I wanted to let any blog followers out there know that I’m now doing short videos on each of my 10 Candida Myths. Visit my YouTube Channel (embedded below) to watch them.
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
Future microbiology. 01/05/2007; 2:141-51.
“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
“…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
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
“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
“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
“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
“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
“…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
“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
“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
“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
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.
“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.
“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.
CATCH UP on more recent posts at our new blog – Candida Plan Blog
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.