Fungal Arthritis

I’ve just added this article to the Candida Library and thought you should know about it since over 40 million Americans are affected by some form of arthritis.

Fungal arthritis

Marta L Cuellar, Luis H Silveira, Luis R Espinoza

Annals of the Rheumatic Diseases 1992

Why This Article Matters

“There is never a lack of research or information available about the pervasiveness of fungal infections in our society today. There is however, a lack of awareness that this is an ongoing problem in society at all ages, as this research article demonstrates. Fungal infections can cause arthritis of any joint in the body. When treated properly, fungal arthritis cases improve and disappear. The use of antibiotics continues to be the primary cause of this problem, followed by, or in conjunction with steroid use. The best approach is to avoid these problems by avoiding use of these medications whenever possible.” – Dr. Jeff McCombs, DC

Excerpted from the research article:

Although healthy subjects may host fungal diseases, various predisposing factors that depress the immune system have been implicated in most patients developing fungal infections or fungal arthritis, or both. Alcoholism, cirrhosis, diabetes, tuberculosis, cancer, prematurity, treatment with corticosteroids, cytotoxic drugs, prolonged use of intravenous antibiotics, intravenous drug abuse, granulocytopenia, and marrow hyperplasia are among the predisposing factors. Neonates are the first group of patients in whom haematogenously originated Candida arthritis can occur. The illness is a hospital acquired disease of sick children with underlying diseases such as the respiratory distress syndrome, and gastrointestinal defects. C albicans, which is responsible for more than 80% of the reported cases, and C tropicalis are the species responsible for this disease. Arthritis is usually present with accompanying metaphysial osteomyelitis. Bone infection might originate from the infected synovium or via the metaphysical vessels. Polyarthritis occurs in most patients and the knee is the joint most often affected. Arthritis originated by haematogenous dissemination beyond the neonatal period is usually a complication of disseminated candidiasis in patients with serious underlying disorders or intravenous drug abusers. C albicans is again the causative organism in about 80% of cases, and C tropicalis is responsible for most of the remaining cases. Two distinct clinical presentations can be observed: (a) acute onset of constitutional and synovial symptoms (about two thirds of patients), with the aetiological diagnosis established within the first week, and (b) indolent presentation, with mild systemic and arthritic symptoms, and delay in the diagnosis for months or years.

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75+ Candida Studies: The Candida Fact Sheet

Introduction

Many of the doctors who have consulted with me have asked for more information and references to better educate themselves, their patients and fellow doctors. To assist them, I gathered together a few of the references that we are including in our online Candida Library. In this article, you’ll find over 75 research references that provide information on how Candida goes from a harmless normal constituent of the gastrointestinal tract to a pathogenic systemic problem that can affect anyone and everyone.  I’m providing this information here for you to become better educated about Candida, like the many doctors with whom I’ve consulted. Pass it along to your family, friends, and doctors, if you feel that it can also assist them in learning and understanding more about a problem that affects virtually everyone. Please click here to download this Candida Fact Sheet as a PDF so you can email or print it out.

Candida Facts

The human digestive tract is said to contain some 100 trillion cells compared to about only 10 trillion human cells in the body. This particular arrangement has led to man being classified as a “super-organism,” whose health is directly related to the function of the thousands of species of micro-organisms that make up the 100 trillion cells in the intestinal tract. For years, research suggested that there were 400-500 species that made up this microbial population. Recent advances in research have now put that number at anywhere from 3,300 to 5,700 or more, ⁽⁹⁾ to upwards of 30,000 species. The intestinal tract houses what has been called “the densest ecosystem on the planet,” and is approximately 25-28 ft long. The surface area of the intestinal tract measures approximately 200 square meters, roughly the size of a tennis court.

Modern medicine states that systemic Candida exists only in immunocompromised individuals, as a result of AIDS, immunosuppressive therapy, such as in organ transplants, or chemotherapy. Science states otherwise, and extends that list to include: diabetes, premature infants, surgical patients; ^(7)(10)(66) hematological malignancies; ⁽⁸⁾ hospitalized patients, especially in Intensive Care Units, or having major injuries;⁽¹⁰⁾ burn victims; ⁽⁵⁴⁾ nutritional deficiencies; ⁽²²⁾ as well as aging. ^{(22)(35)(36)(37)} alcoholism, cirrhosis, tuberculosis, cancer, corticosteroids, marrow hyperplasia;

Researchers continuously broaden the scope of those being affected. Valdimarsson et al. state that there are no common immunological denominators. ⁽¹⁾ may appear following even a slight modification of the host. ⁽⁵⁵⁾ Berg et al. on behalf of Biocodex Pharmaceuticals states that Candida spreads in immunocompetent individuals. ⁽⁶⁸⁾ Senet states that the pathogenic behavior of Candida

The widespread use of antibiotics, which induce neutropenia, an abnormally low number of neutrophils (white blood cells), and immune system suppression is commonly attributed by science to be the most consistent cause of systemic Candida.^{(3)(9)(12)(13)(14)(16)(17)(18)(19)(20)(21)(22)(55)(56)(57)(64)(67)(68)(69)(76)(77)} Corticosteroids suppress immune system function. ^(11)(17)(68) Intestinal homeostasis is critical for human health. ^{(6)(7)(55)(57)(68)(71)}

