The Candida Expert

Archive for the ‘Medicine’ Category

Hydrochloric Acid and Health

Hydrcochloric acid (HCL) is produced in the stomach to aid in activating digestion of foods and protection of the intestinal flora. Excess stomach acid (HCL) has traditionally been treated as a result of low HCL levels that creates cycles of over- and under-production. With the advent of direct-to-consumer marketing by pharmaceutical companies, the public was entrained to believe that this was purely an excess HCL problem that needed to be suppressed with antacids, leaving behind the science, physiology, and wisdom of the body.

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Tryptophan Reduces Intestinal Inflammation

It’s always nice to see good research that helps to clarify simple principles that demonstrate what effectively works and doesn’t work for our bodies. Researchers from Japan, Switzerlan, Germany, Austria, and the Netherlands have discovered the effectiveness of the natural amino acid, Tryptophan in controlling inflammation of the intestinal tract. Such inflammation is associated with malnutrition, diarrhea, Crohn’s, IBS, IBD, and Colitis – http://www.sciencedaily.com/releases/2012/07/120725132133.htm

More than one billion people in poor countries are starving, and malnutrition remains a major problem even in rich countries, making it a leading cause of death in the world. For over a hundred years, doctors have known that a lack of protein in the diet or low levels of amino acids, the building blocks of proteins, can lead to symptoms like diarrhoea, inflamed intestines and other immune system disorders, which weaken the body and can be fatal. However, the molecular mechanism which explains how malnutrition causes such severe symptoms has been largely unexplored.

Now a research group led by Josef Penninger, the director of the Institute of Molecular Biotechnology (IMBA) in Vienna, Austria, in cooperation with Philip Rosenstiel, University of Kiel, Germany, has found a molecular explanation for the increased susceptibility to intestinal inflammation in malnutrition.  The researchers were studying an enzyme which helps to control blood pressure, kidney failure in diabetes, heart failure and lung injury, called the Angiotensin Converting Enzyme 2, or ACE2.  This enzyme was identified as the key receptor for SARS virus infections, but the researchers also discovered an entirely new function.  ACE2 controls the way our intestines take in amino acids from our food, via amino acid transporters, and in particular the uptake of the essential amino acid tryptophan.

Too little tryptophan alters our natural immune system, which changes the types of bacteria which can live in our bowels and guts, leading to higher sensitivity and eventually diarrhoea and inflamed intestines.  Increasing the intake of tryptophan in their diet provided relief for mice suffering from intestinal inflammation. The mixture of bacteria returned to normal, the inflammation died down, and the mice also became less susceptible to new attacks.

“The research shows how the food we eat can directly change the good bacteria in our intestines to bad bacteria and so influence our health”, says Thomas Perlot, the first author of the study. “Our results might also explain nutritional effects that have been known for centuries and provide a molecular link between malnutrition and the bacteria living in our intestines. This discovery could be used in the future to treat patients with a simple regulated diet or by taking tryptophan as a food supplement.  And there is hardly any risk of side effects from artificially increasing an amino acid found in the normal diet.”

Josef Penninger, the lead author, says “I have studied ACE2 for more than 10 years and was completely stunned by this novel link between ACE2 and amino acid balance in the gut. Biology continues to surprise me. Up to a billion people in the world are malnourished, especially the poor and disadvantaged. In Austria alone, around 80,000 people suffer from a chronic inflammatory bowel disease like ulcerative colitis or Crohn’s disease. I hope that our findings have opened a door to a better molecular understanding how malnutrition affects human health. Whether simple tryptophan diets can indeed cure the effects of malnutrition in humans now needs to be carefully tested in clinical trials.”

Common Questions About Candida

Here are three common questions that we get about Candida.

 

1) How Do I Know I Have Candida?

Dr. McCombs analysis of the research, dating back to 1949, shows that if you’ve ever done antibiotics, you’ll have systemic fungal candida. Most people however, won’t have any symptoms of fungal candida infections. Studies that have been done, show that candida albicans can persist undetected in the majority of individuals. For those of you have symptoms already, there’s really no short list of symptoms that would apply as fungal candida can affect every organ, tissue, and cell in the body, depending on several factors.

