Do You Know the Johne’s Disease Status of Your Goat Herd?

While dairy goats generally get the cattle strain of Johne’s disease (also called paratuberculosis),[i] they often do not show the typical signs that are observed in cattle i.e. watery diarrhoea, dehydration and thickened, corrugated intestines.  In goats, the main clinical sign of Johne’s disease is just wasting away. Johne’s disease is caused by bacteria called Mycobacterium avium subspecies paratuberculosis, which is very similar to the bacteria that cause tuberculosis or TB.  

Goats with very poor body condition can have a variety of causes, most often gastro-intestinal parasites or poor quality feed. Johne’s disease in goats also occurs in younger animals that is the case with cattle i.e. as early as 12 months[ii].  Often after the stress of first kidding can cause Johne’s disease clinical signs to start, but kidding can also cause Caprine Arthritis Encephalitis (CAE) which is also a cause of wasting in goats.  A recent study of Johne’s disease in goats in Saudi Arabia found that the only consistent clinical sign was “weight loss despite apparently normal food intake” in adult goats.[iii]

One complication is that goats with Johne’s disease and therefore in poor condition, are more prone to other diseases such as pneumonia, parasitic gastro-enteritis, and digestive disorders.  Thomas (1983)[iv] reported two years of post-mortems of 67 goats from a large UK goat herd in the first two years of Johne’s disease control, which are summarized in the table below: 

However it also goes the other way i.e. goats with Johne’s disease who would have eventually died of this condition can die first of another condition. A survey of deaths in 13 goat herds (10 dairy and 3 meat herds) in Quebec, Canada between 2009/10, found that 29 goats of the 152 post-mortemed had Johne’s disease, but only 16 of these actually died of Johne’s disease.[v]  So just because there is an obvious disease e.g. bloat, it doesn’t mean that Johne’s disease is not also present and could be a predisposing factor.

In a study of goat herds in Norway, PCR tests were performed on bulk milk samples.  It was found that 3.3% of herds which had previous Johne’s disease cases had positive PCRs, but for herds with no history of Johne’s disease there was a 9.1% positive  rate for PCRs.[vi]  This higher level in supposedly “normal” herds indicated that the diagnosis of Johne’s disease had been missed in these latter herds by the herd owners.

Clinical signs reported in goats with Johne’s disease include:

And less often there are the following clinical signs:

Your veterinarian should be asked to perform a post-mortem on all wasting goats and your vet may find the following :

A study in a large US goat herd with a high incidence of Johne’s disease [viii] found the following gross signs during 120 post-mortems on infected goats:

However, a large number of goats with positive diagnostic tests for Johne’s disease had no signs at all visible to the naked eye on post-mortem. This means your vet must send away samples to a laboratory. 

Prevention

Prevention of the introduction of Johne’s disease is by ensuring that all new introductions of goats are from herds that are accredited free of Johne’s disease all goat herds.  Such herds are in a searchable database on the internet (http://edis.animalhealthaustralia.com.au/public.php?page=mapsearch&aha_program=3 ).  However as at 6/2/14 there were only 33 Australian goat herds in the goat Johne’s disease market assurance program. Western Australia is free of Johne’s disease in all species, although recently some cattle herds in the NW of the state have been placed in quarantine after getting Braham cattle from infected herds in Queensland.  Purchasing goats from the Southern part of Western Australia would be safe. In countries without such a scheme, the only option is to close their herd and only introduce new genetics by artificial breeding.[ix] These closed herds must also ensure no cattle, sheep, deer or alpacas or their products (manure, milk etc) are introduced. 

Control

Control of Johne’s disease in an already infected herd is very difficult but would involve improving general hygiene and removal of kids at birth. General hygiene includes using fenceline feeders or keyhole feeders so that there is no faecal contamination of the goats’ feed.  The response bacteria are very resistant to the environment and can survive for 12 months or more.  If destocking to control Johne’s disease, then the property should be destocked for 12 months, but this period must include 2 summers. It has also been suggested that Mycobacterium avium subspecies paratuberculosis bacteria can survive for approximately 150 days in biofilms in livestock waterers[x]  and this has led to a US Department of Agriculture recommendation to chlorinate drinking water or to add 3 tablespoons of chlorine bleach to 100 gallons of livestock trough water every week combined with only using galvanized metal or stainless steel water troughs. Separate boots for kid rearing areas and adult goats is also desirable, as is frequent cleaning of manure for composting for 12 months. Monthly weighing of goats to pick up cases of Johne’s disease has been used overseas, where access to other diagnostic tests has been too difficult or too expensive. As wild rabbits have been shown to have the Johne’s disease bacteria, rabbit control should be part of any control program.[xi][xii]

