Zwarte schimmel veroorzaakt meningitis

 

http://www.toxicmoldfoundation.com/fungus-caused-meningitis.html

Fungus Caused Meningitis? Black Mold

A black mold entering the spines of hundreds of people who received contaminated vaccines for back pain has marked uncharted medical territory.
This fungus, classified as being difficult to diagnose, has never seemingly caused meningitis, until now. It requires at least three months of a treatment that can cause hallucinations. Not only is it unknown when is it safe to stop treating, but there is also no good way to know how to monitor those who fear the fungus, which may be festering silently inside their bodies.
The fungus’ brown-black color signals an armor that helped the mold sneak past the immune defenses of healthy people.
“I don’t think there is a precedent for this kind of thing,” said Dr. Arjun Srinivasan of the Centers for Disease Control and Prevention (CDC). “This is definitely new territory for us.”

Dat noemen ze struisvogelpolitiek. Vraag het maar eens aan de vele mensen die lijden aan Sick Building Syndrome en excruciating headaches hadden vooraleer ze doodziek werden.

Yuppie flu, stress, ... we kennen het al wel. 

http://www.policyholdersofamerica.org/doc/CIRS_PEER_REVIEWED_PAPER.pdf 
Hier het bewijs dat ze het al lang weten. 

Vervuild medicijn in VS te vroeg verdeeld

Door: Redactie
24/10/12 - 04u44  Bron: ad.nl © ap.

Het vervuilde geneesmiddel dat tot nu toe aan 23 Amerikanen het leven heeft gekost, is gedistribueerd voordat de producent de testresultaten binnen had over de veiligheid van het medicijn. Dat hebben de gezondheidsautoriteiten in de staat Massachusetts bekendgemaakt.

Inspecteurs troffen onder meer schimmel aan, een lekkende boiler, sterk vervuilde vloermatten en een slordige sterilisatieprocedure.

Tijdens een inspectie van de New England Compounding Center (NECC) in de plaats Framingham zijn de afgelopen week gebreken geconstateerd die erop lijken te duiden dat de producent de hygiënevoorschriften niet heeft nageleefd. Zo troffen inspecteurs tijdens hun onderzoek van de fabriek onder meer schimmel aan. Ook stuitten ze op sterk vervuilde vloermatten en een lekkende boiler. De manier waarop het bedrijf zijn apparatuur steriliseert, wordt bovendien omschreven als slordig.

308 besmettingen
Het aantal besmettingen ten gevolge van de uitbraak van hersenvliesontsteking (meningitis) is intussen opgelopen tot 308. De uitbraak is zeer waarschijnlijk veroorzaakt door een geneesmiddel dat bij NECC werd vervaardigd, een steroïdencocktail die wordt gebruikt als pijnbestrijder.

Black mold works antiviral

Have you ever wondered why never catch a cold anymore since you have ME or CFS?

Maybe you suffer from mold intoxication. Some people simply cannot eliminate the neurotoxines released by mold. Some bacteria like Lyme, bartonella and babesia produce the same symptoms. Blue green algue, ciguaterae, chlamydia pneumonia, ... yessss same effect.

Sick building syndrome is not a new concept but a severely underestimated factor in ME. Why do doctors don't ever ask you if you have a leaky roof at your work or house, have musty tiles in the bathroom, HVAC at work, did you work as an airhostess,  ... Maybe it is like opening a jar of worms because fixing mold is very expensive.
If it is at your work, change! If it is your house, move! If none of it is possible, think about it again!

Never ever try to remove the mold yourself. Never! You can die from it. Period. Google a professional. Check with your insurance company what can be done.

Minagawa K, Kouzuki S, Yoshimoto J, Kawamura Y, Tani H, Iwata T, Terui Y, Nakai H, Yagi S, Hattori N, Fujiwara T, Kamigauchi T. Stachyflin and acetylstachyflin, novel anti-influenza A virus substances, produced by Stachybotrys (black mold) sp. RF-7260. I. Isolation, structure elucidation and biological activities. J Antibiot (Tokyo). 2002 Feb;55(2):155-64. PMID: 12002997

Two novel compounds, stachyflin and acetylstachyflin, have been isolated by solid-state fermentation of Stachybotrys sp. RF-7260.

Stachyflin showed antiviral activity against influenza A virus (H1N1) in vitro with an IC50 value of 0.003 microM. Acetylstachyflin was about 77-fold less active than stachyflin.