“Commensal organisms, such as Candida albicans, are able to persistently colonize the host without causing symptoms.”
Interactions of the fungal pathogen Candida albicans with the host
Steffen Rupp
Future microbiology. 01/05/2007; 2:141-51.
http://www.researchgate.net/publication/6176804

“The frequencies of the carriage of yeast pathogens and of serum precipitins to a variety of candida antigens among 254 patients generally tended to increase with the length of the patient’s stay in hospital. This trend was observed even though none of the patients investigated showed signs or symptoms of superficial or systemic candidosis.”
Distribution of pathogenic yeasts and humoral antibodies to candida among hospital inpatients.
J Clin Pathol 1980;33:750-756 doi:10.1136/jcp.33.8.750
http://jcp.bmj.com/content/33/8/750.abstract

“…based on the 15 to 25% rate of asymptomatic colonization in healthy adults or adolescents and especially the high asymptomatic vaginal fungal burden in adolescents.
An Intravaginal Live Candida Challenge in Humans Leads to New Hypotheses for the Immunopathogenesis of Vulvovaginal Candidiasis
Infection and Immunity, May 2004, p. 2939-2946, Vol. 72, No. 5
http://iai.asm.org/cgi/content/full/72/5/2939

 

2) What Causes Candida?

“Antibiotic treatment has also been shown to increase the rate of C. albicans isolation
in stool (15; M. Barza, M. Giuliano, and S. Gorbach, Program Abstr. 25th Intersci.”
“Factors identified that facilitate this dissemination include suppression of the intestinal bacterial flora…”
Factors Affecting Colonization and Dissemination of Candida albicans from the Gastrointestinal Tract of Mice
INFECTION AND IMMUNITY, JUlY 1987, p. 1558-1563
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC260558/pdf/iai00091-0028.pdf

“Candida albicans infections often occur during or shortly after antibacterial treatment.”
Influence of fluoroquinolones on phagocytosis and killing of Candida albicans by human polymorphonuclear neutrophils
Thomas Grúger; Caroline Mörler; Norbert Schnitzler; Kerstin Brandenburg; Sabine Nidermajer; Regine Horré; Josef Zúndorf
http://www.informaworld.com/smpp/content~db=all~content=a793116268?words=candida*%7Calbicans

“Risk factors for candidaemia include breakdown of mucosal barriers due to cytotoxic chemotherapy and surgical procedures, neutropenia, changes in the gut flora due to antibiotics, and invasive interventions that breach the skin, such as intravenous lines and drains (Wey et al, 1989).”
The immune response to fungal infections
Shmuel Shoham1 and Stuart M. Levitz
1Section of Infectious Diseases, Washington Hospital Center, Washington, DC, and 2Department of Medicine, Boston Medical Center and
Boston University School of Medicine, Boston, MA, USA
British Journal of Haematology, 129, 569–582
http://www.aspergillus.org.uk/secure/articles/pdfs/shoham05.pdf

“The composition of the microbiota is significantly affected by the use of antibiotics, which are often used extensively,…”
Host immune response to antibiotic perturbation of the microbiota
M Wlodarska and B B Finlay
http://www.nature.com/mi/journal/v3/n2/full/mi2009135a.html

“Mice were pretreated with antibacterial agents to alter their resident microflora, and then orally inoculated with C. glabrata and/or C. albicans. Elimination of detectable cecal bacteria facilitated colonization with both Candida species.”
Comparative abilities of Candida glabrata and Candida albicans to colonize and translocate from the intestinal tract of antibiotic-treated mice
Michelle J. Henry-Stanley; Robb M. Garni; Mary Alice Johnson; Catherine M. Bendel; Carol L. Wells
http://www.informaworld.com/smpp/content~db=all~content=a727729968?words=candida*|albicans*

“…antibiotic therapy has been reported to precede disseminated candidiasis in children.”
Interaction of Candida albicans with Human Leukocytes and Serum
ROBERT I. LEHRER AND MARTIN J. CLINE
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC315286/pdf/jbacter00585-0178.pdf

“Oral antibiotic therapy in humans often leads to colonization and over-growth of the GI tract by C. albicans”
Inhibition of Candida albicans Translocation from the Gastrointestinal Tract of Mice by Oral Administration of Saccharomyces boulardii
R. Berg, P. Bernasconi, D. Fowler, and M. Gautreaux
Dept of Microbiology and Immunology, Lousiana State University Medical Center, Shreveport and BIOCODEX, Montrouge, France
The Journal of Infectious Diseases, Vol. 168, No. 5 (Nov., 1993), pp. 1314-1318
http://www.jstor.org/stable/pdfplus/30113658?tokenId=KxZI8GrRjXWed9JhIfFv

“Antibiotic treatment decreased the total population levels of the indigenous bacterial flora, and predisposed mice to gastrointestinal overgrowth and subsequent dissemination by Candida albicans, C. parapsilosis, C. pseudotropicalis, C. tropicalis, and Torulopsis glabrata.”
Dissemination of yeasts after gastrointestinal inoculation in antibiotic-treated mice
1983, Vol. 21, No. 1 , Pages 27-33
http://informahealthcare.com/doi/abs/10.1080/00362178385380051

“Antibiotic treatment decreased the total population levels of the indigenous bacterial flora and predisposed hamsters to gastrointestinal overgrowth and subsequent systemic dissemination by C. albicans in 86% of the animals.”
Ecology of Candida albicans Gut Colonization: Inhibition of Candida Adhesion, Colonization, and Dissemination from the Gastrointestinal Tract by Bacterial Antagonism
INFECTION AND IMMUNITY, Sept. 1985, p. 654-663
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC261235/pdf/iai00114-0202.pdf

 

3) How Long Does It Take For Candida To Spread In The Body?