The Goat Milk Producers Federation of the UK have a Code of Best Practice for controlling Johne’s disease and this involves annual or more frequent testing of all replacement does, never feeding bulk unpasteurised milk, rearing kids in isolation from adult goats for the first 6 months, vaccination of all young kids, post mortems of all wasting goats and routine PCR testing of bulk milk samples.[xiii]  Norway have taken a different approach and have eliminated Johne’s disease, Caprine Arthritis Encephalitis (CAE) and Caseous Lymphadenitis (CLA) from herds by snatch-birthing kids, rearing separately on cows’ colostrum and milk replacer and then replacing the original adult herd after thorough disinfection of the barns and milking areas.[xiv]

Pasteurization times and temperature treatments for colostrum that kill the CAE virus (i.e. 1 hour at 56 degrees) do not necessarily kills Mycobacterium avium subspecies paratuberculosis (Map) bacteria. The temperature needed may be higher i.e. 135 degrees F for 30 minutes with stirring.[xv]  It has been shown that cows’ colostrum pasteurized to kill the Johne’s disease bacteria will coagulate but this can be overcome by adding water and using a blender and the resultant colostrum is still useful for feeding to calves.[xvi] Alternatively you could access colostrum for an accredited goat or cattle herd and freeze it until needed.

A key component to stopping the spread of Johne’s disease in the Australian goats is the national kid rearing plan, (http://www.animalhealthaustralia.com.au/national/kid/rearing/plan ) with its recommendation to never feed bulk milk to kids and to rear kids on milk replacer or pasteurised bulk milk. The importance of this recommendation is demonstrated by the trial results reported by Storset et al (2001).[xvii] In this trial seven goats were given suspensions of Mycobacterium avium subspecies paratuberculosis in milk replacer three times a week between 5-8 weeks of age for a period of 9 weeks. These seven kids were then observed for 2 years.  Two goats started faecal shedding at 12 months and another two by 2 years of age. When the goats were necropsied at the end of the trial, five of the seven goats had lesions and the bacteria in the intestines and/or the mesenteric lymph nodes. However two animals had no detectable lesions in the distal ilium and colon on necropsy. Admittedly 2 years is a short period for incubating Johne’s disease, as often clinical signs do not appear for some years. However this research shows that subclinical infections i.e. carriers, can easily be missed.

This is backed up by the findings of Thomas (1983),[xviii] who tabulated the age of faecal shedders in a large UK goat herd in the 3 years following diagnosis and initiation of control. His results are shown in the table below: 

Testing

Frequent testing of all adult goats is needed to remove any faecal shedders as quickly as possible. Faecal culture has a specificity of almost 100% but the test takes several weeks (8-10) for the bacteria to grow and this time can be even longer in goats (10-12 weeks). Sensitivity is low in the early stages of infection but approaches 100% in the advances clinical stage. Research has shown that positive culture results were found in 69% of goats with diffuse lesions and from 44.4% of those with focal lesions found on post mortem.[xix] Research completed by Eamens et al (2007) showed that the faecal culture tests on pooled faecal samples could be used for goats and that the recommended dilution was 1 in 25 (i.e. faecal pellets from 2 5 goats could be mixed and tested together) and  a time frame for culture of 10 weeks. This dilution detected 13 out of 16 positive goats.   This dilution was best for reducing costs without a large drop in sensitivity but this is a trade-off between cost and finding all carriers.  Two low shedders were not detected except by individual culture.

