January 23, 2013
Coccidiosis is a protozoan disease that most cattle develop some immunity to, while continuing to shed a few oocysts in their feces. Calves are the most vulnerable because they have the least immunity, particularly if they ingest a high number of immature protozoa in a dirty environment that overwhelm their immune system.
James Hawkins, DVM, Jackson, MS, says young calves kept in a drylot or small pen are most at risk because the environment’s contamination tends to be high.
“People who run into problems with coccidiosis are usually backgrounders who buy small calves from different sources, keep them 90 days or less, and then resell them. They then buy another group of calves and move them into the same facility,” he says.
Gary Zimmerman, veterinary researcher in Livingston, MT, says there are several different genera and many species of pathogenic coccidia, but only a few affect cattle. “There are also different susceptibilities in individual animals to various coccidia. If new animals come into the herd, they may bring coccidia the rest of the herd hasn’t been exposed to,” he says.
All cattle have subclinical infections, which are held in check by host immunity. “There is no cross-species immunity. A calf that’s been exposed to one species and developed immunity to it won’t have immunity to the other species. In addition, coccidia are host-specific. Some producers think cattle get coccidiosis from birds, but it isn’t true,” Zimmerman says.
Floron (Buddy) Faries, Texas A&M AgriLife Extension Service, says the three species of coccidia of most concern in cattle are Eimeria bovis, E.zuernii, and E. auburnensis. “Their ability to produce cattle disease is dependent upon the degree of exposure,” he says.
A calf can handle a few oocysts, but a heavy load is another story. Meanwhile, adult cattle rarely develop the disease, though it can occur in thin, malnourished or severely stressed cows, or those compromised by another cattle disease. All cows, however, carry coccidia in the small and large intestines, Faries explains.
“We distinguish between infection and disease,” Faries says. “When there are no clinical signs, I prefer to call it coccidiasis – simple infection in which coccidia are a normal inhabitant of the intestine. If there is deep damage to the intestinal mucosa, there will be symptoms and it becomes disease – which we call coccidiosis. The definition of disease implies infection and damage, plus clinical symptoms,” Faries says.
“For a parasite to survive in an otherwise immunocompetent host, it must have some mechanism to avoid, evade or suppress immunity,” Zimmerman adds. “Otherwise, the host’s immune system would kill the parasite. But parasites can suppress the immune response directed against them, or create a generalized immune suppression. This is why animals with a heavy parasite load are more susceptible to other pathogens.”
Stress, such as weaning, confinement and cold, wet or hot weather, can hinder the immune system. Nutritional stress also can be a factor, as many cattle experienced during drought in many parts of the country.
“We see more problems in young cattle coming from drought areas,” Hawkins says. “Over the past dozen years, we’ve also started to see more problems in pastured cattle with coccidiosis – which we wouldn’t normally expect – and I’m not sure why.”
Conditions vary for different producers. “Someone buying calves in Florida may have the worst time during a hot, dry summer when calves are stressed by heat and dust,” Hawkins says. In some climates, however, it might be wet, sloppy spring weather that nips baby calves.
The presence of other pathogens, a change in diet, inadequate colostrum for a newborn calf, etc., are host factors that can play a role. Environmental factors include the use of permanent buildings and small pastures year after year, crowding, poor hygiene, adverse weather, transport, frequent regrouping of calves and bringing in new animals.
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In a group exposed to a high level of contamination, all will be infected by the cattle disease, but only some show clinical signs with diarrhea. In some instances, morbidity (proportion of the group showing disease) may be as high as 75%.
“The morbidity and mortality rates of coccidiosis are variable, depending on overall herd health, nutritional and immune status, and external factors such as crowding, weather, exposure to other diseases, and other stressors,” Zimmerman says. “Mortality rate in a group is usually much lower than morbidity, but can be as high as 24%. Even if none of the animals die, the economic impact can be devastating.”
“Oocysts passed in manure are tiny and much smaller than worm eggs,” Faries says. “They aren’t infectious at that stage. They have to sporulate and develop into four cells, each of which has two sporozoites. These eight sporozoites are the infective stage.”
How long it takes for the oocyst to sporulate depends on weather and temperature. “If it’s cooler than 35°F, or hotter than 85°, development is prolonged. But at optimal temperatures, the oocysts form sporozoites in 2-4 days,” Faries says.
Once a calf ingests sporozoites, they invade the lining of small and large intestines, down into the mucosa where they multiply by asexual development.
“Then they form a second stage. These merazoites rupture out of the mucosal cells and invade new cells, multiply again and produce a second generation. This process continues for at least four asexual multiplication cycles. After a few days with all this damage, they re-enter the mucosal lining and form male and female gametes. These unite and secrete a wall around themselves and form an oocyst, which is passed out with feces to start the life cycle again.”
By the time oocysts are detected in a manure sample, damage is underway in the calf’s intestines, and the immune system is kicking in to fight it.
“If the calf is healthy, immunity becomes fairly high fairly quickly and there’s no further damage,” Faries says.
If a calf only ingests a few coccidia, it’s beneficial because it stimulates immunity against that species. This allows a calf to counter a higher level of exposure down the road.
“If a larger number are ingested and there is some damage (signs of coccidiosis), immunity kicks in and shuts down the asexual multiplying and the disease is self-limiting and runs its course. If immunity stays strong, due to good nutrition and good health, the calf won’t get the cattle disease again if exposed again later,” Faries explains.
There is no vaccine against coccidiosis; prevention or treatment consists of traditional products that kill or hinder coccidia. Coccidiocidal compounds include amprolium and sulfas. Preventive drugs are called coccidiostats because they hinder multiplication of coccidia. These include decoquinate and the ionophores.
