Five membered rings containing a NITROGEN atom.
Substances that destroy fungi by suppressing their ability to grow or reproduce. They differ from FUNGICIDES, INDUSTRIAL because they defend against fungi present in human or animal tissues.
The ability of fungi to resist or to become tolerant to chemotherapeutic agents, antifungal agents, or antibiotics. This resistance may be acquired through gene mutation.
Triazole antifungal agent that is used to treat oropharyngeal CANDIDIASIS and cryptococcal MENINGITIS in AIDS.
A triazole antifungal agent that inhibits cytochrome P-450-dependent enzymes required for ERGOSTEROL synthesis.
A unicellular budding fungus which is the principal pathogenic species causing CANDIDIASIS (moniliasis).
A species of MITOSPORIC FUNGI commonly found on the body surface. It causes opportunistic infections especially in immunocompromised patients.
Broad spectrum antifungal agent used for long periods at high doses, especially in immunosuppressed patients.
Triazoles are a class of antifungal drugs that contain a triazole ring in their chemical structure and work by inhibiting the synthesis of ergosterol, an essential component of fungal cell membranes, thereby disrupting the integrity and function of the membrane.
A steroid of interest both because its biosynthesis in FUNGI is a target of ANTIFUNGAL AGENTS, notably AZOLES, and because when it is present in SKIN of animals, ULTRAVIOLET RAYS break a bond to result in ERGOCALCIFEROL.
An imidazole derivative that is commonly used as a topical antifungal agent.
A genus of yeast-like mitosporic Saccharomycetales fungi characterized by producing yeast cells, mycelia, pseudomycelia, and blastophores. It is commonly part of the normal flora of the skin, mouth, intestinal tract, and vagina, but can cause a variety of infections, including CANDIDIASIS; ONYCHOMYCOSIS; vulvovaginal candidiasis (CANDIDIASIS, VULVOVAGINAL), and thrush (see CANDIDIASIS, ORAL). (From Dorland, 28th ed)
An imidazole antifungal agent that is used topically and by intravenous infusion.
Any tests that demonstrate the relative efficacy of different chemotherapeutic agents against specific microorganisms (i.e., bacteria, fungi, viruses).
An imidazole derivative with a broad spectrum of antimycotic activity. It inhibits biosynthesis of the sterol ergostol, an important component of fungal CELL MEMBRANES. Its action leads to increased membrane permeability and apparent disruption of enzyme systems bound to the membrane.
Infection with a fungus of the genus CANDIDA. It is usually a superficial infection of the moist areas of the body and is generally caused by CANDIDA ALBICANS. (Dorland, 27th ed)
A species of imperfect fungi from which the antibiotic fumigatin is obtained. Its spores may cause respiratory infection in birds and mammals.
Chemicals that kill or inhibit the growth of fungi in agricultural applications, on wood, plastics, or other materials, in swimming pools, etc.
Infection of the mucous membranes of the mouth by a fungus of the genus CANDIDA. (Dorland, 27th ed)
Proteins found in any species of fungus.
Macrolide antifungal antibiotic produced by Streptomyces nodosus obtained from soil of the Orinoco river region of Venezuela.
Steroids with a hydroxyl group at C-3 and most of the skeleton of cholestane. Additional carbon atoms may be present in the side chain. (IUPAC Steroid Nomenclature, 1987)
Infections with fungi of the genus ASPERGILLUS.
A superfamily of hundreds of closely related HEMEPROTEINS found throughout the phylogenetic spectrum, from animals, plants, fungi, to bacteria. They include numerous complex monooxygenases (MIXED FUNCTION OXYGENASES). In animals, these P-450 enzymes serve two major functions: (1) biosynthesis of steroids, fatty acids, and bile acids; (2) metabolism of endogenous and a wide variety of exogenous substrates, such as toxins and drugs (BIOTRANSFORMATION). They are classified, according to their sequence similarities rather than functions, into CYP gene families (>40% homology) and subfamilies (>59% homology). For example, enzymes from the CYP1, CYP2, and CYP3 gene families are responsible for most drug metabolism.
Compounds that specifically inhibit STEROL 14-DEMETHYLASE. A variety of azole-derived ANTIFUNGAL AGENTS act through this mechanism.
Cyclic hexapeptides of proline-ornithine-threonine-proline-threonine-serine. The cyclization with a single non-peptide bond can lead them to be incorrectly called DEPSIPEPTIDES, but the echinocandins lack ester links. Antifungal activity is via inhibition of 1,3-beta-glucan synthase production of BETA-GLUCANS.
A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (CYTOSINE; THYMINE; and URACIL) and form the basic structure of the barbiturates.
A species of MITOSPORIC FUNGI that is a major cause of SEPTICEMIA and disseminated CANDIDIASIS, especially in patients with LYMPHOMA; LEUKEMIA; and DIABETES MELLITUS. It is also found as part of the normal human mucocutaneous flora.
The ability of microorganisms, especially bacteria, to resist or to become tolerant to chemotherapeutic agents, antimicrobial agents, or antibiotics. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).
A triterpene that derives from the chair-boat-chair-boat folding of 2,3-oxidosqualene. It is metabolized to CHOLESTEROL and CUCURBITACINS.
A species of the fungus CRYPTOCOCCUS. Its teleomorph is Filobasidiella bacillispora.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in fungi.

Synergic effects of tactolimus and azole antifungal agents against azole-resistant Candida albican strains. (1/584)

We investigated the effects of combining tacrolimus and azole antifungal agents in azole-resistant strains of Candida albicans by comparing the accumulation of [3H]itraconazole. The CDR1-expressing resistant strain C26 accumulated less itraconazole than the CaMDR-expressing resistant strain C40 or the azole-sensitive strain B2630. A CDR1-expressing Saccharomyces cerevisiae mutant, DSY415, showed a marked reduction in the accumulation of both fluconazole and itraconazole. A CaMDR-expressing S. cerevisiae mutant, DSY416, also showed lower accumulation of fluconazole, but not of itraconazole. The addition of sodium azide, an electron-transport chain inhibitor, increased the intracellular accumulation of itraconazole only in the C26 strain, and not in the C40 or B2630 strains. Addition of tacrolimus, an inhibitor of multidrug resistance proteins, resulted in the highest increase in itraconazole accumulation in the C26 strain. The combination of itraconazole and tacrolimus was synergic in azole-resistant C. albicans strains. In the C26 strain, the MIC of itraconazole decreased from >8 to 0.5 mg/L when combined with tacrolimus. Our results showed that two multidrug resistance phenotypes (encoded by the CDR1 and CaMDR genes) in C. albicans have different substrate specificity for azole antifungal agents and that a combination of tacrolimus and azole antifungal agents is effective against azole-resistant strains of C. albicans.  (+info)

Protection of ebselen against anoxic damage of cultured neurons of cerebral cortex. (2/584)

AIM: To study the protective effect of ebselen on anoxic damage of brain cells. METHODS: On d 10 after plating of the cortical neurons from 1-d-old rat, cultures were placed under 95% N2 + 5% CO2 for 2-6 h. Lactate dehydrogenase (LDH) in supernatant, thiobarbituric acid reactive substance (TBARS) and glutathione peroxidase (GSH-Px) activity of neurons were determined. RESULTS: Under anoxia, efflux of LDH and TBARS from cultured neurons increased while GSH-Px activity decreased. Ebselen reduced the efflux of LDH and TBARS in a dose-related manner and increased the total GSH-Px activity. CONCLUSION: Ebselen can protect neurons from anoxic damage.  (+info)

Effects of azole antifungal drugs on the transition from yeast cells to hyphae in susceptible and resistant isolates of the pathogenic yeast Candida albicans. (3/584)

Oral infections caused by the yeast Candida albicans are some of the most frequent and earliest opportunistic infections in human immunodeficiency virus-infected patients. The widespread use of azole antifungal drugs has led to the development of drug resistance, creating a major problem in the treatment of yeast infections in AIDS patients and other immunocompromised individuals. Several molecular mechanisms that contribute to drug resistance have been identified. In C. albicans, the ability to morphologically switch from yeast cells (blastospores) to filamentous forms (hyphae) is an important virulence factor which contributes to the dissemination of Candida in host tissues and which promotes infection and invasion. A positive correlation between the level of antifungal drug resistance and the ability to form hyphae in the presence of azole drugs has been identified. Under hypha-inducing conditions in the presence of an azole drug, resistant clinical isolates form hyphae, while susceptible yeast isolates do not. This correlation is observed in a random sample from a population of susceptible and resistant isolates and is independent of the mechanisms of resistance. 35S-methionine incorporation suggests that growth inhibition is not sufficient to explain the inhibition of hyphal formation, but it may contribute to this inhibition.  (+info)

