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Relevant bibliographies by topics / Candidiasis Pathogenesis

Academic literature on the topic 'Candidiasis Pathogenesis'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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Contents

Journal articles
Dissertations / Theses
Books
Book chapters

Journal articles on the topic "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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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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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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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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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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More sources

Dissertations / Theses on the topic "Candidiasis Pathogenesis":

1

Fox, A. J. "Studies on the pathogenesis and serodiagnosis of systemic candidiasis." Thesis, University of Aberdeen, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377596.

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A mouse model was used to study the pathogenesis of systemic infection by the opportunistic pathogen Candida albicans. Using this model it was demonstrated that C. albicans yeast cells were more pathogenic for mice than hyphal forms. Polymorphonuclear leukocytes were shown to be important in resistance to systemic infection by C. albicans. Studies on conditions which promote germination of C. albicans yeasts showed that maximum numbers of yeast cells produced germ tubes when incubated in tissue culture media at 37°C, by 2 hours. A comparative ultrastructural examination of yeasts, germ tubes and hyphal forms demonstrated marked differences in the thickness and organisation of the cell walls between these forms. Furthermore, germination of C. albicans yeasts was shown to be accompanied by significant release of cell wall antigens. In vitro interactions between mouse polymorphonuclear leukocytes and C. albicans yeasts, germ tubes and hyphae in the absence of serum were examined. Mouse neutrophils were found to adhere readily to the surface of germ tubes and hyphae but not yeasts. This adherence resulted in damage of the fungus. Studies on the degradation of killed C. albicans yeasts following phagocytosis by murine macrophages in vitro, showed that progressive removal of yeast cell wall layers occurred. This was followed by dissolution of the cytoplasmic contents. During this process, cell wall and cytoplasmic antigens were released into the surrounding medium. An enzyme linked immunosorbent assay was developed to measure IgM, IgA and IgG class antibodies to C. albicans mannan and cytoplasmic antigens in patient's sera, and was shown to have diagnostic potential for candida infection. In particular, use of this assay to monitor the kinetics of antibody levels to these antigens was found to be of diagnostic value for immunocompromised patients at risk of candida infection. Finally a number of monoclonal antibodies were produced to C. albicans cytoplasmic proteins and have been partially characterised.

2

Colina, Ana-Rosa. "Role of mucinolytic activity of Candida albicans in the pathogenesis of mucosal and invasive candidiasis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0006/NQ40497.pdf.

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3

Schmidt-Westhausen, Andrea Maria. "Experimentelle Untersuchungen zur Pathogenese und Therapie der oralen Candidiasis bei Immundefizienz." [S.l.] : [s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=962339725.

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4

Schmidt-Westhausen, Andrea Maria. "Experimentelle Untersuchungen zur Pathogenese und Therapie der oralen Candidiasis bei Immundefizienz." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2001. http://dx.doi.org/10.18452/13748.