*

Mari Nakatani, Masahiko Nakamura, Akiyuki Suzuki, Munenori Inoue, and Tadashi Katoh. A New Strategy toward the Total Synthesis of Stachyflin, A Potent Anti-Influenza A Virus Agent: Concise Route to the Tetracyclic Core Structure. Org. Lett., 2002, 4 (25), pp 44834486. PMID: 12465918

A new strategy directed toward the total synthesis of stachyflin, a potent and novel anti-influenza A virus agent isolated from a microorganism, has been presented through the enantioselective synthesis of the tetracyclic core structure. The synthetic method features a BF3Et2O-induced domino epoxide-opening/rearrangement/cyclization reaction as the key step.

*

Minagawa K, Kouzuki S, Tani H, Ishii K, Tanimoto T, Terui Y, Kamigauchi T.. Novel stachyflin derivatives from Stachybotrys sp. RF-7260. Fermentation, isolation, structure elucidation and biological activities. J Antibiot (Tokyo). 2002 Mar;55(3):239-48. PMID: 12014438

Stachybotrys sp. RF-7260 was found to produce stachyflins, novel anti-influenza virus agents, under solid-state fermentation conditions. Feeding DL-lysine to a culture of Stachybotrys sp. RF-7260 induced the formation of the novel compounds, SQ-02-S-L2 and -L1, and feeding DL-valine the formation of SQ-02-S-VI and -V2. The structures of these metabolites were determined by detailed 2D NMR analyses in comparison with acetylstachyflin. SQ-02-S-L2 and -L1 have the lysine moiety and SQ-02-S-V1 has the valine moiety. SQ-02-S-V2 has an amidine moiety instead of the lactam moiety in acetylstachyflin. SQ-02-S-L2, -L1 and -V1, substituted on the lactam amide hydrogen, displayed only a low level of the antiviral activity. However, deacetyl SQ-02-S-V2 showed potent antiviral activity similar to stachyflin.

*

Tani N, Dohi Y, Onji Y, Yonemasu K. Antiviral activity of trichothecene mycotoxins (deoxynivalenol, fusarenon-X, and nivalenol) against herpes simplex virus types 1 and 2. Microbiol Immunol. 1995;39(8):635-7. PMID: 7494505

The effect of trichothecene mycotoxins, deoxynivalenol (DON), fusarenon-X (FX) and nivalenol (NIV), on plaque formation of herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) in HEp-2 cells was examined.

The 50% effective concentrations (EC50) of DON, FX, and NIV for HSV-1 plaque formation were 160, 56, and 120 ng/ml, respectively. Those for HSV-2 plaque formation were 94, 26, and 50 ng/ml, respectively. These three mycotoxins showed about 2-fold higher selectivity to HSV-2 than to HSV-1. Plaque formation of HSV-1 was not inhibited with trichothecenes at concentrations completely inhibiting plaque formation when cells were treated during virus adsorption period or 15 hr before infection.

These results indicate that trichothecenes affect replication of HSV-1 after virus adsorption, but not before or during virus adsorption to the host cells.

*

Sawadjoon S, Kittakoop P, Isaka M, Kirtikara K, Madla S, Thebtaranonth Y. Antiviral and antiplasmodial spirodihydrobenzofuran terpenes from the fungus Stachybotrys nephrospora. Planta Med. 2004 Nov;70(11):1085-7. PMID: 15549667

Two known spirodihydrobenzofuran terpenes (1 and 2) were isolated from a mycelium extract of the fungus Stachybotrys nephrospora BCC 3900. Compound 1 (Mer-NF5003F or stachybotrydial) exhibited potent antiviral activity (the IC50 value of 4.32 microg/mL) comparable to the standard drug, acyclovir, while compound 2 was inactive against the HSV-1 virus. Both 1 and 2 possessed antiplasmodial activity (IC50 values of 0.85 and 0.15 microg/mL for 1 and 2, respectively), and were not toxic towards the Vero cell line. A regiospecific conversion of the dialdehyde 1 to the lactone 2 proceeded simply under acidic conditions.

Signs and Symptoms of Autonomic Dysfunction

Some of the listed symptoms are always present while others occur
when a person with Autonomic Dysfunction has been standing or sitting too long:

-Dizziness

-Lightheadedness

-Vertigo (room spinning or the sensation of spinning)

-Feeling faint (pre-syncope)

-Fainting (syncope)

-Chest pain or pressure

-Excessive fatigue

-Rapid heart rate (tachycardia)

-Stomach pain

-Intestinal cramping

-Nausea

-Vomiting

-Retching

-Exercise Intolerance: becoming short of breath on mild exertion,

having chest pain or palpitations on mild exertion. Having excessive

heart rate during or immediately after exercise. Leg cramps or

numbness of arms and legs during or after mild exercise.

