Happy New Year Doctor!

Rest in peace my dear friend

In Memoriam - Denise de Hoop (Niessie)

Denise de Hoop

08.10.1967 - 28.12.2012

Je hebt een moedige maar oneerlijke
strijd gestreden. Wij zullen nu jouw
strijd voor ME voortzetten.
Niessie, je zal altijd in ons hart blijven.

Rouwbericht
'Ik had nog niet dood gehoeven.' 28.12.12 (volgt).
Een jaar uit het leven van een ME-patiënt. Dagboekfragmenten. 26.11.12
De dood of de Gladiolen. De ziekte ME: ont- of erkenning. 19.11.12
Gebombardeerd tot martelares van ME-patiënten. 15.07.11
Diagnose kanker gemist bij ME-patiënte door psychosomatisch stigma. 02.07.11

In Memoriam

Denise de Hoop
(Niessie)

8 oktober 1967 – 28 december 2012

Vanmorgen bereikte ons het bericht dat Denise
om 7.37 uur overleden is in het hospice van Hoorn.

Zij heeft zich de laatste jaren met heel haar energie en
kracht ingezet om de ernst van ME aan iedereen over
te brengen. En ook het in gebreke blijven van een aantal
artsen en behandelaars, mede door de stigmatisering
die nog steeds op ME als psychosomatische aandoening
rust in Nederland.

Nog geen drie weken geleden moest zij zelfs nog knokken
voor een plek in het hospice, omdat medici haar niet terminaal
genoeg vonden.

Vandaag verschijnt in het Noord-Hollands Dagblad een deze week
afgenomen interview met haar, waarvan de openingszinnen
luiden:

“Ik had nog niet dood gehoeven. Als ik kom te overlijden, vraag ik de mensen om de petitie voor erkenning van ME te tekenen. De artsen hebben mijn tumor te laat ontdekt, doordat ze mij als ME-patiënt niet serieus namen”.

Denises blog op me.net, zal de kern worden van een boek waaraan enkele mensen nu al werken. Het was haar bekend dat dat in de maak is, zodat zij wist dat haar strijd wordt voortgezet.

Wij wensen haar man en beide dochters alle kracht om het grote gemis in hun leven te vullen met de mooie en dierbare herinneringen aan een bewonderenswaardige en diep liefhebbende
vrouw, moeder en vriendin.

 

Bovenstaande in memoriam werd opgesteld door de ME/cvs Vereniging [PDF], waarvoor dank.

How to get rid of neurotoxines?

http://www.lyme-symptoms.com/LymeNeurotoxins.html

Neurotoxins 
of the Borrelia burgdorferi Bacteria What is Neurotoxins: 

A neurotoxin is a poison that acts specifically on nerve cells. Neurotoxins are attracted to the nervous system, are then absorbed by nerve endings and then travel inside the neuron to the cell body. There they disrupt vital functions of the nerve cell. 

Sources of Neurotoxins:

Neurotoxins are caused by heavy metals, Aspartame, MSG, Sodium Nitrite in processed  meats, alcohol, Fluoride, Aluminum Zirconium, paints, cocaine, statins,food additives,viruses, fungi, molds, mycoplasma, enteroviruses, Chlamydia pneumonia, Candida,parasites and protozoans (in the case of Babsiosis)and bacteria (as in the Lyme Bb bacteria) ..to name only a few of the 1178 chemicals officially listed as neurotoxins and the various bacteria's.

Neurotoxin Poison released by the Bb Bacteria :

The Borrelia burgdorferi bacteria, in their life process (living and dying) release nerve poisons/toxins/biotoxins (similar to Clostridium botulinum) and are believed to be the cause, both directly and indirectly, of most, if not all, the symptoms of Lyme disease. These toxins are dumped into the intersitial fluid and circulated throughout the body, until they can either be eliminated by the body or get lodged in areas of weakened tissues or fat cells- all the while causing problems with the nerves and distorting the messages of the nerves to any or all areas of the body.

