A Response from Randy S. Wymore, Ph.D

I want to say that I am grateful that Dr. Randy Wymore has taken the time to address some of the issues I and others have been blogging about (the putida path has been followed by others as well). As soon as I received this I read it in it’s entirety and decided to post it right away for others to read to make it clear to everyone that I am only interested in finding out what Morgellons is and how to get rid of it. If I am wrong in certain areas then I am wrong. In order to identify what Morgellons is it is just as important to rule out the things that it isn’t. Regarding the B. subtilis I did know that the fibers were the bacteria when I used the term “grow” but that’s a minor point.

I will be doing a follow up to my recent blog post on Collembola with about a dozen or so more cases of Collembola infections in humans drawn from medical papers. Dr. Wymore feels that Collembola don’t play a role and that is just fine. I have come into more information that I will post soon on this subject.

I took the contents of this blog post from a forum post so if anyone sees that I am missing any of the original email please make a comment on this blog and I will correct it right away. Again, I want to say that I am very grateful for this response, it wasn’t really a response to me, just to the communtiy to address the issues. If I am chasing rabbits down rabbit holes I certainly want to know about it and spend my time looking at other possibilities. Please be respectful, I wont allow any negative responses to this post as I have a lot of respect for what Dr. Wymore has to say here. We can debate of course. The letter as I saw it is as follows:

---

To the many dozens of people who have emailed me regarding my statement that we detected Psuedomonas a couple of years ago, and the possible connection between that bacterial type and the production of toluene, thank you for your emails.

Since most of you forwarded a link with the discussion of P. putida and toluene, including quotes from me, I thought I would reply to all of you at once. Again, thank you for bringing the link to my attention and sorry for an impersonal bcc group emailing.

I don’t know if this is the original posting, but one link is: Does this identification mean anything? I do not know Morgellons – A Mundane Approach Apparently I say, “I don’t know” more often than I was aware. A preface here: High-context words, acronyms and sentences (AKA ‘techno-babble’) are sometimes viewed as a way of masking the truth, so as to keep information from the masses. I prefer to not use techno-babble unless the audience is familiar with its usage. Unfortunately, I do have to rely on some fairly high-context language to discuss the posting that I have been receiving a steady stream of emails about. The original posting used such language and to clear up confusion about the matter I must use the same language of chemistry and molecular biology. When a person starts making quotes from papers and trying to interpret what they might mean, such language is the only way to separate speculation and misinterpretation from actual meaning. I will put in quote marks sections I quote from the poster or other sources.

Whether it is my argument or anyone else’s, it is important to remember that in a linear argument (where one point leads to the next, and so on) if any assumption of fact or truth is incorrect, then the final conclusion will likely be incorrect.

 

Pseudomonas putida

I was a bit shocked to read that someone going by the name of Mr. Common Sense stated: “…it can also be fed glucose, something readily found in the human body and again the byproduct is toluene,…”.

A reminder here that I am not a microbiologist, but I have read that the bacteria in question had been looked at for the possibility of bioremediation of toxic spills, and in areas where mining had concentrated certain toxins in the soil, such as the Tar Creek site in Oklahoma . On the other hand I have never heard of native bacteria making organic toxic molecules from sugar. That seems intuitively wrong, as life forms tend to use complex organic molecules (sugars, proteins, fats) to 1) generate the useable fuel to keep the organism alive (often ATP) and 2) to manufacture the necessary proteins, membrane components, etc. necessary to keep the organism alive. All life produces some waste products, such as ammonia, urea, carbon dioxide, oxygen, alcohol and hydrogen peroxide as part of their metabolic reactions; which product depends on the kind of organism (bacterial, fungal, plant, bird, fish, mammal, etc.). I could not understand how a simple sugar, like glucose, could be metabolized to generate a complex organic molecule with an aromatic ring like toluene. Neither aerobic nor anaerobic metabolism made sense. So, I decided to look at the news story that was cited in the article (http://news.softpedia.com/news/Bacteria-Eating-Up-Oil-Spills-and-Producing-Biodegradable-Plastic-18787.shtml).

