The Zombie Autopsies: Secret Notebooks from the Apocalypse

by Steven C. Schlozman

  Note the widened sulci and loss of neuronal architecture.

  And there is no doubt about zombies—they can see me, can see all of us. This one even tracks my movements as I walk back to my stool to write.

  We’re moving quickly, but I need to concentrate. I don’t want to miss anything.

  I had to remove the higher brain with a spatula. It was quickest this way, and we need to dig down, get to the hypothalamus as quickly as possible. Surgeons often approach the hypothalamus through the mouth, cutting through the top of the palate, taking a shortcut to the deeper brain structures. We considered this, but our subject must be animate and awake. We need to watch the virus at work, as it actively infects and changes brain function and structure. Anytime these things are animate, they’re biting, chewing, acting as if food were there even when the mouth is empty. We’d lose our way quickly with that kind of movement.

  So we dug down from the top, removing the brain the way you remove soil under a tree to examine the roots. I could sense Blanca’s excitement as the thalamic structures came into view. Below them, she said. It’s called the hypothalamus for a reason. “Hypo-” means “below.” The hypothalamus sits below the thalamus. Easy to lose your orientation when the brain itself is so damaged, so these words have special meaning now. I carefully retracted more tissue, dug just a little bit deeper, and Blanca smiled.

  Some of the hypothalamus seemed preserved, appeared grossly normal and even larger than would be expected. It was as if there were a fence around it, stopping the spongiform changes the way an electric fence holds back an angry dog. To slow something as virulent as the ANSD prions, there would have to be something even more powerful. It would have to alter the pH of the surrounding tissue maybe, make the surroundings more basic, more alkalotic. Something very significant was protecting at least some of the hypothalamus from this plague… We haven’t figured out a good way to stop this disease from spreading throughout the brain, but whatever was in the hypothalamus can. In fact, it seems to me that only another microorganism could do this. Only a separate contagion could even begin this fight, and that means the hypothalamus is infected by something different that we haven’t even considered yet. This is what Blanca was talking about.

  It was tricky to extract the hypothalamus. I had to secure it with forceps and peel the less-formed tissue out of the way. No way to do this except with my fingers and a few instruments. Finally it was loose enough, and I carefully lifted it free with the spatula for Pittman to sketch. It’s hard to recognize it once out of the brain—it looks naked and ill formed. The amygdalae are still down there, buried beneath this mess, but the hypothalamus is extracted and free.

  Hypothalamus quickly loses form once removed from connecting brain tissue.

  I’m trying to get my mind around this. Three contagions operating through a single vector, a single means by which the contagion can infect a given individual. Every germ has its vector—food poisoning comes from contaminated food. Skin infections use direct contact as the primary vector. Hell, until now, prions could only get inside you if you ate them, but now they’re in the air. For ANSD, it’s the air itself; that’s our vector.

  Each cough, each sneeze, each gasp for breath from an infected lung spreads an influenza virus with ANSD prions packaged neatly and efficiently inside the virus itself, but each cough might additionally spread something more. We’ve long known that ANSD was a combination of more than one infective agent. We knew about influenza first and later the prions.

  But could there be a third infectious agent in the same “package”? Could there be something that alters the milieu of specific brain tissues? Could the hypothalamus be protected by a competing contagion? Worse, could all three contagions be symbiotic? Could they be “helping” one another?

  This symbiosis would have to be designed, would have to be planned. This would be engineered carefully, even brilliantly, in a highly technical lab. Nothing like this has ever evolved on its own.

  Gutierrez insisted that we immediately dissect the hypothalamus. She mentioned that some viruses attack only this brain region, but she seemed not to remember that she had already informed me of this hypothesis. She also noted that this brain structure was clearly demarcated, easy to discern. Its architecture was intact. There’s something here, she said. There has to be.

  Additionally, there is something quite large near the inferior, or lower, aspects of the brain that is well demarcated and seems to be pushing the thalamus and hypothalamus upward. Those intact regions maintained their integrity but they were clearly being moved, forced upward in a rhythmic way by whatever sits beneath them.

  Get the sections, Gutierrez said. Get the samples, and I tried to hold my hand steady as I moved the scalpel through the hypothalamus. We need thin slices for examination. We only have one chance once the blade hits the tissue. Gutierrez tried to calm me. You’ve done this, Stanley, and I was thinking the same thing. I’ve taken plenty of brain sections, made thousands of slides.

  But I haven’t done this for a very long time.

  I remembered what my anatomy professor taught me, now more than thirty years ago. Anatomy doesn’t change. Cutting the brain is like cutting bread, he said. Be gentle and confident. Be true with the knife.

