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Johne's Disease Control ProgramMissouri Johne’s Disease Voluntary Control Program Question & Answers

What are the signs of disease?
What causes the signs of disease?
What is the cause of Johne’s disease?
What are the Four Stages of Johne’s Disease in Cattle?
How does Johne’s disease affect the body?
Preventing Introduction of Johne’s disease
What can I do about Johne’s in my herd?
How can some cattle be infected with Johne’s disease, yet not show signs?
What are common sources of Johne’s disease?
Can humans get Johne’s disease?
Is there a treatment?
Is a Johne’s vaccine available?
What should I do if I suspect Johne’s in my herd?
How is Johne’s diagnosed?
What if animals test positive?
What are the economic costs of Johne’s?

What are the signs of disease?
Because of the slow progressive nature of the infection, signs of Johne’s disease may not be seen until years after initial infection. Cattle may be infected for years before they show any signs of disease. When they finally do occur, the signs of Johne’s disease are long-lasting diarrhea and weight loss despite a good appetite. Affected cattle do not generally have a fever. Some infected animals appear malnourished and often weak while others just have chronic diarrhea. The signs of this disease can easily be confused with several other diseases. In the infected cow or heifer, noticeable signs commonly start within a few weeks after a stressful event like calving.

What causes the signs of disease?
The bacteria are taken up by specialized cells in the small intestine called the ileum where nutrients are absorbed from the feed. As the body tries to rid itself of these bacteria, the immune response causes a thickening of the intestinal lining, preventing it from functioning normally. This leads to poor absorption of nutrients and eventual diarrhea. As a result, although animals may be feeling and eating well, they begin to lose weight gradually.

What is the cause of Johne’s disease?
MAP (Mycobacterium avium subspecies paratuberculosis) is 99% genetically related to Mycobacterium avium, but has different phenotypic characteristics such as 1) slower growth, 2) requires the addition of an iron transport chemical known as mycobactin when grown in vitro (outside the body), 3) forms a rough colony when grown on solid agar media, and 4) infects mammals instead of birds. Also, the environmental distribution of MAP is markedly different from that of M. avium, which can produce mycobactin and therefore grow and multiply outside the body.

MAP is a small rod-shaped bacterium that has a rough waxy cell wall with a trilaminar structure. This wall is composed of a thick waxy mixture of unique lipids and polysaccharides but lacks glycolipid antigens on its surface. This kind of cell wall facilitates the mycobacterium’s resistance to physical factor’s (e.g. heat, cold, sunlight, drying, etc.) and common disinfectants. If MAP is found in soil or water samples, it can survive (but not grow and multiply) for over a year after fecal contamination via an infected animal. Johne’s disease is caused by a bacterium named Mycobacterium paratuberculosis. It is a distant relative of the bacterium Mycobacterium bovis (the causative agent of bovine TB and some human TB) but itself does not cause TB.

The bacteria can grow and multiply inside the immune cells of an animal. When the microbe is excreted in the feces, it can contaminate the soil or water. Outside the animal, the organism does not multiply well, if at all, but it can survive over a year in the environment because of its resistance to heat, cold, and drying. Therefore, the primary source of infection is directly from infected animals.

What are the Four Stages of Johne’s Disease in Cattle?
Stage 1 – Silent, subclinical, non-detectable infection. This initial stage of the infection is not apparent and the animal appears normal. It is not possible to diagnose the disease in a live animal at this stage. Typically this stage occurs in calves, and heifers less than two years of age or animals exposed to a small dose of bacteria. There are currently no tests on the market to detect or identify these animals. Eventually, these animals progress to Stage 2.

Stage 2 – Inapparent Carrier Adults. Infected animals at this stage do not show symptoms, yet they shed the organism in their manure. Subclinical shedders typically involving older heifers or adults. These animals may appear healthy, but are shedding enough M. paratuberculosis organisms in their manure to be detected on fecal culture. By shedding organisms, these animals are contaminating the environment. Blood testing may or may not be reliable in detecting these animals.

Stage 3 – Clinical Disease. Animals at this stage show gradual weight loss with intermittent to chronic diarrhea but have a normal appetite. These animals shed billions of organism that contaminate the environment. Any animal with advanced infection, which may have been brought on by a period of stress. These cattle have acute or intermittent, watery, fetid manure. A loss of weight and a drop in milk production are also common signs. Many of these animals continue to eat, and are positive on serologic tests. Signs may last from a few days to a few weeks before these animals progress to Stage 4.

