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Candidemia in adults: Epidemiology, microbiology, and pathogenesis

Candidemia in adults: Epidemiology, microbiology, and pathogenesis
Author:
Jose A Vazquez, MD, FACP, FIDSA
Section Editor:
Carol A Kauffman, MD
Deputy Editor:
Keri K Hall, MD, MS
Literature review current through: Jan 2024.
This topic last updated: Jun 10, 2022.

INTRODUCTION — Candidemia refers to presence of Candida species in the blood. Candida in a blood culture should never be viewed as a contaminant and should prompt evaluation for metastatic infection [1].

Issues related to the epidemiology and pathogenesis of candidemia will be reviewed here. The clinical manifestations, diagnosis, and treatment of candidemia as well as an overview of Candida infections are presented separately. (See "Clinical manifestations and diagnosis of candidemia and invasive candidiasis in adults" and "Management of candidemia and invasive candidiasis in adults" and "Overview of Candida infections".)

EPIDEMIOLOGY — Candidiasis is an increasingly important nosocomial infection in both adults and children, especially those who are cared for in intensive care units (ICUs) [2-11]. (See "Intravascular catheter-related infection: Epidemiology, pathogenesis, and microbiology".)

In most cases, the infecting strain is part of the host's endogenous flora; however, nosocomial acquisition of Candida species also occurs [8].

The organism has spread via contaminated solutions in some cases [8], whereas the hands of health care workers were the probable source in others.

Risk factors for candidemia — Patients at highest risk for development of candidemia include those receiving intensive care and those who are immunocompromised. In some areas of the United States, increasing rates of candidemia among people who inject drugs have been observed [12].

Intensive care — Patients in ICUs account for the greatest number of episodes of candidemia in most hospitals. Surgical units, especially those caring for trauma and burn patients, and neonatal units have the highest rates of Candida infections. Besides the risks associated with the extremes of age and trauma or burns, other factors include [3,9]:

●Central venous catheters

●Total parenteral nutrition

●Broad-spectrum antibiotics

●High APACHE scores

●Acute renal failure, particularly if requiring hemodialysis

●Prior surgery, particularly abdominal surgery

●Gastrointestinal tract perforations and anastomotic leaks

●Pancreatitis

In a prospective multicenter study of 300 ICU patients in France with proven invasive candidiasis, C. albicans was the most common species isolated (57 percent), followed by C. glabrata (17 percent), C. parapsilosis (8 percent), C. krusei (5 percent), and C. tropicalis (5 percent) [13]. In a subsequent study among ICU patients in Europe, North America, Latin America, and Asia, C. albicans was more common (70 percent) than non-albicans species; however, this varied by geographic region, with Latin America demonstrating a higher proportion of non-albicans isolates [14].

Risk factors for candidemia with non-albicans Candida species were assessed in a retrospective case-comparator study of patients with candidemia (non-albicans Candida compared with C. albicans) in the medical and surgical ICUs of two tertiary care hospitals in the United States from 1995 to 2005 [15]. Two significant risk factors for candidemia with non-albicans species were identified on multivariate analysis:

●Fluconazole exposure (odds ratio [OR] 11.6, 95% CI 2.3-58.9)

●Central venous catheter exposure (OR 2.0, 95% CI 1.1-3.5)

A subsequent prospective cohort study that included 179 episodes of ICU-acquired candidemia showed that prior gastrointestinal surgery and systemic antifungal exposure were independently significant variables that were associated with bloodstream infection with both non-albicans Candida species and potentially fluconazole-resistant Candida species [4].

In another prospective cohort study that included 154 cases of ICU-acquired candidemia in non-neutropenic patients, independent risk factors for C. glabrata infection included age >60 years, recent abdominal surgery, interval from ICU admission to first positive blood culture ≤7 days, recent cephalosporin use, solid tumor, and absence of diabetes mellitus [16].

A subsequent 2017 CDC surveillance study performed in 9 states reported that the estimated incidence of candidemia was 7 cases per 100,000 people [17]. Among 1122 Candida isolates submitted, C. albicans accounted for 38 percent, followed by C. glabrata (30 percent), C. parapsilosis (14 percent), and C. tropicalis (7 percent). Thus, non-albicans Candida isolates constituted 51 percent of isolates. Only 6 percent of all Candida isolates were resistant to fluconazole; the highest rates were in C. glabrata (7 percent) and C. parapsilosis (9 percent). This study also documented a low rate (2 percent) of resistance to echinocandin antifungals, most of which occurred in C. glabrata.

These findings may help determine initial empiric therapy for candidemia since patients with non-albicans Candida infection are more likely to have a fluconazole-resistant isolate than those with C. albicans infection. (See "Management of candidemia and invasive candidiasis in adults".)

Immunosuppression — Immunocompromised patients are at special risk for candidemia [9,18]. High-risk groups include:

●Those with hematologic malignancies

●Recipients of solid organ or hematopoietic stem cell transplants

●Those given chemotherapeutic agents, especially those associated with extensive gastrointestinal mucosal damage

Neutropenia is common in these settings, and most transplant recipients are also receiving glucocorticoids as well as several immunosuppressants. Other risk factors include broad-spectrum antibiotics and central venous catheters. However, because of the frequent use of azole or echinocandin prophylaxis in patients with chemotherapy-related neutropenia and after hematopoietic stem cell transplant, candidemia has become less common in these populations.