“Oral-intragastric inoculation of 5-6-day-old mice with yeast of a virulent strain of Candida albicans (CA30) resulted in systemic spread within 30 min after challenge. Histological examinations of the gastrointestinal (GI) tract have shown that the highest frequency of invasion of the mucosa by yeast cells occurred in the region of the jejunum 1-3 h after inoculation. Results of ultrastructural examinations of sites where the fungus invaded the bowel wall suggested that C. albicans yeast cells are capable of progressive extracellular digestion of the intestinal mucus barrier and microvillus layer, followed by intracellular invasion of columnar epithelial cells.”
Morphological aspects of gastrointestinal tract invasion by Candida albicans in the infant mouse.
J Med Vet Mycol. 1988 Jun;26(3):173-85.
http://www.ncbi.nlm.nih.gov/pubmed/3050009

“The pseudomycelium was found to invade animal epithelia at an average rate of 2 microns per hour, penetrating the entire epithelial thickness during 24-48 h. These data have been extrapolated to clinical pathology. On the basis of experimental data and by measuring the epithelial thickness in some human mucous membranes, the presumable periods of total epithelial penetration were calculated which may lead to vascular invasion and create the danger of dissemination. For different human mucous membranes these periods ranged from 22 to 59 h.”
Velocity of Candida albicans invasion into host tissues.
Mycoses ; 34:293-6.
http://www.ophsource.org/periodicals/ophtha/medline/record/MDLN.1803229

“Critical times in the development of infections in optimally challenged BALB/c mice were at 5-10 h (bloodstream fully cleared of fungi), 24 h (start of exponential fungal growth in kidneys) and 48 h (50% of blood cultures become positive.”
Temporal events in the intravenous challenge model for experimental Candida albicans infections in female mice.
Mycoses. 2005 May;48(3):151-61.
http://www.ncbi.nlm.nih.gov/pubmed/15842329

 

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Antibiotics Cause Candida

This article from the Departments of Microbiology and Immunology and Medicine at Albert Einstein College of Medicine is one of the best articles that I’ve read in a while as it addresses the idea and concept of pathogenicity very well. At the same time, I consider it to be an indictment on the poor state of medicine as it is currently practiced. Conversely, it vindicates the centuries old approach to healing as practiced by holistic doctors around the world – http://www.biomedcentral.com/1741-7007/10/6

Pathogen vs. Non-pathogen –

“…this takes us to an ongoing debate that dates back to the late 19th century when the [Pasteur] germ theory of disease was established. …even then it was obvious that neat classifications were problematic, for it was known that a microbe could be attenuated in the laboratory, but virulence could be restored by passage in a host, suggesting that the same microbe could exist in pathogenic and non-pathogenic states.”

Pasteur’s famous confession on is deathbed that he was wrong about his germ theory was in reference to this as he finally realized that the interaction between the host and the microbe was the determining factor for infection, not the microbe itself. Pasteur’s theory was openly opposed by scientists at the time, as they better understood the host-microbe interaction, however Pasteur held a government position allowing him to craft “official” policy (similar to what’s happening at the FDA today). The pharmaceutical industry has found it to be more profitable to market Pasteur’s germ theory, instead of his later understanding and now current science’s opinion, that the host-microbe interaction is the most important consideration.

“…properties conferring pathogenicity depend as much on the host as they do on the microorganism…it was developments in the 20th century that clearly obliterated the hope of ever drawing a clear and unequivocal line of distinction between pathogens and non-pathogens. Beginning in the 1950s the introduction of broad spectrum antimicrobial agents, immunosuppressive therapies, newer types of surgery, including organ transplantation and joint replacement, implantable devices and indwelling catheters, each of which alters host-microbe interactions, turned out to create conditions in which the host became vulnerable to microbes that were previously considered non-pathogenic. As a result, it became apparent that many microbes previously considered non-pathogenic, or rarely pathogenic, such as Staphylococcus epidermis and Candida albicans, could cause serious disease.”

