From 1997 to 2009, 1,862 dermatology, gynaecology, and paediatrics (DGP) associated clinical yeast isolates were analysed for species occurrence, specimen origin and type, (multi-) resistance pattern, and testing period. The top seven of the isolated DGP-associated species remained the same as compared to total medical wards, with Candida albicans (45%) as most frequent pathogen. However, the DGP wards and DGP ICUs showed species-specific profiles; that is, the species distribution is clinic-specific similar and however differs in their percentage from ward to ward. By applying the “one fungus one name” principle, respectively, the appropriate current taxonomic species denominations, it has been shown that no trend to emerging species from 1998 to 2008 could be detected. In particular the frequently isolated non-Candida albicans species isolated in the DGP departments have already been detected in or before 1997. As yeasts are part of the cutaneous microbiota and play an important role as opportunistic pathogens for superficial infections, proper identification of the isolates according to the new nomenclature deems to be essential for specific and calculated antifungal therapy for yeast-like DGP-related infectious agents. 1. Introduction Superficial fungal infections are often chronic and recurring. It has been estimated that approximately 15% of the population has fungal infections of the skin (tinea pedis or athlete’s foot) or nails (onychomycosis) or of the feet. These infections are common in older children and adults [1]. Distal subungual, proximal, subungual, and white superficial onychomycoses are usually caused by dermatophytes, but Candida spp. may be present in all types in less than 1% of these cases [2]. In the past, yeasts are thought to be simply skin contaminants [3]; however, yeasts and nondermatophyte moulds may also cause toenail onychomycosis [4–8]. A higher proportion of yeasts is generally found in onychomycosis, where dermatophytes (68%), yeasts (29%), and moulds (3%) are the most causative fungal pathogens [9]. Some Candida spp. causing onychomycosis were reported to be partly resistant to oral antifungal agents (AFAs). In patients with chronic mucocutaneous infections, the main yeast pathogen is Candida (C.) albicans, but C. tropicalis, C parapsilosis, Issatchenkia (I.) orientalis, and Meyerozyma (M.) guilliermondii may also contribute to these infections [10]. It has been suggested by Clayton and Noble [11] that the spread of yeasts in the hospital ward occurs in a similar way to the spread of Staphylococcus aureus. In
References
[1]
J. C. Gentles and E. G. V. Evans, “Foot infections in swimming baths,” British Medical Journal, vol. 3, no. 5874, pp. 260–262, 1973.
[2]
T. J. Zuber and K. Baddam, “Superficial fungal infection of the skin: where and how it appears help determine therapy,” Postgraduate Medicine, vol. 109, no. 1, pp. 117–132, 2001.
[3]
M. A. Ghannoum, R. A. Hajjeh, R. Scher et al., “A large-scale North American study of fungal isolates from nails: the frequency of onychomycosis, fungal distribution, and antifungal susceptibility patterns,” Journal of the American Academy of Dermatology, vol. 43, no. 4, pp. 641–648, 2000.
[4]
M. M. Walshe and M. P. English, “Fungi in nails,” British Journal of Dermatology, vol. 78, no. 4, pp. 198–207, 1966.
[5]
S. L. Noble, R. C. Forbes, and P. L. Stamm, “Diagnosis and management of common tinea infections,” American Family Physician, vol. 58, no. 1, pp. 163–174, 1998.
[6]
A. K. Gupta and M.-J. Ricci, “Diagnosing onychomycosis,” Dermatologic Clinics, vol. 24, no. 3, pp. 365–369, 2006.
[7]
M. R. Vander Straten, M. A. Hossain, and M. A. Ghannoum, “Cutaneous infections dermatophytosis, onychomycosis, and tinea versicolor,” Infectious Disease Clinics of North America, vol. 17, no. 1, pp. 87–112, 2003.
[8]
E. G. V. Evans, “Resistance of Candida species to antifungal agents used in the treatment of onychomycosis: a review of current problems,” British Journal of Dermatology, Supplement, vol. 141, no. 56, pp. 33–35, 1999.
