Acid-Fast Bacteria Discovered In Prostate Cancer]

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Acid-Fast Bacteria

Discovered In Prostate Cancer

2004 Alan R Cantwell, M.D.

Los Angeles, CA

alancantwell

6-12-4

 

 

 

 

 

 

 

 

 

 

 

Are infectious and unrecognized bacteria involved in the

cause of prostate cancer? Can so-called "cancer microbes" cause cancer?

Is there a connection between prostate cancer and a cancer-causing

virus common in AIDS patients? These controversial questions concerning

the cause of prostate cancer are explored here. In addition,

microphotographs of the newly-discovered bacteria found in prostate

cancer are presented.

 

 

Prostate cancer is the most

common form of cancer in American men, with 230,000 new cases diagnosed

yearly and 30,000 deaths annually (double the number of yearly AIDS

deaths in the U.S. ). This slow-growing cancer primarily affecting

older men. Elderly men with prostate cancer often die from some other

cause.

 

 

Autopsy studies have shown that

by the time men reach age 50, already thirty percent of men have

microscopic evidence of prostate cancer; and at age 80 there is an 80%

chance a man will have this cancer. Standard treatment is surgical

removal of the entire gland (along with a portion of the urethra

contained within it) or a series of radiation treatments to the

prostate. Both procedures often result in urinary incontinence and

impotence.

 

 

Since the late 1980's the PSA

(prostate specific antigen) blood test has been widely used to screen

for prostate cancer. Previously, a rising PSA level of 4 nanograms or

more signified possible cancer. However, a new study in May 2004

indicates that 15% of men with PSA levels less than 4 had cancer when

their prostates were assessed with biopsies. The results of this new

study is causing great controversy in the diagnosis and treatment of

prostate cancer.

 

 

 

 

 

What causes prostate

cancer?

 

 

 

 

 

Like most forms of cancer,

there is no known cause. If the cancer is confined to the prostate a

cure is probable, but once it spreads to other parts of the body, there

is no cure.

An April 2004 report widely

heralded in the media suggests that men who ejaculate more frequently

might lower their risk for prostate cancer. A May 2004 report also

warned that men with a history of sexual promiscuity and

sexually-transmitted diseases were more likely to get prostate cancer.

 

 

 

Acute and chronic inflammation

of the prostate (prostatitis) is a common and painful condition

affecting younger and middle-aged men. The cause of chronic prostatitis

is incompletely understood, although antibiotic therapy is employed in

the majority of cases. A variety of bacteria (staphylococci,

streptococci, corynebacteria, and others) have been cultured from

prostatitis. There is debate whether this ailment is a risk factor for

cancer. Benign prostatic enlargement (hyperplasia) , another common

condition of older men, is not a precursor to carcinoma.

 

 

There is also disagreement

regarding the role of testosterone in the development of prostate

cancer.

 

 

Researchers have recently

cautioned men about ingesting excessive amounts of zinc supplements,

claiming that 100 milligrams of zinc daily could more than double the

risk of prostate cancer. DHEA, another popular supplement, is also

suspect because some fear that the increased levels of testosterone

seen with daily DHEA pills could stimulate the growth of a tiny

prostate tumor that would otherwise have remained dormant.

 

 

 

 

 

 

 

Prostate Cancer and

Kaposi's sarcoma virus infection

 

 

 

 

 

Over the years a number of

viruses (the cytomegalovirus, human papilloma virus, various herpes

viruses, and the hepatitis B virus) have been suspected of causing or

complicating prostate cancer. A very recent report suggests the

Kaposi's sarcoma virus, also known as human herpes virus 8 (HHV-8),

might also be involved .

 

 

The Kaposi's sarcoma virus is

intimately connected with the epidemic of HIV (human immunodeficiency

virus) and AIDS. Prior to the AIDS epidemic in gay men in the late

1970's, so-called "classic" Kaposi's sarcoma (KS) in the U.S. was a

rare cancer tumor found primarily in elderly men of Jewish and Italian

extraction.

 

 

When AIDS began exclusively in

the gay male population in America in the late 1970s, KS skin tumors in

young homosexuals became the "Scarlet Letter" of the new disease. Up to

one-third of AIDS patients now carry the KS virus. When AIDS began, one

in three gay AIDS patients had KS skin lesions. Now, only one in ten

men with AIDS have KS lesions.

