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Bacteria In Heart Disease And Strokes
By Alan Cantwell, MD
© 2009 Alan Cantwell, MD
On June 5, 2009, the Daily Mail (UK) reported the details of the miraculous 'cure' of Russell McPhee, a 49 year old Australian man who had a devastating stroke and was paralyzed for more than two decades. After multiple injections of Botox into his spastic muscles, he was able to walk again.
Before its well-known use on wrinkles, Botox was used for stroke victims to counteract the muscles spasms. However, it is most unusual to get such a positive response after so many years, as in McPhee's case. Interestingly, Botox is Botulinum toxin, a neurotoxic protein produced by the bacterium Clostridium botulinum. It is the most toxic protein known. The intense forced relaxation of his contracted muscles (along with physical therapy) was the key to initiating his 'cure.'
Professor John Olver, one of Australia's top stroke experts, said: "We use Botulinum toxin routinely for patients with spasticity which has been caused by stroke, brain damage or heart disease. But we use it very early on, usually within weeks of a stroke, to prevent the spasticity from becoming a problem. Sometimes the spasticity is so severe we inject those muscles with Botulinum toxin, which relaxes the muscles enough to allow a physiotherapist to strengthen and stretch them. It is unfortunate that this patient had to wait for 20 years and extremely unusual that his treatment was so successful after being immobile for so long. But he's very fortunate that his muscles are strong enough to allow him to be able to walk."
During my many years of research investigating the role of bacteria as possible agents in certain chronic diseases and in cancer, I was curious whether similar bacteria might play a role in heart disease and stroke, or in chronic muscle disease.
There are a few reasons to suspect bacteria in these conditions. First, there is increasing evidence that bacteria (and viruses) may play a heretofore unrecognized role in chronic illness. Second, there is evidence that the blood of both healthy and ill people contain bacteria. And thirdly, there is an intimate connection between stroke, heart disease, and chronic hypertension (high blood pressure).
Bacteria and chronic muscle disease
By Googling "bacteria + muscle disease", one can easily review the evidence for bacteria (particularly pleomorphic cell wall deficient bacteria and mycoplasma) in certain chronic diseases in which muscular weakness, arthritic symptoms and fibrotic changes take place over time. These diseases include rheumatoid arthritis, Lyme disease, chronic fatigue syndrome, and others. Some patients with chronic diseases appear to be helped by long term antibiotic therapy.
Years ago, my autopsy research into the "acid-fast bacteria" discovered in systemic scleroderma convinced me that these microbes were implicated in the muscle, cardiac, and kidney abnormalities that accompany the hardening and thickening of the skin in fatal cases. (Figure 1 shows round tiny granular coccoid-appearing bacteria in the deep portion of the skin in scleroderma.) For more details, Google: "alan cantwell" + scleroderma.
Figure 1: Tiny round granular coccoid-appearing bacteria in the skin of scleroderma.
Bacteria and the blood
Recent research, based on molecular biology, indicates that 90% of the cells of the human body are microbial cells! Despite this amazing new discovery, most physicians do not believe bacteria are involved in any way with the major diseases (heart disease, stroke and cancer) that kill most of us. In addition, most physicians still believe that healthy blood is sterile, that is, free of bacteria.
During the 1970s the late Guido Tedeschi and his colleagues at the University of Camerino in Italy showed than human blood was universally infected staphylococcus-like and streptococcal-like bacteria. In 1977 Domingue and Schlegel confirmed "the existence of a novel bacteriologic system" in the blood. They cultured staphylococcal-like bacteria and filamentous cocco-bacillary forms from 71% of the blood specimens from ill patients; and from 7% of supposedly healthy people. These pleomorphic (variation in size and shape) bacteria grew out of round complex "dense bodies" and developed into "ordinary bacteria." The authors concluded: "These organisms may represent an adaptation of certain bacteria to life in the blood." Their full report, which contains pictures (full-screen) of the bacteria grown from human blood, is online at:
In the 1990's microbiologists Phyllis E Pease and Janice Tallak termed these blood bacteria as "the human bacterial endoparasite." Finnish researchers Kajander et al. describe them as "novel bacteria-like particles," which are staphylococcal-like. Like viruses, these tiny bacterial forms were able to pass through bacterial filters, and were exceedingly difficult to culture. The Finnish team called them "nanobacteria" and proposed a tentative name for the novel agent: Nanobacterium sanquineum.