[9]
C. Mügge, U.-F. Haustein, and P. Nenoff, “Causative agents of onychomycosis—a retrospective study,” Journal der Deutschen Dermatologischen Gesellschaft, vol. 4, no. 3, pp. 218–228, 2006 (German).
[10]
M. A. Hossain and M. A. Ghannoum, “New developments in chemotherapy for non-invasive fungal infections,” Expert Opinion on Investigational Drugs, vol. 10, no. 8, pp. 1501–1511, 2001.
[11]
Y. M. Clayton and W. C. Noble, “Observations on the epidemiology of Candida albicans,” Journal of Clinical Pathology, vol. 19, no. 1, pp. 76–78, 1966.
[12]
W. C. Noble, “The contribution of individual patients to the spread of infection,” British Journal of Dermatology, vol. 85, no. 1, pp. 24–29, 1971.
[13]
D. A. Somerville, “Yeasts in a hospital for patients with skin diseases,” Journal of Hygiene, vol. 70, no. 4, pp. 667–675, 1972.
[14]
M. A. Slavin and A. Chakrabarti, “Opportunistic fungal infections in the Asia-Pacific region,” Medical Mycology, Early Online, pp. 1–8, 2011.
[15]
S. N. Leaw, H. C. Chang, R. Barton, J.-P. Bouchara, and T. C. Chang, “Identification of medically important Candida and non-Candida yeast species by an oligonucleotide array,” Journal of Clinical Microbiology, vol. 45, no. 7, pp. 2220–2229, 2007.
[16]
E. M. Johnson, “Rare and emerging Candida species,” Current Fungal Infection Reports, vol. 3, no. 3, pp. 152–159, 2009.
[17]
M. H. Miceli, J. A. Díaz, and S. A. Lee, “Emerging opportunistic yeast infections,” The Lancet Infectious Diseases, vol. 11, no. 2, pp. 142–151, 2011.
[18]
P. Vandeputte, S. Ferrari, and A. T. Coste, “Antifungal resistance and new strategies to control fungal infections,” International Journal of Microbiology, vol. 2012, Article ID 713687, 26 pages, 2012.
[19]
M. Ruhnke, “Epidemiology of Candida albicans infections and role of non-Candida albicans yeasts,” Current Drug Targets, vol. 7, no. 4, pp. 495–504, 2006.
[20]
S. K. Fridkin, “The changing face of fungal infections in health care settings,” Clinical Infectious Diseases, vol. 41, no. 10, pp. 1455–1460, 2005.
[21]
A. K. Paswan, D. C. Raju, D. K. Singh, S. Khuba, and R. K. Dubey, “Isolation and distribution of Candida species among different clinical situations in critically ill patients: prospective study,” International Journal of Biomedical Research, vol. 3, pp. 120–126, 2012.
[22]
J. H. Meurman, E. Siikala, M. Richardson, and R. Rautema, “Non-Candida albicansCandida yeast of the oral cavity,” Communicating Current Research and Educational Topics and Trends in Applied Microbiology, 2007, http://www.formatex.org/microbio/pdf/pages719-731.pdf.
[23]
F. Gallè, M. Sanguinetti, G. Colella et al., “Oral candidosis: characterization of a sample of recurrent infections and study of resistance determinants,” New Microbiologica, vol. 34, no. 4, pp. 379–389, 2011.
[24]
J. B. Varkey and J. R. Perfect, “Rare and emerging fungal pulmonary infections,” Seminars in Respiratory and Critical Care Medicine, vol. 29, no. 2, pp. 121–131, 2008.
[25]
C. Seebacher, C. D. Abeck, J. Brasch, et al., “Candidiasis of the skin,” Journal der Deutschen Dermatologischen Gesellschaft, vol. 4, pp. 591–596, 2006 (German).
