PANDAS article in the Christian Post

The Christian Post has published my feature on PANDAS – Pediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococci.
There are some great quotes from Susan Swedo, MD, who is often credited with discovering the relationship between psychiatric symptoms and strep throat. I don’t say much about it but I also report some new research regarding the mechanism of action for the strep antibodies in the brain. Crosswalk.com will put it up next week.

37 thoughts on “PANDAS article in the Christian Post”

  2. Very interesting news today from the Stanford team leading the way in the fight to understand narcolepsy. They had already established that the disorder resulted from the autoimmune destruction of a small set of neurons that made hypocretin, a neurotransmitter, but now they seem to have zeroed in on what triggers it:

    “Together with recent findings, these results strongly suggest that winter airway infections such as influenza A (including H1N1), and/or Streptococcus pyogenes are triggers for narcolepsy,” Mignot, a professor of psychiatry and behavioral sciences, and his colleagues wrote in the paper.

    Reminds me of PANDAS and strep.

  4. John Weaver
    Is there evidence floating around that OCD may be caused by strep? I have no doubt it’s something like that but I didn’t know one way or the other if there was evidence yet.

  5. Good article, Warren. Now if we could only persuade nouthetics supporters to admit that OCD may be caused by strep, then we’d be on to something!

  6. Thanks Carole. I’m pretty alert to infections and such. I have a roommate now and her boyfriend is in the military so I am extra cautious with towels around the house. Anyone in an institutional setting can carry it in to the house. Soooo….. plus I have to be careful with my grandmother.

  7. Mary,
    The staphyloccus aureus bug is just one of many strains of staph infections; if a wound/cut/abrasion is just superficial and is cleaned out you’ve likely nothing to worry about.
    Things like blisters, and cuts tend to go deeper than a mere abrasion and it’s when the bug enters a deeper wound that it can spread IF it isn’t tended to with care.
    Of course, diabetics don’t heal as well as others so they are more at risk. When high school kids get a wound, they tend not to pay much attention to it until infection has taken hold. By then, the germ has gone more deeply into the skin, and that offers the risk that it will not remain a local infection. It spreads; there is often swelling and a tell-tale red line from the wound leading toward the heart, and that speaks of it entering the circulatory system which is when the germ can spread throughout the body, leading to big trouble no matter the age of the patient.
    The s. aureaus itself only became hard to get rid of when antibiotics were often used for all kinds of things, and it learned to evolve to avoid being killed off.
    So, just make sure you don’t share things like towels with others, and just be sure to look for any openings in your skin and then cleanse the area often.
    In gyms, I’d use Clorox wipes to wipe off handle bars of exercise bikes and things of that nature. And, were I to use a gym, I’d wait to shower at home rather than at the gym. That’s just me.
    Just about any germ is capable of doing what SA has done. In fact, there is one now that is being spread in hospitals through sheets, tubes, etc. It causes diahrrea, and can kill rather quickly. So, hospitals have begun the same regimen to combat it as they instituted with MRSA. The good news is that in hospitals MRSA has been on the decline from the procedural practices put in place.

  8. Interesting. I live in an urban setting with diverse people. In our county we have had outbreaks at schools. My step sister had it. She is diabetic. I’m sort of a germaphobe. Use paper towels in my bathroom. Don’t go to gyms etc…

  9. Lyn David,
    Wow. You were put through the wringer. Glad you are on the mend.
    Vanco? Yep. Very familiar with it. Drug of last resort–thank God they have it, but wonder how much longer it will work on the superbug and the other superbugs out there.
    Mary,
    MRSA (methylin resistant staphylococcus aureus) is a very common, everyday germ. You can come into contact with it simply going about your day to day business. My sister probably got it off her carpet or kitchen floor. Her blister left her skin open to infection.
    It’s important to always take care to treat cuts and open wounds with hot water, soap, then antibacterial ointments.
    Some places, like locker rooms in schools and gym, are places where the germ is passed from one person who might have it to another (towels, etc.)
    It can lie dormant in one’s lungs, but it rarely is passed from a sneeze or cough unless the person who in on the receiving end has a compromised immune system.
    Bottom line, MRSA is everywhere in your house and elsewhere. It used to be a fairly benign germ but it evolved to virulence when doctors overprescribed antibiotics. These bugs know how to survive.
    I like reading Paul Ewald because he writes about how to get bugs to evolve to benignity.

