Also known as: Paratuberculosis
Caused by M avium subsp. paratuberculosis
Johne's Disease is a contagious and chronic disease of ruminants caused by the bacterium Mycobacterium avium subsp. paratuberculosis. Affected species include cattle, sheep, goats and camelids. The disease is present worldwide with the highest prevalence occurring in dairy cattle. In these animals the disease is responsible for severe economic losses due to reduced reproductive performance, increased susceptibility to disease, reduced milk production and culling losses. Subclinical carriers can occur, shedding organisms in their faeces.
Mycobacterium paratuberculosis is an intracellular pathogen that is spread through herds via faecal-oral transmission, contaminated water and in utero. Young animals less than a year of age are most susceptible to infection and this usually occurs via ingestion of contaminated milk or colostrum. Environmental factors such as overcrowding and poor husbandry may increase the risk of infection.
Following ingestion of M. paratuberculosis and uptake by the Peyer's patches, infection begins in the ileum. M. paratuberculosis infects macrophages in the gastrointestinal tract and lymph nodes leading to a granulomatous inflammatory response. This leads to malabsorption and a protein-losing enteropathy.
The organism is viable in the environment for long periods of time and has a long incubation period with clinical signs appearing in cattle over 2 years of age.
Cattle become infected by the bacteria as calves but do not display the clinical signs of disease until between two and five years of age. In addition animals may be affected subclinically before overt clinical signs are displayed.
In the early stages, the disease is characterised by reduced milk production, reduced reproductive performance and increased susceptibility to infection or disease. There may be intermittent diarrhoea and weight loss.
In the later phases of infection, the clinical signs become more severe. The characteristic clinical signs are of watery 'pipe-stem' diarrhoea and severe wasting (despite maintenance of a good appetite). The disease is progressive and advanced cases may develop submandibular or ventral oedema due to a protein losing enteropathy.
The disease is similar in goats and sheep except diarrhoea is not a feature. It is characterised mainly by weight loss. It may be rapidly fatal with weight loss and diarrhoea in some deer.
Diagnosis is difficult, particularly in the case of subclinical disease as there is no single test that will detect all stages of the disease. Bacterial culture is the most definitive test but is time-consuming, requiring up to sixteen weeks for incubation.
The most commonly used diagnostic test is the ELISA which detects antibodies to M. paratuberculosis in clinically affected animals. This is typically used in combination with post mortem and identification of the classic pathological lesions of the disease. Other commercially available tests include bacterial culture, PCR and agar gel immunodiffusion. Test sensitivity may be increased by using different tests in combination.
Diagnosis in sheep may also be complicated due to the disease occurring in two different types in these animals. Multibacillary disease is associated with large numbers of bacteria in the gut and a high antibody response. Paucibacillary disease is characterised by few or no bacteria within the alimentary tract and is associated with a low antibody response. Due to the different type of immune response occurring with each type of disease, there is no single test available to detect the presence of disease. Definitive diagnosis is provided following post mortem exam, histopathology and culture in order to determine the type of disease present.
Other possible tests include:
- Serology of serum including complement fixation tests
- Histopathology of intestines and lymph nodes
- Isolation and identification of mycobacteria from faeces and tissues
- Ziehl-Neelson-positive smears
- Intradermal tuberculin test
- DNA probes for detection in faeces
Lesions are usually localised to the terminal portion of the ileum. Lymphocytes and macrophages accumulate in the lamina propria and submucosa, resulting in marked thickening and folding of the intestinal wall. The mucosal surface is diffusely thickened with transverse, corrugated rugae which do not disappear when the intestinal wall is stretched. In sheep and goats however, the lesions usually described are nodule formation with necrosis and calcification .
Infected animals may also have enlarged mesenteric lymph nodes.
Several studies have reported an improvement in clinical signs following antimicrobial treatment of affected animals. However the same studies have shown that faecal shedding of the bacterium still occurs following treatment, therefore such treatment does not appear to be currently viable. Control measures are aimed at providing good hygiene and husbandry, maintaining adequate stocking densities and minimising exposure of young animals to the organism. Current recommendations include providing clean, manure-free areas for cows to calve and only administering pasteurised or test-negative colostrum to new born calves. Separation and isolation of calves from affected dams is also recommended.
The disease in mainly controlled by slaughter of affected animals, detection and slaughter of subclinical shedders using faecal culture, DNA probes and ELISA.
Inactivated adjuvanted vaccines are available and reduce shedding of mycobacteria but do not eliminate infection.
|Johne's Disease Learning Resources|
Search for recent publications via CAB Abstract
(CABI log in required)
|Johne’s disease in cattle publications since 2000|
Full Text Articles
Full text articles available from CAB Abstract
(CABI log in required)
|Mycobacterium paratuberculosis/Johne's disease: review & update. Whitlock, R. H.; Eastern States Veterinary Association, Gainesville, USA, Proceedings of the North American Veterinary Conference. Large animal. Volume 19, Orlando, Florida, USA, 8-12 January, 2005, 2005, pp 79-80|
- Jones, T. C., Hunt, R. D., King, N. W. (1997) Veterinary Pathology Wiley-Blackwell
- Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition) Merial
|This article has been peer reviewed but is awaiting expert review. If you would like to help with this, please see more information about expert reviewing.|