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The Wyrms of &alon
15.2 - Polyphagia

15.2 - Polyphagia

There were some things you didn’t bring up in polite conversation. Engoliss’ disease was one of them. That Horosha—a self-confessed Angelical Lassedile—had brought it up spoke volumes about his character. Either he was blissfully free of any qualms toward sexual abuse by the clergy,—in which case, he disgusted me—or his faith was so perfect that he could continue to believe even if the Angel Himself came down and told him that humanity had gotten His message all wrong.

I’d heard of Engoliss’ disease, both because of the neurological fallout it caused, and because the outbreak of Engoliss that had unintentionally elucidated monstrous of sexual abuse of children perpetuated and covered up by the Church behind closed doors. The outbreak had only really come to light in the past decade or so, but it had eked out an existence under the radar, so to speak, for generations. Of the innumerable denominations of the great and holy Lasseditic faith, the only ones that had emerged from the scandal without a blight upon their reputations were the ones which were so liberalized that barely anyone attended them.

The widespread outbreak of chronic Engoliss’ across the country revealed the Church’s quincunx sin: its celibate clergy, whose sexual improprieties spread Engoliss’ among them; its celibate clergy, whose sexual improprieties spread Engoliss’ among the laity; a vainglory so great that the Church would not dare stoop to paying for the treatment of the infected clergymen; a vainglory so great that the laity refused to acknowledge the epidemic or take actions to end it; and a faith whose policy was to shield the abusers from righteous justice and sweep every trace of their abuses into the darkness underneath the proverbial rug.

Engoliss’ disease was caused by a protozoan. The infection could only be spread through contact with bodily fluids, and while it was possible to become infected by being exposed to infected blood on an open wound or a mucous membrane, in practice, the disease was spread almost exclusively through sexual intercourse—vaginal, oral, anal. Following the initial infection, there would be only mild, non-specific symptoms, with one exception: small chancres at the infection site. That was the acute phase. But after a couple of days, those symptoms abated, and then the pathogen would hide away inside the body for decades—thirty years on average, though it could sometimes go up to fifty—at the end of which, the symptoms of chronic Engoliss’ disease would appear. Mood swings set in, followed by decline in organ function—heart, liver, and kidneys. Of course, by then, it was too late for treatment. Memory loss frequently ensued as the mood swings steadily intensified—spirited mania, crushing depression, unquenchable rage. From the time of the first onset of chronic Engloss’ disease, it was a race between multi-organ failure and central nervous system damage to see which would kill the victim first.

Dr. Horosha looked around the room, to see if it was safe to continue. Heggy looked exceptionally troubled—of all the people I knew, only my wife had greater difficulty discussing the Engoliss scandal—but our recent acquisition from Noyoko General was apparently not going to let that deter him from his line of inquiry.

“Moreover,” he continued, “it is well-known that Engoliss is endemic in Trenton. It is not outside the realm of possibility that the Engoliss protozoan underwent mutations thanks to the recent rash of outbreaks in Trenton, due to—”

“—Hold your horses, Dr. Horosha,” Heggy said. “It’s not even lunchtime yet. Let’s belay that level of controversy for a more… appropriate time.”

“Dr. Marteneiss, as devout of an Angelical Lassedile as I am, even I would hardly call it controversial, certainly not from an epidemiological perspective. It is a truth universally acknowledged that the occurrence rate of Engoliss’ disease among seminary-trained clergy of the rank of Luminer or higher is over an order of magnitude greater than that of the general population, due to—”

“—So, what other treatment recommendations do you have for us, Dr. Derric?” Heggy said, cutting off Dr. Horosha altogether.

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Although Dr. Marteneiss wasn’t anywhere near as religious as my wife, she was still dedicated to the Church and its purported integrity, enough that she wouldn’t hesitate to clamp down on any talk that suggested otherwise. It was hard to talk to her about it even in private. For Heggy, I think it was the Church’s sheer institutionality which most mattered to her. She was the most lawful person I’d ever known—in the Alignment Chart sense—and I couldn’t begin to imagine how difficult it must have been for her to swallow the bitter pill of Church’s inner decay.

