Coccidiosis

 

Coccidiosis is an intestinal disease of a number of different species of animals.  The cause is a single celled protozoa that reproduces once inside the animal at an extremely rapid rate. The coccidia are very host specific parasites; cattle coccidian affect only cattle, and coccidian from goats, sheep, dogs or cats will not cause disease in cattle. The major damage that occurs from this organism is the damage to the gut cells as the parasite reproduces.  Multiplication occurs so rapidly, that the final release of oocysts (eggs) into the manure represents over 23 million times the number of eggs the animal originally swallowed.  The eggs are resistant to environmental stress and thus are difficult to completely remove from the environment.  They are frequent contaminants of feed and water, and once ingested by other cattle, the life cycle starts again in a new host.

 The life cycle of coccidia is complicated.  Each oocyst, given 2-3 days passed out of the animal in the manure, will develop 8 sporozoites.  Once ingested by a susceptible victim, the oocyst ruptures releasing the sporozoites.  These then penetrate the lining cells of the small intestines and begin a period of multiplication that destroys intestinal cells as asexual reproduction occurs.  This multiplication results in the release of millions of merozoites to invade the large intestine. It is there that the final stage of sexual reproduction occurs where male and female parasites unite to produce the oocyst and the fertile “egg” appears (albeit microscopic) in the manure. The clinical signs of cocciodiosis generally occur because of this last large intestinal stage, resulting in bloody diarrhea, straining and the passage of clumps of necrotic intestinal lining.  However, because damage can also occur in the small intestine if sufficient intestinal lining cells are destroy, unthriftiness and poor doing cattle can be a result even before oocysts are found in the stool.

 It is estimated that as few as 50000 oocysts ingested by a young susceptible calf can result in severe disease.  While this sounds like a ridiculously large number, bare in mind that these oocysts are microscopic and cannot be seen by the naked eye.  Fifty thousand would occupy only a tiny amount of space.. Furthermore, the eggs are very resistant to enviromental conditions such as heat and cold, and thus remain infective for long periods.  Contamination of feed or water can increase the likelihood of serious infection. The severity of the disease is directly related to the number of oocysts ingested.  In light infections, the damage to the gut is minimal, and because the intestinal epithelial cells replace themselves at such a rapid rate, any damage is quickly repaired.  However, in the case of heavy infections, about 2 weeks after the eggs are consumed, most of the cells at the base of  the intestinal glands are filled with merozoites (asexually reproduced life stages) and gametocytes (life stage with both male and female counterparts in the large intestine that finally result in the production of the oocyst.)When all those cells die and rupture because of their infestation, damage is severe, there is loss of blood, fluid, electrolytes and proteins.  Dead intestinal cells are sloughed and also passed out in the diarrhea.

 Most animals infected with coccidia do not show signs of disease.  This is due to a normally low dose exposure and subsequent immunity to that particular coccidian species. Clinical disease is usually a condition seen in the young; caused by lack of acquired immunity, crowding and/or stress.  Weaning with consolidation of calves into close quarters is the perfect place to expect an outbreak. 

 Signs of coccidiosis are usually worst following stressful periods such as weather changes, weaning, overcrowding, long travel, filthy surroundings or other illnesses such as shipping fever.  In mild cases, animals may be asymptomatic, or may only show mild diarrhea, and exhibit a rough haircoat .  Severely affected animals may have severe, watery diarrhea. General emaciation is not unusual, and weakness may cause the calf to defecate without rising, thus soiling its hindquarters. Straining with defecation is usually evident, and rapid dehydration, weight loss and disinterest in food may also be signs may occur in later stages. The diarrhea may contain blood, mucous and stringy masses of tissue due to the of the epithelium of the intestines.  Death is not unusual.