 

 

Infection with HIV makes

patients more vulnerable to certain cancers, particularly lymphoma, KS,

and uterine cancer. However, prostate cancer in HIV-infected men is

uncommon.

 

 

Although cases of "classic" KS

were first diagnosed in Europe in 1872, the KS virus was only

discovered in 1994 in cases of AIDS-related KS. This KS virus has also

been found in other forms of cancer, such as lymphoma and multiple

myeloma.

 

 

A 2004 study by LJ Hoffman and

associates at the University of Pittsburgh tested the blood of prostate

cancer patients for antibodies to the KS virus antigens. Remarkably,

40% of men from Trinidad and Tobago and 20% of U.S. men tested positive

for antibodies to the KS virus. This was considerably higher than an

age-matched control group of Trinidad men (23%) and American men (5%).

The researchers conclude that the KS virus could play a role in the

development of prostate cancer.

 

 

In the U.S. the general

incidence of KS virus in blood donors is 5%. However, a 2002 study of

Texas blood donors indicated a 15% infection rate.

 

 

The emergence of the KS virus

worldwide indicates the virus has been introduced in recent decades.

The fact that both HIV and the KS virus were initially introduced

exclusively into the gay American population in the late 1970s has

received little comment. One can perhaps easily explain the

introduction of a new HIV virus of supposed African origin, but what is

the explanation for the additional and simultaneous introduction of a

second virus - the KS virus - into gay men?

 

 

At present, the blood supply is

not screened to eliminate donors carrying the KS virus. Gay men, and

any man who has had sex with another man since 1978, are routinely

banned as donors, and all blood is screened for HIV. Yet, KS virus

carriers are not excluded. This alone is good reason for any person

undergoing elective major surgery (like prostate gland removal) to

donate their own blood beforehand in the event that a blood transfusion

is needed during or after surgery.

 

 

 

 

 

 

 

Cancer and the Cancer

Microbe

 

 

 

 

 

Although medical science claims

the cause of most cancers is unknown, there is evidence accumulated

since the late 19th century to show that cancer is a disease caused by

infectious bacteria (not to be confused with viruses which are not

visible microscopically). In 1890 the noted Scottish pathologist

William Russell (1852-1940) discovered round forms in cancer tissue

which he interpreted as "the characteristic organism of cancer." These

forms were subsequently discredited as infectious agents but have

became known to every pathologist as "Russell bodies." (For more

details see, "The Russell Body: The forgotten clue to the bacterial

cause of cancer" at: www.rense.com/general44/russell.htm)

 

 

The most vocal proponent of

bacteria as a cause of cancer was the late Virginia Livingston, M.D. In

1950, Virginia Wuerthele-Caspe Livingston and Eleanor Alexander-Jackson

(a microbiologist), along with John A Anderson (head of the Department

of Bacteriology at Rutgers), James Hillier (head of the electron

microscopy at the RCA Victor Laboratories at Princeton), Roy Allen (a

renowned microscopist), and Lawrence W Smith (author of a well-known

pathology textbook used in medical colleges), all combined their

talents to write a paper entitled "Cultural Properties and

Pathogenicity of Certain Microorganisms Obtained from Various

Proliferative and Neoplastic Diseases," published in the December issue

of The American Journal of the Medical Sciences. The characteristics of

the cancer microbe in blood, tissue, and culture, were described in

detail; and the extreme pleomorphic nature of the organism was revealed

in photos taken with the electron microscope at a magnification of

31,000X. (The ordinary light microscope only magnifies a thousand

times.)

 

 

The cancer microbe, which

Livingston later called Progenitor cryptocides, was filterable through

a pore designed to hold back bacteria, indicating that the smallest

forms of the microbe were indeed "virus-sized." However, with time

these filter-passing were able to grow and revert back to the size of

conventional bacteria.

