Saccharomyces boulardii |
Scientific classification |
Kingdom: |
Fungi |
Phylum: |
Ascomycota |
Subphylum: |
Saccharomycotina |
Class: |
Saccharomycetes |
Order: |
Saccharomycetales |
Family: |
Saccharomycetaceae |
Genus: |
Saccharomyces |
Species: |
S. boulardii |
Binomial name |
Saccharomyces boulardii
Henri Boulard |
Saccharomyces boulardii is a tropical strain of yeast first isolated from lychee and mangosteen fruit in 1923 by French scientist Henri Boulard. It is related to, but distinct from, Saccharomyces cerevisiae in several taxonomic, metabolic, and genetic properties.[1] S. boulardii is sometimes used as a probiotic with the purpose of introducing beneficial active cultures into the large and small intestine, as well as conferring protection against pathogenic microorganisms in the host.[2][3][4] However, in immunocompromised individuals, S. boulardii has been associated with (fungemia) or localized infection, which may be fatal.[5]
Boulard first isolated this yeast after he observed natives of Southeast Asia chewing on the skin of lychee and mangosteen in an attempt to control the symptoms of cholera. In healthy patients, S. boulardii has been shown to be non-pathogenic, non-systemic (it remains in the gastrointestinal tract rather than spreading elsewhere in the body). It grows at the unusually high temperature of 37 °C (98.6 °F).[6]
S. boulardii is often marketed as a probiotic in a lyophilized form and is therefore often referred to as S. boulardii lyo.
Contents
- 1 Medical uses
- 1.1 Acute diarrhea
- 1.2 Recurrent Clostridium difficile infection
- 1.3 Irritable bowel syndrome
- 1.4 Inflammatory bowel disease
- 1.5 Travelers' diarrhea
- 1.6 Antibiotic-associated diarrhea
- 1.7 HIV/AIDS-associated diarrhea
- 2 Mechanisms of action
- 2.1 Antitoxin effects
- 2.2 Antimicrobial effects
- 2.3 Trophic effects on enterocytes
- 2.4 Anti-inflammatory effects
- 2.5 Increased levels of disaccharidases
- 2.6 Increased immune response
- 3 References
Medical uses
There are numerous randomized, double-blind placebo-controlled studies showing the efficacy of S. boulardii in the treatment and prevention of gastrointestinal disorders.[7]
Acute diarrhea
Two studies each showed a significant reduction in the symptoms of acute gastroenteritis in children, versus placebo, by measuring frequency of bowel movements and other criteria.[8][9] Children over three months are recommended to take two doses of 250 mg a day (BID) for five days to treat acute diarrhea. Children under three months are recommended to take half a 250 mg capsule or sachet twice daily for five days.
A prospective placebo-controlled study found a significant reduction in symptoms of diarrhea in adults as well taking 250 mg of S. boulardii twice a day for five days or until symptoms are relieved.[10]
Recurrent Clostridium difficile infection
Administration of two 500 mg doses per day of S. boulardii when given with one of two antibiotics (vancomycin or metronidazole) was found to significantly reduce the rate of recurrent Clostridium difficile (pseudomembranous colitis) infection. No significant benefit was found for prevention of an initial episode of Clostridium difficile-associated disease.[11]
Irritable bowel syndrome
A prospective placebo-controlled study found patients with diarrhea-predominant irritable bowel syndrome (IBS) had a significant reduction on the number and consistency of bowel movements.[12]
Another study in 2011 did not find any change in bowel frequency.[13]
Inflammatory bowel disease
Further benefits to inflammatory bowel disease (IBD) patients have been suggested in the prevention of relapse in Crohn's disease patients currently in remission[14] and benefits to ulcerative colitis patients currently presenting with moderate symptoms.[15] The recommended dosage is three 250 mg[dubious – discuss] capsules a day (TID).[citation needed]
Travelers' diarrhea
Austrian vacationers taking S. boulardii traveling around the world were found to have significantly fewer occurrences of travelers' diarrhea than those taking placebo.[16] A meta-analysis of twelve studies from 1977 to 2005 investigating the efficacy of probiotics found them to be safe and effective for the treatment of travelers' diarrhea, having a pooled relative risk of 0.85 with respect to placebo (between 0.79 and 0.91 with 95% confidence). Three of four studies concerning S. boulardii found it to be an effective treatment. [17] The recommended dosage is one 250 mg[dubious – discuss] capsule or sachet per day (QD).[citation needed]
Antibiotic-associated diarrhea
There is evidence for its use in the prophylactic (preventative) treatment of antibiotic-associated diarrhea (AAD) in adults.[18] There is further evidence for its use to prevent antibiotic-associated diarrhea in children.[19]
HIV/AIDS-associated diarrhea
S. boulardii has been shown to significantly increase the recovery rate of stage IV AIDS patients suffering from diarrhea versus placebo. On average, patients receiving S. boulardii gained weight while the placebo group lost weight over the 18-month trial.[20] There were no reported adverse reaction observed in these immunocompromised patients.
