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When Plants Thrive in the Body 16 Mycotic Infection Summary The hypha is the basic morphologic element of mul- ticellular fungi in the vegetative phase. It is a multi- branched tubular structure subdivided by transverse septa. These structures form a network known as a mycelium. The unicellular hyphae are oval to round, but often adhere together in the form of hypha-like chains (pseudo-hyphae). Most of the fungi that cause disease in humans have only slight pathogenic potential and can only invade tissue in an immuno- compromised host or after destruction of compet- ing bacterial flora. These are known as opportunistic pathogens. Tissue destruction by mycotic patho- gens is partially attributable to toxic fungal products that cause disease by mechanisms that are not al- ways well understood. It is also partially attributable to abnormal immune reactions. Antigens of the fun- gus capsule stimulate a population of B lymphocytes to form antibodies. This leads to precipitating and complement-binding antibodies, whose presence aids in diagnosing these disorders. " The spores of saprophytic fungi such as Asper- gillus, Candida, Coccidioides, and Penicillium cause allergic hypersensitivity reactions in predisposed pa- tients and lead to mycotic allergies. A cell-mediated type IV hypersensitivity reaction also plays a decisive role in combating mycotic infections, as does un- compromised granulocyte function. " Histologic findings of a “ruthlessly proliferative” mycelium that does not respect tissue septa, organ capsules, or vascular walls are common to all infec- tious diseases caused by mycelium-forming fungi (mycoses). The mycelium grows through these structures and typically exhibits a ring-like or sphe- rical pattern of proliferation. Skin Mycoses (Superficial Mycoses) Pathogenesis: Forms of mycosis are differen- tiated according to the pathogen and depth of penetration in the tissue. Superficial epidermal mycosis is infestation of the horny layer of the epidermis with fungus organisms (not dermatophytes or fungi that produce deeper types of mycosis). Cutaneous mycosis refers to infestation of the entire epidermis and/or hair with fungal organisms (pri- marily dermatophytes, which cause dermatophyto- sis, and Candida, which causes candidosis). Dermatophytoses Pathogens (dermatophytes): They only infect tissue containing large amounts of keratin such as the epidermis (Epidermophyton flocco- sum), hair (Trichophyton rubrum), and nails (Trichophyton mentagrophytes). Pathogenesis: Dermatophytoses are the only fungal infections that are spread by human- to-human or animal-to-human contact. Pathogen identification: All dermatophytes are hypho- mycetes and form septated hyphae in the skin lesions they create. These hyphae will be positive in a periodic acid-Schiff reaction (PAS). Clinical presentation and morphology: Dermatomycoses (skin mycoses) are caused by vari- ety of pathogens that produce morphologically simi- lar cutaneous lesions (referred to as a tinea and further specified according to location). These tineas consist of round or oval erythematous rashes that are often concentric ( A). Onychomycosis (nail mycosis) is an infection of the nails of the fingers or toes causing yellowish-white opacification and flaking of the nail ( B). The disor- der begins as distal unguinal, proximal unguinal, or superficial onychomycosis and later progresses to dystrophic onychomycosis. Deep trichophytosis is dermatophytosis with bacte- rial superinfection that results in a suppurative ab- scess-forming inflammation with mycelium at the depth of the hair follicles. Subcutaneous and Mucosal Mycoses General pathogenesis: Fungi grow beyond the epidermis and penetrate into deeper layers of subcutaneous connective tissue through skin wounds. This results in a focal chronic inflam- matory reaction around the mycelium ( C2); granulomatous inflammatory reactions ( C1) may occur in patients with stronger immune systems. Organ and Systemic Mycoses General pathogenesis: Fungal penetration may occur by several mechanisms. Aerogenic penetration leads to fungal bronchitis ( D1) with invasion of the bronchial wall ( D2) progressing to invasion of surrounding pulmonary tissue. Latrogenic penetration of fungi present in the oral flora can occur during endoscopic retrograde cho- langiopancreatography (ERCP). Hematogenous penetration can occur in vascular in- vasion, which may successively lead to fungal vas- culitis ( E), fungemia (fungal sepsis), and fungal colonization of organs such as the liver ( F). Note: The general principle of mycosis due to my- celium-forming fungi involves these elements: Relentless invasion of tissue septa, organ capsules, and vessel walls; Organ invasion ! spherical pattern; Skin invasion ! circular pattern. Riede / Werner, Color Atlas of Pathology © 2004 Thieme All rights reserved. Usage subject to terms and conditions of license.

