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Questions and Answers
What is the primary reason for administering hydrocortisone or acetaminophen along with amphotericin B?
What is the primary reason for administering hydrocortisone or acetaminophen along with amphotericin B?
What is the mechanism by which flucytosine exerts its antifungal effects?
What is the mechanism by which flucytosine exerts its antifungal effects?
Which of the following side effects is most closely associated with prolonged administration of flucytosine?
Which of the following side effects is most closely associated with prolonged administration of flucytosine?
What is a significant drawback of using flucytosine as a standalone treatment?
What is a significant drawback of using flucytosine as a standalone treatment?
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Flucytosine is primarily indicated for use in combination with amphotericin B to treat which of the following conditions?
Flucytosine is primarily indicated for use in combination with amphotericin B to treat which of the following conditions?
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Which conditions are associated with an increased risk of rhinocerebral mucormycosis?
Which conditions are associated with an increased risk of rhinocerebral mucormycosis?
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What is the primary route of infection for thoracic mucormycosis?
What is the primary route of infection for thoracic mucormycosis?
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What is the primary organ involved in both allergic disease and invasive aspergillosis caused by Aspergillus?
What is the primary organ involved in both allergic disease and invasive aspergillosis caused by Aspergillus?
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Which characteristic is specific to allergic bronchopulmonary aspergillosis?
Which characteristic is specific to allergic bronchopulmonary aspergillosis?
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What is a common clinical symptom of rhinocerebral mucormycosis?
What is a common clinical symptom of rhinocerebral mucormycosis?
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Which structural characteristics are indicative of the fungi involved in mucormycosis?
Which structural characteristics are indicative of the fungi involved in mucormycosis?
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What conditions are commonly associated with the development of an aspergilloma?
What conditions are commonly associated with the development of an aspergilloma?
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What is the recommended first-line treatment for mucormycosis?
What is the recommended first-line treatment for mucormycosis?
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Which of the following statements accurately describes the role of gliotoxin?
Which of the following statements accurately describes the role of gliotoxin?
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In which context is invasive pulmonary aspergillosis most likely to occur?
In which context is invasive pulmonary aspergillosis most likely to occur?
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Which symptom can indicate the progression of rhinocerebral mucormycosis?
Which symptom can indicate the progression of rhinocerebral mucormycosis?
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What type of patient is at higher risk for pneumonia caused by Pneumocystis jiroveci?
What type of patient is at higher risk for pneumonia caused by Pneumocystis jiroveci?
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Which symptoms may develop in patients with aspergilloma?
Which symptoms may develop in patients with aspergilloma?
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What type of skin test hypersensitivity is characteristic of allergic bronchopulmonary aspergillosis?
What type of skin test hypersensitivity is characteristic of allergic bronchopulmonary aspergillosis?
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Which clinical finding is a potential consequence of rhinocerebral mucormycosis treatment?
Which clinical finding is a potential consequence of rhinocerebral mucormycosis treatment?
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What is the expected rate of disease progression for rhinocerebral mucormycosis?
What is the expected rate of disease progression for rhinocerebral mucormycosis?
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What type of infections can lead to ischemic necrosis in mucormycosis?
What type of infections can lead to ischemic necrosis in mucormycosis?
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What characterizes the mechanism of action of amphotericin B?
What characterizes the mechanism of action of amphotericin B?
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Which of the following antifungal classes directly interferes with ergosterol synthesis?
Which of the following antifungal classes directly interferes with ergosterol synthesis?
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How does amphotericin B compare to cholesterol in mammalian cells?
How does amphotericin B compare to cholesterol in mammalian cells?
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What is a rare feature of amphotericin B regarding resistance?
What is a rare feature of amphotericin B regarding resistance?
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What is the effect of amphotericin B at low levels?
What is the effect of amphotericin B at low levels?
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What is one key consideration for the administration of amphotericin B?
What is one key consideration for the administration of amphotericin B?
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Which of these systemic mycoses is amphotericin B NOT typically used to treat?
Which of these systemic mycoses is amphotericin B NOT typically used to treat?
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What is the main adverse effect of amphotericin B?
What is the main adverse effect of amphotericin B?
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What distinguishes the echinocandins from other antifungal classes?
