Статті в журналах: "Candidiasis Pathogenesis"

1

Podzorski, Raymond P. "Pathogenesis of Candidiasis." Archives of Surgery 124, no. 11 (November 1, 1989): 1290. http://dx.doi.org/10.1001/archsurg.1989.01410110044009.

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2

van de Veerdonk, Frank L., Bart-Jan Kullberg, and Mihai G. Netea. "Pathogenesis of invasive candidiasis." Current Opinion in Critical Care 16, no. 5 (October 2010): 453–59. http://dx.doi.org/10.1097/mcc.0b013e32833e046e.

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3

Agabian, N., F. C. Odds, D. Poulain, D. R. Soll, and T. C. White. "Pathogenesis of invasive candidiasis." Medical Mycology 32, s1 (January 1994): 229–37. http://dx.doi.org/10.1080/02681219480000861.

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4

Balsdon, M. J. "Candidiasis: Pathogenesis, Diagnosis and Treatment." Sexually Transmitted Infections 69, no. 4 (August 1, 1993): 326–27. http://dx.doi.org/10.1136/sti.69.4.326-b.

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5

Sobel, Jack D. "Pathogenesis of recurrent vulvovaginal candidiasis." Current Infectious Disease Reports 4, no. 6 (December 2002): 514–19. http://dx.doi.org/10.1007/s11908-002-0038-7.

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6

Buralkina, N. A., and O. V. Shabalova. "Vulvovaginal candidiasis: etiology, pathogenesis, diagnosis, treatment." Medical Council, no. 12 (August 31, 2019): 142–45. http://dx.doi.org/10.21518/2079-701x-2019-12-142-145.

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7

Monif, Gilles R. G. "Classification and pathogenesis of vulvovaginal candidiasis." American Journal of Obstetrics and Gynecology 152, no. 7 (August 1985): 935–39. http://dx.doi.org/10.1016/s0002-9378(85)80004-1.

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8

SOBEL, JACK D. "Pathogenesis and Epidemiology of Vulvovaginal Candidiasis." Annals of the New York Academy of Sciences 544, no. 1 Antifungal Dr (December 1988): 547–57. http://dx.doi.org/10.1111/j.1749-6632.1988.tb40450.x.

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9

PUTO, Klementina, Naxhije HILA, and Rexhep SHKURTI. "Oral, Intestinal and Vaginal Candidiasis, Pathogenesis and Clinical Presentation in Elbasan (Albania)." Indian Journal of Applied Research 3, no. 12 (October 1, 2011): 471–73. http://dx.doi.org/10.15373/2249555x/dec2013/144.

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10

Sobel, Jack D. "Epidemiology and pathogenesis of recurrent vulvovaginal candidiasis." American Journal of Obstetrics and Gynecology 152, no. 7 (August 1985): 924–35. http://dx.doi.org/10.1016/s0002-9378(85)80003-x.

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11

Bairamova, G. R., A. S. Amirkhanyan, and V. F. Chernova. "Vulvovaginal Candidiasis: Pathogenesis, Diagnosis, and Treatment Strategy." Doctor.Ru 154, no. 10 (2018): 32–36. http://dx.doi.org/10.31550/1727-2378-2018-154-10-32-36.

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12

Klajn-Laslo, Marija. "Chronic candidiasis - pathogenesis, symptoms, diagnosis and treatment." Zbornik Matice srpske za prirodne nauke, no. 116 (2009): 267–74. http://dx.doi.org/10.2298/zmspn0916267k.

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The yeast named Candida normally colonizes the gut and vagina without causing any sign of its presence. It is a commensal and opportune fungus but in certain conditions it turns to be pathogenic, causing chronic disturbances in any part of the body. The pathogenesis is complex, signs and symptoms are non-specific. The colonisation is difficult to distinguish from invasive disease. The current diagnostic methods do not always allow a definitive diagnosis to be made. Treatment is complex, individual and no protocol can be created. The author tries to give an overview of the Candida related problem.

13

Sobel, J. D. "Pathogenesis and Treatment of Recurrent Vulvovaginal Candidiasis." Clinical Infectious Diseases 14, Supplement_1 (March 1, 1992): S148—S153. http://dx.doi.org/10.1093/clinids/14.supplement_1.s148.

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14

Sohnle, Peter G. "Candidiasis: Pathogenesis, diagnosis and treatment (2nd edn)." Parasitology Today 9, no. 11 (November 1993): 434. http://dx.doi.org/10.1016/0169-4758(93)90058-n.

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15

Tada, Yuhei, and Shin-ya Takahashi. "Study on the Pathogenesis of Congenital Cutaneous Candidiasis." Nippon Ishinkin Gakkai Zasshi 34, no. 4 (1993): 459–69. http://dx.doi.org/10.3314/jjmm.34.459.

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16

Uppuluri, Priya, Ashok K. Chaturvedi, Niketa Jani, Read Pukkila-Worley, Carlos Monteagudo, Eleftherios Mylonakis, Julia R. Köhler, and Jose L. Lopez Ribot. "Physiologic Expression of the Candida albicans Pescadillo Homolog Is Required for Virulence in a Murine Model of Hematogenously Disseminated Candidiasis." Eukaryotic Cell 11, no. 12 (October 26, 2012): 1552–56. http://dx.doi.org/10.1128/ec.00171-12.