In 2002 McLaughlin et al. presented a study entitled "Are there naturally occurring pleomorphic bacteria in the blood of healthy humans?" The researchers were surprised to discover bacteria in the blood "since it is generally acknowledged that the blood stream in healthy humans is a sterile environment, except when there is a breach in the integrity of the tissue membranes." More details on blood bacteria can be found in my article "All human blood is infected with bacteria," posted on the Internet.
In addition, these blood bacteria studies confirm the findings of Gunther Enderlein (1872-1968), Wilhelm Reich (1897-1957), Raymond Royal Rife (1888-1971), Virginia Livingston (1906-1990), Gaston Naessens
(1924- ) and others whose research can be easily googled.
Bacteria and hypertension
Because cryptic bacterial infection of the blood is not accepted by most scientists, there have been no studies correlating infection with hypertension. However, a very recent report (May 16, 2009) suggests that high blood pressure could be caused by a common virus, known as the cytomegalovirus (CMV), a common viral infection affecting between 60 and 99 percent of adults worldwide.
(http://www.sciencedaily.com/releases/2009/05/090514221915.htm) This new study brought together a team of researchers from a variety of disciplines ­ infectious diseases, cardiology, allergy and pathology ­ to look more closely at the issue. Previous controversial studies linked CMV infection to hardening of the arteries (atherosclerosis). Hardening of the arteries leads to hypertension, heart and kidney disease, and stroke.
Bacteria and the Heart
In an autopsy study entitled "Mycobacterial forms in myocardial vascular disease," published in 1965, my mentors Virginia (Wuerthele-Caspe) Livingston and Eleanor Alexander-Jackson first showed acid-fast bacteria in the heart muscle, in the coronary blood vessels and in the aorta. Later, they proposed a vaccine to combat the bacteria they observed not only in heart disease, but also in cancer and degenerative disease as well. A summary of their research can be read by Googling: U.S. Patent # 4692412, which also describes their finding of bacteria in heart disease. Figure 2 shows bacteria in the heart muscle at autopsy in a fatal case of AIDS. Figure 3 shows bacteria in the heart muscle from an autopsied case of lymphoma cancer (mycosis fungoides).
Figure 2: Bacteria in the heart muscle at autopsy in a fatal case of AIDS.
Figure 3: Bacteria in the heart muscle at autopsy in a fatal case of mycosis fungoides (T-cell lymphoma).
In various publications, Livingston and Alexander-Jackson proposed that these microbes were closely related to the acid-fast mycobacteria that cause human tuberculosis. In addition, they discovered that the acid-fast stain was the best staining method to detect these ubiquitous microbes in tissue sections and in laboratory culture. The various (pleomorphic) forms of the microbe can appear as virus-sized forms, as yeast-like forms, and as staphylococcal-like forms. In my experience, they appear most frequently in biopsy and surgical specimens as round coccus-like forms that are found both within and outside of the cells. Only rarely do they appear as acid-fast rod-forms, the typical appearance of the classic form of tuberculosis mycobacteria.
Most recently, in a BBC news report on May 25, 2009, a scientific team, headed by Arne Schaefer at the University of Kiel, found a common gene mutation in patients with periodontitis (gum disease) and in heart attack patients. There were also similarities between the bacteria found in the oral cavity and those in the coronary plaques. One theory is that the bacteria involved in gum disease trigger a low grade inflammatory response throughout the body, resulting in changes in the arteries that can lead to strokes and heart attacks. Another possibility is that the bacteria disturb the way blood vessels dilate directly, since some bacteria can enter the bloodstream. (http://news.bbc.co.uk/2/hi/health/8063512.stm).
Bacteria and strokes
Only recently has there been mild interest in investigating the role of bacteria in strokes. A Google search using key words "bacteria" + "strokes" leads to numerous web articles, such as "Ulcer bacteria linked to stroke', "Bacteria in mouth could predict strokes", "Antibiotics help prevent strokes", etc.
A stroke in the form of a hemorrhage pours blood into the affected areas of the brain and damages the brain cells and nerve connections. A stroke in the form of a clot does not allow blood to get to the cells. Obviously much more research needs to be done in this area. If bacteria are universally present in the blood, they might play a role in stroke formation.
Bacteria in kidney disease
It is well-known that chronic high blood pressure can lead to kidney disease. The role of bacteria (particularly pleomorphic cell wall deficient bacteria) in renal and urinary disease has been extensively studied and pioneered by microbiologist Gerald Domingue, author of Cell Wall Deficient Bacteria (1982). The PubMed website posts his many publications concerning cryptic bacterial infection of the blood, the kidney and the urinary tract. There is also an extensive bio on Domingue on the Wikipedia.