-Visible pooling in arms and legs: Deep purple-red color in fingers

and toes.

-White appearance of fingers. Some present with white patches of skin

on arms and legs.

-Extremely cold hands and feet.

-Numbness of hands and feet.

-Muscle weakness

-Muscle and joint pain

-Tremors or mild shaking of hands

-Frequent headaches or migraine headaches

-Irritability due to decreased blood flow to the brain

-Feeling anxious/Having panic attacks due to increased production of

adrenaline

-Mood changes

-Forgetfullness

-Inability to concentrate or remember (frequently referred to

as "brain fog")

-Inability to tolerate changes in temperature

-Decreased sweating or excessive sweating

-Abnormal deep tendon reflexes may or may not be present.

-Basic neurological exam is normal.

-Intelligence normal when receiving adequate cerebral perfusion.

Less frequently recognized signs and symptoms:

-Insomnia

-Disruption of sleep/wake cycle usually consisting of increased

energy late in the evening and lowest energy level in the morning

irregardless of amount or quality of sleep.

-Central sleep apnea

-Need to sleep 12-14 hours in order to complete simple activities of

daily living.

-Anoxic or convulsive seizures that are not epileptic.

-Frequent need to urinate at night.

-Upon standing feels head is "heavy". This resolves with lying down

or with walking around.

-Decrease in (or absence of) lubricating tears in the eye.

-Sensitivity to bright, florescent light and bright sunlight. Many patients report feeling pre-syncopal in large grocery stores and

department stores that use excessive florescent lighting. Flashing

lights and multi-colored lighting can also produce symptoms.

-Visual distortion: Television screens and computer screens can

appear distorted, especially post-syncopal or pre-syncopal episode.

Flat screens are recommended.

-Distorted depth perception resulting in a feeling of unsteadiness.

Often appears to be "clumsy" or excessively cautious when climbing

stairs, reaching for an object, etc.

-Other visual disturbances include a graying out or blacking out of

the visual field; either partially or completely.

-Decreased awareness of what is in the peripheral visual field. This

often causes the patient to startle because they did not perceive

anyone or anything next to them.

-Frequent "bumping into things". Attributed to a combination of

visual and depth perception deficits.

-Noise sensitivity. Loud or beating sounds can cause pre-syncopal

episodes. Difficulty filtering out sounds. Easily distracted by

sounds.

-Sensitivity to odors, even pleasant smelling chemicals such as

perfume. Odors such as cleaning products, gasoline, strong foods,

etc. may cause extreme nausea, retching, vomiting, dizziness and

headache.

Decrease production of saliva or excessive production of saliva.

-Severe constipation and decreased gut motility.

-Weight gain irregardless of diet modifications.

-Overall slowing of metabolism is common. -Increased metabolism (rare)

-Excessive gut motility leading to chronic diarrhea and weight loss.

(less common)

-Sensitivity to touch. Mild pat on the arm or squeeze of the hand can

cause excruciating pain especially right after an episode or if the

patient has not had enough sleep.

-Decrease sensitivity to pain/touch in certain areas. If standing or

sitting too long causes hands and feet to turn cold and blue, patient

will have decreased sensation in these areas due to poor blood flow.

-Taste and appetite changes. Fruits and other acidic foods may taste

extremely acidic. Foods may taste differently if patient is tired,

stressed, or post-syncopal episode.

-Hair loss due to decreased blood supply to hair folicles.

-Speech disturbances: Inability to finish an expressed thought, loss

of train of thought, "spoonerisms", especially if up and about for 2

hours or more without lying flat and resting.

-Comprehension difficulties. Inability to follow a conversation. May

hear words but is unable to understand their context in the sentence.

Cannot focus on more than one activity at a time. May not realize

they are being addressed. Losses conversation focus when topic is

changed. Is easily distracted from the conversation focus by any

environmental stimuli.

-Memory recall deficits in long and short term memory. Improves with

lying down and resting.

-Abdominal migraines. Severe stomach pain triggered by large meal or

by sitting or standing too long. Usually resolves if patient lies

quietly.

-Drifting to the right or left when walking. Most commonly patients

report drifting to the left. Many patients report always fainting to

the left as well. Appears to be unrelated to hand-dominance, but

further research is needed.