Read more here

Acetylcholine and Dopamine

The effects of Bb bacteria neurotoxins

Neurotoxin Overload

Bb Activity Manifests Symptoms of Lyme Disease

Is it possible to rid the body of neurotoxins:

What is the interstitial fluid?

What is die-Off:

http://www.lyme-symptoms.com/LymeNeurotoxins.html

Role of Chronic Bacterial and Viral Infections

Role of Chronic Bacterial and Viral Infections in Neurodegenerative, Neurobehavioural, Psychiatric, Autoimmune and Fatiguing Illnesses: Part 2

 

Garth L. Nicolson and Jörg Haier

Cite this article as: BJMP 2010;3(1):301 Download PDF

ABSTRACT Chronically ill patients with neurodegenerative and neurobehavioural and psychiatric diseases commonly have systemic and central nervous system bacterial and viral infections. In addition, other chronic illnesses where neurological manifestations are routinely found, such as fatiguing and autoimmune diseases, Lyme disease and Gulf War illnesses, also show systemic bacterial and viral infections that could be important in disease inception, progression or increasing the types/severities of signs and symptoms. Evidence of Mycoplasma species, Chlamydia pneumoniae, Borrelia burgdorferi, human herpesvirus-1, -6 and -7 and other bacterial and viral infections revealed high infection rates in the above illnesses that were not found in controls. Although the specific roles of chronic infections in various diseases and their pathogeneses have not been carefully determined, the data suggest that chronic bacterial and/or viral infections are common features of progressive chronic diseases.

Introduction

 

In the first part of this review we considered neurodegenerative and neurobehavioural diseases and the findings that these diseases commonly are associated with systemic and central nervous system bacterial and viral infections.¹ In this second part we continue with psychiatric diseases, autoimmune diseases, fatiguing illnesses, and other chronic diseases where chronic infections play an important role.

 

Psychiatric diseases

 

Borrelia-associated psychiatric disorders

 

In addition to neurologic and rheumatologic symptoms Borrelia burgdorferi has been associated with several psychiatric manifestations^{2, 3} (see also below). Such infections can invade the central nervous system and may cause or mimic psychiatric disorders or cause a co-morbid condition. A broad range of psychiatric conditions have been associated with Lyme disease, including paranoia, dementia, schizophrenia, bipolar disorder, panic attacks, major depression, anorexia nervosa and obsessive-compulsive disorder.^4-7 For example, depressive states among patients with late Lyme disease are fairly common, ranging from 26% to 66%.³  It is not known whether B. burgdorferi contributes to overall psychiatric morbidity, but undiagnosed chronic Lyme disease caused by this spirochete is considered a differential diagnosis in patients with certain psychiatric symptoms such as depressive symptoms, lack of concentration and fatigue.

 

The neuropsychiatric sequelae of chronic Lyme disease remains unclear. Studies were performed, some on large numbers of patients, to investigate whether a correlation exists between chronic Lyme disease (defined by seropositivity) and psychiatric disorders.^8-11 Interestingly, different results were reported on the association between B. burgdorferi infection and psychiatric morbidity.^8-11 For example, Hájek et al.⁸ compared the prevalence of antibodies to B. burgdorferi in groups of psychiatric patients and healthy subjects. Among the matched pairs, 33% of the psychiatric patients and 19% of the healthy comparison subjects were seropositive. In contrast, Grabe et al.¹¹ did not find an association between Borrelia seropositivity and mental and physical complaints. In 926 consecutive psychiatric patients that were screened for antibodies and compared with 884 simultaneously recruited healthy subjects, seropositive psychiatric patients were found to be significantly younger than seronegative ones, and this was not found in the healthy controls.¹⁰ However, none of the psychiatric diagnostic categories used in this study exhibited a stronger association with seropositivity.¹⁰ These findings suggest a potential association between B. burgdorferi infection and psychiatric morbidity, but fail to identify any specific clinical 'signature' of the infection. This might be due to the very low incidence in an endemic region (0.2%, CI 95% 0.0% to 1.1%) as demonstrated in 517 patients hospitalized for psychiatric diseases.⁹