 Diagnosis is made from a combination of history of illness and sanitation for the herd, clinical signs, gross lesions found at autopsy, and microscopic evaluation of intestinal scraping from the dead animals, or microscopic evaluation of the manure. Diarrhea may precede the heavy discharge of oocysts by several days, and diarrhea may continue passed the discharge of oocysts, thus finding the oocysts in the manure may be difficult.  Likewise, healthy animals may harbor some coccidia, thus simply the act of find the eggs in the stool does not necessarily diagnose the problem as coccidia. Certain species of the many coccidia that affect cattle are more likely to cause sever disease.  Eimeria zuernii and  are the main culprits in cattle. Other species may be present, but are far less likely to be pathogenic.

 So called “nervous coccidiosis” is associated with heavy coccidial infestations. The coccidian (or maybe the host) produce a soluble protein exotoxin that is encephalotoxic. Signs include muscle tremors, convulsions and other central nervous system symptoms. 

 Animals can die from coccidiosis; either directly or from secondary diseases.  While  many very sick animals will recover,  permanent damage to the gut may occur.  Unfortunately, normal animals may harbor the organism, and diarrhea may be present before the eggs are found, adding to confusion in accurate diagnosis.  Susceptibility to infection varies.  Some animals are naturally immune.  Most others will develop immunity with exposure; however, this is just to the strain causing illness.  Many strains exist, and exposure to a new variety can induce disease.  It may be that many animals will carry the parasites and coexist reasonably well with the parasite until severe periods of stress. Older cattle  may break with coccidiosis when brought to a new herd with a novel strain to that individual.

 Clincial coccidiosis, in an animal showing signs of disease, must be treated as soon as possible.  It is best to treat each sick animal individually, but these same treatments  can be used  in a herd situation  Sulfa drugs such as sulfadimethoxine (Albon), sulfamethazine or the vitamin B1 analog amprolium (Corid) are the mainstay of treatment for clinical cocciodiosis and all are excellent .  All can be used as a drench or as a water additive. Most sick calves will still continue to drink water, but if there is any question of the calf’s ability or desire to drink from a communal water supply, that animal should be dosed individually by body weight and the medication administered as a drench directly into the animal’s mouth.  The rest of the exposed animals can be treated with the addition of these medications in the drinking water.  Medicated water should be mixed up once per day. Generally treatment for acute coccidiosis continues for 5-6 days, and all calves in a group of animals should be treated even if some are asymtomatic. Sulfas have the advantage of  providing antibacterial effects for secondary infections that may be associated with coccidiosis, such as pneumonia or bacterial enteritis (gut infection). Amprolium replaces vitamin B1 (thiamine) in the coccidia, interfering with its life cycle. High doses for prolonged periods beyond those recommended can result in thiamine deficiency in treated animals.  Likewise, high doses of thiamine to the animals under treatment can interfere with the efficacy of the drug.  Secondary conditions such as dehydration, bacterial pneumonia may require specific treatment.

 There are several products available to prevent coccidiosis in a group of cattle, before any of them show signs.  These medications must be used for 28 days at a minimum, to ensure that they have a chance to act on the part of the life cycle for which they are effective. Amprolium can be used as a preventative at half the dosage required for treatment. Other useful drugs include the ionophore antibiotics lasalocid (Bovatec) and monensin (Rumensin) and the coccidiostat decoquinate. (Deccox). These are all effective preventatives, given well before signs of disease appear, but with the exception of amprolium at the higher dose, none are effective treatments for clinical disease. The ionophore antibiotics lasalocid and monensin have the advantage of being very good growth promotants.  However, they are usually mixed with grain and they have one incredibly important disadvantage;  they are both highly poisonous to dogs and horses and can be fatal if ingested by the wrong species. If mixed in a grain ration, extreme care should be taken to ensure that horses and dogs have no access to the mix.  Unfortunately,  my dogs (and I am sure that most of yours, if given the opportunity) will steal the grain intended for the weaned calves. If you have horses or dogs, decoquinate or amprolium are much safer options. (Amprolium, for example, is used off-label at the recommendation of some veterinarians, to treat coccidiosis in dogs.)

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