btw. Grapefruit-Seed-Extract is very helpful aganist biofilms (liquid extract!)
I also recommend AMD Syntol compared with nystatin and enzymes such as lubrokinase and serrapeptase.
Biofilm protocol should be taken away from food! I prefere to wake up in the middle of the night and take most of them, then same thing at the morning, 1 hour before breakfast.


Here is a pretty nice biofilm protocol, that i ve found on the internet:

Here is my actual regimen (done 2-3 times a day):

LYSIS - Biofilm Busters / Systemic Enzymes
• Digestive Enzymes - Digest Gold, MRM Digest All
• Nattokinase
• Lumbrokinase
• Serratiopeptidase
• Mucolase (Seaprose-S)
• PRX or ViraStop (has Serra, Protease, Natto, Catalase, Mucolase, etc)
• InterFase
• EDTA (AM and PM doses only)
• Lactoferrin: Nutricillin + Jarrow + LE Apolactoferrin
• NAC
• Berberine Complex (integrative Therapeutics)

(+30mins)
KILLERS - Antimicrobials
• Nystatin / SF722 10-Undecenoic Acid / Kolorex / Herbals
• GI Microb-X
• Iodine-50
• Monolaurin

(+1 hour after antimicrobials)
BINDERS (clean up the debris)
• Chitosan
• Citrus Pectin + lots of water
• Germanium
• Charcoal (PM, 2 hrs away from food)
• Vit C + Triphala (buffer + bile/BB)

Yes, Apo-Lactoferrin.

Polyunsaturated Fatty Acids.! ( Fish Oil )

Biochim Biophys Acta. 2012 Oct;1820(10):1463-8. doi: 10.1016/j.bbagen.2012.05.004. Epub 2012 May 17.
Polyunsaturated fatty acids cause apoptosis in C. albicans and C. dubliniensis biofilms.
Thibane VS, Ells R, Hugo A, Albertyn J, van Rensburg WJ, Van Wyk PW, Kock JL, Pohl CH.
Source
Department of Microbial, Biochemical and Food Biotechnology, University of the Free State, P. O. Box 339, Bloemfontein, 9300, South Africa. thibanev@ufs.ac.za
Abstract
BACKGROUND:
Polyunsaturated fatty acids (PUFAs) have antifungal properties, but the mode by which they induce their action is not always clear. The aim of the study was to investigate apoptosis as a mode of action of antifungal PUFAs (stearidonic acid, eicosapentaenoic acid and docosapentaenoic acid) which are inhibitory towards biofilm formation of C. albicans and C. dubliniensis.
METHODS:
Candida biofilms were grown in the absence or presence of 1mM PUFAs (linoleic acid, stearidonic acid, eicosapentaenoic acid, docosapentaenoic acid) for 48h at 37°C. The effect of these PUFAs on the membrane fatty acid profile and unsaturation index, oxidative stress, mitochondrial transmembrane potential and apoptosis was evaluated.
RESULTS:
When biofilms of C. albicans and C. dubliniensis were exposed to certain PUFAs there was an increase in unsaturation index of the cellular membranes and accumulation of intracellular reactive oxygen species (ROS). This resulted in apoptosis, evidenced by reduced mitochondrial membrane potential and nuclear condensation and fragmentation. The most effective PUFA was stearidonic acid.
CONCLUSIONS:
The resultant cell death of both C. albicans and C. dubliniensis is due to apoptosis.
GENERAL SIGNIFICANCE:
Due to the increase in drug resistance, alternative antifungal drugs are needed. A group of natural antifungal compounds is PUFAs. However, understanding their mechanisms of action is important for further use and development of these compounds as antifungal drugs. This paper provides insight into a possible mode of action of antifungal PUFAs.
Copyright © 2012 Elsevier B.V. All rights reserved.

Carvacrol ( Oil of Oregano )

In vitro activity of terpenes against Candida biofilms.
Dalleau S, Cateau E, Bergès T, Berjeaud JM, Imbert C.
Source
UMR 6008, Université de Poitiers, CNRS, 6 rue de la Milètrie, BP 199, 86034 Poitiers Cedex, France.
Abstract
The antibiofilm activity of 10 terpenes was tested in vitro against three Candida species by 24-h treatment of biofilms aged 1-5 days. Treatment of 24-h-old Candida albicans biofilms with carvacrol, geraniol or thymol (0.06%) resulted in >80% inhibition. Carvacrol (0.03%) inhibition was > or =75% independent of the age of the C. albicans biofilm. Carvacrol (0.125%) inhibition was >75% against Candida glabrata and Candida parapsilosis biofilms. Geraniol (> or =0.125%) and thymol (0.06% or 0.125%) inhibition was >75% against C. parapsilosis biofilms whatever their age. This study demonstrates the antibiofilm activity of terpenes and points out the exceptional efficiency of carvacrol, geraniol and thymol, which could represent candidates in the treatment of candidiasis associated with medical devices.


See this fragment :

Terpenoid phenols have been shown to be efficacious not only on planktonic cells but also on biofilms of Candida albicans that are resistant to many antifungal drugs. Carvacrol demonstrated the strongest antifungal activity against Candida albicans biofilms, with a MIC of <0.03% (9). Furthermore, carvacrol was shown to be effective regardless of the maturity of the biofilm. The terpenoid phenols tested were able to inhibit biofilms of several strains of Candida, including C. albicans, C. glabrata, and C. parapsilosis.