 

 

The microbe was characterized

as pleomorphic, that is, having more than one form and size. The

smallest forms of the organism were virus-like, and the larger

bacterial forms were comparable to what bacteriologists call

"mycoplasma", "L-forms" and "cell-wall deficient forms." The largest

forms of the organism resembled what Russell called "the cancer

parasite." Livingston believed the organism was closely related to the

mycobacteria, the species of acid-fast bacteria that causes

tuberculosis. She claimed the "acid-fast" staining method was essential

to identify the microbe in tissue and in culture.

 

 

In a series of papers

Livingston and her colleagues all continued important cancer microbe

research showing the characteristic "connective tissue parasite" of

cancer, the germ that could be found inside the cell (intracellular)

and outside the cell (extracellular) in all cancers they studied.

Livingston always stressed that the microbe tends to involve the

collagenous (connective) tissue, and the photographs presented here in

prostate cancer confirm that.

 

 

When she died in 1990 at the

age of 84, she was widely regarded as a quack, particularly by the

American Cancer Society which claimed her cancer microbe did not exist.

Likewise, a bulletin published by the National Cancer institute on Nov

30, 1990 stated: "There is no scientific evidence to confirm

Livingston's theories of cancer causation."

 

 

More details covering a century

of cancer microbe research can be found in my book, The Cancer Microbe:

The Hidden Killer in Cancer, AIDS, and Other Immune Diseases (1990) ,

in Cell Wall Deficient Bacteria (1993) by Lida Mattman, Ph.D., in Can

Bacteria Cause Cancer?: Alternative Medicine Confronts Big Science

(1997) by David Hess, and also by initiating a computer search at

www.google.com and typing in "cancer bacteria", "cancer microbe", or

"cancer-associated bacteria."

 

 

Over the past four decades

personal publications in medical journals record the presence of cancer

bacteria in various cancers, including breast cancer, Kaposi's sarcoma,

Hodgkin's disease, mycosis fungoides, as well as in non-cancerous

diseases like scleroderma, lupus erythematosus, and sarcoidosis.

Additional papers on the microbiology of cancer are presented online at

the Journal of Independent Medical Research web site (www.joimr.org).

References and abstracts on 10 cancer microbe medical publications can

be found at the National Library of Medicine's "PubMed" web site

(www.ncbi.nlm.gov/PubMed/). (Type in "Cantwell AR + cancer bacteria".

 

 

 

According to Livingston, the

cancer microbe is present in the blood, tissue, excreta, and body

fluids of all human beings. When the immune system is functioning

normally these microbes did not cause disease. However, when tissue is

damaged or weakened these microbes became aggressive and pathogenic,

producing hardening and thickening of the tissue (such as found in

scleroderma and heart disease), inflammation (autoimmune diseases and

sarcoidosis) and proliferative and cancerous changes. The cancer

microbe is essential to our life biology. When conditions are adverse,

it emerges and reverts to its pathogenic form .

 

 

Livingston's research is

connected with newer microbiologic findings indicating that the blood

of all human beings is infected with a variety of so-called "cell wall

deficient" bacteria. Tiny, virus-like forms of the cancer microbes are

undoubtedly related to the tiniest of newly-discovered bacteria

currently called nanobacteria. These previously neglected and

largely-unstudied nanobacteria, which lie in size between the

normal-sized bacteria and the smallest viruses, are thought to be

involved in a variety of skin and heart ailments presently labeled as

diseases of unknown etiology. An excellent source of up-to-date

nanobacteria research can be found at the Nanobac Pharmaceutical web

site (www.nanobaclabs.com/research ).

 

 

 

 

 

 

 

Detecting Acid-Fast

Cancer Bacteria in Prostate cancer

 

 

 

 

 

In December 2003 my partner of

30 years was diagnosed with prostate cancer. He is a 68 year-old

Italian-American who has always been in good health. His PSA was

abnormally elevated to 9, and a digital rectal examination by the

urologist revealed a hardened area on the right side of the gland.

Multiple biopsies were performed from six areas of the prostate gland

and three were positive for adenocarcinoma.

 

 

Two months before the prostate

cancer diagnosis, he had a skin biopsy performed on a small reddish

skin lesion on the right lower leg. The pathology report was

interpreted as Kaposi's sarcoma. The lesion totally disappeared after

the biopsy site healed and there has been no recurrence.