I will quote below from the article that was also posted in the posting under discussion (bolding is mine):

“…Kevin O’Connorand his colleagues produced a chemical cocktail made up of more than 80 percent styrene oil plus low volumes of other toxicants. Frankly, they haven’t expected that their test bacteria, P. putida CA-3, a special strain of a common soil microbe, would do too well.However, the bacteria managed to turn 64 grams of undistilled styrene oil into nearly 3 grams of additional bacteria. In the process, the bacteria also produced 1.6 grams of a biodegradable plastic called polyhydroxyalkanoates, or PHA.

As a scientist I bolded certain key parts differently than it appears in the post, and here is my take on the story. 1) Dr. Connor fed the bacteria this toxic sludge of styrene oil that the researchers made for the bacteria; 2) this is a lab strain of P. putida, not the P. putida one typically finds in the environment and 3) the waste PHA ws a byproduct of the metabolism. This particular mutant strain was amazingly able to convert the 64 g of toxic sludge into 3 more grams of bacteria & 1.6 g of PHA. This is amazing that these bacteria were able to use toxic organic molecules for fuel and as the building blocks for making their own proteins and other molecules they needed to live. It’s not too surprising that the waste products were PHA, which seems a bit bizarre; that is until you look at the starting fuel. Start out with a toxic soup for the fuel and the waste products will not simply be carbon dioxide and water, the way it would be if the starting fuel were glucose. The point is, that the only reason they are making PHA (and probably other trace organics, including toluene) is precisely because of what they were grown on. Nothing in this press release indicates that the normal environmental strains of P. putida, or the mutant lab strain, maked toluene from normal food sources the bacteria would be consuming in a common setting. More on “normal” in a moment.

Next I read the original research from 1987, that was cited in the posting. It is found in:Biotechnology and Bioengineering, Vol. XXIX, Pp. 873-883 (1987) (http://www3.interscience.wiley.com/cgi-bin/fulltext/107621620/PDFSTART)

The title is:

Production of Toluene cis-Glycol by Pseudomonas putida in Glucose

Fed-Batch CuIture by, Richard 0. Jenkins, Gillian M. Stephens, and Howard Dalton from the

Department of Biological Sciences at the University of Warwick .

In the MATERIALS AND METHODS section, under: Organism and Culture Conditions, the following is found (bolded for emphasis):

“…Organism and Culture Conditions
Wild-type Pseudomonas putida NC 1 B 1 1767, a mutant
strain NG1 (obtained from Dr. S. C. Taylor, ICI,
Billingham, England) lacking the enzyme TCG dehydrogenase
and a mutant strain T5 lacking toluene dioxygenase
activity were used for the investigation. The
organisms were stored in L-broth containing 20% (w/v)
glycerol at – 20°C. The wild-type strain was grown on
toluene in liquid culture as described previously.’2 Mutant
strains were grown at 30°C in a 5-L LH 1000 series
fermenter (L. H. Engineering, Stoke Poges , Bucks,
England). The glucose medium described by Jenkins
and DaltonI2 was used but contained 1.0 g/L NH4Cl
unless otherwise stated. The pH value was maintained
at 6.8 by automatic addition of 1M KOH. Air was
introduced at 2 L/min and stirring was at 400 rpm.

Conversion of Toluene to TCG
Strain NG1 was used for the biotransformation. The
culture was grown overnight to a cell density of AS4
= 2.0-2.4. After depletion of glucose in the medium,
indicated by a rise in the dissolved oxygen concentration,
the pH value of the medium was adjusted to 7.2
and fresh medium, containing 17.4 or 8.7 g/L glucose
but lacking NH4CI, was added at a rate of 1 mL/min.
After 2 h, toluene (19 g/h) was added by passing the
air stream through 300-500 mL of liquid toluene contained
in a 2-L conical flask. When necessary, I-mL
volumes of 10% silicone antifoam A (Sigma Chemicals,
Poole, Dorset , England ) was added. The total volume
of the culture was maintained between 3.0 and 3.5 L…”

 

The authors were looking at metabolic reactions and comparing the wild type with the mutant. The normal wild type strain was actually grown with toluene in the media and the mutant strain had toluene added to the media. A byproduct of toluene metabolism (in those few organisms that can metabolize toluene in the first place) is toluene cis-glycol. Toluene & toluene cis-glycol are not the same thing. In the context of the research discussed above, toluene cis-glycol is a metabolic breakdown product left over when the starting material is toluene.

