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Fungi/Yeast/Molds

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Atifa Ambreen
Atifa Ambreen

Fungi differ from bacteria in that they have a cell wall composed of chitin rather than peptidoglycan, and a cell membrane containing ergosterol rather than cholesterol. There are two main types of fungi: yeasts, which grow as single cells, and molds, which grow as filaments called hyphae. Many medically important fungi can exist as either molds or yeasts depending on temperature. Fungi reproduce both sexually through spores and asexually through budding or formation of conidia. Host defenses against fungi include intact skin and mucous membranes, as well as cell-mediated immunity and antibodies, though fungi do not produce endotoxins or exotox

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Fungi/Yeast/Molds Atifa Ambreen M. Phil, Microbiology
Structure & Growth  Because fungi (yeasts and molds) are eukaryotic organisms whereas bacteria are prokaryotic, they differ in several fundamental respects. Two fungal cell structures are important medically:  The fungal cell wall consists primarily of chitin (not peptidoglycan as in bacteria); thus, fungi are insensitive to antibiotics, such as penicillin, that inhibit peptidoglycan synthesis.  Chitin is a polysaccharide composed of long chains of N- acetylglucosamine. The fungal cell wall contains other polysaccharides as well, the most important of which is -glucan, a long polymer of D-glucose. The medical importance of -glucan is that it is the site of action of the antifungal drug caspofungin.  The fungal cell membrane contains ergosterol, in contrast to the human cell membrane, which contains cholesterol. The selective action of amphotericin B and azole drugs, such as fluconazole and ketoconazole, on fungi is based on this difference in membrane sterols.
Fungi/Yeast/Molds
Types There are two types of fungi: 1. Yeasts 2. Molds. 1. Yeasts grow as single cells that reproduce by asexual budding. 2. Molds grow as long filaments (hyphae) and form a mat (mycelium). Some hyphae form transverse walls (septate hyphae), whereas others do not (nonseptate hyphae). Nonseptate hyphae are multinucleated (coencytic).
Fungi/Yeast/Molds
Important Properties  Several medically important fungi are thermally dimorphic; i.e., they form different structures at different temperatures. They exist as molds in the environment at ambient temperature and as yeasts (or other structures) in human tissues at body temperature.  Most fungi are obligate aerobes; some are facultative anaerobes; but none are obligate anaerobes. All fungi require a preformed organic source of carbon—hence their frequent association with decaying matter. The natural habitat of most fungi is, therefore, the environment. An important exception is Candida albicans, which is part of the normal human flora.
Fungal Reproduction  Some fungi reproduce sexually by mating and forming sexual spores, e.g., zygospores, ascospores, and basidiospores. Zygospores are single large spores with thick walls; ascospores are formed in a sac called ascus; and basidiospores are formed externally on the tip of a pedestal called a basidium. The classification of these fungi is based on their sexual spores. Fungi that do not form sexual spores are termed "imperfect" and are classified as fungi imperfecti.
 Most fungi of medical interest propagate asexually by forming conidia (asexual spores) from the sides or ends of specialized structures (Figure 47–1). The shape, color, and arrangement of conidia aid in the identification of fungi. Some important conidia are  (1) arthrospores, which arise by fragmentation of the ends of hyphae  (2) chlamydospores, which are rounded, thick-walled, and quite resistant.  (3) blastospores, which are formed by the budding process by which yeasts reproduce asexually (some yeasts, e.g., C. albicans, can form multiple buds that do not detach, thus producing sausagelike chains called pseudohyphae, which can be used for identification).  (4) sporangiospores, which are formed within a sac (sporangium) on a stalk by molds such as Rhizopus and Mucor.
