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"When you have eliminated the impossible, what remains, however improbable, is the truth." Sherlock Holmes
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Parasitic Filarial Nematode Worms and Systemic Lupus Eurythematosus
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A THESIS by David f. Nicholls
A PERCEPTION OF TRUTH
In my opinion Lupus is not an autoimmune disease; it is a disease that should not exist. In my opinion autoimmunity is one thing and one thing only. It is a case in which an individual produces antibodies that are directed towards their own cells. These antibodies will be directed to the outer membrane of a normal healthy “self” cell. They will not be directed towards the debris of “self” cells as is believed in Lupus. Thrombocytopenia is a good example of autoimmunity. Our platelets are targeted and eliminated by the adaptive immune system. Antibodies are produced that bind to these cells and label them as pathogenic. The adaptive immune system will do this for the rest of the life of the subject. The adaptive immune system retains a memory of every pathogen it encounters. The platelets are forever labelled as pathogenic. This process is what I term TRUE AUTOIMMUNITY. Sometimes people who have been diagnosed with thrombocytopenia will have their condition resolve itself. That is not true autoimmunity, true autoimmunity cannot resolve itself. It is on or off, all or none.
Lupus is a rather broad spectrum illness. It is referred to as the disease with a thousand faces. Different people will exhibit different symptoms. Doctors currently follow a criterion of 11 clinical manifestations in diagnosing Lupus. In order to be diagnosed with Lupus a subject must meet 4 of 11 possible criteria. My clinical manifestations include anaemia, photosensitivity, non-erosive polyarthritis, positive for antinuclear antibodies or ANA, positive for anti-dsDNA (double stranded DNA) antibodies, positive for antiphospholipid antibodies. Other symptoms include deep vein thrombosis, Raynaud’s phenomena, and acne pustules. To any doctor I would have Lupus.
In 95% of Lupus cases a definitive diagnosis is followed after confirmation of a positive test for ANA coupled with the other criteria. A positive test for antinuclear antibodies is a non-specific test and it is relatively common, even in the healthy population(1). What this test means is that you are producing an antibody towards the nucleus of a cell. It does not tell us what part of the nucleus. A more specific test is incorporated for identification as well as for a quantative result. These tests are called assays. The assays include radioimmunoassay or Farr assay, enzyme-linked immune-absorbent assay(ELISA), and immuno-flourescent assay(IF), to name a few, there are others. The Farr assay is being replaced by the other two assays so that laboratory staff are not exposed to radioactive materials. In any case, all of these test procedures utilize foreign substances to bind the antibodies that are found in your blood. The test for anti-dsDNA(deoxyribonucleic acid) antibodies using the IF assay utilizes dsDNA from a micro-organism known as the Haemoflagellate Crithidia lucilae (1). They use this dsDNA and not yours because this DNA is a pure circular double strand and it is readily available. The back bone of the DNA structure is what these antibodies bind to. The molecular structures of the DNA back bone in all eukaryotic(human) cells are the same.
These assays do not prove autoimmunity. The anti-dsDNA antibody that you produce will bind to your DNA, the DNA of your cousin in Boston and ralphies DNA, your pet dog. It is only ASSUMED to be directed at your DNA because they have not found a pathogen. It is also assumed to be your DNA because this antibody is also found in the healthy population. Healthy people are not sick, they could not have a pathogen, they must be getting rid of their own cellular debris. This must be part of normal cell apoptosis(programmed cell death). These are the perceived truths, but they are wrong. What if the healthy population also has a pathogen? A pathogen that they are asymptomatic(no symptoms) towards. A pathogen whose cellular debris provokes an immune response but the medical community does not recognise this as such. A pathogen that has not been found because they have not utilized the “gold standard” testing method to detect this pathogen. A pathogen known as parasitic filarial nematode worms.
One very important fact that must not be overlooked is the fact of the bias or authority that the innate immune system has over our adaptive immune system when it comes to the elimination of “self” cells, or “self” cell debris. The innate immune system is also referred to as the “primitive immune system”. PRIMITIVE, because it existed before the adaptive immune system. We inherited this immune system from our primate ancestors. The primitive immune system has been removing “self” cells and “self” cell debris for quite some time. Outside of being our front line of defence against pathogens at the point of entrance into our bodies, the primitive immune system is also responsible for “self” cell elimination and tissue repair, this is a primary function. The adaptive immune system plays no such role. It’s sole purpose is elimination of pathogens and when it is activated it is ruthless. It will eliminate all of the pathogen, it will not stop until it has done so.
