This isn’t my usual post about morons (or fucking morons). Nope, this is about the Black Death, caused by the bacterium Yersinia pestis (we’ll get to the morons in a bit). Recent work, published in The Proceedings of the National Academy of Sciences, suggests that the strain of Y. pestis that caused the Black Death is extinct (emphasis mine):
…plague is still around, caused by a bacterium called Yersinia pestis. The Black Death is generally assumed to be an intense pandemic of the same disease. It’s the second of a trilogy that began with the Plague of Justinian in AD 541 and that continues with modern plague, which infects some 2,000 people a year. But some scientists and historians saw features in the Black Death that separates it from other plague pandemics – it spread too quickly, killed too often, recurred too slowly, appeared in different seasons, caused symptoms in different parts of the body, and so on…
It not only confirms the idea that the Black Death was plague, but it might explain why that particular pandemic was so different to the others – it was Y.pestis, but not as we know it….
Many of the Y.pestis sequences came from a plasmid – a ring of DNA that sits apart from the bacterium’s main genome. This one, known as pPCP1, is responsible for many of the features that set Y.pestis apart from its close relatives and contains many of the genes that allow it to grow in human hosts, and spread to new ones. However, pPCP1 wasn’t responsible for the unique nature of the Black Death – the Smithfield sequences were no different to those of modern strains.
However, Schuenemann and Bos also sequenced fragments of the bacterium’s main genome, and these contained two mutations that aren’t found in any known Y.pestis sequences, modern or ancient. This alone suggests that these sequences couldn’t have come from modern bacteria.
It’s unlikely that these two mutations were specifically responsible for the unusual nature of the medieval plague pandemic. After all, neither of them would have led to any changes in the bacterium’s proteins. However, they do suggest that the ancient strain was something different to those we study today, and perhaps one that is no longer around.
So the question is, what might have made the medieval Y. pestis so different than it was even thought to be a different disease altogether? One possible answer could be morons.
These are not your usual morons. Believe it or not, the term morons also refers to genes that are carried by bacterial viruses, often called phage:
My money is on phages, and specifically, those phages morons. Phages are kinda like bacterial ERVs– They are DNA viruses that insert themselves into the bacterial genome, and hijack that bacteria to generate more babby viruses. But phages dont always immediately start making babbies– sometimes they go latent. Its a dog-eat-dog world out there, and sometimes its safer to hide in a warm snuggly bacteria than to be out fending for yourself. But the bacteria have no interest in having this parasitic DNA contaminating their Specially Created genome. So phages bribe them.
Phages can encode for gene groups called morons.
These are viral genes that dont code for anything the virus wants, like structural proteins, or enzymes the virus needs– They are genes that make having the virus around attractive to the bacteria. And few things are more attractive to a pathogen than making you sick, thus spread the bacteria faster than if you werent pooping/oozing/puking/etc.
Leaving aside the issue of whether or not phage-encoded genes are beneficial over the long term, they are a key component in causing disease. The recent E. coli O104:H4 outbreak was, in part, so lethal because of the phage-encoded Shiga toxin (which works in an analogous way to the biowarfare agent ricin–not fun). But phage-encoded genes aren’t the whole story in bacterial pathogenesis.
In the case of the Black Death Y. pestis, it’s not surprising that the plasmid doesn’t appear to differ–the plasmid is critical in colonization of the flea (which spreads the bacterium), not the human disease symptoms*. That doesn’t mean other plasmids won’t be found however. And to jump back to O104:H4, the other critical component is a virulence plasmid that enables the bacterium to adhere to the gut lining. So let’s not rule out the plasmids yet.
The third possibility is gene deletion. This is actually an underrated, yet common phenomenon. In Shigella, which causes bacterial dysentery (and Shigella is actually E. coli), one of the key evolutionary events is the loss of cadaverine production through gene deletion. Cadaverine inhibits the function of the toxin Shigella produces, so eliminating cadaverine production increases the virulence of the infection. This is actually a common theme in Shigella: cadaverine production has been knocked out in each of the Shigella lineages, but it happens in each lineage in a slightly different way (in one lineage, it’s just a little piece of the gene, in others, larger pieces). There also seem to be several other genes which have been lost repeatedly in slightly different ways (e.g., lactose utilization), suggesting these are also important losses. In the bacterium Staphylococcus aureus (the “SA” in MRSA), long term infections are associated with deletions of part of the agr gene which is a ‘master switch’ for a lot of disease-related genes.
So what do I think will be the difference between the Black Death Y. pestis and today’s Y. pestis? Plasmids, gene deletions, or morons?
Yes.
Probably all three.
Including the fucking morons.
*The bacterium is also harmful to the flea, eventually killing it.
mikethemadbiologist