Stage 4 – Advanced Clinical Johne’s Disease – This is the end stage of this disease. Most animals are very thin with fluid diarrhea. Some animals can progress from Stage 2 to Stage 4 in a few weeks. Animals in the advanced stage are weak and emaciated and usually have a profuse diarrhea.

How does Johne’s disease affect the body?
The primary site targeted by Johne’s disease is the lower part of the intestine known as the ileum. The wall of the ileum contains a large number of pockets of lymphoid tissue known as Peyer’s patches that lie just beneath the interior surface of the intestine. Peyer’s patches are clusters of macrophages and lymphocytes that are organized much like lymph nodes. Covering Peyer’s patches are a layer of cells called M cells. These cells function to circulate into the lumen of the intestines where they ingest antigens (bacteria) before returning to the Peyer’s patch to “show” these antigens to the macrophages and lymphocytes. This is a means of “educating” the cells in a young animal about its environment and is a protective mechanism designed to help the animal become immune to pathogens in its environment.

Unfortunately, when M cells bring MAP to the Peyer’s patch, the bacteria finds an ideal place for growth. Macrophages in Peyer’s patches engulf MAP with the intention of destroying the foreign invader, but for reasons that are unclear, these macrophages fail to accomplish this. Inside a macrophage MAP multiplies until it eventually kills the cell, spreads and infects other nearby cells. In time, other parts of the ileum and other regions of the body are teaming with millions of the mycobacteria. How MAP neutralizes or evades the normally efficient bacterial killing mechanisms of the macrophages is unknown.

The animal’s immune system reacts to the MAP invasion by recruiting more macrophages and lymphocytes to the site of the infection. The lymphocytes release a variety of chemical signals, called cytokines, in attempt to increase the bacterial killing power of the macrophages. Macrophages fuse together forming large cells, called multinucleated giant cells, in an apparent attempt to kill the mycobacterium. Infiltration of infected tissues with millions of lymphocytes and macrophages leads to invisible thickening of the intestines. This prevents nutrient absorption and diarrhea results. Late in the infection, antibody production by the animal occurs to MAP in serum of animals and is an indicator that clinical signs of disease and death from the infection will soon follow.

Preventing Introduction of Johne’s Disease
Johne’s disease usually enters a herd when healthy but infected animals are introduced to the herd. Herds that are not infected should take precautions against introduction of Johne’s disease. Such precautions include keeping a closed herd, or requiring replacement animals to come from test negative herds. In 1998, the United States Animal Health Association approved the Voluntary Johne’s Disease Herd Status Program for Cattle (VJDHSP). The VJDHSP provides testing guidelines for states to use to identify cattle herds as low risk for Johne’s disease infection. With numerous tests over several years, herds progress to higher status levels. The higher the status level, the more likely a herd is not infected with Johne’s disease. In April of 2002, USDA-Animal and Plant Health Inspection Services – Veterinary Service incorporated portions of this program into is national program standards: Uniform Program Standards for the Voluntary Bovine Johne’s Disease Control Program (VBJDCP). VBJDCP test negative herds (often referred to as Status Herds) serve as a source of low Johne’s disease risk replacement animals.

Some basic prevention strategies are:

  • Calves, lambs, kids, etc. should be born in a clean environment.
  • Reduce the newborns’ exposure to manure from adult animals by separation when possible.
  • Avoid manure contamination of feed by using feed bunks and not using the same equipment to handle feed and move manure.
  • Avoid manure contamination of water sources where animals drink.
  • For natural colostrum needs of newborn animals, use colostrum from Johne’s negative animals.
  • Do not pool colostrum.
  • Avoid natural nursing and milk feeding whenever possible. Feed an artificial milk replacer or pasteurized milk instead of raw milk to supply the needs of newborns. Never feed pooled milk or waste milk.
  • Thoroughly clean the udder and teats in the environment so if possible, for pastures that have become contaminated, till the ground or graze using non replacement feeder cattle.
  • Identify all females in the herd. Identify and remove, or keep separate all test positive animals.
  • Prevent infection from spreading by culling, or separating offspring of infected mothers as soon as possible.
  • If purchasing herd additions, try to buy from low risk herds. Some herds are enrolled in the Voluntary Bovine Johne’s Disease Control Program to help identify their herd as low risk.

Work with your veterinarian to develop a strategic plan for Johne’s prevention and control for your farm. Consult with them about which Johne’s test is best for your situation and see a test certified diagnostic laboratory.

What Can I Do About Johne’s In My Herd?