-Tend to have mild symptoms of Ehlers-Danlos, but do not necessarily

test positive for the disease. This includes hypermobile joints,

double joints, and soft, velvet-like skin that has little or no

texture.

-Often has another auto-immune disorder.

-Family History of auto-immune disorder or symptoms that resemble

autonomic dysfunction.

-Appears to have more viral illnesses than general population. Often

diagnosed with Chronic Fatigue Immune Dysfunction Syndrome.

I did not compile this list, credit goes to the owners of:

http://www.dysautonomia-eduinfo.org/index.html

Why do you need trace elements?

COPPER: cytochrome oxidase, ceruloplasmin, dopamine beta-hydroxylase, tyrosinase, cytosolic SOD

ZINC: carbonic anhydrase, cytosolic SOD, carboxypeptidase

MOLYBDENUM: xanthine oxidase

SELENIUM: glutathione peroxidase, (antioxidant)

COBALT: vitamin B12, heme synthesis and synthesis and maintenance of myelin

MANGANESE: pyruvate carboxylase, mitochondrial SOD


Wat is SOD?
Wikipedia: Als gevolg van de biologische oxidatieve reacties, kan ook superoxide-ion als bijproduct in cellen ontstaan. Dit is een zeer reactief deeltje, en het wordt dan ook zo snel mogelijk, voor het schade kan aanrichten, door een enzym, (superoxide dismutase), opgeruimd. Superoxide wordt in verband gebracht met allerlei ziekten en het verouderingsproces. Superoxide dismutase dat superoxide laat reageren tot zuurstof en waterstofperoxide, is voor zover bekend het snelste enzym.

What is SOD?
Wikipedia: SOD is an extremely efficient enzyme; it catalyzes the neutralization of superoxide nearly as fast as the two can diffuse together spontaneously in solution. Other proteins, which can be both oxidized and reduced by superoxide, have weak SOD-like activity (e.g. hemoglobin).
While the action of superoxide in the pathogenesis of some conditions is strong, for instance, mice and rats overexpressing CuZnSOD or MnSOD are more resistant to strokes and heart attacks ...

Chronic immune activation

http://imdtheory.blogspot.be/

Abstract: The conclusion of this paper is that non-communicable diseases such as the psychiatric disorders, neurological diseases, autoimmune diseases and other diseases associated with immune system upregulation but not deemed to be autoimmune, such as cardiovascular disease, cancer, type 2 diabetes, porphyria and many others, all arise as a consequence of chronic, aberrant activation of an immune system response which is driven by the transcription factor, nuclear factor kappa beta (NF-kB).

One of the principal functions of the NF-kB immune response is to control intracellular pathogens which establish latency within cells. To achieve this, reactive oxygen species (ROS), such as hydroxyl radical, which are destructive to these pathogens, are generated inside cells. In addition, the cell membrane receptors which are used by these pathogens to gain entry into cells are reduced in number, desensitised, or blocked by antibodies, causing these cells to become hypofunctional. To compensate for this, receptors on other cells may become hyperfunctional.

...

Many of the diseases which are known to be associated with a chronically activated NF-kB driven immune response are also associated with an above average incidence of infection with specific pathogens. I have compiled a list of those pathogens which appear to be most important. They are herpes simplex virus-1, herpes simplex virus-2, human herpes virus-6, cytomegalovirus (herpes family), Epstein-Barr virus (herpes family), varicella zoster (herpes family), mycobacteria, Borna virus, enteroviruses, hepatitis C virus, human papilloma virus, Borrelia bacterium, Toxoplasma gondii protozoon, human endogenous retroviruses, mycoplasma pneumoniae bacterium, Chlamydia pneumoniae bacterium, Helicobacter pylori bacterium, JC virus, Candida albicans fungus and intestinal worms.

This list reveals a crucially important fact. Except for Candida and worms, all these infectious organisms are obligate intracellular parasites which are known to establish latency within cells and can persist in a dormant state for years without causing illness. 

...