[26]
N. S. Ryder, S. Wagner, and I. Leitner, “In vitro activities of terbinafine against cutaneous isolates of Candida albicans and other pathogenic yeasts,” Antimicrobial Agents and Chemotherapy, vol. 42, no. 5, pp. 1057–1061, 1998.
[27]
A. K. Gupta, E. A. Cooper, J. E. Ryder, K. A. Nicol, M. Chow, and M. M. Chaudhry, “Optimal management of fungal infections of the skin, hair, and nails,” American Journal of Clinical Dermatology, vol. 5, no. 4, pp. 225–237, 2004.
[28]
J. M. Achkar and B. C. Fries, “Candida infections of the genitourinary tract,” Clinical Microbiology Reviews, vol. 23, no. 2, pp. 253–273, 2010.
[29]
J. F. Fisher, “Candida urinary tract infections—epidemiology, pathogenesis, diagnosis, and treatment: executive summary,” Clinical Infectious Diseases, vol. 52, no. 6, pp. S429–S432, 2011.
[30]
P. Fournier, C. Schwebel, D. Maubon et al., “Antifungal use influences Candida species distribution and susceptibility in the intensive care unit,” Journal of Antimicrobial Chemotherapy, vol. 66, no. 12, pp. 2880–2886, 2011.
[31]
K. M. Butler and C. J. Baker, “Candida: an increasingly important pathogen in the nursery,” Pediatric Clinics of North America, vol. 35, no. 3, pp. 543–563, 1988.
[32]
D. A. Kaufman, “Challenging issues in neonatal candidiasis,” Current medical research and opinion, vol. 26, no. 7, pp. 1769–1778, 2010.
[33]
A. Diana, M. Epiney, M. Ecoffey, and R. E. Pfister, “White dots on the placenta and red dots on the baby”: congential cutaneous candidiasis—a rare disease of the neonate,” Acta Paediatrica, International Journal of Paediatrics, vol. 93, no. 7, pp. 996–999, 2004.
[34]
D. K. Benjamin Jr., B. J. Stoll, M. G. Gantz et al., “Neonatal candidiasis: epidemiology, risk factors, and clinical judgment,” Pediatrics, vol. 126, no. 4, pp. e865–e873, 2010.
[35]
J. Robinson, “Fungal skin infections in children,” Nursing Standard, vol. 27, pp. 52–54, 2012.
[36]
G. Yousef Ali, E. Hussein, S. S. Algohary, K. Ahmed Rashed, M. Almoghanum, and A. AbdelRahman Khalifa, “Prevalence of Candida colonization in preterm newborns and VLBW in neonatal intensive care unit: role of maternal colonization as a risk factor in transmission of disease,” Journal of Maternal-Fetal and Neonatal Medicine, vol. 25, pp. 789–795, 2012.
[37]
J. E. Baley, R. M. Kliegman, B. Boxerbaum, and A. A. Fanaroff, “Fungal colonization in the very low birth weight infant,” Pediatrics, vol. 78, no. 2, pp. 225–232, 1986.
[38]
K. N. Smolinski, S. S. Shah, P. J. Honig, and A. C. Yan, “Neonatal cutaneous fungal infections,” Current Opinion in Pediatrics, vol. 17, no. 4, pp. 486–493, 2005.
[39]
K. H. Abu-Elteen and M. A. Hamad, “Changing epidemiology of classical and emerging fungal infections: a review,” Jordan Journal of Biological Sciences, vol. 5, pp. 215–230, 2012.
[40]
S. P. DaVeiga, “Epidemiology of atopic dermatitidis: a review,” Allergy and Asthma Proceedings, vol. 33, pp. 227–234, 2012.
[41]
H. C. Williams, “Epidemiology of human atopic dermatitis—seven areas of notable progress and seven areas of notable ignorance,” Veterinary Dermatology, vol. 24, pp. 3-9.e1–3-9.e2, 2013.