Mechanisms of action
Antitoxin effects
S. boulardii secretes a 54 kDa protease, in vivo. This protease has been shown to both degrade toxins A and B, secreted from Clostridium difficile, and inhibit their binding to receptors along the brush border. This leads to a reduction in the enterotoxinic and cytotoxic effects of C. difficile infection.[21]
Antimicrobial effects
Escherichia coli and Salmonella typhimurium, two pathogenic bacteria often associated with acute infectious diarrhea, were shown to strongly adhere to mannose on the surface of S. boulardii via lectin receptors (adhesins). Once the invading microbe is bound to S. boulardii, it is prevented from attaching to the brush border; it is then eliminated from the body during the next bowel movement.[22]
Trophic effects on enterocytes
The hypersecretion of water and electrolytes (including chloride ions), caused by cholera toxin during a Vibrio cholerae infection, can be reduced significantly with the introduction of S. boulardii. A 120 kDa protease secreted by S. boulardii has been observed to have an effect on enterocytes lining the large and small intestinal tract–inhibiting the stimulation of adenylate cyclase, which led to the reduction in enterocytic cyclic adenosine monophosphate (cAMP) production and chloride secretion.[23]
During an E. coli infection, myosin light chain (MLC) is phosphorylated leading to the degradation of the tight junctions between intestinal mucosa enterocytes. S. boulardii has been shown to prevent this phosphorylation, leading to a reduction in mucosal permeability and thus a decrease in the translocation of the pathogenic bacteria.[24]
Polyamines (spermidine and spermine) have been observed to be released from S. boulardii in the rat ileum. Polyamines have been theorized to stimulate the maturation and turnover of small intestine enterocytes.[25]
Anti-inflammatory effects
Interleukin 8 (IL-8) is a proinflammatory cytokine secreted during an E. coli infection in the gut. S. boulardii has been shown to decrease the secretion of IL-8 during an E. coli infection; S. boulardii could have a protective effect in inflammatory bowel disease.[24] Saccharomyces boulardii may exhibit part of its anti-inflammatory potential through modulation of dendritic cell phenotype, function and migration by inhibition of their immune response to bacterial microbial surrogate antigens such as lipopolysaccharide (LPS). A recent study showed that culture of primary human myeloid dendritic cells CD1c+CD11c+CD123- DC (mDC) in the presence of Saccharomyces boulardii culture supernatant (active component molecular weight < 3kDa as evaluated by membrane partition chromatography) significantly reduced expression of the co-stimulatory molecules CD40 and CD80 and the dendritic cell mobilization marker CC-chemokine receptor CCR7 (CD197) induced by the prototypical microbial antigen lipopolysaccharide (LPS). Moreover, secretion key pro-inflammatory cytokines like TNF-α and IL-6 were notably reduced, while the secretion of anti-inflammatory IL-10 did increase. Finally Saccharomyces boulardii supernatant inhibited the proliferation of naïve T-cells in a mixed lymphocyte reaction (MLR) with mDC.[26]
Increased levels of disaccharidases
The trophic effect on enterocytes has been shown to increase levels of disaccharidases such as lactase, sucrase, maltase, glucoamylase, and N-aminopeptidase in the intestinal mucosa of humans and rats. This can lead to the increased breakdown of disaccharides into monosaccharides that can then be absorbed into the bloodstream via enterocytes.[27][28] This can help in the treatment of diarrhoea, as the level of enzymatic activity has diminished and carbohydrate cannot be degraded and absorbed.