PARASITIC FILARIAL NEMATODE WORMS
Parasitic filarial nematode worms infect every life form on this planet. They are very successful. There are 9 known filarial nematode worms where humans are the definitive(only) host. The disease created by these worms is called Filariasis. They are divided into three groups according to the niche within the body that they occupy. The groups are termed Lymphatic Filariasis, Subcutaneous Filariasis, and Serous Cavity Filariasis. Lymphatic Filariasis consists of the worms Wuchereria bancrofti, Brugia malayi, and Brugia timori. They like the lymphatic system such as the lymph nodes. Subcutaneous Filariasis consists of the worms Loa loa, Mansonella streptocerca, Drancunculus medinensus, and Onchocerca volvulus. They like the subcutaneous layer of our skin. Serous Cavity Filariasis consists of the worms Mansonella perstans, and Mansonella ozzardi. They like the deep tissues of the abdomen.
All of these worms have a complicated life cycle, which is primarily composed of 5 stages. All of these worms require an intermediate host for transmission. The intermediate host is termed the Vector. In all cases the Vector is a blood sucking insect, a fly or mosquito, except for one, Drancunculus medinensus is transmitted by ingestion of a micro-crustacean known as a Copepod. After the adult worms mate the female will give birth to live first stage larvae by the thousands. These larvae are called microfilaria. Some microfilaria exhibit periodicity, that is, they are geared to the feeding habits of the vector insect. An example is Loa loa, whose vector is the deerfly. The best time of the day to search for the microfilaria in the blood is between 12:00 and 2:00 in the afternoon, where as with Wuchereria bancrofti, whose vector is the mosquito, 10:00 and 2:00 in the morning are the best times. Mansonella streptocerca and Onchocerca volvulus do not utilize the blood, they can be found in the dermis layer of our skin at any time. Mansonella perstans and M. ozzardi utilize the blood but show no periodicity.
When the first stage larvae are sucked up by the feeding vector insect, they will moult through 2 stages. When they have reached the third stage they are now infectious. When the vector insect takes another blood meal the third stage larvae are injected into the skin of the human host. Over the course of about a year the third stage larvae will moult through 2 more stages and become the adult worm. Generally, we have two conditions of infection, Filariasis and Occult Filariasis. With Occult Filariasis a diagnosis is based on clinical manifestations of the adult worms, no microfilaria can be found in the peripheral blood. These people are termed amicrofilaraemic(allergic). This is in contrast with Filariasis whose diagnosis can be based solely on the direct observation of microfilaria in the peripheral blood. These people are termed microfilaraemic(tolerant). The areas of the world were these worms are considered endemic are areas that are tropical and sub-tropical. It is believed by the medical community that these worms are confined to these geographical locations. It is this perceived truth that prevents me from convincing doctors of what I have found to be the cause of Lupus.
Because these worms are the current problems of developing and under-developed nations their behaviour is poorly understood. They simply do not have the money to carry out the research. A lot is known, molecular biology has come a long ways in the last 25 years, but we still do not know their true behaviour in our bodies. This is primarily the result of us not having the diagnostic machines that are capable of viewing these worms while they are in the body. We simply cannot see them and this is why we have a plague. There is an assumption that these worms are confined to their niche within our bodies, and that is simply not true. There is nowhere in the human body were these worms cannot go. There are no exceptions. The only limiting factor is the size of the worm. Wuchereria Bancrofti will not be able to fit through a venous hole in the bone of the leg if it will not accommodate its size.
THE ILLUSION
I do not wish to come across as a health care, doctor bashing lunatic, but these people and their system have screwed everything up. I have Lupus and it took doctors 2 years of putting things in my butt, down my throat, extracting stuff out of my bones, and even more out of my veins before I was finally diagnosed with a disease that has no cause and no cure. I am infected with parasitic filarial nematode worms, of this, you can be certain. You are infected with parasitic filarial nematode worms, of this, you can be certain. I do not mean you people who have been diagnosed with Lupus, I mean most, if not all of you. That's right, everyone on this planet is infected with filarial nematode worms. You may not be infected to same extent that I am infected, and I may not be infected to the same extent as someone else, but we are all infected. Because of this fact, the incidence of disease, of pathology, is going to increase. More and more people are going to be diagnosed with an illness that has no cause and no cure. This will all stem from an increase in the total worm population within our bodies. As the burden of these worms escalates from continuous exposure, pathology will increase from re-infection. If we do not do something about it, it will soon be out of control, if it is not already so.