Enzymes are frequently seen to be autoantigens in autoimmune diseases and are attacked by antibodies generated by B-cells. About a third of enzymes utilise a metal co-factor, very often iron, which may produce ROS, including hydroxyl radicals. However, virtually all of the enzyme autoantigens I have studied are metalloenzymes which use transition metal ions as a co-factor. The only exception I am aware of is glutamic acid decarboxylase, which utilises pyridoxal phosphate (vitamin B6) as a co-factor and is often an autoantigen in type 1 diabetes. This means that it is the metal or a product of the chemical reactivity of the metal which is attracting the attention of the immune system. The products may be ROS or alterations to the enzymes, co-factors or substrates caused by reactions with ROS. Examples of metalloenzyme autoantigens in autoimmune diseases include thyroid peroxidase (iron in heme) in thyroiditis, tyrosinase (copper) in vitiligo, transglutaminase (manganese) in coeliac disease and cytochrome P450 (iron in heme) in Addison’s disease. The cytochrome P450 superfamily of enzymes are frequent targets of the immune system, with CYPc21 and CYPc17 both antigens in Addison’s disease, CYPc17 and CYPscc in premature menopause, CYPc17 in gonadal failure, CYP1a2 and CYP2a6 in autoimmune polyglandular syndrome type1 and CYP1a2 in halothane hepatitis.




Het document is een pareltje, klik door naar de originele blog!
The original blog is a gem, please click to the original blog!

http://imdtheory.blogspot.be/

Crossreaction between bartonella and chlamydia

J Clin Microbiol. 1997 Sep;35(9):2283-7.

Serological cross-reactions between Bartonella and Chlamydia species: implications for diagnosis.

Maurin M, Eb F, Etienne J, Raoult D.

Source

Unité des Rickettsies, CNRS UPRESA 6020, Université de la Méditerranée, Faculté de Médecine, Marseille, France.

Abstract

Diagnosis of Chlamydia or Bartonella infections continues to rely mainly on serology. However, serological cross-reactions between members of these genera have recently been described. Sera from eight patients originally diagnosed as having Chlamydia pneumoniae endocarditis reacted with both Chlamydia sp. and Bartonella quintana antigens (microimmunofluorescence technique). Adsorption of sera with B. quintana or C. pneumoniae antigens removed anti-C. pneumoniae antibodies, whereas adsorption with C. pneumoniae antigens did not change antibody titers to B. quintana. Western blot analysis confirmed the presence of cross-reacting antigens and showed antibody patterns in all sera to be compatible with a Bartonella infection. These patients were therefore probably suffering from Bartonella-induced rather than Chlamydia-induced endocarditis. In contrast, sera from 10 patients presumed to be suffering from C. pneumoniae pneumonia did not display anti-B. quintana antibodies, although cross-reacting antigens were revealed by Western blotting. This work highlights the possibility that cases of infective Bartonella endocarditis are erroneously diagnosed as chlamydial infections.

http://www.ncbi.nlm.nih.gov/pubmed/9276403

http://ccforum.com/content/15/6/457  

Severe lactic acidosis reversed by thiamine within 24 hours

Karin Amrein^*, Werner Ribitsch, Ronald Otto, Harald C Worm and Rudolf E Stauber

• * Corresponding author: Karin Amrein karin.amrein@yahoo.de

Author Affiliations

Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 15, A-8036 Graz, Austria

For all author emails, please log on.

Critical Care 2011, 15:457 doi:10.1186/cc10495

The electronic version of this article is the complete one and can be found online at: http://ccforum.com/content/15/6/457

Published:

1 December 2011

© 2011 BioMed Central Ltd

Letter

Thiamine is a water-soluble vitamin that plays a pivotal role in carbohydrate metabolism. In acute deficiency, pyruvate accumulates and is metabolized to lactate, and chronic deficiency may cause polyneuropathy and Wernicke encephalopathy. Classic symptoms include mental status change, ophthalmoplegia, and ataxia but are present in only a few patients [1]. Critically ill patients are prone to thiamine deficiency because of preexistent malnutrition, increased consumption in high-carbohydrate nutrition, and accelerated clearance in renal replacement. In retrospective [2] and prospective [3,4] studies, a substantial prevalence of thiamine deficiency has been described in both adult (10% to 20%) and pediatric (28%) patients. Thiamine deficiency may become clinically evident in any type of malnutrition that outlasts thiamine body stores (2 to 3 weeks), including alcoholism, bariatric surgery, or hyperemesis gravidarum, and results in high morbidity and mortality if untreated [1].

