The time between 1346 and 1353 marks the time of the Black death, the largest outbreak of plague in Europe. By the time this epidemic finished running its course, Europe would lose over 60 percent of its population. At the time, the source of this illness was a mystery. Now there is very little doubt that this epidemic catastrophe was the result of an outbreak of bubonic plague.
Bubonic Plague is caused by the bacterium Yersinia pestis that lives in infected fleas that themselves like to find their home on rats. The fleas get from rats to humans, where the bite of an infected flea starts an infection of the lymphatic system. From there infected people go through a series of increasingly horrible symptoms that go from chills and fever, to lymph gland swelling, to gangrene of extremities (fingers, toes, nose, and lips), coma, and ultimately death.
While there is little argument that Yersinia pestis was responsible for the black death, where the plague came from and how it persisted has been highly contentious. Until recently.
Beginning with the sequencing of the Y. pestsis genome, a large collaboration of scientists have used ancient DNA in the teeth of buried plague victims to reconstruct the history of plague worldwide.
The short story, rats in Asia changed their range due to changes in climate. This brought them into closer contact with people. From there, plague carrying rats follow trade routes, and ultimately provide the seeds for all modern outbreaks of plague. This graphic from Spryrou et al. 2016 sums it all up beautifully.
“Map describing dissemination pattern of Y. pestis during the second and third plague pandemics. All strains are depicted as points on the map. Branch 1 strains are in red and include both second pandemic (triangles) and modern (circles) isolates. Positioning of modern strain distribution on the map corresponds to geographic location.Red arrows indicate Branch 1 cycling through Europe during the 14th century, eastward travel out of Europe after the Black Death, and global dissemination from China during the third plague pandemic” Legend abridged and image taken from Spryrou et al. 2016
The plague group is continuing to do really cool work tracing the origins of earlier outbreaks of plague so keep an eye on google scholar! This work features such a cool application of phylogenetic trees that is in line with a growing trend of seeing phylogenetics front and center in human health studies. This foundational component to research makes accurate tree and branch length estimation more important than ever. Luckily there were some great talks showcasing the bleeding-edge of tree inference methods.
I want to focus on one talk in particular. Jake Berv gave a really interesting talk that linked life history to patterns of molecular evolution and what that means for divergence times. By looking at a group of genes in birds, he showed very convincingly that simply choosing large, medium, or small birds can change the divergence times you estimate and gave some compelling evidence that such effects have misled our estimates of avian divergence times.
Jake and Daniel Field published a paper in systematic biology about this last year that I urge you to read.
How old are modern birds? ‘Rocks and clocks’ have long been at odds for an answer, which Berv and Field argue is likely a consequence of a burst of rapid evolution following the K-Pg mass extinction we have failed to model.
Jake and Dan argue that small bodied lineages are more likely to persist after major extinction events, as a result of having faster generation times among other factors. These faster generation times imply faster rates of molecular evolution in many markers that slow when lineages evolve large body size. This type of change in molecular rate can have major impacts on divergence time estimation not just in birds, but any part of the Tree of Life where lineages have heterogeneous molecular rates. Needless to say, but for tracing pathogens across a landscape this could be particularly important. After seeing Jake’s talk, I’ve teamed up with Jake, Dan, and a host of others and helped write a formal review of this phenomenon. Stay tuned!
There were too many good talks and posters to list them all here. Fitting for the theme of this post was Anne Stone’s closing talk on the spread of tuberculosis (TB) to the New World. Similar to the Y. pestis group, Stone used ancient DNA to trace the spread of TB from Africa to South America. Prior to this work, it was thought that TB came from contact with Europeans. However, the archeological record supports the presence of TB in South America prior to any European contact. Using bacterial genomes, Anne’s group was able to bring some resolution to this conflict of hypotheses .
Including TB strains from several candidate non-human hosts provides a really surprising result.
Seals may have brought TB to the new world.
Seals were routinely hunted by humans both in South America and Southern Africa at the same time, making contact and host switching pretty likely. Seals also swim in some cases extreme (> 5000 km) distances which makes for quite the effective transport host!
This hypothesized spread of TB is also in line with a mountain of evidence discussing long distance marine dispersal events giving rise to major biogeographic patterns. Pathogens are not usually considered in these types of conversations which makes this talk all the cooler. All the seals around our boat in Antarctica and Southern Chile earlier this year just got little scarier…
In addition to being packed with excellent talks, the Yokohama venue for SMBE was equally fantastic. I used my jet-lag to my advantage and explored the city at sunrise every morning, and also had a chance for some quick outing with some wonderful friends and colleagues. Here are some photos to wrap-up!