Pine needle blight pathogen gets weaker in New Zealand
6 November 2019
New Zealanders are used to hearing about plant diseases that arrive here and wreak havoc.
But for the first time, a New Zealand study has revealed that one introduced plant pathogen appears to have become weaker since it arrived here 50 years ago – possibly to make sure it doesn’t kill off its host.
The Dothistroma septosporum fungus, which infects pine trees, first appeared in New Zealand in the 1960s. It causes Dothistroma needle blight, one of the worst foliar diseases of pine trees worldwide. Infected trees lose their needles, grow more slowly, and can even die.
In other parts of the world D. septosporum can reproduce sexually, with two individuals mating to produce genetically different offspring. However, only one mating type exists in New Zealand – like having just males or just females – so the fungus reproduces asexually, effectively cloning itself.
Stringent New Zealand biosecurity regulations have helped to ensure that no more introductions of D. septosporum have occurred since the 1960s, so the current pathogen population is essentially a clone originating from that first introduction.
This provides a unique environment for studying its evolution, free from “confounders”, or complicating factors outside the study.
Lead author Prof Rosie Bradshaw, from the Bio-Protection Research Centre and based at Massey University’s Manawatū campus, said that while D. septosporum, like all fungi, reproduced rapidly, the pine trees they lived on were slow-growing and long-lived.
“If the fungus is too virulent, it will kill off its host trees and decrease its chances to move to other host trees, similar to people destroying their own houses,” she said.
In the study published in the scientific journal Microorganisms, researchers compared four isolates of D. septosporum collected in the 1960s with four isolates collected between 2006 and 2013, and two collected in 1991 and 1994. They then infected one-year-old Pinus radiata seedlings with the different isolates.
The fungal strains collected in the 1960s were much more virulent than the strains from the 1990s or 2000s.
“The four isolates collected in the 1960s produced higher levels of the known virulence factor, dothistromin, than any of the isolates collected from the 1990s onwards,” they wrote. “The effect of decade group on dothistromin levels was highly significant.”
This was opposite to what the researchers expected to see from isolates that had been in storage for so long.
Researchers also tested how the fungal strains reacted to copper (the main control method in commercial plantations), and found they had not developed resistance.
“Given that in New Zealand pine forests, trees are sprayed with copper fungicide sprays at most every two to three years, and only when certain thresholds of disease symptoms are exceeded, the selection pressure exerted by these antifungal compounds in the forest environment may be minimal compared to frequently sprayed agricultural crops,” co-author Lindsay Bulman, a science leader at Scion and the Bio-Protection Research Centre, said.
Prof Bradshaw said this was all good news for New Zealand foresters. “It means the disease is not as destructive here as it can be elsewhere, or as it was when it first arrived, and also suggests that copper spray is still an effective control.”
The finding also has significant global implications for forest health, suggesting the potential for incursions of some highly virulent clonal forest pathogens to become less virulent over time, regardless of human intervention, Prof Bradshaw said.
The implications for practical resistance breeding are that, in some situations, even low levels of resistance or tolerance might be sufficient to improve the long-term health of trees.
For the full study, see Reduced Virulence of an Introduced Forest Pathogen over 50 Years, DOI: 10.3390/microorganisms7100420