Formation of azole-resistant Candida albicans by mutation of sterol 14-demethylase P450. (4/584)

The sterol 14-demethylase P450 (CYP51) of a fluconazole-resistant isolate of Candida albicans, DUMC136, showed reduced susceptibility to this azole but with little change in its catalytic activity. Twelve nucleotide substitutions, resulting in four amino acid changes, were identified in the DUMC136 CYP51 gene in comparison with a reported CYP51 sequence from a wild-type, fluconazole-susceptible C. albicans strain. Seven of these substitutions, including all of those causing amino acid changes, were located within a region covering one of the putative substrate recognition sites of the enzyme (SRS-1). Polymorphisms within this region were observed in several C. albicans isolates, and some were found to be CYP51 heterozygotes. Among the amino acid changes occurring in this region, only an alteration of Y132 was common among these fluconazole-resistant isolates, which suggests the importance of this residue to the fluconazole resistance of the target enzyme. DUMC136 and another fluconazole-resistant isolate were homozygotes with respect to CYP51, although the typical wild-type, fluconazole-susceptible C. albicans was a CYP51 heterozygote. These findings suggest that part of the fluconazole-resistant phenotype of C. albicans DUMC136 was acquired through a mutation-prone area of CYP51, an area which might promote the formation of fluconazole-resistant CYP51, along with a mechanism(s) which allows the formation of a homozygote of this altered CYP51 in this diploid pathogenic yeast.  (+info)

When and why a water-soluble antioxidant becomes pro-oxidant during copper-induced low-density lipoprotein oxidation: a study using uric acid. (5/584)

The inclusion of uric acid in the incubation medium during copper-induced low-density lipoprotein (LDL) oxidation exerted either an antioxidant or pro-oxidant effect. The pro-oxidant effect, as mirrored by an enhanced formation of conjugated dienes, lipid peroxides, thiobarbituric acid-reactive substances and increase in negative charge, occurred when uric acid was added late during the inhibitory or lag phase and during the subsequent extensive propagation phase of copper-stimulated LDL oxidation. The pro-oxidant effect of uric acid was specific for copper-induced LDL oxidation and required the presence of copper as either Cu(I) or Cu(II). In addition, it became much more evident when the copper to LDL molar ratio was below a threshold value of approx. 50. In native LDL, the shift between the antioxidant and the pro-oxidant activities was related to the availability of lipid hydroperoxides formed during the early phases of copper-promoted LDL oxidation. The artificial enrichment of isolated LDL with alpha-tocopherol delayed the onset of the pro-oxidant activity of uric acid and also decreased the rate of stimulated lipid peroxidation. However, previous depletion of alpha-tocopherol was not a prerequisite for unmasking the pro-oxidant activity of uric acid, since this became apparent even when alpha-tocopherol was still present in significant amounts (more than 50% of the original values) in LDL. These results suggest, irrespective of the levels of endogenous alpha-tocopherol, that uric acid may enhance LDL oxidation by reducing Cu(II) to Cu(I), thus making more Cu(I) available for subsequent radical decomposition of lipid peroxides and propagation reactions.  (+info)

Optimized expression and catalytic properties of a wheat obtusifoliol 14alpha-demethylase (CYP51) expressed in yeast. Complementation of erg11Delta yeast mutants by plant CYP51. (6/584)

CYP51s form the only family of P450 proteins conserved in evolution from prokaryotes to fungi, plants and mammals. In all eukaryotes, CYP51s catalyse 14alpha-demethylation of sterols. We have recently isolated two CYP51 cDNAs from sorghum [Bak, S., Kahn, R.A., Olsen, C. E. & Halkier, B.A. (1997) Plant J. 11, 191-201] and wheat [Cabello-Hurtado, F., Zimmerlin, A., Rahier, A., Taton, M., DeRose, R., Nedelkina, S., Batard, Y., Durst, F., Pallett, K.E. & Werck-Reichhart, D. (1997) Biophys. Biochem. Res. Commun. 230, 381-385]. Wheat and sorghum CYP51 proteins show a high identity (92%) compared with their identity with their fungal and mammalian orthologues (32-39%). Data obtained with plant microsomes have previously suggested that differences in primary sequences reflect differences in sterol pathways and CYP51 substrate specificities between animals, fungi and plants. To investigate more thoroughly the properties of the plant CYP51, the wheat enzyme was expressed in yeast strains overexpressing different P450 reductases as a fusion with either yeast or plant (sorghum) membrane targeting sequences. The endogenous sterol demethylase gene (ERG11) was then disrupted. A sorghum-wheat fusion protein expressed with the Arabidopsis thaliana reductase ATR1 showed the highest level of expression and activity. The expression induced a marked proliferation of microsomal membranes so as to obtain 70 nmol P450.(L culture)-1, with CYP51 representing 1.5% of microsomal protein. Without disruption of the ERG11 gene, the expression level was fivefold reduced. CYP51 from wheat complemented the ERG11 disruption, as the modified yeasts did not need supplementation with exogenous ergosterol and grew normally under aerobic conditions. The fusion plant enzyme catalysed 14alpha-demethylation of obtusifoliol very actively (Km,app = 197 microm, kcat = 1.2 min-1) and with very strict substrate specificity. No metabolism of lanosterol and eburicol, the substrates of the fungal and mammalian CYP51s, nor metabolism of herbicides and fatty acids was detected in the recombinant yeast microsomes. Surprisingly lanosterol (Ks = 2.2 microM) and eburicol (Ks = 2.5 microm) were found to bind the active site of the plant enzyme with affinities higher than that for obtusifoliol (Ks = 289 microM), giving typical type-I spectra. The amplitudes of these spectra, however, suggested that lanosterol and eburicol were less favourably positioned to be metabolized than obtusifoliol. The recombinant enzyme was also used to test the relative binding constants of two azole compounds, LAB170250F and gamma-ketotriazole, which were previously reported to be potent inhibitors of the plant enzyme. The Ks of plant CYP51 for LAB170250F (0.29 microM) and gamma-ketotriazole (0.40 microM) calculated from the type-II sp2 nitrogen-binding spectra were in better agreement with their reported effects as plant CYP51 inhibitors than values previously determined with plant microsomes. This optimized expression system thus provides an excellent tool for detailed enzymological and mechanistic studies, and for improving the selectivity of inhibitory molecules.  (+info)

Comparison of the toxicity of fluconazole and other azole antifungal drugs to murine and human granulocyte-macrophage progenitor cells in vitro. (7/584)

We studied the inhibitory effects on colony formation by granulocyte-macrophage colony forming units (cfu-gm) of eight azole antifungal agents in vitro. All agents, except fluconazole, inhibited colony formation dose-dependently with 50% inhibitory concentrations (IC50) in the range of 0.78-49 micromol/L in cultures of murine and human bone marrow. For human cells, the IC50 values were 0.553 mg/L for itraconazole, 1.24 mg/L for saperconazole, 2.58 mg/L for clotrimazole, 5.33 mg/L for miconazole, 6.17 mg/L for econazole, 6.27 mg/L for ketoconazole and 8.38 mg/L for oxiconazole. The IC50 of itraconazole for human cfu-gm in vitro was similar to the plasma level of this drug recommended for systemic antifungal therapy (>0.5 mg/L) thus indicating the potential clinical relevance of our data. The IC50 of ketoconazole for human cfu-gm in vitro may be exceeded by plasma levels produced in vivo by high (> or =400 mg) doses, whereas fluconazole failed to reduce colony formation by 50% even at 100 mg/L, a concentration not reached in vivo even after extremely high doses (2000 mg/day). To most of the drugs studied, murine progenitor cells seemed to be less sensitive than the human ones. There was, however, a close correlation between the murine and human log IC50 values of the drugs (r2 = 0.964, P< 0.001), suggesting that cultures of murine bone marrow may be suitable to predict the in-vitro toxicity of azole antifungals to human cfu-gm.  (+info)

The inhibition of mammalian 15-lipoxygenases by the anti-inflammatory drug ebselen: dual-type mechanism involving covalent linkage and alteration of the iron ligand sphere. (8/584)

