Download Saccharomyces boulardiiIs Not Saccharomyces cerevisiae

Correspondence
200
viremia observed in our study [1]. Taken together, the results of
these studies indicate that parvovirus B19 viremia is uncommon
in patients with HIV infection, regardless of the seroprevalence of
B19 in the patient population.
Gary Dubin, Esther Chernak, and Harvey M. Friedman
Division ofInfectious Diseases, Department of Medicine, Hospital of the
University ofPennsylvania, Philadelphia. Pennsylvania
Saccharomyces boulardii Is Not Saccharomyces cerevisiae
SIR- A recent letter by Chia et al. [1] described four patients with
recurrent ClostridiumdifJicile diarrhea who were treated with onequarter ofa l-inch cake of Fleischmann's baker's yeast (Saccharomyces cerevisiae) in addition to either metronidazole or vancomycin. The patients became "relatively asymptomatic," and the authors concluded "that baker's yeast may be an inexpensive and
safe adjunctive therapy ... for patients with relapses of C. difJicile
colitis." There are several problems with this conclusion. The
authors hold the erroneous belief that "Saccharomyces cerevisiae
. . . is synonymous with S. [Saccharomyces] boulardii" and cite
several studies demonstrating the effectiveness of S. boulardii for
the treatment of C. difJicile colitis/diarrhea.
However, S. boulardii is a completely different species of yeast
from baker's, brewer's, or wine yeast, and thus the results of S.
boulardii therapy in the cited clinical studies are not applicable to
S. cerevisiae therapy or to the four case descriptions. S. boulardii
has been shown to be a separate species of Saccharomyces on the
basis of several taxonomic, metabolic, and molecular parameters.
S. boulardii is a wild Saccharomyces strain that does not produce
ascospores or use galactose as a carbon source (as do wild
S. cerevisiae strains). This strain is also given a separate designation by the American Type Culture Collection (ATTC #74012).
S. boulardii has different oxidative utilization and fermentation
patterns that can distinguish it from S. cerevisiae (Professor JeanMarie Bastide, personal communication).
Recent evidence indicates that the mitochondrial DNA fingerprint pattern of S. boulardii is different from those of other Saccharomyces species (P. Nguyen Van, personal communication).
Two other molecular techniques have produced different patterns
for S. boulardii and S. cerevisiae: Southern blots with poly (GT)5o
probes (Professor Y. Barra, personal communication) and SDSPAGE electrophoresis of genomic DNA restriction fragments (P.
Nguyen Van, personal communication). Further investigations
found that S. boulardii does not possess similar ADNmt speciesspecific restriction fragments that are characteristic of S. cerevisiae
Reprints or correspondence: Dr. Lynne V. McFarland, Biocodex, Inc., 1910
Fairview Avenue E., Suite 208, Seattle, Washington 98102.
Clinical Infectious Diseases 1996; 22:200-1
© 1996 by The University of Chicago. All rights reserved.
1058-4838/96/2201-0058$02.00
em
1996; 22 (January)
References
1. Chernak E, Dubin G, Henry D, et a1. Infection due to parvovirus B19 in
patients infected with human immunodeficiency virus. Clin Infect Dis
1995;20:170-3.
2. Schwarz TF, Hottentrager B, Roggendorf M. Prevalence of antibodies to
parvovirus B19 in selected groups of patients and healthy individuals.
Int J Med Microbiol Virol Parasitol Infect Dis 1992;276:437-42.
and that the residual standard deviation of the restriction fragments
of S. boulardii lies outside the model class boundaries of S. cerevisiae [2, 3]. The data above indicate that the identities of these
yeasts are distinct.
S. boulardii is a pharmaceutical biotherapeutic agent that has
been used for years outside of the United States to treat diarrhea
[4 ], but this is not the first time that confusion over the two
yeasts has led to investigations of the potential therapeutic value
of baker's yeast [5, 6]. When the efficacy of the two yeasts was
compared in controlled experiments with use of a standard gnotobiotic mouse model, treatment with S. boulardii showed a significant
protective effect against C. difJicile disease while that with S. cerevisiae did not [6, 7].