The proportion of Candida infections caused by non-albicans Candida species has been rising at many medical centers that care for patients with hematologic malignancies [18,19]. In a retrospective study of 635 patients with candidemia at a cancer center from 1993 to 2003, C. glabrata and C. krusei were the most common causes of candidemia, accounting for 31 and 24 percent of episodes in patients with hematologic malignancy. However, in solid organ transplant recipients, only 18 and 2 percent were caused by these species, respectively. On multivariate analysis, fluconazole prophylaxis was a risk factor for both C. glabrata and C. krusei candidemia, neutropenia was a risk factor for all candidemias, and central venous catheter–related infection was a risk factor for C. parapsilosis candidemia [18].

A large study from 13 European cancer centers that surveyed 145,030 admissions from 2005 to 2009 documented candidemia in 267 patients who had cancer [20]. An equal proportion of episodes were due to C. albicans and non-albicans Candida species, of which the most common were C. tropicalis, C. glabrata, and C. parapsilosis. The proportion of C. glabrata isolates was highest in patients with solid tumors, whereas C. tropicalis and C. krusei were the most common species isolated from patients who had hematologic malignancies or had received a hematopoietic stem cell transplants, respectively.

These findings have important implications for the empiric treatment of candidemia in patients with hematologic malignancy. (See "Management of candidemia and invasive candidiasis in adults".)

Injection drug use — In patients with candidemia who lack typical candidemia risk factors, especially in those who are 19 to 44 years of age and have community-associated candidemia, injection drug use is an important risk factor [12]. In 2017, the CDC conducted population-based surveillance of candidemia in nine states; an increase in the rate of candidemia associated with injection drug use was observed in some counties [12]. Candida endocarditis, a rare complication of candidemia, is strongly associated with intravenous drug use [21,22].

Host factors — Host-specific polymorphisms in toll-like receptors and cytokine pathways likely play a role in determining development of infection with Candida species [9,23,24].

COVID-19-associated candidemia — Given that patients at highest risk for candidemia include those receiving intensive care, it is not surprising that severe COVID-19 is a risk factor for developing candidemia. In a study of 148 ICU patients with COVID-19, 28 (19 percent) developed candidemia and the likelihood increased as the number of days in the ICU increased (50 percent by day 30 of their ICU stay) [25]. In a population-based candidemia surveillance study, 64 (25 percent) of 251 candidemic patients had COVID-19, and candidemia in these cases was largely attributable to receipt of mechanical ventilation and treatment with corticosteroids, immunomodulatory medications, or renal replacement therapy [26]. Antibiotic treatment prior to the diagnosis of candidemia was common, occurring in over 85 percent of cases [25,26]. All-cause mortality for COVID-19 patients with candidemia has ranged from 62 to 84 percent.

MICROBIOLOGY

Prevalence of Candida species — C. albicans has been the predominant bloodstream isolate; however, over the past decade, non-albicans Candida species have been recovered in as many as half of cases [13,27-30].

In a multicenter surveillance study conducted in the United States between 2004 and 2008, 54 percent of 2019 bloodstream isolates represented non-albicans Candida spp and 46 percent represented C. albicans [29]. C. glabrata was responsible for 26 percent of all cases of candidemia, followed by C. parapsilosis (16 percent), C. tropicalis (8 percent), and C. krusei (3 percent).

In one review of Candida species isolated from patients with invasive candidiasis between 2009 and 2017, there was no increase in non-albicans Candida isolates causing invasive disease; C. albicans remained the most common species, accounting for 48 percent of isolates [31]. C. glabrata remained the second-most common species (24 percent) followed by C. parapsilosis (11 percent) and C. tropicalis (7 percent). Other unusual species constituted only 6 percent of isolates.

The incidence of each species varies in different patient populations and geographic regions [29,32-36]. As an example, in Latin America, the most common species to cause bloodstream infection after C. albicans are C. parapsilosis and C. tropicalis, with C. glabrata being isolated much less frequently [32,34,35].

Knowing the prevalence of the non-albicans Candida species is important because susceptibility to antifungal agents varies among the species. As an example, all isolates of C. krusei are fluconazole resistant, and an increasing proportion of C. glabrata are both fluconazole and voriconazole resistant. Additionally, resistance to fluconazole has been found in a small proportion of isolates of C. albicans, C. parapsilosis, and C. tropicalis [37]. Echinocandin resistance among C. glabrata isolates has been reported with increasing frequency from some medical centers, but has not been universally observed [38-40]. (See "Management of candidemia and invasive candidiasis in adults".)

It is postulated that isolation of non-albicans Candida species is related to the selective pressure associated with fluconazole use [41], and some studies provide strong evidence for this association [41-43]. In addition to azole use, there are other factors, such as echinocandin use [43], geography [30,42], age [33], and perhaps other issues [44], that contribute to these trends.