 

In addition to serological data, clinical evidence for the association of psychiatric symptoms and post-Lyme disease has also been investigated. If mental and physical complaints in patients were assessed with the von Zerssen's complaint scale using multivariate analyses, the data revealed that definitions of seropositivity were not associated with increased mental or physical complaints.¹¹ In contrast, if the SF-36 was used to determine Quality of Life (QOL) in post-Lyme patients, the average SF-36 physical component summary (40±9, range 29-44) and mental component summary (39±14, range 23-46) of the QOL assessment were worse than the general USA population, and they could be significantly improved by anti-Lyme antibiotics (46% versus 18%, p=0.007).⁵ Barr et al.¹² examined the relation between complaints of memory disturbance and measures of mood and memory functioning in 55 patients with serological evidence of late-stage Lyme borreliosis. There was a significant correlation between subjective memory ratings and self-reported depression (p<0 .001=".001" 30="30" a="a" affect="affect" and="and" battery="battery" but="but" checklist="checklist" chronic="chronic" disturbance="disturbance" in="in" indicating="indicating" interview="interview" lyme="lyme" memory="memory" negative="negative" neuropsychological="neuropsychological" not="not" objective="objective" of="of" patients.="patients." patients="patients" performance="performance" positive="positive" post-lyme="post-lyme" psychiatric="psychiatric" schedule="schedule" span="span" structured="structured" symptom="symptom" tests="tests" the="the" using="using" with="with">, participants did not appear to have an elevated incidence of psychiatric disorders or psychiatric history.¹³ Their mood, however, was characterized by lowered levels of positive affect and typical levels of negative affect that were similar to affect patterns in individuals with chronic fatigue syndrome (CFS). Similarly, Hasset et al.^{4, 7} reported on 240 consecutive post-Lyme patients who were screened for clinical psychiatric disorders, such as depression and anxiety. After adjusting for age and sex, these disorders were more common in symptomatic patients than in the comparison group (Odds Ratio=3.54, CI 95% 1.97-6.55, p<0 .001=".001" both="both" but="but" comparable="comparable" disorders="disorders" groups.="groups." in="in" personality="personality" span="span" were="were">

 

Although psychiatric co-morbidity and other psychological factors are prominent in post-Lyme patients, it remains uncertain whether these symptoms can be directly attributed to the chronic course of Borrelia infections or to other chronic illness-related factors. 

 

Schizophrenia

 

...

Neuropsychiatric Movement Disorders

 

... As mentioned above, streptococcal infections are likely to play a pivotal role in these syndromes.³⁵

 

The pathogenic mechanism may be secondary to an activation of the immune system, resulting in an autoimmune response. This will be discussed in the next section.

Autoimmune Diseases

 

Infections are associated with various autoimmune conditions.^38-40 Autoimmunity can occur when infections like cell-wall-deficient bacteria are released from cells containing parts of cell membranes that are then seen as part of a bacterial antigen complex, or bacteria can synthesize mimicry antigens (glycolipids, glycoproteins or polysaccharides) that are similar enough in structure (molecular mimicry) to stimulate autoimmune responses against similar host antigens. Alternatively, viral infections can weaken or kill cells and thus release cellular antigens, which can stimulate autoimmune responses, or they can incorporate molecules like gangliosides into their structures.

 

In addition to molecular mimicry, autoimmunity involves several other complex relationships within the host, including inflammatory cytokines, Toll-like receptor signalling, stress or shock proteins, nitric oxide and other stress-related free radicals, among other changes that together result in autoimmune disease.^{38, 39}

 

Guillain-Barré syndrome

 

...