  10. Got me…. a several of people I know have had it, including a couple of cousins. It’s likely what is called community MRSA meaning it is somewhat widespread among the populace. Not everyone who is “colonized” by MRSA develops an infection. So you can get it from someone who is not symptomatic of anything. I had a previous open sore, so it likely was not do difficult to pick it up, I guess.

  12. Warren wrote: Yes. that is how the strep antineuronal antibodies are able to effect the D2 receptors. Infections weaken the blood brain barrier which allow the naughty antibodies past.

    Thanx! It is good to know this old brain is not in decline as yet.

    carole wrote: I have almost lost my sister, a diabetic, twice, to a mrsa infection because she rubbed a blister on her toe, didn’t feel it (neuropathy in her feet and part of her lower legs).

    Yeah, I know how that works. I had MRSA eat into my leg and cause a venous ulcer. It broke open as I was driving across town one day. I didn’t notice until I had stopped at my cousin’s house. I thought the 2 inches of fluid in the footwell of my pickup was something out of the truck… wrong. Lost 9+ pints of blood but I still managed to drive to the hospital and place a cell phone call to the ER for them to come outside and get me. I was on vancomycin for the MRSA for over a month and had a relapse for 2-3 weeks a month later. Then 1-1/2 months later an opportunistic bacteria [C. difficile] struck my gut, that almost killed me.
    But I’m much better now.

  14. carole
    The ramifications of the GNXP article are fascinating. Up to a third of the American population may have an “altered” personality because of a common Toxo infection. The next time you are stuck in traffic and you think to yourself, “these people are all nuts,” you might be right. 😎

  16. Lyn David asked,

    At any rate, if this blood-brain barrier exists is it possible that a breakdown in the barrier is how the auto-immune effect, via strep antibodies, effected?

    I think this is a very interesting question. In my reading, I haven’t come across an answer to it.
    I am thinking how much chance plays a role in if and when we get sick. One easy route of infection is the skin, of course, and it’s the one most of us pay the least attention to. We don’t readily disinfect /tend to a scratch on our body until it heals. I have almost lost my sister, a diabetic, twice, to a mrsa infection because she rubbed a blister on her toe, didn’t feel it (neuropathy in her feet and part of her lower legs). Recently, a similar thing happened to my friend’s husband, he too a diabetic. Lucky for him that with all his problems, the blood infection he had was a staph, but not mrsa. As it is, they treated him with three antibiotics, which did shut down his kidneys and until yesterday, they feared he’d have to have dialysis.
    Other than the skin, I think of the digestive tract or respiratory tracts. Small entry points into the capillaries allow a bug entry–perhaps that’s all that’s needed and a wily bug will fight for survival even if it finds itself someplace “accidentally.” They still don’t know why in a small % of people the polio gut virus made its way to nerve sheathings, maybe because they stopped studying it after preventative measures were found and administered. In some people, did the virus evolve to survive in the sheathings? Or, did they wander there to their own dead end?
    Is it the strategy of these pathogens that can wind up in the brain to do so the way a parasite like toxo does? Or, have they wandered there, swept away by the circulatory system to promiscuously alight elsewhere? Perhaps each bug is different, but one thing is for sure–they struggle mightily to survive no matter where they wind up. Even if they don’t, in some cases, they leave behind damage. In other cases they “appear” to peacefully co-exist with us. I say “appear” because in some people, for example, there appears an immunity to their effects. In others, not so.
    H. pylori lives in a huge % of the human population; in most it appears to cause no noticeable damage; in many, it causes ulcers; in others, it causes stomach cancer.

  17. Lyn David said,

    So antibodies in the brain tissue. Isn’t there supposed to be a blood-brain barrier over which some pathogens or even some chemicals (including drugs) cannot cross.