So the poster’s statement: “…But Pseudomonas Putida can do more than make things out of oil spills, it can also be fed glucose, something readily found in the human body and again the byproduct is toluene,…” is completely false, based on the very articles used to try to justify that claim. The bacteria were directly fed toluene, in the research paper, or fed a mixture of styrene and other toxic substances, based on the news story. P. putida has a couple of genes that allow it the ability to synthesize a dehydrogenase enzyme that can metabolize or break-down toluene & benzene, but it does not make toluene unless it is forced to grow in a toxic media. Given sugar, P. putida happily metabolizes sugar in the normal manner like many other bacteria and does not make toluene.

If it is true that some people have measurable levels of benzene or toluene in their blood, then they are being exposed to it on a regular basis. And, not by bacteria makinig it. It would have to be environmental in nature. Often, toluene is measured indirectly by looking at something called hippuric acid, in urine. Hippuric acid is the metabolite we humans make in the processing of toluene exposure. If a person smokes cigarettes or marijuana, is exposed to moderate second hand smoke, breathes wood smoke or is in contact with creosote, then there will be some toluene in their blood. Not normally enough to interfere with tests for toluene poisoning for someone who works in certain types of industry, but it will be detectable. According to the various federal agencies (http://www.atsdr.cdc.gov/csem/toluene/standards_regulations.html) there is a fairly wide range for airborne toluene that is allowed, or a 1ppm amount of toluene in drinking water. Personally, I think zero toluene would be the best, but for many jobs, and certain sources of drinking water, that is impossible. Toluene clears a human in a few hours to a few days, depending on whether it has gotten into fatty tissue. But, if toluene is there on a repeated basis, then that person is being exposed to toluene regularly and I would want to identify where it is coming from (unless a person is a smoker, in which case there may be no need to look further). As an aside, hippuric acid is the metabolite for multiple benzene/toluene organic compounds & it is not possible to take the end product and say what the original organic toxin was. This is important in the conversation. Is it directly toluene that is being measured, and how, or is it hippuric acid, or some other metabolite. Similar to the way some athletes get busted for taking steroids or growth hormone; it is not always the steroid or growth hormone that is directly measured, but rather a metabolite in the urine. If it is a metabolite, then the best that can be done is to narrow the original organic compound to a class of molecules rather than a specific one.

If I could, I’d like to mention something about Morgellons in general, and my past comments. My previous statement included: “…PCR was performed and the amplified DNA was sent to a commercial sequencing lab to do the DNA sequencing. Two different bacterial species were identified. They were: a) Pseudomonas putida and b) Corynebacterium efficiens. Does this identification mean anything? I do not know. Both of these can cause infections, especially in immunocompromised individuals. Both of these bacterial types are found in soil and can be found in skin. The fact that they grew from fibers that were associated with skin makes it difficult to say if they are related to Morgellons Disease in any meaningful way, or merely normal skin contaminants. Still, these are the only two DNA sequences to be identified so far.”

