全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

Epidemiology and Virulence Determinants including Biofilm Profile of Candida Infections in an ICU in a Tertiary Hospital in India

DOI: 10.1155/2014/303491

Full-Text   Cite this paper   Add to My Lib

Abstract:

The purpose of this prospective study was to isolate, speciate, and determine antifungal susceptibility and virulence patterns of Candida species recovered from the intensive care units (ICUs) in an Indian hospital. Study included 125 medical/postoperative patients admitted to ICU. Identification and speciation of yeast isolates were done by the biochemical methods. Antifungal susceptibility was done by broth microdilution method. Virulence testing of Candida species was done by phospholipase, proteinase, and adherence assay. A total of 103 Candida isolates were isolated; C. tropicalis was the predominant species (40.7%), followed by C. albicans (38.83 %), C. glabrata (11.65%), C. parapsilosis (3.88%), and 1.94% each of C. krusei, C. kefyr, and C. sphaerica. 60 Candida isolates (58.25%) showed resistance to fluconazole, while 7 (6.7%) isolates showed resistance to amphotericin B. Phospholipase and proteinase activities were seen in 73.8% and 55.3% Candida isolates with different species showing a wide range of activities, while 68.9% Candida isolates showed {4+} adherence activity. The present study revealed that nonalbicans Candida species (NAC spp.) caused most of the cases of Candidemia in the ICU patients. The isolation of C. tropicalis from a large number of cases highlights the ability of this pathogen to cause bloodstream infections. The presence of azole resistance is a matter of concern. 1. Introduction Fungal infections are emerging as a problem of significant magnitude in hospitals during the last decade, especially in the ICUs, which are epicenters for infections such as Candidemia and invasive Candida infection (ICI). The escalating problem in ICUs is probably due to an increasing population of immunocompromised patients. A survey of the epidemiology of sepsis conducted in USA revealed that the incidence of fungal sepsis increased threefold between 1979 and 2000 [1]. Fungal infections account for nearly 8% of all nosocomial infections; Candida is the responsible agent in 80% of the cases [2]. Candida species are approximately the fourth most common cause of nosocomial infections in ICUs, according to data from the National Nosocomial Infections Surveillance System and the European Prevalence of Infection in Intensive Care [3]. Critically ill patients who are treated in the ICUs are very susceptible to infections due to acquired defects in host defense mechanisms from the immunosuppressive effect of the underlying disease, recent surgery, trauma, and concurrent drug therapy. Infections occur in 15–40% of all ICU admissions and central venous