Viruses have also been found to be associated with GB.⁴⁰    Examples are: CMV,⁴⁷  HIV,⁴⁸ herpes simplex virus,⁴⁹ West Nile virus,⁵⁰ and HHV-6.⁵¹

 

Paediatric autoimmune neuropsychiatric disorders associated with Streptococci ('PANDAS')

 

Streptococcal infections in children are usually benign and self-limited. In a small percentage of children, however, prominent neurologic and/or psychiatric sequelae can occur. Post-streptococcal basal ganglia dysfunction has been reported with various manifestations, all of which fall into a relatively well-defined symptom complex or syndrome called paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS).⁵²

 

...

Fatiguing illnesses

 

Chronic fatigue syndrome/myalgic encephalomyelitis

 

Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a fatiguing illness characterised by unexplained, persistent long-term disabling fatigue plus additional signs and symptoms, including neurophysiological symptoms.⁶⁵ Brain imaging studies have shown that CFS/ME patients are dysfunctional in their ventral anterior cingulate cortex, and they also have other brain MRI abnormalities.^{66, 67} In addition, CFS/ME patients also have immunological and inflammation abnormalities, such as alternations in natural killer cell function^{68, 69} and cytokine profiles.^{70, 71} In addition, the hypothalamo-pituitary-adrenal axis, which plays a major role in stress responses, appears to be altered in CFS/ME.⁷²

 

Most, if not all, CFS/ME patients have multiple chronic bacterial and viral infections.^73-80   For example, when patients were examined for evidence of multiple, systemic bacterial and viral infections, the Odds Ratio for this was found to be 18 (CI 95% 8.5-37.9, p< 0.001).⁷⁵ In this study CFS/ME patients had a high prevalence of one of four Mycoplasma species (Odds Ratio=13.8, CI 95% 5.8-32.9, p< 0.001) and often showed evidence of co-infections with different Mycoplasma species, C. pneumoniae (Odds Ratio=8.6, CI 95% 1.0-71.1, p< 0.01) and HHV-6 (Odds Ratio=4.5, CI 95% 2.0-10.2, p< 0.001).⁷⁵  In a separate study the presence of these infections was also related to the number and severity of signs and symptoms in CFS/ME patients, including neurological symptoms.⁷⁷ Similarly, Vojdani et al.⁷⁶ found Mycoplasma species in a majority of CFS/ME patients, but this has not been seen in all studies.⁸¹ Interestingly, when European CFS/ME patients were examined for various Mycoplasma species, the most common species found was M. hominis,⁸² whereas in North America the most common species found was M. pneumoniae,^{75, 77} indicating possible regional differences in the types of infections in CFS/ME patients. In addition to Mycoplasma species, CFS/ME patients are also often infected with B. burgdorferi,⁸⁰ and as mentioned above, C. pneumoniae.^{75, 77, 83} 

 

Other infections are also found in CFS/ME patients, such as viral infections: CMV,⁸⁴ parvovirus B19,⁷⁸ enterovirus⁷⁹ and HHV-6.^{75, 77, 85-88} For example, Ablashi et al.⁸⁸ found that 54% of CFS/ME patients had antibodies against HHV-6 early protein, compared to 8% of controls. Similarly, Patnaik et al.⁸⁶ found that 77% of CFS/ME patients were positive for HHV-6 early antigen IgG or IgM antibodies, whereas only 12% of control subjects had IgG or IgM antibodies to HHV-6 early antigen. Recently a new retrovirus, XMRV, was found in mononuclear blood cells of 67% of 101 chronic fatigue syndrome patients compared to only 3.7% of healthy controls. Cell culture experiments determined that the patient-derived virus was infectious and could possibly be transmitted.⁸⁹        

   

Gulf War illnesses

 

