S. Boulardii is not what you think it is

I've seen some posts on this forum expressing concern about whether or not a person should take s. boulardii, since it is known as a prebiotic "yeast."

The fact is that antibiotics (though at times very necessary!) may cause a disease called. C. Diff., and S. Boulardii is one of the only ways to either prevent C. Diff., or to help get over the disease.

So first, S. Boulardii is not the same kind of yeast that causes a "yeast infection," or a Candida overgrowth. It actually prevents Candida.

Also, it's not the same thing as C. Boulardii, which is what is found in Baker's Yeast or Brewer's Yeast.

If you are allergic to all yeasts, then you shouldn't take it. Otherwise, it may save your life. It certainly helped to save mine (along with Bacillus Coagulans, another prebiotic, and hosts of probiotics).

Having survived a drug-resistant C. Diff. (C. Diff. has a 30 % mortality rate), I'm suggesting that by all means, don't (!) avoid it, unless you have a really good reason.

Don't worry, I won't give you any brand names.



Margaret

Margaret,

Really good info! Thank you. My yeast cleanse Probiotic has it in it so it definitely is beneficial against yeast. Glad you are better from C. Diff., very scary.

LC

Oh, and as you can't share the brand, would you let us know the dose you take - how many capsules per day & how many billion cells that are in each capsule. Thanks!!!

So it's more used when someone experiences herxing? That would explain why I haven't been asked yet. Haven't herxed yet.

Be aware, immune suppressed people.. S. Boullardi can also become pathogenic
http://cid.oxfordjournals.org/content/41/11/1559.long

Even in immunocompetant people this can be an issue. Especially in people in antibiotics which many on this board are on.

If you have not extensively treated your gut issues (even if you think you have none.. because if you have lyme, you have gut issues) and completely sealed any leaky gut this is not a probiotic I would take. My .02

No, I very much know what Im talking about and posted a study. Ill paste some of it for you since you didnt click on the link.

http://cid.oxfordjournals.org/content/41/11/1559.long

On the basis of data revealed in our literature search, invasive Saccharomyces infections remain rare among invasive fungal infections, although the incidence has significantly increased since the 1990s. Risk factors associated with invasive Saccharomyces infections are similar to those reported elsewhere for invasive candidiasis, except for treatment with a probiotic containing S. boulardii. It is important to emphasize the role of this biotherapeutic agent, because it was responsible for 40.2% of invasive Saccharomyces infections reported in the literature. In the 5 cases in which S. boulardii was considered to be the etiologic agent, although these patients did not take a probiotic preparation, the similarity of the genotypic profile between S. boulardii isolates from patients and from probiotic preparations strongly suggested nosocomial acquisition, with catheters being a likely portal of entry because of possible contamination through hand transmission [6, 7].

The epidemiologic characteristics of S. cerevisiae infection in human beings is not fully understood. Persistent digestive implantation in healthy volunteers has never been described, suggesting that S. cerevisiae behaves mainly as a transient digestive commensal linked to contaminated food. Thus, the portal of entry for invasive infections is mainly supposed to be digestive. Evidence suggests that nosocomial acquisition of S. cerevisiae can occur, because clusters of identical isolates from patients concurrently hospitalized in the same unit have been described [17]. This is also supported by the increasing rates of colonization among hospitalized patients with hematologic disease who only ingest sterile food not comprised of raw fruits or vegetables [16]. The same conclusion could be drawn for S. boulardii infection in patients who did not receive treatment with a probiotic containing S. boulardii, with intravenous catheters the likely portal of entry . Hand transmission has been suggested in these latter cases .

Saccharomyces infection is clinically indistinguishable from invasive candidiasis, notably because chorioretinitis (fluffy yellow exudates) and esophagitis (yellow-white plaques on an erythematous background) are present in both conditions, and is even indistinguishable from infections due to other microorganisms, such as endocarditis. In addition, patients have nonspecific symptoms that could be related to the underlying disease, and the diagnosis of Saccharomyces infection is often unexpected. Fever, when noted, is present in 75.2% of patients. However, the clinical impact of Saccharomyces infection has been clearly assessed in an immunocompetent patient whose unique predisposing factor was the ingestion of health food containing viable yeasts [25]. The patient developed recurrent fever, malaise with nausea, and night sweats. Yeasts were isolated from bone marrow and urine specimens. The patient recovered when he stopped ingesting health food containing yeasts. The occurrence of deep-site involvement with histologic documentation also underlines the pathogenicity of such yeasts. In these cases, yeasts were most often associated with necrosis [60] and granulomatous reaction [25].

Significant particularities of S. boulardii infections include higher frequency of intensive care unit hospitalization, presence of an indwelling catheter, and intestinal disease. This may either correspond to specific predisposing factors or, more likely, may reflect conditions associated with treatment with a probiotic containing S. boulardii, such as severe digestive disease. The lack of organ involvement and the better prognosis could be due to decreased S. boulardii virulence. Another explanation could be the ability of patients at risk to partly control the infection, given the lower frequency of immunocompromise in this group. S. boulardii showed an intermediate level of virulence in an experimental murine model of invasive infection involving both immunocompetent and immunocompromised mice .