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ABSTRACT Morphogenetic conversions contribute to the pathogenesis of Candida albicans invasive infections. Many studies to date have convincingly demonstrated a link between filamentation and virulence; however, relatively little is known regarding the role of the filament-to-yeast transition during the pathogenesis of invasive candidiasis. We previously identified the C. albicans pescadillo homolog ( PES1 ) as essential during yeast growth and growth of lateral yeast on hyphae but not during hyphal growth. Furthermore, we demonstrated that PES1 is required for virulence in vivo in a Galleria mellonella larva model of candidiasis. Here, we have used a regulatable tetO-PES1 / pes1 strain to assess the contribution of C. albicans PES1 to pathogenesis in the commonly used and clinically relevant murine model of hematogenously disseminated candidiasis. Our results indicate that a physiologically controlled level of PES1 expression is required for full virulence in this animal model, with virulence defects observed both when PES1 is overexpressed and and when it is depleted. The pathogenetic defect of cells depleted of PES1 is not due to a general growth defect, as demonstrated by the fact that PES1 -depleted cells still kill Caenorhabditis elegans as efficiently as the wild type due to hyphal outgrowth through worm tissues. Our results suggest a critical role of lateral yeast growth in the ability of C. albicans to normally proliferate within tissues, as well as a pivotal role for Pes1 in the normal developmental cycle of C. albicans within the mammalian host during infection.

17

de Repentigny, Louis, Daniel Lewandowski, and Paul Jolicoeur. "Immunopathogenesis of Oropharyngeal Candidiasis in Human Immunodeficiency Virus Infection." Clinical Microbiology Reviews 17, no. 4 (October 2004): 729–59. http://dx.doi.org/10.1128/cmr.17.4.729-759.2004.

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SUMMARY Oropharyngeal and esophageal candidiases remain significant causes of morbidity in human immunodeficiency virus (HIV)-infected patients, despite the dramatic ability of antiretroviral therapy to reconstitute immunity. Notable advances have been achieved in understanding, at the molecular level, the relationships between the progression of HIV infection, the acquisition, maintenance, and clonality of oral candidal populations, and the emergence of antifungal resistance. However, the critical immunological defects which are responsible for the onset and maintenance of mucosal candidiasis in patients with HIV infection have not been elucidated. The devastating impact of HIV infection on mucosal Langerhans' cell and CD4+ cell populations is most probably central to the pathogenesis of mucosal candidiasis in HIV-infected patients. However, these defects may be partly compensated by preserved host defense mechanisms (calprotectin, keratinocytes, CD8+ T cells, and phagocytes) which, individually or together, may limit Candida albicans proliferation to the superficial mucosa. The availability of CD4C/HIV transgenic mice expressing HIV-1 in immune cells has provided the opportunity to devise a novel model of mucosal candidiasis that closely mimics the clinical and pathological features of candidal infection in human HIV infection. These transgenic mice allow, for the first time, a precise cause-and-effect analysis of the immunopathogenesis of mucosal candidiasis in HIV infection under controlled conditions in a small laboratory animal.

18

Achkar, Jacqueline M., and Bettina C. Fries. "Candida Infections of the Genitourinary Tract." Clinical Microbiology Reviews 23, no. 2 (April 2010): 253–73. http://dx.doi.org/10.1128/cmr.00076-09.

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SUMMARYAll humans are colonized withCandidaspecies, mostlyCandida albicans, yet some develop diseases due toCandida, among which genitourinary manifestations are extremely common. The forms of genitourinary candidiasis are distinct from each other and affect different populations. While vulvovaginal candidiasis affects mostly healthy women, candiduria occurs typically in elderly, hospitalized, or immunocompromised patients and in neonates. Despite its high incidence and clinical relevance, genitourinary candidiasis is understudied, and therefore, important questions about pathogenesis and treatment guidelines remain to be resolved. In this review, we summarize the current knowledge about genitourinary candidiasis.

19

Darmstadt, G. L., J. G. Dinulos, and Z. Miller. "Congenital Cutaneous Candidiasis: Clinical Presentation, Pathogenesis, and Management Guidelines." PEDIATRICS 105, no. 2 (February 1, 2000): 438–44. http://dx.doi.org/10.1542/peds.105.2.438.

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20

Dąbrowska, Marta, Monika Sienkiewicz, Paweł Kwiatkowski, and Michał Dąbrowski. "Diagnosis and treatment of invasive Candida infections – a review article." Annales Universitatis Mariae Curie-Sklodowska, sectio C – Biologia 73, no. 1 (June 10, 2019): 47. http://dx.doi.org/10.17951/c.2018.73.1.47-59.