  • Risk Assessment: Arrange to have a risk assessment done on your herd by a Johne’s certified veterinarian. This will help you understand what the Johne’s disease risks are in your operation for introduction and/or spread.
  • Management Plan: Next is the development of a management plan with the Johne’s certified veterinarian doing the risk assessment.
  • Testing: If testing is called for in your management plan, then scheduling the testing called for in your management plan is the next step.
  • Renewal: After 12 months, arrange for another risk assessment – management plan (RAMP) to evaluate your progress.

How can some cattle be infected with Johne’s disease, yet not show signs?
Infectious diseases, including Johne’s disease, typically pass through four stages. Stage I is the initial infection. The animal is infected, not showing signs of disease and may be shedding small numbers of microbes into the environment that are not detectable by diagnostic tests. In Stage II, the infection is progressing and the animal still does not show any clinical signs. Nevertheless, the organism is being excreted in very high numbers, probably enough to infect others nearby. Infection is detectable by fecal culture techniques but not often by blood tests. In Stage III, the animal is showing the early signs of disease and many types of diagnostic tests can detect the infection. Stage IV is the obvious clinical disease and readily recognized by the trained observer and detected by diagnostic tests. It may take 2-6 or more years for Johne’s disease to progress through all of these stages.

In some herds with Johne’s disease, animals in all four stages of disease exist. For each animal showing obvious signs of Johne’s disease (Stage IV), 5 to 15 other animals at various stages of infection are not showing signs.

What are common sources of Johne’s disease?
The most common source of infection is feces or manure. While protected in fresh manure, the organism can remain alive in the environment for over a year depending on conditions. Ingestion of manure containing the microbe is the most common way animals become infected.

Johne’s disease typically enters a herd as an infected, but healthy-looking, animal in Stage I. As the disease progresses in that animal, the frequency and number of bacteria being excreted increase. Every day, billions of Johne’s microbes may be excreted from an animal in Stage III or IV of the disease.

Another source of infection is milk from infected dams. The likelihood of Johne’s bacteria being excreted in milk of infected females increases as the disease progresses. Studies suggest that 36% of Stage III and IV cows could have Johne’s microbes in their colostrum. In beef herds, where calves remain with their mothers and nurse daily, the chance for transmission of the infection through colostrum and milk is high. These bacteria may be excreted directly through mother’s milk or it might be present on the outside of the teats in contaminated feces.

Prenatal exposure may be a source of infection for calves. Becoming infected before birth is possible for a fetus, if its mother is in the late stages of disease. Studies have shown that, in disease Stages III and IV in the dam, 8 to 40% of fetuses were infected from their mothers while still in the womb. Risk for infection of the fetus is low from mothers in disease Stages I and II.

Pond water contaminated with infected feces is another potential source of infection. Other possible, but less likely infection sources, are pastures contaminated with infected feces.

Can humans get Johne’s disease?
So far, no epidemiological studies have been published that examine any connection between contact with animals with Johne’s disease and humans who develop Crohn’s Disease, a human illness that in some ways, resembles Johne’s disease. Some recent reports claimed to have cultured the microbe from, or detected its genetic components in, humans. However, the significance of these findings in humans as they relate to any animal disease has yet to be determined.

Is there a treatment?
THERE IS NO TREATMENT FOR JOHNE’S

The key to controlling this disease is prevention. The key to prevention is MANAGEMENT. Testing needs to be one part of a total commitment to eliminating the disease from the herd. Testing will provide the following information:

  • Evaluate absence or the extent of infection.
  • Identify infected animals.
  • Determine the intensity of a control program.
  • Monitor progress of control efforts.

Once the extent of the problem is identified, appropriate management and sanitation procedures will need to be put in place to accomplish the following goals:

  • Prevent highly susceptible newborn calves and young animals from oral manure contamination by infected adults, be it from the dam, the environment, the feed, or the water.
  • Prevent all other susceptible animals from ingesting low levels of infected manure, especially by contamination of feed and water.
  • Reduce the total farm exposure level to M. paratuberculosis by removing the bacteria from the environment and reducing the number of infected animals that are shedding the bacteria.

