Cryptococcus albidus infection in a patient undergoing autologous progenitor cell transplant

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A 51-year-old male with a past medical history of non-insulin dependent diabetes mellitus was diagnosed with a facial peripheral T cell lymphoma. He received local resection, four cycles of CHOP chemotherapy, and involved field radiation therapy (3600 cgy) over six weeks. Seven months later, he presented with left eye ptosis. Bone marrow aspiration with flow cytometric evaluation was consistent with M4 acute myeloid leukemia (AML).
The patient received high-dose cytarabine and daunorubicin with intrathecal thiotepa as induction therapy. During neutropenic periods, he received prophylactic fluconazole and acyclovir. Antimicrobials were utilized during this period, including imipenem, cefepime, vancomycin and Amphotericin B.
Consolidation therapy, including high-dose cytarabine with etoposide, followed two months later. The patient received prophylactic acyclovir and fluconazole. He experienced febrile neutropenic episodes treated with metronidazole, imipenem, amikacin, cefepime and Vancomycin.
Six weeks after consolidation, the patient underwent autologous peripheral progenitor cell transplantation after a busulfan and etoposide preparative regimen. He received diflucan, bactrim and acyclovir prophylaxis. While neutropenic, two consecutive blood cultures in the aerobic specimen were obtained over ten hours, revealing Cryptococcus albidus. A serum assay for cryptococcal antigen was negative. Amphotericin B was begun at 0.6 mg/kg daily for two weeks, followed by oral itraconazole for six weeks. Six further blood cultures were drawn over two weeks which did not grow C. albidus, and cerebrospinal fluid analysis was negative for both cryptococcal antigen as well as encapsulated yeasts using India ink staining techniques.
C. albidus, a member of the non-neoformans species of Cryptococcus, is considered a rare cause of disease (1) whose main portal of entry into the body is through the respiratory tract. Cases of hematogenous dissemination may be seen in patients with defective cell-mediated immunity.
Fourteen previous reported cases of C. albidus infections include six cases of meningitis, five cases of fungemia, two of pulmonary infection and one case of cutaneous involvement. Because of C. albidus’ s predilection for the meninges, all patients suspected of being infected should have an examination of their cerebrospinal fluid in addition to blood assays (1).
This patient’s cryptococcal serum antigen assay was negative. This result is not uncommon. Despite sharing several capsular antigens with Cryptococcus neoformans, as revealed by cross-staining reactions by the fluorescent antibody staining technique, the latex agglutination test is specific for the polysaccharide antigens found on C. neoformans. Thus a negative serum Cryptococcus assay does not rule out infection by species of Cryptococcus other than neoformans. Fungal culture or India ink preparations are the best way to demonstrate C. albidus in both serum and CSF (2).
The treatment for C. albidus is not well defined. Amphotericin B has been modestly effective in the treatment of C. albidus (3,4). In our patient, a dose of 0.6 mg/kg daily of Amphotericin B for two weeks followed by six weeks of oral Itraconazole was used. The total dose of Amphotericin B used in this instance was substantially shorter than in other cases of C. albidus infection with a resultant diminution of treatment toxicity. This antibiotic regimen proved to be successful and no further recurrences of C. albidus occurred.
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