Posts Tagged ‘bacteria’
This is the first post in a 5-part series on the biology of zombies. More info and links to other posts here.
The rise of the zombie in pop culture is typically credited to George Romero’s ghouls from his Night of the Living Dead films, whose dead bodies reanimated with a taste for human flesh define our prototypical zombie. Romero doesn’t give a clear cause for their rise from the grave, with a vague mention in a television broadcast of a satellite returned to Earth from Venus emitting radiation. (Radiation could do anything back then!)
In a behind-the-scenes special about the making of the movie, Romero credits its creation to a short story he had written, “which I basically had ripped off from a Richard Matheson novel called I Am Legend” — a great horror story about Robert Neville, a man fighting for his life in Los Angeles against vampires. But the novel takes the vampire prototype and turns it on its head, with these creatures more recognizable as zombies to us than vampires. They aren’t the sneaky serial-killer types, but are rather stupid and gather in great hordes, and, like zombies, will feed upon one another if they must. (Yes, they have blood!) In an early chapter, Neville reads Bram Stoker’s novel Dracula (as he sips whiskey and listens to Brahms while vampires scream outside his house), describing it as “a hodgepodge of superstitions and soap-opera clichés” compared to his situation at the time.
Most of the standard vampire tropes hold true: they’re sharp-toothed, blood-sucking, repelled by crosses and garlic, and can’t come out in the sunlight. But this is science fiction — there must be a scientific cause for these symptoms! While he’s skeptical of the scientists’ germ theory of vampirism that was proposed before the scientists became vampires themselves, Neville eventually overcomes his “reactionary stubbornness” and gets a microscope. (And Matheson doesn’t leave out the difficulties of microscopy or mounting samples, with Neville throwing his first scope across the room in frustration.)
When he finally gets his slide loaded with a sample of vampiric blood, he is shocked to see a bacterium in the sample — a bacillus, “a tiny rod of protoplasm that moved itself through the blood by means of tiny threads that projected from the cell envelope.” And from there much of the book turns to scientific inquiry with many moments that made me smile, like when Neville so urgently “needs to know!” that he nearly runs out of the house into a vampire horde. Oh, the drive of science! Or when he can’t make the pieces fit into his bacterial model and begins to work himself up into a fury:
He made himself sit down. Trembling and rigid, he sat there and blanked his mind until calm took over. Good Lord, he thought finally, what’s the matter with me? I get an idea, and when it doesn’t explain everything in the first minute, I panic. I must be going crazy.
But over the course of years, performing experiments on captured vampires and their blood samples, as well as doing a lot of hard thinking, Neville manages to explain to himself why the vampires act the way they do. Whether his explanations will be good enough for you is another question.
The bacterial lifecycle
“I dub thee vampiris,” he says to himself when he sees the bacteria for the first time. The bacteria live in the bloodstream of their host and require fresh blood to live, living in a kind of symbiosis (described thus by Neville), with the bacteria generating energy for their hosts. But if there isn’t enough fresh blood around, a bacterium will sporulate, building a cell wall around itself to hide out until better conditions arise. When the host dies, these spores disperse, landing on a new host, with the new source of fresh blood reviving the vampiris bacterium.
In the novel, the bacteria were able to spread rapidly through the population due to dust storms, with the wind blowing the spores everywhere and the dust nicking peoples’ skin and thus creating a way into the body.
Neville’s discussion of bacteriophages is a moment of total scientific inaccuracy which I choose to ignore. His bacteriophages, which he describes as proteins that the bacteria secrete when conditions are poor, cause the bacteria to swell and explode, killing themselves along with the hosts’ cells. The thinking must have been that the bacteria need a way to kill their hosts so that their brethren spores can disperse — however a bacteriophage is not a protein, but rather a virus that infects bacteria.