I will follow up that statement now. We never grew P. putida from any other Morgellons samples from different individuals. Worse still (from my perspective) for the argument the poster is trying to make, even from the same individual, other samples did not give rise to the same bacteria. That’s right, not only do most Morgellons samples not have P. putida associated with them, even other samples from the same person did not. My lab technician does all of the bacterial culturing, so we do not follow what seems to be a dead end; there simply isn’t the time to follow every remote possibility. Can I say with 100% certainty that P. putida is not the cause of Morgellons Disease? No. Can I say that it is unlikely? Yes, and I will explain my thinking. This is only my way of looking at the matter and it may be flawed, but here it is. We have an “either/or” situation. Morgellons is either a single disease/disorder, or it is a syndrome that may have multiple (and even unrelated) causes that simply manifest symptoms that appear similar. There is an example that I have followed over the years and have published papers on the genes/proteins that are involved. The example is the cardiac Long QT Syndrome (LQTS). At one time the there were only two obvious manifestations of LQTS; one was a dominant genetic disorder the other was recessive. In the dominant form, if either parent passed on an abnormal gene, that child would get LQTS. In the recessive form both parents had to pass on the gene & then a child would also have deafness associated with the heart disorder. This was back in the early 1990s. Now, however, multiple genes and variants of LQTS have been characterized and at last count there were LQT1, LQT2, LQT3, LQT4, LQT5, LQT6, LQT7 & LQT8. There may be more in the future. Will there some day be a Morgellons 1, 2, 3, etc.? All with different causes? At the moment, it is hard to picture that due to the fibers and other unusual skin-associated material. If we pretend for a moment that Morgellons is a single condition, then that means whatever is the cause in one person MUST be the cause in everyone. Therefore, the causative agent(s) must be present in all sufferers with Morgellons. If the cause is fungal, bacterial, vector-borne, viral, whatever, then everyone with Morgellons must have that organism present. If it is not biological but is environmental (toxins, chemicals, etc,) then everyone with Morgellons must have had the same kind of exposure; different locations, but the exposure must be present. This is one of the reasons that a proper epidemiological study is needed, to try to find the commonalities between widely geographically spaced individuals. If it were obvious I hope we would have seen it, but there is little in common between the sufferers. Some consume huge amounts of meat while others only eat fish, some are ovo-lacto vegetarian and others still are devout vegans (long predating the onset of Morgellons). Many have been exposed to molds or damp environments and others live in very dry desert settings. Some had been to lakes, oceans or public swimming pools & others wouldn’t touch their big toe in a body of water. Some with Morgellons were avid outdoors enthusiasts and others self-described couch potatoes. Some live in rural settings & others in the midst of urban jungles. Pretty much you can continue on with obvious characteristics that might make sense: dry vs. oily skin, lots of sun vs. very little sun, high fever vs. no sickness prior to onset of symptoms, bottled water vs. tap water vs. well water, have been vaccinated for child-hood disease and those who have not, caffeine consumer vs. no caffeine, alcohol vs. never touch the stuff, and so on. Whatever is common to everyone with Morgellons is not obvious to me. I am not an epidemiologist and cannot do an epidemiology study. This needs an experienced MPH or other advanced degree professional epidemiologist to do this aspect of Morgellons research.

 