C. auris emergence

●Epidemiology − In 2016, the United States Centers for Disease Control and Prevention (CDC) and Public Health England issued warnings about the emergence of a multidrug-resistant Candida species, C. auris [45,46]. This pathogen has caused invasive health care-associated infections, and it has been associated with high mortality rates [45]. This species was first described in 2009 in Japan [47], but, based upon retrospective testing of isolate collections, the earliest known infections occurred in 1996 in South Korea [48]. It has been detected in >30 countries and has been associated with outbreaks at health care facilities [49-56]. New cases continue to be detected.

Molecular typing suggests that the isolates are highly related within each country or region but distinct between continents [57-60]. In the United States, epidemiologic links have been found among most cases [61,62]. Whole-genome sequencing analysis suggests that there have been multiple introductions of C. auris into the United States from other continents (South Asia, South America), followed by local transmission.

In the United States, cases have been reported from multiple states, with most cases occurring in New York City, New Jersey, and Chicago, Illinois [54,63]. Information about reported cases can be found on the CDC's website.

●Risk factors – Risk factors for C. auris infection include underlying medical conditions and extensive exposure to health care facilities (particularly high-acuity skilled nursing facilities such as facilities providing mechanical ventilation) [61].

●Outbreaks – A number of C. auris outbreaks have been described.

•In September 2018, public health authorities in southern California initiated a proactive C. auris surveillance program by pursuing species identification for Candida isolates recovered from urine isolates in patients hospitalized in long-term acute care facilities [64]. The first case of C. auris was identified in February 2019; subsequently, point prevalence surveys at 17 facilities identified a total of 182 cases. Gaps in hand hygiene, transmission-based precautions, and environmental cleaning were identified and addressed; the outbreak was contained to two facilities by October 2019. These findings demonstrate the utility of enhanced laboratory surveillance as well as the importance of public health oversight to reduce the risk for nosocomial C. auris transmission.

•An outbreak of C. auris (including candidemia and central nervous system device-associated infection) in a neurologic ICU in the United Kingdom between 2015 and 2017 was associated with reusable skin-surface axillary temperature probes that had been cleaned with wipes containing quaternary ammonium compound (which has poor activity against Candida species) [65]. The incidence of new cases was reduced after removal of the temperature probes.

●Sites of involvement – C. auris has been cultured from the following sites: blood, urine, respiratory tract, bile, wounds, and central venous catheter tips [61].

●Diagnosis – C. auris requires specialized methods for identification; it could be misidentified as another yeast (most commonly C. haemulonii, but also C. famata, C. sake, C. catenulata, unspecified Candida species, Rhodotorula glutinis, and Saccharomyces cerevisiae) when using traditional biochemical methods [49,50]. (See "Clinical manifestations and diagnosis of candidemia and invasive candidiasis in adults".)

●Treatment – Antifungal susceptibility patterns and treatment recommendations are discussed separately. (See "Management of candidemia and invasive candidiasis in adults".)

●Infection control and prevention – Given concerns about resistance and transmission of C. auris in health care facilities, there are special screening recommendations and infection control precautions for patients who are colonized or infected with C. auris [66,67]. These can be found on the CDC's website.

PATHOGENESIS — There are three major routes by which Candida gain access to the bloodstream:

●Through the gastrointestinal tract mucosal barrier

●Via an intravascular catheter

●From a localized focus of infection, such as pyelonephritis

Gastrointestinal tract — Translocation through the gastrointestinal tract mucosa is probably the most common mechanism for Candida species to enter the bloodstream in both neutropenic patients and in intensive care unit patients. Candida species are part of the normal bowel microbiota; many of the factors noted above lead to overgrowth of yeasts and subsequent egress out of the bowel into the blood. Chemotherapeutic agents that disrupt the intestinal mucosa (mucositis) play a major role in allowing Candida to escape from the bowel in patients with hematologic malignancies [68]. (See "Neutropenic enterocolitis (typhlitis)".)

Intravascular catheters — Intravascular catheters, especially central venous catheters, continue to be an important source for Candida bloodstream infection [3,4,8]. Candida colonization of indwelling vascular devices, especially central catheters, can occur at either the insertion site or the hub and lead to subsequent candidemia. (See "Intravascular catheter-related infection: Epidemiology, pathogenesis, and microbiology".)

Total parenteral nutrition (TPN) is an important risk factor for candidemia. Although the mechanism by which TPN increases the risk of candidemia is not well understood, one in vitro study suggested that the lipid emulsion present in TPN solutions may increase the biofilm formation on the silicone-elastomer catheters and supports growth of C. albicans.

Localized focus — Bloodstream invasion is relatively uncommon from a localized focus of infection but has been well described with ascending Candida urinary tract infection associated with either intrinsic obstruction (eg, from a fungus ball) or extrinsic compression preventing the flow of infected urine. (See "Candida infections of the bladder and kidneys".)

Colonization — Colonization with Candida species is almost always a necessary prerequisite for candidemia and invasive candidiasis. However, colonization alone does not predict which patients will develop fungemia. Other risk factors, as noted above, are needed in addition to colonization. Most patients with Candida colonization and known risk factors do not develop candidemia or invasive candidiasis. (See 'Risk factors for candidemia' above.)