Mammalian lipoxygenases have been implicated in inflammation and atherosclerosis and, thus, lipoxygenase inhibitors may be of pharmacological interest. In cells, lipoxygenases occur in a catalytically silent ground state that requires activation to become active. We found that the seleno-organic drug ebselen [2-phenyl-1, 2-benzisoselenazol-3(2H)-one], which exhibits anti-inflammatory properties, irreversibly inhibited pure rabbit 15-lipoxygenase, with an IC50 in the nM range when preincubated with the enzyme in the absence of fatty acid substrates. Subsequent dialysis, gel filtration, or substrate addition did not restore the enzyme activity, and experiments with [14C]ebselen indicated a covalent linkage of the drug. The presence of sulfhydryl compounds in the incubation mixture prevented both enzyme labeling and inactivation, but we did not see any reactivation when sulfhydryl compounds were added afterward. X-ray absorption studies indicated that ebselen did alter the geometry of the iron ligand sphere, and the data are consistent with an iron complexation by the drug. When fatty acid substrate was present during lipoxygenase-ebselen interaction, the inhibitory potency was strongly reduced and a competitive mode of action was observed. These data suggest that ebselen inactivated the catalytically silent ground-state lipoxygenase irreversibly by covalent linkage and alteration of the iron ligand sphere. In contrast, it functions as a competitive inhibitor of the catalytically active enzyme species. The pharmacological relevance of ebselen as a potential in vivo lipoxygenase inhibitor will be discussed.  (+info)

"Azoles" is a class of antifungal medications that have a similar chemical structure, specifically a five-membered ring containing nitrogen and two carbon atoms (a "azole ring"). The most common azoles used in medicine include:

1. Imidazoles: These include drugs such as clotrimazole, miconazole, and ketoconazole. They are used to treat a variety of fungal infections, including vaginal yeast infections, thrush, and skin infections.
2. Triazoles: These include drugs such as fluconazole, itraconazole, and voriconazole. They are also used to treat fungal infections, but have a broader spectrum of activity than imidazoles and are often used for more serious or systemic infections.

Azoles work by inhibiting the synthesis of ergosterol, an essential component of fungal cell membranes. This leads to increased permeability of the cell membrane, which ultimately results in fungal cell death.

While azoles are generally well-tolerated, they can cause side effects such as nausea, vomiting, and abdominal pain. In addition, some azoles can interact with other medications and affect liver function, so it's important to inform your healthcare provider of all medications you are taking before starting an azole regimen.

Antifungal agents are a type of medication used to treat and prevent fungal infections. These agents work by targeting and disrupting the growth of fungi, which include yeasts, molds, and other types of fungi that can cause illness in humans.

There are several different classes of antifungal agents, including:

1. Azoles: These agents work by inhibiting the synthesis of ergosterol, a key component of fungal cell membranes. Examples of azole antifungals include fluconazole, itraconazole, and voriconazole.
2. Echinocandins: These agents target the fungal cell wall, disrupting its synthesis and leading to fungal cell death. Examples of echinocandins include caspofungin, micafungin, and anidulafungin.
3. Polyenes: These agents bind to ergosterol in the fungal cell membrane, creating pores that lead to fungal cell death. Examples of polyene antifungals include amphotericin B and nystatin.
4. Allylamines: These agents inhibit squalene epoxidase, a key enzyme in ergosterol synthesis. Examples of allylamine antifungals include terbinafine and naftifine.
5. Griseofulvin: This agent disrupts fungal cell division by binding to tubulin, a protein involved in fungal cell mitosis.

Antifungal agents can be administered topically, orally, or intravenously, depending on the severity and location of the infection. It is important to use antifungal agents only as directed by a healthcare professional, as misuse or overuse can lead to resistance and make treatment more difficult.

Fungal drug resistance is a condition where fungi are no longer susceptible to the antifungal drugs that were previously used to treat infections they caused. This can occur due to genetic changes in the fungi that make them less sensitive to the drug's effects, or due to environmental factors that allow the fungi to survive and multiply despite the presence of the drug.

There are several mechanisms by which fungi can develop drug resistance, including:

1. Mutations in genes that encode drug targets: Fungi can acquire mutations in the genes that encode for the proteins or enzymes that the antifungal drugs target. These mutations can alter the structure or function of these targets, making them less susceptible to the drug's effects.
2. Overexpression of efflux pumps: Fungi can increase the expression of genes that encode for efflux pumps, which are proteins that help fungi expel drugs from their cells. This can reduce the intracellular concentration of the drug and make it less effective.
3. Changes in membrane composition: Fungi can alter the composition of their cell membranes to make them less permeable to antifungal drugs, making it more difficult for the drugs to enter the fungal cells and exert their effects.
4. Biofilm formation: Fungi can form biofilms, which are complex communities of microorganisms that adhere to surfaces and are protected by a matrix of extracellular material. Biofilms can make fungi more resistant to antifungal drugs by limiting drug penetration and creating an environment that promotes the development of resistance.

Fungal drug resistance is a significant clinical problem, particularly in patients with weakened immune systems, such as those with HIV/AIDS or cancer. It can lead to treatment failures, increased morbidity and mortality, and higher healthcare costs. To address this issue, there is a need for new antifungal drugs, as well as strategies to prevent and manage drug resistance.

Fluconazole is an antifungal medication used to treat and prevent various fungal infections, such as candidiasis (yeast infections), cryptococcal meningitis, and other fungal infections that affect the mouth, throat, blood, lungs, genital area, and other parts of the body. It works by inhibiting the growth of fungi that cause these infections. Fluconazole is available in various forms, including tablets, capsules, and intravenous (IV) solutions, and is typically prescribed to be taken once daily.

The medical definition of Fluconazole can be found in pharmacological or medical dictionaries, which describe it as a triazole antifungal agent that inhibits fungal cytochrome P450-dependent synthesis of ergosterol, a key component of the fungal cell membrane. This results in increased permeability and leakage of cellular contents, ultimately leading to fungal death. Fluconazole has a broad spectrum of activity against various fungi, including Candida, Cryptococcus, Aspergillus, and others.

It is important to note that while Fluconazole is an effective antifungal medication, it may have side effects and interactions with other medications. Therefore, it should only be used under the guidance of a healthcare professional.

Itraconazole is an antifungal medication used to treat various fungal infections, including blastomycosis, histoplasmosis, aspergillosis, and candidiasis. It works by inhibiting the synthesis of ergosterol, a vital component of fungal cell membranes, thereby disrupting the integrity and function of these membranes. Itraconazole is available in oral and intravenous forms for systemic use and as a topical solution or cream for localized fungal infections.

Medical Definition:
Itraconazole (i-tra-KON-a-zole): A synthetic triazole antifungal agent used to treat various fungal infections, such as blastomycosis, histoplasmosis, aspergillosis, and candidiasis. It inhibits the synthesis of ergosterol, a critical component of fungal cell membranes, leading to disruption of their integrity and function. Itraconazole is available in oral (capsule and solution) and intravenous forms for systemic use and as a topical solution or cream for localized fungal infections.

'Candida albicans' is a species of yeast that is commonly found in the human body, particularly in warm and moist areas such as the mouth, gut, and genital region. It is a part of the normal microbiota and usually does not cause any harm. However, under certain conditions like a weakened immune system, prolonged use of antibiotics or steroids, poor oral hygiene, or diabetes, it can overgrow and cause infections known as candidiasis. These infections can affect various parts of the body including the skin, nails, mouth (thrush), and genital area (yeast infection).

The medical definition of 'Candida albicans' is:

A species of yeast belonging to the genus Candida, which is commonly found as a commensal organism in humans. It can cause opportunistic infections when there is a disruption in the normal microbiota or when the immune system is compromised. The overgrowth of C. albicans can lead to various forms of candidiasis, such as oral thrush, vaginal yeast infection, and invasive candidiasis.

'Candida glabrata' is a species of yeast that is commonly found on the skin and mucous membranes of humans. It is a member of the genus Candida, which includes several species of fungi that can cause infections in humans. C. glabrata is one of the more common causes of candidiasis, or yeast infections, particularly in the mouth (oral thrush) and genital area. It can also cause invasive candidiasis, a serious systemic infection that can affect various organs and tissues in the body. C. glabrata is often resistant to some of the antifungal drugs commonly used to treat Candida infections, making it more difficult to treat.

Ketoconazole is an antifungal medication that is primarily used to treat various fungal infections, including those caused by dermatophytes, Candida, and pityrosporum. It works by inhibiting the synthesis of ergosterol, a crucial component of fungal cell membranes, which leads to increased permeability and ultimately results in fungal cell death.

