Paratuberculosis: Difference between revisions
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== Human risks == |
== Human risks == |
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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. |
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.{{fact}} |
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''M. paratuberculosis'' has never been scientifically proven to cause disease in humans.{{fact}} |
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There are clinical similarities between Johne's disease in ruminants and [[inflammatory bowel disease]] in humans,<ref name="pmid18596984">{{cite journal |author=Juste RA, Elguezabal N, Garrido JM, ''et al'' |title=On the prevalence of M. avium subspecies paratuberculosis DNA in the blood of healthy individuals and patients with inflammatory bowel disease |journal=PLoS ONE |volume=3 |issue=7 |pages=e2537 |year=2008 |pmid=18596984 |pmc=2434204 |doi=10.1371/journal.pone.0002537 |url=http://www.plosone.org/article/info:doi/10.1371/journal.pone.0002537}}</ref> and because of this, a number of researchers, however, contend that the organism is a primary cause of [[Crohn's disease]].{{fact}} |
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==Action and regulations== |
==Action and regulations== |
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Revision as of 19:05, 13 September 2008
| Paratuberculosis | |
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| Specialty | Infectious diseases  |
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. Infections have also been seen in a variety of non-ruminant species including rabbits, foxes and birds. Horses, dogs and non-human primates can be infected experimentally. Paratuberculosis is found worldwide, with Norway, Sweden and some states in Australia the only areas proven to be free of the disease.[1]
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, an acid-fast bacillus often abbreviated 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
In cattle, the main symptoms of paratuberculosis are diarrhoea and wasting. Most cases are seen in 2 to 6 year old animals. The initial symptoms can be subtle and may be limited to weight loss, decreased milk production, or roughening of the hair coat. The diarrhoea is usually thick, without blood, mucus, or epithelial debris, and may be intermittent. Several weeks after the onset of diarrhea, a soft swelling may occur under the jaw. Known as "bottle jaw" or intermandibular edema, this symptom is due to protein loss from the bloodstream into the digestive tract. Paratuberculosis is progressive; affected animals become increasingly emaciated and usually die as the result of dehydration and severe cachexia.
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.
The clinical signs are similar in other ruminants. In sheep and goats, the wool is often damaged and easily shed, and diarrhea is uncommon. In deer, paratuberculosis can be rapidly progressive. Intestinal disease has also been reported in rabbits and non-human primates.
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 reasons 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.
For goats infected with this disease, the most apparent sign of having it is their body wasting away, even with a sufficient diet. If a goat develops Johnes and it has diarrhea, it is most likely going to die. When it has diarrhea, the goat is at the last stages of the disease. Always test your herd once or twice a year to maintain the health of your animals and keep out diseases.
Morbidity and mortality
In an endemic herd, only a minority of the animals develops clinical signs; most animals either eliminate the infection or become asymptomatic carriers. The mortality rate is approximately 1%, but up to 50% of the animals in the herd can be asymptomatically infected, resulting in losses in production. Once the symptoms appear, paratuberculosis is progressive and affected animals eventually die. The percentage of asymptomatic carriers that develops overt disease is unknown.[2]
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.[citation needed]
M. paratuberculosis has never been scientifically proven to cause disease in humans.[citation needed]
There are clinical similarities between Johne's disease in ruminants and inflammatory bowel disease in humans,[3] and because of this, a number of researchers, however, contend that the organism is a primary cause of Crohn's disease.[citation needed]
Action and regulations
Paratuberculosis is a reportable disease in some states of the US[citation needed]. US Federal regulations prohibit culture positive or DNA test-positive animals from being moved across state lines except for slaughter.[citation needed]
References
- ^ Collins M. and Manning E. "Johne's Information Center" The University of Wisconsin-School of Veterinary Medicine. 13 March 2003.
- ^ Paratuberculosis. In the Merck Veterinary Manual, 8th ed. Edited by S. E. Aiello. Whitehouse Station, NJ: Merck and Co. 1998.
- ^ Juste RA, Elguezabal N, Garrido JM; et al. (2008). "On the prevalence of M. avium subspecies paratuberculosis DNA in the blood of healthy individuals and patients with inflammatory bowel disease". PLoS ONE. 3 (7): e2537. doi:10.1371/journal.pone.0002537. PMC 2434204. PMID 18596984.
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