So what exactly is the illusion? How has it been created? The illusion is that we have the evidence for these parasite in our bodies, but it has gone undetected. A parasite that has gone undetected, because developed nations utilize invalid diagnostic testing measures. A parasite that has gone undetected, because the medical community has a perceived truth that these parasites are confined. A parasite that has gone undetected, because the medical community has blantantly been utilizing broad-spectrum antibiotics. I have gone to the doctors, I have told them my self diagnosis, and they have tested me, reluctantly. The first doctor I saw tested me for elevated eosinophils. People who have a filarial nematode infection will sometimes have elevated eosinophils. Elevated eosinophils can also be found in some autoimmune diseases, it is associated with inflammation and a disease flare, this is another perceived truth. If elevated eosinophils are found in autoimmune disease it is treated with steroids. At the time of this test I was taking prednisone, a cortical steroid, naturally the test result was negative. I told the doctor the test would be negative, but I was ignored.
I then visited a tropical disease clinic. They would not even see me because I had not travelled to an endemic region for filarial worms. I live in Canada, I have never left Canada. Canada is almost as far away as one can get from the tropics. There is no damn way I could be infected with a tropical disease, another perceived truth. My next visit was to a hospital. I was treated as if I were psychotic. I was placed in a waiting room with nothing but a bed, a bed that had restraining straps. I was told that I was delusional, that it was all in my head. Parasitic filarial nematode worms are a tropical disease, they cannot exist in Canada, the doctor kindly pointed this out and showed me a map of the regions of the world that are endemic for W. bancrofti. Their test results also came back negative. They used an invalid testing procedure. They withdrew blood from my cephalic vein at my elbow. If the microfilaria are not present in large numbers within the blood they cannot be found with this method. If I am amicrofilaraemic they cannot be found with this method. If I am infected with a worm whose microfilaria does not utilize the blood, they cannot be found with this method. I knew his method of sampling was incorrect and I told him to extract blood from my finger tips. He simply shuck is head “NO”. These are the blockades that I have faced with the medical community.
The only choice available to me was to continue testing my own blood. It was either do this or accept what the doctors were telling me. For about 3 weeks I did believe them and that was not a good time in my life. The testing method that I employed to detect microfilaria in my peripheral blood is known as “the gold standard”. This is a medical term for a perfected procedure. I was searching for the microfilaria of the African eye worm Loa loa. The gold standard testing procedure is a pin prick of the finger. The small drop of blood will be spread across a microscopic glass slide. The slide will then be immersed in alcohol for fixation. After this procedure it will then be immersed in a giemsa stain solution. The giemsa stain will stain the nuclei within the microfilaria and allow identification to the type of microfilaria to take place(figure 1). The sample of blood must come from the finger tips and it must be collected at specific times of the day. For Loa loa that time is between 12:00 and 2:00 in the afternoon.
I have followed these standards studiously, and I did not find what I should have found. What I mean by that is, I did not find what has been found by the medical community for the better part of the last 90 years(figure 1). I found something totally different(figure 2). The different findings really confused me. I was throwing my slide specimens in the garbage because I was not finding what I should be finding. This difference will explain many things. What I have found in my peripheral blood are microfilaria that cannot be identified. They cannot be identified because of the type of immune response that is directed against them. Because this immune response has not been previously recorded it brings into light confirmation of diversity. This diversity is a foundation of elongated pathogenic conflict with humans and filarial nematode worms.
When we humans first encounter a pathogen there will be a known pathological sequence. The pathogen in question will behave in a certain manner in all humans. The subsequent immune response humans will exhibit will also behave in a certain manner. This is the typical scenario upon first contact. When there is a change in this scenario we are witnessing adaptation and in all likelihood it will be a genetic adaptation. This is what has occurred with humans and filarial nematode worms. We have been experiencing change with our immune responses to these worms. What these changes create are sub-populations. What these changes create is diversity and that can only be the result of long term pathogen exposure. This is natural selections finest hour.
The documented cases of filarial infection recognize two scenarios. Microfilaremic persons and amicrofilaraemic persons. Microfilaraemic persons appear to be tolerant to the presence of the microfilaria in the blood or tissues and also to the presence of the adult worms in the tissues. These people will exhibit some inflammatory conditions against these parasites over the course of their infections but they do not tend to develop chronic disease. Amicrofilaraemic persons on the other hand will develop chronic disease. The immune responses exhibited by these persons can have quite debilitating effects. Elephantiasis is good example of chronic disease. This is a condition in which there is a gross enlargement of one or more appendages(an arm or leg). It can result in amputation. These are the documented cases within the endemic regions of known filarial nematode infections. People who are amicrofilaraemic can acquire this condition naturally through their immune system or it can be drug induced. Drugs used to treat filariasis can sterilize adult female worms, embryogenesis of microfilaria can be halted or significantly reduced, which can make a microfilaraemic person into a amicrofilaraemic person.
