Lecturer: Dr. Donal O'Toole
Parasitism is an association between two species in which one species, the parasite, lives on or in a second species, the host, for a significant period of its life as well as obtaining nourishment from it. Technically, pathogenic bacteria and viruses are parasites. In veterinary medicine, parasites are understood in the more restrictive term of being arthropods, helminths and protozoa:
1. Arthropods: e.g., lice and keds
- Round worms � nematodes � e.g., large or small roundworms of horses
- Tapeworms � cestodes
- Flukes - trematodes
3. Protozoa: Unicellular organisms, including several important ones that cause reproductive loss in cattle (Tritrichomonas foetus and Neospora caninum) and abortion in sheep (Toxoplasma gondii).
Economic losses in the United States from parasitic infections of livestock are estimated to cost $3 billion a year. Young animals are more susceptible to infection than adults, and more likely to develop disease. Malnourished or pregnant animals are more disease-prone than well-fed unstressed animals. If anything characterizes that part of the 'disease iceberg' which is out of sight to a livestock owner , it is parasitic disease.
Parasites as a rule differ from bacterial and viral infection in that:
Protozoa are the exception to these generalizations. In lifestyle and consequences, they are more akin to bacteria and viruses: they undergo sexual reproduction in a host, have short generation times, and many cause acute, not chronic, disease. Some parasites are completely dependant on one or two hosts (e.g., Sarcocystis species), whereas others use a host species only briefly (e.g., female mosquito seeking a blood meal). On the bright side, the development of drug resistance has been slower among parasites (especially helminthes) than in bacteria.
Parasitic gastroenteritis (PGE): Infestation by small worms in the abomasum/small intestine is the most important disease complex due to parasites that is seen in Wyoming. The type of disease caused depends on the parasite. In many cases, multiple species are involved in each outbreak. One, Ostertagia spp. causes parasitic abomasitis with protein loss into the lumen (see below). Another, Haemonchus sp., infects the abomasum and is a blood-sucker. There are other genera that can cause problems, in addition to Ostertagia and Haemonchus, such as Trichostrongulus and Cooperia - as an aid in memorization for hapless veterinary students, and using the first letters of each genus, these are sometimes called the HOT Complex. The climate is too cold for Haemonchus spp. most years in most parts of Wyoming. A typical hard winter kills larvae. Various other parasitic nematodes can contribute to protein loss via the small intestine. The time when PGE is most likely to occur in beef cattle (generally as subclinical disease) is after weaning - stocker cattle are the class most at risk from PGE. An important point about PGE in cattle and small ruminants is that TEMPERATURE IS THE PRIMARY DRIVING FORCE FOR THE HATCHING OF EGGS AND DEVELOPMENT OF INFECTIVE LARVAE. Temperartures of 20 - 30 C are optimal for most species. As cattle age, they develop higher resistance and have lower worm burdens than recently weaned calves. The effects of parasitism are generally worse when cattle are subjected to climatic and nutritional stress - this may be the thing that brings out overt clinical disease.
Enteric coccidia: The most important enteric coccidian in cattle is Eimeria zuernii. It causes ill thrift, death and diarrhea in calves aged 3 weeks - 6 months. See below for details.
Tritrichomonas foetus: This is an important protozoal cause of reproductive in cattle in Wyoming. It is reportable to the Wyoming Livestock Board. When we confirm a case in a bull we send the diagnosis along with information about the owner and attending veterinarian to the WLSB, which takes it from there. See below for details.
Liver fluke: The major cause is Fasciola hepatica. Unlike fascioliasis in sheep, the disease in cattle is usually a chronic or subclinical disease. The migrating fluke occasionally trigger fatal hepatic disease when they interact with a clostridial bacterium, resulting in clostridial destruction of part of the liver (so called "black disease"). The mechanism is similar to that which occurs when an injection into muscle, creating an environment in which clostridial spores which are already there can be activated. This is not a major problem in Wyoming due to the absence of appropriate intermediate snail hosts. Fluke are a problem in parts of ID, UT and NV, on the Gulf Coast, and in the Northwest. Cattle coming from fluke-endemic areas should be treated with flukicidal compounds. Aquatic vegetation with the infective stages of the fluke occasionally infect people. Cattle tend to clear themselves of infection ("self cure") and the major expression in them is chronic hepatic disease. Sheep, by contrast, can have acute infections with a fatal outcome.