Tragically, there is little interest in studying the role of pleomorphic, cell wall deficient bacteria in kidney disease. Figure 4 shows such bacteria detected in the kidney in a fatal case of systemic scleroderma. Note the similarity of these round bacterial forms to the bacterial forms depicted in the skin of scleroderma (Figure 1) and in the heart muscles of patients who died of AIDS and cancer (Figures 2 and 3).
Figure 4: Bacteria in the kidney at autopsy in a fatal case of systemic scleroderma.
Perhaps the biggest reason why pleomorphic, cell wall deficient acid-fast bacteria are ignored in human disease is that these microbes are so ubiquitous. Everyone carries them, both in sickness and in health. Physicians are also reluctant to accept that the same type bacteria present in a healthy individual could cause a variety of chronic diseases in sick people.
However, almost all healthy people eventually die of diseases, such as cancer, heart or kidney disease, or suffer a stroke. Livingston was fond of saying "the microbe" was both the giver and the taker of life. I think it is fair to say that we still know very little about the bacteria we carry in our bodies, and the trouble they can cause as we age.
In an October 2009 landmark paper posted on rense.com, entitled "Heart disease; Beyond the stent and the bypass," Lawrence Broxmeyer has summarized a century of little-known research into the role of bacteria, particularly acid-fast tuberculous bacteria, in the development of heart disease. His important findings and conclusions can be found at: http://www.rense.com/general87/stent.htm
Regarding stroke victim Russell McPhee: Why did a bacterial-produced Botox product start a healing? The paralytic product forced a "breaking up" of the tight, constricted muscle. This, along with the message, allows better blood flow to the muscle. Could bacteria be involved in some chronic muscular disease states? I am reminded of an autopsy study of a fatal case of AIDS in which I discovered tiny round bacterial forms in the skeletal muscle (Figure 5). Fatal cases of AIDS are frequently associated with muscle weakness and "wasting."
Figure 5. Bacteria in the skeletal muscle at autopsy in a fatal case of AIDS associated with muscle wasting.
Despite the heretical aspects of this report, I trust it will stimulate other adventurous researchers to search for similar acid-fast bacteria in an attempt to elucidate their precise role in the most common chronic illnesses of man.
Cantwell AR, Kelso DW. Autopsy findings of nonacid-fast bacteria in scleroderma. Dermatologica. 1980;160(2):90-9.
Cantwell AR: Necroscopic findings of variably acid-fast bacteria in a fatal case of acquired immunodeficiency syndrome and Kaposi's sarcoma.. Growth. 1983 Summer;47(2):129-34.
Cantwell AR Jr.Variably acid-fast pleomorphic bacteria as a possible cause of mycosis fungoides. A report of a necropsied case and two living patients. J Dermatol Surg Oncol. 1982 Mar;8(3):203-13.
Domingue GJ, Schlegel JU.Novel bacterial structures in human blood: cultural isolation. Infect Immun. 1977 Feb;15(2):621-7.
Kajander EO, Tahvanainen E, Kuronen I and Ciftcioglu N.
Comparison of staphylococci and novel bacteria-like particles from blood. Zbl. Bakt. Suppl. 26, 1994.
McLaughlin RW, Vali H, Lau PC, Palfree RG, De Ciccio A, Sirois M, Ahmad D, Villemur R, Desrosiers M, Chan EC. Are there naturally occurring pleomorphic bacteria in the blood of healthy humans? J Clin Microbiol. 2002 Dec;40(12):4771-5.
Pease PE, Tallack JE. A permanent endoparasite of man. 1. The silent zoogleal/symplasm/L-form phase. Microbios. 1990;64(260-261):173-80.
Tedeschi GG, Di Iorio EE. Penetration and interaction with haemoglobin of corynebacteria-like microorganisms into erythrocytes in vitro. Experientia. 1979 Mar 15;35(3):330-2.
Tedeschi GG, Bondi A, Paparelli M, Sprovieri G. Electron microscopical evidence of the evolution of corynebacteria-like microorganisms within human erythrocytes. Experientia. 1978 Apr 15;34(4):458-60.
Tedeschi GG, Amici D, Sprovieri G, Vecchi A. Staphylococcus epidermidis in the circulating blood of normal and thrombocytopenic human subjects: immunological data. Experientia. 1976 Dec 15;32(12):1600-2.
Tedeschi GG, Amici D. Mycoplasma-like microorganisms probably related to L forms of bacteria in the blood of healthy persons. Cultural, morphological and histochemical data. Ann Sclavo. 1972 Jul-Aug;14(4):430-42.
Wuerthele-Caspe (Livingston) V, Alexander-Jackson E. Mycobacterial forms in myocardial vascular disease. J Amer Med Wom Assoc. 1965 (20):449-452.
