All it takes is one drop of vermincholie. The substance is a deep, dark green, bearing a rainbow‍-​sheened iridescence where the light dares touch it. Thick, slimey, with the consistency of oil turned to sludge, it lies in wait, stoking an ever‍-​present heat.

The touch of cold air prompts an immediate reaction akin to oxidation or combustion, a patina of grey insulation forming over the liquid’s surface. It is a yolk that grows its own leathery eggshell, a self‍-​incubating egg.

The touch of warm flesh, by contrast, cracks open this skin and out pours vermincholie, seething like always hot oil. It sears flesh acidically and infects that new wound with a viral payload. The affliction? Ovirexia. In its early stages, it overwhelms the immune system with a plague’s virulence. Fever and tremors, but you notice all fluid discharge soon becomes sour and stinging.

If hale and hearty, you can resist it, just as with any disease. It might only take one drop, but further draughts are required to render this fate inescapable.

The true teleology of ovirexia is a unique delirium. The head will ache, dreaming nightmarish notions that writhe and enthrall. The soul itself is infected, a metabolic ritual to catalyze the production of emyra, glowing fruit of the mind and amply‍-​studied alchemical component. Production waxes to a peak each night, in eye‍-​fluttering dreams that leave the heart pounding with climatic intensity. A forced cathexis.

One can almost see the light that glimmers behind the eyes of those in the throes of ovirexia. Emyra is born, mote by mote, and drains like waste into the veins. This metaphysical enrichment renders its victim alluring, ever more delectable to predators hungry for souls. The host now bleeds nectar.

If infected for long enough, emyra builds up throughout your biology‍ ‍‍—‍ in the fat, in the muscles, in each and every tissue. You become a treat at once irresistible and empowering.

Ovirexia is a virus, but it is a disease with a certain pluripotence. Not just a matter of mutation and adaptation (how else could it so relentlessly overwhelm the immune system?) but the genetics prefigures a kind of evolution or ontogenic recapitulation. It does not stop at constructing mere capsids; when the virus grows dense with the conquest of the host, they swell and burgeon and specialize, metamorphosing into cell walls replete with organelles.

One may speak the words spontaneous generation, but far from it; this is a slow process. So many would‍-​be cells promptly commit apoptosis, having suffered too many mutations or simply lacking the epigenetic mandate of heaven. The sequences will be retranscribed again and again, generations crafted then discarded, before a suitable egg cell might emerge.

This could take years. Not quite an inevitability‍ ‍‍—‍ a host may not remain infected for long enough to complete this process, or their infection may not advance to an intense enough stage. But in potentia? Vermincholie is more than a fomite for viruses. This is the foundation and fuel for ovigenesis.

Too easy to misinterpret vermincholie as a mere liquid egg‍ ‍‍—‍ it is moreso the seed that makes a womb of its host.

These are the steps of your enthrallment.

Entiote eggs affix to prey as if glued. As one or many, outside the body or within, whether you were vermincholie’s afflicted womb, or were instead victim to oviposition by a queen’s conception, this gravid froth yields larvae, eager and squirming.

Each hatches and burrows into your flesh, like blowflies or ticks or lice. When you sleep, many will crawl forth to migrate across your body in the fashion of bedbugs, seeking better spots to hide and feed. The ideal would be securing access to your digestive system.

Ovirexia had begotten entiote and likewise does entiote beget ovirexia. The virus warps the host’s chemistry to accommodate its guests. A subtle progression, but it marches in step with the wounds becoming well‍-​populated habitats.

When alone or in scarce company, the larva can complete metamorphosis and depart as a teneral after as little half a moon, though often closer to twice that. The first blightfly from a newly‍-​infested host is a small and unimpressive specimen, living a simple omnivorous life of pollination and blood‍-​sucking, opportunistically dining on fungi and carrion, soon to mate and seek a new host for oviposition.

Yet because this disease adapts the host to entiotic ends, a gravid imago will prefer your changed scent, covered in pheromone‍-​marked scars and stinking of ovirexia.

A single entiote finding a host can multiply again and again until generations of crowding larva pervade the flesh. The odds that a questing worm could arrive at so modest a goal‍ ‍‍—‍ entering the gut‍ ‍‍—‍ would naïvely approach certainty. If nothing else, a self‍-​sustaining infestation is quite difficult to excise. Not without venturing into measures extreme.

Still, we now arrive at the first major fork in this branching evolution. Because if it were merely a matter of eventually reaching the gut, then the dice could be cast indefinitely. But would you host this infestation forever? Could you maintain a social life, surrounded by so many flies swarming necrotic flesh? Could your body endure this strain?