Morgellons & dental work

Still we are left trying to figure out what causes Morgellons and if is it a single disease or multiple diseases/disorders that just by coincidence have virtually identical symptoms. Which brings me to the next item: the proposition that dental work toxins are somehow causing symptoms of Morgellons Disease. Personally, I discounted that idea after a few emails and phone calls for one simple reason. There are a number of younger (and even not so young) individuals who claim to have Morgellons and yet who have never had a cavity, a crown or a root canal in their life. Sadly, I had many cavities throughout the younger part of my life, but now it is not uncommon for children to never have had a single cavity when they hit their teen years. So, if there is even one person with confirmed Morgellons and that person has never had dental work, other than cleanings, then one of two choices must be true: 1) Morgellons is not caused by chemicals associated with dental work or 2) Morgellons is a syndrome with multiple different causes. I chose number 1 as the most likely to be true because there are way more than just one person who have Morgellons & yet have had no fillings or dental crowns. There is another reason and that has to do with a kind of toxic threshold effect. Anything, quite literally anything is toxic in high enough concentrations. As has sadly been true in a couple of high-profile incidents in recent years, even drinking too much water too quickly can be fatal. Water should be the least toxic substance on the planet, but under the right circumstances it is toxic. Alcohol can reduce the incidence of heart disease, or kill a person from alcohol toxicity and the same potassium that people taking some diuretics must take, is the same potassium that has been used in assisted suicides. Selenium deficiency is associated with birth defects & selenium toxicity is associated with birth defects. What determines toxicity of any of the above potential toxins? The amount over a period of time. Everything that is toxic has some level, below which it is no longer toxic. That is why drinking water might be allowed 1ppm of toluene to be present. At that level and lower, even though it is measurably detectable, it is thought to not have any known detrimental effects. Now think of the rate that human blood is pumped around the body. The range for an adult human is around 1 gallon to 3 gallons of blood flow per minute (depending on age and weight). That is over 10,000 gallons of blood flow per week (like a small swimming pool). The amount of any toxic chemicals that can leech out of the dental work & into the blood would be so tiny that if would be less than a drop in a bucket. Even if it cannot directly be excreted in the urine there is likely some liver enzyme that will modify it so that it stays water soluble & can be removed in urine, much like benzene & toluene are modified to hippuric acid & then removed from the body. 1.5 to 2 liters of urine per day can handle a lot of toxins. We’d all be dead as a species a long time ago if we couldn’t handle toxins. Even most fat soluble toxins do not stay in fatty tissues indefinitely. They tend to slowly exit in urine, or if they are volatile enough, sometimes they exit through the lungs. The last piece of evidence is purely anecdotal but over the last 3 years I have communicated with several who claim to have Morgellons & who had gone ahead and replaced their previous dental work with less toxic versions (at huge person cost of money) but had not noticed any improvement in their symptoms even after several months to over a year. As I said, purely anecdotal; but I’m willing to give them the benefit of the doubt.

Don’t get me wrong. I’m not a big fan of toxins. I think zero ppm of toluene or any toxin is a good thing (probably why I filter our “safe” drinking water) and I don’t like the idea of mercury poisoning. Since I do have more than my fair share of old fillings, I once had my hair tested for heavy metals. Happily, the metals tested for were either at too low of levels to be detected, or way below levels that were considered dangerous.

 

Bacterial macrofibers

I am quite interested in bacterial macrofibers and any relationship with Morgellons. The poster brought up B. subtilis by mentioning the following paper:Motions caused by the growth ofBacillus subtilismacrofibres in fluid medium result in new forms of movement of the multicellular structures over solid surfaces, by Neil H. Mendelson1 ,Joelle E. Sarlls2andJohn J. Thwaites3 of the Department of Molecular and Cellular Biology1and Department of Physics2, University of Arizona, PO Box 210106, Tucson, AZ 85721-0106, USA, Gonville and Caius College, Cambridge CB2 1TA, UK2

The poster stated: “…The real reason we want to take a look at Bacillus Subtillus is its ability to grow living, moving fibers. Yes, bacteria growing fibers that move, writhe, and wriggle. I imagine this would feel quite strange under the skin as well.”

Just to make sure that there is no uncertainty here, the bacteria do not grow the fibers. The fibers are the bacteria. In 2006 I spoke with Dr. Mendelson, the first author of the paper in question to get more information. This particular strain of B. subtilis is a mutant strain that has problems with cell wall division. So instead of 1 parent cell going through normal bacterial cell division to give rise to 2 discreet daughter cells, the cells remain adhered to one another. Each round of division continues the process and the large collection of cells continues to elongate until they fold in response to the mechanical forces (think of a rubber band that is twisted & how it will often loop back upon itself). This is mechanical in nature & no additional energy is required. This process continues until a macrofiber made up of hundreds of thousands to millions of bacteria is observed. When the macrofibers get of a certain size the bacteria near the center tend to die & the macrofibers degrade. The bacteria cannot diffuse in the nutrients they need or diffuse out the waste products fast enough to keep them alive for an extended amount of time. Now, please note from the materials & methods section of the paper by Mendelson et al:

“The complex medium TB, consisting of 10 g Bacto Tryptose(Difco), 3 g Bacto Beef Extract (Difco) and 5 g NaCl(l deionized water)-1(Mendelson & Favre, 1987) was usedin static cultures housed either in standard 100 mm diameterplastic Petri dishes or in glass growth chambers constructedfrom 75×25 mm glass microscope slides. The chamber dimensionswere 56x25x13 mm (length, width, height). Right-handedFJ7 fibres were produced by overnight growth in 10 ml TBcontaining 50 mM MgSO4at 20 °C.”

