Candida glabrata is a biofilm-developing yeast (fungus) species that has the potential to cause yeast infections in the mouth, vagina, throat and urinary tract. C. glabrata can also cause systemic infections. C. glabrata lives in the human intestine without harm, however this yeast is an opportunistic pathogen.
If this yeast gets an opportunity to overgrow, it will. C. glabrata is now considered the second-most common cause of Candida infections, increasing in prevalence consistently over time with the use of antifungals.
Symptoms of C. glabrata infection
- Same as for C. albicans generally, but usually a bit less (due to no epithelial cell damage)
- Vulvovaginal infection may have no symptoms
- Compared with C. albicans, abnormal discharge is less frequently observed
- Burns instead of itching found in C. albicans
- Cottage-cheese-type discharge is rare
- Can exist with bacterial vaginosis due to its preference for more alkaline vaginas
- Less inflammation caused by C. glabrata, thus less pain with sex
- Doesn’t usually cause throat and mouth yeast infections, rare
- Can cause Candida infection of the urinary tract, usually asymptomatic but may cause painful urination, frequency, urgency, pelvic discomfort, dark, cloudy, strong-smelling urine
Diagnosis of C. glabrata
Generally C. glabrata and C. albicans look the same, but C. glabrata presents with fewer and less severe symptoms. Microscopy in your doctor’s office may not be able to distinguish between the two yeasts, and may result in a misdiagnosis. C. glabrata infections need immediate attention, so having a quick, reliable diagnosis is important. Also equally important is checking sensitivity and resistance to antifungals to ensure the correct treatment is provided.
Treating C. glabrata using antifungals
C. glabrata is resistant to common antifungals and adapts very quickly to new antibiotics. C. glabrata is mostly resistant to azoles, but is more susceptible to echinocandins, though some resistance is appearing with prior exposure. It has been suggested to use oral posaconazole and echinocandins, though these may be expensive and not approved for vulvovaginal candidiasis.
Order of activity against C. glabrata (-fungins are echinocandins and the rest are -azoles)
Try boric acid as your first stop.
Vaginal boric acid cures up to 70 per cent of C. glabrata infections, however, some countries have banned boric acid. Amphotericin B suppositories are also effective about 70 per cent of the time, against C. glabrata infections that are resistant to azoles.
Topical flucytosine cream alone or with Amphotericin B seems to work, but flucytosine is more expensive. Some lactobacilli species are able to prevent biofilm formation of C. glabrata, but more research is required.
C. glabrata used to be called Torulopsis glabrata and Cryptococcus glabratus, renamed in the 1980s as Candida glabrata. C. glabrata is often acquired in a hospital setting, and anyone with a compromised immune system is at risk. Additionally, anyone treated previously with azole-type antifungals is at greater risk.
There is an association with chronic stress in women and C. glabrata infections. C. glabrata may survive with its biofilm in the penises/foreskin of uncircumcised men and spread to female or male sexual partners. Women undergoing IVF are at risk, and the infection can cause miscarriages.
C. glabrata doesn’t form filamentous (invasive strands) structures that other Candida species develop, to hold and invade tissue. Instead, C. glabrata adheres to our cells and can enter cells, crossing the epithelial barrier without destroying the epithelial cells. We still don’t know how it does this. We can tolerate C. glabrata in our systems without a large immune response or extensive disease, it seems, but it will hang around until its moment to become a disease appears.
C. glabrata capacity to cause infection
It was at this point that C. glabrata was added to the Candida family. C. glabrata is more closely related to baker’s yeast – Saccharomyces cerevisiae, than to Candida albicans, but the yeast – unlike baker’s yeast – can survive in the human body. In fact, C. glabrata has special adhesive molecules on its surface that allow attachment to our cells, and the yeast can multiply within our white blood cells (macrophages) that are supposed to digest and eliminate foreign bacteria.
This means C. glabrata is treatment-resistant and very capable of quickly developing resistance to antifungals. Extensive antifungal treatment is understood to be a key component in the evolution of antifungal resistance in C. glabrata. This results in more infections.
C. glabrata can reorganise its chromosomes and make more copies of large chromosome parts to adapt to antifungals. It does this by duplicating the resistant chromosomes, and by contrast, the opposite is also true: the less drug present, the extra chromosomes drop off. There are some genetic mutations that contribute to C. glabrata antifungal resistance.
People in hospital are more likely to acquire a C. glabrata infection, but women are at risk – more complex vulvovaginal infections. C. glabrata can mix with other pathogenic yeasts such as C. albicans and C. tropicalis.
Contributors of C. glabrata infection
- Frequent courses of antibiotics (disrupts healthy, competitive flora)
- Frequent use of antifungals
- Low immunity
- Injury to tissue (surgery, accident, catheters)
- Equipment with biofilms present, particularly catheters
- Contraception – increases in oestrogen or via IUD biofilms, or general contraception use