Human Anatomy, Physiology, and Medicine. Anything human!
I am not offended by your suggestion that my lesions may be HIV related.
Perhaps you might reread Sabrina's very first post though.
I live in Central London and HIV has affected my life since 1989. Indirectly.
I have lost many friends and shed many tears.
This possibility has already occurred to me.
But I am not HIV positive.
The blood tests I have had on the NHS here show nothing. There is nothing extaordinary about the results apparently, which is why support and treatment options are limited. Many people now have now told you the same thing, so it's time for you to move on.
I can appreciate that I may have aquired Chlamidia Pneumoniae via having a few HIV positive friends but it is an airbourne transmitted disease and almost everybody has been exposed to this pathogen. Infact, I might have picked it up from a pigeon that flew up in surprise as I turned a corner into Trafalgar Square.
It is hard to test for C.Pneumoniae.
I was tested because a doctor researching CFS, Lyme, Fibromyalgia etc etc noticed that it is present in many of his patients.
C. Pneumoniae is part of the genetic makeup of Borrelia too...heres an excerpt to the genome analysis of the pathogenic species B.Burgdorferi.
"Functional classes with low OCs (<0.6): metabolic pathways and transport and other membrane components. Consistent with the picture emerging from other pathogenic bacteria, the genomes of the two spirochetes are noticeably reduced in terms of genes coding for metabolic enzymes, which suggests a general degeneration of metabolic systems that most likely were represented in their common ancestor. However, even in this degenerate state, there are striking differences in the predicted metabolic pathways between T. pallidum and B. burgdorferi, suggesting different adaptation strategies. The common metabolic heritage is largely restricted to the trunk of the glycolytic Embden-Meyerhof pathway, the phosphorylation steps of nucleotide interconversion, and a system for membrane potential generation, namely, the multisubunit V-type ATPase. The latter is the principal energy-generating ATPase in archaea; in bacteria, the V-ATPase subunits are encoded in a single operon that appears to be evolutionarily mobile and shows a scattered distribution, being found, in addition to in the spirochetes, in Chlamydia, Enterococcus, Deinococcus, and Thermus"
http://iai.asm.org/cgi/content/full/68/ ... type=HWCIT
Your analysis is quite accurate. I seem to be working my way back to the original lesion which is on the center(centre) of my scalp.
However, the itching and first lesion started on my left forarm and around my knees.
Itraconazole alone has not removed this. I have used skin softening products containing lactic acid. Exfoliants of all kinds. Diamataceous Earth scrubs. Salt Scrubs. Peppermint Oil and many other products.
Itraconazole stopped the itching on my scalp ...almost. But I knew it was having a profound effect as my appearance and mental state improved quite quickly too.
Itraconazole is more effective than Diflucan I would say.
the article on Lyme and Diflucan is to be found on LymeBusters I think, and is from an interview with a German doctor who treated himself in this way and subsequently many others too.)
Pictures speak louder than words.
You need combined therapy.
Lesions will scar and this will stay.
My advise is as earlier given.
Talk it over with Your GP.
There will be the possibilty of relapse but all that in the mean time is reduced is a pro.
Hi Tam tam,
I would like to thank you once again for helping these people, because no-one else apparently was, partly because their presenting clinical features are, for one reason or another, not easily classified within the taxonomy of medicine as we have come to know and understand it up to now.
It is good that you have repeated your earlier advice, viz. the people who definitely have this apparently novel clinical condition would tend to improve if they were prescribed combination therapy by their doctor. Therefore, they need to discuss the rationale for this with their doctor, so that a decision can be arrived at regarding this.
Do not be afraid to apply what you read about the clinical features of a dermatophyte infection to your own signs and symptoms, which you have alluded to (but rather too briefly) in previous posts.
This is what I meant by you and London searching too high and wide. A lot of it was very intelligent, but it was not direct or precise enough to help you with your specific and clear cut clinical complaints.
Stick to one thing at a time. You mentioned that you observed something in your skin, which someone thought may be 'spider veins', and then Tam said to research apical growth. You then researched some clever science about skin cells in relation to this, but not really in relation to yourself.
What I think is, going by what Tam has said, and what has been alluded to in the videos, is that apical growth is one way that this infection/infestation may slowly grow and spread, and that you might be able to see this, if you know how to look.
I think that I can see some examples of this (possibly past and present) in Hartuk's most helpful and generous photographs.
Dermatophyte infections extend and grow in this way (apical growth), extending into hyphae, then myceliae. I do realise that this infection/infestation is composed of many different elements, (hence the postulated need for combination therapy to be prescribed), but all of the professionals involved in treating it are agreed that a fungal infection is part of it. The mold (dermatophyte) involved may well be genetically modified too, I do not know. What I do know is, even when a person has been 'healed back to source', and the 'principal seat' of infection/infestation is kept as suppressed as possible, the affected person will continue to react badly when in an environment containing mold or active fungal spores.
Therefore, you want the doctor to suggest something that will arrest the apical growth and destroy any live dermatophytes. However, any prescribed regimen of treatment must take account of all of the different elements within the apparent overall infection and infestation.
This is why I think that people should consult Ginger Savely, or a doctor recommended by the MRF.
Although I do not like when people charge money for anything I thought I would pass this along to those that actually have some money to spare. He states it is money back guaruntee..and I do believe him.
So, I am not promoting..just passing along important info. It came to me in an e-mail and it would be unfair not to post it.
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Cyanobacterium= a bacterium that also will grow a mold!
Hence the 1917 confusion.