 

 

In view of the frequent

association of KS with AIDS, an HIV test was performed and was

negative. Thus, his KS diagnosis was consistent with the pre-AIDS

"classic" type of KS which, although rare, is found most often in

elderly Jews and Italians in America. His blood was not tested for the

KS virus. However, blood tests did reveal past asymptomatic infection

with the hepatitis B virus, and he has a history of recurrent skin

infection with herpes simplex virus.

 

 

A prostatectomy, along with

removal of the surrounding lymph nodes, was performed in March 2004.

Microscopic examination of this tissue showed the cancer entirely

confined to the prostate with no cancer detected in the nodes.

Approximately 25% of the gland was involved with invasive

adenocarcinoma. (Cancerous prostate glands removed at surgery often

tend to be multifocal, meaning that more than one part of the gland is

affected by cancer.)

 

 

In view of my previous cancer

microbe studies, I requested that the pathologist supply me with a

Fite-stained tissue section of his prostate tissue. The Fite stain is

an "acid-fast" stain traditionally used for the detection of acid-fast

tuberculosis-type bacteria. The acid-fast stain is essential to detect

cancer-associated bacteria. One of the reasons pathologists do not

identify bacteria in cancer is that the hematoxylin- eosin tissue

stain, routinely employed by pathologists for diagnosis, does not stain

cancer microbes.

 

 

Because bacteria are so small,

it is necessary to study the tissue under oil immersion. That is, a

drop of oil must be put on the slide and the tissue must be studied

carefully using the oil-immersion lens of the light microscope in order

to visualize the material at the highest possible magnification. This

allows tissue examination at the highest magnification possible, a

magnification of 1000 times.

 

 

Having retired from

dermatologic practice a decade ago, I had done absolutely no

microscopic work. Although I had studied various types of cancer

related to dermatology, I had never had the opportunity to study

prostate cancer, the leading cancer of men. I had previously reported

on bacteria in various types of KS. Learning about the association of

the KS virus and prostate cancer, I was determined to see if microbes

could be identified in my partner's cancer, particularly because he had

the rarest of cancers - the non-AIDS related classic form of KS seen in

elderly Italian men .

 

 

For the first 15 minutes of

study I searched the most cancerous area of the gland and found

nothing. However once I searched the connective tissue areas (the

stroma) adjacent to the main tumor mass, the bacteria were easily

detected.

 

 

 

 

 

 

 

 

 

 

 

 

Like bacteria observed in other

forms of cancer, prostate cancer bacteria are primarily observed in the

connective tissue stroma in tightly-packed clusters of round "coccoid"

forms seemingly embedded in a matrix. These microbes can be seen,

although with difficulty, by using the "high power" lens of the

microscope, which magnifies 400 times (Figures 1 and 2). Using oil and

the oil-immersion lens, which allows magnification up to 1000 times,

the organisms are seen more clearly. The forms are primarily seen

packed together in tight units in the connective tissue stroma (Figure

3). Sometimes a cell nucleus is clearly visible in the cluster (Figure

4). Rarely, one can see intracellular forms which suggest short

rod-shaped bacterial forms, rather than the common round coccoid forms

(Figure 5). Extracellular forms that escape from the tight bacterial

clusters can be seen scattered in the connective tissue (Figure 6).

Occasionally larger coccoid forms are seen that are three and

four-times larger than the tiniest round forms. The largest round

spore-like forms seen in Figure 6 are apparently what Russell observed

as his "parasite of cancer."

 

 

The photos emphasize the varied

size and shape of the pleomorphic microbial forms in the prostate, as

well as the preference of the microbe for "collagen" - the "glue"

protein that helps hold together the cells and tissues of the body.

Could this affinity for collagen produce the biochemical change related

to the elevated protein antigen detected by the PSA test for cancer?

Particularly when antigens are often defined as foreign substances

produced by bacteria and viruses.

 

 

 

 

 

 

 

Cancer Microbes and

human blood

 

 

 

 

 

Although doctors and blood

suppliers would like the public to believe that transfused blood is

"safe" and free from harmful infectious agents, in reality human blood

is an aquarium filled with various known and unknown viruses and

bacteria. Currently, healthy blood donors are screened for syphilis,

hepatitis B and C, HIV-1 and 2, and HTLV-1 and 2. However, there is no

routine screening for other known pathogenic viruses, such as

transfusion transmitted virus (TTV), hepatitis G, the KS virus, parvo B

19 virus, and others.

