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zondag 25 november 2012

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.


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


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.

zaterdag 24 november 2012

Severe lactic acidosis reversed by thiamine within 24 hours  

Severe lactic acidosis reversed by thiamine within 24 hours

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

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:

Published:1 December 2011

© 2011 BioMed Central Ltd


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.
thumbnailFigure 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.


We thank Steven Amrein for critical review of the manuscript.


  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 OpenURL
  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 OpenURL
  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 OpenURL
  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 OpenURL
  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  OpenURL

zondag 18 november 2012

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 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.
“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 or call 585-250-9999.
[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
The Center for the Biology of Chronic Disease (CBCD, 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:
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.

zondag 11 november 2012

Chronic Chlamydia pneumonia is treatable

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

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.
(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


More options about treatments can also be found at


vrijdag 2 november 2012

Videotalks by Rich von Konynenburg$%7Bweburl%7D

If you like to learn more about methylation (vit B12, folate, sulphur, gluthation and detox), go to minute 35 in the first film right away!

donderdag 1 november 2012

9 bartonella species known to infect humans

Do Bartonella Infections Cause Agitation, Panic Disorder, and Treatment-Resistant Depression?

In the last 15 years, 9 Bartonella bacteria have been identified that are known to infect humans: B henselae, B elizabethae, B grahamii, B vinsonii subsp. arupensis, B vinsonii subsp. berkhoffii, B grahamii, B washoensis, and, more recently, B koehlerae and B rochalimae.[1620] Currently, the largest national laboratories offer tests for only 2 species[2123] (B quintana and B henselae).

Some Bartonella cases have “atypical” presentations with signs or symptoms lasting more than weeks, causing diverse medical problems. For example, Bartonella can cause vision abnormalities, prolonged fever, joint pain, lung inflammation, respiratory disease, and granulomas throughout the body. It can occasionally cause abdominal pain, liver and spleen tissue abnormalities, thrombocytopenic purpura, bone infection, papules or pustules, maculopapular rashes, arthritis, abscesses,[20, 2430] heart tissue and heart valve problems,[3137] and neurologic illnesses.[3842]
Traditionally, cognitive neurology has been related to some psychiatric illnesses. A search of PubMed with “Bartonella” and the search words “depression,” “mania,” “bipolar,” “major depression,” “depression,” “anxiety,” “panic,” “panic attack,” “psychosis,” and “schizophrenia” yielded the limited journal results below:
  • Depression
  • Dementia
  • Encephalopathy
  • Violent behavior
  • Confusion
  • Combative behavior
  • Substance abuse disorders[4348]


We note that the number of Bartonella species that infect humans currently outpaces the number of Bartonella species that can be tested by top national labs. Some antibiotics seem to have an effect, but dosing and duration are not clearly established or indicated by a broad literature review. Further, clinical improvement and the cessation of symptoms do not always signify complete eradication. That is, it may be possible for a patient to relapse due to a significant medical stress to the body or a decrease in immune system capacity. Of greatest importance, we believe that Bartonella can enter the brain and cause not only well-documented neurologic disorders, but also some psychiatric disorders as well.

How and why herpes virus reactivate

How and why herpes virus reactivate

ScienceDaily (Oct. 31, 2012) — The mere mention of the word "herpes" usually conjures negative images and stereotypes, but most people have been infected with some form of the virus. For most, a sore appears, heals and is forgotten, although the virus remains latent just waiting for the right circumstances to come back. Now, the mystery behind what triggers the virus to become active again is closer to being solved thanks to new research published in the Journal of Leukocyte Biology's November 2012 issue.

In the report, scientists show how the immune system may lose its control over the virus when facing new microbial threats, such as when it must fend off other viral invaders or bacteria.
"Because almost all people are infected by one or more herpes family viruses during their lifetime, the potential impact of these findings are significant," said Charles H. Cook, M.D., FACS, FCCM, director of surgical critical care at The Ohio State University College of Medicine in Columbus, Ohio, and a researcher involved in the work. "We hope that by understanding how these latent viral infections are controlled that we can prevent reactivation events and improve people's lives."
To make this discovery, researchers studied mice with latent herpes family cytomegalovirus (CMV) during severe bacterial infections. They found that T-cells responsible for CMV control were reduced significantly during a new infection with bacteria. This, in effect, reduced the "brakes" which kept the virus under control, allowing the virus to reactivate and cause disease. When the immune system eventually sensed the reactivation, the memory T-cell levels returned to normal, effectively restoring the body's control over the virus.
"Finding ways to control herpes flare ups is important, not only for the health of the person with the virus, but also for preventing its transmission," said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology. "This report highlights the important interplay when we are 'co-infected' with more than one microbe and provides important insights into why the immune system sometimes fails as well as how it can regain control of latent herpes virus infections."