S. cerevisiae has, in immunocompromised mice, been shown to grow at 42°C and to form pseudohyphae [84]. Also, SSD1, which encodes a protein that affects various cellular processes (including maintenance of cell integrity, control of cell cycle, and growth at high temperature), seems to play an important role in the virulence of Saccharomyces organisms [85]. Deletion of this gene leads to a significant increase in virulence for both clinical and plant isolates, as revealed in a mouse model of invasive infection [85]. Alteration in composition and cell wall architecture is supposed to lead to overstimulation of the proinflammatory response. Furthermore, analysis of feral and clinical strains of S. cerevisiae showed similar virulence in a mouse model of infection [85]. Similar to many opportunistic organisms, it is not possible to identify particular features of S. cerevisiae that distinguish between environmental and clinical strains on the basis of virulence-related phenotype [84].

S. cerevisiae exhibits low susceptibility to amphotericin B and to azole derivatives (table 3). Although breakpoints have not been defined for S. cerevisiae, MIC90 for fluconazole and itraconazole are considered to be within the susceptible dose-dependent range defined for C. albicans [86]. One can hypothesize that these drugs may play a role in the emergence of S. cerevisiae. Although data remain scarce, voriconazole seems to exhibit good efficacy against S. cerevisiae, with an MIC90 of <0.25 mg/L. A recent publication reports on the successful outcome with voriconazole therapy for a patient with S. boulardii who did not respond to initial treatment with fluconazole [76]. No published series is available for caspofungin treatment, but preliminary research has demonstrated good efficacy against a limited number of strains (C.H., unpublished data). MIC values for amphotericin B and fluconazole were 0.19 and 32 mg/L, respectively, as determined for 2 clinical isolates of S. boulardii . S. boulardii could not be tested by Etest (AB Biodisk) on casitone or Roswell Park Memorial Institute 1640 agar because of the lack of growth on these media (A.E.-A. and C.H., unpublished data).

Despite this spectrum of susceptibility, a favorable outcome was observed in 63% of cases revealed in our literature search, which is a slightly higher percentage than that reported for cases of invasive candidiasis [87]. Specific data on morbidity were difficult to evaluate, because Saccharomyces infections often occurred in patients with a large number of comorbidities. Use of amphotericin B or fluconazole therapy with central venous catheter removal appeared to be an effective therapeutic option for patients with Saccharomyces infection. Favorable outcome may also be related to the low virulence of this species, a hypothesis that is supported by the absence of significant difference in outcome between immunocompromised and immunocompetent patients.

In conclusion, Saccharomyces organisms are increasingly reported as agents of invasive infection, especially in immunocompromised or critically ill patients. Special caution has to be taken with S. boulardii probiotic preparations, which account for nearly 40% of infection cases.

Post Edited By Moderator (Traveler) : 2/25/2014 6:36:00 PM (GMT-7)

To be fair, the reason why this is an issue for me is that I look at my blood fairly regularly via Darkfield. We knew I had some type of fungi via lab tests but the best we could get is that it was a saphrophyte. I could see plenty of yeast and it was DEFINATELY dimorphic.

Anyway, we decided to hit it with enzymes, herbs, and diflucan....

And add one new probiotic, s. Boullardii.

My blood started doing really funky things. I started seeing budding yeasts.. Thought maybe it was my yeasts going through changes, but I ran out of s. Boullardii and they stopped appearing. I ended up researching s. Boullardii and found out this info.

Tetragram, I've got no beef with you, dear. I simply wanted to make sure people had this information because I don't think s.boullardii is a good thing for everyone.

You have mitigating circumstances with the c diff, I'd rather have a s.boullardii infection then c diff any day if I had to choose. But for others not battling c.diff, I don't know I'd add this probiotic and I really worry about those with picc lines and other central lines who are doing iv abx so I wanted to share the counterpoint.


I'm sorry you are having a hard day today, I hope it gets better.

Actually, doing a little more research and trying to remember, I remembered seeing something called Jarrow at one point, I forget if it was tube feeding or something similar. Doing a google search of it quickly brings up that Jarrows IS Sacchromyces B, and I have found multiple places that both warn of using in those with immunosuppressed systems (which he easily fit after his hypovolemic shock, bad cdiff infection that was fought with vancomycin as well as other powerful, broad spectrum antibiotics), AND multiple warnings against using on people with central lines, which he has had 3 in the past 2 weeks. I guess I should probably make sure the doctors knew those risks, or at least know them next time before they kill someone else.

well, just remember that there are different types of saccharomyces, and one is much more dangerous than the other. However, you may want to check Pathogen's post just to weigh your odds (and risks). Saccharomyces C. is the kind of yeast found in bread, and sometimes your colon can be over populated with bad yeasts, ie sacc. c., just as it can with c. diff. some people are allergic to all yeasts, I think.

Maine, if you stop the s. Boullardi, and your bottom stops itching, then you'll know what the problem is. You may want to try some anti-yeast cream that you can get OTC at the drugstore. Also, may sure you are taking copious amounts of probiotics, other kinds will do fine as well.

Ask your LLND what he thinks too.

You can always use probiotic foods instead of S. boullardi, though the numbers of strains would be smaller. My understanding is that those types of foods are actually prebiotics as well.

My guess is if the S. Boullardi doesn't make you really sick, you're ok?

Margaret

What is it Maine? I think the your LLND suggested you take S. Boulardi so you wouldn't get C. Diff. Otherwise, I give up on the S. Boulardi front, ha ha!

Margaret

i though sacch b was transient and didn't reproduce. or maybe it doesn't produce spores but can still reproduce somehow?

there is a decent wikipedia article on it

it is actually a sub-strain / group of strains of Saccharomyces Cerevisea

"S. boulardii is genetically a grouping of S. cerevisiae strains, sharing >99% genomic relatedness, giving the synonym S. cerevisiae var. boulardii."

https://en.wikipedia.org/wiki/Saccharomyces_boulardii