Increased immune response
S. boulardii induces the secretion of Immunoglobulin A (IgA) in the small intestine of the rat.[29]
References
- ^ Malgoire JY, Bertout S, Renaud F, Bastide JM, Mallié M (2005). "Typing of Saccharomyces cerevisiae clinical strains by using microsatellite sequence polymorphism". J. Clin. Microbiol. 43 (3): 1133–7. doi:10.1128/JCM.43.3.1133-1137.2005. PMC 1081240. PMID 15750073.
- ^ Rajkowska, Katarzyna et al. (April 2012). "Probiotic Activity of Saccharomyces cerevisiae var. boulardii Against Human Pathogens" (PDF). Food Technology and Biotechnology 50: 230–236. Retrieved 18 January 2014.
- ^ Toma, Malda Maija et al. (June 2005). "Effect of Probiotic Yeast on Genotoxicity" (PDF). Food Technology and Biotechnology 43: 301–305. Retrieved 18 January 2014.
- ^ Soccol, Carlos Ricardo et al. (June 2010). "The Potential of Probiotics: A Review" (PDF). Food Technology and Biotechnology 48: 413–434. Retrieved 18 January 2014.
- ^ {{Santino I, Alari A, Bono S, Teti E, Marangi M, Bernardini A, Magrini L, Di Somma S, Teggi A. Saccharomyces cerevisiae fungemia, a possible consequence of the treatment of Clostridium difficile colitis with a probioticum. Int J Immunopathol Pharmacol. 2014 Jan-Mar;27(1):143-6. PubMed PMID 24674691.}}
- ^ McFarland L, Bernasconi P (1993). "Saccharomyces boulardii: a review of an innovative biotherapeutic agent". Microb Ecol Health Dis 6 (4): 157–71. doi:10.3109/08910609309141323.
- ^ Vandenplas Y (July 1999). "Bacteria and yeasts in the treatment of acute and chronic infectious diarrhea. Part II: Yeasts". Clin. Microbiol. Infect. 5 (7): 389–395. doi:10.1111/j.1469-0691.1999.tb00162.x. PMID 11853563.
- ^ Centina-Sauri G, Sierra Basto G (1994). "Therapeutic evaluation of Saccharomyces boulardii in children with acute diarrhea". Ann Pediatr 41: 397–400.
- ^ Kurugöl Z, Koturoğlu G (2005). "Effects of Saccharomyces boulardii in children with acute diarrhoea". Acta Paediatr. 94 (1): 44–7. doi:10.1080/08035250410022521. PMID 15858959.
- ^ Höchter W, Chase D, Hagenhoff G (1990). "Saccharomyces boulardii in acute adult diarrhoea. Efficacy and tolerance of treatment". Münch Med Wochenschr 132: 188–92.
- ^ McFarland L, Surawicz C, Greenberg R (1994). "A randomised placebo-controlled trial of Saccharomyces boulardii in combination with standard antibiotics for Clostridium difficile disease". J Am Med Assoc 271 (24): 1913–8. doi:10.1001/jama.271.24.1913. PMID 8201735.
- ^ Maupas J, Champemont P, Delforge M (1983). "Treatment of irritable bowel syndrome with Saccharomyces boulardii: a double blind, placebo controlled study". Medicine Chirurgie Digestives 12 (1): 77–9.
- ^ [url=http://www.ncbi.nlm.nih.gov/pubmed/21301358]
- ^ Guslandi M, Mezzi G, Sorghi M, Testoni PA (2000). "Saccharomyces boulardii in maintenance treatment of Crohn's disease". Dig. Dis. Sci. 45 (7): 1462–4. doi:10.1023/A:1005588911207. PMID 10961730.
- ^ Guslandi M, Giollo P, Testoni PA (2003). "A pilot trial of Saccharomyces boulardii in ulcerative colitis". European Journal of Gastroenterology & Hepatology 15 (6): 697–8. doi:10.1097/01.meg.0000059138.68845.06. PMID 12840682.
