Liver flukes and redwater disease in Minnesota beef cattle

In North America the primary hosts for F. magna are white-tailed deer and caribou. These flukes can also infect mule deer, elk, moose, bison and other wild ruminants. Domestic cattle, sheep, pigs, horses and llamas can also become infected with deer liver flukes.

Deer liver flukes rarely cause clinical illness in free-ranging deer and do not seem to have a major impact on wild deer populations. These flukes are more of a problem when they infect domestic cattle and sheep.

Infected cattle often do not show clinical signs in early stages of infection or display only mild clinical illness. Mild clinical illness may include decreased milk production and unthrifty offspring. Infection may result in liver condemnation at the slaughterhouse.

In advanced stages of infection, cattle will lose significant body weight, appear lethargic and have a very rough looking hair coat. Once the signs of an advanced infection are present, death from extensive liver damage usually follows.

Sheep are much more severely affected by deer liver flukes and more frequently die from extensive liver damage.

This parasite does not infect humans and meat from infected deer is safe for consumption.

Where deer liver fluke is found

The deer liver fluke is found primarily in five regions in North America: the Great Lakes region, including Minnesota; the Gulf Coast, lower Mississippi, and southern Atlantic seaboard; the northern Pacific coast; the Rocky Mountain trench; and northern Quebec and Labrador.

Life cycle

Transmission and development

The natural host of F. magna is the deer, which is also a reservoir host. Adult flukes live in fibrous capsules within the liver and release eggs that are swept into the intestines and shed in feces. The eggs hatch in water and a free-swimming immature form known as a miracidium emerges. They then penetrate snails (intermediate hosts) where they continue to develop and multiply. Several immature free-swimming cercaria emerge from each infected snail. Cercaria encyst (enclose in a sac) on vegetation; these encysted forms are called metacercaria, which are quite resistant to the elements.

Metacercaria on contaminated vegetation infect new hosts when they are ingested and then migrate through the intestinal wall to the liver, where they become encased in fibrous cysts and develop into adults.

The entire life cycle can be completed within five months under favorable conditions. Low-lying marshy areas, well suited for snail propagation, are ideal sites for fluke development.

In grazing situations, the host is most likely to ingest the metacercaria when grazing near natural surface water which, serve as habitat for the snails. Evidence suggests that consuming hay or other forage produced/stored in a way that allows for contamination with metacercaria can also contribute to infection.

There are different categories of mammalian hosts for deer liver flukes: definitive hosts and dead-end, and aberrant hosts.

• The flukes can complete their life cycle within definitive hosts which include white-tailed deer, elk, caribou, mule deer and fallow deer.

• In dead-end hosts, immature flukes reach the liver but rarely mature and produce eggs. Dead-end hosts include moose, Sika deer, cattle, bison, horses, llamas, alpacas.

• In aberrant hosts, such as bighorn sheep and domestic sheep, immature flukes continue to wander throughout the liver, which can cause extensive liver damage.

Cattle are dead-end hosts and do not contribute to the spread of F. magna.

Symptoms and clinical signs

Most deer infected with F. magna do not show clinical signs.

In definitive and dead-end hosts the F. magna becomes encapsulated within the liver, which prevents further fluke migration and liver damage. When definitive and dead-end hosts are parasitized by a large number of flukes, they may become emaciated, suffer severe liver damage, and sometimes die.

In aberrant hosts, such as bighorn sheep and domestic sheep, immature flukes continue to wander throughout the liver, which can cause extensive liver damage. Clinical signs in aberrant hosts include lethargy, loss of appetite, depression, weight loss and death. In aberrant hosts that have died of deer liver fluke parasitism, necropsy may reveal a swollen, necrotic, hemorrhagic liver with many fluke migration pathways.

Treatment    

• Valbazen® is approved for the treatment of adult (mature) flukes from F. magna in sheep only.

• Valbazen®(Albendazole) at 10 mg/kg, the flukes need to be mature (more than 90 days old) for treatment to be effective.

• Label dose of Valbazen is effective. Increasing the dose does not increase efficacy. However, using 1.5 times label dose may be useful to account for application losses.

• Curatrem® (clorsulon at 7 mg/kg) and Ivermectin Plus (clorsulon at 2 mg/kg) are not labelled for treatment against F. magna infections.

• There are no approved products in the United States approved for the treatment of F. magna in cattle.

Timing of treatment

It is recommended that treatment for F. magna occurs at a time that flukes are mature. It takes approximately 90 days for F. magna flukes to migrate and reach maturity.

To accomplish this, cattle should be treated following heavy killing frost / late fall or early winter is recommended. Retreatment after 90 days may be necessary in heavily infected areas to address potentially immature flukes at time of initial treatment.

Prevention

Limit grazing around wet areas that may contain contaminated vegetation.

Harvested forage (hay bales) should be produced and stored in a manner that do not allow for snails to contaminate and potentially produce infective cysts. The bottom side of hay bales, round bales in particular, are excellent habitat for snails that were picked up with the vegetation during the haying process and stored for winter. If snails are found on the bottom of hay bales, do not feed that hay to livestock.

Some ranchers in endemic areas have claimed that flipping over infected hay bales to expose the snails, thus freezing the snail and killing the fluke cercaria is an effective method of reclaiming affected hay. Although there may be some merit to this practice, there is no clinical evidence to support this as an effective mitigation practice; i.e., we don’t know if freezing the fluke cercaria actually kills it.