What distinguishes the echinocandins from other antifungal classes?
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What is the consequence of amphotericin B's mechanism of action?
What is the consequence of amphotericin B's mechanism of action?
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What is the most probable reason that Aspergillus infection is rare in healthy individuals?
What is the most probable reason that Aspergillus infection is rare in healthy individuals?
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Which treatments are used for aspergilloma?
Which treatments are used for aspergilloma?
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What is the primary diagnostic method for invasive aspergillosis?
What is the primary diagnostic method for invasive aspergillosis?
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What type of exposure control measures are typically taken in bone marrow transplant units?
What type of exposure control measures are typically taken in bone marrow transplant units?
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Which of the following molds is NOT commonly classified as part of the Zygomycetes group?
Which of the following molds is NOT commonly classified as part of the Zygomycetes group?
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Which method of transmission is associated with Aspergillus species?
Which method of transmission is associated with Aspergillus species?
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What form of therapy may be provided prophylactically to patients at risk for invasive aspergillosis?
What form of therapy may be provided prophylactically to patients at risk for invasive aspergillosis?
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In what area are Aspergillus species commonly distributed?
In what area are Aspergillus species commonly distributed?
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What kind of immune cells are primarily responsible for attacking Aspergillus hyphae?
What kind of immune cells are primarily responsible for attacking Aspergillus hyphae?
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Study Notes
Mycosis
- Mycosis is a fungal infection
- Aspergillus, a spectrum of diseases caused by Aspergillus species
- Aspergillus species are ubiquitous saprobes in nature, and aspergillosis occurs globally.
- A. fumigatus is the most common human pathogen, but others like A. flavus, A. niger, and A. terreus can cause disease.
- Aspergillus mold produces conidia that can be aerosolized
- Allergic reactions to conidial antigens can occur in atopic individuals after inhalation.
- Immunocompromised patients, especially those with leukaemia, stem cell transplants, or taking corticosteroids, can have conidia germinate into hyphae invading lungs and other tissues.
Morphology and Identification
- Aspergillus species grow rapidly, producing aerial hyphae and characteristic conidial structures.
- Conidia are formed in basipetal chains.
- Conidiophores have vesicles with phialides enabling the production of basipetal chains of conidia.
- Species are identified based on morphologic differences in conidial structure, size, shape, texture, and color.
- Fluffy colonies appear within 1-2 days and cover the entire plate by day 5, having pigmented growth
- The identification of species is based on differences in the structure of the conidiophore and the arrangement of conidia
Aspergillus fumigatus
- A. fumigatus is a species that often causes aspergillosis in humans.
Morphology and Identification (3)
- Species are identified based on differences in conidiophore structure and conidia arrangement.
- Specific morphology is seen in relation to various Aspergillus species.
Pathogenesis
- In the lungs, alveolar macrophages are able to engulf and destroy conidia.
- Macrophages from corticosteroid-treated or immunocompromised patients have a diminished ability to contain the inoculum.
- Conidia in the lung swell and germinate, producing hyphae that invade preexisting cavities (aspergilloma or fungus ball) or blood vessels.
- Adherence is linked to Aspergillus conidial proteins binding to fibrinogen and laminin.
- Disease progression is related to specific Aspergillus glucans and galactomannans.
- Gliotoxin inhibits phagocyte oxidative killing mechanisms and promotes progression.
- Virulent species produce extracellular elastases, proteinases, and phospholipases.
- Biofilm formation by Aspergillus is linked to infections in medical devices and implants.
Manifestation
- Aspergillus can cause clinical allergies or occasional invasive infections, primarily in the lungs.
- Allergic disease is characterized by eosinophilia and specific IgG.
- Invasive aspergillosis occurs in preexisting pulmonary disease (e.g., tuberculosis, asthma) or immunodeficiencies.
- Aspergillus can invade tissues via branching hyphae.
- Mycelial masses can form a radiologically visible fungus ball (aspergilloma) in preexisting lung cavities.
- Lung tissue invasion can lead to hemoptysis or fistula formation.
- Invasive disease outside of the lungs is rare unless patients are immunocompromised.
- Pneumonia in immunocompromised individuals has a grave prognosis.