Death by stake — an issue of bacterial metabolism
These vampiris bacteria can live with or without oxygen — aerobic or anaerobic metabolisms. In the bloodstream, they live without oxygen, but the second oxygen hits the system, they become parasitic, killing their host. And here’s where the stake comes in: The key to killing these vampires is creating a hole large enough to let oxygen into the bloodstream, causing the host to die immediately due a switch in bacterial metabolism. And when the host dies, the spores are released — and thus we have vampires exploding into dust. Once Neville realizes that it’s an issue of oxygen and not stakes or their material, he switches his method to simply slitting the wrists of the vampires to let oxygen in. “When I think of all the time I used to spend making stakes!” he says.
And why don’t bullets kill vampires? This is some embarrassing fabricated “science:” The bacteria cause the creation of a “powerful body glue” that seals bullet holes as soon as they are formed. (Though this body glue somehow can’t reseal the wrist slits.) The stake creates a large hole and blocks the body glue from resealing it, which is why they are such a potent weapon against vampires.
Other bacteria-based vampire symptoms
Neville read that strong sunlight kills bacteria, which is why vampires can’t go out in sunlight. But without fresh blood, the bacteria can’t create energy — resulting in the coma-like state of the vampires during the day.
One of his first experiments is trying to work out the vampires’ aversion to garlic. After reading that garlic’s potent odor is caused by allyl sulfide, he goes to a chemistry lab and heats mustard oil and potassium sulphide at 100 degrees to create the compound. First he tried injecting it into a vampire — but nothing happened. He expected the bacteria to be killed by the allyl sulfide in a lab experiment, yet again nothing happened! He was so infuriated by this failure of his theory that he downed a bottle of whiskey, broke a bunch of glass, and shredded a mural he painted.
World’s gone to hell. No germs, no science. World’s fallen to the supernatural, it’s a supernatural world. Harper’s Bizarre and Saturday Evening Ghost and Ghoul Housekeeping. ‘Young Dr. Jekyll’ and ‘Dracula’s Other Wife’ and ‘Death Can Be Beautiful’. ‘Don’t be half- staked’ and Smith Brothers’ Coffin Drops.
He stayed drunk for two days and planned on staying drunk till the end of time or the world’s whisky supply, whichever came first.
Yup. Just a normal day in the lab.
He later realized that this chemical in the bloodstream wasn’t enough. It was the actual odor of the garlic that did harm — an allergen that sensitized and repelled the bacteria, and hence their hosts. Tells you something about in vitro and in vivo experiments, am I right?
“The germ also causes, I might add, the growth of the canine teeth,” he mentions once near the end of the novel. Good save, Matheson.
Neville wasn’t satisfied by this theory alone — what about the mirrors and crosses?
A new approach now. Before, he had stubbornly persisted in attributing all vampire phenomena to the germ. If certain of these phenomena did not fit in with the bacilli, he felt inclined to judge their cause as superstition. True, he’d vaguely considered psychological explanations, but he’d never really given much credence to such a possibility. Now, released at last from unyielding preconceptions, he did.
Before society collapsed entirely when vampirism was spreading, in terror people turned to religion to calm their fears — The vampires were cursed by god for their sins, and only by accepting god could you be saved! Neville theorized that when these people, now convinced that evil people were condemned to vampirism, were infected by the bacteria and found that they themselves were vampires, they were driven mad. The mere sight of the cross — a symbol of their rejection — made them want to flee due to their self-hatred.
But the cross doesn’t apply to everyone, he noted. He had one Jewish friend that, as a vampire, was not repelled by the cross. But the sight of the Torah made him run in fright!
Mirrors had a similar effect. Having to actually face the fact that they were vampires visually was enough to drive them nuts and induce them to flee.
Ending teaser (but not a spoiler!)
There are a few other awesome biological references in the novel — including the lymphatic system, medical applications and evolution, which I won’t go into detail about here so you can enjoy the read. But I will tease with this quote, especially appreciating that this book was written in 1954.
He looked into the eyepiece for a long time. Yes, he knew. And the admission of what he saw changed his entire world. How stupid and ineffective he felt for never having foreseen it! Especially after reading the phrase a hundred, a thousand times. But then he ’d never really appreciated it. Such a short phrase it was, but meaning so much.
Bacteria can mutate.