[42]
A. Zinkeviciene, N. Vaiciulioniene, I. Baranauskiene, V. Kvedariene, R. Emuzyte, and D. Citavicius, “Cutaneous yeast microflora in patients with atopic dermatitis,” Central European Journal of Medicine, vol. 6, no. 6, pp. 713–719, 2011.
[43]
H. R. Ashbee and E. G. V. Evans, “Immunology of diseases associated with Malassezia species,” Clinical Microbiology Reviews, vol. 15, no. 1, pp. 21–57, 2002.
[44]
S. M. Yim, J. Y. Kim, J. H. Ko, Y. W. Lee, Y. B. Choe, and K. J. Ahn, “Molecular analysis of malassezia microflora on the skin of the patients with atopic dermatitis,” Annals of Dermatology, vol. 22, no. 1, pp. 41–47, 2010.
[45]
A. F. Schmalreck, M. Lackner, K. Becker, W. Fegeler, V. Czaika, and C. L. Florl, “Phylogenetic relationship matters-antifungal susceptibility among clinically relevant yeast-like fungi,” accepted by AAC for publication.
[46]
V. Czaika, P. Nenoff, A. Gl？ckner, K. Becker, W. Fegeler, and A. F. Schmalreck, “Epidemiology and changes in patient-related factors from 1997 until 2009 in clinical yeast isolates related to dermatology, gynaecology, and paediatrics,” International Journal of Microbiology, vol. 2013, Article ID 703905, 2013.
A. F. Schmalreck, B. Willinger, G. Haase et al., “Species and susceptibility distribution of 1062 clinical yeast isolates to azoles, echinocandins, flucytosine and amphotericin B from a multi-centre study,” Mycoses, vol. 55, no. 3, pp. e124–e137, 2012.
[50]
A. F. Schmalreck, “Empfindlichkeitsprüfung von Fluconazol: Auswertung einer Multizenter-Studie der Arbeitsgemeinschaft “Klinische Mykologie” der Deutschsprachigen Mykologischen Gesellschaft,” Mycoses, vol. 39, supplement 2, pp. 1–11, 1998 (German).
[51]
Rationale für Bewertungskriterien für minimale Hemmkonzentrationen (MHK) und Hemmzonendurchmesser (HZD) von Fluconazol entsprechend DIN 58940 bei klinisch relevanten Sprosspilzen, sowie Festlegung von Fluconazol-(Grenz)-Kontrollwerten für Kontrollst？mme, vol. 157 of DIN-Fachbericht, DIN-Fachbericht, Beuth, Berlin, Germany, 2007, (German).
[52]
J. M. McNeill, F. R. Barrie, W. R. Buck, et al., Eds., International Code of Nomenclature for Algae, Fungi, and Plants (Melbourne Code) Adopted by the Eighteens International Botanical Congress Melbourne, Australia, A.R.G. Ganter, Ruggell, 2012, http://www.imafungus.org/Issue/31/22.pdf.
[53]
L. L. Norvell, “Melbourne approves a new code,” Mycotaxon, vol. 116, pp. 481–490, 2011.
[54]
M. D. Richardson, “Changing patterns and trends in systemic fungal infections,” Journal of Antimicrobial Chemotherapy, vol. 56, no. 1, pp. i5–i11, 2005.
[55]
S. Giri and A. J. Kindo, “A review of Candida species causing blood stream infection,” Indian Journal of Medical Microbiology, vol. 30, pp. 270–278, 2012.
[56]
M. A. Pfaller, L. N. Woosley, S. A. Messer, R. N. Jones, and M. Castanheira, “Significance of molecular identification and antifungal susceptibility of clinically significant yeasts and moulds in a global antifungal surveillance program,” Mycopathologia, vol. 174, pp. 259–271, 2012.
[57]
I. Miranda-Zapico, E. Eraso, J. L. Hernández-Almaraz et al., “Prevalence and antifungal susceptibility patterns of new cryptic species inside the species complexes Candida parapsilosis and Candida glabrata among blood isolates from a Spanish tertiary hospital,” Journal of Antimicrobial Chemotherapy, vol. 66, no. 10, Article ID dkr298, pp. 2315–2322, 2011.
