David Harwood BVetMed, FRCVS.
Senior Vice President Goat Veterinary Society,
Honorary Veterinary Surgeon British Goat Society.

Johne’s disease is a worldwide problem causing clinical disease in many ruminants
including goats, cattle, sheep and deer managed intensively or semi-intensively.
Many wildlife species including rabbits are able to carry and thus maintain localised
infections, and can also spread the organism from unit to unit. It is now recognised
that there are specific cattle and sheep isolates, with most goat infections identified
as cattle strains. Epidemiologically, goats will pick up infection from other goats or
from cattle kept in close association (or from faecal contamination of their
environment). Sheep strains have been identified in goats kept in close association
with infected sheep. It is important to point out that the author has encountered
problems in large commercial dairy herds housed all year – BUT ALSO in small
groups of goats including Pygmy goats
The main causative organism of Johne’s disease in goats is the cattle strain now
referred to as Mycobacterium avium subsp paratuberculosis (often abbreviated to
MAP). Once introduced into a group of goats, uncontrolled infection progressively
becomes established and can be very difficult to eradicate.
Infection is mainly transmitted to young kids under 6 months old, by ingestion of the
organism following faecal contamination of feed and / or water supplies and also
potentially from faecal contamination of the teat and udder while suckling.
Contamination of colostrum and specifically the contamination of pooled colostrum
can readily transmit new infection to a wider group of susceptible kids. There is also
confirmed intra-uterine infection of kids, from dams that are heavily infected in late
pregnancy. Goats older than 6months of age become progressively more resistant
to new infection, although lateral spread even in adult goats may occur if the
environment becomes heavily infected.
Although susceptible to sunlight and desiccation, MAP organisms can reportedly
survive for up to one year on pasture (not forgetting potential maintenance in local
Following infection, there is then an extended incubation period during which the
infected goat will appear fit and healthy. Clinical signs may develop as early as 12
months of age, but more commonly from around 2.5 years old. Before clinical signs
develop, these infected but apparently healthy goats may be shedding organisms in
their faeces, thus adding to the environmental challenge. The stimulus for infection
to become clinical is still poorly understood, but may be linked to stressful insults
such as kidding, transportation, poor nutrition or concurrent disease such as
After infection, MAP localises in the wall of the gut and associated lymph nodes.
This in turn stimulates a local immune response resulting in a progressive thickening
of the gut wall and lymph node enlargement. Depending on a number of factors, a
number of things can happen:
• The infection may be controlled with the goat becoming resistant to infection
with no further shedding or clinical disease.
• The infection may progress to intermittent shedding and sub-clinical disease.
• The disease may become clinical with heavy shedding.
In an endemically infected herd, it is likely that all three manifestations may be
apparent – thus further complicating its control. It is for these reasons that Johne's
disease is referred to as an "iceberg infection" - I.e. for every goat showing clinical
disease, there may be many more appearing perfectly healthy, but carrying the
infection and potentially shedding it.
Serum antibody responses in infected goats prior to the development of clinical signs
are poor, becoming stronger as clinical disease develops. It follows therefore that
serological testing of goats using currently available tests such as the commercially
available ELISA test will effectively result in “false negative” results during this long
period of dormant infection – but an increasingly positive result as clinical disease
Once triggered to develop, clinical signs may go unnoticed initially, but include a
progressive weight loss and reduction in milk yield if lactating, although appetite may
be unaffected. As the condition develops, anaemia and a lack-lustre coat may
become apparent together with sub-mandibular oedema (a feature of the
progressive protein loss that occurs). The diarrhoea associated with disease in
cattle is not a feature of the condition in goats (although it may develop in the
terminal stages).
Differential diagnoses for the combined signs of weight loss, reduced milk yield, and
anaemia in the absence of diarrhoea include the parasites fluke and haemonchosis.
There is no single reliable test that can be used to confirm infection due to the
complexity of the immune response, and the long period of latent infection in
clinically healthy goats.
Live clinically healthy goats (but infected) - most available tests are ineffective during
this phase of disease, there will be little if any antibody response detectable, and the
sporadic shedding of organisms in faeces may be below detectable limits.
Live infected goats in early clinical phase – antibody levels begin to rise, and may
be detectable by e.g. an ELISA test, but false negative results may be widespread
during this phase. Goats may give a positive result on one day, then a negative
result when retested – these goats will invariably retest as positive in time. Faecal
examination using a variety of tests will progressively become more reliable as
clinical signs progress.
Live clinically infected goats – all available tests become more reliable, as the
antibody response becomes stronger and faecal shedding increases.
At post mortem examination, the gut wall thickening evident in the lower jejunum and
ileum is more subtle than that seen in cattle in which “corrugation” and apparent
folding of the mucosal surface is evident. Gut lymph nodes may be grossly enlarged
and oedematous, with caseation and even calcification - a feature of later stage
infections. These lymph node changes are similar to those seen in TB – which must
be considered particularly if goats are located in an area in which TB is widespread
in cattle and local wildlife.
Bulk milk monitoring is becoming more widely available in cattle, and may in time be
available when validated for milking goat herds.
Effective control is difficult to achieve, because of the long incubation period during
which goats are clinically healthy, shedding by these infected goats, and the low
sensitivity of the currently available tests.
Eradication may be a long term aim, but will need considerable commitment by the
herd owner and attending veterinarian. Such an approach would be based
predominantly on regular whole herd testing using available serological tests
supplemented by faecal monitoring – and culling those goats giving a positive result.
This may need to be continued for a number of years to be successful, if two
consecutive negative clear tests are the ultimate aim. An alternative to culling is to
separate positives and negatives into a “clean” and “dirty” herd. National Johne’s
disease monitoring / control schemes are available – giving a structured approach to
Such a control programme must be supported by:
• Prompt identification and removal of clinical cases.
• Minimising faecal contamination of feed and bedding – particularly for young
• Snatching kids and rearing away from adults, feeding colostrum from “known
negative” dams, or using artificial colostrum.
• Avoiding the use of pooled colostrum
• Culling kids born to does developing disease in late pregnancy (due to risk of
in-utero infection.
Control can also be achieved in endemically infected herds by the use of
vaccination, widely available and licensed for use in goats in many countries. It
should be used following manufacturers recommendations in young kids.
Vaccination will result in far fewer clinical cases, increased productivity – but will not
eradicate infection – effectively allowing a unit to continue in production. Vaccination
may interfere with any tuberculosis control programme based on intradermal testing.
There is no known treatment for Johne’s disease