Ketoconazole is available as an oral tablet for systemic use and as a topical cream or shampoo for localized applications. The oral formulation is used to treat severe or invasive fungal infections, while the topical preparations are primarily indicated for skin and scalp infections, such as athlete's foot, ringworm, jock itch, candidiasis, and seborrheic dermatitis.

Common side effects of oral ketoconazole include nausea, vomiting, headache, and altered liver function tests. Rare but serious adverse reactions may include hepatotoxicity, adrenal insufficiency, and interactions with other medications that can affect the metabolism and elimination of drugs. Topical ketoconazole is generally well-tolerated, with local irritation being the most common side effect.

It's important to note that due to its potential for serious liver toxicity and drug-drug interactions, oral ketoconazole has been largely replaced by other antifungal agents, such as fluconazole and itraconazole, which have more favorable safety profiles. Topical ketoconazole remains a valuable option for treating localized fungal infections due to its effectiveness and lower risk of systemic side effects.

Triazoles are a class of antifungal medications that have broad-spectrum activity against various fungi, including yeasts, molds, and dermatophytes. They work by inhibiting the synthesis of ergosterol, an essential component of fungal cell membranes, leading to increased permeability and disruption of fungal growth. Triazoles are commonly used in both systemic and topical formulations for the treatment of various fungal infections, such as candidiasis, aspergillosis, cryptococcosis, and dermatophytoses. Some examples of triazole antifungals include fluconazole, itraconazole, voriconazole, and posaconazole.

Ergosterol is a steroid found in the cell membranes of fungi, which is similar to cholesterol in animals. It plays an important role in maintaining the fluidity and permeability of fungal cell membranes. Ergosterol is also the target of many antifungal medications, which work by disrupting the synthesis of ergosterol or binding to it, leading to increased permeability and eventual death of the fungal cells.

Econazole is an antifungal medication used to treat various fungal infections of the skin, nails, and mucous membranes. It works by inhibiting the synthesis of ergosterol, a key component of fungal cell membranes, thereby weakening the cell membrane and increasing permeability, ultimately leading to fungal cell death.

Econazole is available in various formulations, including creams, lotions, powders, and tablets. It is commonly used to treat conditions such as athlete's foot, jock itch, ringworm, candidiasis (yeast infection), and other fungal skin infections.

It is important to follow the instructions of a healthcare provider when using econazole or any medication, and to report any side effects or concerns promptly.

'Candida' is a type of fungus (a form of yeast) that is commonly found on the skin and inside the body, including in the mouth, throat, gut, and vagina, in small amounts. It is a part of the normal microbiota and usually does not cause any problems. However, an overgrowth of Candida can lead to infections known as candidiasis or thrush. Common sites for these infections include the skin, mouth, throat, and genital areas. Some factors that can contribute to Candida overgrowth are a weakened immune system, certain medications (such as antibiotics and corticosteroids), diabetes, pregnancy, poor oral hygiene, and wearing damp or tight-fitting clothing. Common symptoms of candidiasis include itching, redness, pain, and discharge. Treatment typically involves antifungal medication, either topical or oral, depending on the site and severity of the infection.

Miconazole is an antifungal medication used to treat various fungal infections, including those affecting the skin, mouth, and vagina. According to the Medical Subject Headings (MeSH) database maintained by the National Library of Medicine, miconazole is classified as an imidazole antifungal agent that works by inhibiting the synthesis of ergosterol, a key component of fungal cell membranes. By disrupting the structure and function of the fungal cell membrane, miconazole can help to kill or suppress the growth of fungi, providing therapeutic benefits in patients with fungal infections.

Miconazole is available in various formulations, including creams, ointments, powders, tablets, and vaginal suppositories, and is typically applied or administered topically or vaginally, depending on the site of infection. In some cases, miconazole may also be given intravenously for the treatment of severe systemic fungal infections.

As with any medication, miconazole can have side effects and potential drug interactions, so it is important to use it under the guidance of a healthcare professional. Common side effects of miconazole include skin irritation, redness, and itching at the application site, while more serious side effects may include allergic reactions, liver damage, or changes in heart rhythm. Patients should be sure to inform their healthcare provider of any other medications they are taking, as well as any medical conditions they have, before using miconazole.

Microbial sensitivity tests, also known as antibiotic susceptibility tests (ASTs) or bacterial susceptibility tests, are laboratory procedures used to determine the effectiveness of various antimicrobial agents against specific microorganisms isolated from a patient's infection. These tests help healthcare providers identify which antibiotics will be most effective in treating an infection and which ones should be avoided due to resistance. The results of these tests can guide appropriate antibiotic therapy, minimize the potential for antibiotic resistance, improve clinical outcomes, and reduce unnecessary side effects or toxicity from ineffective antimicrobials.

There are several methods for performing microbial sensitivity tests, including:

1. Disk diffusion method (Kirby-Bauer test): A standardized paper disk containing a predetermined amount of an antibiotic is placed on an agar plate that has been inoculated with the isolated microorganism. After incubation, the zone of inhibition around the disk is measured to determine the susceptibility or resistance of the organism to that particular antibiotic.
2. Broth dilution method: A series of tubes or wells containing decreasing concentrations of an antimicrobial agent are inoculated with a standardized microbial suspension. After incubation, the minimum inhibitory concentration (MIC) is determined by observing the lowest concentration of the antibiotic that prevents visible growth of the organism.
3. Automated systems: These use sophisticated technology to perform both disk diffusion and broth dilution methods automatically, providing rapid and accurate results for a wide range of microorganisms and antimicrobial agents.

The interpretation of microbial sensitivity test results should be done cautiously, considering factors such as the site of infection, pharmacokinetics and pharmacodynamics of the antibiotic, potential toxicity, and local resistance patterns. Regular monitoring of susceptibility patterns and ongoing antimicrobial stewardship programs are essential to ensure optimal use of these tests and to minimize the development of antibiotic resistance.

Clotrimazole is an antifungal medication used to treat various fungal infections such as athlete's foot, jock itch, ringworm, candidiasis (yeast infection), and oral thrush. It works by inhibiting the growth of fungi that cause these infections. Clotrimazole is available in several forms, including creams, lotions, powders, tablets, and lozenges.

The medical definition of Clotrimazole is:

A synthetic antifungal agent belonging to the imidazole class, used topically to treat various fungal infections such as candidiasis, tinea pedis, tinea cruris, and tinea versicolor. It works by inhibiting the biosynthesis of ergosterol, a key component of fungal cell membranes, leading to increased permeability and death of fungal cells.

Candidiasis is a fungal infection caused by Candida species, most commonly Candida albicans. It can affect various parts of the body, including the skin, mucous membranes (such as the mouth and vagina), and internal organs (like the esophagus, lungs, or blood).

The symptoms of candidiasis depend on the location of the infection:

1. Oral thrush: White patches on the tongue, inner cheeks, gums, or roof of the mouth. These patches may be painful and can bleed slightly when scraped.
2. Vaginal yeast infection: Itching, burning, redness, and swelling of the vagina and vulva; thick, white, odorless discharge from the vagina.
3. Esophageal candidiasis: Difficulty swallowing, pain when swallowing, or feeling like food is "stuck" in the throat.
4. Invasive candidiasis: Fever, chills, and other signs of infection; multiple organ involvement may lead to various symptoms depending on the affected organs.

Risk factors for developing candidiasis include diabetes, HIV/AIDS, use of antibiotics or corticosteroids, pregnancy, poor oral hygiene, and wearing tight-fitting clothing that traps moisture. Treatment typically involves antifungal medications, such as fluconazole, nystatin, or clotrimazole, depending on the severity and location of the infection.

'Aspergillus fumigatus' is a species of fungi that belongs to the genus Aspergillus. It is a ubiquitous mold that is commonly found in decaying organic matter, such as leaf litter, compost, and rotting vegetation. This fungus is also known to be present in indoor environments, including air conditioning systems, dust, and water-damaged buildings.

Aspergillus fumigatus is an opportunistic pathogen, which means that it can cause infections in people with weakened immune systems. It can lead to a range of conditions known as aspergillosis, including allergic reactions, lung infections, and invasive infections that can spread to other parts of the body.

The fungus produces small, airborne spores that can be inhaled into the lungs, where they can cause infection. In healthy individuals, the immune system is usually able to eliminate the spores before they can cause harm. However, in people with weakened immune systems, such as those undergoing chemotherapy or organ transplantation, or those with certain underlying medical conditions like asthma or cystic fibrosis, the fungus can establish an infection.

