A chronic debilitating intestinal disease of cattle was recognized in Europe as early as 1826. By 1894 it was recognized as an infectious disease and characterized by Drs. Heinrich Johne (German) and Frothingham (U.S.). Johne’s disease was first described in the U.S. in 1908.
Johne’s disease, also called paratuberculosis, is caused by the bacterium Mycobacterium avium subspecies paratuberculosis, abbreviated MAP. Calves less than six months of age are generally considered to be at the greatest risk of becoming infected with MAP. While the incubation period from time of infection to clinical disease is dependent on the infective dose, it averages about five years. One of the greatest difficulties in controlling Johne’s disease within and between herds, is the presence of animals that shed MAP organisms in their feces before clinical signs become apparent.
It took 70 years before any country began to develop systematic methods to try and stop the spread of paratuberculosis among herds. By then Johne’s was found in over 60 per cent of North American dairy herds and 10 to 15 per cent of beef herds.
MAP is tenacious. Survival in damp, unsanitary conditions extends beyond a year. Direct sunlight and exposure to UV radiation has the greatest impact on MAP survival. The organism is resistant to heat and has been shown to survive high-temperature, short time pasteurization (72 C for 15 seconds) in raw milk.
The discovery of a genetic element unique to M. tuberculosis ushered in a new generation of paratuberculosis research. Identifying a segment of DNA in MAP organisms called IS900 enabled development of genetic tools for detection of MAP without having to cultivate the bacteria under laboratory conditions for 12 to 16 weeks. Through the use of IS900 gene probes, a wealth of information has been learned about MAP’s distribution in the natural environment and the species it infects. Most provocative are reports that M. paratuberculosis is found in the tissues of over half of humans with Crohn’s disease. To date, the exact cause of Crohn’s disease remains unknown.
The actual percentage of infected animals in the population overall is known to be higher in dairy cattle than beef and definitely higher in cull animals tested at slaughter and auction markets.
Animals shedding MAP do so intermittently, but the number of organisms shed is measured in millions. Teats, udders and the calving environment quickly become contaminated. A few individual animals, for reasons yet to be discovered, become “super-shedders” and likely represent the greatest source of MAP contamination in herds. Infected cows shed MAP in colostrum and milk. Transmission during pregnancy has been documented. Up to one-third of calves from cows showing clinical signs of Johne’s disease are infected at birth.
Johne’s disease control must be tailored to specific herds although calving areas and calf rearing practices typically require most of the attention. Typically, MAP infection walks onto a farm with replacement animals. Bulls and replacement heifers can be a source of MAP infections in commercial herds with few questions ever asked about Johne’s disease control at source. The trade in cull dairy cows, dirty trucks hauling heifers bought at auction markets, corral cleaning contractors that move from to farm with little effort to clean equipment between premises and communal grazing arrangements are all points of risk. Efforts to control Johne’s disease have collateral benefits of reducing other diseases.
Researchers continue to look for new vaccine candidates. Limited use of vaccine in the U.S. and in other countries has shown to significantly reduce clinical disease and fecal shedding of MAP, but there are serious drawbacks. Vaccines currently available come with serious injection site reactions, risks to users if accidentally inoculated and complicate interpretation of the diagnostic tests. Genetically engineered sub-unit vaccines with limited side effects will someday greatly enhance Johne’s disease control. Industry’s support of vaccine research needs to be a priority.
Research funding has led to the development of a range of diagnostic tests for use in animals infected with MAP. People often find fault with the lack of definitive tests for paratuberculosis as the reason industry hasn’t progressed as far as it should have with control. There is probably a greater diversity of accurate and affordable tests for paratuberculosis than most other ruminant infectious diseases. The present-day challenge for practitioners is to select the appropriate test for the intended purpose.
In the absence of Johne’s disease being declared a zoonosis, which would trigger compulsory control as it was with brucellosis and TB, the catalyst for Johne’s disease control will probably come from buyers of replacement stock asking for seller reassurances that purchased animals are not MAP-infected. The purebred industry should anticipate this request and establish risk-management protocols with whatever testing is necessary to offer reassurances to buyers. The chain reaction started in the seed stock industry will work its way into the commercial cattle sector and drive change there.
Advances in Johne’s disease control must come. Diseases like BSE taught us all: you can’t un-ring a bell!
— Dr. Ron Clarke prepares this column on behalf of the Western Canadian Association of Bovine Practitioners. Suggestions for future articles can be sent to Canadian Cattlemen ([email protected]) or WCABP ([email protected]).