The Relative Pathogenicity of Candida Krusei and C. Albicans in the Rat Oral Mucosa

Samaranayake, Y. H.; Wu, P. C.; Samaranayake, LP; Ho, Paulo Lee

doi:10.1099/00222615-47-12-1047

Cited by 23 publications

(20 citation statements)

References 36 publications

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“…Other predisposing factors for oral candidiasis that have come under scrutiny in a number of animal models include broad-spectrum antibiotic therapy (5,82,(155)(156)(157), carbohydrate-rich diets (66,154,155), topical use of corticosteroids (47), corticosteroid inhalation (28), trauma (131), iron deficiency (147,185), diabetes (51), xerostomia (1,83,84,119,133), decrease in CD4 ϩ T-cell counts and phagocytic function (31,32), defective T-cell function (16), and immunosuppressive therapy (27,172). Undoubtedly, these studies have helped us to understand the etiology of oral candidiasis and the development of the management protocols that are currently prevalent.…”

Section: Need For and Clinical Relevance Of Animal Modelsmentioning

confidence: 99%

Experimental Oral Candidiasis in Animal Models

2001

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Oral candidiasis is as much the final outcome of the vulnerability of the host as of the virulence of the invading organism. We review here the extensive literature on animal experiments mainly appertaining to the host predisposing factors that initiate and perpetuate these infections. The monkey, rat, and mouse are the choice models for investigating oral candidiasis, but comparisons between the same or different models appear difficult, because of variables such as the study design, the number of animals used, their diet, the differences in Candida strains, and the duration of the studies. These variables notwithstanding, the following could be concluded. (i) The primate model is ideal for investigating Candida-associated denture stomatitis since both erythematous and pseudomembranous lesions have been produced in monkeys with prosthetic plates; they are, however, expensive and difficult to obtain and maintain. (ii) The rat model (both Sprague-Dawley and Wistar) is well proven for observing chronic oral candidal colonization and infection, due to the ease of breeding and handling and their ready availability. (iii) Mice are similar, but in addition there are well characterized variants simulating immunologic and genetic abnormalities (e.g., athymic, euthymic, murine-acquired immune deficiency syndrome, and severe combined immunodeficient models) and hence are used for short-term studies relating the host immune response and oral candidiasis. Nonetheless, an ideal, relatively inexpensive model representative of the human oral environment in ecological and microbiological terms is yet to be described. Until such a model is developed, researchers should pay attention to standardization of the experimental protocols described here to obtain broadly comparable and meaningful data

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Section: Need For and Clinical Relevance Of Animal Modelsmentioning

confidence: 99%

Experimental Oral Candidiasis in Animal Models

2001

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“…The widespread use of fluconazole to treat fungal infections has contributed to the appearance of C. krusei infections, since this species shows intrinsic resistance to this antifungal (22). Candida krusei can form pseudohyphae (11), a feature that might contribute to its virulence (26). Different studies have shown that C. krusei is less virulent than Candida albicans in terms of its adherence to epithelial cells and prosthetic devices, proteolytic potential, and production of phospholipases (10).…”

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confidence: 99%

The Interaction between Candida krusei and Murine Macrophages Results in Multiple Outcomes, Including Intracellular Survival and Escape from Killing

et al. 2011

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Candida krusei is a fungal pathogen of interest for the scientific community for its intrinsic resistance to fluconazole. Little is known about the interaction of this yeast with host immune cells. In this work, we have characterized the outcome of the interaction between C. krusei and murine macrophages. Once C. krusei was internalized, we observed different phenomena. In a macrophage-like cell line, C. krusei survived in a significant number of macrophages and induced filamentation and macrophage explosion. Phagocytosis of C. krusei led to actin polymerization around the yeast cells at the site of entry. Fluorescent specific staining with anti-Lamp1 and LysoTracker indicated that after fungal internalization, there was a phagolysosome maturation defect, a phenomenon that was more efficient when the macrophages phagocytosed killed yeast cells. Using cell line macrophages, we also observed macrophage fusion after cell division. When we used primary resident peritoneal macrophages in addition to macrophage explosion, we also observed a strong chemotaxis of uninfected macrophages to regions where C. krusei-infected macrophages were present. We also noticed yeast transfer phenomena between infected macrophages. Primary macrophages inhibited pseudohypha elongation more efficiently than the macrophage-like cell line, suggesting that C. krusei infection was better controlled by the former macrophages. Primary macrophages induced more tumor necrosis factor alpha (TNF-␣) and interleukin-6 (IL-6) than the macrophage-like cell line. Our results demonstrate that C. krusei can exploit the macrophages for replication, although other different outcomes are also possible, indicating that the interaction of this pathogen with phagocytic cells is very complex and regulated by multiple factors.

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“…Despite the increased morbidity caused by C. krusei, the approaches used in the investigation of mucosal candidosis have focused mainly on the most virulent species, C. albicans, and to our knowledge there are no animal studies pertaining to oral C. krusei infection. It would appear that this is the first documented study on the oral carriage of C. krusei in an animal model (in addition to Samaranayake et al 1998). Samaranayake et al (1998) indicated that C. krusei isolates were able to colonize the rat tongue mucosa, but in smaller numbers than C. albicans, despite the use of equal inocula at an identical frequency and the same conditions.…”

Section: Discussionmentioning

confidence: 99%

“…It would appear that this is the first documented study on the oral carriage of C. krusei in an animal model (in addition to Samaranayake et al 1998). Samaranayake et al (1998) indicated that C. krusei isolates were able to colonize the rat tongue mucosa, but in smaller numbers than C. albicans, despite the use of equal inocula at an identical frequency and the same conditions. The lower oral carriage of C. krusei, in general, may reflect its reduced ability to adhere to buccal epithelial cells when compared with C. albicans.…”

Section: Discussionmentioning

confidence: 99%