The 0.00 Result
The 0.00 Result
A story I didn’t want to write
I was planning to write a different article.
After 17 years of living with a multiple sclerosis diagnosis, after insisting on thorough tests that my doctors thought unnecessary, after trusting math and statistics more than medical authority, after questioning impressions presented without evidence as though they were certainties—I was finally going to write about how my diagnosis was revised. How the data had been there all along. How persistence and probability theory had led me to the truth.
The process took years, not because I was relentlessly pushing, but because I doubted myself. I knew I was biased. I knew I would prefer one diagnosis over the other—the treatable infection over the incurable disease. That awareness made me hesitant. I second-guessed my conclusions. I delayed advocating for what I believed was the right diagnostic course of action, always wondering if my reasoning was motivated by hope rather than evidence.
It should have been an article about trusting math. But also about trusting oneself.
But that’s not the article I’m writing.
The Beginning
In 2005, I traveled to Ghana. Shortly after returning, I developed Katayama fever—a telltale sign of schistosome infection. I received treatment with praziquantel, the standard antiparasitic drug. Case closed, or so everyone thought.
A year later, neurological symptoms appeared. Sensory disturbances. Strange MRI findings. Long, dorsally-located intramedullary lesions with mass effect and contrast enhancement—an atypical pattern for relapsing-remitting MS. But the parasites were gone, they said. The infection was treated. What remained must be something else.
The doctors in 2006 concluded with apparent certainty that the schistosome infection had been eradicated. Years later, I would revisit their reasoning—applying Bayes’ theorem to the evidence they had cited. When I combined the actual probabilities of their diagnostic arguments, the math told a different story. Far from near-certainty, the calculation suggested neuroschistosomiasis was substantially more likely than multiple sclerosis. But at the time, I trusted the experts.
I was diagnosed with multiple sclerosis.
For the next six years, I lived without MS medications—and I was stable. No new lesions. No Uhthoff phenomenon despite saunas and African holidays. In retrospect, this stability without treatment was itself unusual for MS. But I didn’t know that then.
The Decline
In 2012, under stress, I experienced optic neuritis. I started my first disease-modifying therapy. And then something strange happened: I got worse.
Each medication—Copaxone, dimethyl fumarate, Aubagio, Ocrevus—seemed to accelerate my decline. Walking distance dropped from 12 kilometers to under 4. The heat sensitivity I had never experienced suddenly appeared. By 2022, I was using a wheelchair.
I couldn’t prove causation, but the correlation was impossible to ignore. Every immunosuppressive treatment designed to slow MS seemed to be making things worse. What if, I began to wonder, these drugs weren’t helping because I didn’t have what they were designed to treat?
The Evidence
In 2023, a serum PCR test came back positive for schistosome DNA.
Seventeen years after my “treated” infection. The parasites had never left.
The implication was staggering. What if my entire MS diagnosis had been built on a false premise—the assumption that the 2005 infection was cured? What if the immunosuppressive MS therapies had actually allowed the parasites to cause more damage? What if I had been treated for the wrong disease for nearly two decades?
I dove into the literature on neuroschistosomiasis. The clinical picture was plausible. Spinal cord involvement. Granulomatous inflammation. The way prednisolone dramatically improved my symptoms while standard MS treatments made things worse. It all seemed to fit.
The Rollercoaster
What followed was a diagnostic odyssey marked by hope and uncertainty.
A 7-Tesla MRI in September 2025 showed multiple FLAIR-hyperintense lesions with paramagnetic rims and central vein signs. The radiologist’s verdict: “typical for a demyelinating CNS disease.” But we know so little about what chronic neuroschistosomiasis looks like on MRI, especially after 20 years of potentially counterproductive immunosuppressive treatment. The findings were suggestive of MS, yes—but they couldn’t rule out parasitic damage that had been mismanaged for two decades.
I started high-dose prednisolone. My standing improved. Transfers became easier. The medication that should have merely dampened an acute MS relapse seemed to be addressing something more fundamental.
We developed a diagnostic protocol: baseline antibody titers, intensive praziquantel treatment under steroid protection, then cerebrospinal fluid analysis at the optimal window for detecting any schistosome-specific immune response in the central nervous system.
In December 2025, we launched the nuclear option.
