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Volume 8, Number 4—April 2002

Candida dubliniensis Infection, Singapore

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To the Editor: We read with interest the letter by Marriott et al. (1) describing the first case of Candida dubliniensis fungemia in Australia.

We report the first two cases of C. dubliniensis infection in Singapore. We have been using the API 20C AUX on all yeast isolates from blood, sterile fluids, and tissue to screen for C. dubliniensis since May 2000. To our knowledge, this infection has not been previously reported from a Southeast Asian country.

The first patient was a 49-year-old woman with adult polycystic kidney and liver disease; she had mild chronic renal failure and a past history of nephrotic syndrome. She was admitted to the renal unit on May 9, 2001, for management of ascites. A septic workup showed leukocytosis (34.67 x 109/L) with predominance of neutrophils (95%). Blood culture received on May 31 grew yeast with two slightly different forms, one large and one small. The isolates, investigated separately, were germ-tube positive. The API 20C AUX profile for the larger isolate was 6072114 at 48 hours’ incubation (96.2% certainty for C. dubliniensis) and 6072134 for the smaller isolate (99.8% certainty for C. dubliniensis). The yeasts grew well on potato dextrose agar at 35°C but poorly at 42°C and 45°C. In addition, electrophoretic karyotyping with pulsed-field gel electrophoresis showed that both isolates had identical patterns, with eight chromosome fragments, one of which was <1 megabase (Mb), indicating that the two morphologically different strains were the same karyotypically. The pattern obtained was in keeping with results obtained by Jabra-Rizk et al. (2), with C. dubliniensis showing a chromosome-sized band of <1 Mb. For C. albicans, by contrast, all bands were >1 Mb. Five control strains—C. dubliniensis (RCPA Microbiology QAP item 2001:2:7A), C. albicans ATCC 90028, and three clinical strains of C. albicans—were also run together with the two strains; the results obtained were consistent with those of Jabra-Rizk et al. (2). The MIC of the isolates to fluconazole by E-test was 0.75 μg/mL, indicating susceptibility. Disseminated intravascular coagulopathy due to sepsis from a possible ruptured liver cyst developed in the patient. Despite broad-spectrum antibiotics and amphotericin B, hemodialysis, and intensive-care support, she died 5 weeks after admission. Except for C. dubliniensis candidemia, Candida species isolated from the urine and endotracheal secretions (speciation not done), and Acinetobacter baumannii (cultured from the endotracheal secretions and femoral catheter tip), no other important microorganisms were isolated. Peritoneal fluid cultures did not yield any microorganisms.

Soon after the first case, C. dubliniensis was isolated from a sputum culture and bronchial alveolar lavage cultures from a 50-year-old Chinese woman, who had myelodysplastic syndrome and was hospitalized for pneumonia. She had been previously treated with chemotherapy and had multiple admissions for infection. The same phenotypic and karyotypic methods as the first patient were used to identify the isolate. The API 20C AUX profile was 2152134 at 48 hours (98.5% certainty for C. dubliniensis). The MIC of fluconazole by E-test was also 0.75 μg/mL. Pancytopenia developed, and the patient’s condition deteriorated. She died of pneumonia despite transfusions and treatment with broad-spectrum antibiotics and amphotericin B. Microbiologic investigations for bacteria, tuberculosis, pneumocystis, Legionella, and viruses did not yield positive results except for Corynebacterium species in the bronchial alveolar lavage fluid.

Although C. dubliniensis was first associated with oral candidiasis in HIV-infected persons (3), several reports now link the organism to non-HIV patients who were immunosuppressed due to chemotherapy, hematologic malignancy (4), and end-stage liver disease (1). Our two patients were not HIV positive but were immunosuppressed. In vitro susceptibility results showed that our patients should have responded to the usual antifungal treatment. However, they died despite appropriate therapy.



We acknowledge David Ellis for help in confirming the isolates.


Ai Ling Tan, Grace CY Wang, and Yoon Wan Chiu
Author affiliations: Singapore General Hospital, Singapore;



  1. Marriott  D, Laxton  M, Harkness  J. Candida dubliniensis candidemia in Australia. Emerg Infect Dis. 2001;7:479.PubMedGoogle Scholar
  2. Jabra-Rizk  MA, Baqui  AAMA, Kelley  JI, Falkler  WA Jr, Merz  WG, Meiller  TF. Identification of Candida dubliniensis in a prospective study of patients in the United States. J Clin Microbiol. 1999;37:3216.PubMedGoogle Scholar
  3. Sullivan  DJ, Westermemg  TJ, Haynes  KA, Bennett  DE, Coleman  DC. Candida dubliniensis sp. nov.: phenotypic and molecular characterization of a novel species associated with oral candidiasis in HIV-infected individuals. Microbiology. 1995;141:150721.PubMedGoogle Scholar
  4. Meis  JFGM, Ruhnke  M, DePauw  BE, Odds  FC, Siegert  W, Verweij  PE. Candida dubliniensis candidemia in patients with chemotherapy-induced neutropenia and bone marrow transplantation. Emerg Infect Dis. 1999;5:1503.PubMedGoogle Scholar


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DOI: 10.3201/eid0804.010423

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Table of Contents – Volume 8, Number 4—April 2002

Page created: July 15, 2010
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