Clinical findings (Allergic forms)
- Immediate asthmatic reactions can develop in some atopic individuals upon exposure to Aspergillus conidia antigens.
- In other cases, conidia germinate and hyphae colonize the bronchi without invading lung parenchyma.
- This phenomenon is allergic bronchopulmonary aspergillosis (ABPA), characterized by asthma, recurrent chest infiltrates, eosinophilia, and immediate and delayed hypersensitivity reactions.
- Patients often produce sputum with Aspergillus precipitins.
- Massive doses of conidia can lead to extrinsic allergic alveolitis in healthy individuals.
Aspergilloma and Extrapulmonary Colonization
- Aspergilloma develops when inhaled conidia germinate and produce abundant hyphae in existing lung cavities.
- Patients with previous cavitary diseases (e.g., tuberculosis, sarcoidosis, emphysema) are at risk.
- Aspergilloma is usually asymptomatic, but some patients experience cough, dyspnea, weight loss, fatigue, and hemoptysis.
- Localized, noninvasive infections (colonization) by Aspergillus species can infect the nasal sinuses, ear canal, cornea, or nails.
Invasive Aspergillosis
- Following inhalation and germination, invasive disease manifests as an acute pneumonic process.
- Patients at risk include those with lymphocytic or myelogenous leukemia, lymphoma, stem cell transplant recipients, and those taking corticosteroids.
- Symptoms include fever, cough, dyspnea, and hemoptysis.
- Hyphae invade blood vessel lumens and walls, causing thrombosis, infarction, and necrosis.
- Invasive disease can spread from lungs to other organs (GI tract, kidney, liver, brain).
- Severe and rapid progression without treatment carries a poor prognosis.
Abdominal Aspergillosis
- Abdominal aspergillosis involves the liver, spleen, and kidneys in patients who have undergone chemotherapy for acute myeloid leukemia.
- Axial contrast-enhanced CT scans reveal a pseudoaneurysm of the splenic artery and diffuse low-attenuated lesions and cortical enhancement and tiny low attenuated lesions in the kidneys and liver, indicating infarctions.
Laboratory Diagnosis
- Specimens include sputum, respiratory tract specimens, and lung biopsy tissue. Blood samples are rarely positive for Aspergillus.
- Direct microscopic examination of specimens (sputum, tissue samples) with KOH or calcofluor white reveals hyaline, septate hyphae with uniform width (about 4µm) and dichotomous branching.
- Cultures grow rapidly (few days) on most media at room temperature.
Laboratory Diagnosis (2)
- Precipitation tests for A. fumigatus are often positive in cases of aspergilloma or allergic aspergillosis.
- Antibody tests are not useful for invasive aspergillosis, but a serologic test for circulating cell wall galactomannan is diagnostic.
Treatment
- Aspergilloma typically treated with itraconazole or amphotericin B, sometimes requiring surgery.
- Invasive aspergillosis requires rapid administration of amphotericin B or voriconazole (often with cytokine immunotherapy).
- Allergic forms are treated with corticosteroids or disodium chromoglycate.
Immunity
- The efficiency of innate mechanisms is the primary reason for low incidence of Aspergillus infections in healthy people.
- Alveolar macrophages kill conidia; PMNs attack hyphae.
Epidemiology
- Aspergillus species are widespread in nature and found in various environments globally.
- Inhalation of Aspergillus spores is the mode of infection.
- Conidia can disperse via air ducts.
- A. fumigatus was identified in 2012 as the cause of extensive meningitis cases due to contaminated steroid medication injected into the cerebrospinal fluid (CSF).
Control
- Efforts to minimize exposure to Aspergillus conidia are crucial for preventing allergic and invasive disease in susceptible individuals.
- Bone marrow transplant units often employ filtered air systems, patient room monitoring, restrictions on visiting, and other measures to isolate patients and reduce exposure to aspergillus molds.
- Prophylactic low dose amphotericin B or itraconazole may be prescribed for patients at high risk
Zygomycetes and Zygomycosis
- Mucormycosis is a opportunistic infection caused by molds classified in the order Mucorales of the phylum Zygomycota.
- Zygomycosis refers to infections with Zygomycetes, which include species like Absidia, Rhizopus, Cunninghamella, and Mucor.
- These species are soil saprophytes.