Cryptosporidia: This causes diarrhea in young calves, especially dairy calves. We see this in Wyoming but these organisms on there own usually do not cause disease in beef herds.
Sarcocystosis: This is a protozoal cause of abortion in cattle and sheep. In cattle, dogs are the definitive host (= sexual reproduction occurs in that species). It occurs in Wyoming but is uncommon.
Anaplasmosis: Not a major disease in Wyoming cattle, although we diagnose a few cases annually by serology. Anaplasmosis becomes important when people ship native Wyoming cattle to parts of the US where the disease is permanently established (= endemic), such as the southern USA and some western states including California. It is caused by the bacterium Anaplasma marginale. I am including the disease here since it is tick-transmitted. The rickettsial organism lives inside red blood cells, leading to their destruction. The major effect of infection is anemia. The organism is transmitted by specific species of tick as well as by blood-feeding insects (horse and stable flies, and mosquitoes). A less common source of transmission is careless use of blood-contaminated instruments, such as syringes, dehorning saws, castrating knives and tattoo instruments. Calves rarely die of this disease. Typically, disease affects cattle >9 months when they are moved from anaplasmosis-free to anaplasmosis-endemic areas. These animals have no resistance and are highly susceptible to infection. Anemic animals are weak, reluctant to walk or move, and may die acutely when handled or excited. In heavy infections, cattle may be found dead. If you ship cattle to an area where you know the disease occurs annually, they are at especial risk. Acutely infected animals can be treated successfully by antibiotics (e.g., oxytetracycline). Long-acting formulations (30 days) of antibiotics can be used to protect animals during the vector season. To minimize disease, insecticidal ear tags or periodic insecticide use reduces the incidence of clinical anaplasmosis when ticks and other vectors are active. There is a modified live vaccine available for use in California. This should ONLY be used in young animals, as it causes illness and occasionally death in older animals and in pregnant cattle. Killed vaccines used to be available, but are no longer on the market. For interested students, there is a good review of the disease by the Texas Agricultural Extension Service which has details of treatment and prevention.
Neospora caninum: This protozoan is related to Toxoplasma gondii (below). Although a rare cause of abortion in Wyoming, in many dairy states (e.g., CA) it is the leading recognized cause of reproductive wastage (mainly abortion) in cattle. It surpasses BVDV in importance. The role of the dog as a definitive host was identified and established by Drs. Milt McAllister in the Veterinary Sciences department. Other canids (e.g., coyotes) can probably shed the organism.
Sheep are particularly prone to the clinical effects parasites. Reasons are
Parasitic gastroenteritis: This included ostertagiasis (below) and infection with a genus of worms called Nematodirus. Animals with signs of severe parasitism look unthrifty ('wormy'). They may go off feed, suffer weight loss, have diarrhea, and be anemic. Animals with severe blood protein loss develop "bottle jaw", a soft swelling in the jaw and throat area due to loss of protein and resultant edema (= fluid accumulation in extravascular space). Death occurs in severely affected animals. Less severely affected or chronically parasitized sheep show intermittent diarrhea, weight loss/reduced weight gains, reduced wool production, decreased milk yield, and poor reproductive performance.
Enteric coccidia: Coccidiosis is common in Wyoming sheep. Most sheep are infected with multiple different species from an early age. The species vary from minimally pathogenic to highly pathogenic. Young lambs are particularly susceptible to infection/disease. Older animals are tend to be more resistant but are often infected. Clinical coccidiosis is common in young lambs at weaning, in confined conditions, or shortly after entering feedlots. It also occurs in sheep stressed by weather, handling, and shipping.
Lungworm due to Dictyocaulus filaria is less pathogenic than the major lungworm of cattle (D. viviparus) but it can cause losses. Other lungworms such as Protostrongylus stilesi and Muellerius capillaris, while generally nonpathogenic in sheep, can cause severe signs in goats and bighorn sheep. Where sheep co-graze with free ranging bighorn sheep, their ability to transmit lungworms and Pasteurella spp. represents a threat to bighorn flocks. Other predisposing factors are probably involved (e.g., Mycoplasma infection) and the exact role of domestic sheep in oubreaks is disputed by some. Nevertheless, it is one reason why the two species should be kept separate. The WGFD has a program to keep domestic sheep out of "core" bighorn sheep habitat areas, so that losses due to pneumonia complex in bighorn sheep are kept to a minimum.