  I removed four samples of the hypothalamus and passed them to Gutierrez. Two of the samples looked pretty good, the architecture intact, the tissue robust. But the other two samples, the ones from the back of the hypothalamus, looked somewhat worse. It wasn’t noticeable at first, but when I made the cuts the tissue sagged, crumpled, like a tired wall. I mentioned this to Gutierrez and she looked pleased. She wheeled out of the room to see if we had enough power in the generator to work the electron microscope. A solar-powered generator can only do so much when the sky never clears, she said, and she turned to leave, stopping at the door. We might need to power down other resources, she mumbled. It was the first time I had seen her look concerned. Then she turned to me. Find out what’s under the hypothalamus, she instructed. Something’s down there that’s making this tissue move.

  I used my fingers to explore, gently pulling at tissue to insert my hand underneath what remained of the brain. There was something there, without question. It was hard, like clay. Was it a tumor? A fungal infection?

  It moves with the rhythm of the heart, rising and falling with each cardiac contraction. Whatever this is has got to be at least functional tissue, part of the overall organism. And it feels as healthy as the hypothalamus, maybe even more so.

  Dammit, this is “healthy” tissue below the hypothalamus and I can’t correlate it with any expected brain structures. It has to be highly vascularized, it has to have ample blood and oxygen, to be this healthy, to be this tied to the beating heart. With a brain this sick, when even the gross pathology is completely abnormal, anything that remains healthy, anything that actually recruits its own blood supply must be there for a reason. Whatever this tissue is, it is vital to the success of the infection. It might even be central to the behavior of the zombie.

  As Pittman moved closer to study my dissection, whatever it was that I was feeling quickened its pace, seemed alive and alert. The subject flared its nostrils. Jesus, it looked like it could smell him.

  Readers may be alarmed that the subject remains awake during the procedures. It is important that this feature of the process not be confused with a property unique to ANSD Stage IV humanoids. In fact, even noninfected humans in sterile environments will remain alert during open-brain procedures, and the hypersterile environment of the Crypt laboratories was presumably still intermittently functional.

  Blum’s findings, however, remain some of the most perplexing aspects of ANSD pathophysiology. Prion infiltration usually invades much of the brain, and in all cases of successfully examined ANSD subjects, specific brain structures remain preserved or at least relatively preserved.

  If indeed a third contagion exists, its role might be to protect the brain from the rapid degradation that ANSD prions w
ould otherwise generate. This is the first new theory in more than a year, and we’re already looking at ways to investigate its validity. Maybe the key to a cure is to interrupt the protective properties of the third contagion. As Blum correctly notes, this kind of symbiosis—three contagions keeping the host alive, keeping it active, allowing it to spread the disease efficiently and widely—would almost certainly be an engineered plague. In fact, very few countries before the outbreak possessed the necessary technological knowledge to even conceptualize this disease. Our forensic teams are scanning biowarfare intelligence documents for signs of anything resembling even theoretical initiatives regarding ANSD. So far, we have found nothing to implicate any country, organization, or individual, but the process is ongoing.

  5:25 PM

  And that thing, that hardened mass below the hypothalamus?

  I was wrong.

  Not a tumor. Not infection. Robust, almost supernaturally healthy tissue.

  Grotesquely healthy.

  The masses are the amygdalae themselves. The crocodile brains.

  We’re dissecting crocodiles… crocodiles that used to be human.

  We’re dissecting monsters.

  We had planned to keep the subject animate for the entire dissection, but Blanca feels strongly that we need brain stem tissue for analysis. Severing the brain stem will deanimate the subject, but Gutierrez reminded us that additional subjects remain for further animate dissections. We need to know now, she said, why the brain stem stays functional.

  Using nine-inch serrated Yasargil neurosurgical scissors, the brain was removed from the spinal column at the C1 cervical vertebra. As expected, separation of brain stem from spine deanimated the subject, though the pupils remained pinpoint longer than expected. I suspect this was due to a heightened fight-or-flight posture even after initial deanimation. Adrenaline still runs high. The lack of immediate dilatation of the pupils that would be observed in normal human death is consistent with the increased sympathetic nervous system activity that characterizes Stage IV humanoids. Zombies are biologically primed for aggression at both anatomical and molecular levels. As I said, their adrenaline runs very high, even after the brains stop working.

  Removal of amygdaloid material.

  The brain stem itself is remarkable precisely because it looks so normal. It appears entirely intact. Sections were obtained from the pons and the medulla, key components of the brain stem itself, in order to study the reticular system of the subject. They’re called this because of the meshwork, the reticulum of primitive neuronal fibers that intermingle and communicate. These are the parts of the brain stem responsible for keeping us alert and aware.

  I made some rudimentary slides and studied them under the microscope. They’re damaged, but it’s unsettling how normal these samples looked compared with the soup we had to cut through to get these structures.

  There’s no doubt that these things are aware. Until I separated the brain from the rest of the body, it knew we were here. It is awake the way a crocodile waits for its prey. It would have bitten me even with most of its brain removed.