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Ziel der vorliegenden Arbeit war anhand eines Tiermodells zu untersuchen, 1. ob eine Dosis-Wirkungsbeziehung zwischen der Keimmenge und der Entstehung einer oralen C. albicans Infektion besteht, 2. welche zelluläre Immunantwort auf definierte inokulierte Keimmengen stattfindet, 3. ob sich die Adhärenz von C. albicans an murine Epithelzellen durch Spaltprodukte von Muzin (Glykopeptide) verhindern läßt. Material und Methode: Immunkompetente Inzuchtmäuse (Balb/c) (n=27) und Mäuse mit kombiniertem B- und T-Zelldefekt (SCID) (n=30) wurden mit Keimmengen von10^4 bis 10^8 C. albicans-Zellen/10 mikrol des Stammes DSM 3454 oral inokuliert. Darüber hinaus wurden Balb/c Mäuse (n=8) mit 10^8 C. albicans-Zellen in Kombination mit Glykopeptiden und SCID Mäuse (n=8) mit 10^5 C. albicans-Zellen mit Glykopeptiden inokuliert. Eine Zungenhälfte wurde histologisch mittels Periodic-Acid-Schiff (PAS) Reaktion auf Invasion von Hyphen untersucht. Die andere Hälfte wurde mittels Immunperoxidase-Technik auf die Verteilung immunkompetenter Zellen (CD4, CD13, ICAM-1, E-Selectin, CD74, CD80, CD86, CD103) im Epithel und subepithelialen Bindegewebe untersucht. Ergebnisse: Eine Woche post inoculationem fanden sich weder bei Balb/c noch bei SCID Mäusen klinische Zeichen einer oralen Candidiasis. Die histologischen Ergebnisse mittels PAS-Methode zeigten jedoch, daß eine Inokulationsmenge von 10^8 C. albicans-Zellen bei Balb/c Mäusen und 10^8 Keime bei SCID Mäusen zu einer Infektion der Zungenmukosa führte. Das Ausmaß der immunologischen Reaktion war abhängig von der Inokulationsdosis sowie vom Immunstatus der Tiere. Die Ergebnisse der Inokulation von 10^8 C. albicans-Zellen zusammen mit Glykopeptiden zeigten bei 2/8 Balb/c Mäusen eine Hypheninvasion in das Zungenepithel. Bei 0/8 SCID Mäusen wurde nach Inokulation von 10^4 C. albicans-Zellen zusammen mit Glykopeptiden eine Hypheninvasion in das Zungenepithel beobachtet. Die immunhistochemischen Ergebnisse zeigten, daß die Reaktionen des Wirtes auf die Gabe der Keim-Glykopeptidlösung denen ohne Inokulation entsprachen. Schlußfolgerung: Obwohl bei den eingesetzten C. albicans-Mengen keine klinisch manifeste orale Candidiasis vorhanden war, fanden sich in beiden Tierstämmen inapparente Infektionen des Zungenepithel (Hypheninvasion), die immunologische Reaktionen der Zungenmukosa auslösten. Da nach Inokulation von C. albicans-Zellen zusammen mit Glykopeptiden weniger häufig Infektionen nachgewiesen werden konnten als bei Inokulation derselben Keimmenge ohne Glykopeptide und Nebenwirkungen dieser antiadhäsiven Wirkstoffe bisher nicht nachgewiesen wurden, wäre der unterstützende Einsatz von Muzinen oder deren Spaltprodukten bei Patienten mit erhöhtem Candidiasisrisiko zu erwägen.
This study applied an animal model to address the following questions: 1. Does a dose/effect relationship exist between C. albicans load and the emergence of an oral C. albicans infection, 2. which cellular immune response takes place following inoculation with defined pathogen loads, 3. is it possible to inhibit C. albicans adhesion to murine epithelium cells through the local application of mucine metabolites (glycopeptides). Material and methods: Immunocompetent inbred mice (Balb/c) (n=27) and mice with combined B- and T-cell defects (SCID) (n=30) were orally inoculated with pathogen loads between 10^4 and 10^8 C. albicans cells/10 microl (strain DSM 3454). Moreover, Balb/c mice (n=8) were inoculated with 10^8 C. albicans cells in combination with glycopeptides; SCID mice (n=8) were inoculated with 10^5 cells, also in combination with glycopeptides. One half of the tongue tissue was histochemically examined with the Periodic Acid Schiff (PAS) Method for displaying the invasion of hyphae. The other half of the tissue was examined by immune peroxidase technique for analysing the distribution of immunocompetent cells (CD4, CD13, ICAM-1, E-Selectin, CD74, CD80, CD86, CD103) in the epithelial layers and subepithelial connective tissue. Results: One week following the inoculation, neither group's tissue showed clinical signs of oral candidiasis. Following histochemical preparation (PAS-Reaction) the tongue mucosa showed signs of infection (hyphae) with the inoculation dose of 10^8 C. albicans cells in the case of Balb/c mice and a load of 10^5 pathogens in the case of SCID mice. The extent of the immunologic reaction depended both on the inoculation dose given to the animals and on their immune status. The results of an inoculation of 10^8 C. albicans cells in combination with glycopeptides showed hyphae invasion of the tongue epithelium in 2/8 Balb/c mice. Following an inoculation of 10^5 pathogens in combination with glycopeptides hyphae invasion could be demonstrated in 0/8 SCID mice. The results of immunohistochemical studies showed that the host's reaction to combined glycopeptide-pathogen-inoculation correspond to the reaction without inoculation. Conclusion: Despite the lack of clinical signs of oral candidiasis in neither group's tissue, non-apparent infections of the tongue epithelium were evident leading to immunologic reactions of the tongue mucosa. Inoculation of C. albicans cells in combination with glycopeptides resulted in decreased infection rate compared to a corresponding inoculation dose without glycopeptides. As no side effects have been documented for the oral application of these antiadhesive agents, their use as complimentary therapy for patients at an increased risk for oral candidiasis should be considered.

5

Schmidt-Westhausen, Andrea [Verfasser]. "Experimentelle Untersuchungen zur Pathogenese und Therapie der oralen Candidiasis bei Immundefizienz / Andrea Maria Schmidt-Westhausen." Berlin : Humboldt-Universität zu Berlin, 2001. http://d-nb.info/1207666343/34.

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6

Fraser, Michelle (Michelle Lousie). "Systematics of the genus Candida; implications for understanding clinical presentation, mixed infection and antifungal treatment and the influence on strain maintenance and replacement during oral candidiasis in HIV-infected individuals." 2002. http://web4.library.adelaide.edu.au/theses/09PH/09phf8421.pdf.

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"8th July 2002." Includes bibliographical references (leaves 276-308) Examines the systematics (taxonomy, phylogeny, and epiemiology) of the genus Candida using a combination of traditional and contemporary methodologies. Assesses these methods to determine their diagnostic potential to unequivocally identify and characterise species and strains of this medically and dentally important yeast genus.

7

Fraser, Michelle Louise. "Systematics of the genus Candida; implications for understanding clinical presentation, mixed infection and antifungal treatment and the influence on strain maintenance and replacement during oral candidiasis in HIV-infected individuals / by Michelle Fraser." 2002. http://hdl.handle.net/2440/21799.