Abortion due to the protozoan, Toxoplasma gondii. Although rare as a cause of abortion Wyoming, it is one of the most important causes of abortion in sheep worldwide. You may have heard of this disease since it is also infectious for people (below).
Large stronglyes, including Strongylus vulgaris. The life cycles of these parasites will not be covered in detail, but some have extensive and damaging migration routes in the body. Most anthelmintics currently sold are effective against the adult stage of the parasite, but vary in their efficacy against larval stages. Compounds such as ivermectin (e.g., Eqvalan� paste � Merial) and moxidectin (e.g., Quest� Gel � Fort Dodge) kill adults and larvae. They also suppress egg production for extended periods (8 � 12 weeks)
Small strongyles, such as cyathostomes. The advent of good oral paste wormers has made disease due to Strongylus vulgaris largely a thing of the past. Cyathostomosis is now relatively more important as a disease. We periodically see fatal cyathostomosis in Wyoming horses, particularly when large numbers of larvae emerged from arrested development in mucosa of the large bowel. Usually we see this in late winter/early spring. The trigger mechanism is poorly understood. Sometimes recent use of an anthelmintic that kills only adults appears to trigger emergence. The most effective control is achieved by regular use of anthelmintics that kill the encysted larval stages of the parasite. Several products are available that are effective against these. Cyathostomes are resistant to many dewormers unless used at higher dosage rates. This is often not clear on package inserts since they claim efficacy against �small strongyles� without specifying that they mean adults stage, and not the larvae that do most damage. Daily use of pryantel tartrate (e.g., Strongid T� � Pfizer; there are also generic equivalents) will kill ingested larvae. Since the compound does not kill all stages of large strongyles, it should be combined with use of other anthelmintics such as ivermectin.
EPM (equine protozoal myelitis) due to Sarcocystis neurona. This will be covered in more detail elsewhere in this course. The disease is rarely diagnosed in native Wyoming horses, since the source of infection is the opossum. Opossums survive (with frozen toes, ears and noses) only in south-eastern Wyoming. But elsewhere in the USA EPM important � arguably the most important recognized cause of neurological disease in the horse. It is expensive to treat. Fort Dodge has a vaccine for this disease, although its efficacy is questionable. Its use in some states is regulated by state veterinarians.
Ascarids (Parascaris equorum). This is primarily a problem of foals, since horses develop a reasonable immunity and clear ascarids at 18 months of age. Disease is due to migration through lungs as part of their life cycle: it is one of many causes of coughing and nasal discharge in young stock. Very heavy infections of the gut can cause impactions of the gut, and colic. Wormers that kill strongyles also kill ascarids.
Tapeworms: Generally horses tolerate tapeworms well but tapeworms are a common incidental finding at necropsy. Heavy infestations by one tapeworm species that lives at the ileocecal junction has been reported to cause gastrointestinal problems, including colic. Daily worming treatments with compounds such as pryantel tartrate (e.g., Strongid C� � Pfizer; also generic equivalents) reduces egg output and helps control the problem. Horses with heavy burdens of tapeworms may respond to deworming with transient colic and diarrhea - this is rarely fatal.
Control of parasites in horses must be tailored to the premises and the risk of infection. It can have the following components:
Proper manure disposal:
These are discussed together since pathogenesis, treatment and control are similar. Differences are pointed out where present
An important worm parasite of cattle and sheep is Ostertagia, commonly referred to as the brown stomach worm. It is found on the mucosa and gastric glands of the abomasum (the true stomach). Adult worms graze the lining or mucosa and cause irritation and fluid loss, interfering with gastric function. Dyspepsia ("heartburn") results. Feed, especially hot rations such as grain, become poorly tolerated. Feed conversion for weight gain, body maintenance, reproductive fitness and milk production is compromised. Larvae or immature worms invade the gastric glands, which are pits in the lining of the stomach, disrupting normal structure and function of the glands. This compounds the effects of parasitism. Adults lay eggs that are passed in feces and hatch in manure. Microscopic larvae are dispersed, with some trickling deep into the soil and others carried on to surrounding grass. The free-living larvae feed on fungi and other soil and grass microorganisms and represent pasture contamination. When larvae develop to an infective stage, they migrate up blades of grass. Cattle become infected as they graze. After ingestion, infective larvae penetrate gastric glands. Larvae remain in the glands and emerge in relatively small numbers after two to three weeks, and mature so that glandular disruption is minimal and is of less clinical consequence. This is called type 1 ostertagiasis. However, infective larvae picked up in fall in some parts of the country (Northwest, Southeast, Northeast) can undergo arrested development (= inhibited larvae; hypobiosis) and overwinter till late winter (February-March). These larvae rapidly increase in size, emerge in large numbers simultaneously and cause massive destruction to the gastric glands, bringing abomasal function to a virtual halt. The host becomes clinically ill with anemia, bottlejaw, and loss of appetite; this delayed-onset form of disease, which generally occurs in late winter-early spring, is called type 2 ostertagiasis. Some cattle are overwhelmed and die; others are set back for several months before adequate stomach repair can occur.