- Risk factors for infection are acidosis (especially in diabetes mellitus), leukemias, lymphomas, severe burns, immunodeficiencies, and dialysis using deferoxamine.
- Pulmonary disease resulting from mucormycosis is similar to diseases from other fungi.
Rhinocerebral Mycosis
- Rhinocerebral mucormycosis results from germination of sporangiospores in the nasal passages, followed by hyphae invasion of blood vessels.
- The disease can rapidly spread to sinuses, eyes, cranial bones, and brain, leading to tissue damage, and development of edema, hemorrhage, and orbital cellulitis.
- Clinical symptoms begin with headache and could progress to orbital cellulitis, cranial nerve palsy, vascular thrombosis, coma, and death within two weeks.
Thoracic Mucormycosis
- Thoracic mucormycosis follows inhalation of sporangiospores and invasion of lung parenchyma and vasculature.
- Ischemic necrosis causing massive tissue destruction.
- Contamination of wound dressings is possible as an infection source.
Identification
- Direct examination of nasal discharge, tissue, sputum reveals broad hyphae (10-15 µm) with uneven thickness, irregular branching, and sparse septations.
- These fungi grow rapidly on lab media (producing abundant cottony colonies).
- Identification can be based on sporangial structures.
- Treatment includes aggressive surgical debridement, rapid amphotericin B administration, and underlying disease control.
Pneumocystis jiroveci
- Causes pneumonia in immunocompromised patients, rarely disseminated.
- Thought to be a protozoan, but molecular studies show a close relationship to ascomycetes.
- P. jiroveci is the human species; P. carinii is found only in rats.
- Before chemoprophylaxis, P. jiroveci was a major cause of death among AIDS patients.
- Incidence has significantly decreased, but increasing infections in organs like the spleen, lymph nodes, and bone marrow are observed.
- Morphological characteristics include distinct forms: thin-walled trophozoites and thick-walled cysts with four to eight nuclei; these structures can be stained with silver stains, toluidine blue, and calcofluor white.
- P. jiroveci typically grows tightly clumped in the lungs and is confined to the alveolar epithelium.
- Cysts and trophozoites are typically observed in clinical specimens.
- P. jiroveci surface glycoprotein can be detected in sera.
Pneumocystis
- P. jiroveci causes lethal pneumonia in immunocompromised patients, especially those with AIDS.
- It is an extracellular pathogen.
- Growth in the lung is limited to the alveolar epithelium.
- Observed stages are trophic, precysts, and cysts. Filamentous forms are not seen.
Characteristic of Pneumocystis
- The trophocytic form has a cell wall and cytoplasmic membrane enclosing nucleus and mitochondria.
- The precyst matures and nuclei divide, forming eight spores within a structure that forms a cyst.
- Cysts contain an eccentric nucleus and single mitochondrion.
- The cell wall lacks typical fungal rigidity; N-acetylglucosamine is present, but cholesterol is the dominant sterol.
Current insights into the biology and pathogenesis
- Asexual and sexual reproduction stages are detailed.
- (Asexual) Nucleus and mitochondria are seen in the stages.
- (Sexual) Haploid and diploid precysts and conjugation processes are seen.
Manifestation (Pneumocystis pneumonia)
- Pneumocystis pneumonia begins insidiously with mild fever or malaise in compromised immune patients.
- Signs in the lungs include cough, shortness of breath, progressive cyanosis, and hypoxia, potentially leading to death within three to four weeks.
- Lesions outside the lungs are becoming more frequent, including lymph nodes, bone marrow, spleen, liver, eyes, thyroid, adrenal glands, gastrointestinal tract, and kidneys.
Epidemiology (Pneumocystis)
- P. jiroveci exists worldwide in humans and animals.
- Antibodies are common.
- Transmission via airborne route is probable. A common complication of immunocompromised states, AIDS patients are at high risk.
Pathogenesis (Pneumocystis)
- Pneumocystis is a low-virulence organism.
- Disease in healthy individuals with normal T lymphocytes is infrequent.
- Major surface glycoprotein (Msg) acts as an attachment ligand with host proteins (fibronectin, vitronectin, surfactants).
- Histologically, pneumocystis pneumonia is characterized by alveolar exudate.
