Treatment for Candida krusei Infections
Candida krusei is intrinsically resistant to fluconazole and should never be treated with this agent 1, 2. The treatment approach depends critically on the site and severity of infection.
Invasive Candidiasis/Candidemia
First-Line Treatment
An echinocandin is the preferred first-line therapy for C. krusei candidemia and invasive infections 3:
- Caspofungin: 70 mg loading dose, then 50 mg daily 3
- Micafungin: 100 mg daily 3
- Anidulafungin: 200 mg loading dose, then 100 mg daily 3
Both C. krusei and C. glabrata demonstrate excellent susceptibility to echinocandins, making this class the optimal choice 3.
Alternative Options
Amphotericin B deoxycholate (1.0 mg/kg/day) is the preferred alternative when echinocandins cannot be used 3. However, some C. krusei isolates demonstrate resistance to amphotericin B, and this agent requires intravenous administration with associated toxicity 3.
Lipid formulations of amphotericin B (3-5 mg/kg daily) are reasonable alternatives if there is intolerance, limited availability, or resistance to other agents 3.
Step-Down Therapy
Voriconazole (400 mg twice daily for 2 doses, then 200 mg twice daily) is recommended as step-down oral therapy for selected cases of C. krusei candidemia once the patient is clinically stable 3. Voriconazole is licensed in Europe for treatment of fluconazole-resistant serious invasive Candida infections including C. krusei 3.
Essential Adjunctive Measures
- Remove central venous catheters as early as possible when the source is presumed to be the catheter 3
- Perform follow-up blood cultures daily or every other day to establish clearance 3
- Continue treatment for 2 weeks after documented clearance from bloodstream and resolution of symptoms 3
- Perform dilated ophthalmological examination within the first week after diagnosis in all nonneutropenic patients 3
Urinary Tract Infections
Assessment
First determine whether C. krusei in urine represents true infection requiring treatment versus asymptomatic candiduria 4. Treatment is warranted for:
- Symptomatic patients with cystitis or pyelonephritis 4
- High-risk groups: neutropenic patients, very low birth-weight infants, patients undergoing urologic procedures 4
Treatment Approach
Amphotericin B deoxycholate (0.3-0.6 mg/kg daily for 1-7 days) is first-line treatment for C. krusei UTI 4. This agent achieves adequate urinary concentrations and maintains activity against most C. krusei isolates 3.
Key management principles:
- Remove indwelling bladder catheter if present 4
- Eliminate any urinary tract obstruction 4
- For cystitis only: Amphotericin B bladder irrigation (50 mg/L sterile water daily for 5 days) combined with endoscopic removal of obstructing lesions if present 3
Duration and Monitoring
- Cystitis: 2 weeks of treatment 4
- Pyelonephritis: 2 weeks with documented symptom resolution and negative cultures 4
- Repeat urine cultures to document clearance 4
Alternative for UTI
Echinocandins have poor urinary excretion and are generally ineffective for UTI 3. However, there is emerging evidence supporting increased-dose micafungin (150 mg daily) for chronic symptomatic C. krusei UTI, particularly in transplant recipients where amphotericin B toxicity is problematic 5. This remains an off-label approach with limited data.
Critical Pitfalls to Avoid
- Never use fluconazole for C. krusei—it exhibits intrinsic resistance 1, 2, 6
- Avoid lipid formulations of amphotericin B for UTI—they do not achieve adequate urinary concentrations 3
- Do not use flucytosine as monotherapy for C. krusei—it lacks activity against this species 3
- Echinocandins are ineffective for UTI due to minimal urinary excretion, except possibly at higher doses in select cases 3, 5
Special Populations
In hematologic patients with C. krusei candidemia, rapidly remove the catheter regardless of species 3. The treatment algorithm remains the same with echinocandins as first-line therapy 3.
For neonates with disseminated C. krusei infection, amphotericin B deoxycholate is preferred due to low toxicity in this population and lack of pharmacokinetic data for echinocandins 3.