We report the case of a 56-year-old man with profound lactic acidosis that resolved rapidly after thiamine infusion. He was admitted because of a decreased level of consciousness (Glasgow Coma Scale score of 6). Vital signs, including blood pressure, heart rate, and oxygen saturation, were normal. Besides reporting regular alcohol consumption, relatives reported recent progressive weakness and 5-kg weight loss. Laboratory findings on admission were remarkable for moderate hypoglycemia and metabolic acidosis - pH of 6.87, base excess of -29.5, partial pressure of carbon dioxide (pCO₂) of 14 mm Hg - with a high anion gap (37 mmol/L) that was attributed to severe hyperlactatemia (21 mmol/L). After intravenous glucose administration, the patient was transferred to the intensive care unit, where he received sodium bicarbonate and 1,500 mL of lactate-free isotonic crystalloids. Within the next few hours, lactate levels increased further while pH slowly improved. Clinically, thiamine deficiency was suspected after other causes of hyperlactatemia, such as hypoxia and hepatic failure, were excluded. After administration of 300 mg of intravenous thiamine, hyperlactatemia normalized rapidly (Figure 1). Unfortunately, the patient suffered persistent neurocognitive deficits.

Figure 1. Lactate levels during the first 24 hours. IV, intravenous.

Thiamine deficiency may cause unspecific neurologic symptoms. Glucose administration or feeding may aggravate depletion. Thiamine deficiency is an underdiagnosed cause of lactic acidosis, although treatment is safe, inexpensive, and readily available. Current guidelines on parenteral nutrition recommend a daily intravenous dose of 100 to 300 mg of thiamine during the first 3 days in the intensive care unit when deficiency is a possibility (grade B) [5]. In conclusion, although its clinical significance has been known for decades, thiamine deficiency remains an under-recognized condition. Intensivists should have an increased awareness of this problem and a low threshold to infuse high-dose thiamine. Future prospective studies to define the optimal dose and duration of treatment are warranted.

Competing interests

The authors declare that they have no competing interests and that the data presented have not been published previously, except in abstract form.

Acknowledgements

We thank Steven Amrein for critical review of the manuscript.

References

1. Sechi G, Serra A: Wernicke's encephalopathy: new clinical settings and recent advances in diagnosis and management.
   Lancet Neurol 2007, 6:442-455. PubMed Abstract | Publisher Full Text
   
2. Cruickshank AM, Telfer AB, Shenkin A: Thiamine deficiency in the critically ill.
   Intensive Care Med 1988, 14:384-387. PubMed Abstract | Publisher Full Text
   
3. Lima LF, Leite HP, Taddei JA: Low blood thiamine concentrations in children upon admission to the intensive care unit: risk factors and prognostic significance.
   Am J Clin Nutr 2011, 93:57-61. PubMed Abstract | Publisher Full Text
   
4. Donnino MW, Carney E, Cocchi MN, Barbash I, Chase M, Joyce N, Chou PP, Ngo L: Thiamine deficiency in critically ill patients with sepsis.
   J Crit Care 2010, 25:576-581. PubMed Abstract | Publisher Full Text
   
5. Singer P, Berger MM, Van den Berghe G, Biolo G, Calder P, Forbes A, Griffiths R, Kreyman G, Leverve X, Pichard C, ESPEN: ESPEN Guidelines on Parenteral Nutrition: intensive care.
   Clin Nutr 2009, 28:387-400. PubMed Abstract | Publisher Full Text

http://ccforum.com/content/15/6/457 

Chronic latent (!) viruses cause disease

Latent Viruses Cause Disease; CBCD Explains

Many scientists believe that latent viruses can only cause disease if reactivated. This is simply untrue.

