AJR 2001; 177:721
© American Roentgen Ray Society
A Fungus by Another Name
Candida glabrata
Lisa Corrente and
Michael A. Sadler
St. Vincent's Hospital and Medical Center New York, NY
10011
Fungemia is a well-described and often life-threatening complication in the
patient with a compromised immune system. Systemic blood cultures most often
grow Candida albicans
[1]. The emergence of
non—Candida albicans species, such as Candida
glabrata, are of increasing concern for the medical community
[2]. Candida species,
except C. glabrata (also referred to as Torulopsis
glabrata), appear in tissue as both yeast and pseudohyphae. In any single
lesion, only one form may be present. With C. glabrata, only yeast
cells are present. Visceral lesions are characterized by necrosis and a
neutrophilic inflammatory response. Neutrophils kill Candida yeast
cells and damage segments of pseudohyphae in vitro, and visceral candidiasis
complicates neutropenia, suggesting a major role for the neutrophil in host
defense against this fungus. Visceral lesions show a preference for kidney,
brain, spleen, heart, eye, and liver
[3]. C. glabrata is
now considered the second most common cause of fungal sepsis
[1]. We report a patient with
C. glabrata sepsis presenting with splenic involvement on CT scans.
To our knowledge, this entity has not been previously described in the
radiology literature.
A 35-year-old HIV-positive woman presented with pancreatitis and diabetic
ketoacidosis. The patient showed signs of sepsis on admission through the
emergency department and underwent emergent IV contrastenhanced CT of the
abdomen and pelvis. This study (not shown) was consistent with pancreatitis,
and no splenic lesions were identified. The patient continued to develop
complications associated with sepsis for a period of 3 months after her
emergency admission. Subsequent complaints of abdominal pain prompted the
performance of a repeated CT scanning of the abdomen and pelvis. The findings
revealed a single low-attenuation lesion within a spleen of normal size
(Fig. 3A). An infectious cause
for this lesion could not be excluded. On an empirical basis, broad-spectrum
antibiotic therapy and amphotericin B (AmBisome; Fujisawa, Deerfield, IL) were
administered. Shortly thereafter, blood cultures grew C.
glabrata.
A follow-up contrast-enhanced CT scan of the abdomen and pelvis obtained 2
weeks later showed interval improvement of the low-attenuation splenic lesion.
The antifungal sensitivities to C. glabrata were reviewed, and the
medication was changed to itraconazole (Sporanox; Janssen, Titusville, NJ).
Treatment was continued on the basis of the CT findings because blood cultures
failed to provide evidence of C. glabrata. Four weeks after the
administration of antifungal therapy, another CT scan showed resolution of the
splenic lesion (Fig. 3B). After
multiple repeated negative blood cultures and significant clinical
improvement, the patient was discharged with itraconazole medication.
C. glabrata must be considered in all patients with compromised
immune systems who are not responding to empiric antifungal therapy.
References
-
Nguyen MH, Peacock JE, Morris AJ, et al. The changing face of
candidemia: emergence of non Candida albicans species and antifungal
resistance. Am J Med
1996;100:617
-623[Medline]
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Darwin P, Mergner W, Thuluvath P. Torulopsis glabrata
fungemia as a complication of a clotted transjugular intrahepatic
portosystemic shunt. Liver Transpl Surg
1998;4:89
-90[Medline]
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Bennett JH. Candidiasis. In: Isselbacher KJ, Braunwald E, Wilson
JD, Martin JB, Fauci AS, Kasper DL, eds. Harrison's Principles of
Internal Medicine. New York: McGraw-Hill,
1994: 860-861
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