    The bbb was once thought to provide the ultimate protection from pathogens; its “protective” qualities have in the past thwarted efforts to directly target things like brain tumors with chemical treatments. Lately, however, there is great hope that understanding what the bbb can defend against and what it cannot has begun to offer great hope for targeted, more effective treatment of tumors that can’t be reached by surgery. They hope to eliminate the need for surgery altogether if they can learn the techniques to deliver the medicines effectively.
    Studying how viruses themselves manage to cross the bbb have helped give researchers ideas. Viruses which have gotten that far have a much greater chance of getting through the cells of the bbb because of their molecular structure and because they are smaller than bacterium; further, they seem quite adept at quickly evolving and able to use molecular mimickry, for example. They can disguise themselves to allow themselves a “pass” in sometimes.
    Also, the important hypothalamus (not that any part of the brain is unimportant, I suppose) is not even completed protected by the bbb, maybe because its job is to receive information from so many areas of the body to receive information that some parts of it have remained unprotected. Perhaps we have not yet evolved to the point that our hypothalamus can both block out the dangerous while still receiving all the inputs from our body it needs to run the systems it controls. The bugs sometimes out evolve us.
    This isn’t the best source, Wikipedia, but it was the handiest:

    The hypothalamus is bounded in part by specialized brain regions that lack an effective blood-brain barrier; the capillary endothelium at these sites is fenestrated to allow free passage of even large proteins and other molecules.

  18. Infections weaken the blood brain barrier which allow the naughty antibodies past.

    WOW! So theoretically speaking that might be happening all the time.
    —
    If I understood the Toxoplasma/Schiz article from today the microbe crosses the BBB and makes cysts in the brain. And it’s common! That’s crazy.

  19. @Drowssap & Lynn David – Yes. that is how the strep antineuronal antibodies are able to effect the D2 receptors. Infections weaken the blood brain barrier which allow the naughty antibodies past.

  20. What I find interesting is that 10 years ago everyone believed this stuff was genetic. 30 years ago everyone believed it was the parents fault.
    Times are changing.

  22. Interesting timing on the PANDAS article.
    A group of scientists believe they have discovered why Toxoplasma triggers Schizophrenia and Bipolar disorder.

    Toxoplasmosis, which is transmitted via cat faeces (found on unwashed vegetables) and raw or undercooked infected meat, is relatively common, with 10-20% of the UK population and 22% of the US population estimated to carry the parasite as cysts.
    —
    The team from the University of Leeds’ Faculty of Biological Sciences has shown that the parasite may play a role in the development of these disorders by affecting the production of dopamine — the chemical that relays messages in the brain controlling aspects of movement, cognition and behaviour.
    —
    “In addition, the ability of the parasite to make dopamine implies a potential link with other neurological conditions such as Parkinson’s Disease, Tourette’s syndrome and attention deficit disorders, says Dr McConkey. “We’d like to extend our research to look at this possibility more closely.”

  23. Drowssap,

    News flash     – I’ll quote this, because it’s interesting and it’s from today:

    Scientists have discovered how the toxoplasmosis parasite may trigger the development of schizophrenia and other bipolar disorders.
    The team from the University of Leeds’ Faculty of Biological Sciences (UK) has shown that the parasite may play a role in the development of these disorders by affecting the production of dopamine – the chemical that relays messages in the brain controlling aspects of movement, cognition and behaviour.
    Toxoplasmosis, which is transmitted via cat faeces (found on unwashed vegetables) and raw or undercooked infected meat, is relatively common, with 10-20% of the UK population and 22% of the US population estimated to carry the parasite as cysts. Most people with the parasite are healthy, but for those who are immune-suppressed – and particularly for pregnant women – there are significant health risks that can occasionally be fatal.
    Dr Glenn McConkey, lead researcher on the project, says: “Toxoplasmosis changes some of the chemical messages in the brain, and these changes can have an enormous effect on behaviour. Studies have shown there is a direct statistical link between incidences of schizophrenia and toxoplasmosis infection and our study is the first step in discovering why there is this link.”
    The parasite infects the brain by forming a cyst within its cells and produces an enzyme called tyrosine hydroxylase, which is needed to make dopamine. Dopamine’s role in mood, sociability, attention, motivation and sleep patterns are well documented and schizophrenia has long been associated with dopamine, which is the target of all schizophrenia drugs on the market.
    The team has recently received $250,000 (£160,000) to progress its research from the US-based Stanley Medical Research Institute, which focuses on mental health conditions and has a particular emphasis on bipolar illnesses.
    Dr McConkey says: “It’s highly unlikely that we will find one definitive trigger for schizophrenia as there are many factors involved, but our studies will provide a clue to how toxoplasmosis infection – which is more common than you might think – can impact on the development of the condition in some individuals.
    “In addition, the ability of the parasite to make dopamine implies a potential link with other neurological conditions such as Parkinson’s Disease, Tourette’s syndrome and attention deficit disorders, says Dr McConkey. “We’d like to extend our research to look at this possibility more closely.”