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<p>Candida albicans is the most common cause of fungal infections worldwide. Invasive candidiasis comprises candidemia and deep-seated candidiasis. Most yeast invasive infections are endogenous with a high mortality. Pathogenesis of candidiasis depends on avoiding host immune responses, as well as the virulence factors of the fungus enabling colonization and invasion of tissues. Adequate source control and antifungal therapy administered within a short time is critical to get a better prognosis. The emergence of drug resistance and the side effects of currently available antifungals are becoming the major problem in the management of Candida spp. infection.</p>

21

Bendel, Catherine M. "Colonization and epithelial adhesion in the pathogenesis of neonatal candidiasis." Seminars in Perinatology 27, no. 5 (October 2003): 357–64. http://dx.doi.org/10.1016/s0146-0005(03)00059-4.

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22

Kamai, Yasuki, Mikie Kubota, Yoko Kamai, Tsunemichi Hosokawa, Takashi Fukuoka, and Scott G. Filler. "New Model of Oropharyngeal Candidiasis in Mice." Antimicrobial Agents and Chemotherapy 45, no. 11 (November 1, 2001): 3195–97. http://dx.doi.org/10.1128/aac.45.11.3195-3197.2001.

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ABSTRACT We established a straightforward murine model of oropharyngeal candidiasis. Mice were immunosuppressed with cortisone acetate, anesthetized, and then inoculated by placing cotton wool balls saturated with Candida albicans sublingually for 2 h. A prolonged, reproducible infection was induced. This model may be useful for antifungal screening or pathogenesis studies.

23

Kamai, Yasuki, Mikie Kubota, Yoko Kamai, Tsunemichi Hosokawa, Takashi Fukuoka, and Scott G. Filler. "Contribution of Candida albicans ALS1 to the Pathogenesis of Experimental Oropharyngeal Candidiasis." Infection and Immunity 70, no. 9 (September 2002): 5256–58. http://dx.doi.org/10.1128/iai.70.9.5256-5258.2002.

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ABSTRACT We investigated the contribution of Candida albicans ALS1, which encodes a candidal adhesin, to the pathogenesis of experimental murine oropharyngeal candidiasis. Our results indicate that the ALS1 gene product is important for the adherence of the organism to the oral mucosa during the early stage of the infection.

24

Matthews, R., and J. Burnie. "The epidemiology and pathogenesis of candidiasis: Applications in prevention and treatment." Bulletin de l'Institut Pasteur 96, no. 4 (October 1998): 249–56. http://dx.doi.org/10.1016/s0020-2452(99)80005-0.

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25

Spellberg, Brad. "Novel Insights into Disseminated Candidiasis: Pathogenesis Research and Clinical Experience Converge." PLoS Pathogens 4, no. 2 (2008): e38. http://dx.doi.org/10.1371/journal.ppat.0040038.

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26

Ashman, RB, and JM Papadimitriou. "Murine Candidiasis. Pathogenesis and host responses in genetically distinct inbred mice." Immunology and Cell Biology 65, no. 2 (April 1987): 163–71. http://dx.doi.org/10.1038/icb.1987.18.

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27

Allen, C. M., F. M. Beck, F. A. Lurie, and H. M. Pinsky. "Role of tetracycline in pathogenesis of chronic candidiasis of rat tongues." Infection and Immunity 47, no. 2 (1985): 480–83. http://dx.doi.org/10.1128/iai.47.2.480-483.1985.

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28

Murakov, S. V., E. V. Vladimirova, V. P. Kovalyk, Y. A. Markova, A. A. Vladimirov, U. A. Stromskaya, D. I. Makeeva, and S. A. Popkov. "State-of-the-art of vulvovaginal candidiasis: etiopathogenesis, diagnosis, and treatment." Russian Medical Inquiry 4, no. 10 (2020): 625–31. http://dx.doi.org/10.32364/2587-6821-2020-4-10-625-631.

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During the reproductive age, 75% of women experience at least one episode of vulvovaginal candidiasis (VVC) and 40–50% of women experience two or more episodes. Recurrent VVC is referred to as at least four episodes of the disease within a 12-month period. The aim of this paper is to review the etiology, pathogenesis, clinical signs, diagnosis, and treatment for VVC. Both domestic and foreign published data are analyzed. It is now recognized that urogenital disorders and systemic comorbidities are the key predisposing factors to recurrent VVC. Other risk factors include the use of broad-spectrum antibiotics, immunosuppressants, and hormone replacement therapy, endocrine disorders, and intestinal Candida persistence. Intravaginal medications are the preferred treatment for VVC. A 6-month maintenance therapy reduces the rate of VVC recurrences by 90%. Further studies on the etiopathogenesis of recurrent VVC will improve treatment efficacy. KEYWORDS: vulvovaginal candidiasis, recurrent vulvovaginal candidiasis, vulvovaginal candidiasis, Candida albicans, non-albicans Candida, Candida spp., Lactobacilli, vaginal colonization resistance. FOR CITATION: Murakov S.V., Vladimirova E.V., Kovalyk V.P. et al. State-of-the-art of vulvovaginal candidiasis: etiopathogenesis, diagnosis, and treatment. Russian Medical Inquiry. 2020;4(10):625–631. DOI: 10.32364/2587-6821-2020-4-10-625-631.

