Posts Tagged ‘Lawrence Broxmeyer M.D.’

ALZHEIMER’S DISEASE: WHICH GERM IS IT?

October 9, 2016

NEW RELEASE………..

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Abstract:

Recent literature shows a controversial new push to tie microorganisms to Alzheimer’s disease (AD) ― which despite the protests of some, is badly needed. Indeed there is a good chance that Alzheimer’s is caused by a microbe. Study after study, in which scientists have injected human Alzheimer-diseased brain tissue into mice and other laboratory animals that later developed the disease have left little doubt that Alzheimer’s arises from an infectious process. So the proper focus of the present debate regarding AD should not be ‘is there an infectious process or processes behind Alzheimer’s?’…….. but rather ‘which one?’ Clearly, whatever the infectious cause behind Alzheimer’s is, it must be a disease that is statistically widespread in the world today and that was also prevalent at the time of Dr. Alzheimer. Presently, in America alone, more than 5 million people, to varying degrees, have lost their memory or cognition to this challenging disease.

Specifically mentioned to this point as possible causes have been: [1] herpes simplex virus type 1 (HSV-I), [2] Chlamydia pneumoniae, and [3] several types of spirochetes. Also mentioned is [4] fungal infection in the AD brain as well.

Mawanda and Wallace’s review (2013) gave seven annotated references as to why Herpes Simplex virus type 1 (HSV-1) “remains questionable” as a cause for Alzheimer’s; nine studies referenced as to why there was “no evidence to suggest an association between Chlamydia pneumoniae infection and AD pathogenesis”; and six “rigorous studies which found no evidence to suggest that spirochetal B. Burgdorferi, is “causally linked to AD” Wallace also mentioned that although Riviere et al. found oral spirochetal Treponema, including T. denticola, T. pectinovorum, T. vincentii, T. amylovorum, T. maltophilum, T. medium, and T. socranskii in a significantly higher proportion of postmortem brain specimens from AD cases than controls. These results have, however, according to Mawanda and Wallace’s review, not been replicated.

As for fungal forms found in the Alzheimer’s brain, this is nothing new. Oskar Fischer, the co-discoverer of Alzheimer’s disease, saw such forms in 1907. But Fischer knew that they were related to Streptothrix, a germ with both bacterial and fungal properties often confused with tuberculosis. The disease actinomycosis was at one time referred to interchangeably with its older bacterial name, the “Streptotriches” (the plural form of Streptothrix). Fischer used such older nomenclature in describing certain forms he saw under his microscope. Furthermore, regarding the thick, black, club-shaped “Drüsen” in Oskar Fischer’s 1907 drawing of senile plaque ― at the time, it was widely acknowledged that such drüsen could result from either infection with Streptothrix, now known as actinomycosis (aktinomycesdruse), a rare disease in humans, or tuberculosis, a disease that by 1882, as Alzheimer prepared to leave for Berlin for his medical education, was understood to be far and away the leading cause of infectious death in Europe. And just ten years before Oskar Fischer found Actinomycosis-like Streptothrix in Alzheimer’s cerebral plaque, Babèş and immunologist Levaditi reported in “On the Actinomycotic Shape of the Tuberculous Bacilli” that typical Actinomyces-like clusters [Drüsen] with clubs appeared in the tissue of rabbits inoculated with tubercle bacilli beneath the dura mater of their brains. Once introduced into the brain this way, reported Babes, TB bacilli not only branched out like the Actinomycosis such as Streptothrix, but they developed rosettes that were identical to the “drüsen” that Oskar Fischer spotted in Alzheimer’s plaque.

What Mawanda and Wallace did maintain however was the emerging evidence that supported an infectious pathogen and two prime suspects for Amyloid beta deposition to the extent that it was going on in Alzheimer’s. This book discusses one of them.