Infections caused by Aspergillus fumigatus can be difficult to treat, and treatment options may include antifungal medications, surgery, or a combination of both. Prompt diagnosis and treatment are essential for improving outcomes in people with aspergillosis.

Industrial fungicides are antimicrobial agents used to prevent, destroy, or inhibit the growth of fungi and their spores in industrial settings. These can include uses in manufacturing processes, packaging materials, textiles, paints, and other industrial products. They work by interfering with the cellular structure or metabolic processes of fungi, thereby preventing their growth or reproduction. Examples of industrial fungicides include:

* Sodium hypochlorite (bleach)
* Formaldehyde
* Glutaraldehyde
* Quaternary ammonium compounds
* Peracetic acid
* Chlorhexidine
* Iodophors

It's important to note that some of these fungicides can be harmful or toxic to humans and other organisms, so they must be used with caution and in accordance with safety guidelines.

Oral candidiasis is a medical condition characterized by an infection of the oral mucous membranes caused by the Candida fungus species, most commonly Candida albicans. It is also known as thrush or oral thrush. The infection typically appears as white, creamy, or yellowish patches or plaques on the tongue, inner cheeks, roof of the mouth, gums, and sometimes on the tonsils or back of the throat. These lesions can be painful, causing soreness, burning sensations, and difficulty swallowing. Oral candidiasis can affect people of all ages; however, it is more commonly seen in infants, elderly individuals, and those with weakened immune systems due to illness or medication use. Various factors such as poor oral hygiene, dentures, smoking, dry mouth, and certain medical conditions like diabetes or HIV/AIDS can increase the risk of developing oral candidiasis. Treatment usually involves antifungal medications in the form of topical creams, lozenges, or oral solutions, depending on the severity and underlying cause of the infection.

Fungal proteins are a type of protein that is specifically produced and present in fungi, which are a group of eukaryotic organisms that include microorganisms such as yeasts and molds. These proteins play various roles in the growth, development, and survival of fungi. They can be involved in the structure and function of fungal cells, metabolism, pathogenesis, and other cellular processes. Some fungal proteins can also have important implications for human health, both in terms of their potential use as therapeutic targets and as allergens or toxins that can cause disease.

Fungal proteins can be classified into different categories based on their functions, such as enzymes, structural proteins, signaling proteins, and toxins. Enzymes are proteins that catalyze chemical reactions in fungal cells, while structural proteins provide support and protection for the cell. Signaling proteins are involved in communication between cells and regulation of various cellular processes, and toxins are proteins that can cause harm to other organisms, including humans.

Understanding the structure and function of fungal proteins is important for developing new treatments for fungal infections, as well as for understanding the basic biology of fungi. Research on fungal proteins has led to the development of several antifungal drugs that target specific fungal enzymes or other proteins, providing effective treatment options for a range of fungal diseases. Additionally, further study of fungal proteins may reveal new targets for drug development and help improve our ability to diagnose and treat fungal infections.

Amphotericin B is an antifungal medication used to treat serious and often life-threatening fungal infections. It works by binding to the ergosterol in the fungal cell membrane, creating pores that lead to the loss of essential cell components and ultimately cell death.

The medical definition of Amphotericin B is:

A polyene antifungal agent derived from Streptomyces nodosus, with a broad spectrum of activity against various fungi, including Candida, Aspergillus, Cryptococcus, and Histoplasma capsulatum. Amphotericin B is used to treat systemic fungal infections, such as histoplasmosis, cryptococcosis, candidiasis, and aspergillosis, among others. It may be administered intravenously or topically, depending on the formulation and the site of infection.

Adverse effects associated with Amphotericin B include infusion-related reactions (such as fever, chills, and hypotension), nephrotoxicity, electrolyte imbalances, and anemia. These side effects are often dose-dependent and may be managed through careful monitoring and adjustment of the dosing regimen.

Sterols are a type of organic compound that is derived from steroids and found in the cell membranes of organisms. In animals, including humans, cholesterol is the most well-known sterol. Sterols help to maintain the structural integrity and fluidity of cell membranes, and they also play important roles as precursors for the synthesis of various hormones and other signaling molecules. Phytosterols are plant sterols that have been shown to have cholesterol-lowering effects in humans when consumed in sufficient amounts.

Aspergillosis is a medical condition that is caused by the infection of the Aspergillus fungi. This fungus is commonly found in decaying organic matter, such as leaf litter and compost piles, and can also be found in some indoor environments like air conditioning systems and old buildings with water damage.

There are several types of aspergillosis, including:

1. Allergic bronchopulmonary aspergillosis (ABPA): This type of aspergillosis occurs when a person's immune system overreacts to the Aspergillus fungi, causing inflammation in the airways and lungs. ABPA is often seen in people with asthma or cystic fibrosis.
2. Invasive aspergillosis: This is a serious and potentially life-threatening condition that occurs when the Aspergillus fungi invade the bloodstream and spread to other organs, such as the brain, heart, or kidneys. Invasive aspergillosis typically affects people with weakened immune systems, such as those undergoing chemotherapy or organ transplantation.
3. Aspergilloma: Also known as a "fungus ball," an aspergilloma is a growth of the Aspergillus fungi that forms in a preexisting lung cavity, such as one caused by previous lung disease or injury. While an aspergilloma itself is not typically harmful, it can cause symptoms like coughing up blood or chest pain if it grows too large or becomes infected.

Symptoms of aspergillosis can vary depending on the type and severity of the infection. Treatment may include antifungal medications, surgery to remove the fungal growth, or management of underlying conditions that increase the risk of infection.

The Cytochrome P-450 (CYP450) enzyme system is a group of enzymes found primarily in the liver, but also in other organs such as the intestines, lungs, and skin. These enzymes play a crucial role in the metabolism and biotransformation of various substances, including drugs, environmental toxins, and endogenous compounds like hormones and fatty acids.

The name "Cytochrome P-450" refers to the unique property of these enzymes to bind to carbon monoxide (CO) and form a complex that absorbs light at a wavelength of 450 nm, which can be detected spectrophotometrically.

The CYP450 enzyme system is involved in Phase I metabolism of xenobiotics, where it catalyzes oxidation reactions such as hydroxylation, dealkylation, and epoxidation. These reactions introduce functional groups into the substrate molecule, which can then undergo further modifications by other enzymes during Phase II metabolism.

There are several families and subfamilies of CYP450 enzymes, each with distinct substrate specificities and functions. Some of the most important CYP450 enzymes include:

1. CYP3A4: This is the most abundant CYP450 enzyme in the human liver and is involved in the metabolism of approximately 50% of all drugs. It also metabolizes various endogenous compounds like steroids, bile acids, and vitamin D.
2. CYP2D6: This enzyme is responsible for the metabolism of many psychotropic drugs, including antidepressants, antipsychotics, and beta-blockers. It also metabolizes some endogenous compounds like dopamine and serotonin.
3. CYP2C9: This enzyme plays a significant role in the metabolism of warfarin, phenytoin, and nonsteroidal anti-inflammatory drugs (NSAIDs).
4. CYP2C19: This enzyme is involved in the metabolism of proton pump inhibitors, antidepressants, and clopidogrel.
5. CYP2E1: This enzyme metabolizes various xenobiotics like alcohol, acetaminophen, and carbon tetrachloride, as well as some endogenous compounds like fatty acids and prostaglandins.

Genetic polymorphisms in CYP450 enzymes can significantly affect drug metabolism and response, leading to interindividual variability in drug efficacy and toxicity. Understanding the role of CYP450 enzymes in drug metabolism is crucial for optimizing pharmacotherapy and minimizing adverse effects.

14-alpha Demethylase Inhibitors are a class of antifungal medications that work by inhibiting the enzyme 14-alpha demethylase, which is essential for the synthesis of ergosterol, a critical component of fungal cell membranes. By inhibiting this enzyme, the drugs disrupt the structure and function of the fungal cell membrane, leading to fungal cell death.

Examples of 14-alpha Demethylase Inhibitors include:

* Fluconazole (Diflucan)
* Itraconazole (Sporanox)
* Ketoconazole (Nizoral)
* Posaconazole (Noxafil)
* Voriconazole (Vfend)

These medications are used to treat a variety of fungal infections, including candidiasis, aspergillosis, and cryptococcosis. However, they can also have significant drug-drug interactions and toxicities, so their use must be monitored closely by healthcare professionals.