Fungi/Yeast/Molds
Key Points:  fungi that are human pathogens, it should be remembered that fungi are used in the production of important foods, e.g., bread, cheese, wine, and beer. Fungi are also responsible for the spoilage of certain foods. Because molds can grow in a drier, more acidic, and higher-osmotic-pressure environment than bacteria, they tend to be involved in the spoilage of fruits, grains, vegetables, and jams.
Pathogenesis  The response to infection with many fungi is the formation of granulomas. Granulomas are produced in the major systemic fungal diseases, e.g., coccidioidomycosis, histoplasmosis, and blastomycosis, as well as several others. The cell-mediated immune response is involved in granuloma formation. Acute suppuration, characterized by the presence of neutrophils in the exudate, also occurs in certain fungal diseases such as aspergillosis and sporotrichosis. Fungi do not have endotoxin in their cell walls and do not produce bacterial- type exotoxins.  Activation of the cell-mediated immune system results in a delayed hypersensitivity skin test response to certain fungal antigens injected intradermally. A positive skin test indicates exposure to the fungal antigen. It does not imply current infection, because the exposure may have occurred in the past. A negative skin test makes the diagnosis unlikely unless the patient is immunocompromised. Because most people carry Candida as part of the normal flora, skin testing with Candida antigens can be used to determine whether cell-mediated immunity is normal.
Fungi/Yeast/Molds
 Intact skin is an effective host defense against certain fungi (e.g., Candida, dermatophytes), but if the skin is damaged, organisms can become established. The normal flora of the skin and mucous membranes suppress fungi. When the normal flora is inhibited, e.g., by antibiotics, overgrowth of fungi such as C. albicans can occur.  In the respiratory tract, the important host defenses are the mucous membranes of the nasopharynx, which trap inhaled fungal spores, and alveolar macrophages. Circulating IgG and IgM are produced in response to fungal infection, but their role in protection from disease is uncertain.
Fungal Toxins & Allergies  Ingestion of Amanita mushrooms causes liver necrosis due to the presence of two fungal toxins, amanitin and phylloidin. Amanitin inhibits the RNA polymerase that synthesizes cellular mRNA.  Ingestion of peanuts and grains contaminated with Aspergillus flavus causes liver cancer due to the presence of aflatoxin. Aflatoxin epoxide induces a mutation in the p53 gene that results in a loss of the p53 tumor suppressor protein.  Inhalation of the spores of Aspergillus fumigatus can cause allergic bronchopulmonary aspergillosis. This is an IgE-mediated immediate hypersensitivity response.
Fungi/Yeast/Molds
Antifungal Therapy  The drugs used to treat bacterial diseases have no effect on fungal diseases. For example, penicillins and aminoglycosides inhibit the growth of many bacteria but do not affect the growth of fungi. This difference is explained by the presence of certain structures in bacteria, e.g., peptidoglycan and 70S ribosomes, that are absent in fungi.  The most effective antifungal drugs, amphotericin B and the various azoles, exploit the presence of ergosterol in fungal cell membranes that is not found in bacterial or human cell membranes. Amphotericin B disrupts fungal cell membranes at the site of ergosterol and azole drugs inhibit the synthesis of ergosterol, which is an essential component of fungal membranes. Another antifungal drug, caspofungin , inhibits the synthesis of -glucan, which is found in fungal cell walls but not in bacterial cell walls. Human cells do not have a cell wall.  There is no clinically significant resistance to antifungal drugs.
Fungi/Yeast/Molds

