About Johne's Disease

The cause of Johne's disease

Johne’s Disease (JD) is caused by a bacteria (Mycobacterium avium subspecies paratuberculosis – or MAP for short). It was successfully isolated first by german veterinarians Dr H A Johne and Dr L Frothingham in 1894. It is a very close relative of the bacteria that causes tuberculosis in cattle (M. bovis). Today JD is a significant animal health issue world wide in developed livestock industries, particularly dairy, sheep, and deer. It can also be found in the environment and in some species of wildlife.

Impact On the New Zealand deer industry

JD was first diagnosed in farmed deer in New Zealand in 1979. It spread through the deer farming industry with greater speed and more severe animal health consequences than have been seen in other farmed species.  

In 2011 an economic analyisis indicated that the deer industry lost about 9 million dollars each year. The loss is primarily due to deaths occurring on farm, sub-optimal production in sub-clinically affected finishing stock and very slightly lower reproductive performance in infected breeding stock.

To put this in perspective, JD related financial loss to the industry is about $30 for every deer processed.

Host range

Ruminant species are the main hosts for MAP.  From a farming perspective the most important hosts are deer, sheep and cattle, but the organism can also be found in a wide range of other ruminants and, occasionally, non-ruminant species.

JD affects farmed animals worldwide. The disease is probably more of a problem in farmed ruminants than in wild ruminants because of the higher density of animals on farms, which leads to higher contact rates between infected and susceptible animals and higher levels of contamination than would be found in the wild.

Disease process

JD affects the small intestine.  Typically, the bacteria enters the young deer by ingestion of infected faeces or milk and is then taken into the host’s own cells near the small intestine. The bacteria then sits dormant until triggered to multiply. The exact trigger(s) are not well understood and could range from various stresses like nutrition, climate, social stress, long distance transport and parasite burden. The trigger may also be influenced by the genotype of the animal.

Once triggered, the bacteria multiply and the host's immune system responds in an attempt to control the growing infection. The struggle between the bacteria and the host causes the wall of the intestine to thicken and this reduces the ability of the host to absorb nutrients from its food. Diarrhoea and weight loss result. The infection begins to spread from the small intestine into the nearby lymph nodes causing Tb-like lesions. On occasion, lesions caused by MAP can be found in lymph nodes elsewhere in the body but this is usually associated with severe infection.

The duration of the disease process, from when multiplication starts until death of the host, can be as short as four to six weeks, but it can also draw out to many months or even years if the host gains better control of the infection. Even though the host may control the disease there are very very few cases where it seems to eradicate the infection.    

Clinical signs

Early signs

  • Decreased weight gain relative to herd mates
  • Diarrhoea – typically green sticky faecal pasting, often containing hundreds or even thousands of MAP/gram
  • Weight loss and ill thrift
  • Rough, light coloured coat with patchy hairloss
  • Retention of winter coat
  • Muscle loss, particularly over the loin

Late clinical signs

  • Diarrhoea containing millions or more MAP/gram
  • MAP shed in the milk of hinds
  • Emaciation
  • Swelling under the jaw and brisket
  • Death usually within weeks

 

Affected deer tend to remain alert and maintain their appetite.

Shedding of the bacteria is generally greater in more heavily diseased animals but this is not always the case. Sometimes apparently healthy animals can shed huge numbers of MAP in healthy looking faeces, while emaciated animals with severe diarrhoea may shed very few bacteria.

Other animal health conditions that can look like JD

Other animal health conditions that have similar clinical signs to JD are

  • Yersiniosis
  • Gastrointestinal parasitism/worms
  • Avian tuberculosis
  • Bovine tuberculosis
  • Copper deficiency
  • Inadequate nutrition
  • Fading elk/Wapiti syndrome
  • Chronic Malignant Catarrhal Fever
  • Faulty teeth

How do I know if JD is in my deer?

If you see deer in your herd losing weight with diarrhoea JD needs to be ruled out as the cause, as these symptoms may be due to many things. To rule out JD, get your veterinarian to confirm a diagnosis. For Johne’s disease the diagnosis is based on a combination of the following tools:

  • examination of the affected deer, possibly including post-mortem
  • blood testing a group of animals
  • discussing the history of the property
  • discussing the source of the deer

Johne’s Management Limited has established a network of veterinarians with specialist training in Johne’s disease to help.

Can I control Johne’s disease in my deer?

Yes.

Johne’s disease can be successfully and cost effectively controlled.

  • Controlling JD will save you money and make your farming business more profitable.
  • Controlling JD will improve the animal health status of your deer.
  • Controlling JD on your farm is your part in an industry wide effort to control this disease.
  • Controlling JD will reduce stress on the farmer.

Experience with the Deer Industry ‘Making a DIFFerence’ Focus Farms has demonstrated successful control and a cost-benefit analysis has shown it’s well worth the relatively low costs involved (see the Deer Industry News, issues 46 and 49).

Controlling JD is not as simple as giving an injection or a pill so JML has established a network of veterinarians with specialist training in JD to help make an on-farm control programmes [link].  

Controlling JD will take a small but firm commitment on the farmer’s part to stick with the programme. But the programme will work. And the solution is achievable.

 

A control programme will involve the following steps:

  • Determine the extent of Johne’s disease in your herd
  • Culling test-positive deer
  • Maintain a closed herd (do not bring deer in, but if you must, ensure they are JD-test negative)
  • Tweak management of young deer to minimise their chance of infection

It will take a little work each year for several years to really minimise JD but after that, vigilance and some targeted monitoring are all that is required to ensure it stays minimised.

The bottom line is more animals, heavier sooner and better which is exactly the aim for the New Zealand Deer Industry.

How is JD spread?

The main way that JD spreads between farms is through the trading of healthy looking but infected deer.

The main way that JD is transmitted between individual animals is when young calves ingest infected faeces or milk. This is most likely when it is suckling from an infected hind (calves may suckle from hinds other than their mother) but can also happen when grazing contaminated pasture or eating contaminated supplementary feeds. The calf’s gut system matures in the months post birth and this process is likely to make it particularly susceptible to infection by MAP.

Calves may also be infected before birth in the uterus.

Drinking water contaminated with MAP infected faeces is another potential source of infection.

There is no transmission risk through nose-to-nose contact through fences.

Wildlife are not considered a major source of transmission of JD. It’s true that the bacteria can be found in multiple wildlife species in New Zealand including rabbits, hedgehogs, ferrets, cats and gulls but the realistic chances of transmission from them to young calves is low compared to transmission from infected hinds or contaminated feed or water.  

The importance of transmission of JD between deer and other species of livestock is not yet well understood.

JD in young deer and mature deer

JD manifests differently depending on the age of the deer. In weaner deer major outbreaks of disease can occur causing scouring, weight loss and death in up to 25% of the affected mob during the first winter of life. It is not clearly understood whether these outbreaks are due to infection passing between the weaners, or whether they were all infected at an earlier date then experience a common stress (like those associated with weaning, social mixing, overcrowding, nutritional and climatic stress in winter) causing disease.

In comparison, the disease in adult deer is usually seen as one-off cases in small herds or in the tail end of large mobs of animals, often after unusually stressful conditions.