Read if you have: Vaginal Yeast Infections, Topical Facial Rashes, Topical Skin Rashes/Excema/Psoriasis/Daiper Rash, Foot Rot, Toenail Fungus, Perioral Dermatitus, Skin Ulcers.
For several weeks now I’ve been researching this idea of a synergistic or symbiotic relationship between Candida Albicans/fungi and a bacterial infection. Over and over, on this forum, and through personal experience or relationships, I have come across conditions that do not respond to anti-fungal/anti-yeast, or antibacterial/antibiotic treatments. I’ve cringed over horrid stories of advanced cases of Vaginosis so painful and deteriorating the subject cannot sit down and is facing surgical removal of the vagina! Others who have “rashes” that will not go away no matter how many different salves, balms, creams, and diets are implemented. I am under the impression that this “condition” is becoming more and more prevalent in our society. I’m beginning to miss the good old days when a yeast infection was just a yeast infection.
Some of our research uncovered a “test” done to discover whether or not fungi and bacteria can work together. To make a lot of difficult text short and readable; the doctors doing this experiment discovered that Candida Albicans can circle and “protect” a topical bacterial infection, keeping the area weakened and susceptible to reoccurring bacterial infection. Likewise, the infectious bacteria will feed on, and open the flesh to provide a low-oxygen environment for the Candida fungi to safely maintain. Whether these two are synergistic, or merely opportunistic, is undetermined, but the outcome is clear: a situation that cannot be treated successfully with antibiotics or anti-fungals.
A topical fungal-bacterial infection will usually worsen when coated with a salve or cream which blocks off oxygen exposure. Both fungi and bacteria are considered to be anaerobic; which means, they prefer low oxygen environments.
Aerobic topical flora exist in large numbers on the surface of your skin to maintain skin-health. These flora/natural bacteria flourish in high oxygen environments. Some anaerobic bacteria also exist naturally, but when anaerobic yeast and “bad” bacteria take over an area, it is the aerobic flora that you want to strengthen and aid.
?According to my understanding, when an anti-fungal ointment is applied, the anaerobic fungi are combatted by the anti-fungal chemicals, but the aerobic flora are also killed in the low oxygen environment under the ointment. This leaves the area vacant of natural defenses. And, the bacterial infection is untouched, even worsened, as it can thrive in low oxygen, and now has no aerobic adversaries.
Are you following my war-saga? Keep reading: there is an answer to this problem!
In some situations the doctor will identify the bacterial infection and an antibiotic will be administered. As expected, the infection will die down. However, the fungi is still present, and even stronger as the antibiotics have killed the good bacteria as well, and lowered your immune system. The fungi keep the area weakened and festering so that as soon as the flood of antibiotics is over, the bacterial infection can return, this time more resistant than ever.
The recovery of Candida albicans along with bacteria from the abdomen in the setting of peritonitis is becoming increasingly common. It is not known whether the interactions between the fungal and bacterial elements of these infections are synergistic, competitive, or neutral. To study this question, we have examined the effects of both the addition of C. albicans to a solely bacterial infection caused by Escherichia coli and Bacteroides fragilis, and the deletion of various components of this system using directed antimicrobial therapy. In a mixed infection, both C. albicans and bacteria contributed to mortality, since only the combination of cefoxitin and amphotericin B improved survival (from 50% to 90%). The addition of C. albicans to the bacterial inoculum increased the recovery of abscesses, but only to the number seen with fungal infection alone, implying two fairly independent processes. Although the number of bacteria recovered from abscesses at 10 days postinfection was unchanged with the addition of fungi, the deletion of the bacterial component of mixed infections led to the overgrowth of C. albicans. We conclude that this model of mixed C. albicans/E. coli/B. fragilis peritonitis is best characterized as two nonsynergistic, parallel infections with incomplete competition, allowing the survival of all three organisms to eventual abscess formation.
In clinical candidiasis, Candida albicans is frequently
found with Staphylococcus aureus and Streptococcus spe-
cies (2, 7, 10, 11, 14-20, 23). In addition, S. aureus has been
found to be a frequent opportunist in experimentally induced
candidiasis (19). In vitro, C. albicans has been found to
enhance the growth of a number of bacteria, including S.
aureus (18, 22).
In previous reports from this laboratory, we described
enhancement by C. albicans of S. aureus, Serratia marces-
cens, and Streptococcus faecalis in the establishment of
experimental infection in mice when fungi and bacteria were
inoculated intraperitoneally (i.p.) (4). Moreover, a synergis-
tic effect of C. albicans and S. aureus on mouse mortality (3,
5) has been reported. The present study was designed to
examine further the nature of this synergistic interaction.
The following questions were addressed. Would Candida
stimulation of bacterial infection take place if the two
pathogens were introduced at different sites? Would species
other than C. albicans or heat-inactivated C. albicans ex-
hibit a protective effect on bacteria injected at the same
time? What is the physical relationship and growth pattern of
C. albicans and S. aureus in the tissues when introduced