It is now increasingly

recognized that everyone's blood contains bacteria. Some of the species

of blood bacteria (staphylococci, streptococci, corynebacteria) are

similar to the kinds of bacteria found on the skin. However, these

types of bacteria are also closely related, if not identical, to what

are generally and loosely termed "cancer-associated bacteria", as

reported by various investigators over the decades. Except for the

bacteria that cause syphilis, "healthy" blood is not screened for any

of these bacterial agents. Blood suppliers also ignore a host of tiny

and difficult-to-culture "nanobacteria", which are newly-recognized

normal constituents of the blood.

 

 

The origin of cancer microbes

in cancer tissue may very well be derived from blood bacteria. The

microbiology of cancer, although ignored by science, will ultimately

have to be explored in relationship to the equally-ignored microbiology

of human blood.

 

 

 

 

 

 

 

Cancer: One disease or

many?

 

 

 

The cancer establishment

believes that cancer is not one disease but many different diseases,

each with their special risk factors, and each with their own special

treatment. However, if bacteria turn out to be the cause, cancer may

prove to be essentially one disease and not many different ones. For

example, tuberculosis bacterial infection confined to the skin is a

very different clinical disease from extensive tuberculosis infection

of the lungs. Yet both diseases are the same because they are caused by

the same agent- and they are treated with the same drugs.

 

 

Breast cancer and Kaposi's

sarcoma are considered very different diseases. However, cancer

bacteria have been reported in both diseases. Figures 7 shows the

appearance of variably-sized intracellular coccoid forms in breast

cancer (infiltrating ductal carcinoma), and Figure 8 shows the

acid-fast stained appearance of Staphylococcus epidermidis cultured

from the tumor when it metastasized to the skin. The size of some of

the coccoid forms in the tumor is exactly the size and shape of the

staphylococci bacteria cultured from the tumor. In addition, the

presence of pink and red "acid-fast spicules" sprouting from coccoid

bodies seen in the staphylococcus culture is most unusual. However,

Livingston and Alexander ­Jackson showed exactly the same type of

acid-fast spicule growth in culture from the urine of a cancer patient

in their 1970 paper (their Figure 12A). This research regarding "a

specific type of organism cultivated from malignancy" was presented at

the New York Academy of Sciences in November 1969. These two women

repeatedly claimed the cancer microbe was related to the acid-fast

mycobacteria that cause tuberculosis - and that the acid-fast stain was

the key to identifying this microbe.

 

 

Figure 9 shows coccoid forms

within a skin lesion of KS in a patient near death from AIDS. Figure 10

shows the appearance of Streptococcus G cultured from his blood shortly

before death. If one compares the size and shape of the blood

streptococci, they appear similar in size and shape to the coccoid

forms seen deep in the skin of a KS tumor .

 

 

Until the recent study

associating the KS virus with prostate cancer, there was no

relationship between KS and prostate cancer. Likewise, mammary gland

breast cancer and prostate cancer (found exclusively in men) seemingly

have nothing in common except they are the most common forms of cancer

(other than skin cancer) in women and men. Both the mammary and the

prostate glands are secretory glands that excrete externally, and both

glands and both cancers are hormone-fueled. But the pleomorphic coccoid

forms seen in both cancers are similar in appearance, suggesting that

bacteria are involved in the production of both these "different"

cancers.

 

 

If one studies the microbiology

of cancer, it is apparent that cancer microbes provoke not only cancer,

but also a variety of tissue responses, including fibrosis and

thickening of the connective tissue (as in scleroderma), cellular

infiltrations (as seen in autoimmune diseases), and the formation of

tumors. The fact that similar-appearing bacteria can be identified in

acid-fast stained tissue sections of so many different types of

diseases makes them admittedly an unprecedented type of infectious

agent.

 

 

 

 

 

 

 

Why does the medical

establishment ignore cancer microbe research?

 

 

 

 

 

Despite a century of credible

cancer microbe research, the medical profession generally ignores all

aspects of research implicating bacteria in cancer. One exception is

the 1982 discovery of certain bacteria in the stomach (Helicobacter

pylori) that are now accepted as the cause of stomach ulcers that can

sometimes progress to cancer and gastric lymphoma.