No, and thus the infestation operates on a clock.

So what happens if the larvae had achieved the goal and breached the digestive system? Or better yet, if the eggs were lucky enough to hatch there in the first place‍ ‍‍—‍ perhaps because the hosts food came laced with this gift?

A few will reach the intestines and grow fat there, unconstrained by any need to move or hide. Much less work to be done‍ ‍‍—‍ now one can simply gorge oneself on the hosts’ meals (a theft which encourages the host to eat more and more) while one steadily grows longer and thicker. Eventually, there are enough larvae crowding the guts for the stomach to bulge. But that doesn’t mean the growth will cease.

Imagos can continue depositing eggs and thus larvae even after the host wanes in the strength or ability or willingness to keep feeding. But the same scent‍-​cue that advertised your body as a promising oviposition site can instead deter further additions.

Even after no more space remains in the gut, your accumulated brood can simply burst outward and infest the other internal organs. Naturally, no host will survive long with a chest so full of hungry spawn unleashed; maggotslime drowns your lungs and your ribs burst while the heart is devoured.

This is a natural, ideal process of infestion‍ ‍‍—‍ the parasitoid lifecycle.

A special note is to be made of alternatives to the gut. It’s the ideal, but it’s not the only place the maggots can take up residence. The reproductive system could provide refuge‍ ‍‍—‍ mainly in cases where the host has a womb. Advanced manipulation of hormones may even persuade the body to direct nutrients to the passenger of its own accord.

Nor is this the only possible outcome of the larvae arriving in the digestive system, but before explaining the alternative, it is illustrative to examine what happens if the larvae do not achieve this.

So: suppose they never make it to the intestines. This means all must survive by subtly draining blood and fat deposits. What exactly happens next depends on the host’s response.

Most obviously, you may notice the bites, a growing weakness and fatigue, the inflamed sickness of an immune system expelling invaders. You’ll grow weary of the swarms of blood‍-​sucking flies so relentlessly in pursuit. If you examine yourself carefully, you will notice the wounds, the blisters‍ ‍‍—‍ you might even catch a worm in the midst of its wriggle‍-​scurry across an exposed stretch of skin, darting to the cover of a patch of hair.

When you scratch at the wounds, tear out and squish any larvae you spot, wipe yourself clean, you are creating selection pressure for the larvae to adapt and hide from notice.

Thus, energy will be diverted from just feeding on the host to camouflage. This already happens on a chemical level‍ ‍‍—‍ sucking up genes and hormones to imitate the chemical signature of your biology, avoiding the immune system’s notice‍ ‍‍—‍ and eventually it also happens on a physiological level.

The metabolism of the larvae slows down, hibernating patiently instead of pupating. The pattern and rate of feeding both become intermittent and cryptic.

At an extreme, the worms will devour the host’s muscles, hooking on attachment sites with teeth and tail‍-​spikes, or cutting open your vessels and transfusion‍-​routing your blood through a larva.

Alone, the larvae would struggle to achieve this substitution (it’s quite the feat of coordination and ingenuity), but with the stigmergy of several generations of entiotes, crafting prosthetics like nests?

Piece by piece, your flesh stops being your own. It still responds to your nerve signals‍ ‍‍—‍ for now, so long as that aligns with the agenda of all. Behave yourself well, and you earn consideration as sibling to the worms within; you await a profounder pupation‍ ‍‍—‍ to be transformation free from this flesh.

This is the fusomorphic lifecycle. It is the high road to total assimilation.

But again, the word is adaptation‍ ‍‍—‍ it cannot happen if there’s no need for it to happen. You may have seen depictions of patients with necrotic wounds that have decayed to the point of having maggots visible in exposed cavities. And of course, those awareness campaigns telling you to check for suspicious lumps wouldn’t be necessary if everyone noticed these things. It is entirely possible, given the right host in the wrong circumstances, for the infestation to develop to an advanced stage essentially untreated.

Thus, the maggots may aggregate into a tumor‍-​nest and extract nutrients with little if any pretense of mutualism.

Now, this scenario easily mirrors one of the cases we’ll discuss later on, so what’s essential for a unique outcome here is that eventually, this affliction becomes taxing enough that either the host is forced to finally seek treatment for it, or the host begins to outright fail in gathering sufficient nutrients for the parasite.

Importantly, this all must happen while there is still resources for the entiote to extract; the infestation remains larval and anticipatory. A milestone common to all these advanced routes of infestation is that the pupation halts and synchronizes.