SUMMARY

●Candida in a blood culture should never be viewed as a contaminant and should always prompt a search for the source of the fungemia. For many patients, candidemia is a manifestation of disseminated candidiasis, whereas for others it reflects colonization of an indwelling intravenous catheter and subsequent introduction into the bloodstream. (See 'Introduction' above.)

●Candidiasis is an increasingly important nosocomial infection in both adults and children, especially those who are cared for in intensive care units (ICUs). (See 'Epidemiology' above.)

●Although the infecting strain is most often part of the host's endogenous flora, nosocomial acquisition of Candida species has been described. (See 'Epidemiology' above.)

●Non-albicans species of Candida account for approximately half of all bloodstream and invasive candidiasis infections. Most prominent have been C. glabrata and C. parapsilosis, followed by C. tropicalis and C. krusei. All C. krusei are fluconazole resistant, and an increasing proportion of C. glabrata are both fluconazole and voriconazole resistant. In addition, echinocandin resistance among C. glabrata isolates is being reported with increasing frequency from certain medical centers. (See 'Prevalence of Candida species' above.)

●In 2016, the United States Centers for Disease Control and Prevention and Public Health England issued warnings about the emergence of a multidrug-resistant Candida species, C. auris. It has been detected in >30 countries and has been associated with outbreaks at health care facilities. New cases continue to be detected. (See 'C. auris emergence' above.)

●Patients in the ICU and those who are immunocompromised (eg, patients with hematologic malignancies, patients with coronavirus disease 2019 [COVID-19], solid organ and hematopoietic stem cell transplant recipients) are at greatest risk for the development of candidemia. Host-specific polymorphisms in toll-like receptors and cytokine pathways likely play a role in determining development of infection with Candida species. (See 'Risk factors for candidemia' above.)

●There are three major routes by which Candida gain access to the bloodstream: through the gastrointestinal tract mucosal barrier, via an intravascular catheter, and from a localized focus of infection, such as pyelonephritis. (See 'Pathogenesis' above.)

●Translocation via the lymphatics through the gastrointestinal tract mucosa is probably the most common mechanism for Candida species to enter the bloodstream in both immunocompromised patients (eg, those receiving chemotherapy who are neutropenic) and in ICU patients. Candida species are part of the normal bowel microbiota; many factors lead to overgrowth of yeasts and subsequent egress out of the bowel into the blood. Chemotherapeutic agents that disrupt the intestinal mucosa play a major role in allowing Candida to escape from the bowel in patients with hematologic malignancies. (See 'Gastrointestinal tract' above.)

●Intravascular catheters, especially central venous catheters, continue to be an important source for Candida bloodstream infection. Candida colonization of indwelling vascular devices, especially central catheters, can occur at either the insertion site or the hub and lead to subsequent candidemia. (See 'Intravascular catheters' above.)

●Colonization with Candida species is almost always a necessary prerequisite for candidemia and invasive candidiasis. However, colonization alone does not predict which patients will develop fungemia. Other risk factors are needed in addition to colonization. Even with risk factors and colonization with Candida species, most patients do not become candidemic. (See 'Colonization' above.)