Available on Amazon: Alzheimer’s Disease – How Its Bacterial Cause Was Found And Then Discarded

Introductory YouTube Video: click here

Introductory chapter article is on: Academia.edu

 

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RENSE.COM: EBOLA vs African TB ― OR HOW TO HIDE A DIAGNOSIS BEHIND A FEVER

November 20, 2014

 Dr. Lawrence Broxmeyer, MD

 

The CDC has quietly lowered its “critical temperature” protocols for detecting a fever ‘characteristic’ for Ebola after one health care worker slid by with a low-grade fever ― yet tested Ebola positive ― So……
“We changed to 100.4 after the first nurse presented to hospital with symptoms of disease and her temp was not the 101.5 that Ebola patients usually present when they are having vomiting diarrhea, etcetera,” CDC spokesman Thomas Skinner told the Daily Caller.
Etcetera. Etcetera. What Skinner meant is their Ebola temperature criteria has been changed to a temperature of 100.4ºF or above.
Anyway 100.4° (or above) sounds like a nice round number. So let’s examine it.
On the National Health Service’s website, put up by the UK government, the now magically designated temperature of100.4ºF or above also appears ― but not for Ebola. They are describing temperatures characteristic for tuberculosis. (http://www.nhs.uk/Conditions/Tuberculosis/Pages/Symptoms.aspx)

And, it might be added, temperatures characteristic for a dozen-and-a-half other illnesses.
So much for the use of temperature as an Ebola criteria.

Subsequently, by October the 20th ― World Health Organization (WHO) claimed Nigeria, which used to have the highest ‘Ebola’ death rate of any country in the world (See: http://rense.com/general96/ebooraf.html – “Ebola-free” Great, but does that they can say the same about the Ebola-like symptoms originating from the African strains of tuberculosis ― namely Mycobacterium tuberculosis and Mycobacterium africanum ― still raging over there? Will they next proclaim West Africa “Tuberculosis-free?”

Extrapulmonary (outside of the lungs) tuberculosis is the most frequent cause of a prolonged Fever of Unknown Origin (FUO) and has been for a long, long time.1,2
And in patients returning from areas where tuberculosis and malaria are
Common ― such as Africa ― the index of suspicion for these diseases should be elevated.
The current question………………… is it?
REFERENCES:

1. Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL, Casademont J. Harrison’s Principles of Internal Medicine. 16th Edition. 2004. McGraw-Hill Professional Publishing. 2680 pp
2. Roth AR, Basello GM. Approach to the adult patient with fever of unknown origin.Am Fam Physician. 2003 Dec 1;68(11):2223-8.

See also:

http://www.rense.com/general96/ebotbinter.html  Ebola & African TB – An Interview With Dr. Lawrence Broxmeyer, MD Part 1  Jeff Rense Dr. Lawrence Broxmeyer, MD 11-6-14
http://www.rense.com/general96/eboaf2.html
Ebola & African TB – An Interview With Dr. Lawrence Broxmeyer, MD Part 2
http://www.rense.com/general96/ebolareal.html
Is The Ebola Virus Real? From Dr. Lawrence Broxmeyer, M.D. © U.S. Library of Congress All rights reserved 11-9-14

Hello world!

August 14, 2012

These are the manuscripts, thoughts and laboratory results of physician/researcher Lawrence Broxmeyer, M.D.. As a medical investigator and author, his mission is and has always been to push out the boundaries of what is known towards those of what is conceivable. What he writes, along a historical time-frame is both compelling and well-documented addressing some of the most challenging problems in medicine today, among them AIDS, Alzheimer’s disease, Parkinson’s disease, autism, cancer, diabetes, heart disease, HIV, influenza, the Pandemic of 1918, TSE, the Transmissible Spongioform Encephalopathies, tuberculosis, Jakob-Cruezfeldt disease, mad-cow disease, phage therapy and recent mycobacterial research.  If you are expecting to read the parroting of present medical orthodoxy, you might be disappointed. If on the other hand, you are not entirely satisfied with certain areas of present day dogma and the results they bring, you might find Broxmeyer’s ideas absorbing. Anyway, let us begin………….