[58]
K. Alby and R. J. Bennett, “Sexual reproduction in the Candida clade: cryptic cycles, diverse mechanisms, and alternative functions,” Cellular and Molecular Life Sciences, vol. 67, no. 19, pp. 3275–3285, 2010.
[59]
A. Tragiannidis, W. Fegeler, G. Rellensmann et al., “Candidaemia in a European Paediatric University Hospital: a 10-year observational study,” Clinical Microbiology and Infection, vol. 18, no. 2, pp. E27–E30, 2012.
[60]
K. Paredes, D. A. Sutton, J. Cano et al., “Molecular identification and antifungal susceptibility testing of clinical isolates of the Candida rugosa species complex and proposal of the new species Candida neorugosa,” Journal of Clinical Microbiology, vol. 50, pp. 2397–2403, 2012.
[61]
G. Morace, E. Borghi, R. Latta, et al., “Antifungal susceptibility of invasive yeast isolates in Italy: the GIIA3 study in critically ill patients,” BMC Infectious Diseases, vol. 11, p. 130, 2011.
[62]
M. A. Pfaller, D. J. Diekema, D. L. Gibbs et al., “Results from the artemis disk global antifungal surveillance study, 1997 to 2007: a 10.5-year analysis of susceptibilities of Candida species to fluconazole and voriconazole as determined by CLSI standardized disk diffusion,” Journal of Clinical Microbiology, vol. 48, no. 4, pp. 1366–1377, 2010.
[63]
M. B.-V. Zepelin, L. Kunz, R. Rüchel, U. Reichard, M. Weig, and U. Gro？, “Epidemiology and antifungal susceptibilities of Candida spp. to six antifungal agents: results from a surveillance study on fungaemia in Germany from July 2004 to August 2005,” Journal of Antimicrobial Chemotherapy, vol. 60, no. 2, pp. 424–428, 2007.
[64]
R. Fleck, A. Dietz, and H. Hof, “In vitro susceptibility of Candida species to five antifungal agents in a German university hospital assessed by the reference broth microdilution method and Etest,” Journal of Antimicrobial Chemotherapy, vol. 59, no. 4, pp. 767–771, 2007.
[65]
C. Lass-Fl？rl, “The changing face of epidemiology of invasive fungal disease in Europe,” Mycoses, vol. 52, no. 3, pp. 197–205, 2009.
[66]
A. C. Rodloff, D. Koch, and R. Schaumann, “Epidemiology and antifungal resistance in invasive candidiasis,” European Journal of Medical Research, vol. 16, no. 4, pp. 187–195, 2011.
[67]
P. Billie and J. Marchetti, “Diagnosis of invasive candidiasis in the ICU,” Annals of Intensive Care, vol. 1, p. 37, 2011.
[68]
O. Leroy, J.-P. Gangneux, P. Montravers et al., “Epidemiology, management, and risk factors for death of invasive Candida infections in critical care: a multicenter, prospective, observational study in France (2005-2006),” Critical Care Medicine, vol. 37, no. 5, pp. 1612–1618, 2009.
[69]
G. Ece, P. Samlioglu, G. Akkoclu, S. Atalay, and S. Kose, “The evaluation of the distribution of yeast like fungi,” International Journal of Medical Sciences, vol. 9, pp. 617–620, 2012.
[70]
C. Paulo, C. Mour？o, P. M. Veiga et al., “Retrospective analysis of clinical yeast isolates in a hospital in the centre of Portugal: spectrum and revision of the identification procedures,” Medical Mycology, vol. 47, no. 8, pp. 836–844, 2009.
[71]
C. Geffers and P. Gastmeier, “Nosocomial infections and multidrug-resistant organisms in Germany: epidemiological data from KISS (The Hospital Infection Surveillance System),” ？rzteblatt International, vol. 108, no. 6, pp. 87–93, 2011 (German).
