Ruminant species (hoofed herbivores with four-chambered stomachs that chew their cud) are the natural host for and most affected by Mycobacterium avium ss. paratuberculosis (MAP). All genera of this diverse and numerous taxonomic group are believed susceptible to infection (“pseudo-ruminants” such as camelids as well). In these species the infection eventually proceeds to gastrointestinal disease and death. This is true for domestic agriculture ruminants (such as cattle, sheep and goats), ruminant wildlife in captivity (e.g. addax, eland, and muntjac) plus free-ranging ruminants including bison, moufflon and guanaco. Cases of Johne’s disease (the clinical illness that appears months to years after initial infection by MAP in young animals) have been reported in every country in the world that has tested for it. The infection can spread from one ruminant species (for instance cattle) to another (goats, sheep, etc.).
Non-ruminant species (omnivores, carnivores) are infrequently infected, and few of these infections have been shown to progress to either clinical illness or systemic pathology. In these “atypical” hosts (such as fox, stoat, badger, raven, etc.) the organism is believed to be acquired through eating infected prey*. While insufficient research has been completed to make any firm conclusions, it is believed that these non-ruminant species are “dead-end” hosts i.e. that the infection is not shed in the feces or milk to represent a risk of transmission and that offspring do not become infected in utero. There have been a few reports MAP infecting pigs, horses, and nonhuman primates. (See the Zoonosis section for a discussion of whether MAP represents a health risk for humans).
One non-ruminant type of animal does appear affected by MAP infection: rabbits and hares. There has been extensive investigation of a location in Scotland where rabbits have not only been infected by the same strain as MAP as found in the dairy cattle sharing pasture, but appear to maintain the infection in subsequent generations without re-infection from cattle or the environment. In some of these rabbits, MAP caused pathologic lesions resembling Johne’s disease. MAP infection of rabbits and hares in other countries has been reported as well, but subsequent disease is rarely described and these populations do not appear to be reservoirs of the infection as is seen in Scotland.
Johne's disease has steadily dispersed around the world with the global trade in animals. First recognized in Europe, it has now been reported on every continent in a variety of species. Up to 68% of dairy herds and 8% of beef herds in the United States were found to have evidence of the infection in a recent study. Prevalence estimates in other domestic species are not available due to limited testing and reporting, but virtually all ruminant animal industries list Johne’s disease as a common problem.
Cases of Johne's disease have been reported in both captive and free-ranging wildlife, but the infection is much more common in farmed ruminants due to prevailing animal husbandry methods that result in high animal density and multiple routes of concentrated MAP exposure for youngstock.
Clinical Johne’s disease has also been reported on occasion in other free-ranging ungulate species including Rocky Mountain bighorn sheep (Ovis canadensis canadensis), Rocky Mountain goats (Oreamnos americanus), as well as free-ranging red (Cervus elaphus hippelaphus) and fallow deer in Europe. A quicker progression from infection to clinical signs is reported in farmed cervids (red deer or elk) than bovids, with animals less than two years of age rapidly losing weight, developing severe pathology and dying of the infection.
Infected tule elk (Cervus elaphus nannodes) were first detected in 1979 at the Point Reyes National Seashore (PRNS) reserve, California. The infection has been confirmed in adult animals since that time but reserve managers report no obvious overall effect on herd health or reproduction due to Johne’s disease. Surveys in Arkansas and Montana/Wyoming elk did not reveal indicators of MAP infection in these free-ranging populations. MAP infection was first diagnosed in an endangered Florida Key deer (a subspecies of white-tailed deer; Odocoileus virginianus clavium) in 1996 and subsequent surveys indicate that the organism persists in the Key deer population and environment at a low prevalence. Its distribution is limited to a relatively small geographic area within their range. A clinical case in a two-year old male white-tailed deer in Virginia lead to subsequent surveillance; no additional cases or infected animals were found in that study.
Johne’s disease is present in at least several herds of bison in the United States, both farmed and free-ranging. A serologic survey of banked sera collected over multiple years from free-ranging bison managed in four western national parks did not indicate the presence of MAP infection in these populations. In Canada, surveillance of bison with PCR produced positive results in several herds, but the organism has yet to be recovered from any fecal sample.
Free-ranging guanacos (Lama guanicoe) on Tierra del Fuego Island, Chile were found to be shedding MAP at a low prevalence in a recent report. (The economic basis of this region is livestock production; Johne’s disease has not been reported in sheep or cattle in the area but surveillance for the infection is not performed.) Paratuberculosis in camelids under domestic husbandry has also been reported, including alpacas (Lama pacos) in Australia, and camels (Camelus dromedarius) from Egypt and Saudi Arabia.
MAP is an obligate animal pathogen. This means that the only place it multiplies in nature is inside an animal (ruminant). Most specifically, it is inside cells that are part of the animal's immune system called macrophages. When MAP leaves an animal, for example when shed in the feces, it can survive at low numbers for a long time (up to a year) in environments such as soil and water, but it cannot multiply there. Consequently, the primary source of infection is infected animals’ manure (and the resultant contaminated environment) and milk.
Experimental infection studies indicate 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), for example, by crossing barn corridors in the path of a contaminated keeper’s boot 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 this environmental contamination presents a risk to wildlife via contaminated feed and water.
As MAP infection progresses in an animal, the frequency and number of bacteria being excreted increases. Cattle produce more than 100 pounds of manure a day and what to do with it is a big problem for the agriculture industry. This contaminated manure may be used as fertilizer for crops, be injected into the soil, be placed in a (leaky) lagoon, or run off pastures or fields into streams, ponds and groundwater. This means that the environmental burden of MAP can increase, and can spread beyond herd premises. For more detailed information on the survival characteristics of MAPsee the part of this website called "Biology of MAP”.
Milk from infected dams is a second source of MAP infection. Just as with fecal shedding, the likelihood of MAP being excreted into milk increases with time as the infection progresses. MAP may be excreted directly into the mother's milk and/or the surface of the teats might be contaminated with infected manure.
Most MAP transmission occurs from adult infected animals to young calves, kids or fawns through the fecal-oral route. The organism is swallowed in manure-contaminated milk, water or feed; sometimes manure is swallowed directly before the calf even hits the ground. MAP is also shed directly into the milk and colostrum of infected dams in later stages of infection, providing another route of exposure for susceptible young animals. Once established in a population, Johne's disease can be expected to spread more quickly in species producing twins or triplets (e.g. small ruminants) as opposed to single offspring since a greater percentage of the flock/herd is at a susceptible age and more animals are exposed to an infected dam.
Another transmission route is in utero: a fetus may become acquire the infection from its infected dam before it is born. The clearest example of this was an embryo transfer case managed under the strictest of research biosecurity conditions to prevent any exposure to MAP after birth (e.g., C-section birth and removed immediately from recipient cow, colostrum and milk collected from a different cow that was repeatedly test-negative bottle-fed, hay from uninfected herd pastures, etc.). While the embryo recipient cow was Johne’s disease test negative at the start of the pregnancy, it became strong ELISA-positive result in month six. After the C-section, the recipient cow was proven infected at necropsy. Two years later, the (very valuable) embryo calf was ELISA-positive and MAP infection was confirmed at necropsy. The recipient cow had been purchased from a herd with a history of Johne’s disease.
There is no transmission risk through nose-to-nose fence line contact (unless contaminated manure is sluicing under the fence), through sneezed aerosols, or via artificial insemination or natural breeding.