Three things of note in that protocol, 1) the very specific formula necessary for the bacteria, 2) the addition of the MgSO4 & 3) the temperature of 20 °C. The bacteria are not hard to grow but to get them to grow as macrofibers is not trivial in the least bit. If the formula of the media is not right, the temperature not right or there is movement (shaking) they will grow, but they will not twist up into the macrofibers. We succeeded in growing a macrofiber from bacteria cultured off of a Morgellons sample once. My research associate spent months trying to get it to happen again and we could not. The bacteria that formed the macrofiber was not one single bacterium. It was a mixture of a bacillus and cocci. We could never purify the 2 strains away from one another even when we had microbiologists help us. It is intriguing and puzzling. But, since we did not see this combination of two different classes of bacteria in other Morgellons samples, it seems unlikely to be the cause of Morgellons. Some day I would like to revisit this, but for now it seems like it would be a waste of the limited time that is available. B. subtilis is not something that has shown up in multiple different samples from different people. I mentioned that no energy other than the twisted (stored) mechanical energy is necessary for formation of the macro-fibers. The movement is a phenomenon of the experimental conditions in the paper under question. They would not do that under the skin. They could not form in human blood, lymphatic fluid or extracellular fluid; the bacteria could live & might form a biofilm, but they wouldn’t form fibers. The pH, chemistry and temperature are all wrong for bacterial macrofiber formation. Even if they somehow could form, the viscosity of the fluid, the presence of our cells, connective tissue, iron in blood, etc. would prevent the fibers from moving. It would require much more than stored mechanical energy to move bacterial macro-fibers around through human skin. It would require a fair bit of ATP (or equivalent) energy molecule to accomplish that much work. Something the cells don’t have considering that by the time a macro-fiber is big enough to see with the naked eye, the central bacteria are dying due to lack of energy molecules & the fact that they are being bathed in toxic waste that cannot diffuse away fast enough to keep them alive.

 

Collembola & DNA

The original poster that I am responding to made the following statement: “Now, the mere fact that Dr. Wymore couldn’t find any Collembola DNA doesn’t surprise me as I think that it would be a very difficult task indeed. The Oklahoma (NPA) study went to great lengths just to identify “whole” Collembola that were lying around in their skin scrapings, in fact, they were initially all overlooked, but later found.” Bolding of words was by me.

The poster seems to imply that finding a whole organism is easier than amplifying DNA from an organism. This is exactly backwards from the actual situation. To visually recognize an organism requires that much of the organism be present. To PCR DNA requires a few cells to be present. I don’t know how many cells there are in Collembola, but since it has an entire digestive tract, reproductive system, neurons and muscles (to name some tissues), there are undoubtedly many cells. If such an organism was moving around through human tissue it would shed cells. No two ways around it. At the very least it would shed digestive system cells in its feces. In theory, one can amplify DNA from 1 single cell. Our forensics faculty/students have amplified DNA from handprints on a door-knob (not too many cells there). Now, I don’t presume that I can amplify DNA from 1 single cell; I’ve never tried that & possibly would fail. But amplifying DNA from a few cells is something we can do. We accidentally amplified DNA from an algal contaminant in our deionized lab water. This algae was contaminated at a very low level. No more than 1 organism per drop (5-20 microliters). So, at the most, there were 5-10 cells in the amount of water that was used for PCR. At the low end it might actually have been from a single cell. The Collembola primers that are used to amplify the DNA are particularly useful and detect a gene that is found in every one of the tens of thousands of different Collembola species. The primers we had made are the primers that many of the evolutionary studies about Collembola utilized. If there are still 10,000 more varieties of Collembola, or more, left to be characterized, they will work on all of them. Certain genes are conserved in all related organisms. The gene in question is even more conserved than most. Even if there were many mutations in this gene, we would still be able to amplify the DNA. If there is an arthropod in the skin of Morgellons patients it is not something that we have been able to detect at the molecular level. In contrast, PCR from the skin of an individual with scabies, has multiple published reports where the DNA of the scabies-causing mite was amplified. The process does work, and it is much more sensitive than microscopy. Our normal big problem is contamination; not difficulty in detection. At times PCR is TOO sensitive and we have to sort through a positive result to make sure that we did not accidentally contaminate the samples with a “positive control”. I therefore, do still maintain that if Collembola were causative in Morgellons, then the fibers or other shed material or scrapings or punch biopsies would have revealed that information by the presence of Collembola DNA.

