Johne's disease
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| Johne's disease Classification and external resources | |
| DiseasesDB | 33739 |
|---|---|
| MeSH | D010283 |
Johne's disease (pronounced "yo-knees") is a contagious, chronic and sometimes fatal infection that affects primarily the small intestine of ruminants. A ruminant is any hooved animal that digests its food in two steps, first by eating the raw material then regurgitating and eating a semi-digested form known as cud. Ruminants include cattle, goats, sheep, camels, llamas, giraffes, bison, buffalo, deer, wildebeest, and antelope. All ruminants are susceptible to Johne's disease, which is sometimes called paratuberculosis. The disease is worldwide in distribution.
Bacterium
The disease, discovered by Heinrich A. Johne, a German bacteriologist and veterinarian, in 1905, is caused by a bacterium named Mycobacterium avium subspecies paratuberculosis; often the name is abbreviated as MAP. MAP is akin to but distinct from Mycobacterium tuberculosis, the main cause of tuberculosis in humans, and Mycobacterium bovis, the main cause of tuberculosis in cows and occasionally also in humans. MAP is 99 percent genetically related to Mycobacterium avium, but has different phenotypic characteristics such as
- slower growth,
- requires the addition of an iron transport chemical known as mycobactin when grown in vitro (outside the body)
- forms a rough colony when grown on solid agar media, and
- 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.
Symptoms
Signs of Johne's disease include weight loss and diarrhea with a normal appetite. Several weeks after the onset of diarrhea, a soft swelling may occur under the jaw (bottle jaw). Bottle jaw or intermandibular edema is due to protein loss from the bloodstream into the digestive tract. Animals at this stage of the disease will not live very long, perhaps a few weeks at most.
Signs are rarely evident until two or more years after the initial infection, which usually occurs shortly after birth. Animals are most susceptible to the infection in the first year of life. Newborns most often become infected by swallowing small amounts of infected manure from the birthing environment or udder of the mother. In addition, newborns may become infected while in the uterus or by swallowing bacteria passed in milk and colostrum. Animals exposed at an older age, or exposed to a very small dose of bacteria at a young age, are not likely to develop clinical disease until they are much older than two years.
Clinical characteristics
The primary site targeted by Johne's disease is the lower part of the intestine know 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 M. paratuberculosis to the Peyer's patch, the bacteria finds an ideal place for growth. Macrophages in Peyer's patches engulf M. paratuberculosis for the purpose of destroying the foreign invader, but for reason that are unclear, these macrophages fail to do this. Inside a macrophage, M. paratuberculosis 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 teeming with millions of the mycobacteria. How M. paratuberculosis neutralizes or evades the normally efficient bacterial killing mechanisms of the macrophages is unknown, although the unusually resistant cell wall of mycobacteria likely plays an important role.
The animal's immune system reacts to the M. paratuberculosis invasion by recruiting more macrophages and lymphocytes to the site of the infection. The lymphocytes release a variety of chemicals 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 visible thickening of the intestines. This prevents nutrient absorption and diarrhea results. Late in the infection, antibody production by the animal occurs to M. paratuberculosis in serum of animals and is an indicator that clinical signs of disease and death from the infection will soon follow.
Human risks
Studies performed in the United States, the UK, and the Czech Republic demonstrate that pasteurization is capable of a 7 log reduction of M. paratuberculosis in milk. M. paratuberculosis has never been scientifically proven to causes disease in humans; however a number of researchers contend that the organism is a primary cause of Crohn's disease citing clinical similarities between Johne's disease in ruminants and Crohn's disease in humans.
External references
- USDA Johne's resource page
- University of Wisconsin School of Veterinary Medicine Johne's Information Center
- Open Directory Categoryde:Paratuberkulose
is:Garnaveiki ja:ヨーネ病 nl:Paratuberculose
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
