A pathogen killing our iconic kauri has likely been quietly lurking in New Zealand for hundreds of years – a finding that’s led some scientists to ponder new questions about precisely how humans have influenced the rapid rise of dieback disease.
Kauri dieback disease – caused by a fungus-like pathogen that can be spread on muddy boots and equipment – has become an increasing threat to our ancient taonga over the past decade.
It’s now been recorded across Auckland, Waikato, Coromandel and Northland, notably in the hugely important Waipoua Forest – home to our most famous kauri, Tane Mahuta – and most recently in the Bay of Islands’ Puketi Forest.
This year, the Government earmarked $28 million for a new National Pest Management Plan to protect kauri – the strongest form of protection available under the Biosecurity Act 1993 to combat the disease.
New research suggests that, rather than having been introduced to the country over recent decades, the pathogen, named Phytophthora agathidicida, has been here for at least 300 years – and possibly millennia.
While the study, published in major journal PLOS One, suggested a move away from an “introduced pathogen narrative”, it doesn’t mean efforts to combat it are a lost cause, says the scientist who led it.
Over time, researchers have been able to learn more about how the pathogen senses its host, how quickly it can move through water-logged soils toward new ones, and how its presence can be linked with differences in soil microbial communities.
Yet, more than a decade on from its first detection, there remains no cure – and the scourge continues to kill most, if not all, the kauri it infects.
Study leader Dr Richard Winkworth, a plant geneticist at Massey University and Ampersand Technologies, said it had been assumed the pathogen had come to the country recently, but this theory had never been formally tested.
“The idea has, however, become ingrained in the research strategy, management actions, and, ultimately, public perception.”
Winkworth said colleagues had suggested better understanding the pathogen’s history here was unimportant and a distraction from fighting it – but he contended the origin question was a critical one.
“Assuming recent arrival has consequences,” he said.
“For example, this assumption allows us to interpret new sites of disease expression in terms of pathogen spread.
“Importantly, this is not the same as having documented spread empirically nor could we then use the rapid spread of disease as evidence supporting recent arrival.”
To examine when the pathogen arrived in New Zealand, he and colleagues assembled complete mitochondrial genome sequences for 16 collections of the pathogen from across the known range of the disease.
Using these DNA sequences and information from a related species about how fast the sequences change, the team had calculated the age of their last common ancestor.
“For you and your brother or sister, your mother is your last common mitochondrial ancestor, and for you and a cousin, it is your grandmother,” Winkworth explained.
“We take this same idea, but rather than think about generations we consider time.”
By examining the genetic diversity in the sample, the researchers not only found that the last common ancestor for their sample of the pathogen was about 300 years old, but also that their sample contained four genetic groups each with a different geographically distribution.
“This combination of observations is not expected of a post-1945 introduction and instead points to the pathogen having been diversifying in New Zealand for hundreds of years.”
The analysis doesn’t explicitly test when the pathogen arrived, but since it appears to have been diversifying in New Zealand for three centuries, he said we have to assume it must have arrived even earlier.
“Data available for related species puts an upper limit on the arrival at perhaps several thousand years.”
If the incursion was recent, he noted, it made sense to assume our role was mainly that of transmission – moving the pathogen from place to place through human movement.
“However, if the pathogen has been here for a longer period of time then our role in disease expression may go beyond that of a vector,” he said.
“One alternative is that kauri and the pathogen have co-existed for hundreds or even thousands of years and that the rapid increase in numbers of diseased sites over the last 20 years or so reflects human-induced environmental change.”
Potential culprits included pressures like deforestation, higher recreational use, and climate change – or perhaps a combination of them.
“This is why understanding pathogen arrival is not a distraction,” he said.
“Focusing our management and science strategies around spread and vectoring makes sense if we could be confident introduction was relatively recent.
“But if the pathogen has been here longer then we need to look at broadening the focus of our management and science programmes.”
He also pointed to two areas that required more research.
One was getting a better understanding of where the pathogen occurs and how important landscape-scale movement of the pathogen was.
The other was working out how the genetic diversity of the pathogen was distributed.
“These areas are important in terms of confirming just how long the pathogen has been here and should also help us to understand the patterns and timing of pathogen movement,” he said.
“Understanding pathogen diversity is also important from a management perspective, especially if the different groups differ in ways that affect how virulent they are or effective a particular intervention might be.”
“There is still much to learn but our results suggest that we should not continue to simply assume that the pathogen is a recently arrived pathogen that is rapidly spreading through the forest.
“If our science and management is to be robust we should at least consider the potential impacts of the alternative.”
Winkworth said it was important that the study’s findings weren’t taken to imply that the disease couldn’t be beaten – a view that might lead more people to flout the current rules.
“The take-home from this study should be that, as we learn more about the pathogen, we can and should adapt our approach to dealing with it. The study does not mean kauri are doomed, but it also shouldn’t remain business as usual,” he said.
“It’s the nature of learning about a problem and trying to address it all at once.
“In much the same way as we are doing with Covid-19, we need to learn more about this pathogen whilst at the same time improving our response based on what we learn.”
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