I would correct the 3rd line to “Beginning in the late 1940s” as that was when antibiotics were introduced and there was a significant jump in fungal Candida albicans cases. The early 1950s saw an even more significant jump in candida albicans cases, along with a strong push in research around candida infections and resulting conditions, as antibiotic use continued to escalate. Of those therapies listed above, it was antibiotic use that created the most significant change. Here we start to see why the medical profession isn’t readily willing to look at systemic fungal Candida as a result of antibiotic use. The widespread use of antibiotics creates an even greater problem by altering the host’s ability to resist infections that are created by their use. Antibiotics empower the pathogen and weaken the host. Some antibiotics have been implicated as a direct trigger for then conversion of the normal yeast form of Candida to it’s pathogenic fungal form. Most research shows that it alters the host terrain, creating the conditions necessary to cause the yeast-fungal conversion.

“Antibiotics make people more vulnerable to microbe-mediated damage because they alter the microbiota, or the normal microbial flora, and the balanced relationships between the microbes that reside in the mucosal niches in the body and the host structures that support these communities. Surgery can have the same effect by removing or altering normal mucosal and cutaneous barriers to infection. So the effects of antibiotics and surgery enhance the pathogenicity of microbes that do not ordinarily cause damage or disease in normal microbial communities, or intact mucosal and cutaneous surfaces, by making the host more susceptible to damage or invasion.”

Is there any more that needs to be said? Thank you Albert Einstein College! You do your namesake great credit. I would like to say more, however. Antibiotic use is not only associated with these immediate effects, but they can permanently alter the make-up of the intestinal flora, and are being implicated in more serious diseases and conditions such as life-threatening colitis, diabetes, cancers, obesity, and a host of as yet other unknown diseases – http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0060280

“many microbes that cause disease are already present in the individual and the individual is thus already ‘infected’. This is exemplified by microbes such as staphylococci and Candida spp., which are actually present in most individuals, but only cause disease in some. This also applies to many other microbes, including those to which an individual is immune, either through prior infection or through vaccination, as immune individuals are recognized as being resistant to the capacity of a microbe to cause disease.”

Health is a state of constant vigilance and maintenance. When you consider that most everyone already carries a heavy body burden of tens of thousands of chemicals and heavy metals from the environment, foods, and water from past exposures, and is constantly faced with even more, it becomes clearer how maintaining health has become an challenge.

“…when a host is immune, pathogenicity is not expressed. What is important to recognize is that pathogenicity and virulence are microbial properties that can only be expressed in a susceptible host.”

Health is a state of constant vigilance and maintenance. Worth repeating.

“…pathogenicity is an outcome of host-microbe interaction and is thus inextricably linked to characteristics of the host as well as those of the microbe. Rather than distinguishing commensals from pathogens/non-pathogens, the immune system of healthy hosts actually depends on these microbes. Commensals (also called the microbiota) are acquired by infection soon after birth, after which they establish residence in mucosal niches where they replicate, and there is increasing evidence that the microbiota play a crucial role in the development of the immune system and that the immune response to the bacteria in mucosal niches helps maintain barriers to invasion on surfaces exposed to potentially harmful microorganisms. The commensal bacteria themselves do no harm, provided that the immune system and mucosal barriers remain normal and intact. The immune system provides a large variety of tools – cells and molecules – that recognize, react to and control microbial growth and invasion, often in a manner that does not result in host damage or disease, and when this happens, there is no readout. In this instance, the immune system might be thought to have distinguished a pathogen from a non-pathogen, but in fact, it simply controls microbial growth and/or invasion in a manner that does not translate into microbial pathogenicity.”

The intestinal tract is an ecosystem composed of bacteria and other micro-organisms. As a whole, it doesn’t matter if some are pathogenic and some are commensal/friendly. They all exist in a harmonious state, as long as the host is healthy. Antibiotics disrupt this harmony.

“An interesting paradox occurs in the case of two bacteria that produce toxins generally regarded as factors increasing the virulence of the microbe: staphylococci that produce a so-called leukocidin, and pneumococci that produce a toxin called pneumolysin. Because these toxins also activate the innate immune response, bacteria that do not produce them can sometimes be more pathogenic than bacteria that do. Thus, when the immune response to a microbe is insufficient, microbial factors can cause damage, and when microbial factors fail to stimulate the immune system, the microbe can disseminate and cause disease.”

The standard medical approach is to see everything as bad and the body doesn’t know what its doing, regardless of what science continues to reveal. It’s not a black and white picture, it’s everything taken as a whole. These type of paradoxes in the human body are present everywhere. As I constantly point out to people when I lecture, we know about 1% of what goes on in the human body.

“At the other end of the spectrum, when the immune response to a microbe is too exuberant, it can be the immune response itself that is responsible for the pathology. When damage occurs in this setting, it is most commonly due to detrimental inflammation and can occur whether the microbe is controlled or contained or not.”