Faecal smears stained with a special stain that only stains Mycobacterium avium subspecies paratuberculosis a special colourcan give a rapid result, but have low sensitivity and specificity. It has been suggested that faecal smears can only be used in advanced clinical cases as an interim diagnosis.[xx]  False positives can occur if the environment is heavily contaminated by faeces from heavy shedders.[xxi] There is also a skin test with an intradermal injection of johnin, similar to the tuberculin test, but this test has only very limited value.[xxii]

Initially Compliment Fixation or CF tests were used in goats and this was the test used when Johne’s disease was first reported in Australian goats.[xxiii]  Then  Agar Gel Immuno-Diffusion or AGID tests were developed as the diagnostic test for goats e.g. when 331 goats were tested in Western Australia as part of the surveillance for proof of freedom from Johne’s disease.[xxiv] ELISA tests were developed and these have better sensitivity and specificity in cattle than other earlier serological tests.  Research in the USA with dairy goats compared ELISA  tests using sera and individual milk samples and found that the sensitivity was 64% compared with 48% respectively to faecal cultures. However a RIRDC study compared the AGID and ELISA tests and found the ELISA detected more cases of Johne’s disease in goats.[xxv]   ELISA tests are the serological tests mentioned in the Goat Market Assurance Program or MAP (http://www.animalhealthaustralia.com.au/wp-content/uploads/2011/04/GoatMAP-manual.pdf). Also mentioned in this MAP is the PCR test, which is a DNA based test and which is now widely used in cattle.  A recent study looked at using ultrasound examination to detect enlarged gut lymph nodes and/or thickened intestinal walls but these changes were only detected in 94% and 80% of goats with Johne’s disease respectively.[xxvi]

There is no test that identifies the goats that are in the early stage of incubating Johne’s disease. Goats with Johne’s disease can be classified into four stages as summarized in the table below:[xxvii] 

The number of identified goat herds with Johne’s disease and reported by Animal Health Australia reports is very low and this could be due to the Caprine Arthritis Encephalitis (CAE) control program that involved snatch birthing kids and raising in isolation on milk replacers. CAE and Johne’s disease control methods are very similar.   However, goats can become infected with Johne’s disease from both cattle and to a less extent, sheep with this disease. All dairy goat owners in states such as Victoria and Tasmania, where Johne’s disease is prevalent, should keep Johne’s disease in their mind if there is loss of body condition in adult goats. Don’t just think your goats have worms. Remember also that the sheep strain, while less likely to infect goats, is also less likely to develop severe clinical signs, positive blood tests or be positive on faecal culture.[xxviii]

 All goat keepers must arrange for any wasting goat to be seen by a vet and if necessary, post-mortemed.    The Australian New Zealand Sub-Committee on Animal Health Laboratory Standards has recommendations for vets who suspect Johne’s disease as to the samples that are needed or the laboratory can advise.  This means extra costs but these tests are essential.

I would recommend that all goat keepers look at this PowerPoint & audio combination about the devastation that Johne’s disease caused in a Saanen goat herd in Chile over many years without any diagnosis.  This will convince any goat keeper of the need to have wasting goats post-mortemed by a vet.  See http://www.johnes.org/presentations/Diagnosis/Maine-DVMs-Cases.m4v

Only when an accurate diagnosis is obtained can any goat owner initiate the correct control program and start on the way to recovery. A Johne’s disease vaccination program can then be started which will delay clinical signs and shedding, although it won’t prevent cases of Johne’s disease. Your veterinarian can advise on the best ways to control Johne’s disease and together you can do a plan to eventually eliminate this terrible disease. Ignoring the cause of wasting in your goats, just delays control as eventually Johne’s disease will resurface and become an even more severe problem. If you sell stock, eventually the Johne’s disease will be traced back to your herd. 

Cook, K. L., J. S. Britt and C. H. Bolster (2010). "Survival of Mycobacterium avium subsp. paratuberculosis in biofilms on livestock watering trough materials." Vet Microbiol141(1-2): 103-109.

Corpa, J. M., J. Garrido, J. F. Garcia Marin and V. Perez (2000). "Classification of lesions observed in natural cases of paratuberculosis in goats." J Comp Pathol122(4): 255-265.

Debien, E., P. Helie, S. Buczinski, A. Leboeuf, D. Belanger and R. Drolet (2013). "Proportional mortality: A study of 152 goats submitted for necropsy from 13 goat herds in Quebec, with a special focus on caseous lymphadenitis." Can Vet J54(6): 581-587.

Djonne, B., M. R. Jensen, I. R. Grant and G. Holstad (2003). "Detection by immunomagnetic PCR of Mycobacterium avium subsp. paratuberculosis in milk from dairy goats in Norway." Vet Microbiol92(1-2): 135-143.