[This article was originally published in NEXUS NEW TIMES, September 2009. Alan Cantwell M.D. is a retired dermatologist. He is the author of The Cancer Microbe: The Hidden Killer in Cancer, AIDS, and Other Immune Diseases, and Four Women Against Cancer: Bacteria, Cancer and the Origin of Life, both published by Aries Rising Press, PO Box 29532, Los Angeles, CA 90029 (www.ariesrisingpress.com). His books are available from Amazon.com and via Book Clearing House at 1-800-431-1579.
Email address: alancantwell@sbcglobal.net
ADDENDUM: The following is a description of the bacteria discovered within the heart and blood vessels by Virginia Livingston and Eleanor Alexander-Jackson, and illustrated in their 1965 paper (cited above). The description is included in their U.S. Patent #4692412 (issued on Sept 8. 1987) , in which their "autogenous vaccine" invention was proposed to stimulate the immune system against the build-up of these pleomorphic acid-fast bacteria. My figures 2 and 3 in the above paper showing bacteria in the heart muscle are strikingly similar to those microphotographs showing "acid-fast organisms in heart muscle" in their 1965 paper.
(In) "Mycobacterial Forms in Myocardial Vascular Disease", Virginia Wuerthele-Caspe Livingston and Eleanor Alexander-Jackson, (1965) proposes the theory that there are microbic bodies in the lesions of heart diseases and that they are especially numerous in the areas where the blood vessels have ruptured. Until recently the theory has been the coronary blood vessels of the heart are narrowed due to arteriosclerosis, and that fatty deposit in the wall of the vessels, and overweight are the determining factors in this type of heart disease. Now the medical researchers are becoming aware of the fact that the blood vessels themselves are often not involved so much as the supporting tissues and muscles of the heart so that the heart vessels rupture due to extrinsic factors outside the vessel rather than from intrinsic disease. This is particularly true of patients with collagen diseases such as scleroderma and lupus erythematosus. Vascular and myocardial pathology is related to chronic low-grade infection by the mycobacterium-like organisms (Cryptocides).
Degenerative changes occur in coronary heart disease in the presence of the invasive mycobacterial parasite cryptocides.
Postmorten heart sections of 6 patients with coronary and aortic disease were stained by the Fite modification of the Ziehl-Neelsen technique (for demonstrating Lepra bacilli in sections) using Kinyoun's carbon-fuchsin, and compared with sections of the same involved areas stained with conventional H and E. Eight predominant types of lesions were observed in the myocardium
1. PERIVASCULAR CHANGES AROUND THE SMALL CORONARY VESSELS. In the loose connective tissues numerous small acid-fast bodies can be seen.
2. CELLULAR INFILTRATION. This is frequently seen not only around the vessels but between the muscle fibers as well. These cells consists almost entirely of mononuclear types, predominantly lymphocytes, while large mononuclear phagocytes laden with organisms plasma and other mononuclear cells are present in relatively large number.
3. FIBROBLASTIC INFILTRATION. The presence of these organisms appears to stimulate the formation of fibroblasts. In some areas, the muscle fibers and interstitial tissues appear to be replaced by fibroblasts.
4. INFARCTION. Where there has been an infarct, there may be a softened central area with numerous small acid-fast cocci and coccobacilli present in the collagenous hemorrhagic softened area.
5. NECROSIS. Necrotic changes may involve the blood vessels. Striking degenerative changes of the vessel walls are observed as illustrated not only by the sections of coronary vessels but also by the sections of involved aorta. Proliferative changes may involve the endothelium, with invasion of the endothelial cells, and are accompanied by thickening and narrowing of the wall. Hairlike filaments of the organisms were seen protruding into the lumen. These changes are also present in the vasa vasorum of the aorta.
6. THROMBOSIS AND RECANALIZATION. Some areas of recanalization were observed in heart, liver, and spleen.
7. CHANGES IN THE ELASTIC LAYER OF THE AORTA. The elastic fibrils have lost their identity and have become collagenized with loss of structure. As scar tissue forms, cholesterol-like plaques occur. It seems possible that deposits may be derived in part from the fatty envelopes of these organisms. In other tissue where masses of the organisms have proliferated, polyhedral crystals resembling cholesterol have been observed.
8. CHANGES IN THE HEART MUSCLE. Individual nuclei of the heart muscle are frequently parasitized, and replaced by small acid-fast globoidal bodies. The muscle fibers themselves appear in a state of gradual digestion and disintegration by both minute and larger acid-fast forms.
All of the above can be treated and detected by this invention
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