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Cheng, Shaoji, Cornelius J. Clancy, Mary Ann Checkley, Zongde Zhang, Karen L. Wozniak, Kalpathi R. Seshan, Hong Yan Jia, Paul Fidel, Garry Cole, and M. Hong Nguyen. "The Role of Candida albicans NOT5 in Virulence Depends upon Diverse Host Factors In Vivo." Infection and Immunity 73, no. 11 (November 2005): 7190–97. http://dx.doi.org/10.1128/iai.73.11.7190-7197.2005.

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ABSTRACT We previously identified Candida albicans Not5p as an immunogenic protein expressed during oropharyngeal candidiasis (OPC). In this study, we demonstrate that C. albicans NOT5 reverses the growth defects of a Saccharomyces cerevisiae not5 mutant strain at 37°C, suggesting that the genes share at least some functional equivalence. We implicate C. albicans NOT5 in the pathogenesis of disseminated candidiasis (DC) induced by intravenous infection among neutropenic and nonimmunosuppressed mice, as well as in that of OPC in mice immunosuppressed with corticosteroids. We find no role in virulence, however, among neutropenic and corticosteroid-suppressed mice with DC resulting from gastrointestinal translocation, nor do we implicate the gene in vulvovaginal candidiasis among mice in pseudoestrus. These findings suggest that the role of NOT5 in virulence depends on the specific in vivo environment and is influenced by diverse factors such as tissue site, portal of entry, and the status of host defenses. NOT5 is necessary for normal adherence to colonic and cervical epithelial cells in vitro, demonstrating that such assays cannot fully replicate disease processes in vivo. Lastly, antibody responses against Not5p do not differ in the sera of patients with OPC, patients with DC, and healthy controls, suggesting that the protein is associated with both commensalism and the pathogenesis of disease.

30

Rosati, Diletta, Mariolina Bruno, Martin Jaeger, Jaap ten Oever, and Mihai G. Netea. "Recurrent Vulvovaginal Candidiasis: An Immunological Perspective." Microorganisms 8, no. 2 (January 21, 2020): 144. http://dx.doi.org/10.3390/microorganisms8020144.

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Vulvovaginal candidiasis (VVC) is a widespread vaginal infection primarily caused by Candida albicans. VVC affects up to 75% of women of childbearing age once in their life, and up to 9% of women in different populations experience more than three episodes per year, which is defined as recurrent vulvovaginal candidiasis (RVVC). RVVC results in diminished quality of life as well as increased associated healthcare costs. For a long time, VVC has been considered the outcome of inadequate host defenses against Candida colonization, as in the case of primary immunodeficiencies associated with persistent fungal infections and insufficient clearance. Intensive research in recent decades has led to a new hypothesis that points toward a local mucosal overreaction of the immune system rather than a defective host response to Candida colonization. This review provides an overview of the current understanding of the host immune response in VVC pathogenesis and suggests that a tightly regulated fungus–host–microbiota interplay might exert a protective role against recurrent Candida infections.

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Galocha, Mónica, Pedro Pais, Mafalda Cavalheiro, Diana Pereira, Romeu Viana, and Miguel C. Teixeira. "Divergent Approaches to Virulence in C. albicans and C. glabrata: Two Sides of the Same Coin." International Journal of Molecular Sciences 20, no. 9 (May 11, 2019): 2345. http://dx.doi.org/10.3390/ijms20092345.

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Candida albicans and Candida glabrata are the two most prevalent etiologic agents of candidiasis worldwide. Although both are recognized as pathogenic, their choice of virulence traits is highly divergent. Indeed, it appears that these different approaches to fungal virulence may be equally successful in causing human candidiasis. In this review, the virulence mechanisms employed by C. albicans and C. glabrata are analyzed, with emphasis on the differences between the two systems. Pathogenesis features considered in this paper include dimorphic growth, secreted enzymes and signaling molecules, and stress resistance mechanisms. The consequences of these traits in tissue invasion, biofilm formation, immune system evasion, and macrophage escape, in a species dependent manner, are discussed. This review highlights the observation that C. albicans and C. glabrata follow different paths leading to a similar outcome. It also highlights the lack of knowledge on some of the specific mechanisms underlying C. glabrata pathogenesis, which deserve future scrutiny.

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Beketova, G., N. Savychuk, and A. Savychuk. "Acute and recurrent oral candidiasis under experimental conditions: characteristics of its pathogenesis." Health of Society 5, no. 1-2 (June 1, 2016): 24–36. http://dx.doi.org/10.22141/2306-2436.5.1-2.2016.121236.

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Papadimitriou, J. M., and R. B. Ashman. "The pathogenesis of acute systemic candidiasis in a susceptible inbred mouse strain." Journal of Pathology 150, no. 4 (December 1986): 257–65. http://dx.doi.org/10.1002/path.1711500405.

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34

Lynch, M. E., J. D. Sobel, and P. L. Fidel. "Role of antifungal drug resistance in the pathogenesis of recurrent vulvovaginal candidiasis." Medical Mycology 34, no. 5 (January 1996): 337–39. http://dx.doi.org/10.1080/02681219680000571.

