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Management and Control of Goat Coccidia

A. David Scarfe



Coccidiosis can be one of the most economically important diseases in many livestock species. It can be especially devastating to recently weaned kids and, occasionally, cause losses in other age groups. Coccidia are everywhere; it is nearly impossible to find a goat without some coccidia. However, the presence of coccidia in the intestines of an individual does not mean the animal is actually suffering from coccidiosis. Coccidia only cause disease when their numbers become so great that pathological damage is done to the host. Usually poor management is the reason why coccidia numbers increase excessively; thus, coccidiosis may be considered a man-made disease. This also suggests that coccidiosis can be adequately managed. Unfortunately, two forms of the disease are frequently present, one in which the clinical signs are obvious, the other in which no immediately obvious signs are evident. It was thought for many years that the coccidia of sheep and goats were interchangeable between those species, but now it appears that most, if not all, coccidia species are unique to their host. Coccidia from chickens will not infect goats.

The objective of this article is to give goat producers sufficient information to adequately understand the organisms and the disease they can cause. Such understanding is necessary to control and prevent coccidiosis and to reduce or prevent acute and chronic losses. The typical life cycle of coccidia will be described in order to understand where damage is done and why changes in management may be useful. The forms of the disease and how to recognize and diagnose them will be discussed along with treatment and control measures, and a list of available drugs for the control and treatment of coccidiosis will be provided.

Coccidia Life Cycles
It should be clearly recognized that among the internal parasites of goats coccidia are only one of the many parasites of economic importance. Others include round worms (nematodes), flukes (trematodes), tape-worms (cestodes) and a myrad of bacteria, viruses and other organisms. Each type of parasite has a different life cycle, affects the host in different ways and is controlled with different drugs and management schemes.

Basic knowledge of the life cycle of coccidia is necessary to understand the damage done to the host (goat) and to demonstrate why control is so difficult. While several species of coccidia may inhabit the intestines of goats, two species are important pathogens and can cause serious damage: Eimeria ninakohlyakimovae and E. arlongi. Coccidia are intracellular parasites. They live and grow within cells lining the gastrointestinal tracts of their hosts. The oocyst, an egg-like structure, is passed in the feces of infected hosts. When first passed, the oocyst is not infective; it must first undergo a period of development (sporulation) in the environment which takes 2-3 days.

Oxygen and moisture are required for sporulation (the formation of sporozoites within the oocyst). The time required for development is temperature-dependent. In general, the warmer the weather, the faster the development, unless the temperature is high enough to kill the organism.

After sporulation, the oocysts are very resistant to environmental conditions and ordinary disinfectants will not kill them. Extreme desiccation or direct sunlight are about the only environmental factors that are detrimental to sporulated oocysts, and a sporulated occyst may survive for a year or longer if protected from direct sunlight. Therefore, areas under feed bunks and around water troughs may harbor infective oocysts for prolonged period of time.

When a susceptible goat ingests sporulated oocysts, sporozoites are released and enter cells lining its intestine. Within these cells, the organism becomes a schizont or meront, which grows to many times its original size.

Sporocysts escape from the oocyst, invade cells lining the intestinal tract. Asexually produced meroziotes will reinvade more host cells. Some of the merozoites act like eggs and sperm, fuse and the resulting oocyles are shed in the feces. These become "spores" and become infective in 2 to 3 days. The entire life cycle takes about 14 days. Clinical signs of disease depends on how may intestinal cells are damaged by invading organisms (modified after Wright, 1989).

The schizont undergoes asexual reproduction producing a large number of daughter cells called merozoites. The number of merozoites produced within each meront varies from about a dozen to more than a hundred thousand, depending upon the species of coccidia involved. Each of the merozoites released from a schizont has the capability to enter a new host cell where a new schizont is once more formed and, subsequently, another generation of merozoites. The number of generations of meront formation is unique to each coccidian species. After a predetermined number of generations, the merozoites differentiate into male and female gametes and fertilization of fusion of these gametes form an oocyte within a host cell. The oocyte is then passed in the feces, completing the life cycle in about 2 weeks.

Various species of coccidia parasitize different areas of the intestinal tract, utilizing specific types of host cells. Some invade only mature epithelial cells, others only cells of underlying tissues. Each species has different reproductive patterns. There are varying numbers of generations of asexual reproduction, and if more merozoites are produced per meront, then more host cells are invaded. It is for these reasons that some species of coccidia are much more likely to cause disease than others.

Pathological Changes Induced by Coccidia
The damage done to the host is essentially that of intestinal cell destruction, which occurs when any coccidian stage leaves the host cell. Potentially, one oocyst ingested may lead to the production of a million or more oocysts which are passed in the feces 2 to 3 weeks later. This also means that one oocyte ingested potentially destroys millions of intestinal cells. The host cells affected most often are epithelial cells lining the gut which transport nutrients and fluids into the body. If these cells are damaged, blood or plasma may leak into the lumen of the gut. The damage may also allow bacteria from the intestine to enter the blood stream and invade other tissues. If the individual does not die of blood loss, dehydration, or bacterial septicemia, the cells will be replaced at least to some extent by scar tissue or by a increased turnover of epithelial cells. The latter form short, flattened villi or large polyps with rapidly proliferating epithelial cells that are not as efficient in absorbing nutrients from the intestine. This causes the host to become unthrifty.