GWI is a syndrome similar to CFS/ME.⁹⁰ In most GWI patients the variable incubation time, ranging from months to years after presumed exposure, the cyclic nature of the relapsing fevers and the other chronic signs and symptoms, and their subsequent appearance in immediate family members, are consistent with an infectious process.^{90, 91} GWI patients were exposed to a variety of toxic materials including chemicals, radiochemicals and biologicals so not all patients are likely to have infections as their main clinical problem. Neurological symptoms are common in GWI cases.⁹⁰ Baumzweiger and Grove⁹² have described GWI as neuro-immune disorder that involves the central, peripheral and autonomic nervous systems as well as the immune system. They attribute a major source of the illness to brainstem damage and central, peripheral and cranial nerve dysfunction from demyelination. They found GWI patients have muscle spasms, memory and attention deficits, ataxia and increased muscle tone.⁹²

 

Bacterial infections were a common finding in many GWI patients.⁹⁰ Mycoplasmal infections were found in about one-half of GWI patients, and more than 80% of these cases were PCR positive for M. fermentans.^{90, 91, 93-95} In studies of over 1,500 U.S. and British veterans with GWI, approximately 45% of GWI patients have PCR evidence of such infections, compared to 6% in the non-deployed, healthy population. Other infections found in GWI cases at much lower incidence were Y. pestis, Coxiella burnetii and Brucella species.⁹⁰

 

When we examined the immediate family members of veterans with GWI who became sick only after the veteran returned to the home, we found that >53% had positive tests for mycoplasmal infections and showed symptoms of CFS/ME. Among the CFS/ME-symptomatic family members, most (>80%) had the same Mycoplasma fermentans infection as the GWI patients compared to the few non-symptomatic family members who had similar infections (Odds Ratio=16.9, CI 95% 6.0-47.6, p<0 .001=".001" sup="sup">91

 In contrast, in the few non-symptomatic family members that tested Mycoplasma-positive, the Mycoplasma species were often different from the species found in the Gulf War Illness patients (M. fermentans).   The most sensible conclusion is that veterans came home with M. fermentans infections and then transmitted these infections to immediate family members.⁹¹

 

Some other infectious diseases with neurological aspects

 

Lyme Disease

 

Lyme disease is caused by a tick bite and the entry of the spiral-shaped spirochete B. burgdorferi as well as other co-infections.⁹⁶ Lyme disease is the most common tick-borne disease in North America. After incubation for a few days to a month, the Borrelia spirochete and co-infections migrate through the subcutaneous tissues into the lymph and blood where they can travel to near and distant host sites, including the central nervous system.^{3, 97-99}  Transplacental transmission of B. burgdorferi and co-infections can occur in pregnant animals, including humans, and blood-borne transmission to humans by blood transfusion is likely but unproven. The tick-borne co-infections associated with Lyme disease can and usually do appear clinically at the same time, complicating clinical dignoses.¹⁰⁰

 

Lyme disease signs and symptoms eventually overlap with the signs and symptoms of other chronic illnesses, and patients are often diagnosed with illnesses like CFS/ME, chronic arthritis or a neurological disease.^{80, 97-100} About one-third of cases with Lyme disease start with the appearance of a round, red, bulls-eye skin rash (erythema migrans) at the site of the tick bite, usually within 3-30 days.¹⁰⁰ Within days to weeks mild flu-like symptoms can occur that include shaking chills, intermittent fevers and local lymph node swelling. After this localised phase, which can last weeks to months, the infection can spread to other sites resulting in disseminated disease. In the disseminated (late) phase patients present with malaise, fatigue, fever and chills, headaches, stiff neck, facial nerve palsies (Bell’s palsy) and muscle and joint pain, and other signs and symptoms.^100-104

 