Cobblestone lesions are found on the lining of the abomasum at necropsy and the normally thin folds of the stomach will be edematous (= waterlogged). The cobblestone appearance is caused by irreparable damage of the gastric glands.
To prevent ostertagiosis (parasitic gastritis), strategic deworming can be used to attacks the parasite cycle on a seasonal basis prior to occurrence of disruptive damage to the host. With inhibited larvae are present, a dewormer with both adulticidal and larvicidal effects needs to be administered. Dewormers with this property include the benzimidazoles or "white" dewormers such as albendazole (Valbazen�), fenbendazole (Safeguard�, Panacur�), oxfendazole (Synantic�) and ivermectin (Ivomec�). Incoming stocker calves and cattle to be finished in feedlots may originate from many places. They should be dewormed on arrival with an adulticide-larvicide dewormer.
No one-size-fits-all approach to parasitic gastroenteritis in cattle and sheep. A control program has to be tailored to the level of risk in the flock or herd, particularly the type of grazing practices, and local climate. Components for an effective control program can include:
Enteric coccidiosis is a disease of cattle and sheep aged 2 weeks � 1 year old. Multiple species infect cattle. Not all are pathogenic, so when we receive feces for egg (more correctly, oocyst) counts in the laboratory we distinguish highly pathogenic from less pathogenic species based on the shape and size of oocysts. In cattle the important ones are E zuernii and E bovis. The typical syndrome is chronic or subclinical disease in groups of grower animals. Calves are unthrifty with soiled rear quarters. In light infections, cattle appear healthy and oocysts are present in normally-formed feces, and feed efficiency is reduced. The most characteristic sign of clinical coccidiosis is watery feces, with little or no blood. Animals show only slight discomfort for a few days. Severe infections are less common, but we see outbreaks every year in Wyoming operations, particularly where there is crowding and poor hygiene. This can occur in well managed operations, including the UW beef farm. Severely affected cattle develop diarrhea, which consists of watery bloody fluid, that may continue for >1 wk, or thin feces with blood and mucus. Cattle may develop a fever, become anorectic, depressed, dehydrated and lose weight. Straining (tenesmus) is common. DIARRHEA MINIMAL IN COCCIDIOSIS AND THEREFORE MAY NOT BE OBSERVED. During acute disease, some cattle die immediately whereas others die later due to secondary complications, particularly pneumonia. Cattle surviving severe illness can have appreciable weight loss that is not quickly regained, or they remain stunted. Calves with concurrent infections (e.g., coronavirus) are more severely affected than calves with coccidial infections alone. Management factors, such as protection from weather stress, housing, feeding practices, and how animals are grouped, are important determinants of coccidiosis in Essentially all cattle in Wyoming have a subclinical infection with coccidia. The trick is to make sure that levels do not build up so that disease occurs - trying to get on top of an outbreak of coccidiosis in calves is difficult, time consuming, expensive and frustrating. Although typically seen in older calves (>1 month), I've seen this as a fatal disease in calves as young as 2 weeks. When it occurs this young, this signals a heavily contaminated environment and infection at or shortly after birth.