Crohn’s, IBS, IBD, and Colitis are good examples of this. Some authors have stated that most autoimmune diseases originate with imbalances in the intestinal tract.

“There is no difference between an opportunistic pathogen and any other kind of pathogen. Both are microbes and both have the potential to cause damage/disease in a host. The definition that is often used for opportunistic pathogens is that these microbes cause disease in people with impaired immunity but not in normal individuals. However, this definition is purely operational: the same microbe – consider Candida albicans and Staphylococcus epidermidis – can cause disease in one individual but live harmlessly in others, which means that the same microbe would be called an opportunist in one individual and a commensal in another. Indeed, the identification of certain microbes as a cause of disease in certain hosts can unmask or be a sentinel for an underlying immunodeficiency.”

Another way to look at this is, “if you have an infection, it’s diagnostic of a deficient or altered immune response.” One of the most consistent effects of antibiotic use is suppression of the immune system. It doesn’t make sense to suppress the immune system further, when it is already struggling. The reason that most doctors use it and most people continue to turn to its use is that it suppresses the normal immune response that causes the common symptoms of fevers, aches, and pains. It is the suppression of the normal inflammatory response that makes people “feel” better, but at the same time alters the natural healing process of the body. This process is necessary to promote ongoing immune function and improvement of health in the body. Pharmaceutical companies through advertising have raised a generation of doctors and consumers believing that we shouldn’t have to deal with that. We need to quit interfering with the body’s normal healing process by using drugs.

“…there are only microbes and hosts and the outcomes of their interactions, which include commensalism, colonization, latency and disease. Hence, attempts to classify microbes as pathogens, non-pathogens, opportunists, commensals and so forth are misguided because they attribute a property to the microbe that is instead a function of the host, the microbe, and their interaction.”

The entire approach of antibiotic use is severely questioned with the above statement. Antibiotics destroy the balance of the host leaving us susceptible to any number of pathogens, along with newly created antibiotic-resistant superbugs. Antibiotic resistance is now classified as the 3rd leading threat to human health by the World Health Organization (WHO). Antibiotics are connected to life-threatening colitis, diabetes, obesity, and cancers. Antibiotics are part of the problem.

“Pathogenicity and virulence are emergent properties, meaning that they cannot be predicted directly from the properties of the microorganism. The environment, an individual host or population of hosts and/or an individual microbe or population of microbes can change independently, or as a function of complex interactions, including those between environment and host, host and microbe, microbe and environment, and all three. Thus, microbial pathogenicity is intrinsically unpredictable. Host and microbial characteristics are subject to predictable and unpredictable changes prompted by known, unknown, and random environmental, immunological, and other factors. Thus, as it is an outcome of host-microbe interaction whereby each entity is subject to independent and dependent changes at any point in time, pathogenicity is an emergent property.”

This paragraph brings into question the use of vaccines as effective therapies, as well as all antimicrobial drugs. I think that it also points out the reversibility of conditions and diseases by improving host-microbe interactions, not destroying them.

“…however, neither the complexity nor the variability or randomness that occurs in nature occurs or can be recapitulated in models systems. Thus, while predictions on how given (known) variables might affect the potential for a (new) microbe to be pathogenic in a given (known) population might be possible, such predictions are only possible in the context of available knowledge and paradigms. This being the case, prediction of the emergence of new microbes with the potential for pathogenicity will always be subject to severe limitations.”

This paragraph, along with the preceding one, are important because it explains why infectious agents like the H5N1 Bird flu have never materialized into the epidemic that pharmaceutical companies would have us believe in order to get us to use their vaccines. In general, it implicates all vaccines. This paragraph also points out how limited current science is, even though we’re always being lead to believe that the “authorities” are knowledgeable beyond any doubt and we should do whatever they say or recommend. Obviously not. Just say, “No!”

Excerpts from:
Q&A: What is a pathogen? A question that begs the point
Liise-anne Pirofski and Arturo Casadevall
Departments of Microbiology and Immunology and Medicine (Division of Infectious Diseases) of the Albert Einstein College of Medicine and Montefiore Medical Center, 1300 Morris Park Ave, Bronx, NY 10461, USA
BMC Biology 2012, 10:6

 

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Candida, Fruit, and Dr. McCombs Candida Plan

When I developed the McCombs Plan about 20 years ago, I was fortunate enough NOT to be familiar with the anti-candida programs or books that were around. That meant that I could discover for myself what worked and what didn’t work for my patients. Three years later, I started getting questions from my patients about why this or why not that.