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35

Huston, David P. "Defects in Interleukin-17 Immunity in the Pathogenesis of Chronic Mucocutaneous Candidiasis." Current Allergy and Asthma Reports 11, no. 5 (July 16, 2011): 342–44. http://dx.doi.org/10.1007/s11882-011-0209-4.

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36

de Cássia Orlandi Sardi, Janaina, Diego Romário Silva, Paula Cristina Anibal, Julianna Joanna Carvalho Moraes de Campos Baldin, Suellen Rodrigues Ramalho, Pedro Luiz Rosalen, Maria Ligia Rodrigues Macedo, and José Francisco Hofling. "Vulvovaginal Candidiasis: Epidemiology and Risk Factors, Pathogenesis, Resistance, and New Therapeutic Options." Current Fungal Infection Reports 15, no. 1 (February 22, 2021): 32–40. http://dx.doi.org/10.1007/s12281-021-00415-9.

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37

Bokor-Bratic, Marija. "Oral candidiasis-adhesion of non-albicans Candida species." Zbornik Matice srpske za prirodne nauke, no. 114 (2008): 69–78. http://dx.doi.org/10.2298/zmspn0814069b.

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Oral candidiasis is an opportunistic infection caused primarily by Candida albicans. However, in recent years, species of non-albicans Candida have been implicated more frequently in mucosal infection. Candida species usually reside as commensal organisms and are part of normal oral microflora. Determining exactly how transformation from commensal to pathogen takes place and how it can be prevented is continuous challenge for clinical doctors. Candidal adherence to mucosal surfaces is considered as a critical initial step in the pathogenesis of oral candidiasis. Acrylic dentures, acting as reservoirs, play an important role in increasing the risk from Candida colonisation. Thus, this review discusses what is currently known about the adhesion of non-albicans Candida species of oral origin to buccal epithelial cells and denture acrylics.

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Khodavandi, Alireza, Fahimeh Alizadeh, and Mahsa Jafarzadeh. "Synergistic Interaction of Fluconazole/Amphotericin B on Inhibition of Enzymes Contributes to the Pathogenesis of Candida Tropicalis." Pharmaceutical Sciences 24, no. 4 (December 30, 2018): 280–90. http://dx.doi.org/10.15171/ps.2018.41.

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Background: Candidiasis has gained much attention in recent decades due to its increasing prevalence in immunocompromised patients. Usually, antifungals such as fluconazole and amphotricin B are used for treatment of candidiasis, but one of the major clinical problems is the emergence of antifungal resistance. Combination antifungal therapy is one of the most commonly used methods to alleviate the problem of antifungal resistance. Methods: The effect of fluconazole alone and in combination with amphotericin B on C. tropicalis isolates were performed using the Clinical and Laboratory Standards Institute (CLSI) reference method. Eventually hypha formation, time kill study, proteinase and phospholipase activity and expression of PLB and SAP2 genes were carried out to investigate the enzymes inhibitory properties of antifungal tested against C. tropicalis. Results: Results showed the significant synergic effect of fluconazole in combination with amphotericin B in inhibiting the growth of C. tropicalis isolates, with fractional inhibitory concentration indices ranging from 0.06 to 0.5. The combination of fluconazole with amphotericin B reduced the number of yeast form and inhibited the yeast to hyphae transition in C. tropicalis. The antifungals tested were able to show the effect of down regulating expression of the selected genes significantly in fluconazole/amphotericin B ranging from 1.42- to 2.27-fold. Conclusion: Our results demonstrated that the synergistic interaction of fluconazole/amphotericin B would be worth exploring for the management of candidiasis. In addition, PLB and SAP2 genes could be probable molecular targets in the synergistic interaction of fluconazole/amphotericin B in C. tropicalis.

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Shirani, Kiana, Zahra Allameh, and Azadeh Moshtzan. "Identification of etiologic agents of recurrent vulvovaginal candidiasis in patients from Isfahan, Iran." Immunopathologia Persa 7, no. 2 (September 10, 2020): e18-e18. http://dx.doi.org/10.34172/ipp.2021.18.

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Introduction: Occurrence of vulvovaginal candidiasis (VVC), as a common condition in women of childbearing age, is increasing all over the world as a result of extensive use of antibiotics and antifungal drugs. Objectives: In the present study to gain the up-to-date information on involved species and the prevalence of the recurrent vulvovaginal candidiasis (RVVC) in Isfahan, Iran, we assessed the etiologic agents of aforementioned disease in women referred to the Al-Zahra hospital (Isfahan, Iran). Furthermore, we surveyed the possible relationship between age, education and marital status with prevalence of albicans and non-albicans candidiasis. Patients and Methods: Our study was conducted on subjects who were admitted to the gynecology and midwifery clinic between September 2017 and August 2018 and had clinical presentations of vulvovaginitis. Sampling of 100 women was done using sterile swab. Samples were transferred to the hospital laboratory for cellular and molecular investigations. Results:Candida albicans was the main pathogen involved in the pathogenesis of RVVC and Candida glabrata is the second most common pathogen. Moreover, none of the 100 cases that we tested were infected with Candida krusei. We found a meaningful relationship between age and RVVC triggered by Candida albicans (P<0.05) but there was no significant relationship between age and RVVC that triggered by non-albicans fungi. There was no meaningful correlation between levels of education, number of children and types of delivery with RVVC that infected by various albicans and non-albicans candidiasis (P>0.05). Conclusion:Candidaalbicans was the main pathogen involved in the pathogenesis of RVVC in Isfahan while Candida glabrata is the second most common pathogen. Despite their high cost, molecular methods have high value in accurate diagnosis of the RVVC.

