Johne's disease is a chronic enteritis of ruminants caused by the aerobic bacterium Mycobacterium avium paratuberculosis (MAP).MAP is thought to be unable to multiply outside a host, although the organism remains viable for long periods in the environment, surviving for nine months in faeces. 

Despite probably underreporting the disease is widely distributed worldwide and causes substantial economic losses through death and loss of productivity during the prolonged preclinical stage. The disease has remained a problem for so long because of the absence of a simple, accurate diagnostic test.

 

Causes 

Mycobacterium avium paratuberculosis (MAP)

MAP is spread via faeces and milk and potentially via the placenta in pregnant animals and the semen in infected bulls. It is excreted by infected animals before clinical signs appear, although bacteria numbers increase once clinical signs have developed. It is believed that most infections occur during the first day of life of a calf and originate from the dam.

There is a large potential reservoir of MAP in the environment as Johne’s disease and carriage of MAP has been reported in a number of domestic and wildlife species including sheep, goats, rabbits, deer and cats.

Cattle have been reported to show a lack of avoidance of pasture contaminated with rabbit faeces, therefore, theoretically, this may be a route of disease spread.

The main risk factor associated with Johne’s disease in a herd is buying-in cattle with application of manure to pasture and access to feed by wildlife also considered risk factors.

Other risk factors associated with clinical disease are recently calving, possibly as immunity is compromised and Jersey breed cattle.

After ingestion with faeces or milk, MAP invades the lymphatic tissue in the mucosa of the small intestine, where it multiplies over the next 2-3 months and spreads to the draining mesenteric lymph nodes. The outcome of the infection depends on both the ability of the host to mount a cell-mediated immune response and the dose of the initial infection. 

Effects

The course of the infection depends on the host's response. The initial infection may be overcome, or the infection may persist for many months or years with intestinal lesions slowly progressing until they interfere with normal function.

In response to chronic infection, the distal small intestine, especially the ileum, becomes thickened with a concurrent increase in permeability. There is loss of plasma proteins into the lumen and malabsorption of amino acids.

Faeces may be soft and pasty or more classically the animal may show signs of homogenous diarrhoea. Anaemia occurs in some animals. Animals are usually bright and have a good appetite until the disease reaches advanced stages and animals become emaciated and weak. Clinical disease is normally seen in animals over two years of age.

Due to the long incubation period, disease is often sub-clinical and direct effects on production and welfare are often masked, hence it may appear difficult to justify large investment in control programmes. Johne’s disease has been associated with reduced milk production, an increased number of days empty and increased culling of infected cows in dairy herds. The main economic loss due to Johne’s infection in dairy herds is due to reduced milk production from clinically and sub-clinically affected cows.

 Note:

Recently, Johne's disease has been implicated in the development of Crohne's disease in humans, as it has been shown that MAP can be isolated from some lesions of Crohne’s. Additionally. both MAP DNA and viable MAP have been isolated from both raw and pasteurised milk from a number of countries.

The consensus opinion currently is that there is insufficient evidence to prove or disprove that MAP is the cause of Crohne’s. However, it would seen prudent to limit the prevalence of Johne’s disease from a public health perspective (both real and perceived risk) and from an animal health and welfare perspective.

A detailed source of information on all aspects of Johne’s disease, including the potential public health issues can be found at the Johne’s Information Centre website.

Diagnosis

The accuracy of all tests for Johne’s disease are not ideal, therefore it is extremely difficult to be precise about disease status due to the poor sensitivity of many of the tests and the change in likelihood of obtaining a positive diagnosis with disease progression in individual animals.

For most commercial dairy herds, a bulk milk ELISA is the first step in any control program, and for beef herds a herd serum ELISA on all herd animals aged 2 years and older.

Results are most reliable for herds confirmed to be infected by isolation of MAP from at least one animal. The percentage of a herd that is ELISA-positive for MAP (apparent prevalence) should be doubled to get a rough estimate of the true prevalence of Johne’s (given a test sensitivity of roughly 50%, only half of infected animals test positive).

Using the ELISA or any other test for Johne’s to estimate herd prevalence of MAP infection is only possible in herds that do not routinely test and cull test-positive animals.

Prevalence of Johne’s will be underestimated by a whole herd ELISA once the cattle in advanced stages of MAP infection have been removed.

Testing using the ELISA may be of therefore be of most value in high prevalence herds due to the low sensitivity of the ELISA test.

In order to maximise the efficiency of testing for Johne’s disease it may be best to target sampling to those herds where risk assessment deems them to be at highest risk of disease entering.

The poor sensitivity of the ELISA may not be, in practical terms, a large a problem in relation to control as might be first considered. This is because of two factors.

Firstly, the prime concern in relation to control is to remove the infected animals that are shedding. As an increase in shedding is related to an increase likelihood of detection by ELISA the cattle that present the greatest risk to the herd should still be detected.

Secondly a test that was 100% sensitive would potentially reveal so many positives that the potential for culling all such animals may not be a viable proposition. 

Subsequent herd tests should occur within a year (there is some indication that annual test may provide little advantage over removing clinically diseased animals) and that six monthly testing is preferable. Testing of the herd should be continued after the cull. The closed herd strategy, may reduce the risk of the disease entering the herd.

This information was taken from:

http://www.vetsweb.com/diseases/johnes-disease-d234.html

 

For more information see:

http://www.organicvet.co.uk/Cattleweb/disease/johne/johne1.htm