I made a mental note to ask Dr. Derric at some point in the future about what he thought of the Engoliss scandal. If he gave a half-decent response, maybe there was still some hope for him yet.

“I’m glad you asked,” Jonan said. He advanced to the next slide of his presentation.

The heading on the wall changed to Immunostimulants — Our Ace in the Hole.

“In addition to the enzyme inhibiting drugs, I think it is essential that we consider the array of immunostimulating therapies that have been developed for treatment of systemic fungal infections.”

“Now wait just a minute, Jonan,” Ani said, “immunostimulants are meant to help people with compromised immune systems—cancer patients, organ transplant recipients, and the like.”

“I think it’s worth a shot,” Jonan said, “and we’re in no position to look a gift horse in the mouth. There’s a whole spectrum of new and emerging therapies meant to strengthen the immune system in people suffering from systemic fungal infections.” Terms spelled themselves out on the wall, one bullet point at a time. “We’ve got macrophage colony stimulating factor, interferon-γ, and cytokine therapy—specifically Granulocyte Colony-Stimulating Factor (G-CSF) and Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF). It might very well be the case that the reason for the virulence and severity of NFP-20 is because the infection deleteriously affects our immune systems.”

“This… this all seems very advanced,” I said, trying my best to contribute. To say that I felt out of my element would be an understatement, to say the least.

“But isn’t there also the chance that immunostimulants could cause patients’ immune systems to overreact and damage their bodies in the crossfire of their attacks against the infection?” Ani asked.

Horosha nodded. “Indeed, viral infection can, in certain cases, lead to hypercytokinemia, where the body’s own defenses can cause severe damage to multiple organs, often leading to death.”

“Cytokine storms are a valid concern,” Jonan said, “thankfully, synthetic variants of GM-CSF have been developed to preferentially stimulate the growth of either the pro-inflammatory or anti-inflammatory varieties of macrophage, and the latter works to counteract pro-inflammatory chemical signals by secretion of the appropriate interleukins. So, in the event patients’ immune systems happen to get out of control, we can just stimulate the growth of these ‘calming’ macrophages and bring things back to normal.”

Dr. Horosha laughed—a single, strong guffaw. “I am not easily impressed, Dr. Derric, but you appear to be the exemplary exception."

“I’d like to double check your sources myself, Jonan,” Ani said, “just to be safe.”

“Speaking of antifungals,” Heggy said, “what’s our plan of attack going to be? What’s our ground game?”

“What do you mean?” I asked.

“You always gotta be careful with internally administered antifungals,” Heggy replied, “especially with patients with pre-existing conditions. Like Jonan said, most orally or internally administered antifungals come with risks, not to mention some significant side-effects. Intestines, liver, kidneys,” she glanced at Jonan, “what Dr. Derric mentioned.”

“We should prescribe with discretion,” Dr. Horosha said, “and we should be taking into account the circumstances of individual patients.”

“After miforol, I think bluzepinab and gimotlin are probably our best bet,” Jonan said, “in addition to the standard meds. Also, we’d be remiss if we didn’t keep ulfinact on the table.”

Ulfinact?

Once again, my mind flashed back to my medical school days—this time, to a neuropharmacology seminar. Ulfinact was one of the few medications capable of treating Nodding Sickness. The arsenic-based drug was able to penetrate the blood-brain barrier, and thereby attack the protozoa responsible for the otherwise terminal disease.

“Isn’t ulfinact an arsenic compound?” I asked.

“That it is, Doc.” Jonan nodded. “But… look at the bright side: testing a wide spectrum of drugs on different patients will expedite the determination of which medications work best.”

“So… broad spectrum antifungals and immunostimulants,” Heggy said. “Anything else?”

“Yes,” Ani answered, wryly, “the wonderful worlds of PPE and Quarantine protocol.”

Oh joy…