Praziquantel—the antiparasitic drug—is normally given for a single day. That’s usually enough to kill the worms. I took it for three consecutive days, 6 grams each day. But we didn’t stop there. We added cimetidine and grapefruit juice—both known to inhibit the liver enzymes that break down praziquantel, dramatically boosting blood levels of the drug. This wasn’t a standard treatment. This was scorched earth. If any schistosomes remained anywhere in my body, this protocol would annihilate them.
We measured antibody titers before this assault. If living parasites or eggs were killed, the dying organisms would release antigens, and antibody levels would rise in response. This would be the proof.
The Test
On January 12, 2026, four weeks after the antiparasitic treatment, I underwent a lumbar puncture. The timing was deliberate: if there were schistosomes in my central nervous system, the post-treatment period would show elevated antibodies against them in the cerebrospinal fluid.
The results painted a clear picture—just not the one I was hoping for.
Despite being on 75 mg of prednisolone daily (which suppressed my systemic immune markers significantly), my cerebrospinal fluid showed massive intrathecal antibody production: 29% local IgA synthesis, 27% local IgM synthesis. My central nervous system was actively producing antibodies against something.
Then came the Swiss Tropical Institute results.
First, the serum antibodies: the titers before and after the intensive praziquantel treatment had not significantly changed. No spike. No immune response to dying parasites. The nuclear attack had found no targets. There was nothing to kill because there was nothing there.
But the definitive answer came from the cerebrospinal fluid:
Schistosome antibodies in the central nervous system:
- ELISA Adult Antigen: 0.00
- ELISA Egg Antigen: 0.00
- IFAT: negative
Zero. Not weakly positive. Not borderline. Zero.
What the Numbers Mean
The logic is inescapable. My central nervous system is producing a massive inflammatory response—IgA and IgM antibodies nearly three times the normal rate—despite heavy immunosuppression. But those antibodies are not directed against schistosome antigens.
The unchanged serum titers mean the nuclear assault was unnecessary—there were no parasites to kill. The faint positive serum results are nothing more than immunological memory of the 2005 exposure. The parasites are not in my brain. They are not in my spinal cord. They are not responsible for my neurological disease.
The 0.00 result doesn’t leave room for interpretation.
Diagnosis: Multiple Sclerosis
After years of uncertainty, the diagnosis is now definitive: I have multiple sclerosis.
Not the typical kind. My immune pattern is unusual—IgA and IgM dominant rather than the classic IgG pattern. My oligoclonal bands changed type between 2023 and 2026. My blood-brain barrier remains intact despite active inflammation. The disease doesn’t quite fit the textbook.
But it is MS.
What Now
The high-dose prednisolone is being tapered—it was protecting against a threat that wasn’t there.
I’m back to facing the disease I was told I had 20 years ago. The same disease I questioned, doubted, and sought alternatives to. The same disease whose treatments seemed to make me worse between 2012 and 2022.
I don’t regret pushing for answers. The positive serum PCR in 2023 was real evidence that demanded investigation. The diagnostic uncertainty needed resolution. Now it is resolved.
But what I hadn’t fully appreciated was how much I had been living in suspension. With the parasite hypothesis, there was always a future state to wait for: after the diagnosis is confirmed, after the treatment works, after the inflammation subsides. Major life decisions could be postponed. Planning could wait. Everything was contingent on a resolution that would change everything.
Now I have that resolution—just not the one I wanted.
There is no dramatic recovery on the horizon. Instead, I face the questions I had been deferring. How long will I be able to travel alone? Will I be able to travel alone again? How much assistance will I need in the years ahead? These are no longer hypotheticals to be answered “after treatment.” They are the terrain I must navigate now.
And I’m navigating with massively reduced bandwidth. The disease takes not just mobility but energy—and time. Hours for sleeping, hours for exercising, hours just to get dressed. Every day requires conscious choices about how to spend what capacity remains. Not everything can be pursued. Not every goal is realistic. I have to choose—really choose—what matters enough to warrant the cost.
The Hope That Wasn’t
I had hoped to write about a misdiagnosis corrected. About how trusting data over authority revealed the truth. About a treatable infection masquerading as an incurable disease.
That narrative would have been satisfying. It would have validated years of questioning. It would have offered a path to healing.
Instead, I’m writing about the limits of hope. About how sometimes the evidence leads you back to where you started. About how even the most rigorous diagnostic pursuit can confirm what you didn’t want to believe.
The 0.00 result is unambiguous. And so I move forward—not toward the cure I imagined, but into the reality I have.
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