- ^ Kollaritsch H, Kemsner P, Wiedermann G, Scheiner O (1989). "Prevention of traveler's diarrhoea. Comparison of different non-antibiotic preparations". Travel Med Int: 9–17.
- ^ McFarland LV (2007). "Meta-analysis of probiotics for the prevention of traveler's diarrhea". Travel Med Infect Dis 5 (2): 97–105. doi:10.1016/j.tmaid.2005.10.003. PMID 17298915.
- ^ McFarland LV, Surawicz CM, Greenberg RN et al. (1995). "Prevention of beta-lactam-associated diarrhea by Saccharomyces boulardii compared with placebo". Am. J. Gastroenterol. 90 (3): 439–48. PMID 7872284.
- ^ Kotowska M, Albrecht P, Szajewska H (2005). "Saccharomyces boulardii in the prevention of antibiotic-associated diarrhoea in children: a randomized double-blind placebo-controlled trial". Aliment. Pharmacol. Ther. 21 (5): 583–90. doi:10.1111/j.1365-2036.2005.02356.x. PMID 15740542.
- ^ Saint-Marc T, Blehaut H, Musial C, Touraine J (1995). "AIDS related diarrhea: a double-blind trial of Saccharomyces boulardii". Sem Hôsp Paris 71: 735–41.
- ^ Castagliuolo I, Riegler MF, Valenick L, LaMont JT, Pothoulakis C (1999). "Saccharomyces boulardii protease inhibits the effects of Clostridium difficile toxins A and B in human colonic mucosa". Infect. Immun. 67 (1): 302–7. PMC 96311. PMID 9864230.
- ^ Gedek BR (1999). "Adherence of Escherichia coli serogroup O 157 and the Salmonella typhimurium mutant DT 104 to the surface of Saccharomyces boulardii". Mycoses 42 (4): 261–4. doi:10.1046/j.1439-0507.1999.00449.x. PMID 10424093.
- ^ Czerucka D, Rampal P (1999). "Effect of Saccharomyces boulardii on cAMP- and Ca2+ -dependent Cl- secretion in T84 cells". Dig. Dis. Sci. 44 (11): 2359–68. doi:10.1023/A:1026689628136. PMID 10573387.
- ^ a b Dahan S, Dalmasso G, Imbert V, Peyron JF, Rampal P, Czerucka D (2003). "Saccharomyces boulardii interferes with enterohemorrhagic Escherichia coli-induced signaling pathways in T84 cells". Infect. Immun. 71 (2): 766–73. doi:10.1128/IAI.71.2.766-773.2003. PMC 145355. PMID 12540556.
- ^ Buts JP, De Keyser N, De Raedemaeker L (1994). "Saccharomyces boulardii enhances rat intestinal enzyme expression by endoluminal release of polyamines". Pediatr. Res. 36 (4): 522–7. doi:10.1203/00006450-199410000-00019. PMID 7816529.
- ^ Thomas S, Przesdzing I, Metzke D, Schmitz J, Radbruch A, Baumgart DC (2009). "Saccharomyces boulardii inhibits lipopolysaccharide-induced activation of human dendritic cells and T cell proliferation". Clin Exp Immunol. 155 (1): 78–87. doi:10.1111/j.1365-2249.2009.03878.x. PMC 2673744. PMID 19161443.
- ^ Buts JP, Bernasconi P, Van Craynest MP, Maldague P, De Meyer R (1986). "Response of human and rat small intestinal mucosa to oral administration of Saccharomyces boulardii". Pediatr. Res. 20 (2): 192–6. doi:10.1203/00006450-198602000-00020. PMID 3080730.
- ^ Zaouche A, Loukil C, De Lagausie P et al. (2000). "Effects of oral Saccharomyces boulardii on bacterial overgrowth, translocation, and intestinal adaptation after small-bowel resection in rats". Scand. J. Gastroenterol. 35 (2): 160–5. doi:10.1080/003655200750024326. PMID 10720113.
- ^ Buts JP, Bernasconi P, Vaerman JP, Dive C (1990). "Stimulation of secretory IgA and secretory component of immunoglobulins in small intestine of rats treated with Saccharomyces boulardii". Dig. Dis. Sci. 35 (2): 251–6. doi:10.1007/BF01536771. PMID 2302983.