Like this, the larvae can coordinate and achieve several instars of growth beyond what’s necessary for simple metamorphosis. Yet postponing the life cycle like this presents a vulnerability; if critically threatened, the larvae have sacrificed the ability to quickly mature and escape. (Or at all: those molded into fusomorphic function can no longer undergo normal pupation.)

As a result, the parasite will be forced to divert resources from extraction and growth toward self‍-​preservation, or even reinvestment in the host’s survival. This can mean synthesizing hormones like dopamine and adrenaline to motivate behavior, and it can mean repairing atrophied muscles and necrotic flesh with the same techniques of replacement‍-​imitation outlined in the fusomorphic lifecycle.

But this outcome is a bit different. What distinguishes it is that here, the parasite isn’t hiding, nor is one integrating into the hosts’ biology. Rather, one is colonizing you. The parasite has centralized in the tumor‍-​nest, and only extends larva‍-​tendrils into the the limbs or hormone‍-​signals into the bloodstream as something more akin to puppetry.

So that serves as a decent enough name for this: the quasicolonial lifecycle. A callous and abortive faux‍-​assimilation.

But remember that first fork in the road? We didn’t finish exploring the other branch.

So, imagine the larvae had arrived to a secure place deep within the body. This naturally implies that while a few are living out the easy life inside the guts, one’s sisters are still scraping by outside. How does the other half live?

In most cases, the intestinal larvae will secrete covert hormonal messages into the blood, coordinating the colonies elsewhere in the host. If there are larvae in the gut, these hormones will suppress the formation of any rival tumor‍-​nests‍ ‍‍—‍ which are just pale imitation of the gut‍-​palace, after all.

This means that remaining larvae will be directed toward fusomorphic behavior. This can easily transition toward the quasicolonial or outright fusomorphic, especially if the environment demands parasitic adaptation to survive, or the host makes an effort to get rid of the infestation. (But I repeat myself.)

Still, unique behavior can emerge in cases where the host is accommodating and the environment fruitful. This mean balancing on a knife’s edge. The parasite must grow integrated enough into the hosts’ biology to render self‍-​destructive the prospect of outright parasitoidism, yet not so intertwined as to advance to total assimilation. It remains a pampered guest‍ ‍‍—‍ free to leave at one’s whim.

This is the ovitransitive lifecycle. Generation after generation of entiote imago can be nurtured in the same host.

Thus defined, these are the four major modalities, but the nature of a such a flexible lifecycle is that possibilities still abound.

A fifth mode, subtlest of all, can be most clearly outlined now that these last three have been defined. Quasicolonialism implies a certain usurpation of the nervous system; fusomorphism implies a total conversation of all limbs and organs; ovitransitivity implies a kind of independence from the body.

If those absolutes are not achieved? If the parasite is limited by the host, if the transformation‍-​conquest reaches a stalemate, if the larvae grow too used to the shelter and indulgence of the body? You could almost imagine it the transplant of a new organ, a xenograft. This is the endosymbiotic lifecycle.

We can continue: what happens if the host is lackluster‍ ‍‍—‍ in biomass (obviating parasitoidism) or in knowledge (obviating assimilation)‍ ‍‍—‍ and the parasite would prefer a mulligan? Larvae simply infest flesh; should one be lucky, one can migrate to a new host. Luck, or cunning: a host could be molded into vector replete with larvae and manipulated into infesting others.

But if all victims remain viscerally in contact? Fusomorphsis is, at its core, the weaving of new anatomy‍ ‍‍—‍ what might result from entiotes able to freely slither and insinuate between many hosts? (It’s there in the name; fusomorphosis happens because the because the boundaries between organisms are so easily blurred.)

But we are getting ahead of ourselves.

Now that we’ve enumerated various outcomes, let us finally illustrate the most important difference between them all. We have concerned ourselves with larvae‍ ‍‍—‍ one is left to wonder, then, what complexities await upon chrysalis and emergence. Is the unimpressive blightfly the destiny of this species?

Far from it: the gropings of swarmling imagos are best considered an intermediate life‍-​stage, a kind of metaphorical larvae transitional toward the true acme of entiotes.

Grasshoppers, when great in number, instead give rise to locust swarms. When a larva entiote finds itself crowded and drinks in the appropriate pheromonal cue from the blood, one will postpone one’s pupation.

All will ruthlessly extract and extract, all will grow and mutate, and when all is ready, the final chrysalis, half‍-​woven and half‍-​secreted, will engulf the entire agonized corpse‍-​to‍-​be. All larvae deliquesce into an incestuous, indeterminate soup of biology from which shall spring a colonial chimera organism.

The plague summoned by this ritual is what we call the chrylurk.

And she will need more hosts to feed on and lay in.