Rochester, New York (PRWEB) June 13, 2012 

The Center for the Biology of Chronic Disease (CBCD) has learned that Medpagetoday.com has published a story regarding the reactivation of latent viruses. The story focuses on the ability of the latent Epstein Barr virus (EBV) to reactivate and begin replicating itself…which in turn can spark inflammation in Multiple Sclerosis.
Many scientists believe that latent viruses can only cause disease if reactivated. Reactivation means that the virus begins to produce all of its proteins and make copies of itself on a large scale. In contrast, Dr. Polansky’s discovery says that viruses can cause disease while still latent, that is, without being reactivated.
The Theory of Microcompetition, as put forward by Dr. Hanan Polansky in his highly acclaimed “Purple Book” entitled “Microcompetition with Foreign DNA and the Origin of Chronic Disease,” explains how latent viruses can cause many major diseases. One of these viruses is the Epstein Barr virus, and one of these diseases is cancer.
Why is this important? Because most people who have an EBV infection do not know it. They harbor a latent infection that shows no symptoms, which are associated with reactivation. These people should be careful. They are at risk of developing cancer even if they don’t see the usual EBV symptoms.
Latent viruses replicate on a small scale even when they are not reactivated. This is something overlooked by many in the medical field today. As stated by Dr. Hanan Polansky, the latent EBV virus microcompetes with human genes for limited genetic resources, and as a result, can drive the human genes to malfunction, and cause disease.
Some scientists wrongly believe that if a virus is latent, then it is harmless. A latent virus is not dead. It continues to express some of its proteins and therefore to microcompete with human genes.
Consider the paper entitled “Human Cytomegalovirus Persistence” published February 13, 2012 in the journal, Cellular Microbiology. [1]
“Both the chronic and latent states of infection contribute to HCMV persistence and to the high HCMV seroprevalence worldwide. The chronic infection is poorly defined molecularly, but clinically manifests as low-level virus shedding over extended periods of time and often in the absence of symptoms.”
A virus is still shedding copies of itself during the latent phase, meaning it still replicates, and still microcompetes.
The same paper goes on to say: “Transcripts and proteins encoded from a region encompassing the major immediate early region are detected in hematopoietic cells following infection in vitro as well as in latently infected individuals.” (Kondo et al., 1996; Landini et al., 2000).
What does it all mean? Latent viruses such as the Epstein Barr virus continue to replicate, and therefore can cause disease even without reactivation, or while still latent.
Listen to Dr. Polansky describing his discovery during a recent interview by clicking on the following link.
http://dl.dropbox.com/u/41576890/02.06.12%20HHH%20Polansky%20Interview%20.mp3
“The key to your health is to reduce the level of latent viruses in your body to harmless levels.” – Dr. Hanan Polansky
So how does one reduce latent EBV?
It’s not easy. There are two traditional ways to attack the latent EBV virus: through vaccines and through antiviral medications. A vaccine is still in the early stages of development, and “There are…no regulatory agency-approved treatments for EBV-related diseases,” according to a study published in the Journal of Antimicrobial Chemotherapy. [2]
This means that currently there are no vaccines or drugs on the market to combat the active virus, let alone the latent virus.
However, the CBCD would like to point out a natural product designed to target the latent form of the virus. The name of that natural product is Gene-Eden-VIR. The CBCD encourages people infected with latent EBV to learn more about Gene-Eden-VIR.
For more information on the Center for the Biology of Chronic Disease, or to schedule an interview with one of our researchers, please visit http://www.cbcd.net or call 585-250-9999.
References:
[1] Goodrum F, Caviness K, Zagallo P. “Human Cytomegalovirus Persistence”, Cellular Microbiology, May 14, 2012
[2 Gershburg E., Pagano Joseph S., “Epstein Barr Virus Infections: Prospects for Treatment”, Journal of Antimicrobial Chemotherapy, 2005
http://jac.oxfordjournals.org/content/56/2/277.full
The Center for the Biology of Chronic Disease (CBCD, http://www.cbcd.net) is a research center recognized by the IRS as a 501(c)(3) non-for-profit organization. The mission of the CBCD is to advance the research on the biology of chronic diseases, and to accelerate the discovery of treatments for these diseases.
We invite biologists, virologists, scientists everywhere to download Dr. Polansky’s book, “Microcompetition with Foreign DNA and the Origin of Chronic Disease” here: http://cbcd.net/
The CBCD published the “Purple” book by Dr. Hanan Polansky.
The book presents Dr. Polansky’s highly acclaimed scientific theory on the relationship between the DNA of latent (chronic) viruses and the onset of chronic diseases. Dr. Polansky’s book is available as a free download from the CBCD website.

Chronic Chlamydia pneumonia is treatable

http://cid.oxfordjournals.org/content/29/2/452

Chronic Chlamydia pneumoniae Infection: A Treatable Cause of Chronic Fatigue Syndrome

Chronic fatigue syndrome (CFS), an elusive and controversial
illness, has been a difficult management problem for clinicians. A
number of infectious agents have been implicated as the cause of
CFS, although consistent and compelling evidence is still lacking
[1]. Few well-documented infections could cause persistent inflammatory
reaction leading to the symptomatology of CFS [2, 3].
Chlamydia pneumoniae is a common cause of respiratory infection
 and has been demonstrated within plaques of the coronary arteries
years after initial infection [4]. Recently demonstrated replication
of C. pneumoniae within human macrophages and endothelial cells
[5] and a potent inducer of proinflammatory cytokines, such as
TNF-a and IL-1 [6], raised the possibility of chronic infection that
leads to persistent inflammatory response. A previous study failed
to demonstrate elevated titers of antibody to C. pneumoniae in 50
patients with CFS [7], although fatigue is a common symptom
reported by patients for whom sputum cultures are persistently
positive for C. pneumoniae [8].

