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1
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
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Isobolographic in vitro interactions of fluconazole with citrus essential oils against Cladosporium cladosporioides

100%
Wroblewska-Luczka P.
Journal of Pre-Clinical and Clinical Research
|
2021
|
tom 15
|
nr 1
2
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
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Additivity interactions between fluconazole and citrus essential oils to Aspergillus fumigatus

72%
Wroblewska-Luczka P., Luszczki J.
Journal of Pre-Clinical and Clinical Research
|
2021
|
tom 15
|
nr 3
3
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
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Detection of cross-resistance between methotrexate and azoles in Candida albicans and Meyerozyma guilliermondii: an in vitro study

72%
Karuga F. F., Goralska K., Brzezianska-Lasota E.
Acta Mycologica
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2021
|
tom 56
|
nr 1
4
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
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Yeasts isolated from frequently in-patients and out-patients

72%
Dynowska M., Ejdys E., Biedunkiewicz A., Kubiak D., Sucharzewska E., Roslan M.
Annals of Parasitology
|
2014
|
tom 60
|
nr 3
The paper is a part of a general mycological monitoring study of nosocomial infections. Differences in the species composition and drug resistance of fungi isolated from in-patients and out-patients prompted an analysis of this topic. The studies were conducted with fungi from the collection of the Department of Mycology, University of Warmia and Mazury in Olsztyn, that were isolated from the oral cavity, sputum, bronchoscopic fluid, anus and skin from 100 in-patients and 100 out-patients. Laboratory analyses, including species categorization of fungi, were performed according to routine mycological diagnostics. Drug sensitivity to fluconazole and nystatin was tested with the disc diffusion method. In the group of in-patients, a wider taxonomic diversity of fungi (12 species) was found in comparison with the out-patients (7 species) and 31 cases of multifocal infections were recorded, while in the second group the number of the latter was only six. In all patients, C. albicans were predominant, constituting the largest proportion in focal infections in all patients and in multifocal infections in the in-patients. In the latter, over a half of the examined individuals were resistant to fluconazole (C. glabrata and C. krusei – 80%, C. tropicalis and S. capsularis – 60%, C. guilliermondii – 50%) and nystatin (T. beigelii – 80%, C. krusei and C. tropicalis – 50%). Substantially lower drug resistance of fungi was recorded in the out-patients. The hospital environment is an abundant reservoir of different fungal species with significantly greater expansiveness and aggressiveness compared to the environment outside a hospital.
5
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Cutaneous leishmaniasis mimicking granulomatous cheilitis and treated successfully with oral fluconazole in a boy

72%
Serarslan G., Aksakal M.
Annals of Parasitology
|
2015
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tom 61
|
nr 3
Cutaneous leishmaniasis is a protozoan infectious disease and widespread in Mediterranean basin including Turkey. Lesions usually start with erythematous papules, gradually enlarges and afterwards it ulcerates. We present a 12-year-old boy with diffuse persistent lip swelling mimicking granulomatous cheilitis. Systemic glucantime was started. However, severe hypotension and bradycardia was developed after injection. Oral fluconazole was started and the lesion resolved completely. Cutaneous leishmaniasis can have varied clinical manifestations and should be suspected especially in endemic areas. Oral fluconazole seems to be safe and effective treatment modality in paediatric cases.
6
Content available remote

Effect of Candida colonization on human ulcerative colitis and the healing of inflammatory changes of the colon in the experimental model of colitis ulcerosa

58%
Zwolinska-Wcislo M., Brzozowski T., Budak A., Kwiecien S., Sliwowski Z., Drozdowicz D., Trojanowska D., Rudnicka-Sosin L., Mach T., Konturek S. J., Pawlik W. W.
Journal of Physiology and Pharmacology
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2009
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tom 60
|
nr 1
107-118
The influence of fungal colonization on the course of ulcerative colitis (UC) has not been thoroughly studied. We determined the activity of the disease using clinical, endoscopic and histological index (IACH) criteria in UC patients with fungal colonization and the healing process of UC induced by an intrarectal administration of trinitrobenzene sulfonic acid (TNBS) in rats infected with Candida, without and with antifungal (fluconazole) or probiotic (lacidofil) treatment. The intensity of the healing of the colonic lesions was assessed by macro- and microscopic criteria as well as functional alterations in colonic blood flow (CBF). Myeloperoxidase (MPO) content and plasma proinflammatory cytokines IL-1ß and TNF- levels were evaluated. Candida more frequently colonized patients with a history of UC within a 5-year period, when compared with those of shorter duration of IBS. Among Candida strains colonizing intestinal mucosa, Candida albicans was identified in 91% of cases. Significant inhibition of the UC activity index as reflected by clinical, endoscopical and histological criteria was observed in the Candida group treated with fluconazole, when compared to that without antifungal treatment. In the animal model, Candida infection significantly delayed the healing of TNBS-induced UC, decreased the CBF and raised the plasma IL-1ß and TNF- levels, with these effects reversed by fluconazole or lacidofil treatment. We conclude that 1) Candida delays healing of UC in both humans and that induced by TNBS in rats, and 2) antifungal therapy and probiotic treatment during Candida infection could be beneficial in the restoration and healing of colonic damage in UC.
7

Antifungal susceptibility of yeasts isolated from secrection of inflamed mammary glands in cows

58%
Wawron W., Bochniarz M., Dabrowski R.
Polish Journal of Veterinary Sciences
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2010
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tom 13
|
nr 3
8

Mechanisms of resistance to azole antifungals

58%
Marichal P., Bossche H. V.
Acta Biochimica Polonica
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1995
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tom 42
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nr 4
Until the late eighties, clinical resistance to azole antifungals was a rare pheno­menon. Only a few cases of resistance to ketoconazole were found in patients with chronic mucocutaneous candidiasis (CMC). The spread of AIDS and the widespread prophylactic and therapeutic use of the hydrophilic azole compound fluconazole resulted both in the selection and induction of resistant strains and in a shift in the nature of the infecting organisms. Most azole antifungals such as itraconazole, ketoconazole and fluconazole are active against a variety of fungal diseases. However, the concentration needed to inhibit growth is dependent on the nature of the infecting species. Mucor spp., e.g., are almost insensitive to present available azole compounds and can be regarded as intrinsically resistant to azole treatment. Physicochemical features, such as the hydrophobicity and pKa, of a given azole, define whether or not it will be active or cross-resistant against a given species. Fluconazole is almost inactive against Candida krusei and Aspergillus fumigatus, whereas the lipophilic itraconazole is active against these species. A third type of resistance is acquired or induced resistance. This is the most contro­versial type because, even within a given species, organisms may differ in their response to the same azole. For these strains, convincing evidence can only be obtained when there is a genotypically related strain, which does not show resistance. In a limited number of biochemical or molecular biological studies the mechanisms of resistance have been investigated at the molecular level. These studies show that resistance can occur when there is an insufficient intracellular content of the azole. This can be due to impermeability problems, inactivated uptake systems or, and more likely, the presence of active multidrug resistance gene products of the P-glycoprotein type. Alteration or overexpression of the target for azole antifungals, the cytochrome P450-dependent 14 a-demethylase, also induces resistance. The nature and amount of the accumulating sterols also are of great importance for azole-induced growth inhi­bition. This may explain why mutations in other enzymes of the ergosterol bio­synthesis pathway, e.g. the A5-6 desaturase, can contribute to azole resistance.
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