Chronic Wasting Disease

A misfolded protein. The phrase harkens back to wrinkled dress shirts, drunkenly rumpled into the wrong drawer, more than it does a progressive degeneration of the brain, unfurling out of sight like a sleight of hand trick.

Of course, deer affected by Chronic wasting disease have no inebriated anecdotes such as these to forget, no stories of returning from wild nights out too sloshed or too stoned to fold their clothes. Memories of drunk drivers plowing through herd mates might be most analogous to such recollections, as they slip from a doe’s mind like drool from her plague slackened mouth.

Simply put, misfolded proteins, or prions, are normal proteins with their shapes gone awry, so swollen with sickness that they cannot help but strangle their neighbor proteins to the same point of malformation, mirroring their own disfigured bodies, their horribly squashed figures. Here, the words bodies and figures must not be taken as synonymous with living creatures, for prions are not alive. They do not contain DNA or RNA. Every being, from viruses and parasites to newborn fawns still pink with afterbirth, must check one or the other three- lettered box to be placed in a category with the living. Chronic wasting disease is not some malevolent, sentient varmint hell-bent on annihilation, but a contagion of mutation. There is no evil beast doing the killing; the prions merely inhabit, set up shop, and make a few modifications. It is the deer’s cells themselves that turn a terrible shape of death upon the animal.

There are stages to dying from the inside out. Such an invasion’s demise takes time.

The infiltration of prions becomes more apparent the longer the proteins incubate, the longer the deer unknowingly houses a suburb of the deformed, festering things in their central or peripheral nervous system. It’s not as if an early diagnosis is imperative, anyways. A definitive labeling of the disease can only be made postmortem, so there’s no need to stamp a CWD seal on the animal at the onset of any off-putting behavior.

Loss of fear toward people is one of the first subtle characteristics of the deer on its way to decay. It is human nature to mistake this early sign of a spreading infection for a woodland creature’s enchanting friendliness, a chance Bambi-esque encounter, some deep-seated level of understanding from one species to another. But if an approach is made with little to no inhibition and the deer is slack jawed and glassy eyed, CWD is far more likely to be the culprit than any folkloric crack of magic.

Some steps in the direction of death are conspicuous, displayed by virtue of ribs visible through emaciated frames or fur coats so shaggy and tufted, they resemble feathers. These symptoms, worn on the deer’s body like shirtsleeves or a suffocating second skin, are often accompanied by postural stoops: gaits punctuated by staggers, heads draping off crooked, flower stem necks low enough to graze the grass, ears that wilt as they do the same. An increase in fluids occurs on all fronts; excessive salivation is accompanied by heightened thirst, is accompanied by frequent urination. For the deer unable to bend his legs and maneuver his neck downwards to meet the stream, these are utterly unmeetable urges.

Even so, increasingly blatant proof of unwellness may be written off as the byproduct of a particularly cruel winter, and affairs of the mouth and bladder were once accounted for by such shallow explanations as emotional state. (See: Hippocrates fretting about the body’s liquid humors.) It ultimately matters not whether the deer’s maladies are given their proper name or placed under the correct causal umbrella. By the time any speculation is made, it is already too late.

Once the deer exhibits noticeable signs of disease, it is undeniable that the prions started their interior renovations long before the illness-inducing endeavors were reaped. Likely, the shapeshifting proteins made themselves at home well over a year before the mammal visually began to deteriorate. They silently constructed a settlement of squatters, lurking behind preexisting cells soon to be subdued. A year’s worth of work, the prions’ overdue inside job, is sowed within the deer’s final months.

There is no known cure. Autopsies of deer ravaged with the disease reveal brains riddled with holes, like pulverized sponges.

Chronic wasting disease belongs to the same sadistic family tree as mad cow disease, Alzheimer’s, and Parkinson’s, alongside a handful of other morbid neurodegenerative disorders. Such a roster carries with it some commonalities: loss of memory, loss of control, loss of self. Human understanding of said phenomena, though not all encompassing, is assumingly far vaster than deer’s comprehension of neurodegeneration. Especially that of a fifteen-month-old fawn, the youngest noted case of an animal succumbing to the sickness. In comparison to a human lifespan, this creature would barely have been a teenager.

It's incomprehensible, the fear that must be felt by the deer with a brain turned to holey mush. Does a mother doe, in bewilderment thick as fog, forget a fawn she had in tow? Does a broad-chested buck, once proud to sport his antlered crown, fail in lifting his head to see which way he stumbles? What is it like to forget as an animal, when forgetting itself is a foreign concept?

Though the disease’s methods of spreading (direct contact between animals, bodily fluids contaminating food and water sources) are scientifically understood, its origin is beyond human insight. There is no knowledge regarding how the augmentative, sleeper agent proteins came into existence. Research mostly seeks to uncover a cure for the illness, a yet fruitless pursuit, and make certain that people are free from the danger of wasting away like the withering deer. Currently, the disorder leads solely animals to slaughter, (its jettisoned carcasses somehow still safe to make into venison steak or stew) but experimentation on human susceptibility involves injecting rodents with brain tissue extracted from infected cadavers. The lab mice, with their human adjacent genes, pay the price of bearing such an ideal genetic code for precautionary testing. An ironic redistribution of evil.

Say a prion metamorphosizes, finds a way to sidestep species lines. Say the disease’s days of staying in the deer’s lane are over. Say it takes on people as a new renovation, tries driving through the bodies of humans next, like a haphazard station wagon pummeling roadkill, a collection of red stains upon its bumper. Surely, no fault could be pinned to a mere misfolded protein, unalive as it is. But maybe fault can be credited when there exists a purposeful administration of suffering for the sake of another species’ survival; when the disparity of sentience is vast, and an understanding of what it means to forget is all but universal.