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Candida krusei was first discovered in 1839 by Langenbeck from a patient with typhus, 75 years later Castellani proposed the suggestion that C. krusei may cause disease in humans. Since then, it has been generally considered as a commensal in warm-blooded animals with low pathogenicity and virulence. In humans, C. krusei is generally considered to be a transient commensal and is infrequently isolated from mucosal surfaces. However, since 1960s there has been an increase in the number of reports of C. krusei as a human pathogen.
In contrast to most other ovoid shaped Candida spp., C. krusei cells are generally elongated in a feature similar to C. kefir (formerly C. pseudotropicalis) amongst clinically important Candida spp. C. krusei has various colony morphology. It has a multilayered cell wall consisting of an outer irregular coat of flocculent material, an electron-dense zone, a granular layer, a less granular layer, a thin layer of dense granules and another sparsely granular layer outside the trilaminar cell membrane. The mannan component of the C. krusei cell wall has been shown to be different from other Candida spp. in containing (1-2) and (1-6) side chains in the ratio of 3 : 1 as being lightly branched. Such differences may account for the variable behavior of C. krusei in biological fluids such as saliva and bronchial lavage fluid comparing with other Candida spp.
C. krusei has two basic morphological forms, yeast and pseudohyphae and both are often present simultaneously in growing cultures and not easily separated. C. krusei grows at a 37°C but can withstand temperature up to 45°C. C. krusei can grow in vitamin-free media even though most common Candida spp. requires biotin or additional vitamin for growth. C. krusei ferments and assimilates glucose only as carbohydrate.
Like C. auris, C. krusei can adhere to abiotic surfaces but not to the same extent as C. albicans. Although adhesion to host surfaces is essential for colonization and invasion, C. krusei is able to colonize readily to inert surfaces such as implants and catheters by virtue of its cell surface hydrophobicity. Less pathogenic species – C. parapsilosis, C. pseudotropicalis (now C. kelvr) and C. glabrata – usually produce significantly less biofilm than the more pathogenic C. albicans, but C. krusei produced the most extensive biofilm on the surfaces of polyvinyl chloride catheter disks regardless of the growth medium. This could demonstrate the very high cell surface hydrophobicity and adherence of C. krusei to inert plastic surfaces, which may then have other species, facilitated biofilm development. C. krusei does not adhere to buccal epithelial cells whereas C. tropicalis, C. parapsilosis, C. guilliermondii and C. kefir do.
The susceptibility to lysozyme, an antimicrobial enzyme produced in phagosomes has been used as a method to assess the microbial virulence. Such tests indicate that the susceptibility to lysozyme of C. krusei > C. parapsilosis > C. tropicalis > C. guilliermondii > C. albicans > C. glabrata, the latter being the most resistant to lysozyme. Interesting when pre-incubated in sucrose-supplemented media, C. krusei became highly sensitive to lysozyme as compared to than C. albians.
Pathogen Profile: Diploid, does not belong to CTG clade, Genome sequence available, antifungal resistance is moderate – high.
C. kefir was first found in dairy products such as fermented milk, cheese, and yoghurt. It has been isolated from a kefir sample in 1909, named as Saccharomyces fragilis at first, then C. pseudotropicali and finally been reclassified as Kluyveromyces marxianus with its teleomorph. C. kefir has been rarely the cause of candidiasis.
The first case of invasive C. kefir (C. pseudotropicalis) was identified in a 58-year-old female with metastatic adenocarcinoma of the brest. C. kefir represents < 1% isolates of Candida spp. from clinical specimens. It has been reported to colonize oral cavities, gastrointestinal tract and urinary tract. However, the published cases of invasive C. kefir infections are few. All infected patients were immunocompromised and had several potential risk factors.
These emerging pathogens of the Candida species themselves are not more virulent than C. albicans. Therefore, it is generally thought that their conversion from commensalism to parasitism is largely determined by the host immune status.
Candida lusitaniae was firstly isolated from warm-blooded animals and was shown to cause opportunistic infections in humans in 1979. It is distinguished by the resistance to Amphotericin B among Candida species. Studies has showed that C. lusitaniae has similar ability to colonize individuals and opportunistically infected in immune-compromised patients however does develop differently in vivo from other species in terms of resistance to Amphotericin B.
Candida tropicalis was identified as the most prevalent NAC pathogen in Candida spps. In compromised mice and human patients, C. tropicalis isolates appeared to have increased virulence. Secreted aspartyl proteinase 5 and 9 (SAP5 and SAP9) antigens are expressed by C. tropicalis. Invasive C. tropicalis infections were found more frequently in acute leukemia or bone marrow transplants patients may indicate that polymorphonuclear leukocytes are the first defense line against of C. tropicalis. Overexpression of CtERG11 gene mutations in C. tropicalis could cause acquired resistance to azoles.
Candida dubliniensis is a species of chlamydospore- and germ tube-positive yeast, primarily recovered from HIV-infected individuals and AIDS patients. It grows well at 30 and 37°C but not 42°C. C. dubliniensis is unable to express b-glucosidase activity.
Candida parapsilosis has increased in significance and prevalence over the past 2 decades. The infections are mainly associated with prosthetic devices and catheters, especially in the nosocomial spread. Risk factors of C. parapsilosis infections include the hydrolytic enzymes secretion, prosthetics adhesion, and biofilm formation.
Candida guillermondii is the sixth frequently isolated Candida species, an emerging pathogen in Latin America that rarely causes invasive candidiasis. However, it has been reported to exhibits reduced susceptibility to fluconazole thus further study of the anti-drug mechanism is required.
Candida lypolitica isolates formed narrow, multi-branched, true hyphae on cornmeal-Tween 80 agars. C. lipolytica is a weakly virulent pathogen that is most clearly vascular catheter-related. It is sensitive to Amphotericin B and Ketoconazole ion vitro.
Candida rugosa was quite rarely a cause of invasive candidemia, however recently, with isolates shown to be an increasing cause of fungal infections especially in Latin America. Besides, C. rugosa appears decreased susceptibility to fluconazole with various patterns following geographic regions.
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