[72]
O. Marchetti, J. Bille, U. Fluckiger et al., “Epidemiology of candidemia in Swiss tertiary care hospitals: secular trends, 1991–2000,” Clinical Infectious Diseases, vol. 38, no. 3, pp. 311–320, 2004.
[73]
M. H. Nguyen, J. E. Peacock Jr., A. J. Morris et al., “The changing face of candidemia: emergence of non-Candida albicans species and antifungal resistance,” American Journal of Medicine, vol. 100, no. 6, pp. 617–623, 1996.
[74]
R. Latha, R. Sasikala, N. Muruganandam, and R. Venkatesh Babu, “Study on the shifting patterns of non Candida albicans Candida in lower respiratory tract infections and evaluation of the CHROM agar in identification of the Candida species,” Journal of Microbiology and Biotechnology Research, vol. 1, pp. 113–119, 2011.
[75]
M. Bassetti, E. Righi, A. Costa et al., “Epidemiological trends in nosocomial candidemia in intensive care,” BMC Infectious Diseases, vol. 6, 2006.
[76]
M. Méan, O. Marchetti, and T. Calandra, “Bench-to-bedside review: Candida infections in the intensive care unit,” Critical Care, vol. 12, no. 1, article 204, 2008.
[77]
O. Romeo and G. Criseo, “Molecular epidemiology of Candida albicans and its closely related yeasts Candida dubliniensis and Candida africana,” Journal of Clinical Microbiology, vol. 47, no. 1, pp. 212–214, 2009.
[78]
R. Gumral, B. Sancak, A. B. Guzel, M. A. Sara？li, and M. Ilkit, “Lack of Candida africana and Candida dubliniensis in Vaginal Candida albicans Isolates in Turkey using HWP1 gene polymorphisms,” Mycopathologia, vol. 172, no. 1, pp. 73–76, 2011.
[79]
N. E. Nnadi, G. M. Ayanbimpe, F. Scordino et al., “Isolation and molecular characterization of Candida africana from Jos, Nigeria,” Mycology, vol. 50, pp. 765–757, 2012.
[80]
H.-J. Tietz, M. Hopp, A. Schmalreck, W. Sterry, and V. Czaika, “Candida africana sp. nov., a new human pathogen or a variant of Candida albicans?” Mycoses, vol. 44, no. 11-12, pp. 437–445, 2001.
[81]
A. Forche, G. Sch？nian, Y. Gr？ser, R. Vilgalys, and T. G. Mitchell, “Genetic structure of typical and atypical populations of Candida albicans from Africa,” Fungal Genetics and Biology, vol. 28, no. 2, pp. 107–125, 1999.
[82]
A. F. Schmalreck, P. Tr？nkle, E. Vanca, and R. Blaschke-Hellmessen, “Differenzierung und Charakterisierung von humanpathogenen Hefen (Candida albicans, Exophiala dermatitidis) und tierpathogenen Algen (Prototheca spp.) mittels Fourier-Transform-Infrarot-Spektroskopie (FT-IR) im Vergleich zu konventionellen Methoden,” Mycoses, vol. 41, supplement 1, pp. 71–77, 1998.
[83]
H. Hof, U. Eigner, T. Maier, and P. Staib, “Differentiation of Candida dubliniensis from Candida albicans by means of MALDI-TOF mass spectrometry,” Clinical Laboratory, vol. 58, pp. 927–931, 2012.
[84]
A. M. Borman, A. Szekely, and E. M. Johnson EM, “Epidemiology, antifungal susceptibility and pathogenicity of Candida africana isolates from the United Kingdom,” Journal of Clinical Microbiology, vol. 51, Article ID 233035, pp. 967–972, 2013.