 

 

The most influential physician

condemning cancer-associated bacteria was James Ewing, a noted American

pathologist and author of the widely read textbook, Neoplastic Diseases

(1919), in which he wrote that "few competent observers consider it

(the parasitic theory) as a possible explanation in cancer." In Ewing's

view, cancer did not act like an infection. Therefore, he reasoned

microbes could not possibly cause cancer. As a result of his edict, few

doctors dared to contradict Ewing by continuing cancer microbe

research.

 

 

Ewing co-founded the American

Cancer Society in 1913 and in the 1930's he was the director of

Memorial Hospital, now better known as Memorial Sloan-Kettering Cancer

Center in New York City, one of the most prestigious cancer hospitals

in the world. Ewing died in 1943 from bladder cancer, at the age of 76.

 

 

 

Although bacteria were

dismissed as causative agents one hundred years ago, viruses are now

considered as likely causes of cancer - despite Ewing's contention that

cancer did not act like an infectious disease. What the pathologist did

not know is that pleomorphic cancer microbes have characteristics of

both bacteria and viruses and were not visible with routine staining

methods . Although physicians now easily accept the idea of

microscopically invisible viruses in cancer, they seem unable to

conceive of a microscopically visible bacterial agent in cancer.

 

 

 

Undoubtedly, the acceptance of

cancer bacteria would put cancer research and treatment into a tailspin

cancer chemotherapy and radiation would have to be reevaluated as a

rational treatment for bacterial infection. Because current antibiotics

cannot rid the body of cancer-causing bacteria, this would necessitate

the development of new cancer treatments designed to minimize this

infection.

 

 

It may be left to future

medical historians to explain why cancer microbe research has been

ignored for so many years, despite the millions of cancer deaths yearly

and the billions spent on cancer research.

 

 

In the meantime, as a retired

physician I will continue to bug (pun intended) my colleagues in

medicine to search for acid-fast bacteria as I and other cancer microbe

researchers in the past have done. The only requirements are an

acid-fast stained histopathologic slide of the malignant tissue, a drop

of oil, the use of the oil-immersion lens, a little patience, and an

open mind.

 

 

To ignore cancer bacteria

because a powerful pathologist once told his students a century ago

that there were no microbes to be found in cancer is simply irrational

and bad science. Re-search means to search again. After many decades of

failure to uncover a cause for cancer, surely it is time for a second

look at bacteria that can be easily found in this dread disease.

 

 

 

 

 

 

Legend for Photographs

 

 

 

Figure 1: Tissue section from

prostate adenocarcinoma showing, in center, a cluster of tightly-packed

intracellular blue-stained coccoid forms. Fite (acid-fast) stain,

magnification x 400 ("high power").

 

 

Figure 2: Prostate cancer. In

center, additional focus of intracellular blue-stained coccoid forms.

Fite stain, magnification x 400 ("high power").

 

 

 

 

Figure 3. Prostate cancer.

Tightly-packed cluster of blue and pink-stained coccoid forms in the

connective tissue stroma. Fite stain, magnification x 1000 (highest

magnification), in oil.

Figure 4. Prostate cancer.

Loosely-packed intracellular blue-stained coccoid forms. Fite stain,

magnification x1000, in oil.

 

 

Figure 5. Prostate cancer. Rare

cluster of loosely-packed intracellular and extracellular coccoid and

tiny rod-shaped forms. Fite stain, magnification x1000, in oil.

 

 

Figure 6. Prostate cancer. On

right, a cluster of larger coccoid forms. On left, scattered larger

extracellular coccoid forms in the connective tissue stroma.

These forms could be compatible

with "Russell bodies" - which Russell believed were "the characteristic

organism of cancer." Fite stain, magnification x1000, in oil.

 

 

Figure 7. Breast cancer. In

center, intracellular, tightly-packed variably-sized coccoid forms.

Kinyoun's (acid-fast) stain. magnification x 1000, in oil.