Over the past 3 years, we encountered 10 of 171 patients with
symptoms of chronic fatigue who had elevated titers of antibody to
C. pneumoniae long after initial respiratory infection. Most patients
had favorable clinical and serological responses to a 1- to
2-months course of azithromycin therapy, although relapse was
common. The clinical symptoms of and titers of antibody to
C. pneumoniae for our 10 patients over the course of treatment are
summarized in table 1.
A 32-year-old female developed pharyngitis, cough, cervical
lymphadenopathy, low-grade fevers, severe fatigue, and myalgia
in January 1993 (patient 1). A medical evaluation showed a normal
complete blood cell count and normal results of thyroid function
test and serum chemistry analysis. IgG antibody to Epstein-Barr
virus was positive. During the following 3 years, the patient had
frequent relapses of severe fatigue, diffuse myalgia, night sweats,
pharyngitis, headaches, insomnia, and painful, swollen cervical
lymph nodes (especially following exertion) that resulted in total
disability.
Repeated evaluation in August 1996 revealed small nontender
anterior cervical lymph nodes. Results of routine laboratory studies
and serologies for several viruses were unremarkable. The titer of
IgG antibody to C. pneumoniae was 1:256. Magnesium sulfate
injections and salt loading failed to alleviate symptoms. One
month later, when the patient was having increasing fatigue, the
titer of antibody to C. pneumoniae rose to 1:1,024. Azithromycin
(500 mg) was administered by mouth the first day, followed by
250-mg doses for the subsequent 4 days. The patient’s condition
improved by day 3 of therapy, although her symptoms relapsed 12
days later.
Similar improvement and relapse followed a second 5-day
course of azithromycin treatment. Thereafter, 250 mg of azithromycin
was given daily for a total of 30 days; this therapeutic
course resulted in a marked decrease in her symptoms. She returned
to full-time work as a manager at her company and maintained
an energy level of 8–9 of 10 for the next 2 years. Follow-up
antibody titers are shown in table 1.
Most of our patients had symptoms referable to the upper or
lower respiratory tracts, but radiographic studies of the sinuses
and chest were unremarkable. Seven of the 10 patients had high
levels of total antibody to C. pneumoniae 0.5 to 3 years following
an episode of symptomatic respiratory infection. Three
patients had low antibody titers of 1:128 and 1:256, but their
symptoms did decrease with antibiotic therapy. Low or absent
antibody response to C. pneumoniae was documented for patients
with persistently positive respiratory cultures [8]. Comparatively,
the mean titers 6 SD for 90 controls were 32 6 36
(range, ,8 or 4 to 256). Only two of 19 fatigued patients with
reciprocal titers between 32 to 64 responded to 1 month of
azithromycin treatment (data not shown).
The spontaneous rise of titers for several patients correlated with
an increased severity of fatigue and a concomitant increase in
respiratory symptoms. This observation suggests that relapses of
symptoms could be due to persistent infection with periodic reactivation
rather than reinfection. All of the patients with relapses
responded to additional azithromycin treatment.
C. pneumoniae is a common copathogen in patients with respiratory
infection [9]. Symptoms of acute purulent sinusitis and mastoiditis
in patients 7 and 8, respectively, did decrease after 2–3 weeks of
ceftriaxone treatment, but severe fatigue persisted for the next 2 years;
fatigue resolved only after 2 months of azithromycin treatment.
Recently, Falck et al. [10] found C. pneumoniae DNA in throat
secretions from 10 of 11 patients with chronic rhinorrhea, fatigue,
and throat biopsies positive for C. pneumoniae. Seventy percent of
the patients had elevated titers of IgG (1:512) or IgA (1:128)
antibody. All of their patients responded to prolonged courses of
macrolide therapy, but symptoms frequently recurred.
Collectively, these results suggest that C. pneumoniae is an
uncommon yet treatable cause of chronic fatigue. The sensitivity,
specificity, and interlaboratory variability of the DNA test will
need to be better defined. Although seemingly less sensitive and
prone to interlaboratory variation, the widely available microimmunofluorescence
test may be a practical screening test for this
entity before throat biopsy is performed.

John K. S. Chia and Laura Y. Chia
Torrance Memorial Medical Center, Torrance, California

Source: http://cid.oxfordjournals.org/content/29/2/452

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