  1. Fridkin SK. The changing face of fungal infections in health care settings. Clin Infect Dis 2005; 41:1455.
  2. Wisplinghoff H, Bischoff T, Tallent SM, et al. Nosocomial bloodstream infections in US hospitals: analysis of 24,179 cases from a prospective nationwide surveillance study. Clin Infect Dis 2004; 39:309.
  3. Chow JK, Golan Y, Ruthazer R, et al. Risk factors for albicans and non-albicans candidemia in the intensive care unit. Crit Care Med 2008; 36:1993.
  4. Playford EG, Marriott D, Nguyen Q, et al. Candidemia in nonneutropenic critically ill patients: risk factors for non-albicans Candida spp. Crit Care Med 2008; 36:2034.
  5. Playford EG, Nimmo GR, Tilse M, Sorrell TC. Increasing incidence of candidaemia: long-term epidemiological trends, Queensland, Australia, 1999-2008. J Hosp Infect 2010; 76:46.
  6. Zaoutis TE, Argon J, Chu J, et al. The epidemiology and attributable outcomes of candidemia in adults and children hospitalized in the United States: a propensity analysis. Clin Infect Dis 2005; 41:1232.
  7. Arendrup MC, Fuursted K, Gahrn-Hansen B, et al. Semi-national surveillance of fungaemia in Denmark 2004-2006: increasing incidence of fungaemia and numbers of isolates with reduced azole susceptibility. Clin Microbiol Infect 2008; 14:487.
  8. Pfaller MA, Diekema DJ. Epidemiology of invasive candidiasis: a persistent public health problem. Clin Microbiol Rev 2007; 20:133.
  9. Kullberg BJ, Arendrup MC. Invasive Candidiasis. N Engl J Med 2015; 373:1445.
  10. Kollef M, Micek S, Hampton N, et al. Septic shock attributed to Candida infection: importance of empiric therapy and source control. Clin Infect Dis 2012; 54:1739.
  11. León C, Alvarez-Lerma F, Ruiz-Santana S, et al. Fungal colonization and/or infection in non-neutropenic critically ill patients: results of the EPCAN observational study. Eur J Clin Microbiol Infect Dis 2009; 28:233.
  12. Zhang AY, Shrum S, Williams S, et al. The Changing Epidemiology of Candidemia in the United States: Injection Drug Use as an Increasingly Common Risk Factor-Active Surveillance in Selected Sites, United States, 2014-2017. Clin Infect Dis 2020; 71:1732.
  13. Leroy O, Gangneux JP, Montravers P, 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). Crit Care Med 2009; 37:1612.
  14. Kett DH, Azoulay E, Echeverria PM, et al. Candida bloodstream infections in intensive care units: analysis of the extended prevalence of infection in intensive care unit study. Crit Care Med 2011; 39:665.
  15. Chow JK, Golan Y, Ruthazer R, et al. Factors associated with candidemia caused by non-albicans Candida species versus Candida albicans in the intensive care unit. Clin Infect Dis 2008; 46:1206.
  16. Cohen Y, Karoubi P, Adrie C, et al. Early prediction of Candida glabrata fungemia in nonneutropenic critically ill patients. Crit Care Med 2010; 38:826.
  17. Tsay SV, Mu Y, Williams S, et al. Burden of Candidemia in the United States, 2017. Clin Infect Dis 2020; 71:e449.
  18. Hachem R, Hanna H, Kontoyiannis D, et al. The changing epidemiology of invasive candidiasis: Candida glabrata and Candida krusei as the leading causes of candidemia in hematologic malignancy. Cancer 2008; 112:2493.
  19. Pfaller MA, Diekema DJ, Rinaldi MG, et al. Results from the ARTEMIS DISK Global Antifungal Surveillance Study: a 6.5-year analysis of susceptibilities of Candida and other yeast species to fluconazole and voriconazole by standardized disk diffusion testing. J Clin Microbiol 2005; 43:5848.
  20. Cornely OA, Gachot B, Akan H, et al. Epidemiology and outcome of fungemia in a cancer Cohort of the Infectious Diseases Group (IDG) of the European Organization for Research and Treatment of Cancer (EORTC 65031). Clin Infect Dis 2015; 61:324.
  21. Sankar NP, Thakarar K, Rokas KE. Candida Infective Endocarditis During the Infectious Diseases and Substance Use Disorder Syndemic: A Six-Year Case Series. Open Forum Infect Dis 2020; 7:ofaa142.
  22. Morelli MK, Veve MP, Lorson W, Shorman MA. Candida spp. infective endocarditis: Characteristics and outcomes of twenty patients with a focus on injection drug use as a predisposing risk factor. Mycoses 2021; 64:181.
  23. Johnson MD, Plantinga TS, van de Vosse E, et al. Cytokine gene polymorphisms and the outcome of invasive candidiasis: a prospective cohort study. Clin Infect Dis 2012; 54:502.
  24. Plantinga TS, Johnson MD, Scott WK, et al. Toll-like receptor 1 polymorphisms increase susceptibility to candidemia. J Infect Dis 2012; 205:934.
  25. Arastehfar A, Ünal N, Hoşbul T, et al. Candidemia Among Coronavirus Disease 2019 Patients in Turkey Admitted to Intensive Care Units: A Retrospective Multicenter Study. Open Forum Infect Dis 2022; 9:ofac078.
  26. Seagle EE, Jackson BR, Lockhart SR, et al. The Landscape of Candidemia During the Coronavirus Disease 2019 (COVID-19) Pandemic. Clin Infect Dis 2022; 74:802.
  27. Almirante B, Rodríguez D, Cuenca-Estrella M, et al. Epidemiology, risk factors, and prognosis of Candida parapsilosis bloodstream infections: case-control population-based surveillance study of patients in Barcelona, Spain, from 2002 to 2003. J Clin Microbiol 2006; 44:1681.
  28. Messer SA, Jones RN, Fritsche TR. International surveillance of Candida spp. and Aspergillus spp.: report from the SENTRY Antimicrobial Surveillance Program (2003). J Clin Microbiol 2006; 44:1782.
  29. Horn DL, Neofytos D, Anaissie EJ, et al. Epidemiology and outcomes of candidemia in 2019 patients: data from the prospective antifungal therapy alliance registry. Clin Infect Dis 2009; 48:1695.
  30. Colombo AL, de Almeida Júnior JN, Slavin MA, et al. Candida and invasive mould diseases in non-neutropenic critically ill patients and patients with haematological cancer. Lancet Infect Dis 2017; 17:e344.
  31. Ricotta EE, Lai YL, Babiker A, et al. Invasive Candidiasis Species Distribution and Trends, United States, 2009-2017. J Infect Dis 2021; 223:1295.
  32. Nucci M, Queiroz-Telles F, Tobón AM, et al. Epidemiology of opportunistic fungal infections in Latin America. Clin Infect Dis 2010; 51:561.
  33. Diekema DJ, Messer SA, Brueggemann AB, et al. Epidemiology of candidemia: 3-year results from the emerging infections and the epidemiology of Iowa organisms study. J Clin Microbiol 2002; 40:1298.
  34. Pfaller MA, Moet GJ, Messer SA, et al. Geographic variations in species distribution and echinocandin and azole antifungal resistance rates among Candida bloodstream infection isolates: report from the SENTRY Antimicrobial Surveillance Program (2008 to 2009). J Clin Microbiol 2011; 49:396.
