Reply To: Latero-Flora(Brevibacillus Laterosporous) Chitinase producer?

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dvjorge
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jameskep;30314 wrote: I think the chitin inhibitors are more designed for fungal form of candida. From what I remember the fungal form of candida contains much more chitin than the yeast form of candida? So maybe you did not have fungal candida in your small intestine? Thats maybe why the lufenuron did not work for you as well. Its hard to say if the lufenuron or B. Laterosporous even reaches the colon. I think Lufenuron is a chitin inhibitor, whereas the B.Lat actually secretes direct chitinase. Seems like two slightly different animals. I did take 5 of the B. Lat capsules and definetly noticed it doing something to the Candida. Time will only tell if its a waste of $$ or not. I like the idea of supplements that interfere with chitin, because the chitin seems to give “fungal” candida its strong cell membrane and the strong defense to its chain formation.

Agree. Multi-step approach is needed for candida yeast+candida fungal form. Multi approach is needed for the small intestine and the colon because there are a lot of anti-fungals that do not make its way to the colon.

Yes, Lufenuron didn’t work in my case. The relevant aspect of it was I tried it together with some other powerful antifungals such as Amp B , Lamisil, and Fluconazole.
I have read that Lufenuron has poor activity against candida species. However, the new outcoming resistant some candida species are developing to the Echinocandins can be reversed after adding a chitin inhibitor. This demonstrates that drug combinations are the best way to treat it.
It may worth to try BOD probiotic with some form of antifungal that targets ergoesterol.
BOD has some other mechanisms of fungal inhibition beside the chitinase production.
Jorge.

Candida albicans cells with increased cell wall chitin have reduced echinocandin susceptibility in vitro. The aim of this study was to investigate whether C. albicans cells with elevated chitin levels have reduced echinocandin susceptibility in vivo. BALB/c mice were infected with C. albicans cells with normal chitin levels and compared to mice infected with high-chitin cells. Caspofungin therapy was initiated at 24 h postinfection. Mice infected with chitin-normal cells were successfully treated with caspofungin, as indicated by reduced kidney fungal burdens, reduced weight loss, and decreased C. albicans density in kidney lesions. In contrast, mice infected with high-chitin C. albicans cells were less susceptible to caspofungin, as they had higher kidney fungal burdens and greater weight loss during early infection. Cells recovered from mouse kidneys at 24 h postinfection with high-chitin cells had 1.6-fold higher chitin levels than cells from mice infected with chitin-normal cells and maintained a significantly reduced susceptibility to caspofungin when tested in vitro. At 48 h postinfection, caspofungin treatment induced a further increase in chitin content of C. albicans cells harvested from kidneys compared to saline treatment. Some of the recovered clones had acquired, at a low frequency, a point mutation in FKS1 resulting in a S645Y amino acid substitution, a mutation known to confer echinocandin resistance. This occurred even in cells that had not been exposed to caspofungin. Our results suggest that the efficacy of caspofungin against C. albicans was reduced in vivo due to either elevation of chitin levels in the cell wall or acquisition of FKS1 point mutations.

See this fragment :
This study explored the in vitro anti-Candida activity of drug
combinations from four classes: the polyenes, second-generation
triazoles, echinocandins and nikkomycins. While both the
polyenes and triazoles act on the fungal cell membrane,
although through different mechanisms, the echinocandins and
nikkomycins affect the cell wall, interfering with the synthesis
of glucan and chitin, respectively.
1,3
Our data show that combining voriconazole or caspofungin with nikkomycin Z resulted in
a synergistic effect. To the best of our knowledge, the specific
drug combinations used in our study against C. albicans have
not been described before. Whether combinations of antifungals
with different modes of activity could enhance the therapeutic
efficacy beyond that of monotherapy should be corroborated in
animal models, leading eventually to use in humans.