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Lazzarin, Adriano, Caterina Uberti-Foppa, Massimo Galli, Paolo Crocchiolo, and Mauro Moroni. "Pulmonary Candidiasis in a Heroin Addict: Some Remarks on its Aetiology and Pathogenesis." Addiction 80, no. 1 (March 1985): 103–4. http://dx.doi.org/10.1111/j.1360-0443.1985.tb05296.x.

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41

Willems, Hubertine M. E., Salman S. Ahmed, Junyan Liu, Zhenbo Xu, and Brian M. Peters. "Vulvovaginal Candidiasis: A Current Understanding and Burning Questions." Journal of Fungi 6, no. 1 (February 25, 2020): 27. http://dx.doi.org/10.3390/jof6010027.

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Candida albicans, along with other closely related Candida species, are the primary causative agents of vulvovaginal candidiasis (VVC)—a multifactorial infectious disease of the lower female reproductive tract resulting in pathologic inflammation. Unlike other forms of candidiasis, VVC is a disease of immunocompetent and otherwise healthy women, most predominant during their child-bearing years. While VVC is non-lethal, its high global incidence and profound negative impact on quality-of-life necessitates further understanding of the host and fungal factors that drive disease pathogenesis. In this review, we cover the current state of our understanding of the epidemiology, host response, fungal pathogenicity mechanisms, impact of the microbiome, and novel approaches to treatment of this most prevalent human candidal infection. We also offer insight into the latest advancements in the VVC field and identify important questions that still remain.

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Bertolini, Martinna, and Anna Dongari-Bagtzoglou. "The Dysbiosis and Inter-Kingdom Synergy Model in Oropharyngeal Candidiasis, a New Perspective in Pathogenesis." Journal of Fungi 5, no. 4 (September 21, 2019): 87. http://dx.doi.org/10.3390/jof5040087.

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As more information emerges on oral microbiota using advanced sequencing methodologies, it is imperative to examine how organisms modulate the capacity of each other to colonize or trigger infection. Most mouse models of oral C. albicans infection have focused on interactions with single bacterial species. Thus, little is known about the microbiome-mediated interactions that control the switch of C. albicans from commensalism to infection. Evidence is accumulating that in immunosuppression where mucosal candidiasis is more prevalent, there is an altered oral bacterial microbiome with reduced diversity, but not an altered mycobiome. Oropharyngeal candidiasis in immunosuppressed humans and mice is associated with a further reduction in oral bacterial diversity and a dysbiotic shift with significant enrichment of streptococcal and enterococcal species. Our recent studies in a cancer chemotherapy mouse model supported the combined profound effect of immunosuppression and C. albicans in reducing oral bacterial diversity and provided the first direct evidence that these changes contribute to pathogenesis, representing dysbiosis. There is still a gap in understanding the relationship between Candida and the oral bacterial microbiome. We propose that certain oral commensal bacteria contribute to fungal pathogenesis and we identify gaps in our understanding of the mechanisms involved in this cooperative virulence.

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Cheng, Shaoji, Cornelius J. Clancy, Douglas J. Hartman, Binghua Hao, and M. Hong Nguyen. "Candida glabrata Intra-Abdominal Candidiasis Is Characterized by Persistence within the Peritoneal Cavity and Abscesses." Infection and Immunity 82, no. 7 (May 5, 2014): 3015–22. http://dx.doi.org/10.1128/iai.00062-14.

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ABSTRACTThe pathogenesis ofCandida glabratainfections is poorly understood. We studied the pathogenesis of intra-abdominal candidiasis (IAC) in mice that were infected intraperitoneally withC. glabrataand sterile feces.C. glabrataBG2 (5 × 108CFU) caused a 100% mortality rate. Sublethal inocula of BG2 (1 × 108or 1 × 107CFU) caused peritonitis that progressed to abscesses. Three clinicalC. glabratastrains (5 × 108CFU) caused 80 to 100% mortality rates, while a fourth (strain 346) caused a 29% mortality rate. Following sublethal inocula (1 × 107CFU), the intra-abscess burdens of virulent strain 356 were ∼1 log greater than those of strain 346. AC. glabrataΔplb1-2mutant (phospholipase B genes disrupted) killed mice as well as BG2 did. When sublethal inocula were used, however, the Δplb1-2mutant was associated with more rapid abscess resolution and lower intra-abscess burdens; these findings were reversed byPLB1andPLB2reinsertion. The Δplb1-2mutant was also more susceptible than BG2 to killing by human neutrophilsin vitro. BG2 and the Δplb1-2mutant were indistinguishable during hematogenously disseminated candidiasis.C. albicansSC5314 was more virulent thanC. glabrataBG2 during IAC, causing a 100% mortality rate following a challenge with 5 × 107CFU. In contrast, a sublethal inoculum (1 × 107CFU) of BG2 caused less neutrophil infiltration and greater burdens in peritoneal fluid than SC5314 did and abscesses that persisted longer and contained greater burdens. In conclusion, a mouse model ofC. glabrataIAC mimics disease in humans and distinguishes the relative virulence of clinical and gene disruption strains.C. glabratadiffered fromC. albicansduring IAC by being less lethal and eliciting dampened neutrophil responses but resulting in more persistent peritonitis and abscesses.