  35. Colombo AL, Guimarães T, Silva LR, et al. Prospective observational study of candidemia in São Paulo, Brazil: incidence rate, epidemiology, and predictors of mortality. Infect Control Hosp Epidemiol 2007; 28:570.
  36. Fortún J, Martín-Dávila P, Gómez-García de la Pedrosa E, et al. Emerging trends in candidemia: a higher incidence but a similar outcome. J Infect 2012; 65:64.
  37. Oxman DA, Chow JK, Frendl G, et al. Candidaemia associated with decreased in vitro fluconazole susceptibility: is Candida speciation predictive of the susceptibility pattern? J Antimicrob Chemother 2010; 65:1460.
  38. Alexander BD, Johnson MD, Pfeiffer CD, et al. Increasing echinocandin resistance in Candida glabrata: clinical failure correlates with presence of FKS mutations and elevated minimum inhibitory concentrations. Clin Infect Dis 2013; 56:1724.
  39. Castanheira M, Woosley LN, Messer SA, et al. Frequency of fks mutations among Candida glabrata isolates from a 10-year global collection of bloodstream infection isolates. Antimicrob Agents Chemother 2014; 58:577.
  40. Lewis JS 2nd, Wiederhold NP, Wickes BL, et al. Rapid emergence of echinocandin resistance in Candida glabrata resulting in clinical and microbiologic failure. Antimicrob Agents Chemother 2013; 57:4559.
  41. Abbas J, Bodey GP, Hanna HA, et al. Candida krusei fungemia. An escalating serious infection in immunocompromised patients. Arch Intern Med 2000; 160:2659.
  42. Cuenca-Estrella M, Rodriguez D, Almirante B, et al. In vitro susceptibilities of bloodstream isolates of Candida species to six antifungal agents: results from a population-based active surveillance programme, Barcelona, Spain, 2002-2003. J Antimicrob Chemother 2005; 55:194.
  43. Lortholary O, Desnos-Ollivier M, Sitbon K, et al. Recent exposure to caspofungin or fluconazole influences the epidemiology of candidemia: a prospective multicenter study involving 2,441 patients. Antimicrob Agents Chemother 2011; 55:532.
  44. Lin MY, Carmeli Y, Zumsteg J, et al. Prior antimicrobial therapy and risk for hospital-acquired Candida glabrata and Candida krusei fungemia: a case-case-control study. Antimicrob Agents Chemother 2005; 49:4555.
  45. Centers for Disease Control and Prevention. Clinical Alert to U.S. Healthcare Facilities - Global Emergence of Invasive Infections Caused by the Multidrug-Resistant Yeast Candida auris. https://www.cdc.gov/fungal/diseases/candidiasis/candida-auris-alert.html (Accessed on July 08, 2016).
  46. Public Health England. Candida auris identified in England. https://www.gov.uk/government/publications/candida-auris-emergence-in-england/candida-auris-identified-in-england (Accessed on July 08, 2016).
  47. Satoh K, Makimura K, Hasumi Y, et al. Candida auris sp. nov., a novel ascomycetous yeast isolated from the external ear canal of an inpatient in a Japanese hospital. Microbiol Immunol 2009; 53:41.
  48. Lee WG, Shin JH, Uh Y, et al. First three reported cases of nosocomial fungemia caused by Candida auris. J Clin Microbiol 2011; 49:3139.
  49. Tsay S, Kallen A, Jackson BR, et al. Approach to the Investigation and Management of Patients With Candida auris, an Emerging Multidrug-Resistant Yeast. Clin Infect Dis 2018; 66:306.
  50. Lamoth F, Kontoyiannis DP. The Candida auris Alert: Facts and Perspectives. J Infect Dis 2018; 217:516.
  51. Kohlenberg A, Struelens MJ, Monnet DL, et al. Candida auris: epidemiological situation, laboratory capacity and preparedness in European Union and European Economic Area countries, 2013 to 2017. Euro Surveill 2018; 23.
  52. Escandón P, Cáceres DH, Espinosa-Bode A, et al. Notes from the Field: Surveillance for Candida auris - Colombia, September 2016-May 2017. MMWR Morb Mortal Wkly Rep 2018; 67:459.
  53. Adams E, Quinn M, Tsay S, et al. Candida auris in Healthcare Facilities, New York, USA, 2013-2017. Emerg Infect Dis 2018; 24:1816.
  54. Centers for Disease Control and Prevention. Tracking Candida auris. https://www.cdc.gov/fungal/diseases/candidiasis/tracking-c-auris.html (Accessed on November 30, 2019).
  55. Vallabhaneni S, Jackson BR, Chiller TM. Candida auris: An Emerging Antimicrobial Resistance Threat. Ann Intern Med 2019; 171:432.
  56. Bradley SF. What Is Known About Candida auris. JAMA 2019; 322:1510.
  57. Vallabhaneni S, Kallen A, Tsay S, et al. Investigation of the First Seven Reported Cases of Candida auris, a Globally Emerging Invasive, Multidrug-Resistant Fungus - United States, May 2013-August 2016. MMWR Morb Mortal Wkly Rep 2016; 65:1234.
  58. Lockhart SR, Etienne KA, Vallabhaneni S, et al. Simultaneous Emergence of Multidrug-Resistant Candida auris on 3 Continents Confirmed by Whole-Genome Sequencing and Epidemiological Analyses. Clin Infect Dis 2017; 64:134.
  59. Jeffery-Smith A, Taori SK, Schelenz S, et al. Candida auris: a Review of the Literature. Clin Microbiol Rev 2018; 31.
  60. Escandón P, Chow NA, Caceres DH, et al. Molecular Epidemiology of Candida auris in Colombia Reveals a Highly Related, Countrywide Colonization With Regional Patterns in Amphotericin B Resistance. Clin Infect Dis 2019; 68:15.
  61. Tsay S, Welsh RM, Adams EH, et al. Notes from the Field: Ongoing Transmission of Candida auris in Health Care Facilities - United States, June 2016-May 2017. MMWR Morb Mortal Wkly Rep 2017; 66:514.
  62. Chow NA, Gade L, Tsay SV, et al. Multiple introductions and subsequent transmission of multidrug-resistant Candida auris in the USA: a molecular epidemiological survey. Lancet Infect Dis 2018; 18:1377.
  63. Ostrowsky B, Greenko J, Adams E, et al. Candida auris Isolates Resistant to Three Classes of Antifungal Medications - New York, 2019. MMWR Morb Mortal Wkly Rep 2020; 69:6.
  64. Karmarkar EN, O'Donnell K, Prestel C, et al. Rapid Assessment and Containment of Candida auris Transmission in Postacute Care Settings-Orange County, California, 2019. Ann Intern Med 2021; 174:1554.
  65. Eyre DW, Sheppard AE, Madder H, et al. A Candida auris Outbreak and Its Control in an Intensive Care Setting. N Engl J Med 2018; 379:1322.
  66. Centers for Disease Control and Prevention. Recommendations for infection control for Candida auris. https://www.cdc.gov/fungal/diseases/candidiasis/c-auris-infection-control.html (Accessed on April 10, 2019).
  67. Centers for Disease Control and Prevention. Screening for Candida auris colonization. https://www.cdc.gov/fungal/candida-auris/c-auris-screening.html (Accessed on April 10, 2019).
  68. Velasco E, Bigni R. A prospective cohort study evaluating the prognostic impact of clinical characteristics and comorbid conditions of hospitalized adult and pediatric cancer patients with candidemia. Eur J Clin Microbiol Infect Dis 2008; 27:1071.
Topic 2442 Version 42.0

