[With the re-organisation of the New Zealand rural media and the demise of NZ Farmer for which I previously wrote, this is the first of a new series of fortnightly articles I will be writing for Farmers Weekly and also published at http://www.interest.co.nz. Whereas my articles in Stuff (online and in their hardcopy newspapers ) are about rural issues, but largely for an urban audience, the Farmers Weekly articles are primarily for farmers and those more directly involved in rural matters.]
A key message from the Ministry of Primary Industries (MPI) has been “generally prolonged or repeated contact with infected animals is required for the disease to be transmitted” (MPI website). Another key message has been that the disease has only been here since the end of 2015.
Bringing those two supposed facts together, it seems surprising that the disease has progressed so quickly in just two years from the so-called index farm in Southland to at least 52 infected farms, with many additional farms still being traced.
Surely, one of the two supposed facts cannot be correct.
Back in May, it was the incongruity between these supposed facts that led Biosecurity Head Roger Smith to tell a Parliamentary Committee that the blow-out rate of infected properties was outside the numbers that MPI had considered likely. This will also have been an influence in the perspective of four out of 10 Technical Advisory Group (TAG) members in mid-May that eradication was no longer technically feasible, let alone practical.
It is debatable as to which of the two supposed facts is wrong. There is evidence either way. It could even be both.
There is surely one situation where Mycoplasma bovis is highly contagious and that is through infected milk. If we are to eradicate this disease, then farmers must not feed calves with unpasteurised milk from their ‘hospital herd’.
With hindsight, the disease would probably have spread much less if it were not for the feeding of hospital milk. Almost certainly, this is the fastest way the disease spreads, although looking forward, service bulls are the other big risk. Given the testing the semen companies are now doing, artificial insemination is a much smaller risk.
MPI is saying that all of the infected herds relate to animal movements from the so-called Southland index farm, but the farmers with infected herds that I am talking to are not convinced. Some of them blame over the fence interactions or other transient contact, but the picture there is not clear.
There is another key problem with the theory that all transmission is related to recent animal movements. This problem is that some of the animal movement traces have led to positive tests, but the suspect farms of origin have subsequently tested clean on multiple occasions. It seems therefore that the disease may have already been there on the receival farm from another source. It all gets very confusing.
I find the overall pattern of identified infections more consistent with the notion that it has been in New Zealand for quite some time, with somewhere between 2008 and 2013 being the most plausible explanation.
Each week I get more people ringing me to talk about evidence that the disease was here up to ten years ago. Typically, this is for situations where it is only now that they have put two and two together and said, ‘Aha, this explains things that we could not put our finger on at the time, despite seeking veterinary assistance’.
In some cases, there may be post-event rationalisation, but other cases seem convincing. If there is a common element to them, it is large-framed Holstein-Friesians with imported genetics, including both semen and embryos as possibilities for the original source. The convincing cases include udder blow-out, cold quarter mastitis and arthritis in cows, and lots of calf deaths. Feeding hospital milk to calves also comes into it.
Currently, there are possibilities that the original source could have been another Southland farm, where the farmer was himself an importer of semen (not just a user of imported semen). This farmer had major calf rearing problems around 2008 despite using all accepted protocols.
This farmer subsequently left the country when he got into major financial stress, and the herd was dispersed around Southland and Canterbury. One of the receival herds is believed to be the same farm that MPI currently regards as the index farm.
Clinical problems in adult cattle have still only been identified on two infected farms out of more than 50 farms known to be infected. Everywhere else the disease has been a sleeper. It is only when other stress factors come into play that Mycoplasma bovis shows itself to the farmer. If only a few animals are infected, then the chances of identification or even asymptomatic shedding are low.
One case study I am aware of is where the farm became suspect seven months ago but MPI is still trying to confirm whether or not it is positive. The antibody tests suggest strongly that it is infected, but antibody testing is riddled with false positives. False negatives can also occur. I have seen antibody lab reports for multiple cows from this farm that have gone from positive on one test to negative on the next, and vice versa.
Multiple PCR tests on this farm have also gone negative, but I have said to that farmer that based on the antibody tests, if MPI keep on testing then they are likely to eventually find a positive. This is also the experience of American vets, who say that in America if you test enough then you will eventually find it.
One of the TAG members has pointed out in a private communication that all of the overseas experience is about finding clinical cases and not sub clinicals. That illustrates how we are in new territory in New Zealand.
Some weeks back, I was criticised by MPI response Director Geoff Gwyn for my report of Gilbert van Reenen’s literature review of cross-species transfer. Gwyn conceded that Mycoplasma bovis could transfer to other species, but he said they were dead-end hosts. As such, the MPI perspective is that there is no risk.
However, MPI itself states in some written materials that it can cause mild infection in sheep and goats, and the research literature suggests this could be a reservoir back to cattle. There are few certainties in this game.
In that earlier article (archived here), where I stated that cross-species transmission was proven, I also said there was genuine debate as to the risks of this in the New Zealand situation. I still hold to that position. I don’t think Geoff Gwyn was correct to be so sure of his facts.
There remains a view within MPI and also amongst some vets that farmer messaging should be kept simple to reduce anxiety. My experience is that farmers want the full story, with all uncertainties out on the table.
However, I am pleased that at last MPI is showing interest in exploring evidence that it was here prior to the end of 2015 rather than being dismissive thereof. For the first time, I am having productive conversations with MPI.
To date, the counter argument against the need for these investigations has been MPI’s confidence from their genetic clock analyses. But as two geneticists have said to me in recent days, and I have myself been arguing, that conclusion is dodgy.
Accordingly, there is a need to intensively test specific farms in both islands that are linked to historical suspicious disease outbreaks. Some but not all of these farms can be identified. It only takes one to be confirmed as Mycoplasma bovis and the big picture changes.