Acute Flaccid Myelitis
Quick, what looks like polio, can be mistaken for polio, but gets almost zero press?
Why, it’s AFM, or acute flaccid myelitis.
Briefly, children coming down with a stomach bug can become paralyzed. Yep, paralyzed. So why aren’t we more upset? Because public health officials tell us it’s very rare.
How rare? We’re not sure, because we don’t monitor stomach flu in the U.S.
But let’s take rareness as a justification for non-concern.
Remember Zika virus? How we lost our minds over that disease? Any idea how many people died of Zika in the U.S.? Maybe one?
Or pick the most recent recall of all romaine lettuce in the U.S. and Canada. How many people died of that outbreak? No one. Only 32 people even got sick.
So rarity is not a reason for not publicizing a disease that is by all accounts more common and has worse long term effects.
AFM is nasty, and hopefully we can stop it before it becomes more common.
Where did AFM come from?
This isn’t a new issue, it’s an ongoing story from a few years back. As a country, the U.S. stopped screening for paralysis since polio cases stopped. But after hearing a few case reports, California started screening again in 2012. Out of two hundred reported cases, California public health determined 59 patients had AFM. Of these, two older patients died. The average patient was around nine years old, and after almost a year of follow-up, only 7 had fully recovered from the paralysis.
That’s bad, because it sounds a lot like while we’ve been focused on one cause of childhood paralysis, we entirely ignored another.
Children who continue to have weakness will have that weakness even after the brain and spinal cord are cleared of lesions. Following 8 children for over a year in Colorado, most showed continued atrophy of their muscles.
So, what do we know about AFM?
- 90% of patients had a respiratory or stomach flu before getting AFM.
- AFM also occurs in the fall, between August and October, so tons of kids are going to have respiratory illnesses around that time.
- While we’d like to think we had a culprit, it’s not that likely. “We detected coxsackievirus A16, EV-A71, and EV-D68 in the spinal fluid of four of 484 confirmed cases of AFM since 2014, which points to the cause of their AFM. For all other patients, no pathogen (germ) has been detected in their spinal fluid to confirm a cause.”
- To translate into English, we’ve got something that attacks the spinal cord. In less than 1% of cases we found something, but we’re going to keep going with that because we don’t have any better ideas.
- But we do know AFM is not polio virus.
- AFM has occurred in 46 states and DC.
- Most reported cases are children.
But I need to ask, if you were an older person who came down with partial paralysis, would you think AFM or stroke? My thoughts exactly. So we’re going to see a major over-reporting of stroke and an underreporting of AFM as the population ages. Look for stroke victims making an extremely rapid recovery.
If we believe that AFM is caused by a specific virus, EV-D68, then we have to look at how common that virus is. According to European researchers, there were 699 cases of EV-D68 confirmed worldwide from 1962 to 2013. That’s not a common virus at all. It also makes it sound a lot more deadly than the CDC wants us to think.“From 2009 to 2013, a total of 79 cases were reported in the US, with generally mild symptoms, followed by 1,153 cases in 2014” If, out of those few cases, 59 people got severely ill, then EV-D68 has a severe illness rate that exceeds polio’s 5%. “AFM was diagnosed in 10.4% (120/1,153) of cases in the US and five cases of neurological illness were associated with EV-D68 in Canada.”
That’s extremely scary. But it’s far more likely that EV-D68 is far more common and just really underreported.
What’s interesting about the cases of AFM that have continued is that the muscles affected are the proximal muscles, the ones nearest the core. In most cases the distal muscles, like fingers and toes, are less affected. That says the attack is targeting very specific areas, and not areas specific to the brain but more likely to the base of the brain and the spinal column. “AFM results from damage to the 2nd motor neuron without involvement of the 1st motor neuron or sensory afferent nerves; thus only motor function is affected.” But the weakness continues even after the brain lesions heal. So what we’re dealing with are anti-muscle antibodies? Some kind of continued autoimmune response to the body’s muscles long after the virus has left the body? But the results for autoimmune tests are mixed.
What Can We Do About It (Besides Sneezing Into Our Elbows)?
Since we lack full understanding of what’s happening, we have to treat acutely for now.
The best culprit we have is EV-D68. Mouse studies do show it is capable of causing AFM. They also show that some of the common treatments may make the situation worse. Non-specific antivirals and steroids fall into this category.
In contrast, “In our respiratory model, treatment with guanidine provides a two-log reduction in lung virus titers, reduces MCP-1 and IL-6, and prevents histological lesions in the lungs. Importantly, viremia is prevented by early treatment with guanidine.”
Where can we get this miracle product that could stop potential paralysis? Guanidine is a normal product of protein breakdown in the body, and is dumped out in the urine. Which means, of course, that it’s a prescription-only drug that you need to ask your doctor to give you. The good news is that the cost is around $10 for a 30 day supply, though if my child was acutely ill, I’d want the hospital putting this in IV.
Treating AFM with guanidine would be highly experimental, but likely much less damaging than giving steroids (which suppress the immune system and its ability to fight the virus). Guanidine is already prescribed to treat muscle weakness, but only for a another disease.