Johne’s Disease (Paratuberculosis)

In this episode, Dr. Lottie covers everything about Johne’s disease (also known as paratuberculosis) from the MAP pathogen itself and what clinical signs you may see, to how we can control infection and what Johne’s means for public health

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Timeline:
00:00 Intro
00:45 Case
02:36 Aetiology & Pathogenesis
06:26 Clinical Signs
09:18 Diagnosis
14:46 Treatment
15:59 Prevention
18:42 Impact of Johne’s
21:01 Key Points
22:32 Outro

Recommended Reading:

• Johne’s Disease in Canada – Parts I and II Part I is an overview of clinical signs, how the disease develops, and common di gnostic approaches then part II focuss on the economic impact of the disease and control methods . Canadian Veterinary Journal (2006), Vol 47(9), pp 874–882 and Canadian Veterinary Journal (2006), Vol 47(11), pp 1089–1099.
• Mycobacterium avium subsp. paratuberculosis in Veterinary Medicine  A very readable but detailed explanation of the bacterium itself and how it behaves. Clinical Microbiology Reviews (2001).
• Veterinary Medicine: A Textbook of the Diseases of Cattle, Horses, Sheep, Pigs and Goats (11th Edition)  Great cattle textbook chapter on paratuberculosis Constable, Hinchcliff, Done & Grünberg — pp. 552–572

References

• Tiwari, A., VanLeeuwen, J.A., McKenna, S.L.B., Keefe, G.P. & Barkema, H.W. (2006) ‘Johne’s disease in Canada Part I: Clinical symptoms, pathophysiology, diagnosis, and prevalence in dairy herds’, Canadian Veterinary Journal, 47(9), pp. 874–882.
• McKenna, S.L.B., Keefe, G.P., Tiwari, A., VanLeeuwen, J.A. & Barkema, H.W. (2006) ‘Johne’s disease in Canada Part II: Disease impacts, risk factors, and control programs for dairy producers’, Canadian Veterinary Journal, 47(11), pp. 1089–1099.
• Harris, N.B. & Barletta, R.G. (2001) ‘Mycobacterium avium subsp. paratuberculosis in Veterinary Medicine’, Clinical Microbiology Reviews, 14(3), pp. 489–512. doi: 10.1128/CMR.14.3.489-512.2001.
• Constable, P.D., Hinchcliff, K.W., Done, S.H. & Grünberg, W. (2017) Veterinary Medicine: A Textbook of the Diseases of Cattle, Horses, Sheep, Pigs and Goats. 11th ed. Elsevier, pp. 552–572.
• Sweeney, R.W., Collins, M.T., Koets, A.P., McGuirk, S.M. & Roussel, A.J. (2012) ‘Paratuberculosis (Johne’s Disease) in Cattle and Other Susceptible Species’, Journal of Veterinary Internal Medicine, 26(6), pp. 1239–1250. doi: 10.1111/j.1939-1676.2012.01019.x.
• Rathnaiah, G., Zinniel, D.K., Bannantine, J.P., Stabel, J.R., Gröhn, Y.T., Collins, M.T. & Barletta, R.G. (2017) ‘Pathogenesis, Molecular Genetics, and Genomics of Mycobacterium avium subsp. paratuberculosis’, Frontiers in Veterinary Science, 4, 187. doi: 10.3389/fvets.2017.00187.
• Beard, P.M., Daniels, M.J., Henderson, D., Pirie, A., Rudge, K., Buxton, D., Rhind, S., Greig, A., Hutchings, M.R., McKendrick, I., Stevenson, K. & Sharp, J.M. (2001) ‘Paratuberculosis infection of nonruminant wildlife in Scotland’, Journal of Clinical Microbiology, 39(4), pp. 1517–1521. doi: 10.1128/JCM.39.4.1517-1521.2001.
• Whittington, R., Donat, K., Weber, M.F. et al. (2019) ‘Control of paratuberculosis: who, why and how. A review of 48 countries’, BMC Veterinary Research, 15, 198. doi: 10.1186/s12917-019-1943-4.
• World Organisation for Animal Health (WOAH) (2024) Paratuberculosis. Available at: https://www.woah.org/en/disease/paratuberculosis/ (Accessed: 30th October 2025).
• Fecteau, M.E. (2018) ‘Paratuberculosis in cattle’, Veterinary Clinics of North America: Food Animal Practice, 34(1), pp. 209–222. doi: 10.1016/j.cvfa.2017.10.011

Current Vet is an educational podcast intended for veterinary students, veterinary professionals, and individuals with an interest in veterinary medicine.