Ellis, T. M., R. T. Norris, P. Martin, R. H. Casey and C. D. Hawkins (1998). "Evidence for freedom from Johne's disease in cattle and goats in Western Australia." Aust Vet J76(9): 630-633.

Gezon, H. M., H. D. Bither, H. C. Gibbs, E. J. Acker, L. A. Hanson, J. K. Thompson and R. D. Jorgenson (1988). "Identification and control of paratuberculosis in a large goat herd." Am J Vet Res49(11): 1817-1823.

Gwozdz, J. M. (2010). Paratuberculosis (Johne's disease). Australian New Zealand Standard Diagnostic Techniques, Subcommittee on Animal Health Laboratory Standards

Jones, P. H. (2003). "Paratuberculosis in goats " Goat Veterinary Society Journal19: 4-10.

Khodakaram Tafti, A. and K. Rashidi (2000). "The Pathology of Goat Paratuberculosis: Gross and Histopathological Lesions in the Intestines and Mesenteric Lymph Nodes." Journal of Veterinary Medicine, Series B47(7): 487-495.

Lenghaus, C., R. T. Badman and J. C. Gillick (1977). "JOHNES DISEASE IN GOATS." Australian Veterinary Journal53(9): 460-460.

Lindheim, D. (2013). The Norwegian Healtier Goats project. Goat Milk Quality - Regional IGA Conference Tromsø, Norway, International Goat Association.

Maio, E., T. Carta, A. Balseiro, I. A. Sevilla, A. Romano, J. A. Ortiz, M. Vieira-Pinto, J. M. Garrido, J. M. P. de la Lastra and C. Gortázar (2011). "Paratuberculosis in European wild rabbits from the Iberian Peninsula." Research in Veterinary Science91(2): 212-218.

Manning, E. J., H. F. Cushing, S. Hietala and C. B. Wolf (2007). "Impact of Corynebacterium pseudotuberculosis infection on serologic surveillance for Johne's disease in goats." J Vet Diagn Invest19(2): 187-190.

Manning, E. J. B. and E. Patton. "Johne's Disease Management Concepts for Owners."   Retrieved 8/1/14, 2014, from http://www.johnes.org/presentations//General/Goats/Goats.html.

Meylan, M., D. M. Rings, W. P. Shulaw, J. J. Kowalski, S. Bech-Nielsen and G. F. Hoffsis (1996). "Survival of Mycobacterium paratuberculosis and preservation of immunoglobulin G in bovine colostrum under experimental conditions simulating pasteurization." Am J Vet Res57(11): 1580-1585.

Stewart, D. J., J. A. Vaughan, P. L. Stiles, P. J. Noske, M. L. Tizard, S. J. Prowse, W. P. Michalski, K. L. Butler and S. L. Jones (2006). "A long-term study in Angora goats experimentally infected with Mycobacterium avium subsp. paratuberculosis: clinical disease, faecal culture and immunological studies." Vet Microbiol113(1-2): 13-24.

Storset, A. K., H. J. Hasvold, M. Valheim, H. Brun-Hansen, G. Berntsen, S. K. Whist, B. Djonne, C. M. Press, G. Holstad and H. J. Larsen (2001). "Subclinical paratuberculosis in goats following experimental infection. An immunological and microbiological study." Vet Immunol Immunopathol80(3-4): 271-287.

Tharwat, M., F. Al-Sobayil, M. Hashad and S. Buczinski (2012). "Transabdominal ultrasonographic findings in goats with paratuberculosis." Can Vet J53(10): 1063-1070.

Thomas, G. W. (1983). "Johne's Disease:An Investigation in a Large Goat Herd." Goat Veterinary Society Journal4(2): 29-31.

Whittington, R. J., G. J. Eamens and D. V. Cousins (2003). "Specificity of absorbed ELISA and agar gel immuno-diffusion tests for paratuberculosis in goats with observations about use of these tests in infected goats." Australian Veterinary Journal81(1-2): 71-75.

Whittington, R. J., I. B. Marsh, P. J. Taylor, D. J. Marshall, C. Taragel and L. A. Reddacliff (2003). "Isolation of Mycobacterium avium subsp paratuberculosis from environmental samples collected from farms before and after destocking sheep with paratuberculosis." Australian Veterinary Journal81(9): 559-563.