The documented cases of persons who are not native to the endemic regions and who upon visiting these regions contract filarial infection tend to exhibit more allergic qualities to these parasites. Although they will experience the same symptoms there will be a more severe reaction of these symptoms. All of these documented cases clearly show that there is already diversity amongst us humans, but there is also diversity amongst the filarial nematodes. It will be a two way street, we adapt to an adaptation that the worms have acquired who in turn adapt to our adaptation. It is a vicious circle and this is the result of long term exposure.
Human filarial nematode worms have been extracted from humans that simple express on the epicuticle the normal antigenic molecules that are present on all living cells. These molecules compose their glycocalyx(slime coat) and consist of polysaccharides and glycolipids, I call this the primitive state. They have also been found to have other molecules that are not of their making. They have been found to also express a human serum(blood) molecule known as Albumin(2). Human serum albumin is a protein within our bloods plasma and it is produced by our livers. It is the most abundant plasma protein, immunoglobulins(antibodies) are the next abundant protein. Albumin acts for us as a transport molecule. It aids other proteins such as vitamins, hormones, and antibiotics by binding to them and getting them to where they need to go, namely our cells. The adaptation by the worms to have host serum albumin adhere to their epicuticles has not yet been defined, but clearly it is an adaptation that provides nutrient deliver and may also provide immune system evasion. This is an adaptation of the worm and it is a resent phenomenon, we are just now beginning to see adaptation on the part of humans in a sub-population that suffer from analbuminenia. These people produce little or no albumin(3). These are all documented and published articles of medical research that clearly display diversity amongst parasite and host. What I found in my peripheral blood cannot be explained by any of these documented cases. I am exhibiting a different immune response to these parasites.
I must make one thing quite clear to begin with. Lupus, as I have come to know it from observation of my illness as well as observations from my peripheral blood is a multiple filarial nematode SPECIES infection. I have different species, but for some of us who have lupus we may have only one species. There will be diversity, both in the type of worm and in the type of immune response. You may have a greater number of one species and I may have a greater number of a different species. The immune response that I have encountered has not been previously recorded against filarial nematodes. It is undocumented, and this immune response is a beauty.
The immune responses originate from proteins that are produced by our livers and our adipocytes(fat cells and debated), these proteins are C-reactive protein, and Matrix metalloproteinases. C-reactive protein does something that is truly exceptional, truly phenomenal. C-reactive protein can solubilize(dissolve) nuclear materials. That is a very unique feature and this process has been previously documented in vitro(in glass)(4), this paper is important because it directly references to lupus. One of the more difficult nuclear substances to solubilize is chromatin or DNA. C-reactive protein can dissolve this substance. The way it works for eradication of microfilaria is for C-reactive protein to encompass the pathogen(figure 2). It then goes to work by activating the complement system. The complement system is a biochemical cascade which attacks surfaces of foreign cells. It is a major component of the innate immune system. The microfilaria that I am finding are encompassed by C-reactive protein, I have the images. The microfilaria that are encompassed by C-reactive protein appear fuzzy. As if there is a slime coating around the microfilaria. The nuclei that are inside the cuticle stain with giemsa but are indistinguishable as to their species. Because the solubilization is in process, it is ongoing, the nuclei are essentially mush, a jumbled mass of dissolving nuclear material. What I have also been finding are what appear to be a skeleton. A conclusion that I have come to is that this must be the result from C-reactive protein. It dissolves the inner nuclear materials(figure 3) but not the outer cuticle of microfilaria, but I do believe this debris is eventually gotten rid of in a secondary attack, and this is were the Matrix metalloproteinases comes in(figure 4,5).
The immune response carried out by C-reactive protein, does not produce antinuclear antibodies in a direct fashion. C-reactive proteins are not capable of presenting the nuclear antigens to the adaptive immune system. The antigenic properties of these nuclei are dissolved and contained within this protein(figure 3). Once all of the nuclear materials are absorbed into the C-reactive protein, this protein will then un-encompass the microfilaria cuticle. The C-reactive protein laden with nuclear debris will be cleared from the body through macrophages scavenging this waste product. We can now see why antinuclear antibodies are produced. Macrophages will have to follow procedure and present the nuclear antigens to the adaptive immune system, which in turn produces antibodies to this nuclear debris. The de-nucleated cuticle will be left in the tissues. Matrix metalloproteinases now comes into play, it will form into an aggulation(clumping) within the tissues and it will engulf the de-nucleated microfilaria cuticle(figure 4,5). Matrix metalloproteinases belong to the family of proteases and are capable of degrading all kinds of extracellular matrix proteins(5). The cuticle of microfilaria have a molecular composition of a protein called collagen. Collagen is also the primary cellular constituent in the dermis layer of our skin. If the dermis layer of skin becomes injured, Matrix metalloproteinases will breakdown the damaged collagen fibres and rid them from the body.
