Primary cutaneous cryptococcosis (PCC) caused rapidly progressive cellulitis with suspected flexor tendon sheath involvement and extensive tissue destruction requiring amputation in a patient, even without clinically apparent systemic dissemination.
Researchers described an 81-year-old male patient with transfusion-dependent myelodysplastic syndrome (MDS) who developed severe infection of his right middle finger following a splinter injury. His medical history included type 2 diabetes mellitus, hypertension, and actinic keratosis. He was not receiving chemotherapy, corticosteroids, or immunosuppressive therapy.
The case focused on the progression of PCC from a presumed inoculation site into deeper soft tissues, with clinical and operative findings suggesting flexor tendon sheath involvement. Additional observations included identification of the fungal pathogen, extent of tissue destruction, assessment for systemic dissemination, and clinical response to surgical and antifungal treatment.
The patient developed a small bruise-like lesion on the palmar aspect of his right middle finger, followed by pain, swelling, erythema, and blood-filled blisters. On admission, laboratory testing showed a white blood cell count of 13.8 × 10⁹/L, a neutrophil count of 12.2 × 10⁹/L, and a C-reactive protein level of 96 mg/L. Blood cultures were negative, and hand radiography demonstrated no bony destruction.
Empiric intravenous antibiotics were initiated, and urgent surgical exploration was performed on hospital day 1. Examination revealed murky fluid within the flexor tendon sheath, although no frank pus or tissue necrosis was evident. Routine bacterial cultures showed no growth after 48 hours.
Despite treatment, the infection progressed rapidly. By hospital day 4, extensive finger necrosis, purulent discharge, and digital arterial thrombosis necessitated amputation through the proximal interphalangeal joint. Persistent inflammation required additional debridement and bone shortening on day 7, with further surgical procedures subsequently performed because of poor wound healing.
Fungal cultures grew Cryptococcusneoformans, subsequently confirmed by a reference mycology laboratory. Histopathologic examination demonstrated encapsulated yeast forms with narrow-based budding, supporting the diagnosis of cryptococcal infection. Although clinical and intraoperative findings were consistent with flexor tendon sheath involvement, specimens were not specifically identified as originating from the tendon sheath, preventing direct microbiological confirmation of cryptococcaltenosynovitis.
Despite extensive local tissue destruction, the patient reported no respiratory or neurologic symptoms, and chest radiography was normal. Serum cryptococcal antigen testing was negative on 2 occasions, supporting localized infection rather than secondary cutaneous cryptococcosis resulting from systemic dissemination.
Initial antifungal treatment consisted of oral itraconazole 200 mg every 12 hours for 2 weeks while definitive fungal identification was pending. Following confirmation of C neoformans and susceptibility testing, treatment was changed to oral fluconazole 800 mg daily because of its more predictable systemic exposure.
After 7 weeks of fluconazole treatment, the dose was reduced to 400 mg daily and continued for another 2 weeks. Therapy was discontinued after 9 weeks because of intolerable gastrointestinal adverse effects and evidence of clinical resolution. At the 12-week assessment, the wound had healed with scarring and no signs of active infection. The patient remained well 6 months posttreatment, without reported wound breakdown or systemic illness.
The patient's underlying MDS may have contributed to the aggressive clinical presentation through impaired immune function, even without neutropenia or immunosuppressive treatment. However, neutrophil function and cellular immunity were not directly assessed, leaving the disease's contribution uncertain.
Although repeatedly negative serum cryptococcal antigen tests and the absence of systemic symptoms supported localized infection, lumbar puncture and chest computed tomography were not performed, preventing definitive exclusion of occult dissemination. Direct microbiological confirmation of tendon sheath infection was unavailable. The combined use of surgery and antifungal therapy prevented determination of the independent contribution of either intervention to recovery.
PCC should be considered in progressive cellulitis or suspected flexor tendon sheath infection that does not respond to conventional antibacterial treatment, particularly following environmental trauma. The researchers emphasized early deep-tissue sampling for fungal culture and histopathology, assessment for systemic dissemination, and timely multidisciplinary management when extensive local tissue involvement is suspected.
"Combined antifungal and surgical treatment may be appropriate in selected patients with extensive or progressive local disease," wrote lead study author Julia Gleeson, MBBS. of the Department of Microbiology at Wirral University Teaching Hospital National Health Service Foundation Trust, and colleagues.
The study authors reported no conflicts of interest.
Source: Cureus