References

1 : The changing face of fungal infections in health care settings.

2 : Nosocomial bloodstream infections in US hospitals: analysis of 24,179 cases from a prospective nationwide surveillance study.

3 : Risk factors for albicans and non-albicans candidemia in the intensive care unit.

4 : Candidemia in nonneutropenic critically ill patients: risk factors for non-albicans Candida spp.

5 : Increasing incidence of candidaemia: long-term epidemiological trends, Queensland, Australia, 1999-2008.

6 : The epidemiology and attributable outcomes of candidemia in adults and children hospitalized in the United States: a propensity analysis.

7 : Semi-national surveillance of fungaemia in Denmark 2004-2006: increasing incidence of fungaemia and numbers of isolates with reduced azole susceptibility.

8 : Epidemiology of invasive candidiasis: a persistent public health problem.

9 : Invasive Candidiasis.

10 : Septic shock attributed to Candida infection: importance of empiric therapy and source control.

11 : Fungal colonization and/or infection in non-neutropenic critically ill patients: results of the EPCAN observational study.

12 : The Changing Epidemiology of Candidemia in the United States: Injection Drug Use as an Increasingly Common Risk Factor-Active Surveillance in Selected Sites, United States, 2014-2017.

13 : Epidemiology, management, and risk factors for death of invasive Candida infections in critical care: a multicenter, prospective, observational study in France (2005-2006).

14 : Candida bloodstream infections in intensive care units: analysis of the extended prevalence of infection in intensive care unit study.

15 : Factors associated with candidemia caused by non-albicans Candida species versus Candida albicans in the intensive care unit.

16 : Early prediction of Candida glabrata fungemia in nonneutropenic critically ill patients.

17 : Burden of Candidemia in the United States, 2017.

18 : The changing epidemiology of invasive candidiasis: Candida glabrata and Candida krusei as the leading causes of candidemia in hematologic malignancy.

19 : Results from the ARTEMIS DISK Global Antifungal Surveillance Study: a 6.5-year analysis of susceptibilities of Candida and other yeast species to fluconazole and voriconazole by standardized disk diffusion testing.

20 : Epidemiology and outcome of fungemia in a cancer Cohort of the Infectious Diseases Group (IDG) of the European Organization for Research and Treatment of Cancer (EORTC 65031).

21 : Candida Infective Endocarditis During the Infectious Diseases and Substance Use Disorder Syndemic: A Six-Year Case Series.

22 : Candida spp. infective endocarditis: Characteristics and outcomes of twenty patients with a focus on injection drug use as a predisposing risk factor.

23 : Cytokine gene polymorphisms and the outcome of invasive candidiasis: a prospective cohort study.