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Any clinical cases discussed in this podcast are fictional, and are designed to reflect typical or likely clinical scenarios for educational purposes. They do not represent specific real-life cases, clients, or animals.

While every effort is made to ensure accuracy and alignment with current evidence at the time of publication, veterinary medicine is a rapidly evolving field, and recommendations may change over time

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Host

Dr. Lottie Wilkinson

Creator and host of the Current Vet podcast

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In each episode, Dr. Lottie breaks down clinical conditions, cases, and concepts across species, focusing on pathophysiology, decision-making, diagnostics, and what actually matters in practice. It’s the kind of context that makes your knowledge finally click.

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Intro

​Hello, hello, and welcome back to Current Vet, the podcast that makes veterinary medicine simple. I'm your host, Dr. Lottie, and today we are talking about Johne's disease, also known as para tuberculosis.

It's a chronic progressive disease that we most commonly see in cows, but it can also occur in small ruminants, camelids and wildlife species like deer.

Johne's can be frustrating to diagnose and manage. It develops slowly, and by the time clinical signs appear, the disease has usually been present in the animal and in the herd for years. But as always, let's start with a case.

Case

You are on a routine visit to one of your biggest dairy farms. This is a housed high yield herd of around 3000 girls.

The Farm manager has asked you to check an older cow, one of their reliable producers. She's five years old, multiparous, and has historically performed extremely well over the last few weeks. Her milk yield has declined gradually, and she's also losing weight despite being on a good ration.

A few of the farm hands have noticed her feces are looser than normal, but they haven't noticed profuse or watery diarrhea. On exam, you note that she is bright and alert. No fever, no abnormalities in her heart rate, respirate or any respiratory efforts, and no abnormal sounds heard in any of her lung fields.

Her body condition score is at a two out of five. The manager tells you that she's 120 days in milk and you palpate under the jaw for a pulse and feel mild pitting edema. You ask about worming history and she's been treated routinely. There's been no recent calving issues. No other cows are currently showing similar signs, but the manager mentions that a couple of cows last year just never bounced back and were eventually culled.

So we currently have an older cow presenting with gradual weight loss, intermittent diarrhea, a drop in milk yield, and mild submandibular edema.
Our differential at this point are gonna be things like parm, which still needs to be a consideration, even in cows who have been treated prophylactically. Liver disease, neoplasia, and of course Johne's. If it is Johne's, however, the infection likely, began as a calf and there's a risk that a lot of the rest of the herd are also sub clinically infected.

Aetiology & Pathogenesis

But let's get into what Johne's is and how it's possible that our gal is only now showing signs if she became infected years ago. So Johne's is caused by bacteria called mycobacterium avium, subspecies para tuberculosis, which is a huge mouthful to say. So it's also known as MAP for short, and just like other mycobacteria, it is a slow growing, acid fast bacteria that has a thick waxy cell wall.

While cows are the species most often seen with Johne's, the true host range is incredibly broad. So it encompasses things like small ruminants, camelids, buffalo, wild ruminants, deer, reindeer, antelope, and so many others. And there's even evidence that it can infect non ruminant species like foxes, rabbits, badgers, rodents, and some birds.

So this is truly a global disease and one that is very difficult to control. The key thing to understand about para tuberculosis is that infection progresses very slowly, it almost always begins early in life, but the disease doesn't become clinically apparent until years later. Calves pick up MAP from contaminated colostrum or pooled milk feces from infected adults, calving pens, bedding, shared feeding equipment, manure, contaminated tets, or from the environment.

Adult cows can be infected, but infection is most likely to occur when they are neonatal and in young calves up to around six months of age. And this is thought to be because the calf immune system is less developed than in the adult bovine. And the fact that the intestines are more permeable in early life may play a role once infected.