Treatment: Anticoccidial drugs may prevent parasite invasion of cells and impair development. Some are designed for the treatment of coccidiosis in the face of an outbreak or for prevention when appropriate conditions prevail. Amprolium (Corid�) is administered in water or in medicated feed for five days for treatment and 21 days for prevention. Antimicrobial agents like some of the sulfa drugs can also be used for treatment (sulfadimethoxine - Albon� boluses - Pfizer, Inc.). By contrast, decoquinate (Deccox� - Alpharma) is for the prevention of coccidiosis and is fed for at least 28 days during an exposure or if one is anticipated. Lasalocid (Bovatec� Premix) is also used for control Because oocyst production is not directly affected by anticoccidial drugs, oocysts may continue to be passed for a short period following treatment. Anticoccidial drugs are primarily coccidiostatic (inhibiting the parasite) rather than coccidiocidal (killing the parasite). As result, resumption of shedding may occur for a short time but with fewer oocysts produced and passed. If contamination is minimized, reinfections will be lighter, of less clinical consequence and will allow for immune response One benefit of coccidiostats is improved feed efficiency and rate of gain. Some coccidiostats, formulated into feed at low concentrations, can themselves cause problems if the feed manufacturer makes a mistake. Ionophore coccidiostats (monensin and lasalocid) cause sudden weakness, recumbency and death of cattle and sheep, due to their ability to cause necrosis of skeletal muscle and the heart. The WSVL can perform feed analysis for these ionophores, if you suspect this has happened. It's uncommon, but such episodes can cause spectacular wrecks, affecting half or more of the animals that are accidentally poisoned. Reputable companies investigate the situation and make amends. Non-reputable companies do no or limited analysis of the analysis and will claim that their product was not at fault. If you get into a situation like this, get the company to use a laboratory you trust and has no commercial relationship with the manufacturer. This should ensure a thorough investigation is done. As an aside, be careful feeding ionophore coccidiostat-laced feed to monogastric species. The margin of safety in horses is narrow.
Cryptosporidiosis is a cause of diarrhea in young calves (3 weeks old or less), commonly as a cofactor. It is generally a self-limiting watery diarrhea. The important one in calves is C. parvum, which infects the lower part of the small intestine and is significantly associated with diarrhea. Parvum is derived from the Latin word for small (as in parvovirus, the cause of "parvo" in dogs). There are several other agents in cattle, such as C. andersoni which infects lining cells of the abomasum and is probably not a significant cause of disease, and C bovis, which infects older calves, is considered non-pathogenic, and results in large numbers of oocytes in feces
C. parvum infects other ruminant species (sheep, goats, deer) and - importantly - people. Immunity is short-lived and incomplete, but age-related resistance develops. Calves become re-infected so that recurring infections can occur. Cryptosporidiosis is a zoonotic disease. In 1993 the largest waterborne outbreak of diarrhea due to a parasite occurred when 400,000 people in the city of Milwaukee became infected. It was not clear whether animals were the source, since the species that infects people, C. hominis, also infects calves and is microscopically indistinguishable from C. parvum. There is a confusion in the scientific literature about the identification of cryptosporidia species and the extent to which animals contribute to human disease. 13 species of the organism exist. Some, from humans, cats, dogs, rodents, and turkeys, infect people. If you are involved in an outbreak of cryptosporidiosis in calves, remember you may be infected (watery diarrhea). It is a rite of passage for veterinary students to acquire infection in veterinary teaching hospitals from sick calves. Unlike the enteric coccidia, cryptosporidial oocytes are immediately infectious as they are shed by the calf. Currently the only way to tell the diarrhea-inducing, zoonotic type oocytes in calves (C. parvum) from apathogenic non-zoonotic types (such as C. bovis) is by DNA testing - few laboratories offer this.
Treatment: There is no approved medical treatment other than keeping calves hydrated. These calves should survive, provided there is no complicating infection with other agents. Oocysts are hardy, but can be killed by desiccation, and 5% ammonia or 10% formalin solutions. Currently there are no effective drugs labeled for elimination of the parasite. However, decoquinate (see above) administered orally at 4.5x the label dosage for 1-3 weeks has promise as a method for treating affected calves. Good hygiene decreases the likelihood of disease and helps prevent reinfection.
Human health implications: The CDC web site has information on the human disease. Identifying whether animals are the source of infection is constrained by scientific disagreement about identifying individual species. Regulatory control of Cryptosporidium spp. in water by the EPA and other agencies is expensive. Human outbreaks are routinely blamed on agricultural operations. There is an excellent but long review of the importance of accurately identifying whether species are of human or animal origin in the January 2004 issue of Clinical Microbiology Reviews.