References

[1]  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.
[2]  J. E. Edwards Jr., “Invasive Candida infections: evolution of a fungal pathogen,” The New England Journal of Medicine, vol. 324, no. 15, pp. 1060–1062, 1991.
[3]  C. M. Beck-Sague and W. R. Jarvis, “Secular trends in the epidemiology of nosocomial fungal infections in the United States, 1980–1990,” Journal of Infectious Diseases, vol. 167, no. 5, pp. 1247–1251, 1993.
[4]  V. Mohandas and M. Ballal, “Biofilm as virulence marker in Candida isolated from blood,” World Journal of Medical Sciences, vol. 2, no. 1, pp. 46–48, 2007.
[5]  J. H. Shin, S. J. Kee, M. G. Shin et al., “Biofilm production by isolates of Candida species recovered from nonneutropenic patients: comparison of bloodstream isolates with isolates from other sources,” Journal of Clinical Microbiology, vol. 40, no. 4, pp. 1244–1248, 2002.
[6]  P. Eggimann, J. Garbino, and D. Pittet, “Management of Candida species infections in critically ill patients,” The Lancet Infectious Diseases, vol. 3, no. 12, pp. 772–785, 2003.
[7]  E. W. Koneman, S. D. Allen, W. M. Janda, et al., “Mycology,” in Color Atlas and Textbook of Diagnostic Microbiology, pp. 983–1057, Lippincott Williams and Wilkins, Philadelphia, Pa, USA, 5th edition, 1997.
[8]  Clinical and Laboratory Standards Institute, “Reference method for broth dilution antifungal susceptibility testing of yeasts, Approved Standard—third edition,” CLSI Document M27-A3, Clinical and Laboratory Standards Institute (CLSI), 2008.
[9]  V. Mohandas and M. Ballal, “Proteinase and phospholipase activity as virulence factors in Candida species isolated from blood,” Revista Iberoamericana de Micologia, vol. 25, no. 4, pp. 208–210, 2008.
[10]  Y. H. Samaranayake, R. S. Dassanayake, J. A. M. S. Jayatilake et al., “Phospholipase B enzyme expression is not associated with other virulence attributes in Candida albicans isolates from patients with human immunodeficiency virus infection,” Journal of Medical Microbiology, vol. 54, no. 6, pp. 583–593, 2005.
[11]  M. L. Branchini, M. A. Pfaller, J. Rhine-Chalberg, T. Frempong, and H. D. Isenberg, “Genotypic variation and slime production among blood and catheter isolates of Candida parapsilosis,” Journal of Clinical Microbiology, vol. 32, no. 2, pp. 452–456, 1994.
[12]  G. P. Dureja, “Nosocomial Infections in Intensive Care Unit: a study,” Hospital Today, vol. 11, pp. 695–699, 2001.
[13]  J. Freeman and J. E. McGonan Jr., “Methodological issues in hospital epidemiology: rates, core finding and interpretation,” Reviews of Infectious Diseases, vol. 3, pp. 668–677, 1981.
[14]  E. R. M. Sydnor and T. M. Perl, “Hospital epidemiology and infection control in acute-care settings,” Clinical Microbiology Reviews, vol. 24, no. 1, pp. 141–173, 2011.
[15]  P. H. Chandrasekar, J. A. Kruse, and M. F. Mathews, “Nosocomial infection among patients in different types of intensive care units at a city hospital,” Critical Care Medicine, vol. 14, no. 5, pp. 508–510, 1986.
[16]  A. Chakrabarti, K. Singh, and S. Das, “Changing face of nosocomial Candidemia,” Indian Journal of Medical Microbiology, vol. 17, pp. 160–166, 1999.
[17]  I. Xess, N. Jain, F. Hasan, P. Mandal, and U. Banerjee, “Epidemiology of candidemia in a tertiary care centre of North India: 5-year study,” Infection, vol. 35, no. 4, pp. 256–259, 2007.
[18]  R. I. Singh, I. Xess, P. Mathur, B. Behera, B. Gupta, and M. C. Misra, “Epidemiology of candidaemia in critically ill trauma patients: experiences of a level I trauma centre in North India,” Journal of Medical Microbiology, vol. 60, no. 3, pp. 342–348, 2011.
[19]  R. J. Kothavade, M. M. Kura, A. G. Valand, and M. H. Panthaki, “Candida tropicalis: its prevalence, pathogenicity and increasing resistance to fluconazole,” Journal of Medical Microbiology, vol. 59, no. 8, pp. 873–880, 2010.
[20]  M. Bassetti, E. Righi, A. Costa, et al., “Epidemiological trends in nosocomial candidemia in intensive care,” BMC Infectious Diseases, vol. 6, article 21, 2006.
[21]  S. Giri and A. J. Kindo, “A review of Candida species causing blood stream infection,” International Journal of Medical Microbiology, vol. 30, no. 3, pp. 270–278, 2012.
