Peter Watson describes Johnes Disease and explains how it is becoming increasingly prevalent in the UK and the approaches that are recommended in order to control it.
Johnes Disease is named after Heinrich Johne, a German veterinary surgeon and microbiologist, who first described it. It is caused by a bacterium, Mycobacterium avium paratuberculosis or MAP, which is related to the bacteria which cause human, bovine and avian tuberculosis. Johnes disease mainly affects ruminants including cattle, sheep and goats. But it can also infect other mammals including rabbits, foxes, birds and sub human primates. Rabbits are thought to be of significance in maintaining a wild reservoir of infection. The prevalence of Johnes in the UK is increasing and attempts are being made to control the disease.
The usual route of infection is by ingestion of the bacteria which then grow in the intestinal walls, causing diarrhoea and wasting. Infection is thought to take place at or shortly after birth by direct ingestion from the teat skin and environment, but animals may also be infected by colostrum and milk and pre natally in the uterus prior to birth. Many exposed animals will mount an effective immune response and MAP will not become established, others will become persisently infected excretors of MAP without developing clinical disease and the minority (5 – 10%) will succumb to the full disease. Cattle showing clinical signs do not recover. Affected animals slowly waste away and may show signs of “bottle jaw” as a result of low blood protein levels. In sheep and goats the loss of coat may be the most obvious clinical sign and an affected animal may recover to some extent.
MAP bacteria are found in the terminal part of the small intestine (ileum) in the lymphatic tissue known as Peyers patches which are important in providing immunity to intestinal organisms. MAP avoids the normal destructive mechanisms and invades the lymphastic tissue. From here it can spread around the body. Infected animals carry and release immense numbers of bacteria in faeces, this can occur for many months before clinical disease becomes apparent thus seriously contaminating the environment. Infection causes thickening of the intestinal wall, preventing nutrients from being absorbed and leading to the diarrhoea. The high levels of environmental contamination from the diarrhoea, coupled with increased production of bacteria as a result of the stress of pregnancy creates a very high risk of spread in calving pens. The bacteria can also survive for long periods (> 1 year) in manure.
Apart from the wasting and eventual death of clinically affected cattle, productivity is also lost before the disease becomes clinically apparent, resulting in significant economic loss even if only a low percentage of the herd are clinically affected at any time.
MAP can also interfere with the intra-dermal tuberculin test used to detect bovine tb and the interpretation of the results.
Unlike Mycobacterium bovis, the cause of bovine tuberculosis, MAP is not inactivated by the normal temperatures used to pasteurise milk. The simularity of the lesions to those of Crohn’s disease in humans and the detection of MAP DNA in some affected people has led to speculation as to whether MAP may be involved in some way, but the evidence is inconclusive and a link not proven.
In order to control any disease one must have reliable, sensitive and specific tests to identify infected animals. Tests available for MAP include bacterial culture from faeces. This test is both specific and sensitive, it is reliable in large herds and identifies sub clinically infected animals. It is slow (up to 16 weeks to culture), expensive and may not detect animals shedding low numbers of organisms. Milk can also be cultured. Heavy excretors can be identified by staining faecal smears with selective stains, but this is not sensitive and considered unreliable. Serological ELISA tests are available which are specific, but not very sensitive. These are based on blood or milk samples and are quick and relatively cheap, but they only detect a percentage of infected animals.
Control of Johnes is difficult and can be costly, but there are a number of voluntary schemes running in the UK. These are based on a test and cull principle, with close attention being paid to calf hygiene which is the single most cost effective measure to prevent spread on a farm. Avoidance of cross suckling and the use of pooled colostrum is also important in preventing spread of the disease.
In general a two tier approach is recommended. Firstly testing to identify infected herds and individuals and finding herds free of the disease, followed by appropriate isolation and culling. Implementation of strict biosecurity at the farm gate should be followed by high hygiene standards and repeated testing to reduce incidence or maintain freedom from the disease. In dairy herds the standard approach is to perform a herd ELISA test of all animals over 2 years. The percentage found positive should be doubled to gain a better estimate of infection in the herd, due to lack of test sensitivity. Removal of confirmed infected animals should follow if economically feasible. Subsequent testing within a year (preferably 6 monthly) and removal of suspected clinically diseased animals will reduce the incidence in the herd over time. There are many spin off benefits as improved calf hygiene will reduce losses in the calves and the enhanced biosecurity will also have economic benefits with other diseases.
For more information please contact Brian Merrell on 07748 182886 or email brian.merrell@adas.co.uk.