“If the calves are doing okay, we should let it run its course, instead of treating it and shutting down the asexual multiplication – which would interfere with development of immunity,” Faries says. “But if some calves are passing blood, with watery diarrhea, shedding some mucosal lining, or are anemic, weak and dehydrated because they can’t absorb fluid and nutrients, they need supportive treatment,” he adds.
These calves need treatment to shut down multiplication of coccidia, along with supplemental fluids and nutrients. Serious cases need intravenous therapy if the intestine is too damaged to absorb oral fluid and electrolytes.
Several products are effective for treating coccidiosis; these include amprolium (Amprol® or Corid®), as well as decoquinate (Deccox®). “These work well if infection is still in the asexual stage. Some of the sulfonamides, such as sulfaquinoxalene, are also still used,” Faries says.
If calves are brought into a contaminated facility, such as weaning pens or a feedlot, they may break with coccidiosis within four weeks unless administered a coccidostat.
“A preventive drug would be fed at a low level during that period. Some producers give every new group of calves 21 days or more of a preventive level of Corid,” Hawkins says. “The label for Corid as a preventive is 21 days at half the treatment dose (which is given for five days),” he says.
Ionophores, such as monensin (Rumensin®) and lasalocid (Bovatec®), are often given to feedlot-age calves because they help increase feed efficiency and also act as a mild coccidostat, hindering multiplication of coccidia.
Joe Dedrickson, DVM and Merial’s field director of veterinary services, considers Corid, which is labeled for prevention and treatment of coccidiosis, as being “probably the best treatment for calves exhibiting symptoms, and Deccox for control is probably the next choice.” Deccox, which is labeled for prevention but not treatment, prevents immature coccidia from growing while the calf heals, and is unique because it’s safe at any level and not toxic to mammals and birds. Meanwhile, monensin and lasalocid are also labeled for prevention of coccidiosis, while sulfaquinoxaline and sulfamethazine are labeled for both treatment and control.
The key to preventing outbreaks is minimizing heavy fecal contamination of the environment. Corrals, pens, small pastures used year after year with cattle confined for calving, breeding, weaning, etc., are high-risk environments for cattle disease. It helps to keep cattle spread out.
“Many producers confine cattle for calving to allow monitoring. Even if they move pairs out of the maternity trap into a larger pasture when calves are a few days old, the young calves have already picked up oocysts,” Faries says. If a calf nurses a dirty udder or lies in manure and licks himself, he ingests oocysts.
He says one ranch with a chronic problem addressed it by developing two maternity areas, which they alternate for use each year. The “off” year allows dry hot weather to sterilize the pen, leaving it fairly clean for use in alternate years.
“Another risk is congregating cattle in the same feeding area. If you use round bales and never move the feeders, or feed hay on the ground in the same high places in the field, manure builds up,” Faries says.
Diagnosis of coccidiosis
If a calf has bloody diarrhea, the veterinarian may take a fecal sample and do a flotation test for coccidia. Whether you find them or not, however, doesn’t mean much.
“By the time a calf has diarrhea, it’s almost past the time when that calf is passing a lot of oocysts,” says Joe Dedrickson, Merial field director of veterinary services. A lack of oocysts doesn’t necessarily mean the calf doesn’t have coccidiosis; if he’s had bloody diarrhea for several days, most of the oocysts may already be passed.
“And if we find oocysts, they may not be the cause of the problem,” adds Faries. “Often, coccidiosis is suspected because the test was positive for oocysts. If there are large numbers of a pathogenic type, however, with a history of coccidiosis on the ranch, and an environment optimum for spread, we will probably call it coccidiosis.”
A calf with coccidiosis occasionally shows nervous signs that can vary from twitching to incoordination, loss of balance, and even seizures.
“This syndrome isn’t completely understood,” says Gary Zimmerman, veterinary researcher in Livingston, MT. “Some researchers believe it’s not due to the coccidia themselves, but mineral depletion from the damaged and compromised intestinal tract. Neurotoxins have also been suggested as a cause.”
Such nervous signs occur in 10%-30% of calves with coccidiosis. Joe Dedrickson, Merial’s field director of veterinary services, says parasitologists and diagnostic labs use the term “nervous enteritis” for the condition, since it’s associated with enteritis, which is inflammation of the intestines.
The condition can be difficult to treat. “Calves may respond and look better, and you think the drug worked, but it’s probably the supportive treatment – intravenous (IV) fluids, dextrose, etc., – that helped,” Dedrickson says. Traditional drugs may help, however, by removing coccidia.
Some animals in a coccidiosis outbreak may be weak from diarrhea, dehydration and anemia. If they stagger or go down and have trouble getting up, this may be mistaken for nervous coccidiosis.
“Actual nervous coccidiosis syndrome is dramatic, however,” Dedrickson says. “If these animals become excited, they go into convulsions, drop to the ground and kick; muscles become rigid. If a calf goes down, and you give him thiamin and dextrose IV, oral electrolytes, get him upright so he won’t bloat, and leave him alone – he’s usually gotten up and rejoined the herd when you come back an hour later.”
You may think you did a miracle cure, but the calf simply got over the seizure.
“The convulsions may be dramatic, but if you let them be calm and quiet for awhile, they become normal again. The death rate when you see nervous signs is fairly high, however; more than half generally die in the next few days. They get up and look good, but the next morning you find them dead,” probably of another seizure, Dedrickson says.
Heather Thomas is a rancher and freelance writer based in Salmon, ID.
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