Johne’s disease prevention, diagnosis remains a challenge

Johne’s disease has long been recognized as an economically important disease in dairy cattle, but it actually affects a wide variety of ruminants.


Other species that it affects in-clude beef cattle, sheep, goats, llamas, alpacas and wildlife such as deer, bison, elk and antelope. 


The disease is caused by mycobacterium avium subspecies paratuberculosis (MAP), a master of evading the immune system. The bacteria is able to avoid white blood cells and cause tremendous inflammation. 


The intestines eventually become so thick that nutrients cannot be absorbed. The affected animal loses weight and may eventually die from the infection. There are no effective treatments. 


Clinical signs of Johne’s in cattle include weight loss, diarrhea and bottle jaw and typically occur in cattle between the ages of two and six. Other diseases look similar, including coccidiosis, parasitism and several mineral deficiencies. 


Sheep and goats affected with Johne’s show different signs. They are often afflicted with weight loss and poor wool quality but not diarrhea. 


Johne’s is found worldwide and causes the most trouble where intensive animal production is practised. 


MAP is spread primarily through feces, although fetuses can be infected while still within the uterus. Animals younger than weaning age are most susceptible to infection and are typically exposed to the bacteria by eating feces-contaminated feed. 


The severity of the disease seems to depend on the amount of bacteria with which an animal is infected. 


Scottish researchers said in a recent edition of the Veterinary Journal that they have identified a link between wild rabbits and Johne’s. They found that farms with more infected rabbits were more likely to have trouble controlling Johne’s in their herds. 


The finding suggests that wildlife reservoirs may play a key role in controlling the disease at the farm level. 


Problems with diagnosis and prevention remain the biggest impairment to effectively managing Johne’s at the herd or flock level. 


Inexpensive and safe vaccines are available to prevent other diseases such as clostridial infections, but Johne’s is much more complicated to manage. 


Growing the bacteria from feces is the standard way to confirm infection in a suspected case, but it is technically challenging and can take up to six months. 


DNA testing is rapid and takes only a few days to get results, but it is not a magic bullet in Johne’s. 


As well, infected animals can live for years before showing signs of illness.


Clinical cases of Johne’s represent the tip of the iceberg at the herd level. Only a small percentage of the infected animals develop clinical disease, while the rest live as bacteria factories, shedding MAP in their feces and providing ample opportunity for spread to other herd mates. 


The structure of MAP’s cell wall makes it remarkably resistant to en-vironmental conditions that would kill other types of bacteria, including heat, acidity, drying and chemical disinfectants. 


Meanwhile, human health re-searchers are grappling with the controversial question of whether MAP is related to Crohn’s disease in humans. 


This debilitating condition is a form of chronic inflammatory bowl disease, which has been linked to the same bacterium that causes Johne’s in animals. 


MAP is shed in the milk of infected cows and it has been proposed that contaminated milk may be the route through which humans become infected. 


MAP is also known to rarely infect non-ruminant species such as dogs and cats, so it isn’t surprising that it would also make the jump to infecting humans. 


However, this issue requires further research to definitively establish the cause and effect relationship.


Dr. Jamie Rothenburger is a veterinary pathology resident at the Western College of Veterinary Medicine, University of Saskatchewan.