Its a synthetic micro organism and a lot seems to be hung in its "tree".
c.q the micro organism is informed with a multiple set genes derived from plant, parasite, maybe bird but for sure mammal and higher primate.
All now represents one (1)
A new entity with multiple expression.
Its an entity because it is environmentally resistant c.q will proliferate outside the lab.
Under favorable conditions it will grow back multi cellular expression.
The human body provides this type of strata.
The process is bacterial load depending.
Hi Tam tam,
I understand the concept of the cloned microorganism (cyano) being like a tree, with multiple set genes from plants, parasites, possibly bird, all 'informing' it, e.g. all swirling about in the 'sap', each having their role to play, and, the higher the bacterial load is allowed to get, the stronger and more resilient the whole process becomes.
What I do not understand at all is the reference to genes being included from a mammal and/or a higher primate.
Could you please explain?
Why are you so certain about this?
Could you say why it is significant?
Is it anything to do with the helminths being also part of this syndrome? (A bit like the systemic insect technology associated with the plant technology maybe?)
I realise that the helminths would not be the main reason whatsoever for inclusion of the gene sets from the mammal and/or higher primate.
There will be a much more important reasion than that, I think. But I absolutely do not understand that bit, although I think it might be crucial.
Maybe this will help:
Correlated evolution between host immunity and parasite life histories in primates and oxyurid parasites
Maturation time is a pivotal life-history trait of parasitic nematodes, determining adult body size, as well as daily and total fecundity. Recent theoretical work has emphasized the influence of prematurational mortality on the optimal values of age and size at maturity in nematodes. Eosinophils are a family of white blood cells often associated with infections by parasitic nematodes. Although the role of eosinophils in nematode resistance is controversial, recent work has suggested that the action of these immune effectors might be limited to the larval stages of the parasite. If eosinophils act on larval survival, one might predict, in line with theoretical models, that nematode species living in hosts with large eosinophil numbers should show reduced age and size at maturity. We tested this prediction using the association between the pinworms (Oxyuridae, Nematoda) and their primate hosts. Pinworms are highly host specific and are expected to be involved in a coevolutionary process with their hosts. We found that the body size of female parasites was negatively correlated with eosinophil concentration, whereas the concentration of two other leucocyte families--neutrophils and lymphocytes--was unrelated to female body size. Egg size of parasites also decreased with host eosinophil concentration, independently of female size. Male body size was unrelated to host immune parameters. Primates with the highest immune defence, therefore, harbour small female pinworms laying small eggs. These results are in agreement with theoretical expectations and suggest that life histories of oxyurid parasites covary with the immune defence of their hosts. Our findings illustrate the potential for host immune defence as a factor driving parasite life-history evolution.
Sorry, probably not. I misread your question to Tam...your was about Genes.
And here is a new one for me to see. It is about the trypansomes.
Newly Discovered Protein An Important Tool For Sleeping Sickness Research
WOODS HOLE, MA -- Sixty million people in 36 countries of sub-Saharan Africa are threatened daily by a deadly parasitic disease known as African sleeping sickness. The disease is caused by organisms called trypanosomes, which are spread by the tsetse fly. African sleeping sickness affects approximately 500,000 people in sub-Saharan Africa, a quarter of whom will die this year. Because the trypanosome has an exceptional genetic strategy for evading the human immune system and resisting treatment, the current treatment for this disease is melarsoprol, an antiquated drug with terrible side effects, including death.
In the February issue (Volume 17, Issue 3) of the journal Molecular Cell, scientists in the Marine Biological Laboratory's (MBL's) Josephine Bay Paul Center for Comparative Molecular Biology and Evolution report their discovery of a protein called JBP2, which will help them test their hypothesis that a uniquely modified DNA base called base J is a key component of the trypanosome's mechanism for evading the immune system. If the hypothesis is correct, it will bring scientists closer to developing a more effective drug for treating African sleeping sickness.
The trypanosome evades the human immune system because it is coated with a surface antigen called variant surface glycoprotein (VSG). The human body makes antibodies for VSG, but trypanosomes randomly switch to another antigen when the organisms divide and reproduce. Trypanosomes whose VSG has switched evade the antibodies the human immune system made to fight the original antigen, thus assuring the long-term survival of these parasites within their hosts. The trypanosome has approximately 1,000 different VSG genes, but only expresses one at a time while the others are somehow silenced. This genetic trick, called antigenic variation, has severely limited sleeping sickness treatment options and essentially ruled out the possibility of a vaccine.
MBL trypanosome experts in Robert Sabatini's lab hypothesize that base J (beta-D-glucosylhydroxymethyluracil) may play an important role in the gene silencing process behind antigenic variation. With the goal of learning how the organism regulates the process of antigenic variation, the scientists have been trying to understand how the trypanosome makes base J.
The discovery of JBP2, a member of a protein family that helps control DNA-related functions, is a significant breakthrough in this quest because Sabatini and his colleagues were able to demonstrate that the protein is the key regulator of base J synthesis. This will provide the scientists a new tool to elucidate the biological function of this unique modified DNA base in the regulation of antigenic variation.
If base J does indeed play a role in the gene silencing that enables the trypanosome to change its antigen coating, the discovery of JBP2 may one day enable scientists to create a drug that prevents the manufacture of base J, affecting the trypanosome's ability to vary its antigenic coating, and therefore allowing the human immune system to kill it.
Understanding trypanosomes at the molecular level is key to fighting African sleeping sickness and diseases caused by similar parasites.
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