Some sources define "paratuberculosis" by the lack of Mycobacterium tuberculosis, rather than the presence of any specific infectious agent, leaving ambiguous the appropriateness of the term to describe Buruli ulcer or Lady Windermere syndrome.
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.
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.
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.
M. paratuberculosis has never been scientifically proven to cause disease in humans.
There are clinical similarities between Johne's disease in ruminants and inflammatory bowel disease in humans, and because of this, some researchers contend that the organism is a cause of Crohn's disease.
EXOTIC ENTRIES ON REPORTABLE DISEASE LIST OLDER ILLNESSES NOW CONSIDERED COMMON HAVE BEEN DROPPED, AND NEW DEADLY VIRUSES HAVE BEEN ADDED.(FRONT)
Dec 10, 2007; Byline: DAVID WAHLBERG firstname.lastname@example.org 608-252-6125 Scratch cat scratch disease off the list of illnesses doctors must...