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Mallya, Sachidananda, and Shrikara Mallya. "Candida and Oral Candidosis—A Review." Journal of Health and Allied Sciences NU 09, no. 02 (April 2019): 39–44. http://dx.doi.org/10.1055/s-0039-1695651.

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AbstractOral candidiasis (also called candidosis) is an opportunistic infection affecting the oral mucosa. These lesions are very common and caused by yeast Candida albicans. C. albicans are normal component of oral microflora and around 30 to 50% carry these organisms. The rate of carriage increases with advancing age of the patient. C. albicans are recovered from patient’s mouth over the age of 60 years. Other species such as C. glabrata, C. tropicalis, C. guilliermondii, and C. krusei are infrequently but consistently isolated. Oral candidosis can be classified into primary and secondary candidiasis. The factors involved in the pathogenicity of C. albicans have been reviewed. The pathogenesis of different biotypes and strains of C. albicans varies. A relationship has been suggested between the adherence of C. albicans to surfaces and its ability to colonize and cause disease. An important aspect of the pathogenicity of C. albicans may be its nonspecific affinity and binding to acrylic resin and other plastics. The factors affecting adhesion of yeasts, related to yeast cells, related to host cells and environmental factors, and the main factors which increase the susceptibility of oral candidiasis have been reviewed. The different types of oral lesions, their identification by different methods, management, and treatment of oral candidiasis also have been highlighted.Oral candidosis as a common opportunistic infection has gained importance after the discovery of human immunodeficiency virus infection. Candidiasis was always an endogenous infection. There are few cases of exogenous infection in intravenous drug abusers and contact lens users. Esophageal candidiasis is the earliest and most cases of lesions seen in acquired immunodeficiency syndrome patient. The diagnosis and reporting of oral candidiasis should be done with utmost care. The finding of yeast cells in large numbers and presence of pseudohyphae indicate invasion and causative agent of infection. The diagnosis of Candida infection can be confirmed by various techniques and recently discovered advanced methods.The confirmation of Candida infection depends on clinical diagnosis, proper collection of specimen, and careful evaluation in methodology and reporting.

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JACOB, LISA S., CATHERINE M. FLAITZ, C. MARK NICHOLS, and M. JOHN HICKS. "ROLE OF DENTINAL CARIOUS LESIONS IN THE PATHOGENESIS OF ORAL CANDIDIASIS IN HIV INFECTION." Journal of the American Dental Association 129, no. 2 (February 1998): 187–94. http://dx.doi.org/10.14219/jada.archive.1998.0176.

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46

Grubb, Sarah E. W., Craig Murdoch, Peter E. Sudbery, Stephen P. Saville, Jose L. Lopez-Ribot, and Martin H. Thornhill. "Candida albicans-Endothelial Cell Interactions: a Key Step in the Pathogenesis of Systemic Candidiasis." Infection and Immunity 76, no. 10 (June 23, 2008): 4370–77. http://dx.doi.org/10.1128/iai.00332-08.

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47

Fidel, Paul L., Junko Yano, Shannon K. Esher, and Mairi C. Noverr. "Applying the Host-Microbe Damage Response Framework to Candida Pathogenesis: Current and Prospective Strategies to Reduce Damage." Journal of Fungi 6, no. 1 (March 11, 2020): 35. http://dx.doi.org/10.3390/jof6010035.

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Disease is a complex outcome that can occur as a result of pathogen-mediated damage, host-mediated damage or both. This has led to the revolutionary concept of the damage response framework (DRF) that defines microbial virulence as a function of host immunity. The DRF outlines six scenarios (classes) of host damage or beneficial outcomes, depending on the microbe and the strength of the immune response. Candida albicans is uniquely adapted to its human host and can exist as either a commensal, colonizing various anatomical sites without causing notable damage, or as a pathogen, with the ability to cause a diverse array of diseases, ranging from mucosal to invasive systemic infections that result in varying levels of microbe-mediated and/or host-mediated damage. We recently categorized six different forms of candidiasis (oropharyngeal, hematogenous, intra-abdominal, gastrointestinal, denture stomatitis, and vulvovaginitis) into independent DRF classes, supporting a contemporary view of unique mechanisms of pathogenesis for these Candida infections. In this review, we summarize the evidence for the pathogenesis of these various forms of candidiasis in the context of the DRF with the further intent to provide insights into strategies to achieve a level of host response or outcome otherwise, that limits host damage.