Cis 2 decenoic acid.

I can think about any decanoic acid such as undecenoic acid (sf-722) See this :

Blocking of Candida albicans biofilm formation by cis-2-dodecenoic acid and trans-2-dodecenoic acid
YuQian Zhang1,†, Chen Cai1,†, YuXiang Yang1, Lixing Weng1 and LianHui Wang2
+ Author Affiliations

1Department of Microbiology and Microbial Engineering, School of Life Sciences, Fudan University, Shanghai 200433, PR China
2Institute of Advanced Materials, Nanjing University of Posts and Telecommunications, Nanjing, Jiangsu, 210046, PR China
Correspondence
Lixing Weng wenglixing@fudan.edu.cn LianHui Wang iamlhwang@njupt.edu.cn
Received 14 December 2010.
Accepted 18 July 2011.

Next Section
Abstract

Candida is an important opportunistic human fungal pathogen. Infections caused by Candida albicans are related to the formation of a biofilm. The biofilm enhances the resistance of the C. albicans defence system, increases its resistance to antifungal drugs and induces increased drug tolerance, making clinical care more challenging. The in vitro activity of cis-2-dodecenoic acid (BDSF; a diffusible signal factor from Burkholderia cenocepacia) and trans-2-dodecenoic acid (trans-BDSF) against C. albicans growth, germ-tube germination and biofilm formation was estimated by absorbance measurements and microscopic assessments. C. albicans biofilms were prepared using a static microtitre plate model. Quantitative analysis of biofilm formation was performed using a 2,3-bis(2-methoxy-4-nitro-5-sulfo-phenyl)-2H-tetrazolium-5-carboxanilide reduction assay to evaluate the effect of different concentrations of BDSF and trans-BDSF at different stages of biofilm formation. Reductions in biofilm structure and formation were visualized by inverted microscopy. Real-time RT-PCR was employed to estimate the mRNA expression levels of the hyphae-specific genes HWP1 and ALS3. It was found that 30 µM of either BDSF or trans-BDSF reduced germ-tube formation by approximately 70 % without inhibiting yeast growth. Yeast growth was strongly repressed by the exogenous addition of 300 µM BDSF and trans-BDSF at 0 and 1 h after cell attachment, with biofilm formation being reduced by approximately 90 and 60 %, respectively. BDSF and trans-BDSF were more effective against biofilm formation than farnesol and the diffusible signal factor cis-11-methyl-2-dodecenoic acid. None of the four drugs was able to destroy pre-formed biofilms. Real-time RT-PCR analysis showed that HWP1 was downregulated by approximately 90 % and ALS3 was downregulated by 70–80 % by 60 µM BDSF and trans-BDSF, implying that BDSF and trans-BDSF block C. albicans biofilm formation by interfering with the morphological switch. These results suggest that BDSF and trans-BDSF are potentially useful therapeutic agents worthy of further study.


EDTA

Mycopathologia. 2007 Dec;164(6):301-6. Epub 2007 Oct 2.
Inhibition on Candida albicans biofilm formation using divalent cation chelators (EDTA).
Ramage G, Wickes BL, López-Ribot JL.
Source
Section of Infection and Immunity, Glasgow Dental School and Hospital, The University of Glasgow, Glasgow, UK.
Abstract
Candida albicans can readily form biofilms on both inanimate and biological surfaces. In this study we investigated a means of inhibiting biofilm formation using EDTA (Ethylenediaminetetra-acetic acid), a divalent cation chelating agent, which has been shown to affect C. albicans filamentation. Candida albicans biofilms were formed in 96-well microtitre plates. Cells were allowed to adhere for 1, 2, and 4 h at 37 degrees C, washed in PBS, and then treated with different concentrations of EDTA (0, 2.5, 25, and 250 mM). EDTA was also added to the standardized suspension prior to adding to the microtiter plate and to a preformed 24 h biofilm. All plates were then incubated at 37 degrees C for an additional 24 h to allow for biofilm formation. The extent and characteristics of biofilm formation were then microscopically assessed and with a semi-quantitative colorimetric technique based on the use of an XTT-reduction assay. Northern blot analysis of the hyphal wall protein (HWP1) expression was also monitored in planktonic and biofilm cells treated with EDTA. Microscopic analysis and colorimetric readings revealed that filamentation and biofilm formation were inhibited by EDTA in a concentration dependent manner. However, preformed biofilms were minimally affected by EDTA (maximum of 31% reduction at 250 mM). The HWP1 gene expression was reduced in EDTA-treated planktonic and biofilm samples. These results indicate that EDTA inhibits C. albicans biofilm formation are most likely through its inhibitory effect on filamentation and indicates the potential therapeutic effects of EDTA. This compound may serve a non-toxic means of preventing biofilm formation on infections with a C. albicans biofilm etiology.

I don't have information regarding to S. Boulardii and Candida Albicans biofilms. S. Boulardii produces Capryc Acid that interferes with candida adhesion to the tissues and is also antifungal, however, it looks like it doesn't affect the Boulardii.

Jorge.