There are three responses an animal can have. Firstly, the immune system controls the infection. Basically, the animal doesn't become affected. Secondly, the immune system partially controls infection, but the animal becomes a carrier and can shed bacteria. Well. Thirdly, the bacteria persists in the intestines and the animal will eventually become clinically affected.

When MAP is ingested, it travels to the small intestine, mainly the ileum where it crosses the gut wall and is taken up by macrophages. However, in the animals with an insufficient immune response. Instead of being destroyed by macrophages, MAP survives in these cells by preventing phagosome lysosome fusion and replicates inside them so that the host's immune response can't clear the infection, macrophages then travel to the local lymph nodes where infection persists, as well as in the intestinal mucosa. This leads to a chronically progressive granular Marti enteritis, which develops over two to five years until it becomes clinically apparent.

So by the time an animal is clinically affected, they have likely already been shedding the bacteria into the environment for up to 18 months. This, and the fact that MAP can survive in the environment for up to a year means that by the time Johne's is diagnosed, there is likely to be many, many more cases on the farm that just aren't yet clinically apparent.

It is estimated that for every clinical case of Johne's 15 to 25, other animals in the herd are sub clinically infected. So when we diagnose Johne's, we should immediately be broadening our perspective from the individual case to a herd level problem.

Clinical Signs

So let's talk about how Johne's disease presents. We start to see Johne's in adult cows at around two to six years old, and that's because this is the end stage of that long incubation period. So the classic presentation is progressive weight loss despite a normal or even increased appetite, chronic watery diarrhea, that's typically homogenous, not bloody and non fettered, so it doesn't actually really smell.

There's a gradual drop in milk yield, which is often noticed before diarrhea develops. In early cases, diarrhea can be intermittent, but over time it becomes continuous, sometimes described really nicely as pipestream or water hose consistency. So that is not a cow that you want to be standing behind.

As protein is lost in the diarrhea, hypo protein anemia develops, and that is why we can see submandibular edema, also known as bottle jaw. So despite all this diarrhea, these cows are usually bright alerts and non paraic. So that's actually a really helpful differentiator from other causes of diarrhea, for example, salmonella, where you'd expect pyrexia and systemic illness. So that key clinical pattern is gonna be bright eating well losing weight with persistent watery diarrhea. In small ruminants, Johne's disease less commonly causes diarrhea. And instead, we might see progressive weight loss and emaciation as the key clinical sign alongside poor fleece or coat quality.

In deer, kalos and other wildlife, the disease can progress more rapidly and become clinical in animals of a younger age. Again, seeing that weight loss and diarrhea as the key clinical signs.

Let's quickly go through a couple of differentials that we are going to rule out to make sure that we definitely have Johne's. So first we have chronic parasitism, so things like ostertagiasis, then chronic salmonella is on the list. But remember that those cows are often febrile, dull, and systemically unwell, which can help to distinguish them from Johne's.

Copper deficiency, especially in certain soils and environments or in areas that are high in molybdenum. But this tends to affect multiple animals in the herd simultaneously, and it should improve when copper is supplemented in the diet.
Lymphoma, perhaps associated with bovine leukemia virus we're looking for things like ventral edema, weight loss, and enlarged peripheral lymph nodes with this one and amyloidosis, which is rare, but it does cause a protein losing enteropathy and edema similar to our Johne's presentation.

Diagnosis

So let's come back to our cow. Of course, Johne's is high on our differential list, but how might we confirm it and make sure that it isn't one of our other differentials causing disease? The best way to divide the tests that we can do for Johne's is into tests that detect the organism itself and those that detect the host immune response to infection.

So first, for organism detection, we have fecal culture.

This is a very specific test for MAP, so if it's positive and you see mycobacteria in that culture, that cow is very likely to be infected. But the limitations are that MAP grows exceptionally slowly, and results can take up to 16 weeks to come back, and that's really not useful when we're trying to make medical decisions and herd health plans.

