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.