I won’t be debating the issues above even if some choose to spend time doing so. These are my opinions. Everyone is free to form whatever hypothesis about Morgellons that they wish. I don’t know (I just had to say that once more) what causes Morgellons. I will keep working through the research one step at a time. When something common to most with Morgellons is identified, the information will be made available as soon as I am convinced of the relevance. Clinicians and those suffering from Morgellons will know long before a publication is out. To do otherwise would be immoral in my opinion.

For the record, if someone that I send this email to chooses to post it, that is fine; as long as the entire content is posted. One caveat; wading through the P. putida paper took quite a while, so this email wasn’t edited or “proofed”, so please, no one take me to task for spelling or grammar errors. I hope I communicated my thoughts, but there is no more time to deal with other details in the original posting or my own words for that matter. Time for me to move on to the matters at hand. Based on past experience, if this email does get posted I will receive a couple hundred emails in the next week or so. Please don’t take offense if I do not respond. I won’t have time to do so.

Some of what I do know (or at least what I think if a philosopher argues with the word “know):

Morgellons is a physical pathology. It is not a simple subset of a psychiatric disorder Multiple forensic tests (FTIR, mass-spec, etc) at multiple locations have confirmed that the Morgellons fibers are not identifiable as a known compound. The fibers are a fairly pure organic compound containing: carbon (single & double bonds), hydrogen, nitrogen, oxygen, at least one methyl group, maybe a sulfur group and a few unclear FTIR peaks. They are quite heat resistant and not dissolvable in lab-type solvents or detergents. The red & blue colors of the analyzed fibers are neither dyes nor pigments in any conventional sense.

Attempts to use fixatives for EM analysis have been ongoing for months ( have not been trivial lab exercises) and will hopefully yield results in the near future. Thanks to a large donation outside commercial labs will be doing analyses that we cannot do “inhouse” as soon as non-trivial details can be worked out. We are looking at a possible connection with Agro-bacterium. Multiple physicians are participating in this.

Morgellons is not a skin disease. It is a systemic condition affecting multiple organs. It does not seem to be highly contagious. People who “fight Morgellons” seem to do better than those who isolate themselves and resign themselves to a downward spiral. This is true of most chronic conditions. Just an observation.

Cure is a word I am hesitant to use, but I have met one person who has been symptom free for about 3 years after discontinuing treatment. That person reported that they did a long-term course of high-dose antibiotic, anti-fungal and anti-helmenthic meds. Several people have claimed to be cured, but this is the only one I have personally met that has remained symptom-free for multiple years after discontinuing all treatments. I am not a physician and can give no recommendations for treatment. This person was not seen or treated by any physicians at OSU-CHS. I am merely passing this information on as a personal observation. I will keep working to try to identify the cause of Morgellons. At the moment I have no research-based, front-runners for the cause.

With respect,

RSW

Randy S. Wymore, Ph.D.
Director, OSU-CHS Center for the Investigation of Morgellons Disease
Associate Professor of Pharmacology
Oklahoma State University
Center for Health Sciences