Bacterial vampirism: it’s awesome!
I’m no expert, but this was the only example of vampirism being caused by bacteria that I could find. This novel certainly inspired many later stories of plague-based apocalypse and biological transmission of zombie-ism, but, after a few decades of focusing on radioactivity and biological warfare, the genre switched straight to viruses (to be discussed later this week) and never went the bacterial track.
But there’s plenty of good reason to consider bacteria and other spore-based organisms when developing your zombie mythology, especially since there are a number of examples in nature (also to be discussed later). It’s an underexploited transmission mechanism! Get on it, filmmakers.
And one final note — I Am Legend is really awesome and you should read it. Trust me — there is MUCH to enjoy despite what you’ve read here. This is really a novel about human loneliness, perseverance, and our definition of normalcy, after all.
“Taxonomy and classification are funny,” my father joked recently, “because the organisms being classified really don’t care what they are. We’re the only ones who care!”
Well, at least I thought it was a good joke. And it speaks to a certain truth: humans generally are obsessed with organizing and putting things into categories. It is evident in the way we divide our music into genres (“Is this chillwave or witch house?”) or put our pants in a different drawer than our shirts. This may seem silly, but, with our consciousness and perception, we need to categorize in order to make sense of our world, to generalize, and, well, to help us find things.
Long before any ideas of natural selection and evolution as we know them now, people were trying to organize the natural world around them. In 350 BCE, Aristotle published his History of Animals, which attempted to categorize the various “natures” of animals based on their characteristics. For example, he identified what we now know as arthropods as animals that do not have blood and, “if they have feet, have many” (French 1994). Some of his categorizations were not so on-par; for example, he placed foxes and snakes in the same category because they both burrow underground and thus have “sympathetic natures.” Accurate or not, the effort is there: making sense of the world through categorization.
Although we’ve been at it for a long time, we are not close to being finished identifying all extant species, much less cataloging them. Just this week it was announced that, due to double-counts, the estimate of the number of flowering plant species will be cut by 600,000. 600,000! And those are just the plants that are living today, excluding all the known and unknown species that have gone extinct.
It would be easy to say, “whatever, who cares about the extinct ones? If I’m categorizing to make sense of the world, I want to pay attention to the world I’m living in. Leave the past in the past, man!” But if people view the world as stories as I believe we do, we need this history of organisms to construct our narrative1.
And, in particular, we need to know the history of our own species: where do we fit into the puzzle? How far back can we trace our own ancestors? When I was 14, I was taught that we are part of the Animal Kingdom, one of the five kingdoms of life. When I was 17, I was instead taught the three domain system: the Bacteria, the Archaea, and the Eukarya, a classification developed by the microbiologist Carl Woese in the late 1970s. This new system organized the world based on cell type, in particular dividing the Monera, which previously described all single-celled life, into the Bacteria and the Archaea, which are each single-celled but have many differences in structure. (See this great post by Labrat for more information on their distinction.) No longer were we humans described as “animals” as in ancient times, but rather based on an ancient ancestor, the first to embody the type of cell that makes up our bodies.
In the three-domain system, we eukaryotes are more closely related to the archaea, but evolved separately from a common ancestor (sister lineages). We evolved a unique nucleus composed of specific proteins, and later acquired mitochondria or plastids from bacteria through endosymbiosis. However, a different hypothesis has arisen in the past couple of decades: the 2-domain system. In this system, the Eukarya are even more closely related to the Archaea. In fact, we are a subgroup, having evolved from a singular lineage within the Archaea. A mere secondary domain, replacing Eukarya as a “primary domain” or sister lineage as put forth in the 3-domain system.
Why is the 2-domain system being considered at all? The Archaea and Eukarya share many of the same components of their genetic information systems, such as over 30 ribosomal proteins, RNA polymerases, transciption factors, promoters to initiate transcription of the genome, and replication enzymes (Gribaldo et al. 2010). A general tenet of constructing phylogenies, evolutionary trees through time, is that the simpler answer is usually better. Proponents of the 2-domain system argue that it is simpler for these genetic pathways to have evolved once in the older domain, the Archaea, and been retained in the newer subdomain, the Eukarya. Proponents of the 3-domain system hold that these systems evolved earlier before the lineages split and were preserved in both the groups over time.