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Naglik, Julian R., George Newport, Theodore C. White, Lynette L. Fernandes-Naglik, John S. Greenspan, Deborah Greenspan, Simon P. Sweet, Stephen J. Challacombe, and Nina Agabian. "In Vivo Analysis of Secreted Aspartyl Proteinase Expression in Human Oral Candidiasis." Infection and Immunity 67, no. 5 (May 1, 1999): 2482–90. http://dx.doi.org/10.1128/iai.67.5.2482-2490.1999.

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ABSTRACT Secreted aspartyl proteinases are putative virulence factors inCandida infections. Candida albicans possesses at least nine members of a SAP gene family, all of which have been sequenced. Although the expression of the SAPgenes has been extensively characterized under laboratory growth conditions, no studies have analyzed in detail the in vivo expression of these proteinases in human oral colonization and infection. We have developed a reliable and sensitive procedure to detect C. albicans mRNA from whole saliva of patients with oral C. albicans infection and those with asymptomaticCandida carriage. The reverse transcription-PCR protocol was used to determine which of the SAP1 to SAP7genes are expressed by C. albicans during colonization and infection of the oral cavity. SAP2 and the SAP4to SAP6 subfamily were the predominant proteinase genes expressed in the oral cavities of both Candida carriers and patients with oral candidiasis; SAP4, SAP5, orSAP6 mRNA was detected in all subjects. SAP1and SAP3 transcripts were observed only in patients with oral candidiasis. SAP7 mRNA expression, which has never been demonstrated under laboratory conditions, was detected in several of the patient samples. All seven SAP genes were simultaneously expressed in some patients with oral candidiasis. This is the first detailed study showing that the SAP gene family is expressed by C. albicans during colonization and infection in humans and that C. albicans infection is associated with the differential expression of individualSAP genes which may be involved in the pathogenesis of oral candidiasis.

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Badrane, Hassan, Shaoji Cheng, M. Hong Nguyen, Hong Yan Jia, Zongde Zhang, Nghe Weisner, and Cornelius J. Clancy. "Candida albicans IRS4 contributes to hyphal formation and virulence after the initial stages of disseminated candidiasis." Microbiology 151, no. 9 (September 1, 2005): 2923–31. http://dx.doi.org/10.1099/mic.0.27998-0.

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Candida albicans is a common cause of mucosal and bloodstream infections. As a screening strategy to identify novel candidal virulence factors, sera recovered from HIV-infected patients with active oropharyngeal candidiasis (OPC) were previously used to probe a C. albicans genomic expression library. IRS4 was identified as a gene that encodes an immunogenic protein. In the present study, the presence of IRS4 transcripts was verified within OPC pseudomembranes recovered from patients. Having confirmed that the gene is expressed during human candidiasis, gene disruption strains were created and this implicated IRS4 in diverse processes, including hyphal formation on solid media and under embedded conditions, cell wall integrity and structure, and adherence to human epithelial cells in vitro. IRS4 disruption, however, did not influence hyphal formation or virulence in a murine model of OPC. Rather, the gene was found to be necessary for normal morphogenesis and full virulence during murine intravenously disseminated candidiasis (DC). IRS4's effects on hyphal formation and virulence during DC were not evident on the first day after intravenous inoculation, even though transcripts were detected within murine kidneys. After 4 days, however, an irs4 null mutant strain was associated with attenuated mortality, diminished tissue burdens, less extensive infections, impaired C. albicans hyphal formation and decreased kidney damage. Taken together, these findings suggest that IRS4 makes distinct temporal-spatial contributions to the pathogenesis of candidiasis, which appear to vary between different tissue sites as well as within a given tissue over time.

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Bow, Eric J., Gerald Evans, Jeff Fuller, Michel Laverdière, Coleman Rotstein, Robert Rennie, Stephen D. Shafran, et al. "Canadian Clinical Practice Guidelines for Invasive Candidiasis in Adults." Canadian Journal of Infectious Diseases and Medical Microbiology 21, no. 4 (2010): e122-e150. http://dx.doi.org/10.1155/2010/357076.

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Candidemia and invasive candidiasis (C/IC) are life-threatening opportunistic infections that add excess morbidity, mortality and cost to the management of patients with a range of potentially curable underlying conditions. The Association of Medical Microbiology and Infectious Disease Canada developed evidence-based guidelines for the approach to the diagnosis and management of these infections in the ever-increasing population of at-risk adult patients in the health care system. Over the past few years, a new and broader understanding of the epidemiology and pathogenesis of C/IC has emerged and has been coupled with the availability of new antifungal agents and defined strategies for targeting groups at risk including, but not limited to, acute leukemia patients, hematopoietic stem cell transplants and solid organ transplants, and critical care unit patients. Accordingly, these guidelines have focused on patients at risk for C/IC, and on approaches of prevention, early therapy for suspected but unproven infection, and targeted therapy for probable and proven infection.

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