Clinical Signs of Coccidiosis
As with other parasitic diseases, the clinical signs may vary between animals and on occasion may appear vague. In general, two forms of the disease should be recognized: the acute (or clinical) form and the chronic (subclinical) form. In the clinical form, obvious signs of the disease are suddenly seen. In the subclinical form, progressive, but slow and unseen, damage is done. In reality there is a continuum between these forms and occasionally animals will be seen to occasionally spontaneously break with clinical signs which then resolve themselves without intervention. In these cases, acute disease is seen while chronic coccidiosis is continuously occurring.

Acute coccidiosis
The primary clinical signs of disease are directly related to the degree of intestinal mucosa (lining) destruction. The first signs of disease are usually a sudden onset of severe diarrhea with foul smelling, fluid feces often containing mucus and blood. The blood may appear as a dark tarry staining of the feces or as streaks. In particularly severe cases, the stool may consist almost entirely of large clots of blood. The perineum and tail are usually stained with blood-stained feces. Occasionally severe straining may be seen, with possible rectal prolapse.

Affected animals may also have a slightly evaluated body temperature but usually the temperature is normal or subnormal (under 104F). Depending on the loss of blood from enteric hemorrhage, the animal may be anemic with pale nucosa (mucus membranes), be weak, stagger and, occasionally, have difficulty breathing. Dehydration is common, but may not be severe if animals continue to drink.

There is usually a decrease in appetite in animals with clinical coccidiosis. Decreased appetite and, occasionally, failure to eat may last 5-6 days during the acute phase of disease. Some animals undergo a long convalescent period during which feed consumption and body weight gains are subnormal. In mild cases which may not show dysentery, some diarrhea and a reduced growth rate is usually seen. Subclinical cases (those showing no diarrhea) show inferior growth rates and chronic anemia. In groups of kids raised and fed in crowded conditions, the symptoms over a 1-3 week period may include inferior growth rates, gradual onset of weakness, inappetence, recumbency, emaciation and sometimes death. Signs of diarrhea may not be obvious.

Clinical coccidiosis can be precipitated by stress and overcrowding. Young, recently weaned animals that have been moved into an overcrowded pen or had a sudden change in diet or experienced inclement weather are the most susceptible hosts. Disease occurs when a susceptible goat ingests a large number of oocysts of a pathogenic species of coccidia during a short period of time or when stress overwhelms the host's immune system. An example of a situation in which waning immunity and stress lead to coccidiosis is one that often occurs in the late winter in Angora goats. Does are shorn prior to kidding; then if rain occurs following shearing, the goats may become hypothermic. To prevent this, a rancher will pen the goats. With overcrowding and shearing and weather stress, coccidiosis frequently results; it can also happen to meat goats.

Kids which have been brought off pastures with little or no prior exposure to coccidia are very susceptible to acute clinical coccidiosis when mingled in cramped conditions because they have very little immunity or resistance. They may develop the acute disease and mortality rate may reach 50% or more. Contrarily, some animals never show clinical or subclinical signs even though large numbers of oocytes are found in their feces.

Diarrhea, dysentery, or lack of weight gain may be due to numerous causes other than coccidiosis. For an accurate diagnosis of coccidiosis, clinical signs should be correlated with oocyte fecal counts. As indicated above, the presence of oocytes does not indicate disease, as coccidia are normally present in most goats, but heavy coccidia infection usually produces large numbers of oocytes. There is usually a lag of 14-18 days between a massive ingestion and the presence of oocytes in the feces. There is also a delay of 2-4 days between when dysentery or diarrhea begins and when oocytes are found in the feces. It is, therefore, best to evaluate the feces of several individuals over several days to fully assess the coccidia burden.

A count of over 5000 oocytes/g of feces is considered significant. While counts below 5000/g do not ordinarily suggest a clinical infestation, they may indicate a potential source of severe infestation if environmental conditions become favorable for rapid spread. In severe outbreaks, counts in excess of 100,000/g are common but still need to be correlated with clinical signs because similar counts may also be encountered occasionally in clinically normal animals.

If a herd showing apparent clinical coccidiosis does not respond to prevention or treatment programs, it is wise to pursue further diagnostic techniques to differentiate between other gastrointestinal diseases such as salmonellosis, intestinal helminthiasis (worms), overeating disease, E. coli enteritis, or Crytosporidium and viral infections.

Fortunately, resistance to the organisms does occur. This resistance is an acquired immunity that is specific to each species of coccidia encountered. However, when we speak of immunity to coccidia, as with worms, we think of immunity as being free from disease, not freedom from infection. The resistance is relative in that it may prevent the establishment of the organism or retard its ability to reproduce. However, the apparently short duration of protection makes it impractical to develop an effective vaccine against coccidia in mammals at this time. Resistance can be overridden by excessive numbers of organisms and by stress such as weaning, changes in feed, weather changes, shipping, other diseases, or lactation.