Spreading F. magna

A big concern for livestock producers is assessing whether F. magna can be spread to currently unaffected areas through the transportation of livestock and feedstuffs from affected areas. The movement of infected cattle cannot spread F. magna as they are a dead-end hosts.

F. magna depends upon the distribution of an intermediate host, the lymnaeid snail. Even though infected feedstuffs are often moved throughout the country, these infections will not propagate unless the intermediate host snails are present.   

Redwater disease in cattle (bacillary hemoglobinuria)

Bacillary hemoglobinuria, also known as redwater disease, is often associated with deer liver fluke infestations in Minnesota and the Great Lakes region. Bacillary hemoglobinuria is an acute, infectious, toxic disease that primarily affects young cattle on pasture (but may also affect sheep).

It is caused by the bacteria Clostridium haemolyticum which is a soil-borne bacterium that can survive a long time in contaminated soil or in bones of infected carcasses. The bacteria spores are ingested and are naturally found in the rumen and liver of healthy cattle.

It is not until there is local liver damage and necrosis (usually caused by a migrating liver fluke infection or much less commonly due to a high nitrate diet) that the bacteria spores germinate into vegetative cells that multiply and produce toxins that destroy the red blood cells in the body.

Symptoms and clinical signs

Cattle may be suddenly found dead but usually have a sudden onset of fever, severe depression, abdominal pain and trouble breathing. The gums of the teeth (mucous membranes) and sclera (white portion) of the eye may look pale (anemic) or yellow color (jaundice/icteric) with pinpoint red blood spots (petechia). They may also have dark purple/red “port wine” colored urine (hemoglobinuria).

The duration of clinical signs can vary from no signs (the cow acting as an immune carrier of the disease) to 12 hours in a pregnant cow to three to four days in other cattle. The death rate in untreated animals can be as high as 95 percent.

Diagnosis

• Bacillary hemoglobinuria can be diagnosed by clinical signs and post mortem findings but can be confirmed through lab tests by either isolating the bacteria from the liver (by culture, fluorescent antibody or immunohistochemistry), or the toxin from in the liver or abdominal cavity fluid.

• Proper diagnosis is important as there are other diseases that may present similarly including anaplasmosis, anthrax, bracken fern poisoning and leptospirosis.

Treatment

Early treatment with penicillin or oxytetracycline is essential as the bacteria are restricted to areas of liver damage and the more liver damage there is, the less blood supply there will be to transport the antibiotics to where they are needed (reducing the effectiveness of treatment). Depending on the severity of the disease, IV fluid therapy and/or blood transfusion may also be required.

Prevention

The best way to prevent this disease is to vaccinate (a primer and booster vaccine) against Clostridium haemolyticum (found within the eight-way vaccine). Other control methods include rotating pastures and controlling liver fluke infections.

Where the common liver fluke is found

The common liver fluke of cattle is found mainly in Florida, Louisiana, the gulf coast of Texas, parts of California, Hawaii, the coastal Pacific Northwest and some river valleys and irrigated pasture in the Northwest as far east as Montana. It is not found in Minnesota.

Although this fluke can infect some wildlife species such as deer and small ruminants such as sheep and goats, cattle are the main host and continued environmental contamination by cattle is required to perpetuate the infection.

Life cycle

Adult F. hepatica lives in the bile ducts of the liver and eggs are passed through the bile into the feces and back into the environment. When these eggs are deposited in warm moist environment they hatch and develop into free-swimming organisms (miracidium) which invade a particular type of snail (Lymnaea) where they develop further.

Once infected, snails shed a tadpole like organism (cercaria) which then migrates onto green plants where they form a protective cyst (metacercaria) and are consumed by grazing animals. The cysts will die off after the water recedes and hot dry summer conditions arrive since these cysts are very susceptible to dry conditions.

Snails survive cold winters or hot dry periods by burying themselves in the mud and waiting until favorable conditions return. Infected snails often release the cercaria in the spring when they emerge from the mud as temperatures begin to warm up and spring rains bring moisture which helps the infection process.

Moving fluke-infected cattle to feedlots or areas of the country where Lymnaeid snails are not present to complete the life cycle helps prevent the spread of infection.

Habitat

High rainfall areas, irrigation or wetlands are required for fluke transmission and for the survival of the intermediate snail host. Snails do not survive well in light loam or sandy soil; therefore, the presence of liver flukes in Gulf States like Mississippi and Alabama is limited or non-existent. Also, snails cannot survive in acid soils such as peat soil. Snails prefer neutral, well buffered heavy clay soils such as those found in Louisiana. Snails survive in shallow depressions in fields, springs, seeps and slough that hold water over 180 days per year. Sustained heat and summer droughts ends infection season.

Treatment

FDA approved treatment for F. hepatica:    

• Curatrem® (clorsulon at 7 mg/kg): more than 56-day old immature and mature flukes

• Ivermectin plus (clorsulon at 2 mg/kg): Mature flukes only (more than 90 days old)

• Valbazen® (albendazole at 10 mg/kg): Mature flukes only (more than 90 days old)

For successful treatment of F. hepatica, flukicides approved for treatment of F. hepatica will be required. Curatrem® (clorsulon at 7 mg/kg) will be effective against both juvenile and mature F. hepatica specimen. Therefore, treatment can begin 56 days after expected exposure. Ivomec Plus®  (ivermectin plus clorsulon at 2 mg/kg) and Valbazen®, (albendazole at 10 mg/kg) however, are only effective against mature F. hepatica, therefore, treatment should occur after 90 days of expected exposure.