Pothoulakis et al. [8] reported that a mechanism of action of S.
boulardii may involve the release of a trypsin-like protease that
inhibits binding of the C. difJicile toxin A receptor as well as
intestinal secretion and inflammation caused by toxin A in rat
intestinal loops in vivo. These authors also tested the ability of a
protease-releasing strain of S. cerevisiae in the same animal model
under identical experimental conditions and found no significant
protection either from toxin A-associated diarrhea or from increased intestinal permeability (c. Pothoulakis and J. T. LaMont,
personal communication).
The conclusion reached by Chia et al. should be viewed with
skepticism in light of the evidence that these two yeasts have
distinct biochemical and molecular profiles and that only one of
them, S. boulardii, has proven therapeutic value. The clinical recommendation by Chia et al. based on four case reports is unwarranted and dangerous in that patients who have recurrent C. difJicile
disease may be misled into taking readily available baker's yeast
instead of seeking proven effective therapy for their disease.
Lynne V. McFarland
Biocodex, Inc., Seattle, Washington
References
1. Chia lKS, Chan SM, Goldstein H. Baker's yeast as adjunctive therapy
for relapses of Clostridium difficile diarrhea [letter]. Clin Infect Dis
1995;20:1581.
2. Guillamon lM, Barrio E, Huetra T, Querol A. Rapid characterization of
four species of the Saccharomyces sensu stricto complex according to
mitochondrial DNA patterns. Int J Syst Bacteriol 1994;44:708-14.
3. Cardinali G, Martini A. Electrophoretic karyotypes of authentic strains of
the sensu stricto group of the genus Saccharomyces. Int J Syst Bacteriol
1994;44:791-7.
cm
1996;22 (January)
Correspondence
201
4. Mcfarland LV, Bernasconi P. Saccharomyces boulardii: a review of an
innovative biotherapeutic agent. Microbial Ecology in Health and Disease
1993;6:157-71.
5. Schellenberg D, Bonington A, Champion CM, Lancaster R, Webb S, Main 1.
Treatment of Clostridium difficile diarrhoea with brewer's yeast [letter].
Lancet 1994;343:171-2.
6. Pecquet S, Guillaumin 0, Tancrede C, Andremont A. Kinetics of Saccharomyces cerevisiae elimination from the intestines of human volunteers
and effect of this yeast on resistance to microbial colonization in gnotobiotic mice. Appl Environ Microbioll991;57:3049-51.
7. Corthier G, Dubos F, Ducluzeau R. Prevention of Clostridium difficile
induced mortality in gnotobiotic mice by Saccharomyces boulardii. Can
J MicrobioI1986;31:894-6.
8. Pothoulakis C, Kelly CP, Joshi MA, et al. Saccharomyces boulardii inhibits
Clostridium difficile toxin A binding and enterotoxicity in rat ileum.
Gastroenterology 1993; 104:1108-15.
Brewer's Yeast as a Cause of Infection
infections are well described in the literature, journals are unlikely
to accept additional, essentially repetitive case reports. Thus, the
true incidence and prevalence of saccharomyces infections are
unknown.
I would strongly discourage the use of brewer's yeast in any
patient, as it is unproven and potentially dangerous therapy.
Sir-A statement in Dr. Chia's letter, "S. [accharomyces] cerevisiae is an essentially nonpathogenic yeast that in rare cases has
caused vaginitis . . . and fungemia in severely immunocompromised patients" [1] is not supported by a careful review of the
literature. It has long been appreciated that ingested microorganisms can traverse the lining of the gut of experimental animals
and disseminate [2, 3]. Oral administration of yeast solutions to
a healthy subject has produced fungemia and funguria [4 ]. Jensen
and Smith described a nonimmunocompromised individual who
ingested >2.5 gld of brewer's yeast and developed disseminated
S. cerevisiae infection [5].
Multiple articles, including two published in this journal, attest
to a variety of infections caused by S. cerevisiae [6-11]. Most,
but not all, of these patients were immunosuppressed.