[85]
O. Romeo and G. Criseo, “First molecular method for discriminating between Candida africana, Candida albicans, and Candida dubliniensis by using hwp1 gene,” Diagnostic Microbiology and Infectious Disease, vol. 62, no. 2, pp. 230–233, 2008.
[86]
R. Alonso-Vargas, L. Elorduy, E. Eraso et al., “Isolation of Candida africana, probable atypical strains of Candida albicans, from a patient with vaginitis,” Medical Mycology, vol. 46, no. 2, pp. 167–170, 2008.
[87]
F. Leliaert, D. R. Smith, H. Moreau et al., “Phylogeny and molecular evolution of the green algae,” Critical Reviews in Plant Sciences, vol. 31, no. 1, pp. 1–46, 2012.
[88]
C. Lass-Fl？rl and A. Mayr, “Human protothecosis,” Clinical Microbiology Reviews, vol. 20, no. 2, pp. 230–242, 2007.
[89]
U. Roesler, A. M？ller, A. Hensel, D. Baumann, and U. Truyen, “Diversity within the current algal species Prototheca zopfii: a proposal for two Prototheca zopfii genotypes and description of a novel species, Prototheca blaschkeae sp. nov,” International Journal of Systematic and Evolutionary Microbiology, vol. 56, no. 6, pp. 1419–1425, 2006.
[90]
A. Kalinowska-Pujdak, A. Schmalreck, U.-F. Haustein, and P. Nenoff, “Species differentiation of yeasts of the genus Malassezia with Fourier transform infrared spectroscopy,” Hautarzt, vol. 57, no. 2, pp. 127–136, 2006 (German).
[91]
V. Petry, F. Tanhausen, L. Weiss, T. Milan, A. Mezzari, and M. B. Weber, “Identification of Malassezia yeast species isolated from patients with pityriasis versicolor,” Anais Brasileiros de Dermatologia, vol. 86, no. 4, pp. 803–806, 2011.
[92]
H. K. Park, M.-H. Ha, S.-G. Park, M. N. Kim, B. J. Kim, and W. Kim, “Characterization of the fungal microbiota (mycobiome) in healthy and dandruff-afflicted human scalps,” PLoS ONE, vol. 7, no. 2, Article ID e32847, 2012.
[93]
E. Zhang, T. Sugita, R. Tsuboi, T. Yamazaki, and K. Makimura, “The opportunistic yeast pathogen Trichosporon asahii colonizes the skin of healthy individuals: analysis of 380 healthy individuals by age and gender using a nested polymerase chain reaction assay,” Microbiology and Immunology, vol. 55, no. 7, pp. 483–488, 2011.
[94]
B. Ozhak-Baysan, D. Ogunc, D. Colak et al., “Distribution and antifungal susceptibility of Candida species causing nosocomial candiduria,” Medical Mycology, vol. 50, pp. 529–532, 2012.
[95]
W. Mendling and J. Brasch, “Guideline vulvovaginal candidosis (2010) of the german society for gynecology and obstetrics, the working group for infections and infectimmunology in gynecology and obstetrics, the german society of dermatology, the board of german dermatologists and the german speaking mycological society,” Mycoses, vol. 55, no. 3, pp. 1–13, 2012.
[96]
E. M. Kojic and R. O. Darouiche, “Candida infections of medical devices,” Clinical Microbiology Reviews, vol. 17, no. 2, pp. 255–267, 2004.
[97]
C. Von Eiff, B. Jansen, W. Kohnen, and K. Becker, “Infections associated with medical devices: pathogenesis, management and prophylaxis,” Drugs, vol. 65, no. 2, pp. 179–214, 2005.
[98]
G. Ramage, R. Rajendran, L. Sherry, and C. Williams, “Fungal biofilm resistance,” International Journal of Microbiology, vol. 2012, Article ID 528521, 14 pages, 2012.
[99]
B. Havlickova, V. A. Czaika, and M. Friedrich, “Epidemiological trends in skin mycoses worldwide,” Mycoses, vol. 51, no. 4, pp. 2–15, 2008.