[22]  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.
[23]  P. M. Punithavathy, K. Nalina, and T. Menon, “Antifungal susceptibility testing of Candida tropicalis biofilms against fluconazole using calorimetric indicator resazurin,” Indian Journal of Pathology and Microbiology, vol. 55, no. 1, pp. 72–74, 2012.
[24]  S. C. Deorukhkar and S. Saini, “Species distribution and antifungal susceptibility profile of Candida species isolated from blood stream infections,” Journal of Evolution of Medical and Dental Sciences, vol. 1, no. 3, pp. 241–249, 2012.
[25]  A. Kothari and V. Sagar, “Epidemiology of Candida bloodstream infections in a tertiary care institute in India,” Indian Journal of Medical Microbiology, vol. 27, no. 2, pp. 171–172, 2009.
[26]  C. P. G. Kumar, T. Sundararajan, T. Menon, and M. Venkatadesikalu, “Candidosis in children with onco-hematological diseases in Chennai, South India,” Japanese Journal of Infectious Diseases, vol. 58, no. 4, pp. 218–221, 2005.
[27]  J. F. Ernst and A. Schmidt, Dimorphism in Human Pathogenic and A Pathogenic Yeasts, S. Karger AG, Basel, Switzerland, 2000.
[28]  O. Abaci and A. Haliki-Uztan, “Investigation of the susceptibility of Candida species isolated from denture wearers to different antifungal antibiotics,” African Journal of Microbiology Research, vol. 5, no. 12, pp. 1398–1403, 2011.
[29]  V. Mohandas and M. Ballal, “Distribution of Candida Species in different clinical samples and their virulence: biofilm formation, proteinase and phospholipase production: a study on hospitalized patients in Southern India,” Journal of Global Infectious Diseases, vol. 3, no. 1, pp. 4–8, 2011.
[30]  S. S. A. Al-Nedaithy, “Spectrum and proteinase production of yeasts causing vaginitis in Saudi Arabian women,” Medical Science Monitor, vol. 8, no. 7, pp. CR498–CR501, 2002.
[31]  M. F. Price, I. D. Wilkinson, and L. O. Gentry, “Plate method for detection of phospholipase activity in Candida albicans,” Sabouraudia Journal of Medical and Veterinary Mycology, vol. 20, no. 1, pp. 7–14, 1982.
[32]  T. Wu, L. P. Samaranayake, B. Y. Cao, and J. Wang, “In-vitro proteinase production by oral Candida albicans isolates from individuals with and without HIV infection and its attenuation by antimycotic agents,” Journal of Medical Microbiology, vol. 44, no. 4, pp. 311–316, 1996.
[33]  A. S. Ibrahim, F. Mirbod, S. G. Filler et al., “Evidence implicating phospholipase as a virulence factor of Candida albicans,” Infection and Immunity, vol. 63, no. 5, pp. 1993–1998, 1995.
[34]  M. Negri, M. Martins, M. Henriques, T. I. E. Svidzinski, J. Azeredo, and R. Oliveira, “Examination of potential virulence factors of Candida tropicalis clinical isolates from hospitalized patients,” Mycopathologia, vol. 169, no. 3, pp. 175–182, 2010.
[35]  A. D. Júnior Jr., A. F. Silva, F. C. Rosa, S. G. Monteiro, P. de Maria Silva Figueiredo, and C. de Andrade Monteiro, “In vitro diferential activity of phospholipases and acid proteinases of clinical isolates of Candida,” Revista da Sociedade Brasileira de Medicina Tropical, vol. 44, no. 3, pp. 334–338, 2011.
[36]  F. Hasan, I. Xess, X. Wang, N. Jain, and B. C. Fries, “Biofilm formation in clinical Candida isolates and its association with virulence,” Microbes and Infection, vol. 11, no. 8-9, pp. 753–761, 2009.
[37]  A. K. Pathak, S. Sharma, and P. Shrivastva, “Multi-species biofilm of Candida albicans and non-Candida albicans Candida species on acrylic substrate,” Journal of Applied Oral Science, vol. 20, no. 1, pp. 70–75, 2012.
[38]  A. Kumar, V. C. Thakur, S. Thakur, et al., “Phenotypic characterization and in vitro examination of potential virulence factors of Candida species isolated from blood stream infection,” World Journal of Science and Technology, vol. 1, no. 10, pp. 38–42, 2011.
[39]  S. P. Hawser and L. J. Douglas, “Biofilm formation by Candida species on the surface of catheter materials in vitro,” Infection and Immunity, vol. 62, no. 3, pp. 915–921, 1994.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133