  24. Lynn David

    is it possible that a breakdown in the barrier is how the auto-immune effect

    I’m not an expert but I don’t think that’s necessary. Schizophrenia which hits 1% of the population appears to be triggered in much the same way. I don’t think that many developing babies already have a breakdown in the blood brain barrier.
    Maternal Flu Linked To Schizophrenia, Autism In Child

  25. Lynn David,
    It might be that genetics would make some more prone to get the infection than others.
    Here’s an example I’ve just come across:
    Overmethylated immune system genes, especially for cytokines, can impact on stress regulation and make a child more aggressive. Canadian researchers found that can be the result of a mother’s behaviour during the perinatal period.
    So, if a mother’s behaviours can impact methylation, then the child can be more or less vulnerable to infections. The conclusion is my own.

  26. Dang that notifications box….. sometimes it auto-fills, sometimes it doesn’t….

  27. Really good read… I couldn’t put it down! 😉
    Honest, it flowed. So antibodies in the brain tissue. Isn’t there supposed to be a blood-brain barrier over which some pathogens or even some chemicals (including drugs) cannot cross. But I am basing this idea in my reading of chemotherapies for a cancer I had, but that was way back in 1984 so the science may have changed.
    At any rate, if this blood-brain barrier exists is it possible that a breakdown in the barrier is how the auto-immune effect, via strep antibodies, effected? It might explain why a small percentage of those infected by strep develop PANDAS. But then antibodies might have free reign in the brain…..

  28. Jayhuck

    Its also interesting that the microbes ability to start the process towards diabetes took place in children already disposed to the disease.

    As in PANDAS genes probably influence susceptability for a variety of reasons. I didn’t catch the fact that a virus could prevent Diabetes but it’s certainly possible. It probably has the same effect as a vaccine. Exposure to Herpes is thought to confer some immunity to plague and other bacteria.
    As far as PANDAS is concerned I believe there are several different Strep Throat vaccines in the works.
    Google Search: Strep throat vaccine

  29. Warren,
    I was just curious – ooops, looks like, judging from your response to Katie, we don’t know what happens long-term. I wasn’t sure if the on and off (sawtooth) pattern ever eventually subsided – do the antibodies continue crossing the blood-brain barrier doing this kind of damage forever?

  31. @Jayhuck: They recover from the infection (strep) but the antibodies remain in the blood and cross the blood-brain barrier upon subsequent infections. Thus, children have a saw-toothed pattern of symptoms; acute onset and then wane for awhile and then back again.

  32. Warren,
    I may have read your article too quickly, but it sounds like the kids were able to recover from the infection after a period of time!?

  33. Drowssap –
    Thanks for sharing that study. I found one part particularly interesting:

    Professor Adrian Bone from the University of Brighton said, “viruses have been shown to be capable of both inducing and preventing the development of diabetes.”

    Its also interesting that the microbes ability to start the process towards diabetes took place in children already disposed to the disease.

    1. Katie – No, not yet. Dr. Swedo is following a group of PANDAS kids as are others but it is unclear if this sets off a chronic scenario. One good prognostic issue is that most adults (95%) become immune to strep, eliminating the need to create antibodies. Any chronicity would come from earlier damage to the receptors.

  35. BTW, if there are any mom’s out there Type 1 Diabetes appears to work the same way as PANDAS. Microbes sneak into the body and when the immune system gets wise to the break-in it goes crazy and starts machine gunning the bodies Beta Cells as well as the invader. Over the course of about a year the Beta Cells are all dead and Diabetes sets in. The microbe in question is called an Enterovirus. It’s spread orally through contaminated food or bodily fluids. Apparently it can also survive in chlorinated swimming pools. EEEEeeeeee.
    Study Of Human Pancreases Links Virus To Cause Of Type 1 Diabetes

  36. Outstanding article! I doubt 1 person in 1000 is aware that something like PANDAS is possible.
    —

    Normally when the strep bacteria enter the body, they defend themselves by mimicking healthy cells and elude detection by the immune system.

    Molecular Mimicry… the bane of human existence!

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