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"8th July 2002."
Includes bibliographical references (leaves 276-308)
vi, 308, [57] leaves : charts ; 30 cm.
Title page, contents and abstract only. The complete thesis in print form is available from the University Library.
Examines the systematics (taxonomy, phylogeny, and epiemiology) of the genus Candida using a combination of traditional and contemporary methodologies. Assesses these methods to determine their diagnostic potential to unequivocally identify and characterise species and strains of this medically and dentally important yeast genus.
Thesis (Ph.D.)--University of Adelaide, Dept. of Dentistry, 2002

8

Schmidt-Westhausen, Andrea [Verfasser]. "Experimentelle Untersuchungen zur Pathogenese und Therapie der oralen Candidiasis bei Immundefizienz / vorgelegt von Andrea Maria Schmidt-Westhausen." 2000. http://d-nb.info/962339725/34.

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Books on the topic "Candidiasis Pathogenesis":

1

Saltarelli, Cora G. Candida albicans: The pathogenic fungus. New York: Hemisphere Pub. Corp., 1989.

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2

1934-, Bodey Gerald P., ed. Candidiasis: Pathogenesis, diagnosis, and treatment. 2nd ed. New York: Raven Press, 1993.

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3

Bodey, Gerald P. Candidiasis: Pathogenesis, Diagnosis, and Treatment. 2nd ed. Raven Pr, 1992.

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4

Maziarz, Eileen K., and John R. Perfect. Fungal infections of the kidney and those associated with renal failure, dialysis, and renal transplantation. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0029.

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Fungal infections involving the kidney are often a manifestation of disseminated fungal infection, although primary renal fungal infections do occur, usually from a lower urinary tract source or in the setting of renal transplantation. Candida spp. cause the vast majority of these infections and are the representative pathogen for understanding the pathogenesis of these types of infections. The risk factors and mycology of acute renal candidiasis reflect those of invasive candidiasis. Unique risk factors are observed in chronic renal candidiasis, which manifests differently and requires distinct management approaches. This chapter discusses the spectrum of invasive mycoses involving the kidney, as well as those associated with chronic renal failure, dialysis, and renal transplantation.

5

Sobel, Jack D. Genito-urinary fungal infections. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0027.

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The predominant fungal causes of genitourinary disease are Candida spp.; other fungal genera are uncommon pathogens in both sexes. Vulvovaginal candidiasis affects millions of women worldwide—and includes acute sporadic, recurrent, and chronic syndromes—and considerable progress has been made in understanding its pathophysiology and hence the best therapy. Therapeutic options are still limited, however, and misdiagnosis is common. In contrast, urinary tract candidiasis reflects an entirely different pathogenesis and clinical expression affecting a predominantly hospital-based older population. Candida organisms are extremely difficult to eradicate from often complicated urinary tract infections. Non-Candida fungal species reach the kidney and prostate by the bloodstream rather than the ascending route taken by Candida spp. In women, not infrequently, there is simultaneous lower genital tract and urinary tract infection, requiring attention to both systems.

6

Guhad, Faisal Abdi. Development and Validation of a Localized Murine Candidiasis Model: The Pathogenesis, Chemotherapy and Defense Mechanisms to Candida Mastitis in the Lactating ... Summaries of Uppsala Dissertations, 829). Uppsala Universitet, 1999.

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7

Hube, Bernhard, and Oliver Kurzai. Candida species. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0011.

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Most pathogenic Candida species are members of the microbiota, but also cause superficial or invasive infections. C. albicans is predominant, followed by C. glabrata, C. parapsilosis, and C. tropicalis. C. albicans is polymorphic and grows as yeast, pseudohyphae, or hyphae. The cell wall has multiple functions in pathogenesis. Metabolism and nutrient up-take strategies facilitate growth in multiple niches within the host. Drug resistance is an intrinsic property of C. glabrata and C. krusei, but can be developed by C. albicans and other Candida species during antifungal therapy. Pathogenicity mechanisms include host cell attachment, invasion, and destructive activities; immune evasion; and biofilm production. A disbalanced microbiota and impaired immunity favour superficial infections, and disturbance of the mucosal barriers, together with compromised immunity, enables Candida to invade the human bloodstream and cause invasive infection. Even with antifungal therapy (e.g. azoles or echinocandins), disseminated candidiasis has a high mortality (40–50%).

Book chapters on the topic "Candidiasis Pathogenesis":

1

Filler, Scott G., and John E. Edwards. "Chronic Mucocutaneous Candidiasis." In Infectious Agents and Pathogenesis, 117–33. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4899-2400-1_5.

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2

Walsh, Thomas J., Emmanuel Roilides, Karoll Cortez, and Caron Lyman. "Molecular Immunopathogenesis of Innate Host Defense against Chronic Disseminated (Hepatosplenic) Candidiasis." In Molecular Principles of Fungal Pathogenesis, 583–88. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555815776.ch39.

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3

"Vaccines, Antibodies, in Candidiasis." In Fungal Pathogenesis, 343–70. CRC Press, 2001. http://dx.doi.org/10.1201/9781482270907-27.

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