 

 

Figure 8. Smear from culture of

Staphylococcus epidermidis isolated from skin metastasis of original

breast cancer shown in Figure 7. In addition to myriads of

staphylococci, there are 5 areas of deep blue-stained granules from

which emanate acid-fast pink and red spicules. According to Livingston,

this is a characteristic of bacteria isolated from cancer. Note the

similar size and shape of the cocci to the coccoid forms seen in the

original tumor in Fugure 7. Ziehl-Nielson (acid-fast) stain,

magnification x 1000, in oil.

 

 

Figure 9. AIDS-related Kaposi's

sarcoma of the skin. Several clusters of blue-stained coccoid forms in

the deep dermis of the skin. Fite stain, magnification x 1000, in oil.

 

 

 

Figure 10. Streptococcus G

isolated from the blood of a fatal case of AIDS and AIDS-related

Kaposi's sarcoma. The size and shape of the streptococci are similar in

size and shape to the coccoid forms seen in the KS lesion shortly

before death. Ziehl-Nielson (acid-fast) stain, magnification x1000, in

oil.

 

 

 

 

References:

 

 

Alexander-Jackson E. A specific

type of microorganism isolated from animal and human cancer:

bacteriology of the organism. Growth. 1954 Mar;18(1):37-51.

 

 

Baillargeon J, Deng JH, Hettler

E, Harrison C, Grady JJ, Korte LG, Alexander J, Montalvo E, Jenson HB,

Gao SJ. Seroprevalence of Kaposi's sarcoma-associated herpesvirus

infection among blood donors from Texas. Ann Epidemiol. 2001

Oct;11(7):512-8.

 

 

Cantwell AR, Craggs E, Wilson

JW, Swatek F. Acid-fast bacteria as a possible cause of scleroderma.

Dermatologica. 1968: 136:141-150.

 

 

Cantwell AR Jr, Kelso DW.

Microbial findings in cancers of the breast and in their metastases to

the skin. Implications for etiology. J Dermatol Surg Oncol. 1981

Jun;7(6):483-91.

 

 

Cantwell AR Jr, Kelso DW.

Microbial findings in cancers of the breast and in their metastases to

the skin. Implications for etiology. J Dermatol Surg Oncol. 1981

Jun;7(6):483-91.

 

 

Cantwell AR, Kelso DW, Jones

JE. Histologic observations of coccoid forms suggestive of cell wall

deficient bacteria in cutaneous and systemic lupus erythematosus. Int J

Dermatol. 1982 Nov;21(9):526-37.

 

 

Cantwell AR Jr, Kelso DW.

Variably acid-fast bacteria in a fatal case of Hodgkin's disease. Arch

Dermatol. 1984 Mar;120(3):401-2.

 

 

Cantwell AR. Histologic

observations of variably acid-fast pleomorphic bacteria in systemic

sarcoidosis: a report of 3 cases. Growth. 1982 Summer;46(2):113-25.

 

 

 

Cantwell AR. Variably acid-fast

cell wall-deficient bacteria as a possible cause of dermatologic

disease. In, Domingue GJ (Ed). Cell Wall Deficient Bacteria. Reading:

Addison-Wesley Publishing Co; 1982. Pp. 321-360.

 

 

Cantwell AR, Rowe L. African

"eosinophilic bodies" in vivo in two American men with Kaposi's sarcoma

and AIDS. J Dermatol Surg Oncol. 1985 Apr;11(4):408-12.

 

 

Cantwell A. The Cancer Microbe.

Los Angeles: Aries Rising Press; 1990.

 

 

Diller IC, Diller WF.

Intracellular acid-fast organisms isolated from malignant tissues.

Trans Amer Micr Soc. 1965; 84:138-148.

 

 

Ewing J. The parasitic theory.

In, Ewing J (Ed), Neoplastic Diseases (Ed 1); Philadelphia: Saunders;

1919. Pp 114-126.

 

 

Gaylord HR. The protozoon of

cancer. Amer J Med Sci. 1901;121:501-539.

 

 

Glover TJ. The bacteriology of

cancer. Canada Lancet Pract. 1930; 75:92-111.

 

 

Hess D. Can Bacteria Cause

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Acknowledgement: Microscopist

James D. Solliday of Santa Ana, CA, performed the microphotography on

the prostate tissue sections.

 

 

 

 

 

 

 

 

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