The Footrot Strategic Plan has been one of the great biosecurity successes of the NSW state animal health service.
It was relatively unique in the fact that there was very little government money involved in the actual program and there were no incentives of compensation schemes for the producers, all things that the textbooks proclaim are essential for successful disease control programs.
The big thing that the strategic plan offered was hope. The technical aspects of footrot eradication had been known, and in many cases achieved, for over 50 years, but the strategic plan offered the hope that it would be possible to eradicate footrot from an individual flock and not reintroduce it with purchases or strays.
One of the ironies of the NSW Footrot Strategic Plan was that it was formulated partly in response to a similar plan in Victoria that promised to have all of Victoria as a Footrot Protected Area by 2001. The plan was developed over a period of time in consultation with producers and industry bodies and was launched with widespread support from government, producers and industry.The reason that the NSW plan succeeded whilst the Victorian plan faltered was the commitment of NSW producers to fund the bulk of the program through their Pastures Protection Board rates while a request by the Victorian government for producers to partly fund the footrot control program through a levy was rejected. The Victorian government of the time took the view that if footrot were not important enough to producers for them to fund some of the program there was no justification in putting taxpayers' money towards it.
The other great stimulus for the plan was the success of the Ournie Group: a group of producers in the upper Murray who, with a lot of help from Rob Walker the Regional Veterinary Officer, had eradicated footrot from their area. The group approach became one of the cornerstones of the plan.
The first integrated approach to footrot was by Nobby Clark, the Veterinary Inspector at Armidale. Footrot had become a significant problem as pasture improvement in New England made conditions more conducive to its spread, so he started a district eradication program. The New England Protected Area was proclaimed in the early 1960s and remained the only footrot protected area of NSW until 1989.
Once the Footrot Strategic Plan was launched it was embraced by almost all sheep producers. There were significant improvements in sheep handlers, inspection techniques and treatment as the program progressed.
Because the clinical expression of footrot is dependent on the ability of the organism to produce elastase, the environmental conditions that produce water maceration of the hoof and enhance survival of the organisms on the ground, and the resistance of the sheep, the expression of footrot has always been a bone of contention.
The line between benign and virulent footrot (and in its day, intermediate footrot) has always been somewhat subjective. This led to "Riverina Scald" that was an innocuous foot condition that never caused any problems unless it happened to rain! That meant that in 1939, 1956, 1973 and 1988 footrot miraculously appeared in western sheep stations that never brought any sheep in. Fortunately the late 80s and early 90s were wet years in the Riverina so there was little debate about the nature of the disease while we were working in the station country.
Similar stories involved "Monaro Scald" where sheep on the Monaro had relatively mild disease but when they were taken to the eastern Riverina they broke down with virulent footrot.
Laboratory testing helped us to get a handle on these strains. Initially the test looked at elastase production and virulence was classified according to how long a particular strain of "K organism"/Fusiformis nodosus/Bacteroides nodosus/Dichelobacter nodosus took to clear the fragments of sheep hoof from hoof agar culture media. If it took less than 7 days it was classed virulent, 7-21 days was intermediate and >21 days was benign.
This has been replaced by indirect tests. Gelatin gel thermostability became the definitive test for virulence but there was an increasing number of strains of footrot that were gelatine gel stable but behaved as benign in the field.
Strains of D nodosus that were gel-stable but field-benign have been found to carry a gene group called integrase A (intA). A PCR was developed for this gene group and has become the accepted test for strains of D nododus that were gel-stable but field-benign.
Treatments for footrot have also evolved from careful paring and standing in formalin. Antibiotics are valuable to treat infected sheep during dry periods. The soaking footbaths such as Footrite® and Radicate® were useful to cure and prevent footrot during wet periods.
As always there has been a lot of cost-cutting with plenty of home-brew penetrating footbaths and off-label antibiotics being used to save money.
When vaccines were first introduced in the 1970s they worked well or not at all. An increase in the number of serotypes in the vaccines broadened their coverage at the cost of effectiveness to the extent that they fell into disrepute.
The lack of an effective footrot program in Victoria means that there is a constant threat of reintroduction of the infection, particularly to southern NSW.
We have picked the low-hanging fruit so that the infections remaining in NSW are those classed as benign. Some of them are truly benign, but some of them are further up the scale towards virulent. Because virulence is a clinical judgement in NSW, there will be variation in how an individual strain is classified depending on the season, soil type, pasture, and animal factors. In the wet autumn and winter of 2014 there were quite a few infections that appeared to be virulent although lab testing implied that the strain was benign. Subsequent behaviour of the infection appears to support the latter diagnosis. Some of these infections were even seen in the western Riverina where benign footrot does not appear to persist.
We are struggling with these strains in the twilight zone. If they cause disease most years to the same extent as they did in 2014 they cannot be ignored, but history would suggest that it is very difficult to eradicate benign footrot. If they go back to causing mostly 2-score lesions with an occasional 3c or 4 we can go back to living with them.
There are some diagnostic and treatment options in the pipeline that may or may not reduce the need to spend the summer tipping up sheep.
Strain-specific vaccines have shown significant improvement over previous less specific or more broadly based vaccines, even to the extent of being capable of eradicating footrot (Dhungyel et al 2008). This may be of significant value when wet summers preclude a traditional eradication program and may even replace it.
An apparently more specific gene for virulence has been described and a rapid colorimetric PCR is in the pipeline (Cave pers com). This will significantly improve the diagnosis of virulent footrot.
On the other hand we are still a long way from understanding benign footrot. How can an infection that does not cause under-run, and therefore a carrier pocket, persist from year to year? What is the lesion that we are missing when we eradicate virulent footrot but are left with benign footrot?
When we first started our attempt to eradicate footrot from NSW many people said that we were mad. They were probably right. On the other hand when they said that we could not do it they were probably wrong. The NSW Footrot Strategic Plan remains a template for an effective animal disease control program. Less well-structured programs since have undermined the morale and image of the NSW public livestock health service, but we must not let that cause us to relax on this program: the benefits in welfare and production and trading options cannot be underestimated. The association of the NSW public livestock health service with this program has also been invaluable and we need to persist if we are to retain credibility.