Candida glabrata and Candida krusei are specific types of yeast, belonging to the broader category of fungi. These yeasts are typically part of the normal microbial community in humans, residing in areas like the gastrointestinal tract and mucous membranes. While usually harmless, they can become opportunistic pathogens, causing infections when host conditions change. The prevalence of non-albicans Candida species, including C. glabrata and C. krusei, has been increasing.
Unique Challenges and Symptoms
These two Candida species present particular challenges in clinical settings due to their characteristic resistance profiles to common antifungal medications. Candida krusei exhibits intrinsic resistance to fluconazole, a widely used azole antifungal drug. This means C. krusei is naturally less susceptible to fluconazole’s effects from the outset. Candida glabrata often displays decreased susceptibility and can readily develop acquired resistance during treatment, frequently linked to mutations that increase drug efflux.
The symptoms of candidiasis caused by C. glabrata and C. krusei are similar to those of other Candida species, but their drug resistance can lead to more persistent or severe infections. Infections can manifest in various ways, ranging from superficial to systemic. Common presentations include bloodstream infections, known as candidemia, which may cause fever and chills.
Urinary tract infections (UTIs) are also frequent, particularly with C. glabrata, leading to symptoms such as a frequent urge to urinate, painful urination, or cloudy urine. Oral candidiasis, or thrush, appears as white, creamy patches on the tongue or inner cheeks, while genital infections, like vaginal yeast infections, cause itching, burning, and discharge.
Populations at Risk
Certain host factors significantly increase an individual’s susceptibility to infections caused by Candida glabrata and Candida krusei. Immunocompromised individuals represent a primary risk group, including those undergoing chemotherapy for cancer, organ transplant recipients, and people with advanced HIV. These patients have weakened immune systems, allowing Candida species to overgrow and cause disease.
Patients with prolonged hospital stays, especially those admitted to intensive care units (ICUs), face an elevated risk. The hospital environment, with its invasive procedures and exposure to pathogens, increases infection risk. The presence of indwelling medical devices, such as central venous catheters or urinary catheters, further increases susceptibility by providing surfaces for Candida biofilms to form and act as entry points for infection.
Additionally, prior extensive treatment with broad-spectrum antibiotics can disrupt the body’s natural microbial balance, allowing Candida to proliferate unchecked. Similarly, previous or prolonged exposure to azole antifungal drugs, particularly fluconazole, can select for more resistant Candida species like C. glabrata and C. krusei, leading to their emergence as causative agents of infection.
Diagnostic Process
Identifying infections caused by Candida glabrata and Candida krusei begins with obtaining a clinical sample from the suspected site of infection. This could involve a blood sample for suspected candidemia, a urine sample for a urinary tract infection, or a swab from mucosal surfaces. These samples are then sent to a laboratory for mycological culture, where the yeast is grown in a controlled environment for identification.
Identifying the specific Candida species (e.g., C. glabrata or C. krusei) is important for guiding appropriate treatment. Following species identification, Antifungal Susceptibility Testing (AST) is performed. AST typically involves measuring the minimum inhibitory concentration (MIC) of various antifungal drugs.
Specialized Treatment Strategies
Given their common resistance profiles, standard antifungal therapies like fluconazole are often ineffective. Fluconazole is not recommended for C. krusei due to its intrinsic resistance, and C. glabrata can develop resistance, making it a less reliable option.
Instead, the echinocandin class of antifungal drugs, which includes medications like caspofungin, micafungin, and anidulafungin, is frequently recommended as a first-line treatment for invasive infections caused by these species. Echinocandins work by inhibiting the synthesis of a key component of the fungal cell wall, leading to cell death. These agents show strong activity against both C. glabrata and C. krusei.
For severe or complicated infections, or when echinocandins are not suitable, amphotericin B, particularly its lipid formulations, serves as another potent alternative. Amphotericin B acts by binding to ergosterol, a sterol found in the fungal cell membrane, disrupting its integrity. Antifungal susceptibility testing heavily influences the choice of therapy, ensuring the most effective medication is selected.