Agatha M. Thrash, M.D.
Fungal or mycotic infections are commonly caused by opportunistic yeast-like fungi. These infections most often afflict persons with a depressed immunological system, including those with diabetes, leukemia and other cancers, kidney disease, and long term users of steroids and antibiotics. Patients undergoing anti-cancer chemotherapy and post organ transplants are most susceptible to opportunistic fungi.1
Most of the fifty or more forms of fungi that can cause human disease are in yeast form. The most common of these is Candida albicans which can cause systemic candidiasis, C. endocarditis, C. meningitis and a host of other infections. Candidiasis, also known as moniliasis or thrush can result in both superficial disease in healthy persons and widespread systemic disease in patients with compromised resistance. Candida is also a normal inhabitant of the female genital tract and a major cause of vaginitis.
Candida endocarditis is related to intravascular trauma and resembles bacterial disease with fever, heart murmurs, and anemia. The basic lesion is a vegetation composed of fibrin masses and mesh, and usually develops in the valve. Heart valves that are deformed or damaged by previous disease are more predisposed to infection as are trauma sites in the mural endocardium.2
Yeast-like fungi are often resistant to antibiotics and difficult to control in those with depressed immune systems. Likewise, healthy individuals often experience superficial and unpleasant fungus infections like mouth thrush and vaginitis. Besides the many types of Candida, there are a few other common opportunistic fungi. Aspergillus, for example, can grow as a “fungus ball” in the lung and can become invasive—attacking the brain, kidney or heart valves. Another is Cryptococcus which causes a type of meningitis and encephalitis.
At this time the most common treatment of fungal infections include the use of fungicidal drugs like Amphotericin B, Flucytosine, and Nystatin. Unfortunately, the adverse reactions to the drugs used are often serious and can cause kidney damage, fever, nausea, rashes, and an array of systemic reactions. Many of these drugs are also ineffectual to accompanying bacterial infections.
For these reasons there has been a growing interest in the use of garlic as a natural fungistat. Garlic’s active component allicin (allyl-allylthiosulfinate)3 is both an antifungal and antibacterial agent with little or no side effects. Allicin inhibits the organism’s metabolic enzymes, especially those with reactive -SH groups, and inactivates proteins by oxidation of essential thiols.4 Allicin has been shown to interfere with the reproduction and growth of fungus without affecting the host organism.5
Much of the favorable research on garlic concerns its ability to combat opportunistic and infectious fungus. Atkins and Moore6 tested garlic against C. albicans isolates from active vaginal yeast infections and 20 other yeast-like fungi. When tested in vitro at body temp. (37°C) all Candida species had a Minimum Inhibitory Concentration of 1:512 and an MLC of 1:128. They concluded that garlic was markedly inhibitory to all isolates of yeast-like fungi tested, including species of Cryptococcus, Rhodatorula, Torulopsis and Trichosporum. They also sited Kabelik’s study wherein garlic extract was more effective against pathogenic yeasts than was Nystatin.7
Other research, by Tansey & Appleton, used garlic to inhibit the growth of 20 pathogenic fungi in human and animal cultures.8 Growth in the garlic treated cultures was markedly suppressed compared to controls over a 21 day period. When allicin was isolated from the garlic and tested against Candida, Cryptococcus, and Aspergillus, it showed a large area of inhibition at relatively low concentrations.9 It was shown that allicin inhibits both germination of spores and growth of hyphae, with MIC remaining constant after 3 days. The MIC for Candida and Cryptococcus was 3.13–6.25 ug/ml, and 12.5 ug/ml for Aspergillus. Although allicin is regarded as a fungistat, at a concentration approximately 4 times the MIC, allicin was fungicidal. It was also observed that allicin was comparatively stable in the presence of blood and gastric juices, and most effective in an acidic environment.
An extensive study by Barone suggests that allicin is garlic’s major anticandidal component, and identifies its mode of action. Barone showed garlic extract effective against 39 of 41 isolates of fungi and found that at concentrations which are inhibitory to C. albicans, yet garlic extract was not toxic to mammalian cells. He concluded that the action of allicin may be twofold and provide a model system for chemotherapy of C. albicans infections. Allicin first attacks the essential protein sulfhydryl groups, resulting in stasis or cell death. Secondly, it enhances the yeast-mycilial conversion (C. albicans is dimorphic) resulting in a decrease in virulence.
When comparing garlic to commonly prescribed drugs, Barone concluded, “Observation suggests that natural resistance of clinical strains of C. albicans to the active component of garlic does not occur at high frequency, if at all.” This aspect could be a significant consideration; for nearly 50% of C. albicans strains tested were resistant at prescribed human tolerance levels to the antifungal agent 5-fluorocytosine.
In a clinical study done in China, 16 cases of cryptococcal meningitis treated with garlic were observed.10 Treatment was successful in 11 (68.75%) of the patients treated with garlic alone. It was concluded that garlic was especially effective in early cases, and in most cases superior to Amphotericin B against cryptococcal meningitis.
Because of its non-toxicity and natural bacteriostatic properties, garlic serves as an ideal replacement of drugs used to fight fungal infections. Also, since garlic is most effective on the preventative level, it can be recommended for daily use. The benefits of garlic supplementation can be shared by the chronically ill and healthy persons alike.
The Physician’s Drug Manual, 1981, Doubleday & Company, Inc. Garden City, N.Y.
The Merck Manual, Thirteenth Edition, 1977, Merck Sharp & Dohme Research Labs., Rahway, N. J.
Cavallito, C.J.; Buck, J.S.; Suter, C.M., Journal of the American Chemical Society, 1944, 66, 1954.
Barone, Frank E.; Tansey, Michael, R., Mycologia, Vol. 69, 1977, pp. 793-825.
Hanna, Michelle, M; Allicin, Effect on Bacterial, Fungal & Tumor Cell Growth, U.C. Davis, 1981.
Moore, Gary S.; Atkins, Robin D., Mycologia, Vol. 69, 1977, pp. 341-348.
Kabelik, J. 1970, Parmazie 25: 266 in Chemi Abst. 73:117, 1971.
Appleton, Judith A.; Tansey, Michael R., Mycologia, Vol. 67, 1975 pp. 882-885.
Yarnada, Y.; Deizo, A.; Antimicrobial Agents & Chemotherapy, Apr. 1977, pp. 743-749.
Dept. of Neurology, Hunan Medical College, Changsha. Chinese Medical Journal, 93(2): 123-126, 1980.
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