The disseminated (late) phase of Lyme disease is a chronic, persistent disease with ophthalmic, cardiac, musculoskeletal, central nervous system and internal organ invasion. When it involves the central and peripheral nervous systems, it is often termed neuroborreliosis.^{100, 104} At this late stage, arthritis, neurological impairment with memory and cognitive loss, cardiac problems  (such as myocarditis, endocarditis causing palpitations, pain, bradycardia, hypertension) and severe chronic fatigue are usually apparent.^{80, 100-102} The signs and symptoms of the chronic (late) phase of the disease usually overlap with other chronic conditions, such as CFS/ME, chronic arthritis, as well as neurodegenerative diseases, causing confusion in the diagnosis and treatment of the chronic phase in patients with Lyme Disease.^{80, 97, 100, 105} Patients with late stage neuroborreliosis exhibit neuropathologic and neuropsychiatric disease similar to some of the neurodegenerative diseases discussed in previous sections.¹

 

Diagnostic laboratory testing for Lyme disease at various clinical stages is not fool-proof, and experts often use a checklist of signs and symptoms and potential exposures, along with multiple laboratory tests to diagnose Lyme disease.¹⁰⁴ The laboratory tests include serology, Western blot analysis of B.burgdorferi associated bands, PCR analysis of blood and the nonspecific decrease in CD-57 natural killer cells. Unfortunately, similar to other intracellular bacteria, Borrelia spirochetes are not always released into the blood circulation or other body fluids, making the very sensitive PCR method less than reliable for diagnosing Lyme Borrelia with blood samples. Lebech and Hansen¹⁰⁶ found that only 40% of cerebrospinal fluid samples from patients with Lyme neuroborreliosis were positive for B. burgdorferi by PCR.

 

Co-infections in Lyme disease are important but, in general, have not received the attention that B. burgdorferi attracts. Some of the Lyme Disease co-infections on their own, such as M. fermentans, have been shown to produce signs and symptoms comparable to B. burgdorferi infections.^{80, 102}

 

The most common co-infections found in Lyme disease are species of Mycoplasma, mostly M. fermentans, present in a majority of cases.^{80, 103, 107}   In some cases multiple mycoplasmal infections are present in patients with Lyme disease,⁸⁰ while other common co-infections include Ehrlichia species, Bartonella species and Babesia species. Such co-infections are present in 10-40% of cases.^{103, 104, 108-112} Ehrlichia and Bartonella species are usually found along with Mycoplasma species in Lyme disease.^{94, 98, 108-111} Bartonella species, such as B. henselae,¹¹¹ which also causes cat-scratch disease,¹¹³ are often found in neurological cases of Lyme disease.^{100, 111}

 

Protozoan co-infections have been found with B. burgdorferi, such as intracellular Babesia species.^{100, 108, 109, 112, 114} The combination of Borrelia, Mycoplasma and Babesia infections can be lethal in some patients, and ~7% of patients can have disseminated intravascular coagulation, acute respiratory distress syndrome and heart failure.¹⁰⁹

 

Brucellosis

 

^...

 

Final comments to part 2

 

The progression, and in some cases, the inception of many chronic diseases are probably elicited by various bacterial and viral infections.^{1, 39, 40, 119} Even if infections are not directly involved in the pathogenesis of these diseases, patients with chronic conditions are at risk of a variety of opportunistic infections that could result in co-morbid conditions or promote disease progression. Infections can complicate diagnosis and treatment, and patients with late-stage disease with complex neurological manifestations, such as meningitis, encephalitis, peripheral neuropathy, psychiatric conditions, or with other signs and symptoms could have infections that are not recognized or treated.

 

Patients with chronic diseases are particularly difficult to treat using single modality approaches, and this is particularly true for patients who also have multiple chronic infections.^{103, 109} The multi-focal nature of chronic diseases and the fact that often treatments are given to suppress signs and symptoms, rather than treat causes of the disease or its progression, have resulted in incomplete or ineffective treatments. On the other hand, even if the causes of chronic diseases are known, by the time therapeutic intervention is undertaken, it may be entirely too late to use approaches that should work on the disease if chronic infections were not present. Moreover, if complex, chronic infections are ignored or left untreated, recovery may be difficult, if not impossible to achieve.