The Plan as it had been developed was very successful from the beginning and is still the original Plan as it is laid out today. One of the common questions that I received was why – http://candidaplan.com/blog/432/candida-fruit-and-dr-mccombs-candida-plan/

Does Candida Know When To Attack

There is always a wealth of information coming forth that helps to provide greater clarity on how candida becomes problematic in the body. This recent study, as reported in Science Daily, provides some good information and some confusing information. I’ll add some editorial throughout the article – http://www.sciencedaily.com/releases/2012/07/120724153651.htm

The opportunistic fungal pathogen Candida albicans inconspicuously lives in our bodies until it senses that we are weak when it quickly adapts to go on the offensive. The fungus, known for causing yeast and other minor infections, also causes a sometimes-fatal infection known as candidemia in immunocompromised patients An in vivo study, published in mBio, demonstrates how C. albicanscan distinguish between a healthy and an unhealthy host and alter its physiology to attack. [There are several factors that cause the conversion of the normal yeast form of candida to its pathogenic, problematic fungal form – pH, temperature, antibiotics, bacterial cell wall components, etc., The phrase, “senses we are weak” isn’t something that I have ever seen in scientific studies, but it may be another way to state immunsuppression. Even so, I have yet to see that listed as a trigger for yeast-to-fungal conversion. Immunosuppression can play a role in the spread of candida, but some studies indicate that it isn’t a pre-requisite for this to happen. Candidemia is another term for fungal sepsis, or blood-borne fungal infection. Sepsis is one of the top 10 or 11 leading causes of death in the United States, depending on year of reference, and fungal candida causes over 50% of that].

“The ability of the fungus to sense the immune status of its host may be key to its ability to colonize harmlessly in some people but become a deadly pathogen in others,” said Jessica V. Pierce, BA, PhD student in the molecular microbiology program at the Sackler School of Graduate Biomedical Sciences at Tufts. [This is an interesting quote from an author in the study. It can be taken a couple of different ways. It might be interpreted that she is stating that it spreads throughout the body in its fungal form in the presence of an intact immune system, but doesn’t create any imbalances. That would be ignoring a lot of other research that demonstrates how the fungal form of candida creates many imbalances within the body. It has been shown to spread through the body without the immune system being compromised. A second interpretation and the one that I believe she is stating is that as a fungus, it colonizes the digestive tract harmlessly or pathogenically depending on the host immune status. That would ignore the fact that candida colonizes the intestinal tract in its yeast form. It may not be much of a differentiation, but it can be misleading as the fungal form is problematic and the yeast form isn’t.]

“Effective detection and treatment of disease in immunocompromised patients could potentially work by targeting the levels of a protein, Efg1p, that we found influenced the growth of Candida albicans inside the host,” she continued. [As stated before, there are several factors that cause the conversion of yeast-to-fungus. Efg1 has been identified previously as part of the internal mechanism that regulates the yeast-to-hyphal conversion and back again. It’s not the only part and its presence may not be a good indicator of fungal infections, as it can exist in the yeast form also.]

The researchers knew from previous research that Efg1p influences the expression of genes that regulate how harmful a fungal cell can become. Surprisingly, the investigators found that lower Efg1p levels allow the fungal cells to grow to high levels inside a host. Higher levels of the protein result in less growth. [Would the high levels be associated with it’s yeast form and the low levels with its fungal form. That can be a good reason for differentiating between yeast and fungus and not referring to both forms as though they were fungal.]

To examine how the immune status could affect the growth of C. albicans within a host, the researchers fed both healthy and immunocompromised mice equal amounts of two fungal strains containing two different levels of the Efg1p protein.

Fecal pellets from the mice were tested to determine which strain of fungi thrived. In a healthy host, the fungal cells with higher levels of the protein predominated.

In immunocompromised mice, the fungal cells with lower levels of the protein flourished. The researchers noted that lack of interactions with immune cells in the intestinal tract most likely caused the necessary environmental conditions favoring fungal cells that express lower levels of the protein, resulting in fungal overgrowth and setting the stage for systemic infection.

“By having a mixed population with some high Efg1p cells and some low Efg1p cells, the fungus can adjust its physiology to remain benign or become harmful when it colonizes hosts with varying immune statuses. These findings are important because they provide the first steps toward developing more effective methods for detecting and treating serious and stubborn infections caused by Candida albicans, such as candidemia,” said Carol A. Kumamoto, PhD, professor of molecular biology and microbiology at Tufts University School of Medicine and member of the molecular microbiology and genetics program faculties at the Sackler School of Graduate Biomedical Sciences.

