Invasive species suck.
Humans intentionally or unintentionally introduce some organism into a new environment... and shit hits the fan. Whether its zebra mussels in the Great Lakes or rabbits in Australia, invasive species wreak havoc on their 'new homes'.
There are lots of reasons for this, but there are only three reasons Im interested in:
1. The organism escapes from a pathogen in its native environment. No more pathogen, more reproduction.
2. The organism introduces a pathogen into its new environment. Organism has coevolved with this pathogen for ages, native organisms cant deal with it, invasive species kills off its new competitors.
3. Everyone is infected with the same pathogen, but get different diseases.
I never ever thought of #3 before I read this paper (been out for ages, but this is the first Ive heard of it!)
Pathogen-induced reversal of native dominance in a grassland community
Native California grasses are perennials . Since Europeans colonized Cali, the native perennial grasses have been wiped out by European annual grasses.
Well, okay, so the European annuals are 'more fit', so they can reproduce more, and thats why their kickin perennial butt, right? Survival of the fittest, *yawn*
Except apparently, the European annuals arent more fit. Experimentally, the native perennials are better suited for the California ecosystem.
What?? The 'most fit' grasses arent dominating the landscape?? They arent out-competing the invading European grass??? Evilution is wrong! The Designer changed His mind and doesnt want native grasses growing in Cali anymore! Crumbling! Darwinism is CRUMBLING!!!!
Well, no. There is one thing in nature that can explain why the 'less fit' species are out-competing the 'more fit': viruses.
What if both the native and invasive grasses are infected with a virus, everybody is sick... but the 'more fit' grasses get so sick, they turn 'less fit'?
So researchers just tried something:
If Cali and Euro grasses were left 'pathogen free', Cali grasses out-competed Euro grasses. Totally what we would have expected, more fit grass out-competes less fit. Hurray.
HOWEVER, if you introduce a virus into the system, in this case, barley yellow dwarf virus, the European annuals take over!
Annual grass invasion combined with aphid preferences for annual grasses alters disease dynamics by increasing transmission rates and disease prevalence in perennial grasses. Before annual grass invasion, some perennial grasses remained uninfected each season, whereas in a mixed annual-perennial community, all perennials become infected in the first year, such that virtually no healthy perennials are seen at the end of any growing season...
... BYDV infection has several compounding negative effects on perennials that have survived their first year. First, infection halves the lifespan of adult perennials. Reduced survival to the subsequent year (ÏPI), compounded by reduced fecundity (εp), depresses the lifetime net seed production of an adult perennial (e.g., from 330 to 75 seeds per plant) to a level insufficient for an infected adult perennial to replace itself if all of its offspring were to be infected at germination. Finally, because perennial adults are superior to annuals in competition for light and nutrients, loss of perennial biomass reduces interspecific competitive pressure on annuals. Thus, the disease is more detrimental to the long-lived perennial life history than to the annual grass life history; this permits annuals to increase in relative abundance, which further amplifies viral incidence.
This virus has a detrimental effect on European annuals, but its not the end of the world. But 'no big whoop' problems for annuals turn into Big Problems for perennials, and THATS why these 'more fit' grasses arent taking care of the invasive species problem themselves!
Neatoooo!
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I found this very interesting thanks for posting
Abbie, this is a cool article, and I have a dumb question. Regarding:
I looked at (as in read the abstract) the article and found this:
, checked the article reference (14) which included this:
OK, stupid question now: Is this a correct understanding of the situation:
Native organisms (call them A) which carry native pathogens that are detrimental to other native organisms (call the other native organisms B), don't normally get close enough to B such that the pathogen can jump from A to B, because A doesn't like to eat (or whatever) B. Introduction of a B-like foreign organism (call it C) is very attractive to A. So in pursuing the new C, A gets close enough to B to transmit the pathogen. The pathogen "knows" how to successfully infect B, but not C. So B, although being more fit for the environment, is fucked.
Another dumb question: As B dies off from the pathogen and C prospers, wouldn't evolutionary theory predict that, over time, the pathogen would "learn" how to infect C? And that C would "learn" to adapt to the environment and resist the pathogen's new "talent"? Key point being time.
I may be an idiot here, but is this not similar to the way we view sickle cell anemia?
Malaria kills in africa
Those with sickle cell anemia are immunologically more robust against malaria
In africa they are 'better'
Sickle cell RBCs are not as good of an RBC as normal ones
In an environment without malaria sickle cell anemia is a bad trait.
So in malaria infested areas the less fit survive better.
or have i simplified all of this beyond reasonable comprehension?
Abbie, I'm going to hire you to start writing my headlines for me.
Very cool. Reminds me of the review article on viruses that came out in Cell a couple-few issues ago, discussing the prevalence of a variety of viruses in the human population impacts the immune system ("Redefining Chronic Viral Infections").
The authors went so far as to note that some percentage of differences in immune responses that we chalk up to species variation (e.g. mouse vs human) may actually be due to absence vs. presence of different virus communities.
There's also some mega-cool work on the effect of age-of-acquisition of epstein barr virus and subsequent immune response, including malaria susceptibility. That's a case where the reason everyone-gets-the-same-virus but different diseases result isn't because a subpopulation is more susceptible to to the virus, but because the virus is spread differently depending on host lifecycle.
It cuts both ways. Pathogen escape has allowed North American cherry trees to become an incredibly invasive weed in Europe - which is further ironic as cherry trees are considered extremely valuable here (e.g. for furniture).
Excellent article, thanks for pointing it out!
Techskeptic - you're sort of write about sickle cell and malaria... here's how it works.
Having one copy of the mutated hemoglobin gene is the best - it protects against malaria (harder to suck up by mosquitoes I believe) and doesn't cause sickle cell (the other, wild type, hemoglobin gene protects you). So regions where malaria is endemic select for individuals who have a copy of each. Unfortunately having a copy of each means your offspring may have sickle cell if they inherit mutated forms from both parents. Damned if you do, damned if you don't. Sickle Cell Anemia and Genetic Fence-Sitting.
A couple of clarifying points from the comments (and article). All best estimates suggest that BYDV is a non-native pathogen. So this is a double invasion whammy.
Second, one reason that annuals do better when the virus is prevalent is that they spend a lot less of their lifespan infected--The virus is not transmitted vertically so when annual seeds germinate in the spring, they are uninfected, while most perennials continue to be infected year after year.
you wrote a very good paper. its wasnt boring like most research stuff is. thanks for helping me out