Habitat cascade dynamics are just part of what I’m investigating here in New Zealand. The other topic of research is a bit harder to pin down— it falls under the wonderfully vague term, “science communication”, and describes everything from scientific publications to outreach for school children to graphic design and chats in the grocery store and beyond.
Last night, my friend Lydia and I ventured into the field for science communication research. We attended “Gene Genie”, a genetics-focused panel discussion put on by the Royal Society of New Zealand. The theme was genetics and disease; the host, BBC correspondent and self-identified “recovering geneticist” Adam Rutherford; the panelists, experts in cancer, heart disease, and infectious disease.
The majority of the discussion was supplied by the cancer and heart disease researchers (with expert moderation by Adam Rutherford), and there was much to be learned in what they shared on sifting through the genome in search of disease markers and therapies. Besides that, the questions raised by the public during the Q-and-A period illuminated all of our best/worst sci-fi hopes/fears (can you really clone my dog? In ten years, will it be common practice to sequence your child’s genome before their birth? Can artificial intelligence be used to do this research for us?).
Still, Lydia and I felt a bit unsatisfied by the end of the talk. A zoologist and ecologist, respectively, we were perhaps less interested in the individual genetic risk factors of heart disease or cancer, and more interested in how the diseases in our environment move around and between human, animal, and plant populations. Basically: we wanted panelist Nigel French, the infectious disease expert who focuses on veterinary and plant medicine, to speak more.
Luckily, that’s exactly what that meandering-about time following a talk can provide. I approached Dr. French with a question on tracking disease arrival in New Zealand. Because this is a small and isolated island, a lot of pathogens (I should specify: pathogens that are actively monitored by humans) have only arrived recently. Take Escherichia coli, the consistently prevalent and occasionally fiendish bacterium. Non-toxic strains of E. coli are important inhabitants of our own healthy microbiome, but dangerous strains can colonize livestock guts. If the feces of these animals contaminate human water and veggie sources, resulting outbreaks of nasty E. coli infection can lead to sickness, death, and loss of confidence in food safety (remember the Chipotle crisis in 2015?).
So E. coli, needless to say, attracts a lot of interest, and a lot of research. An international community of researchers are dedicated to unraveling different strains and understanding the movement and evolution of this pathogen. But, like most things in New Zealand, the E. coli situation here is unique.
The history of New Zealand E. coli can be uncovered in the bacterial genome. When you analyze the genomes of a broad sample of New Zealand’s pathogenic E. coli population, three distinct clusters emerge. These three clusters represent three strains of pathogenic bacteria, and three separate introductions of the bacteria to New Zealand. When you track the differences between the genomes of these strains versus the most similar international strains, you can see that these bacteria likely arrived in New Zealand in between 1970 and 1990— which happens to be a period when live cattle imports into the country were increasing to keep up with its burgeoning meat industry. The theory, then, is that E. coli was carried to the country in the guts of these live cattle.
Demonstrating how pathogens like E. coli are getting into the country is essential in trying to stem the flow. Live cattle imports have become much more highly regulated in the past few decades, and likely because of this, the overall E. coli strain count in New Zealand has remained low compared to other livestock-breeding countries. Take the U.K., for example: it has 10 or 12 strains of the pathogenic bug, compared to New Zealand’s three. As Dr. French told me, this pattern of a relative paucity of strains holds for other pathogens in New Zealand, too. This is an isolated island, and the microbes haven’t gotten here. And while there are arguably a lot of benefits to New Zealand becoming more and more connected to the global environment, when it comes to pathogens, maintaining that isolation means this nation might act as a refuge from many infectious diseases.
There’s a sticking point here, though: isolated islands with new colonizers tend to favor high rates of evolution and the development of new strains and species (see: Darwin and the Galapagos finch beak diversity). This is likely to hold just as true for E. coli as Galapagos finches. With active surveillance, we can track the evolution of the E. coli strains as they adapt to the unique landscape (and cattlescape) of New Zealand. That adaptation might make E. coli a more effective pathogen, which would be bad news for human and cattle populations. This sort of genome surveillance work is being carried out by folks like Dr. French and the team at the Infectious Disease Research Center.
Let’s hope their findings are well-communicated, so we can all keep following along.
Until next time,