As well as this, the bacteria will only be found in feces in actively shedding animals. So even if our girl is infected, she may not be shedding the bacteria, and therefore a culture is gonna come back with a false negative result. We can also see false positives if the fecal sample is contaminated, which is very likely on a farm known to be affected with Johne's, or if there's what's known as the pass through effect where cows might have ingested the bacteria, but their immune response has been adequate and the bacteria are just being excreted in the feces, regardless of whether the cow actually becomes clinically ill or not.

So it's an excellent test in theory, but it's slow and it's really not very convenient for field practice. Next, for organism detection, we have fecal PCR, which detects MAP DNA. It is faster than culture and it takes days rather than weeks. And it can be used to quantify the bacteria in the sample and detect which animals are particularly heavy shedders, or if there are very high levels in pooled vehicle samples.

So the farm is likely to be heavily affected, but again, this test relies on bacteria being shed in the feces so they can be detected. There's also the issue of possible cross reaction with other microbacteria species present in the sample, which can give a false positive result.

So PCR is fast and useful, but maybe not great for catching these subclinical cases.

Moving on to detecting the host's immune response. We have an ELISA test. So we can do this with either milk or serum samples, and this is gonna look for antibodies produced by the body to fight the bacteria off. Problem with this one though, is the infected cows aren't going to seroconvert until they're in the later stage of disease.

So for our cows that are clinically affected, we would expect a positive eisa. But if we wanted to screen possible subclinical cases or potentially early stage disease, the results are likely to be negative regardless of whether the animal is truly infected or not. In dairy herds milk Ely is commonly used as it's a really convenient screening test and many labs will run it alongside monthly milk recordings.
But just remember a negative, Eliza does not rule out infection. And finally we can do postmortem exams and tissue histopathology to detect that organism again if we have animals that have been cold. So some gross findings that we'd expect to see include a thickened and corrugated intestinal wall enlarged mesenteric lymph nodes.

And if we take a tissue sample for microscopy, we would use a zeal Nielsen stain, and we should find acid-fast. Microbacteria clumped within macrophages. The best place to take a diagnostic tissue sample from is the ileocecal valve. This is gonna be the most definitive diagnostic test, but it obviously is only feasible once a cow is cued or dies.

So what is actually going to be practical on farm? The most realistic diagnostic flow for our cow in this case is gonna be to run a milk or serum. Eliza and a fecal PCR. This gives both confirmation and an idea of how infectious she is.

And for the rest of the herd, we are not gonna go looking for every infected animal. Instead we assess the herd status and transmission risk. And the simplest, most cost effective starting point is the environmental pulled fecal, PCR. So if we collect samples from calving pens, alleyways, and manure collection points.

If that test comes back positive, we know that MAP is circulating in the herd and we need a control plan

for ongoing monitoring for the herd, we can do milk ELIZA screening for the milking cows. Confirm any positive tests with a fecal PCR. Coal high sheds early and really focus on management changes for our calves. But without intervention, Johne's is going to continue to be a problem for a long, long time.

So what are the next steps for this farm?

Treatment

So without beating around the bush, we cannot cure Johne's disease. There is no antibiotic or drug that will eliminate MAP. Once infection is established, and while there are some available antibiotics that can achieve temporary clinical improvement, the animal will remain a shedder and all that prolonging their life does is increase the amount of bacteria that they are able to shed into the environment.

The possible drugs include is Rifampin, menin and CLO famine, but they do not eliminate infection, and they aren't actually licensed for this use. As we said before, they just extend that period of shedding and increase the risk of transmission to the rest of the herd. So stating the obvious, these treatments are not recommended. This means that the most appropriate and kind action for our clinical cow is to cull her at the earliest practical opportunity. Disease will only continue to progress and her condition will worsen in addition to the problem that she will put the rest of the herd at risk if she isn't cold.

Prevention

But what we can do for this farm is work on a herd health plan to minimize the risk posed to the rest of the herd.

Johne’s is a disease that you control at the calf level as infections are most likely to occur in the first few months of life. So our priority is to stop new infections and not to attempt to treat cows that already infected. There are three core pillars of Johne's control. So one is to identify and remove infected animals.

