The aim of this presentation is to illustrate the nature of spread of Bovine Johnes Disease (BJD) in a NSW north coast dairy environment. It highlights limitations of serology as an eradication tool and the frustrations of attempting to eradicate a Mycobacterial disease with a long incubation period.
This case spans
The herd is a commercial and stud Jersey herd located on the Richmond River floodplain.
The previous owner had BJD diagnosed in 1987 in a 4 year old Jersey bull; introduced as a calf from Victoria. The current owner purchased the property and some of the herd in 1990.
Subsequently the herd had a traceback in 1992 and then another traceback in 1994. Both the traces were cows that had been born on the property in 1987. Both had been sold in 1992. A typical test program requiring three negative herd tests, each two years apart was commenced.
On the basis of these tests the herd was given a clearance for BJD and was enrolled on the Market Assurance Program (BJD MAP) with a commitment to future testing and auditing.
In all a total of 4 negative whole herd tests were achieved, followed by 4 negative part herd tests of 50 head. These were conducted over a period of over 15 years.
In March 2006 a cow was moved off the farm to a local property. In May 2006 samples were taken by a private practitioner because the cow had developed scours. The following month the cow died. In September 2006 BJD culture on the faeces returned a positive result.
The owner of the herd was shocked, having been on the BJDMAP for over 10 years and having had a negative Maintenance Test of 50 head only the month before.
A whole herd test was conducted in September 2006 with 16 ELISA positive/456 tested. Of these 14 were found to be infected on faecal culture. Several cows had early clinical signs of BJD. Including the trace there were 15 infected cattle in the herd that year.
A total of 4 whole herd tests and 4 part herd tests over a period of over 15 years had failed to detect the infection.
In an attempt to resolve this dilemma data was collected on the ages of the infected cattle and the ages of the cattle sampled for the Maintenance Test. The history of the herd and its management was also studied.
The year of birth of an infected animal is critical in understanding when BJD has spread. Calves in their first 12 months of life are the most susceptible cattle to pick up the infection. The year of birth acts as an indicator that the environment of the calf was contaminated with the BJD organism at that time. It also serves as a marker that infected animals in the herd were shedding the organism at the time.
The level of contamination of the environment with M. avium subsp. paratuberculosis on a given property is not constant, but is a reflection of a number of variables including;
The period when environmental contamination is at its highest level could be termed a ‘shed period’, reflecting when faecal shedding by the infected animal/s is greatest.
My experience has been that shed periods tend to rise and fall in a herd. In the first decade or two after the introduction of infection, periods of peak shedding may be separated by periods of several years in which shedding will be low or nonexistent. These intervals match the incubation period for those individual animals with the disease. The same may be true for herds that for whatever reason maintain a low level of infection.
In those herds in which the disease becomes well established with the progress of time, the number of infected cattle rises and I suspect that the distinct ‘peaks and troughs’ become blurred. In this situation calves may be at risk at any time if they are exposed to the faeces of adult cattle.
In this herd an analysis of the year of birth of the cattle confirmed with infection shows a distinct pattern. Because of the level of testing in this herd, there is a reasonable degree of confidence that there should have not been too many other infected cattle in the past 3 decades.
|Year of Birth||Infection Pattern and Possible Conclusions|
|1984||The first diagnosed case, bull born in Victoria & introduced onto the farm as a young calf. Developed clinical signs and therefore was a shedder in 1987. Conclusion- source of infection not clear; the bull was infected either from the property of origin, or on the property of destination. We will call the bull: Case A.|
|1987||2 infected cows (Case B & C) born; sold in 1992 and breakdown, one in 1992, the other in 1994. Conclusion - the bull was diagnosed in 1987 and therefore needs to be considered the prime suspect as the source of infection for the two cows.|
|1994||2 infected cows (Case D & E) born. One was detected in the 2006 herd test. The other developed clinical signs within 2 months of leaving herd in 2006. Conclusion - Source uncertain. We know that there was shedding in 1992 from one or both of the above cows (B or C). Pasture contamination should only last 12 months after infected animals are removed, and both B & C had left the property early in 1992. There had been a full herd test in 1992 and in 1994 with negative results. My conclusion is that there had to be an infected, incubating, but ELISA negative animal present in the herd at the time of 1992 test, for there to have been pasture contamination in 1994. This animal had probably been culled by the time of the 1994 test.|
|1998||1 infected cow (F) born. Infection was detected on the 2006 herd test. Conclusion - Source uncertain. There had to be pasture contamination in 1998 at the time that F was born, and yet a full herd test in late 1997 was negative. Perhaps the shedder responsible had been culled just prior to the 1997 test, and it was the remaining environmental contamination that was the source. Alternatively, the shedder had been present for the test and was seronegative at the time.|
From the 2006 herd test we also know that the following infected animals were born in;
|2000||3 infected born|
|2001||7 infected born|
|2002||1 infected born|
|2004||1 infected born|
1. Clearly the neat pattern of shed period matching the incubation period has broken down as the infection became more established in the herd and the prevalence rose (see Graph 1).
2. There was obviously a high degree of exposure during 2001, with 7 animals infected.
3. The ELISA test had low sensitivity. If full herd tests failed to pick up infected animals on the 1992, 1994, 1996 and 1997 tests, the subsequent 4 part herd tests had no chance.
4. The mean age of the 18 cattle detected with BJD in this herd was 5.6 years (see Graph 2). In my experience BJD is not a disease of aged cattle, but of the middle aged. The bias in the maintenance tests was toward older cattle; mean age of 8.0 (see Graph 3) which may help account for why they were missed.
There are several features of the herd, its management and the property which were conducive to the spread of BJD.