 

At the moment the evidence that particular or specific types of infections are responsible for the inception or pathogenesis of chronic diseases is inconclusive.¹¹⁹ One of the problems that arises in trying to prove this hypothesis is that not all patients appear to have similar chronic infections. Some individuals can harbour chronic infections without any observable signs or symptoms. Although the incidence of chronic infections of the types discussed in this review in symptom-free individuals is generally very low, usually only a few percent,^{74-76, 120} that does not prove that they are important in pathogenesis. Since patients with chronic diseases have been identified that do not have easily diagnosed chronic infections, most researchers have concluded that infections are not involved in the pathogenesis of chronic diseases. Unfortunately, the tools available to find chronic infections are not optimal, and many patients are likely go undiagnosed with chronic infections for purely technical reasons.^{1, 119-121}

 

In the history of medicine animal models of disease have provided useful information that could not be obtained through clinical studies alone. Indeed, the field of chronic diseases could benefit from the greater use of relevant animal models. We suggest that to be useful, the pathogenesis of the animal models of disease must be similar to the pathogenesis of human disease and the animal models must have a similar response to therapy as humans. Thus such models are only relevant if they closely mimic human disease and its response to treatment. For example, the infection of non-human primates with neuropathologic microorganisms, such as Mycoplasma fermentans, resulted in brain infections and fatal diseases with clinically typical neurological signs and symptoms.¹²² These primates also respond to therapies that have been used successfully to treat humans.^{93, 123} Thus this particular model may be useful if it can be reproucibly infected with specific microorganisms and later develop neurological signs and symptoms that closely mimic chronic human neurological diseases.   Future efforts to determine the relationship between specific infections and the pathogenesis of various chronic diseases may well depend on the further development of relevant animal models. 

Competing Interests None declared Author Details GARTH L. NICOLSON, Department of Molecular Pathology, The Institute for Molecular Medicine, Huntington Beach, California 92647, USA JORG HAIER, Department of General and Visceral Surgery, University Hospital, Münster 48149, Germany CORRESSPONDENCE: PROF. GARTH L. NICOLSON, Office of the President, The Institute for Molecular Medicine, P.O. Box 9355, S. Laguna Beach, California, 92652 USA. Website: www.immed.org Email: gnicolson@immed.org

References

 

Controversial Illness is Real and Treatable

Research Shows Controversial Illness is Real and Treatable

CHARLESTON, S.C., July 27 /PRNewswire/ -- Today, Policyholders of America (POA) released a consensus statement written by treating physicians and researchers in the field on the mechanism and treatment of illness found in people sickened by exposure to water-damaged buildings. This illness has been the subject of heated debate that has resulted in harsh allegations being lobbed at patients by experts hired by industry to cast doubt on the legitimacy of the illness. Today however, so-called "Sick Building Syndrome" is now unveiled to be very real; it's a chronic inflammatory illness that is easily identified with available lab testing and treatable using FDA-approved medications.  The research paper is the first in the field written by physicians with experience treating the illness.  Thorough and rigorous, the paper references governmental agency opinions, current published literature and an extensive review of patient data that has made this subject a political and legal hot potato obstructing patient care.   

Nearly six months ago, a distinguished and credentialed panel of medical doctors and researchers, all from outside of POA's membership, were assembled and charged with developing a consensus statement on the diagnosis and treatment of a growing public health problem across America:  illness acquired from water-damaged buildings. The consensus statement was then peer-reviewed by other medical doctors and researchers.  The research paper is being released to help physicians and their patients understand the mechanisms, symptoms, diagnosis and treatment protocols available for sickened patients.  

After reviewing hundreds of peer reviewed studies, analyzing hard data from research conducted on thousands of patients, and incorporating published results of treatment of thousands of patients, the authors embarked on this massive assignment with eyes wide open -- knowing that if the resulting research did not lessen liability of the powerful stakeholders involved, industry would likely attempt to discredit the findings.  