Eukaryotes also share many genes with the Bacteria, even more than with the Archaea. Do these genes “even out the score” and support the 3-domain system, or were they acquired as a remnant of bacterial endosymbiosis? An early edition PNAS paper (2010) by James Cotton and James McInerney of the National University of Ireland argues its title: “Eukaryotic genes of archaebacterial origin are more important than the more numerous eubacterial genes, irrespective of function.”
The authors compared every gene in the yeast genome to bacterial and archaeal genomes, finding that 952 genes have bacterial homologues, while 216 show homology to archaeal genes. Using these genes, they performed two main tests. First, they examined how frequently each of these genes killed the cell when deleted from the genome – a test to see just how imperative each is to the cell’s survival. They found that lethal genes are twice as likely to be of archaeal origin than bacterial origin, giving the Archaea one “important point” in their book. Second, they looked at how frequently these genes were actually transcribed, or copied into a form from which they can be made into proteins. Using RNAseq, they found that there was significantly more expression of genes with archaeal homologues than bacterial. Another “important point” for Archaea.
This study seems to support the 2-domain hypothesis: the genes that come from Archaea are used more frequently and are more necessary for cell survival, despite being fewer in number than Bacterial genes. But remember: both systems of taxonomy support the idea that Eukarya are more closely related to Archaea. Importance is merely a factor of correlation, not evolutionary causation. It provides evidence that the two domains are related, but not the direct evolution of Eukarya from the line of Archaea.
These lineages have been diverging from one another for at least 2.5 billion years – it seems like a bit of a stretch to be doing genomic studies at all! Think of all the mutations and changes that have been made in the DNA over those 2.5 billion years, obscuring the true relationships and further separating these domains morphologically. A review coming out next month in Nature Reviews Microbiology goes through a number of studies that attempted to analyze eukaryotic evolution and found that none drew a strong conclusion, or even found conflicting results, “despite analyzing largely overlapping data sets of universal genes.” They conclude that “it is premature to label any one of these analyses as definitive” and that these large-scale genomic studies have “not yet yielded a resolution to this debate and ha[ve], if anything, intensified it.”
Even if we did know the truth, what would this mean for the “story of human evolution” I was babbling on about earlier? Well, it means that we’re Archaea deep down! Those badasses who live in hot springs and sulfur! We had the potential to be hardy, tough organisms, but instead we’re frail and get cold really easily and get hunger pangs after just a few hours…
More than anything, the fact that this debate exists in the first place gives us a great perspective on our story. Under 2500 years ago, Aristotle categorized foxes and snakes together. Now, we’re splitting hairs over the type of ancient cell that foxes, snakes, and ourselves evolved from over 2.5 billion years ago. It provides the history of our progress. And look how far we’ve come!
1 Of course there are many applications for studying evolution beyond a desire to learn about our own history. This 2005 interview with Massimo Pigliucci, an evolutionary biologist at SUNY Stony Brook, and the 1998 collective paper “Evolution, Science and Society: Evolutionary Biology and the National Research Agenda” are good places to start.
NOTE: Molecular evolution is incredibly hard to explain (in my opinion), and I did my best to do so in English. If you have any questions or think some parts need clarification, please let me know in the comments or write me at hannah.waters [at] gmail.com. I’d really appreciate it! Thanks!
Cotton, J., & McInerney, J. (2010). Eukaryotic genes of archaebacterial origin are more important than the more numerous eubacterial genes, irrespective of function Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1000265107
French, Roger. Ancient Natural History. New York: Routledge, 1994.
Gribaldo S, Poole AM, Daubin V, Forterre P, & Brochier-Armanet C (2010). The origin of eukaryotes and their relationship with the Archaea: are we at a phylogenomic impasse? Nature reviews. Microbiology, 8 (10), 743-52 PMID: 20844558