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Fungi/Yeast/Molds

  • 2. Structure & Growth  Because fungi (yeasts and molds) are eukaryotic organisms whereas bacteria are prokaryotic, they differ in several fundamental respects. Two fungal cell structures are important medically:  The fungal cell wall consists primarily of chitin (not peptidoglycan as in bacteria); thus, fungi are insensitive to antibiotics, such as penicillin, that inhibit peptidoglycan synthesis.  Chitin is a polysaccharide composed of long chains of N- acetylglucosamine. The fungal cell wall contains other polysaccharides as well, the most important of which is -glucan, a long polymer of D-glucose. The medical importance of -glucan is that it is the site of action of the antifungal drug caspofungin.  The fungal cell membrane contains ergosterol, in contrast to the human cell membrane, which contains cholesterol. The selective action of amphotericin B and azole drugs, such as fluconazole and ketoconazole, on fungi is based on this difference in membrane sterols.
  • 4. Types There are two types of fungi: 1. Yeasts 2. Molds. 1. Yeasts grow as single cells that reproduce by asexual budding. 2. Molds grow as long filaments (hyphae) and form a mat (mycelium). Some hyphae form transverse walls (septate hyphae), whereas others do not (nonseptate hyphae). Nonseptate hyphae are multinucleated (coencytic).
  • 6. Important Properties  Several medically important fungi are thermally dimorphic; i.e., they form different structures at different temperatures. They exist as molds in the environment at ambient temperature and as yeasts (or other structures) in human tissues at body temperature.  Most fungi are obligate aerobes; some are facultative anaerobes; but none are obligate anaerobes. All fungi require a preformed organic source of carbon—hence their frequent association with decaying matter. The natural habitat of most fungi is, therefore, the environment. An important exception is Candida albicans, which is part of the normal human flora.
  • 7. Fungal Reproduction  Some fungi reproduce sexually by mating and forming sexual spores, e.g., zygospores, ascospores, and basidiospores. Zygospores are single large spores with thick walls; ascospores are formed in a sac called ascus; and basidiospores are formed externally on the tip of a pedestal called a basidium. The classification of these fungi is based on their sexual spores. Fungi that do not form sexual spores are termed "imperfect" and are classified as fungi imperfecti.
  • 8.  Most fungi of medical interest propagate asexually by forming conidia (asexual spores) from the sides or ends of specialized structures (Figure 47–1). The shape, color, and arrangement of conidia aid in the identification of fungi. Some important conidia are  (1) arthrospores, which arise by fragmentation of the ends of hyphae  (2) chlamydospores, which are rounded, thick-walled, and quite resistant.  (3) blastospores, which are formed by the budding process by which yeasts reproduce asexually (some yeasts, e.g., C. albicans, can form multiple buds that do not detach, thus producing sausagelike chains called pseudohyphae, which can be used for identification).  (4) sporangiospores, which are formed within a sac (sporangium) on a stalk by molds such as Rhizopus and Mucor.
  • 10. Key Points:  fungi that are human pathogens, it should be remembered that fungi are used in the production of important foods, e.g., bread, cheese, wine, and beer. Fungi are also responsible for the spoilage of certain foods. Because molds can grow in a drier, more acidic, and higher-osmotic-pressure environment than bacteria, they tend to be involved in the spoilage of fruits, grains, vegetables, and jams.
  • 11. Pathogenesis  The response to infection with many fungi is the formation of granulomas. Granulomas are produced in the major systemic fungal diseases, e.g., coccidioidomycosis, histoplasmosis, and blastomycosis, as well as several others. The cell-mediated immune response is involved in granuloma formation. Acute suppuration, characterized by the presence of neutrophils in the exudate, also occurs in certain fungal diseases such as aspergillosis and sporotrichosis. Fungi do not have endotoxin in their cell walls and do not produce bacterial- type exotoxins.  Activation of the cell-mediated immune system results in a delayed hypersensitivity skin test response to certain fungal antigens injected intradermally. A positive skin test indicates exposure to the fungal antigen. It does not imply current infection, because the exposure may have occurred in the past. A negative skin test makes the diagnosis unlikely unless the patient is immunocompromised. Because most people carry Candida as part of the normal flora, skin testing with Candida antigens can be used to determine whether cell-mediated immunity is normal.
  • 13.  Intact skin is an effective host defense against certain fungi (e.g., Candida, dermatophytes), but if the skin is damaged, organisms can become established. The normal flora of the skin and mucous membranes suppress fungi. When the normal flora is inhibited, e.g., by antibiotics, overgrowth of fungi such as C. albicans can occur.  In the respiratory tract, the important host defenses are the mucous membranes of the nasopharynx, which trap inhaled fungal spores, and alveolar macrophages. Circulating IgG and IgM are produced in response to fungal infection, but their role in protection from disease is uncertain.
  • 14. Fungal Toxins & Allergies  Ingestion of Amanita mushrooms causes liver necrosis due to the presence of two fungal toxins, amanitin and phylloidin. Amanitin inhibits the RNA polymerase that synthesizes cellular mRNA.  Ingestion of peanuts and grains contaminated with Aspergillus flavus causes liver cancer due to the presence of aflatoxin. Aflatoxin epoxide induces a mutation in the p53 gene that results in a loss of the p53 tumor suppressor protein.  Inhalation of the spores of Aspergillus fumigatus can cause allergic bronchopulmonary aspergillosis. This is an IgE-mediated immediate hypersensitivity response.
  • 16. Antifungal Therapy  The drugs used to treat bacterial diseases have no effect on fungal diseases. For example, penicillins and aminoglycosides inhibit the growth of many bacteria but do not affect the growth of fungi. This difference is explained by the presence of certain structures in bacteria, e.g., peptidoglycan and 70S ribosomes, that are absent in fungi.  The most effective antifungal drugs, amphotericin B and the various azoles, exploit the presence of ergosterol in fungal cell membranes that is not found in bacterial or human cell membranes. Amphotericin B disrupts fungal cell membranes at the site of ergosterol and azole drugs inhibit the synthesis of ergosterol, which is an essential component of fungal membranes. Another antifungal drug, caspofungin , inhibits the synthesis of -glucan, which is found in fungal cell walls but not in bacterial cell walls. Human cells do not have a cell wall.  There is no clinically significant resistance to antifungal drugs.