Coccidiosis, if it doesn't kill the animal, is usually a self-limiting disease and clinical signs usually subside spontaneously. If damage to the intestine is not too severe, natural immunity will reduce, but not eliminate, the number of coccidia living in the gut. Early in outbreaks, changes in management (see below) usually reduce the rate of development of new cases.

Several chemotherapeutic agents have been recommended for both the control and treatment of coccidiosis. These are summarized in Table 1. In an outbreak, clinically affected animals should be isolated, and an attempt should be made to reduce overcrowding in pens and corals. All feedbunks and water supplies should be situated or constructed to reduce fecal contamination or prevent animals walking in feed bunks. Animals should not be fed on the ground. If placed in isolation, soiled bedding in stalls or pens should be removed frequently and clean bedding should be added as needed. This should reduce continuous reinfection.

To prevent secondary gastrointestinal bacterial infections, antibiotic therapy may be advisable. Intestinal protectants which coat damaged intestinal mucosa may assist recovery from severe enteritis. Severe cases requiring rehydration via electrolytes should receive oral or parenteral therapy as necessary.

One or more of the coccidostats known to be effective in reducing or inhibiting coccidia in the intestine (Table 1) should be used in combination with supportive therapy and good management practices. Combinations of sulfonamides (e.g., sulfamethazine, sulfaquinoxaline) and ionophores (monensin, lasalocid) may be helpful to simultaneously reduce coccidia and secondary bacterial infections. While sulfonamides have been used for more than 40 years for the prevention and treatment of coccidiosis per se, resistance to many of these drugs by coccidia is widespread and they are no longer as effective as they once were. These drugs do not kill coccidia directly but inhibit their growth an proliferation. If the infection can be moderated sufficiently with coccidiostat use, the goat's immunity to coccidia will develop and suppress further development.

Amprolium and monensin presently appear to be the most popular with goat breeders. Monensin has been found to be of value in preventing coccidiosis in Angora goats at levels that also increase feed efficacy. While most coccidostats are only approved for use in cattle, sheep or other species, monensin has recently been approved for use in Angora goats in the United States. A similar drug, lasalocid, is approved for use in sheep and an unrelated compound, decoquinate, has been shown to be effective against coccidia in sheep.

The obvious solution to problems resulting from coccidiosis is to prevent susceptible animals from ingesting large numbers of oocysts. Sanitation, dry weather, sunlight, water troughs that cannot be defecated into and don't overflow, and feeders that infected animals can't walk in, all help in prevention of disease. These conditions are only rarely achieved. While good sanitation will help prevent disease, these measures will not entirely preclude an outbreak of coccidiosis unless extremely rigorous precautions are taken.

Coccidiosis can be controlled most practically by limiting exposure to coccidia, by reducing stress on the animals, and by the use of a coccidiostat when exposure is imminent. The fact that most coccidiostats do not kill but interfere with the reproductive potential of coccidia allows enough antigenic stimulation of the immune system to increase resistance while the goat is protected by the drug. When the coccidiostat is removed from the diet, resistance to disease will be maintained as long as exposure to the coccidia continues.

Utilizing feeds that contain coccidiostats prior to the outbreak of disease may be essential in crowded conditions. Susceptible goats exposed to moderate numbers of oocysts will seldom develop signs of disease. However, because of their lack of resistance, they will produce millions of oocysts in their feces. These oocysts will then contaminate the feed and water supplies in sufficient numbers to fatally expose susceptible goats.

To be most effective, coccidiostats should be give early in the coccidian lifecycle and before massive infections overwhelm the goat. Use of the drugs should begin prior to anticipated susceptible times. In some cases, producers start prophylactic use of coccidiostats in pregnant females several weeks prior to kidding and continue until about 60 days postpartum. Kids are started on coccidiostats in creep rations and continue until after the stress of weaning has subsided. In confinement situations their use may be continued until animals are marketed. In most cases, solid immunity develops in pasture kids, except in situations where there is contaminated kidding ground and severe overstocking. In cases where new animals are introduced into a herd, the producer should treat the incoming animals with the control dose of a coccidiostat prior to mixing animals. This should reduce the incidence of stress-related coccidiosis in the incoming animals and reduce contamination of existing facilities.

The most economical way to deal with coccidiosis is to medicate the feed or water supplies with the chemotherapeutic of choice and also avoid overcrowding, nutritional disorders, weaning and other stresses. If necessary, clinical cases can be treated on an individual basis. Routine prophylactic medication of feed, salt-protein blocks or water usually prevents severe outbreaks. Care should be taken to ensure good mixing of the drugs and that the proper doses are adhered to. Continued use of coccidiostats will, over a period of time, lessen the number of oocysts passed into the environment for as long as that coccidiostat is effective. However, the continued use of the coccidiostat against a population of parasites will eventually lead to resistance to the coccidiostat. It is unlikely that alternating drugs will be of much value in preventing coccidiosis. It is advisable that constant monitoring of coccidiostats be practiced so that large numbers of oocysts are not passed into the environment and "at risk" goats receive an overwhelming exposure.
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