Candida tropicalis: its prevalence, pathogenicity and increasing resistance to fluconazole

被引:219
作者
Kothavade, Rajendra J. [1 ]
Kura, M. M. [2 ,3 ]
Valand, Arvind G. [3 ,4 ]
Panthaki, M. H. [5 ,6 ]
机构
[1] EPCOR, Microbiol Sect, WQA Lab, Edmonton, AB T5K 0S5, Canada
[2] Grant Med Coll, Dept Dermatol, Bombay 400008, Maharashtra, India
[3] Sir JJ Grp Hosp, Bombay 400008, Maharashtra, India
[4] Grant Med Coll, Dept Pathol, Bombay 400008, Maharashtra, India
[5] Sir HN Hosp, Dept Immunocytobiol & Pathol, Bombay 400004, Maharashtra, India
[6] Med Res Ctr, Bombay 400004, Maharashtra, India
关键词
CHRONIC MUCOCUTANEOUS CANDIDIASIS; LIVER-TRANSPLANT RECIPIENTS; FUNGAL-INFECTIONS; AZOLE RESISTANCE; RISK-FACTORS; PHOSPHOLIPASE-ACTIVITY; MOLECULAR MECHANISMS; VAGINAL CANDIDIASIS; CLINICAL SPECIMENS; AMPHOTERICIN-B;
D O I
10.1099/jmm.0.013227-0
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Candida tropicalis has been identified as the most prevalent pathogenic yeast species of the Candida-non-albicans group. Historically, Candida albicans has been the major species responsible for causing candidiasis in immunocompromised and immunocompetent patients. However, infections (candidiasis) due to C. tropicalis have increased dramatically on a global scale thus proclaiming this organism to be an emerging pathogenic yeast. The reasons for this organism's dominance and its resistance to fluconazole have been difficult to elucidate. In addition, the mechanism of this organism's pathogenicity and the consequent immune response remain to be clarified. This paper describes certain predisposing factors potentially responsible for these characteristics and presents a 'root cause analysis' to explain the increasing prevalence of C. tropicalis in developed and undeveloped countries, as well as the organism's acquired drug resistance. Control measures against fluconazole resistance in clinical management have also been discussed.
引用
收藏
页码:873 / 880
页数:8
相关论文
共 66 条
  • [1] Brief exposure to antimycotics reduces the extracellular phospholipase activity of Candida albicans and Candida tropicalis
    Anil, S
    Samaranayake, LP
    [J]. CHEMOTHERAPY, 2003, 49 (05) : 243 - 247
  • [2] [Anonymous], ANTIFUNGAL DRUG THER
  • [3] BORG M, 1990, J MED VET MYCOL, V28, P3
  • [4] The expression of the secreted aspartyl proteinases Sap4 to Sap6 from Candida albicans in murine macrophages
    Borg-von Zepelin, M
    Beggah, S
    Boggian, K
    Sanglard, D
    Monod, M
    [J]. MOLECULAR MICROBIOLOGY, 1998, 28 (03) : 543 - 554
  • [5] Mechanisms of azole resistance in petite mutants of Candida glabrata
    Brun, S
    Bergès, T
    Poupard, P
    Vauzelle-Moreau, C
    Renier, G
    Chabasse, D
    Bouchara, JP
    [J]. ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, 2004, 48 (05) : 1788 - 1796
  • [6] BUESCHING WJ, 1979, J CLIN MICROBIOL, V9, P565
  • [7] MUCOSAL AND SYSTEMIC CANDIDIASIS IN CONGENITALLY IMMUNODEFICIENT MICE
    CANTORNA, MT
    BALISH, E
    [J]. INFECTION AND IMMUNITY, 1990, 58 (04) : 1093 - 1100
  • [8] CLARK RA, 1995, J ACQ IMMUN DEF SYND, V9, P43
  • [9] Epidemiology, risk factors, and outcomes of Candida albicans versus non-albicans candidemia in nonneutropenic patients
    Davis, Susan L.
    Vazquez, Jose A.
    McKinnon, Peggy S.
    [J]. ANNALS OF PHARMACOTHERAPY, 2007, 41 (04) : 568 - 573
  • [10] Disseminated Candida tropicalis in a patient with chronic mucocutaneous candidiasis
    Dixon, TC
    Steinbach, WJ
    Benjamin, DK
    Williams, LW
    Myers, LA
    [J]. SOUTHERN MEDICAL JOURNAL, 2004, 97 (08) : 788 - 790