What is the cause of Johne's disease?
Johne's disease is caused by a bacterium named Mycobacterium avium subspecies paratuberculosis; often the name is abbreviated as M. paratuberculosis or MAP. M. paratuberculosis is akin to, but not genetically related to Mycobacterium tuberculosis and Mycobacterium bovis, the bacterium that cause tuberculosis in humans. MAP is 99 percent 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 multiple outside the body.
MAP is a small (0.5 x 1.5 microns) 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 multiple) for over a year after fecal contamination via an infected animal.
How does Johne's disease affect the body?
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 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 reason that are unclear, these macrophages fail to do this. Inside a macrophage MAP multiples 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 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 MAP in serum of animals and is an indicator that clinical signs of disease and death from the infection will soon follow.