The immune system and “good bacteria” within the body act to regulate the size of C. albicans fungal populations in healthy individuals. When the immune system is compromised, the fungus can spread throughout the body. Candidemia, i.e. blood-borne Candida, is the fourth most common blood infection among hospitalized patients in the United States and is found in immunocompromised patients such as babies, those with catheters, and the critically ill. [Here we see the authors state that it is the immune system and the “good bacteria” that help to regulate the candida populations. This would be a very strong statement against the use of antibiotics, as antibiotics destroy the “good bacteria” and suppress the immune system. With Sepsis being one of the top causes of death in the United States and over 50% of that being due to fungal candida, much of that can be prevented by not using antibiotics. That would eliminate sepsis as a leading cause of death and fungal candida as the 4th leading cause of hospital infections. Throughout this article I didn’t see any differentiation between the yeast and fungal forms of candida and I didn’t find it mentioned in the original abstract either. Many studies seem to be limited in the breadth of understanding of candida and the vast amount of past research. Through other studies, it has already been established that immunosuppression is not necessary for the spread of candida. For more research on this, view the Candida Facts Sheet article.  Tests can only serve as indicators, not absolute measures of function in the body. Targeting something like Efg1 doesn’t seem to be a promising advancement in the understanding or treatment of candida. If the purpose is to create another target for antifungal medications, it must be remembered that all medications contain far more harmful effects than beneficial effects. One common effect of antifungal medications  is immunosuppression.

More on Bacillus subtilis

Here’s a list of antibiotics that Bacillus subtilis is used with. It’s effects are against aerobic and non-aerobic bacteria. There is no differentiating between good and bad bacteria, as some people are lead to believe. That differentiation is something put out by the pharmaceuitical companies and MDs. The warrior model of destroying this and that as used in medicine, is antiquated and has been so many decades. The “holistic” approach used by many people is just a variation on the medical warriot model, whereby medications are substituted with something else to bring about destruction. The approach to destroying anything in the body, fails to consider that in doing so, we are destroying ourselves in the process. It’s okay if you want to support those groups, it’s just that the information is misleading.

All bacteria in a balanced system benefit the system. Create the balance and you also create the safeguards against anything that shouldn’t be there. Destroy that balance and you’ll see health start to slip away as the ecosystem starts to collapse into chaos.

As you’ll see below, Bacillus subtilis has been associated with food poisoning, disease conditions, and has been tested for biological applications as a biolgical agent.

Bacillus subtilis is the basis for many antibiotics due to its strong antibacterial function. This antibacterial function will create imbalance within the body by destroying bacteria. It also has a strong antifungal effect and is the basis for antifungal medications, but these, as we know, create other imbalances.

You’ll see below this list of B. subtilis-based antibiotics some more information on B. subtilis. It’s not a risk-free choice. Whatever your decision, make it an informed choice.


B. subtilis
does produce an extracellular toxin known as subtilisin. Although subtilisin has very low toxigenic properties (Gill, 1982), this proteinaceous compound is capable of causing allergic reactions in individuals who are repeatedly exposed to it (Edberg, 1991). Sensitization of workers to subtilisin may be a problem in fermentation facilities where exposure to high concentration of this compound may occur. Exposure limits to subtilisin are regulated by Occupational Safety and Health Administration (OSHA) (29 CFR 1900, et seq.)Biotechnology Program Under Toxic Substances Control Act (TSCA)

Bacillus subtilis Final Risk Assessment

III. HAZARD ASSESSMENT

A. Human Health Hazards

1. Colonization

B. subtilis is widely distributed throughout the environment, particularly in soil, air, and decomposing plant residue. It has shown a capacity to grow over a wide range of temperatures including that of the human body (Claus and Berkeley, 1986). However, B. subtilis does not appear to have any specialized attachment mechanisms typically found in organisms capable of colonizing humans (Edberg, 1991). Given its ubiquity in nature and the environmental conditions under which it is capable of surviving, B. subtilis could be expected to temporarily inhabit the skin and gastrointestinal tract of humans, but it is doubtful that this organism would colonize other sites in the human body (Edberg, 1991).

2. Gene Transfer

The transfer of gene sequences between strains of B. subtilis has been demonstrated when the strains were grown together in soil (Graham and Istock, 1979). In addition, Klier et al. (1983) demonstrated the ability of B. subtilis and B. thuringiensis to exchange high frequency transfer plasmids. Other studies have shown that B. subtilis has the ability to express and secrete toxins or components of the toxins that were acquired from other microorganisms through such transfers of genetic material. B. subtilis expressed subunits of toxins from Bordatella pertussis (Saris et al., 1990a, 1990b), as well as subunits of diphtheria toxin (Hemila et al., 1989) and pneumolysin A pneumococcal toxin (Taira et al., 1989). Although B. subtilis does not appear to possess indigenous virulence factor genes, it is theoretically possible that it may acquire such genes from other bacteria, particularly from closely related bacteria within the genus.