With the research now concluded, the mysterious illness now has a name: Chronic Inflammatory Response Syndrome or "CIRS", and when the cause of the illness can be directly linked to a water-damaged building, or  ("WDB"), it is called "CIRS-WDB".

Says Co-Author, Ritchie Shoemaker , MD, of Pocomoke, Maryland, "This statement builds consensus by debunking false ideas about illness from water-damaged buildings and establishes the basis by which practicing physicians can assess the complex illnesses these patients experience. We don't have to guess what might be wrong when we have the labs to prove what is abnormal.  Patients don't have to suffer any longer after being given incorrect diagnoses such as allergy, stress or depression."

Co-authors included Laura Mark MD from Williamsburg, Virginia; Scott McMahon MD from Roswell, New Mexico; Jack Thrasher PhD of Oakland, California and Carl Grimes HHS, CIEC, President of the Indoor Air Quality Association, from Denver, Colorado.

The 161-page research paper can be found, in its entirety, at: http://www.policyholdersofamerica.org/doc/CIRS_PEER_REVIEWED_PAPER.pdf

A layperson's summary of the research paper follows:  

• CIRS-WDB is a multisystem, multi-symptom illness acquired following exposure to the interior environment of WDB.  It exists as a recognizable syndrome that is identifiable and treatable;
• CIRS-WDB is identified as immunologic in origin, with differential inflammatory responses seen according to (i) genetic susceptibility and (ii) unique aspects of host innate immune responses.
• CIRS-WDB consistently involves loss of normal control of inflammation and the resulting "inflammation gone wild."
• Treatment of human illness that is acquired following exposure to the interior environment of WDB involves a series of steps, each correcting the physiologic problems one by one.  
• CIRS-WDB can be readily identified by current methods of clinical diagnoses. This process of diagnosis is supported by (i) identification of unique subsets ("clusters") of symptoms found in epidemiologic cohorts of affected patients; (ii) identification of unique groupings of biomarkers, such as genetic markers, neuropeptides, inflammatory markers, and autoimmune findings.
• Patients with CIRS-WDB are often given incorrect diagnoses such as depression, stress, allergy, fibromyalgia, Post Traumatic Stress Disorder, and somatization.  Those conditions, when actually present, will not improve with therapies employed in CIRS-WDB.  
• CIRS-WDB is acquired primarily from inhalation of microbial products that are contaminants found in the complex mixture of WDB.  
• Re-exposure of previously affected patients will bring about immunological host responses that are enhanced in their rapidity of onset and magnitude, such that these patients are "sicker, quicker."  

Melinda Ballard , POA's president said, "About 25% of our members have experienced health effects after exposure to toxigenic mold and other organisms in their homes and of those, the vast majority put on the treatment protocol outlined in this paper have reported back to us that their symptoms have either subsided or vanished altogether. While our experience with these members is purely anecdotal, this research paper is not; the findings are irrefutable.  Most importantly, the rigorous science in the paper offers hope to so many who are in desperate need of an effective and inexpensive treatment. 

POA is a nonprofit educational organization that, at no charge, helps policyholders receive adequate payment when a property insurance claim is filed. Since it was founded in 2001, more than 2.5 million people have joined, an unfortunate reflection on the manner in which claims are often handled by insurance companies. Its web address is: www.policyholdersofamerica.org. POA is a member of ACHEMMIC (the Action Committee on the Health Effects of Mold, Microbes and Indoor Contaminants), a group of scientists, researchers, physicians, indoor air quality experts, environmental engineers, industrial hygienists, structural engineers, teachers and advocates working to advance the understanding of the health effects of mold, microbes and indoor contaminants. ACHEMMIC's website is www.achemmic.com.

MEDIA ONLY CONTACT:
Melinda Ballard
Policyholders of America
(843) 367-4574

SOURCE Policyholders of America


RELATED LINKS
http://www.policyholdersofamerica.org

PR Newswire (http://s.tt/1bJ00)

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.

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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.

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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.

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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