Sobel et al. [12] described nine patients with vaginitis due to
S. cerevisiae. None had ingested brewer's yeast. The isolates were
resistant to fluconazole and were relatively more resistant to other
azoles. The authors state that "Together with the recent increase
in numbers of immunosuppressed hosts, there has been a dramatic
increase in reports of invasive diseases caused by Saccharomyces
species.. . . These diseases include fungemia, endocarditis, pneumonia, and infections of the urinary tract and skin in elderly,
debilitated, or compromised patients . . . particularly those with
AIDS.. . . It is apparent that Saccharomyces species are independently capable, in highly susceptible hosts, of inducing disease
and contributing to mortality."
How often this yeast produces disease and how frequently such
disease is associated with exogenous ingestion or other exposure
is unknown. As with most infections, the interaction between inoculum, virulence, and host defense is the important determinant
in the development of disease. Once individual saccharomyces
Reprints or correspondence: Dr. David L. Smith, Infectious Disease Associates of Kansas City, 2316 East Meyer Boulevard, Kansas City, Missouri 64132.
Clinical Infectious Diseases 1996;22:201
© 1996 by The University of Chicago. All rights reserved.
1058--4838/96/2201-0059$02.00
David L. Smith
Infectious Disease Associates of Kansas City.
Kansas City, Missouri
References
1. Chia JKS, Chan SM, Goldstein H. Baker's yeast as adjunctive therapy
for relapses of Clostridium difficile diarrhea [letter]. Clin Infect Dis
1995;20:1581.
2. Wolochow H, Hildebrand GJ, Lamanna C. Translocation of microorganisms
across the intestinal wall of the rat: effect of microbial size and concentration. Infect Dis 1961; 116:523-8.
3. Kennedy MJ, Volz PA. Dissemination of yeast after gastrointestinal inoculation in antibiotic treated mice. Sabouraudia 1983;21:27-33.
4. Krause W, Matheis H, WulfK. Fungemia and funguria after oral administration of Candida albicans. Lancet 1969; 1:598-9.
5. Jensen DP, Smith DL. Fever of unknown origin secondary to brewers yeast
ingestion. Arch Intern Med 1976; 136:332-3.
6. Aucott IN, Fayen J, Grossnicklas H, Morrissey A, Lederman MM, Salata
RA. Invasive infection with Saccharomyces cerevisiae: report of three
cases and review. Rev Infect Dis 1990; 12:406-11.
7. Oriol A, Ribera JM, Arnal J, Milla F, Batlle M, Feliu E. Saccharomyces
cerevisiae septicemia in a patient with myelodysplastic syndrome [letter]. Am J Hematol 1993;43:325-6.
8. Chertow GM, Marcantonio ER, Wells RG. Saccharomyces cerevisiae empyema in a patient with esophago-pleural fistula complicating variceal
sclerotherapy. Chest 1991;99:1518-9.
9. Snyder S. Peritonitis due to Saccharomyces cerevisiae in a patient on CAPO
[letter]. Perit Dial Int 1992; 12:77-8.
10. Bonnay S, Darchis JP, Veyssier P. Saccharomyces cerevisiae septicaemia
in a cancer patient. Medecine et Maladies Infectieuses 1991;21 :73.
11. Doyle MG, Pickering LK, O'Brien N, Hoots K. Saccharomyces cerevisiae
infection in a patient with acquired immunodeficiency syndrome. Pediatr
Infect Dis J 1990; 9:850-1.
12. Sobel JD, Vazquez J, Lynch M, Meriwether C, Zervos MJ. Vaginitis
due to Saccharomyces cerevisiae: epidemiology, clinical aspects, and
therapy. Clin Infect Dis 1993; 16:93-9.