Diagnosis (Pneumocystis)
- Specimen sources may include bronchoalveolar lavage, lung tissue biopsies, and sputum.
- Staining techniques for examining specimens include Giemsa, toluidine blue, methenamine silver, and calcofluor white.
- Cysts or trophozoites are indicative of the presence of the organism.
- A monoclonal antibody-based fluorescent examination technique is available.
Immunity, Treatment, and Prophylaxis (Pneumocystis)
- Cell-mediated immunity likely plays a significant role in resistance to P. jiroveci.
- Treatment of acute pneumocystis pneumonia typically involves trimethoprim-sulfamethoxazole or pentamidine isethionate.
- Prophylaxis may involve daily TMP-SMZ or aerosolized pentamidine.
Epidemiology (Pneumocystis)
- A natural reservoir for P. jiroveci hasn't been identified.
- The organism is an obligate member of the normal flora.
- Persons at risk are given chemoprophylaxis.
- Transmission by aerosols may be possible.
Other opportunistic mycoses
- Individuals with weakened host defenses are vulnerable to infections from various saprobic molds, producing airborne spores.
- Opportunistic mycoses, including candidiasis, aspergillosis, and mucormycosis, are less commonly seen.
- Advances in medicine have resulted in an increased number of patients with compromised immunity who may become infected by non-pathogenic fungi.
- Some infections are geographically restricted, like Penicillium marneffei in Asia and AIDS patients.
- Antifungal antibiotics are used frequently, which contributes to the selection of resistant fungal species and strains.
Antifungal prophylaxis
- Opportunistic mycoses are increasing, particularly in immunocompromised patients with hematologic dyscrasias, hematopoietic stem cell recipients, solid organ recipients, or those on cytotoxic or corticosteroid therapy.
- No single standard for administering antifungal prophylaxis exists.
- Oral fluconazole is a common choice; others use short courses of low-dose amphotericin B.
Antifungal chemotherapy
- There are limited but increasing antifungal drugs.
- Most drugs have limitations, including side effects, narrow spectrum, and poor tissue penetration, and the development of resistant fungi.
- Promising new antifungal drugs are being studied, but efficacy and suitability as targets are still being evaluated.
- Fungal and human cells share similar cellular and molecular processes, presenting difficulties in targeting unique fungal elements.
Mechanisms of action of antifungal drugs
- Polyenes (amphotericin B, nystatin) bind to fungal cell membrane ergosterol, altering membrane permeability.
- Azoles inhibit ergosterol synthesis.
- Echinocandins inhibit cell wall beta-glucan synthesis.
- Griseofulvin interferes with microtubule assembly.
- Other antifungal drugs are under investigation.
Amphotericin B
- The most effective drug for severe systemic mycoses.
- Broad-spectrum, but development of resistance is rare.
- Mechanism of action involves complex formation with fungal membrane ergosterol, inducing membrane damage and leakage.
- Greater affinity for ergosterol than cholesterol.
- Binding to ergosterol can alter membrane fluidity, forming pores, and leading to loss of small molecules and ions.
- Unlike many antifungals, this is cidal, not just fungistatic.
- Weak binding to mammalian cholesterol is thought to contribute to toxicity.
- At low levels, amphotericin B exhibits immunestimulatory effects.
Mechanism of action (Amphotericin B)
- Amphotericin B strongly binds to ergosterol in the fungal cell membrane disrupting membrane fluidity and permeability, which can lead to the release of cellular components.
- In contrast to mammalian cells, which use cholesterol as the predominant sterol in cellular membranes.
- It is cidal, unlike most other antifungals, which may be fungistatic.
Indications (Amphotericin B)
- Amphotericin B has a broad spectrum of activity against several systemic mycoses, including coccidioidomycosis, blastomycosis, histoplasmosis, sporotrichosis, cryptococcosis, aspergillosis, and candidiasis.
- Treatment efficacy is influenced by dose, administration rate, site of infection, patient immune status, and intrinsic pathogen susceptibility.
- Poor penetration into the central nervous system and the joints. Intrathecal and intraarticular administration may be necessary for particular cases.
- Often combined with other drugs for treating certain infections, like cryptococcosis and flucytosine combination is used.
Side effects (Amphotericin B)
- All patients experience adverse reactions, though they are minimized with new lipid preparations.
