccidia. Our conclusion was that coccidiosis prevention, in weaned calves that are minimally exposed to coccidia may have important production benefits.