  Just above the brain stem, it looks like the cerebellar tissue is somewhat affected by spongiform changes but not entirely liquefied. Because the cerebellum helps with balance and coordination, this also makes sense. Anyone who’s ever been drunk knows what it’s like to try to walk without a healthy cerebellum. It’s a remarkable structure, constantly making minuscule changes, a computer really, devoted among other things to keeping our gait fluid and smooth. One of my professors in medical school used to call the act of walking “a series of catastrophes narrowly averted.” Your cerebellum averts the catastrophe, he explained. It keeps you on your feet, helps you to recover even before you’re about to stumble.

  ANSD tries to get at the cerebellum; I can see the damaged tissue, but the changes aren’t nearly as stark as in the higher brain regions. Slower degenerative processes in the cerebellum explain the initially intact gait of the infected, even though they all become increasingly unbalanced with time. That’s why they hold their arms out in front of their bodies: for balance and increased coordination. They just want to remain upright, on their feet. But the process continues, the cerebellum degrades, liquefies. Virtually all late-stage ANSD humanoids ambulate via crawling.

  The nearby hippocampal tissue also looks pretty good. Sure, it doesn’t look entirely healthy, but it looks functional. Because the hippocampus stores memory, this seems to explain those rare instances in which Stage IV humanoids seem to “remember.” There are numerous controversial reports detailing how zombies purportedly return to where they’ve previously fed.

  Gutierrez immediately began preparing the hypothalamus for study. She was careful to separate different hypothalamic regions—the ventral part was placed at one end of her work space, the medial at another, and the dorsal at the far end. She was sweating, working quickly. Her brow was furrowed and she kept stopping to wipe sweat from her eyes with the back of her hand.

  Zombies are always hungry, she said. They’re never sated. Why?

  I hope to hell we find out who did this, and I hope to hell that person is still alive.

  Whoever did this is as deranged as he is brilliant, and if we’re lucky, we’ll find him and understand the disease, his disease, that much better. Whoever made ANSD might have made an antidote as well.

  Or maybe not…

  We never developed a good antidote for radiation, but we made enough bombs to destroy the world about a hundred times over. Let’s hope our evil scientist had something besides destruction in mind.

  We dissected the eyes and optic nerves from the rest of the brain.

  I placed the eyes next to a measuring tape for Pittman to sketch. They appear normal in length and thickness, so it looks like the pathogen spares the eyes, just as it does other sensory organs. Again, this tells me that whatever made this virus meant for its host to see, to track its prey, to kill. It’s almost as if this were a botched attempt at creating a weapon. An army of these things could overwhelm almost anything.

  Signals from the brain to the muscles of the eye are probably at least somewhat disrupted—hard to imagine what they actually see—but this at least explains why zombies often misjudge the speed of their food or the distance they need to lunge. Still, they don’t need to be accurate. Just relentless. One zombie isn’t a problem, but a hundred zombies are bound to catch up with you. I think we are beginning to understand that ANSD is efficient and utilitarian. It preserves just what it needs to survive.

  Removal of intact eyes and optic nerves.

  When we first realized the scope of the pandemic, we weren’t ready. ANSD brain material was already so damaged, so frail. Conventional chemicals, routine laboratory preservatives intended to keep tissue samples intact proved too caustic for specimens taken from the infected.

  We thought we could go forward right away with all the tools, with the technological knowledge that we already had. We didn’t stop to consider that this was something novel, something we’d never seen before. When it became clear in those early days that our technology wasn’t fit to study the outbreak, a cottage industry of new laboratory equipment and chemicals developed directly from the need to better study these things. Industries finally came up with fixatives that could preserve ANSD-infected tissue without damaging it. For a very brief time, some companies got very, very wealthy.

  None of that matters now.

  Tomorrow we’ll open up the thorax and abdomen. Nothing says this virus only takes our brains—if we can find signs of infection, or protection for that matter, in the heart, the lungs, the gastrointestinal tract…

  If the brain is this damaged, then we need to understand why the rest of the body doesn’t give up. Complex organisms this sick shouldn’t last. Until recently, anything whose brain looked like what we’ve seen would have died quickly and completely even with the most advanced life support. But these things walk! They ambulate and feed, and presumably their hearts somehow
get blood to the vital organs, the lungs move air, their digestive tracts absorb at least some nutritional content. It would be good to know why—we might find areas of vulnerability that we haven’t yet considered…

  Think about it. Influenza usually kills by pneumonia. It usually drowns the lungs with pus and we suffocate, coughing until there’s no more air to cough.

  These things breathe.

  They cough and they sputter, but they continue to respire. Air goes in and air goes out. How the hell does that happen with anything this sick?

  I need to see the lungs. The disease is spread through respiratory droplets. We learned this early in the outbreak. People spread influenza through coughing, through blowing their nose, and in the beginning this looked just like influenza.

  Except almost every strain of influenza encounters natural immunity, and no one is immune to ANSD. It may look like influenza, but it behaves differently. Again, it behaves like someone accounted for the inherent immunities of naturally occurring viruses. It behaves like someone wanted it to be this bad.