Much has been accomplished in understanding the interplay of MAP and its host in recent years using as new tools the genome of MAP and the many cellular, proteomic and reagents and assays recently developed. Despite this progress, core questions about MAP pathology remain unanswered:
Here is a summary of our current knowledge about the impact of a MAP infection for an infected member of a wildlife species:
The target for MAP is the ruminant (such as an elk, bison, sheep etc.) gastrointestinal tract. The most distal section, the ileum, is the primary site for infection. Ruminants swallow the organism (via MAP-contaminated milk, water or feed) which then invades through specialized ileal tissue called Peyer’s patches to enter immune cells (macrophages) in the tissue. Experimental infection studies estimate that an infective oral dose for young cattle, deer and goats is 4 x106 CFU (i.e. total 200 mg wet weight pelleted MAP). Therefore the risk for infection of a susceptible ruminant (i.e. less than 6 months old) by crossing barn corridors in the path of a contaminated keeper’s boot, for example, or traversing a road driven upon by a veterinary truck that had crossed a pasture containing infected adult animals is low. However, given that infected cattle may shed 106 CFU per gram of manure, in some circumstances environmental contamination presents a risk to wildlife via contaminated feed and water.
This microscopic infection of macrophages in the small intestinal persists for years without triggering any systemic response from the animal’s immune system i.e., the animal is infected isn’t sick and isn’t responding to the infection in any visible way. At some point MAP spreads to lymph nodes flanking the gastrointestinal tract (the mesenteric nodes); later, for reasons not yet understood, the infection spreads throughout the ruminant. Clinical symptoms of Johne’s disease usually begin to appear at this point, and the adult animal only now, often years after infection, reliably produces the signal of the infection detectable by blood tests (anti-MAP antibody in the serum and milk; unfortunately, few antibody assays are validated for wildlife species.)
Throughout this long sub-clinical phase (estimated at 2-10 years) when the animal is apparently healthy although infected, it is capable of transmitting the infection by shedding MAP intermittently in milk and manure. When observable signs of illness finally begin, the rate and amount of shedding increases and the animal represents an ever greater risk to its own offspring and other young animals.Infection of non-ruminant species is believed also to occur by swallowing MAP, for example carnivorous animals eating infected prey (e.g. stoat eating a rabbit infected through grazing contaminated grass) or an omnivore swallowing contaminated feed (crow pecking at seeds in contaminated rations). While evidence of infection (e.g. isolation of MAP from tissue) can be demonstrated, it is believed rare that the infection damages the intestinal tract or causes clinical disease of a non-ruminant.