Echinocandins are a class of antifungal medications that inhibit the synthesis of 1,3-β-D-glucan, a key component of the fungal cell wall. This results in osmotic instability and ultimately leads to fungal cell death. Echinocandins are commonly used to treat invasive fungal infections caused by Candida species and Aspergillus species. The three drugs in this class that are approved for use in humans are caspofungin, micafungin, and anidulafungin.

Here's a brief overview of each drug:

1. Caspofungin (Cancidas, Cancidas-W): This is the first echinocandin to be approved for use in humans. It is indicated for the treatment of invasive candidiasis, including candidemia, acute disseminated candidiasis, and other forms of Candida infections. Caspofungin is also approved for the prevention of Candida infections in patients undergoing hematopoietic stem cell transplantation.
2. Micafungin (Mycamine): This echinocandin is approved for the treatment of candidemia, esophageal candidiasis, and other forms of Candida infections. It is also used for the prevention of Candida infections in patients undergoing hematopoietic stem cell transplantation.
3. Anidulafungin (Eraxis): This echinocandin is approved for the treatment of esophageal candidiasis and candidemia, as well as other forms of Candida infections. It is also used for the prevention of Candida infections in patients undergoing hematopoietic stem cell transplantation.

Echinocandins have a broad spectrum of activity against many fungal species, including those that are resistant to other classes of antifungal medications. They are generally well-tolerated and have a low incidence of drug interactions. However, they should be used with caution in patients with hepatic impairment, as their metabolism may be affected by liver dysfunction.

Pyrimidines are heterocyclic aromatic organic compounds similar to benzene and pyridine, containing two nitrogen atoms at positions 1 and 3 of the six-member ring. They are one of the two types of nucleobases found in nucleic acids, the other being purines. The pyrimidine bases include cytosine (C) and thymine (T) in DNA, and uracil (U) in RNA, which pair with guanine (G) and adenine (A), respectively, through hydrogen bonding to form the double helix structure of nucleic acids. Pyrimidines are also found in many other biomolecules and have various roles in cellular metabolism and genetic regulation.

'Candida tropicalis' is a species of yeast that can be found normally in certain environments, including the human body (such as the skin, mouth, and digestive system). However, it can also cause infections in people with weakened immune systems or underlying medical conditions. These infections can occur in various parts of the body, including the bloodstream, urinary tract, and skin.

Like other Candida species, C. tropicalis is a type of fungus that reproduces by budding, forming oval-shaped cells. It is often resistant to certain antifungal medications, which can make infections more difficult to treat. Proper diagnosis and treatment, usually with antifungal drugs, are essential for managing C. tropicalis infections.

Microbial drug resistance is a significant medical issue that refers to the ability of microorganisms (such as bacteria, viruses, fungi, or parasites) to withstand or survive exposure to drugs or medications designed to kill them or limit their growth. This phenomenon has become a major global health concern, particularly in the context of bacterial infections, where it is also known as antibiotic resistance.

Drug resistance arises due to genetic changes in microorganisms that enable them to modify or bypass the effects of antimicrobial agents. These genetic alterations can be caused by mutations or the acquisition of resistance genes through horizontal gene transfer. The resistant microbes then replicate and multiply, forming populations that are increasingly difficult to eradicate with conventional treatments.

The consequences of drug-resistant infections include increased morbidity, mortality, healthcare costs, and the potential for widespread outbreaks. Factors contributing to the emergence and spread of microbial drug resistance include the overuse or misuse of antimicrobials, poor infection control practices, and inadequate surveillance systems.

To address this challenge, it is crucial to promote prudent antibiotic use, strengthen infection prevention and control measures, develop new antimicrobial agents, and invest in research to better understand the mechanisms underlying drug resistance.

Lanosterol is a steroid that is an intermediate in the biosynthetic pathway of cholesterol in animals and other eukaryotic organisms. It's a complex organic molecule with a structure based on four fused hydrocarbon rings, and it plays a crucial role in maintaining the integrity and function of cell membranes.

In the biosynthetic pathway, lanosterol is produced from squalene through a series of enzymatic reactions. Lanosterol then undergoes several additional steps, including the removal of three methyl groups and the reduction of two double bonds, to form cholesterol.

Abnormal levels or structure of lanosterol have been implicated in certain genetic disorders, such as lamellar ichthyosis type 3 and congenital hemidysplasia with ichthyosiform erythroderma and limb defects (CHILD) syndrome.

'Cryptococcus gattii' is a species of encapsulated, yeast-like fungi belonging to the family Tremellaceae. It is an environmental pathogen that can cause pulmonary and central nervous system infections in humans and animals. The organism is typically found in soil and on trees in tropical and subtropical regions, but it has also been identified in temperate climates. Infection usually occurs through inhalation of the spores or desiccated yeast cells.

The disease caused by 'Cryptococcus gattii' is called cryptococcosis, which can manifest as a pulmonary infection (pneumonia) or a disseminated infection involving the central nervous system (meningitis). The symptoms of cryptococcosis may include cough, chest pain, fever, night sweats, weight loss, headache, stiff neck, confusion, and altered mental status.

Risk factors for developing cryptococcosis caused by 'Cryptococcus gattii' include underlying lung disease, immunosuppression (such as HIV/AIDS), and exposure to the fungus in endemic areas. Diagnosis typically involves microscopic examination of clinical specimens (e.g., sputum, cerebrospinal fluid) and culture isolation of the organism, followed by confirmation using biochemical or molecular methods. Treatment usually consists of antifungal therapy with agents such as amphotericin B and fluconazole.

Gene expression regulation in fungi refers to the complex cellular processes that control the production of proteins and other functional gene products in response to various internal and external stimuli. This regulation is crucial for normal growth, development, and adaptation of fungal cells to changing environmental conditions.

In fungi, gene expression is regulated at multiple levels, including transcriptional, post-transcriptional, translational, and post-translational modifications. Key regulatory mechanisms include:

1. Transcription factors (TFs): These proteins bind to specific DNA sequences in the promoter regions of target genes and either activate or repress their transcription. Fungi have a diverse array of TFs that respond to various signals, such as nutrient availability, stress, developmental cues, and quorum sensing.
2. Chromatin remodeling: The organization and compaction of DNA into chromatin can influence gene expression. Fungi utilize ATP-dependent chromatin remodeling complexes and histone modifying enzymes to alter chromatin structure, thereby facilitating or inhibiting the access of transcriptional machinery to genes.
3. Non-coding RNAs: Small non-coding RNAs (sncRNAs) play a role in post-transcriptional regulation of gene expression in fungi. These sncRNAs can guide RNA-induced transcriptional silencing (RITS) complexes to specific target loci, leading to the repression of gene expression through histone modifications and DNA methylation.
4. Alternative splicing: Fungi employ alternative splicing mechanisms to generate multiple mRNA isoforms from a single gene, thereby increasing proteome diversity. This process can be regulated by RNA-binding proteins that recognize specific sequence motifs in pre-mRNAs and promote or inhibit splicing events.
5. Protein stability and activity: Post-translational modifications (PTMs) of proteins, such as phosphorylation, ubiquitination, and sumoylation, can influence their stability, localization, and activity. These PTMs play a crucial role in regulating various cellular processes, including signal transduction, stress response, and cell cycle progression.

Understanding the complex interplay between these regulatory mechanisms is essential for elucidating the molecular basis of fungal development, pathogenesis, and drug resistance. This knowledge can be harnessed to develop novel strategies for combating fungal infections and improving agricultural productivity.