Fungal infection and mesomycetozoea (B35–B49, 110–118)
|
|
Superficial and
cutaneous
(dermatomycosis):
Tinea = skin;
Piedra (exothrix/
endothrix) = hair |
Ascomycota |
Dermatophyte
(Dermatophytosis) |
By location |
- Tinea barbae/tinea capitis
- Tinea corporis
- Tinea cruris
- Tinea manuum
- Tinea pedis (athlete's foot)
- Tinea unguium/onychomycosis
- White superficial onychomycosis
- Distal subungual onychomycosis
- Proximal subungual onychomycosis
- Tinea corporis gladiatorum
- Tinea faciei
- Tinea imbricata
- Tinea incognito
- Favus
|
|
By organism |
- Epidermophyton floccosum
- Microsporum canis
- Microsporum audouinii
- Trichophyton interdigitale/mentagrophytes
- Trichophyton tonsurans
- Trichophyton schoenleini
- Trichophyton rubrum
|
|
|
Other |
- Hortaea werneckii
- Piedraia hortae
|
|
|
Basidiomycota |
- Malassezia furfur
- Tinea versicolor
- Pityrosporum folliculitis
- Trichosporon
|
|
|
Subcutaneous,
systemic,
and opportunistic |
Ascomycota |
Dimorphic
(yeast+mold) |
Onygenales |
- Coccidioides immitis/Coccidioides posadasii
- Coccidioidomycosis
- Disseminated coccidioidomycosis
- Primary cutaneous coccidioidomycosis. Primary pulmonary coccidioidomycosis
- Histoplasma capsulatum
- Histoplasmosis
- Primary cutaneous histoplasmosis
- Primary pulmonary histoplasmosis
- Progressive disseminated histoplasmosis
- Histoplasma duboisii
- Lacazia loboi
- Paracoccidioides brasiliensis
|
|
Other |
- Blastomyces dermatitidis
- Blastomycosis
- North American blastomycosis
- South American blastomycosis
- Sporothrix schenckii
- Penicillium marneffei
|
|
|
Yeast-like |
- Candida albicans
- Candidiasis
- Oral
- Esophageal
- Vulvovaginal
- Chronic mucocutaneous
- Antibiotic candidiasis
- Candidal intertrigo
- Candidal onychomycosis
- Candidal paronychia
- Candidid
- Diaper candidiasis
- Congenital cutaneous candidiasis
- Perianal candidiasis
- Systemic candidiasis
- Erosio interdigitalis blastomycetica
- C. glabrata
- C. tropicalis
- C. lusitaniae
- Pneumocystis jirovecii
- Pneumocystosis
- Pneumocystis pneumonia
|
|
Mold-like |
- Aspergillus
- Aspergillosis
- Aspergilloma
- Allergic bronchopulmonary aspergillosis
- Primary cutaneous aspergillosis
- Exophiala jeanselmei
- Fonsecaea pedrosoi/Fonsecaea compacta/Phialophora verrucosa
- Geotrichum candidum
- Pseudallescheria boydii
|
|
|
Basidiomycota |
- Cryptococcus neoformans
- Cryptococcosis
- Trichosporon spp
- Trichosporonosis
|
|
Zygomycota
(Zygomycosis) |
Mucorales
(Mucormycosis) |
- Rhizopus oryzae
- Mucor indicus
- Lichtheimia corymbifera
- Syncephalastrum racemosum
- Apophysomyces variabilis
|
|
Entomophthorales
(Entomophthoramycosis) |
- Basidiobolus ranarum
- Conidiobolus coronatus/Conidiobolus incongruus
|
|
|
Microsporidia
(Microsporidiosis) |
- Enterocytozoon bieneusi/Encephalitozoon intestinalis
|
|
|
Mesomycetozoea |
|
|
Ungrouped |
- Alternariosis
- Fungal folliculitis
- Fusarium
- Granuloma gluteale infantum
- Hyalohyphomycosis
- Otomycosis
- Phaeohyphomycosis
|
|
Index of fungal disease
|
|
Description |
|
|
Disease |
|
|
Treatment |
|
|
|