Specific recommendations: The specifics and intensity of a Johne’s disease control strategy in cattle will vary with the individual farm situation. To be relevant and effective it must be designed to fit the immediate and future goals of the farm, and available resources. Although many specific methods can be used, they must involve some or all of the following:

  • Management of newborn calves and young animals is critical and is the most effective place to put the effort.
  • Calves should be born in an area that is dry, clean of manure, and well bedded. Clean teats and udders are a must. The calving area needs to be restricted and used strictly for maternity. It is best if you can remove newborn calves from the dam immediately, eliminating the chance to ingest manure in attempts to find the udder and nurse.
  • Feed newborns colostrum, ideally within one to two hours, from only healthy appearing dams, who are less likely to pass M. paratuberculosis into the udder and milk.
  • Milk replacer eliminates the risk of possible infection from feeding whole or pooled milk to calves. Replacer should be seriously considered especially in herds with significant infection.
  • Young calves and heifers should be housed separate from adults and should have no direct contact with manure from adult cattle. Separate facilities are ideal but sections protected by partitions, dry alleyways or buffer zones, or low traffic zones are effective.
  • DO NOT contaminate feed or feed mangers with manure from feet or equipment.

Management to prevent low levels of exposure in all older animals is important:

  • Prevent manure contamination of feed and waterers. DO NOT use the same loader or equipment to clean manure and to load feed. DO NOT walk in the feed bunks. Eliminate or fence animals out of natural water sources that they drink, that are also slow moving or stagnant, and collect run-off containing manure that animals stand in.
  • SANITATION has no substitute. Remove manure as thoroughly and often as possible. Always strive for more often. Spread manure on cropland, not on pasture to be harvested or grazed the same season.
  • Identifying and removing infected animals and their manure is necessary to reduce the risk of continued exposure for ALL animals.
  • Test the herd to identify infected animals that are, or probably will be shedding the bacteria. Based on the elevation of results, infected animals should be culled as heavily as economics permit. The most severe should be culled first.
  • Manage all animals as if they are infected, and all manure as if guilty. This management attitude works all the time, and is especially important if testing and early culling is not practical.
  • Reduce the risk of introducing infected animals into the herd, especially when elimination of the infection is the goal.
  • Be cautious and investigate animals to be purchased. Purchase animals from test negative herds, or, in discussions with the owner, confirm the herd has no signs of Johne’s. Reduce risk by prior testing with serology or by fecal culture immediately when animals arrive.

Is a Johne’s vaccine available?
A killed vaccine is available. However, it will not prevent an animal from becoming infected or shedding. Johne’s vaccine is prohibited in Missouri.

What should I do if I suspect Johne’s in my herd?
Contact your local veterinarian who can help develop a comprehensive management plan to reduce the disease. Additional information is available from the Missouri Department of Agriculture or the University of Missouri College of Veterinary Medicine.

How is Johne’s diagnosed?
The best detector of Johne’s is a fecal culture test. This method is slow – requiring 4 to 8 weeks of culture time in the laboratory. Blood tests, while less accurate than culture, are faster and less expensive. Blood and milk testing can be used most effectively to confirm clinical (Stage III and IV) or test a group of animals in a herd. Neither method is an effective test for very young animals (Stage I). Johne’s disease is most accurately diagnosed by examining the lower small intestine and associated lymph nodes in a dead animal.

What if animals test positive?
Animals that test positive on fecal culture should be sold to slaughter as soon as possible. Animals that test positive on blood tests and are not showing clinical signs should be tested by the fecal culture method to confirm the infection.

What are the economic costs of Johne’s?
The economic impact of Johne’s varies widely from herd to herd. The number of animals involved and how long the disease goes undetected are major factors which determine the course of the disease. Dairy producers generally see the effects of Johne’s in their herds more quickly than do beef producers. Milk production may drop as much as 1500 pounds per cow. As the disease progresses, animals lose weight and produce lower quality milk. Increased culling and higher mortality also contribute to the economic drain on the infected farms.

A low-Johne’s clinical herd (fewer than 10% of the cull cows showing symptoms) results in about a $40 milk-loss per animal; the loss climbs to $227 in high-Johne’s clinical herds (those with greater than 10% of culls with signs). DHIA records report about $243 profit per head for the same year.

Failure to recognize the progression of Johne’s prevents early, aggressive culling of infected animals, which is needed to reduce the contamination and exposure within the herd. Culling of animals, before the disease progresses to advanced stages with a severe loss of body condition, will provide greater salvage value and less loss to the owner. The median price received for culls in good condition is reported to be about $400; $250 per head for those in poor condition.

These losses also interfere with the development and selection of genetic replacements. Reports indicate a lot of breeding animals are sold out of infected herds. Increased culling rates and lack of readily available genetic selection results in increased replacement costs. This can vary greatly, depending upon their source and quality, but will be close to $1700 per head.

Veterinary expenses will also be greater for infected herds. The additional diagnosis, testing and consultation fees will negatively impact a herd’s potential to return a profit.

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