Names of azoles maintain the prefix upon reduction (e.g., pyrazoline, pyrazolidine). The numbering of ring atoms in azoles ... Azoles are a class of five-membered heterocyclic compounds containing a nitrogen atom and at least one other non-carbon atom (i ... Azoles at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Nomenclature, IUPAC (CS1: long volume value, ... One, and only one, lone pair of electrons from each heteroatom in the ring is part of the aromatic bonding in an azole. ...
Drug-Drug Interactions in Treatment Using Azole Antifungal Agents. JAMA. 2016 Jun 21. 315 (23):2622. [QxMD MEDLINE Link]. ...
PLOS Pathogens publishes Open Access research and commentary that significantly advance the understanding of pathogens and how they interact with host organisms. Get Started ...
... Harpenden (GB), 2010-12-07/09. Introduction and Background ... Lecture Session II Azole sensitivity monitoring of Septoria populations [Chair: Anne-Sophie Walker] ... CYP51 paralogues and azole sensitivity in Rhynchosporium secalis. Hawkins N*, Cools H*, Shaw M (University of Reading), ... Despite intensive use for more than 30 years, azoles (triazoles and imidazoles) still provide broad effective control in many ...
Azoles are five-membered cyclic compounds containing one or more heteroatoms in the ring, at least one of which must be ... Heteroaromatic Nitrogen Compounds: The Azoles K. Schofield Azoles are five-membered cyclic compounds containing one or more ...
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Azoles:. Azoles, such as ketoconazole found in Nizoral, are a class of antifungal agents commonly used as broad-spectrum ... Azoles are effective against a wide range of fungal infections and are available in multiple forms, including oral tablets, ... Azoles, such as ketoconazole, are commonly used as broad-spectrum antifungal agents that inhibit the synthesis of ergosterol, ... Azoles, such as ketoconazole in Nizoral, are commonly used as broad-spectrum antifungal agents, inhibiting the synthesis of ...
Azoles. ERG11 snp. Disclaimer:. The resistance mechanisms listed were identified by analysis of whole genome sequence using the ...
Organic Photoredox Catalyzed Direct Hydroamination of Ynamides with Azoles ... By using an organocatalytic photoredox system, a direct method to construct a diverse of (Z)-α-azole enamides from ynamides and ...
New azole antifungal agents described by Zambon. Dec. 4, 1996. No Comments ...
... ... Synthesis of some new hybride molecules containing several azole moieties and investigation of their biological activities. ...
The selection of azoles depends to a flammable glomerulonephritis.. I also take paxil along with it for anxiety.. My ...
Systemic azoles can also be used. Surgical debridement or removal of the affected nail is also a consideration for cases that ...
Azole antifungals Ketoconazole increased the plasma concentrations of intravenous midazolam by 5-fold while the terminal half- ...
Compound B8 exhibited excellent in vitro and in vivo antifungal potency in combination with fluconazole against azole-resistant ... of Pyrazolone Carbothioamide Derivatives as Inhibitors of the Pdr1-KIX Interaction for Combinational Treatment of Azole- ...
Before taking fluconazole, tell your doctor or pharmacist if you are allergic to it; or to other azole antifungal drugs (such ... It belongs to a class of drugs called azole antifungals. It works by stopping the growth of certain types of fungus. ...
The development of systemically available azoles such as fluconazole and itraconazole, the emergence of mold active azoles such ... nearly uniformly have low MICs to olorofim (Du Pre et al., 2018). This includes azole resistant (including A. terreus and ... The comparator arm in this study is a combination of oral azole and trimethoprim-sulfamethoxazole. The same 400mg/200mg dosing ... The target enzyme of the tetrazoles (14-alpha demethylase), including oteseconazole is the same as for other azoles, however ...
Alternatives for azole therapy are a little less studied, and its a little less clear what the alternative should be. ... Obviously those guidelines are quite dated, and a number of newer azoles are now available. Is itraconazole still your go-to ... Some of the newer azoles you mentioned are really appealing. Posaconazole gets into the CNS quite well, and isavuconazole also ... been good studies that have shown that individuals who are treated with an azole to begin with vs step-down therapy to an azole ...
azole antifungal medications (e.g., fluconazole, itraconazole, ketoconazole). *barbiturates (e.g., butalbital, phenobarbital) ...
Chloroquine sensitizes biofilms of Candida albicans to antifungal azoles 2013 School of Life Sciences, SRTM University, Nanded ... CI: Copyright (c) 2013; JID: 9812937; 0 (Antifungal Agents); 0 (Azoles); 0 (Echinocandins); 7XU7A7DROE (Amphotericin B); ...
Azoles represent the mainstay of antifungal drugs, and their mode of action involves the binding mode of these molecules to the ... Also, 2a showed activity towards azole-resistant strains. This finding is very interesting since the primary target of 2a is ...
azole antifungals (e.g. itraconazole, itraconazole, or voriconazole). *some antibiotics and antiviral medicines (e.g. ...
azole antifungals (e.g., fluconazole, voriconazole). *beta-adrenergic blockers (e.g., atenolol, propranolol, sotalol) ...
Categories: Azoles Image Types: Photo, Illustrations, Video, Color, Black&White, PublicDomain, CopyrightRestricted 3 images ...
Posaconazole is in a class of medications called azole antifungals. It works by slowing the growth of fungi that cause ...
Azoles [C0000436]. ClassyFire subclass:. Imidazoles [C0000078]. ClassyFire direct parent:. Imidazolyl carboxylic acids and ...
Extensive drug interactions for clarithromycin, fluoroquinolones, azole antifungals and rifampicin. Many antibiotics increase ...
Azole levels in the fabs effluent were reduced by 64% - a decrease of 7,260 lbs. This eased the local publicly owned treatment ... works (POTW) concern regarding incoming azole concentrations.. The program stabilized chemistry within the fabs PCW system, ...
TOM CHILLER: Well, certainly Candida dubliniensis can be a very Azole resistant species, so Im not, in the sense of the C. ... Next? So about 90% were resistant to the azoles, the fluconazole, voriconazole, itraconazole, antifungals. Next? Around 30% or ... our initial studies all of the patients were Candida auris was isolated they were on an Azoles, mainly fluconazole, and you can ...
  • Within the category of azole antifungal medication, there are two sub-categories: imidazoles and triazoles. (medicalnewstoday.com)
  • Azoles, such as ketoconazole, are commonly used as broad-spectrum antifungal agents that inhibit the synthesis of ergosterol, an essential component of the fungal cell membrane. (securingpharma.com)
  • It provides convenience and accessibility for patients and is classified as an azole antifungal drug. (securingpharma.com)
  • The separation of azole antifungal chiral compounds has gaining much interests since 1980's as they possess different biological, pharmaceutical, and pharmacokinetic behaviors at various toxicity levels. (um.edu.my)
  • Compound B8 exhibited excellent in vitro and in vivo antifungal potency in combination with fluconazole against azole -resistant C. glabrata. (bvsalud.org)
  • Minimum spanning tree comparing genotypic relatedness of clinical azole- resistant Aspergillus fumigatus isolates carrying TR34/L98H alteration in the CYP 51A gene from Iran with those reported from European countries. (cdc.gov)
  • Azole resistance in Aspergillus fumigatus isolates from the ARTEMIS global surveillance study is primarily due to the TR/L98H mutation in the cyp51A gene. (cdc.gov)
  • In recent years acquired azole resistance in Aspergillus fumigatus has been increasingly reported and a dominant mechanism of resistance (TR34/L98H) was found in clinical and environmental isolates.The aim of the present study was to investigate the prevalence of azole resistance in environmental A. fumigatus isolates collected in Northern Italy. (unimi.it)
  • INTRODUCTION: The frequency in detection of azole-resistant Aspergillus fumigatus isolates has increased since 2010. (unl.pt)
  • The implication of these findings could have a major impact on future recommendations and due to the significance of the problem an EPPO Workshop on azole fungicides and Septoria leaf blotch control, was held on 2010-12-07/09 at Rothamsted Research (Harpenden, GB). (eppo.int)
  • Are azole fungicides losing ground against Septoria wheat disease? (rothamsted.ac.uk)
  • There has been a recent rapid decline in the efficacy of some, but not all, azole fungicides in controlling the Septoria leaf blotch pathogen of wheat, Mycosphaerella graminicola. (rothamsted.ac.uk)
  • Emergence of azole resistance in Aspergillus fumigatus and spread of a single resistance mechanism. (cdc.gov)
  • Environmental surveillance of the emergence of azole-resistant A. fumigatus sensu stricto strains is needed, to ensure proper and timely implementation of control policies that may have a positive impact on public and occupational health. (unl.pt)