16 When Plants Thrive in the Body Mycotic Infection · Subcutaneous and Mucosal Mycoses General pathogenesis: Fungi grow beyond the epidermis and penetrate into deeper layers of subcutaneous

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When Plants Thrive in the Body16 Mycotic InfectionSummary

The hypha is the basic morphologic element of mul-ticellular fungi in the vegetative phase. It is a multi-branched tubular structure subdivided by transversesepta. These structures form a network known as amycelium. The unicellular hyphae are oval to round,but often adhere together in the form of hypha-likechains (pseudo-hyphae). Most of the fungi thatcause disease in humans have only slight pathogenicpotential and can only invade tissue in an immuno-compromised host or after destruction of compet-ing bacterial flora. These are known as opportunisticpathogens. Tissue destruction by mycotic patho-gens is partially attributable to toxic fungal productsthat cause disease by mechanisms that are not al-ways well understood. It is also partially attributableto abnormal immune reactions. Antigens of the fun-gus capsule stimulate a population of B lymphocytes

to form antibodies. This leads to precipitating andcomplement-binding antibodies, whose presenceaids in diagnosing these disorders." The spores of saprophytic fungi such as Asper-gillus, Candida, Coccidioides, and Penicillium causeallergic hypersensitivity reactions in predisposed pa-tients and lead to mycotic allergies. A cell-mediatedtype IV hypersensitivity reaction also plays a decisiverole in combating mycotic infections, as does un-compromised granulocyte function." Histologic findings of a “ruthlessly proliferative”mycelium that does not respect tissue septa, organcapsules, or vascular walls are common to all infec-tious diseases caused by mycelium-forming fungi(mycoses). The mycelium grows through thesestructures and typically exhibits a ring-like or sphe-rical pattern of proliferation.

Skin Mycoses (Superficial Mycoses)

Pathogenesis: Forms of mycosis are differen-tiated according to the pathogen and depth ofpenetration in the tissue.

— Superficial epidermal mycosis is infestation of thehorny layer of the epidermis with fungus organisms(not dermatophytes or fungi that produce deepertypes of mycosis).

— Cutaneous mycosis refers to infestation of the entireepidermis and/or hair with fungal organisms (pri-marily dermatophytes, which cause dermatophyto-sis, and Candida, which causes candidosis).

Dermatophytoses

Pathogens (dermatophytes): They only infecttissue containing large amounts of keratinsuch as the epidermis (Epidermophyton flocco-sum), hair (Trichophyton rubrum), and nails(Trichophyton mentagrophytes).

Pathogenesis: Dermatophytoses are the onlyfungal infections that are spread by human-to-human or animal-to-human contact.

Pathogen identification: All dermatophytes are hypho-mycetes and form septated hyphae in the skin lesionsthey create. These hyphae will be positive in a periodicacid-Schiff reaction (PAS).

Clinical presentation and morphology:Dermatomycoses (skin mycoses) are caused by vari-ety of pathogens that produce morphologically simi-lar cutaneous lesions (referred to as a tinea andfurther specified according to location). These tineasconsist of round or oval erythematous rashes that areoften concentric ( A).Onychomycosis (nail mycosis) is an infection of thenails of the fingers or toes causing yellowish-whiteopacification and flaking of the nail ( B). The disor-der begins as distal unguinal, proximal unguinal, or

superficial onychomycosis and later progresses todystrophic onychomycosis.Deep trichophytosis is dermatophytosis with bacte-rial superinfection that results in a suppurative ab-scess-forming inflammation with mycelium at thedepth of the hair follicles.

Subcutaneous and Mucosal Mycoses

General pathogenesis: Fungi grow beyond theepidermis and penetrate into deeper layers ofsubcutaneous connective tissue through skinwounds. This results in a focal chronic inflam-matory reaction around the mycelium ( C2);granulomatous inflammatory reactions ( C1)may occur in patients with stronger immunesystems.

Organ and Systemic Mycoses

General pathogenesis: Fungal penetration mayoccur by several mechanisms.

— Aerogenic penetration leads to fungal bronchitis( D1) with invasion of the bronchial wall ( D2)progressing to invasion of surrounding pulmonarytissue.

— Latrogenic penetration of fungi present in the oralflora can occur during endoscopic retrograde cho-langiopancreatography (ERCP).

— Hematogenous penetration can occur in vascular in-vasion, which may successively lead to fungal vas-culitis ( E), fungemia (fungal sepsis), and fungalcolonization of organs such as the liver ( F).

Note: The general principle of mycosis due tomy-celium-forming fungi involves these elements:

– Relentless invasion of tissue septa, organ capsules,and vessel walls;

– Organ invasion ! spherical pattern;– Skin invasion ! circular pattern.

Riede / Werner, Color Atlas of Pathology © 2004 ThiemeAll rights reserved. Usage subject to terms and conditions of license.

C Granulomatous fungal inflammation (PAS) x 15

E Hematogenous fungal infection (vasculitis)(Grocott-silver stain) x 25

A Dermatomycosis

D Aerogenic fungal infection (fungal bronchitis)(Grocott-silver stain) x 25

F Hematogenous fungal infection (fungal sepsis in the liver; PAS) x 75

B Onychomycosis in a black patient

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Thieme S.257-285.MON 02.06.2004 09:18 Uhr Seite 7

Riede / Werner, Color Atlas of Pathology © 2004 ThiemeAll rights reserved. Usage subject to terms and conditions of license.