24 : Toll-like receptor 1 polymorphisms increase susceptibility to candidemia.

25 : Candidemia Among Coronavirus Disease 2019 Patients in Turkey Admitted to Intensive Care Units: A Retrospective Multicenter Study.

26 : The Landscape of Candidemia During the Coronavirus Disease 2019 (COVID-19) Pandemic.

27 : Epidemiology, risk factors, and prognosis of Candida parapsilosis bloodstream infections: case-control population-based surveillance study of patients in Barcelona, Spain, from 2002 to 2003.

28 : International surveillance of Candida spp. and Aspergillus spp.: report from the SENTRY Antimicrobial Surveillance Program (2003).

29 : Epidemiology and outcomes of candidemia in 2019 patients: data from the prospective antifungal therapy alliance registry.

30 : Candida and invasive mould diseases in non-neutropenic critically ill patients and patients with haematological cancer.

31 : Invasive Candidiasis Species Distribution and Trends, United States, 2009-2017.

32 : Epidemiology of opportunistic fungal infections in Latin America.

33 : Epidemiology of candidemia: 3-year results from the emerging infections and the epidemiology of Iowa organisms study.

34 : Geographic variations in species distribution and echinocandin and azole antifungal resistance rates among Candida bloodstream infection isolates: report from the SENTRY Antimicrobial Surveillance Program (2008 to 2009).

35 : Prospective observational study of candidemia in São Paulo, Brazil: incidence rate, epidemiology, and predictors of mortality.

36 : Emerging trends in candidemia: a higher incidence but a similar outcome.

37 : Candidaemia associated with decreased in vitro fluconazole susceptibility: is Candida speciation predictive of the susceptibility pattern?

38 : Increasing echinocandin resistance in Candida glabrata: clinical failure correlates with presence of FKS mutations and elevated minimum inhibitory concentrations.

39 : Frequency of fks mutations among Candida glabrata isolates from a 10-year global collection of bloodstream infection isolates.

40 : Rapid emergence of echinocandin resistance in Candida glabrata resulting in clinical and microbiologic failure.

41 : Candida krusei fungemia. An escalating serious infection in immunocompromised patients.

42 : In vitro susceptibilities of bloodstream isolates of Candida species to six antifungal agents: results from a population-based active surveillance programme, Barcelona, Spain, 2002-2003.

43 : Recent exposure to caspofungin or fluconazole influences the epidemiology of candidemia: a prospective multicenter study involving 2,441 patients.

44 : Prior antimicrobial therapy and risk for hospital-acquired Candida glabrata and Candida krusei fungemia: a case-case-control study.

45 : Prior antimicrobial therapy and risk for hospital-acquired Candida glabrata and Candida krusei fungemia: a case-case-control study.

46 : Prior antimicrobial therapy and risk for hospital-acquired Candida glabrata and Candida krusei fungemia: a case-case-control study.

47 : Candida auris sp. nov., a novel ascomycetous yeast isolated from the external ear canal of an inpatient in a Japanese hospital.

48 : First three reported cases of nosocomial fungemia caused by Candida auris.

49 : Approach to the Investigation and Management of Patients With Candida auris, an Emerging Multidrug-Resistant Yeast.

50 : The Candida auris Alert: Facts and Perspectives.

51 : Candida auris: epidemiological situation, laboratory capacity and preparedness in European Union and European Economic Area countries, 2013 to 2017.

52 : Notes from the Field: Surveillance for Candida auris - Colombia, September 2016-May 2017.

53 : Candida auris in Healthcare Facilities, New York, USA, 2013-2017.

54 : Candida auris in Healthcare Facilities, New York, USA, 2013-2017.

55 : Candida auris: An Emerging Antimicrobial Resistance Threat.

56 : What Is Known About Candida auris.

57 : Investigation of the First Seven Reported Cases of Candida auris, a Globally Emerging Invasive, Multidrug-Resistant Fungus - United States, May 2013-August 2016.

58 : Simultaneous Emergence of Multidrug-Resistant Candida auris on 3 Continents Confirmed by Whole-Genome Sequencing and Epidemiological Analyses.

59 : Candida auris: a Review of the Literature.

60 : Molecular Epidemiology of Candida auris in Colombia Reveals a Highly Related, Countrywide Colonization With Regional Patterns in Amphotericin B Resistance.

61 : Notes from the Field: Ongoing Transmission of Candida auris in Health Care Facilities - United States, June 2016-May 2017.

62 : Multiple introductions and subsequent transmission of multidrug-resistant Candida auris in the USA: a molecular epidemiological survey.

63 : Candida auris Isolates Resistant to Three Classes of Antifungal Medications - New York, 2019.

64 : Rapid Assessment and Containment of Candida auris Transmission in Postacute Care Settings-Orange County, California, 2019.

65 : A Candida auris Outbreak and Its Control in an Intensive Care Setting.

66 : A Candida auris Outbreak and Its Control in an Intensive Care Setting.

67 : A Candida auris Outbreak and Its Control in an Intensive Care Setting.

68 : A prospective cohort study evaluating the prognostic impact of clinical characteristics and comorbid conditions of hospitalized adult and pediatric cancer patients with candidemia.

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