3. Toxin Production

A review of the literature by Edberg (1991) failed to reveal the production of toxins by B. subtilis. Although it has been associated with outbreaks of food poisoning (Gilbert et al., 1981 and Kramer et al., 1982 as cited by Logan, 1988), the exact nature of its involvement has not been established. B. subtilis, like other closely related species in the genus, B. licheniformis, B. pumulis, and B. megaterium, have been shown to be capable of producing lecithinase, an enzyme which disrupts membranes of mammalian cells. However, there has not been any correlation between lecithinase production and human disease in B. subtilis.

4. Measure of the Degree of Virulence

B. subtilis appears to have a low degree of virulence to humans. It does not produce significant quantities of extracellular enzymes or possess other virulence factors that would predispose it to cause infection (Edberg, 1991). There are a number of reports where B. subtilis has been isolated from human infections. Earlier literature contains references to infections caused by B. subtilis. However, as previously stated,the term B. subtilis was synonymous for any aerobic sporeforming bacilli, and quite possibly, many of these infections were associated with B. cereus. In a recent British review article, Logan (1988) cites more recent cases of B. subtilis infections in which identification of the bacterium appeared reliable. Infections include a case of endocarditis in a drug abuse patient; fatal pneumonia and bacteremia in three leukemic patients; septicemia in a patient with breast cancer; and infection of a necrotic axillary tumor in another breast cancer patient. Isolation of B. subtilis was also made from surgical wound-drainage sites, from a subphrenic abscess from a breast prosthesis, and from two ventriculo-atrial shunt infections (as cited by Logan, 1988).

Reviews of Bacillus infections from several major hospitals suggest that B. subtilis is an organism with low virulence. Idhe and Armstrong (1973) reported that Bacillus infections were encountered only twelve times over a 6-1/2 year period. Species identification of these Bacillus infections was not made. In another hospital study over a 6-yr. period, only two of the 24 cases of bacteremia caused by Bacillus (of a total of 1,038 cases) were due to B. subtilis (as cited by Edberg, 1991). Many of these patients were immunocompromised or had long term indwelling foreign bodies such as a Hickman catheter.

B. subtilis has also been implicated in several cases of food poisoning (Gilbert et al., 1981 and Kramer et al., 1982 as cited by Logan, 1988).

As previously mentioned, B. subtilis produces a number of enzymes, including subtilisin, for use in laundry detergent products. There have been a number of cases of allergic or hypersensitivity reactions, including dermatitis and respiratory distress after the use of these laundry products (Norris et al., 1981).

5. Conclusions

B. subtilis is not a human pathogen, nor is it toxigenic like some other members of the genus. The virulence characteristics of the microorganism are low. According to Edberg (1991) either the number of microorganisms challenging the individual must be very high or the immune status of the individual very low in order for infection with B. subtilis to occur.

B. Environmental Hazards

3. Hazards to Other Microorganisms

B. subtilis has been shown to produce a wide variety of antibacterial and antifungal compounds (Katz and Demain, 1977; Korzybski et al., 1978). It produces novel antibiotics such as difficidin and oxydifficidin that have activity against a wide spectrum of aerobic and anaerobic bacteria (Zimmerman et al., 1987) as well as more common antibiotics such as bacitracin, bacillin, and bacillomycin B (Parry et al., 1983). The use of B. subtilis as a biocontrol agent of fungal plant pathogens is being investigated because of the effects of antifungal compounds on Monilinia fructicola (McKeen et al., 1986), Aspergillus flavus and A. parasiticus (Kimura and Hirano, 1988), and Rhizoctonia (Loeffler et al., 1986).

Although B. subtilis produces a variety of antibiotic compounds in culture media, the importance of antibiotic production in the environment is unknown (Alexander, 1977).

B. subtilisis not a frank human pathogen, but has on several occasions been isolated from human infections. Infections attributed to B. subtilis include bacteremia, endocarditis, pneumonia, and septicemia. However, these infections were found in patients in compromised immune states. There must be immunosuppression of the host followed by inoculation in high numbers before infection with B. subtilis canoccur. There also have been several reported cases of food poisoning attributed to large numbers of B. subtilis contaminated food. B. subtilis does not produce significant quantities of extracellular enzymes or other factors that would predispose it to cause infection. Unlike several other species in the genus, B. subtilis is not consider toxigenic. B. subtilis does produce the extracellular enzyme subtilisin that has been reported to cause allergic or hypersensitivity reactions in individuals repeatedly exposed to it.

In conclusion, the use of B. subtilis in fermentation facilities for the production of enzymes or specialty chemicals has low risk. Although not completely innocuous, the industrial use of B. subtilis presents low risk of adverse effects to human health or the environment.

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