There are lot of different classes of proteases for the degradation of collagen and this is because there are different types of collagen. The process of collagen degradation is regulated by two systems. These systems are called the renin-angiotensin and kallikrein-kininogen systems. Your genotype, what nature has given you, will be a dictator to the type of enzymes that these systems will produce to regulate your immune response. It is a very complicated process and it is beyond the scope of this paper. The mechanics of the type of immune response I have descirbed has been previously studied by medical scientists with reference to autoimmune disease, particularly MMP-2 and MMP-9. The one thing these studies have lacked is a reference to a pathogenic cause.
I have been able to find microfilaria in my peripheral blood, but very few. Why are the medical community unable to do the same? Extraction of large blood samples from large veins will yield negative results. This fact I have clearly established. In nursing medical texts and online medical protocols for the collection of blood in preparation of thin blood smears, nurses are instructed to NOT utilize the first drop of blood that appears after the lancet as pierced the skin(6). They discard this drop of blood because its main constituents will be the interstitial fluid from the dermis layer of skin. They are preparing thin blood smears to examine the constituents of the peripheral blood from the capillaries not the interstitial tissues. I have found that this first drop of blood is crucial to detection of microfilaria presence. Microfilaria reside in the interstitial tissues of the dermis layer of our skin, they do not reside in the capillaries. When I have prepared my slides, I have made a smear with the first drop of blood and also with the subsequent drops of blood. Microfilaria can only be detected on the thin smears of the first drop of blood. I do not find microfilaria on the smears prepared with the subsequent drops of blood. The microfilaria that are residents in the dermis layer of skin become vacated from these tissues in the first drop of blood. If the microfilaria load is not present in large numbers, the subsequent drops of blood will be negative for microfilaria presence.
I have made an accusation that the healthy population is also infected. Proof to this claim resides in the fact that they are producing antinuclear antibodies, just like lupus. Further proof also resides in, of all places, a drug addict. There is a street drug known as crystal methamphetamine. It is a derivative of speed. Persons who inject this drug into their veins are normal healthy individuals. They develop a drug addiction which is not normal, nor is it healthy, but they are not physically sick. These people after injecting this drug develop sores on their bodies. These sores are the result of them scratching at what doctors call "imaginary bugs on their skin". They really have bugs, only they are not on their skin, they are in their skin. This drug, when injected also influences filarial nematode worms. It causes them to go into hyperactivity in the dermis layer of skin. This hyperactivity can be felt by the nerve endings in the epidermis. It will be very, very itchy.
CONCLUSION
So there you have it, explanations to our immune responses, explanations to our faulty diagnostic practices, images of peripheral blood specimens providing evidence to the pathogenic cause of Lupus. References to published medical articles of established scientific research that will substantiate my claim as to the type of immune response carried out by our bodies in response to filarial nematode infection. Parasitic filarial nematode worms are causing my illness, as well as, yours. I have come to the conclusion that I am amicrofilaraemic(allergic) to the microfilaria, it is why I do not find larger numbers of microfilaria in my peripheral blood. As for the adult worm, here, I am microfilaraemic(tolerant). Nature has still not a found a way to deal with this macro-organism. There is no circulating antigen within our blood. C-reactive protein readily binds to the antigenic molecules of the microfilaria. This is the factor that renders us amicrofilaraemic, I am also amicrofilaraemic because of drug therapy. I have taken a broad spectrum antibiotic called tetracycline. This antibiotic renders the adult female worm of Onchocerca volvulus to near sterility. Onchocerca volvulus is dependent on a intracellular bacteria called Wolbachia. This bacteria acts as the mitochondria within the eggs when it comes to embryogenesis. When this bacteria is eliminated, so is the engine behind embryogenesis, tetracycline's kill this bacteria.
Lupus is a disease that I have intimately come to know. Through observation of what was occurring within my body I have now come to the conclusion that Lupus is a filarial nematode worm infection of two species. Those species are Onchocerca volvulus and Mansonella streptocerca. Onchocerca volvulus is a very large worm, the female is some 18 inches long but very thin, Mansonella streptocerca is a very small worm about 1 inch long. With the type of immune response carried out by our bodies systems, we do not suffer the chronic disease consequences that are prevalent within the endemic regions of known filarial nematode infections. I am not sure if that is a blessing or a curse. The truth is now on the table, what is your perception of this truth, what is your reality?
What…do…you…believe????????????
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