  • Microsatellite typing of 6 STR loci demonstrated identical patterns for two of the three azole-resistant isolates from Iran, but the TR34/L98H isolates from Iran did not cluster with those from the Netherlands and other European countries, indicating no close genetic relatedness. (cdc.gov)
  • High prevalence of azole-resistant Aspergillus fumigatus in adults with cystic fibrosis exposed to itraconazole. (cdc.gov)
  • Azole resistant isolates were detected in 12.7% of the soil samples and in 20.7% of the soil samples containing A. fumigatus. (unimi.it)
  • These findings, together with the occurrence of resistant clinical isolates, suggest that azole resistance should be considered in primary patient care. (unimi.it)
  • Azole-resistant Aspergillus fumigatus in the environment of Northern Italy, May 2011 to June 2012 / A. Prigitano, V. Venier, M. Cogliati, G. De Lorenzis, M.C. Esposto, A.M. Tortorano. (unimi.it)
  • RESULTS: Overall, 8.1% of isolates were able to grow in the presence of at least one azole, and 3% (isolated from the air in a dairy and from filtering respiratory protective devices in a waste sorting industry) were pan-azole-resistant, bearing the TR34/L98H mutation. (unl.pt)
  • Discovery of Pyrazolone Carbothioamide Derivatives as Inhibitors of the Pdr1-KIX Interaction for Combinational Treatment of Azole-Resistant Candidiasis. (bvsalud.org)
  • Frequency and evolution of azole resistance in Aspergillus fumigatus associated with treatment failure. (cdc.gov)
  • Aspergillus species and other molds in respiratory samples from patients with cystic fibrosis: a laboratory-based study with focus on Aspergillus fumigatus azole resistance. (cdc.gov)
  • Posaconazole is in a class of medications called azole antifungals. (medlineplus.gov)
  • Despite intensive use for more than 30 years, azoles (triazoles and imidazoles) still provide broad effective control in many areas. (eppo.int)
  • By using an organocatalytic photoredox system, a direct method to construct a diverse of (Z)-α-azole enamides from ynamides and pyrazoles, as well as triazoles, benzotriazoles, indazoles, and tetrazoles, is developed, thus providing a concise route to heterocyclic motifs common in medicinal agents. (chemrxiv.org)
  • Azoles are a class of five-membered heterocyclic compounds containing a nitrogen atom and at least one other non-carbon atom (i.e. nitrogen, sulfur, or oxygen) as part of the ring. (wikipedia.org)
  • big problem because the azoles are the only class of drugs that we've got that we can give orally to patients with aspergillosis. (cdc.gov)
  • This article incorporates material from the Citizendium article "Azole", which is licensed under the Creative Commons Attribution-ShareAlike 3.0 Unported License but not under the GFDL. (wikipedia.org)
  • In this study, wood dust from the sanding of micronized copper azole -treated lumber (MCA) was compared to sanding dust from solubilized copper azole-treated wood (CA-C) and untreated yellow pine (UYP). (cdc.gov)
  • Although several cryptic species within the Fumigati section show intrinsic resistance to azoles, one factor driving (acquired) resistance is selective pressure deriving from the extensive use of azoles. (unl.pt)
  • Minimum spanning tree comparing genotypic relatedness of clinical azole- resistant Aspergillus fumigatus isolates carrying TR34/L98H alteration in the CYP 51A gene from Iran with those reported from European countries. (cdc.gov)
  • Emergence of azole resistance in Aspergillus fumigatus and spread of a single resistance mechanism. (cdc.gov)
  • Frequency and evolution of azole resistance in Aspergillus fumigatus associated with treatment failure. (cdc.gov)
  • Aspergillus species and other molds in respiratory samples from patients with cystic fibrosis: a laboratory-based study with focus on Aspergillus fumigatus azole resistance. (cdc.gov)
  • High prevalence of azole-resistant Aspergillus fumigatus in adults with cystic fibrosis exposed to itraconazole. (cdc.gov)
  • Azole resistance in Aspergillus fumigatus isolates from the ARTEMIS global surveillance study is primarily due to the TR/L98H mutation in the cyp51A gene. (cdc.gov)
  • The in vivo efficacy of inravenous formulation of POS was assessed against infection with two isolates: a wild type (MIC, 0.031mg/L) and an azole-resistant A. fumigatus (MIC, 0.5 mg/L) harboring TR34/L98H mutation in Cyp-51A gene. (nih.gov)
  • Dynam- for treatment of Aspergillus diseases and wild-type A. fumigatus isolates ics of antibodies against hypodermin C are the mold-active azole antifungal examined in this study, according to in reindeer infested with the reindeer drugs ( 1 ). (cdc.gov)
  • mutations in A. fumigatus confer azole Technical Appendix Table 1. (cdc.gov)
  • In a multicenter study, we determined a prevalence rate of 4% for azole-resistant Aspergillus fumigatus in Taiwan. (cdc.gov)
  • Worldwide emergence of azole-resistant Aspergillus fumigatus since the late 2000s threatens human health ( 1 ). (cdc.gov)
  • To delineate the influence of clinical and environmental use of azoles on resistance, we conducted a multicenter study that investigated 375 A. fumigatus sensu stricto isolates collected during August 2011-March 2018 from 297 patients at 11 hospitals in Taiwan ( Appendix Table 1, Figure 1). (cdc.gov)
  • 1 medical azoles (itraconazole, voriconazole, posaconazole, and isavuconazole) were defined as azole-resistant A. fumigatus and examined for resistance mechanisms, microsatellite-based phylogenetic relatedness, and growth rates following previously described methods ( 3 , 4 ). (cdc.gov)
  • Overall, 19 isolates from 12 patients were azole-resistant A. fumigatus . (cdc.gov)
  • Ten (83.3%) patients harbored azole-resistant A. fumigatus that had environmental mutations, including TR 34 /L98H (5 isolates, 5 patients), TR 34 /L98H/S297T/F495I (7 isolates, 4 patients), and TR 46 /Y121F/T289A (1 isolate) mutations. (cdc.gov)
  • This observation is consistent with the estimated global prevalence of azole resistance in Aspergillus (3%-6%) and the predominance of environmental resistance mechanisms in azole-resistant A. fumigatus ( 1 , 5 ). (cdc.gov)
  • A high mortality rate observed for azole-resistant aspergillosis necessitates diagnostic stewardship in healthcare and antifungal stewardship in the environment. (cdc.gov)
  • Microsatellite typing of 6 STR loci demonstrated identical patterns for two of the three azole-resistant isolates from Iran, but the TR34/L98H isolates from Iran did not cluster with those from the Netherlands and other European countries, indicating no close genetic relatedness. (cdc.gov)
  • Trapping oes- tibility testing of clinical Aspergil- azole-resistant isolates from Iran, but trid parasites of reindeer: the response lus isolates is not common in many the TR /L98H isolates from Iran did of Cephenemyia trompe and Hypo- centers worldwide, the prevalence of 34 not cluster with those from the Neth- derma tarandi to baited traps. (cdc.gov)
  • In 2016, a Danish study published in the Journal of the American Medical Association ( JAMA ) reported an increased risk of miscarriage associated with low-dose oral fluconazole exposure compared with no exposure or with topical azole exposure. (umn.edu)
  • the target for azole antifungal drugs. (cdc.gov)
  • Summary Azoles are antifungal agents widely-used in clinical applications and agriculture. (nih.gov)
  • 8. Syrdalen P, Stenkula S. Ophthalmo- of azole resistance in clinical A. fumig- (online Technical Appendix Figure). (cdc.gov)
  • We confirmed the presence of azole resistance by using the Clinical Laboratory Standard Institute method ( Appendix Table 1) ( 2 ). (cdc.gov)
  • This study investigated the fate of two commonly occurring azole compounds in an anammox enrichment culture. (arizona.edu)
  • Our wood post caps are protected by Copper Azole Type B (CA-B), an EPA-registered pesticide containing copper and azole compounds to protect it from termite attack and decay. (deckorators.com)
  • For the development of new systemically acting, oral antifungal azoles, it is of key importance to compare them with ketoconazole, the first available drug in this therapeutic class. (nih.gov)
  • These results show intravenous formulation of posaconazole provide higher exposure than the oral suspension for treatment of azole-resistant IA. (nih.gov)
  • A dose-response relationship was observed regardless of the underlying azole-resistance mechanism. (nih.gov)
  • Azole resistance is thought to be resistant phenotype. (cdc.gov)
  • Resistance emerged mainly from the environment (TR 34 /L98H, TR 34 /L98H/S297T/F495I, and TR 46 /Y121F/T289A mutations) but occasionally during azole treatment. (cdc.gov)
  • The mechanism of action of azoles is blocking the synthesis of ergosterol, the primary sterol in the fungal cell membrane. (medscape.com)
  • While the mechanisms are unresolved, azoles induce changes in the embryo that resemble excess bioavailability of all-trans retinoic acid (RA) due to similarities in adverse morphological and molecular phenotypes. (nih.gov)
  • abstract = "Azoles are contaminants of emerging concern. (arizona.edu)
  • Luliconazole is in a class of antifungal medications called azoles. (medlineplus.gov)
  • Despite evident exposures in humans, the developmental health risks associated with azole exposures during pregnancy remains undefined. (nih.gov)
  • The azoles are a group of synthetic antimycotic agents with a broad spectrum of activity. (medscape.com)