Trichomoniasis is a venereal disease of cattle caused by a fragile protozoan. It is characterized by early fetal death and infertility, resulting in extended calving intervals. Distribution is worldwide. It is relatively common in WY, especially in grazing associations. It is state-regulated in WY and UT, and other states are thinking about introducing control rules. The causative organism is Trichomonas (Tritrichomonas) foetus which is related to the human vaginal trichomonad. At one end are three flagella, hence the genus name (= three hairs). Although T. foetus survives freezing in semen, it is killed by drying or high temperatures. For all intents and purposes it is completely dependant on the bull or the cow to survive - it cannot do so in the natural environment Trichomonas foetus is found in the genital tracts of cattle. When cows are bred naturally by an infected bull, 30-90% become infected. Bulls of all ages can remain infected indefinitely, but this is less likely in younger males. By contrast, most cows are free of infection within 3 months of breeding. However, immunity is brief (why might this be?) so that reinfection can occur. Transmission also occurs when the semen from infected bulls is used for artificial insemination.
The most common sign is infertility caused by embryonic death. The embryo is rarely found, so the impression is that many cows did not hold to service. The end result is repeat breeding and an extended calving season. Fetal death and abortions can occur but are not as common as losses earlier in gestation. In 16 years in WY, I've diagnosed trichmoniasis in fetal calves less than five times - this reflects the rarity with which fetuses are found. Pyometra (= pus-filled uterus) occasionally develops after breeding. Confirmation depends on isolation of T. foetus and/or by PCR testing. Control efforts are targeted at bulls because they are the most likely carriers; flush samples are taken from their penis to examine for the parasite. Studies suggest that 90-95% of infected bulls will be positive on culture. THREE successive cultures at weekly intervals are needed to detect ~99.5% of infected bulls. Recently the WLSB agreed that ONE test - provided it was done by polymerase chain reaction - can be used per bull for regulatory purposes. There are commercial test kits to check for T. foetus (In-Pouch� TF - Biomed Diagnostics) which are used by veterinarians as in-clinic tests.
Treatment: Various compounds have been used to treat bulls. None is both safe and effective.
Control: This is done by testing of test-eligible bulls and in accordance with the Chapter 15 rules of the Wyoming Livestock Board. All non-virgin bulls offered for sale in Wyoming as breeding stock must be tested at least once before they change hands. New bulls on common grazing allotments must also test negative. The best time to test for infection is immediately after the breeding season. Bulls that go through a fence and mix with a neighbor�s cattle must also be tested at the bull owner�s expense. If an infected bull is identified he cannot be sold and must be reported to the state veterinarian, as well as to the grazing association within a specified period. The herd is quarantined and positive bulls are V-branded on one side of the tailhead. If a V-branded bull is moved off the property, it must go a designated slaughter plant. Remaining bulls in the herd have to be tested and remain in quarantine until they test negative on three occasions. Females can only be moved out of the infected herd with the approval of the state veterinarian. Interestingly, cats can be infected by Trichomonas (Tritrichomonas) foetus where it sets up a chronic diarrhea. We've seen this in cats in Wyoming, but there does not appear to be any association with the disease in cattle.
Toxoplasmosis is uncommon as a cause of abortion in Wyoming flocks but in much of the world, including the American Midwest, it is one of the most common causes. It is dues to the protozoan Toxoplasma gondii, for which cats are the definitive host. In cats it acts like a non-pathogenic enteric coccidian. It is shed as oocysts in feces. Toxoplasma abortion in ewes occurs after they ingest of feed or water contaminated with oocyst-laden cat feces. Toxoplasmosis generally does not cause clinical symptoms or detrimental effects in open, healthy ewes. In stressed and immunosuppressed ewes, neurological symptoms and death can occur. The result of toxoplasmosis in pregnant ewes varies with the age of gestation. Infection in the first two months results in embryonic death and resorption. Infection at mid-gestation results in abortion and infection. Infection in late gestation results in abortions, stillbirths, mummies or weak lambs. Abortion losses attributable to T. gondii can involve from five (5%) to fifty (50%) percent of the flock, with typical losses averaging 15 - 20% percent of the lamp crop.
Treatment: There are no vaccines, treatment, or specific control methods for toxoplasmosis.
Control: Farm cats should be kept them away from pregnant sheep and their feed. Ewes that abort should be immediately isolated (regardless of identified cause). The area in which abortion occurred should be cleaned and disinfected. The relative rarity of the disease in Wyoming is presumably due to physical separation of cats from flocks