Candida has been shown to be capable of causing systemic immuno-suppression via its cell wall proteins, ⁽²⁾ TLR2-mediated IL-10 release, ⁽³⁰⁾ protease cleaving of leukocyte integrin CD11/CD18, ^{(25)(31)(34)(62)(63)} and intracellular components. ⁽⁷²⁾

Candida can manipulate inflammatory responses as needed ^(31)(32) and inflammatory responses can have systemic effects. ^{(44)(45)(46)(47)}

Candida has the ability to destroy immune cells, ^{(3)(23)(24)(26)(49)} hide from the immune system, ^(4)(19) adapt to the inner environment of immune cells, ^(5)(38)(39) resist and suppress ROI and NO production of immune cells, ^{(15)(16)(27)(43)} destroy binding sites and receptors of immune cells, ^{(25)(31)(33)(34)} manipulate immune responses, ^{(28)(53)(70)(74)} and affect immune cell structure. ^(42)(73)

Stress can cause accumulation of iron at the luminal surface of intestinal cells ⁽⁷⁵⁾ and iron overload leads to impaired neutrophil function. ⁽¹⁴⁾ Stress can lead to immunosuppression facilitating the spread of Candida. ⁽⁵⁵⁾ Sanchez et al. discuss the affect of starches vs. sugars on the immune system response to Candida. ⁽²⁹⁾

Macrophages, which are widely distributed immune system cells that play an indispensable role in homeostasis and defense, and are cells that function as a first line of defense against invading microorganisms, are historically ineffective against Candida albicans. ^(40)(41)

While evidence suggests that intestinal Dendritic Cells are critical for regulation of immunity in the gut, ⁽⁵⁰⁾ Dendritic Cells are poor in both intracellular killing and damaging of C. albicans hyphae, ⁽⁴⁸⁾ and only kill as effectively as macrophages. ⁽⁵¹⁾ Ingestion of hyphae by Dendritic Cells inhibits Th1 immune responses. ⁽⁵²⁾

Candida Albicans’ Secreted Aspartyl Proteases (SAPs) are a highly specific family of enzymes that assists in its ability to cause disease in the body. SAPs are believed to play a role in Candida’s ability to induce inflammation, invade and breakdown tissue barriers, digest proteins for nutrients, destroy and evade immune defenses, and spread throughout the body. ^{(25)(33)(34)(58)(59)(60)(61)(62)(63)(65)} Research has shown that the destructive effects of protease enzymes are associated with diabetes, hypertension, and immune system suppression. ^{(25)(31)(34)(62)}

Additional enzymes secreted by Candida albicans include phospholipases, lipases, glucoamylases, phosphatases, and β-N-acetylglucosaminidase.

Conclusion

As impressive as I find the above research to be, it is just a small representation of the research on Candida albicans and its effects in humans. With over 26,000 studies on Candida albicans since the introduction of antibiotics in the late 1940s, there is much more to be analyzed and reported. What is readily apparent from this data is the fact that systemic fungal Candida infections are a common occurrence in most individuals as a result of antibiotic use and other contributing factors.

– Dr. Jeffrey McCombs, DC

References

1. Immunological phenomena associated with chronic mucocutaneous candidiasis have recently been intensively studied by many workers (reviewed by Kirkpatrick, Rich & Bennett, 1971). The results have shown that there is no common immunological denominator in this disease. The most common finding, however, is defective cellular immunity, which may or may not be accompanied by failure of in vitro lymphocyte transformation.

Immunological Feautures in a Case of Chronic Granulomatous Candidiasis and its Treatment with Transfer Factor

H. VALDIMARSSON, C. B. S. WOOD, J. R. HOBBS AND P. J. L. HOLT

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1553624/pdf/clinexpimmunol00295-0003.pdf

2. The ability of Candida albicans to establish an infection involves multiple components of this fungal pathogen, but its ability to persist in host tissue may involve primarily the immunosuppressive property of a major cell wall glycoprotein, mannan. Mannan and oligosaccharide fragments of mannan are potent inhibitors of cell-mediated immunity and appear to reproduce the immune deficit of patients with the mucocutaneous form of candidiasis. However, neither the exact structures of these inhibitory species nor their mechanisms of action have yet been clearly defined. Different investigators have proposed that mannan or mannan catabolites act upon monocytes or suppressor T lymphocytes, but research from unrelated areas has provided still other possibilities for consideration. These include interference with cytokine activities, lymphocyte-monocyte interactions, and leukocyte homing. To stimulate further research of the immunosuppressive property of C. albicans mannan, we have reviewed (i) the relationship of mannan to other antigens and virulence factors of the fungus; (ii) the chemistry of mannan, together with methods for preparation of mannan and mannan fragments; and (iii) the historical evidence for immunosuppression by Candida mannan and the mechanisms currently proposed for this property; and (iv) we have speculated upon still other mechanisms by which mannan might influence host defense functions. It is possible that understanding the immunosuppressive effects of mannan will provide clues to novel therapies for candidiasis that will enhance the efficacy of both available and future anti-Candida agents. Immunosuppressive properties observed for isolated Candida mannan and its catabolites in vivo and in vitro provide additional evidence that fungal mannan is responsible for patient immune dysfunction.

Candida mannan: chemistry, suppression of cell-mediated immunity, and possible mechanisms of action.

R D Nelson, N Shibata, R P Podzorski, and M J Herron

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC358175/

 

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