Two is to protect calves, and three is to prevent Johne's being introduced into the herd from outside. So how are we going to identify and remove high risk individuals? And we do this with ELIZA tests on milk or blood, and then confirm any positive tests with a fecal PCR, and then culling any confirmed cases for calf management, the key principles are going to be calf in clean, dedicated maternity pens.

If calves are born to suspected or positive cows. Remove the calf immediately after birth. Do not let them drink any milk or colostrum.

Then you can feed either milk, replacer, or pasteurized milk from the herd. Rare young stocks separately from adult cows for at least the first year of the herd health plan to minimize transmission to the young stock.

And then we also need to make sure that manure is not contaminating key areas like water troughs, feed bunks, and bedding areas. Finally, is stopping bringing Johne's into the herd. So we can do this by only buying from low risk or confirmed negative herds. By requesting herd level, yoni status, and not just test results from individuals, avoiding markets and mixed source heifers whenever possible.

And by making sure that all farm staff adhere to strict biosecurity protocols using foot dips, having designated clothing and using PPE, especially if they're working with both adults and young stock. While there are some vaccines available, they are not recommended for use and are under strict control.

Vaccinating animals will minimize the severity of disease, but it won't prevent infection entirely, and these vaccinated animals can still shed bacteria. Vaccines also interfere with the diagnostic tests, making it more difficult to identify truly infected animals.

Impact of Johne's

Before we wrap up, I just wanna talk about the impact that Johne's can have on farms and public health. It can be one of the most financially significant infectious diseases that farms face. And remember that we said for every one clinical cow, there may be 15 to 25 subclinical cases.

The typical losses that dairy herds face are estimated at 40 to $200 per cow per year, depending on the herd size and disease prevalence. And these losses are gonna be from reduced milk yield, reduced fertility, which means that more services are needed per conception, and there are longer calving intervals.
Cows have a poorer body condition and a lower slaughter value, and they're gonna be increased culling and replacement costs, and this is gonna be a major drag on herd performance and farm profitability. We then also need to consider the effects the onlys has on how a farm has to operate.

So things like reevaluating, calving, facilities, changing their colostrum protocols, changing young stock housing. Increasing testing and making strategic culling decisions, and all of these are gonna have a huge impact on, of course, profits, but also on staff and their morale. In terms of public health, there is an ongoing debate on whether the bacteria that causes Johne's may actually be responsible for causing Crohn's disease in humans.

So MAP has been found in milk, in feces, in the environment, and occasionally in meat from affected animals. We also know that MAP can survive pasteurization under certain conditions, especially if the bacterial load is really high. So undercooked meat, raw milk, and environmental exposure are all potential transmission routes to humans.

So is Johne's actually linked to Crohn's or not? There are definitely strong similarities between both diseases and MAP bacteria have been detected in many Crohn's patients, but causation hasn't been conclusively proven, and it's still an active area of research.

Key Points

So let's go through the key takeaways that you have to know about Johne's disease. Johne's is caused by Mycobacterium Avium, paratuberculosis, which is a slow growing hardy microbacterium.

Carbs are usually infected in the first few months of life through contaminated colostrum milk or manure, but clinical disease doesn't appear until years later. Infection is typically seen as progressive weight loss despite a good appetite and with intermittent or persistent watery diarrhea. Diagnosis can be tricky because of this long incubation period and variable immune response.

But a fecal PCR or culture can be used to detect bacteria in feces, either in individuals or in pulled samples. And ELIZA on milk or serum samples are most useful for herd monitoring. There is no cure and affected cows should be cued. Prevention is absolutely key, and the three aims for this are to identify and remove infected animals, protect calves from becoming infected, and then prevent the bacteria being brought onto the farm.

The last thing to know is that there is a potential link between Crohn's disease in humans and Johne's in animals, but it has not been definitively proven.

Outro

and that is Johne's disease. If you found this episode helpful, follow or subscribe so you don't miss our future episodes, and please share it with a friend or colleague who needs to hear it too.

You can find us over on Instagram and TikTok @veterinaryvista, and if you'd like to hear a specific topic, just let us know. All our references and recommended reading will be linked in the show notes as always. Thank you for listening to Current Vet and I'll see you next time.