- Common acute reactions include fever, chills, dyspnea, and hypotension which can be alleviated with hydrocortisone/acetaminophen.
- Chronic side effects, primarily nephrotoxicity, are frequent and cause hypokalemia, anemia, renal tubular acidosis, and headache in some patients.
Flucytosine
- 5-fluorocytosine is an antifungal compound used for treating cryptococcosis and candidiasis often in combination with amphotericin B.
- Effective against several dematiaceous fungal infections.
- It penetrates all tissues, including CSF.
Mechanism of action (Flucytosine)
- Flucytosine is transported into fungal cells by permeases.
- Fungi convert flucytosine into 5-fluorouracil, which inhibits thymidylate synthetase.
- Mammalian cells lack cytosine deaminase, protecting them from flucytosine's toxic effects.
- The fungistatic drug is less effective since resistant mutants surge quickly.
Indications (Flucytosine)
- Primarily used in combination with amphotericin B to treat cryptococcosis and candidiasis.
- Clinical trials show it can help in cases of cryptococcal meningitis.
- Combination with amphotericin B can prolong the effectiveness, limit/delay resistant mutant development.
- Effective against other dematiaceous fungal infections.
Side effects (Flucytosine)
- Relatively well-tolerated itself; but conversion to fluorouracil is highly toxic, and prolonged administration can cause bone marrow suppression, hair loss, and liver abnormalities.
- Conversion by enteric bacteria to fluorouracil may lead to colitis.
Azoles
- Imidazole and triazole antifungal drugs (ketoconazole, fluconazole, voriconazole, itraconazole)
- Oral antifungal agents used for systemic and localized fungal infections.
- Often supplant amphotericin B in milder cases due to oral administration and reduced toxicity.
- These drugs act by inhibiting ergosterol synthesis.
Mechanism of action (Azoles)
- Azoles act to inhibit ergosterol synthesis in fungal cells.
- Various azole drugs are formulated with differing efficacy, availability, kinetics and side effect profiles.
- Azoles are fungistatic
Indications (Azoles)
- Ketoconazole is useful for chronic mucocutaneous candida, dermatophytosis; nonmeningeal blastomycosis, coccidioidomycosis, paracoccidioidomycosis, and histoplasmosis.
- Fluconazole has good penetration of the central nervous system and is utilized for cryptococcal and coccidioidal meningitis.
- Itraconazole is now common first-line treatment for histoplasmosis, blastomycosis, coccidioidomycosis, paracoccidioidomycosis, aspergillosis, and chromomycosis. -It is also effective against onychomycosis.
Side effects (Azoles)
- Ketoconazole is the most toxic azole, often used for treating fungal infections.
- Therapeutic doses can inhibit testosterone/cortisol synthesis affecting libido, impotence, menstrual irregularity, or adrenal insufficiency.
- Fluconazole and itraconazole at recommended therapeutic doses do not cause significant impairment issues in mammalian steroidogenesis.
- Hepatotoxicity and asymptomatic increases in liver function test readings may accompany all azoles.
- Voriconazole can cause a reversible visual impairment.
Topical antifungal agents
- Nystatin
- A polyene antibiotic structurally related to amphotericin B, with a similar mode of action.
- Used topically for treating local candidal infections, including mouth and vaginal areas.
- Can also suppress subclinical esophageal candidiasis and gastrointestinal candidal overgrowth.
- Relatively non-toxic when used for topical infections. Usually not used parenterally due to toxic effects.
Topical antifungal agents (2)
- Various azoles (clotrimazole, miconazole, econazole, butaconazole, tioconazole, terconazole) available as topical formulations.
- These azoles are effective against tinea pedis, tinea corporis, tinea cruris, tinea versicolor, and cutaneous candidiasis (applied to skin).
- Also used for vulvovaginal candidiasis (applied to vaginal area).
- Clotrimazole can be used as an oral troche to treat oral and esophageal thrush in immunocompetent patients.
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Description
Test your knowledge on antifungal treatments, particularly flucytosine and its use in combination with amphotericin B. This quiz covers the mechanisms of action, side effects, and specific conditions related to various fungal infections. Prepare for questions on allergic responses and mucormycosis as well.
