what factors could cause opportunistic mycoses to be a growing medical problem

General Concepts

Classification of Mycoses

The clinical nomenclatures used for the mycoses are based on the (1) site of the infection, (2) route of acquisition of the pathogen, and (3) blazon of virulence exhibited by the fungus.

Classification Based on Site

Mycoses are classified every bit superficial, cutaneous, subcutaneous, or systemic (deep) infections depending on the type and degree of tissue involvement and the host response to the pathogen.

Classification Based on Route of Acquisition

Infecting fungi may be either exogenous or endogenous. Routes of entry for exogenous fungi include airborne, cutaneous or percutaneous. Endogenous infection involves colonization by a fellow member of the normal flora or reactivation of a previous infection.

Nomenclature Based on Virulence

Chief pathogens can establish infections in normal hosts. Opportunistic pathogens crusade disease in individuals with compromised host defense mechanisms.

Epidemiology

The chief pathogens have relatively well-defined geographic ranges; the opportunistic fungi are ubiquitous.

Introduction

Electric current magnitude and problems of mycoses

Fungal infections or mycoses cause a wide range of diseases in humans. Mycoses range in extent from superficial infections involving the outer layer of the stratum corneum of the peel to disseminated infection involving the brain, heart, lungs, liver, spleen, and kidneys. The range of patients at hazard for invasive fungal infections continues to expand beyond the normal host to embrace patients with the caused immunodeficiency syndrome; those immunosuppressed due to therapy for cancer and organ transplantation, and those undergoing major surgical procedures. Each of these patient populations has a high gamble of developing invasive fungal infections. As the population at gamble continues to expand so also does the spectrum of opportunistic fungal pathogens infecting these patients also keep to increase. Many of the deeply invasive mycoses are difficult to diagnose early and often difficult to treat finer. The development of new approaches to diagnosis and treatment of invasive fungal infections is the bailiwick of intensive enquiry.

Concepts of nomenclature

Fungal infections may be classified according to the site of infection, route of acquisition, and type of virulence. When classified according to the site of infection, fungal infections are designated as superficial, cutaneous, subcutaneous, and deep (Fig. 75-1). Superficial mycoses are limited to the stratum corneum and essentially elicit no inflammation. Cutaneous infections involve the integument and its appendages, including hair and nails. Infection may involve the stratum corneum or deeper layers of the epidermis. Inflammation of the skin is elicited by the organism or its products. Subcutaneous mycoses include a range of unlike infections characterized by infection of the subcutaneous tissues unremarkably at the point of traumatic inoculation. An inflammatory response develops in the subcutaneous tissue frequently with extension into the epidermis. Deep mycoses involve the lungs, intestinal viscera, bones and or central nervous system. The most common portals of entry are the respiratory tract, alimentary canal, and blood vessels (Fig. 75-2).

Effigy 75-ane

Master tissue sites of deep mycoses in comparison to those of the superficial, cutaneous, and subcutaneous mycoses.

Figure 75-2

Portals of entry of pathogenic and opportunistic fungi causing deep mycoses.

When classified according to the route of conquering, a fungal infection may be designated every bit exogenous or endogenous in origin. If classified as exogenous, an infecting organism may be transmitted past airborne, cutaneous, or percutaneous routes. An endogenously-acquired fungal infection may be acquired from colonization or reactivation of a fungus from a latent infection. Fungi may be classified also co-ordinate to virulence, equally master pathogens or as opportunistic pathogens. A master pathogen may establish infection in an immunologically normal host; whereas, an opportunistic pathogen requires some compromise of host defenses in order for infection to become established.

Superficial and Cutaneous Mycoses

Superficial Mycoses include the post-obit fungal infections and their etiological amanuensis: blackness piedra (Piedraia hortae), white piedra (Trichosporon beigelii), pityriasis versicolor (Malassezia furfur), and tinea nigra (Phaeoannellomyces werneckii). Pityriasis versicolor is a common superficial mycosis, which is characterized by hypopigmentation or hyperpigmentation of skin of the neck, shoulders, chest, and back. Pityriasis versicolor is due to Malassezia furfur which involves simply the superficial keratin layer. Blackness piedra is a superficial mycosis due to Piedraia hortae which is manifested past a small firm black nodule involving the hair shaft. Past comparing, white piedra due to T beigelii is characterized by a soft, friable, biscuit nodule of the distal ends of hair shafts. Tinea nigra most typically presents equally a chocolate-brown to blackness silver nitrate-like stain on the palm of the manus or sole of the pes.

Cutaneous Mycoses may exist classified as dermatophytoses or dermatomycoses. Dermatophytoses are caused by the agents of the genera Epidermophyton, Microsporum, and Trichophyton. Dermatomycoses are cutaneous infections due to other fungi, the most common of which are Candida spp. The dermatophytoses are characterized by an anatomic site-specificity according to genera. For example, Epidermophyton floccosum infects only skin and nails, but does non infect hair shafts and follicles. Whereas, Microsporum spp. infect hair and skin, but do non involve nails. Trichophyton spp. may infect hair, pare, and nails.

Subcutaneous Mycoses

In that location are three full general types of subcutaneous mycoses: chromoblastomycosis, mycetoma, and sporotrichosis. All appear to be caused by traumatic inoculation of the etiological fungi into the subcutaneous tissue. Chromoblastomycosis is a subcutaneous mycosis characterized by verrucoid lesions of the peel (usually of the lower extremities); histological examination reveals muriform cells (with perpendicular septations) or so-called "copper pennies" that are characteristic of this infection. Chromoblastomycosis is generally express to the subcutaneous tissue with no involvement of bone, tendon, or musculus. Past comparison, mycetoma is a suppurative and granulomatous subcutaneous mycosis, which is subversive of contiguous bone, tendon, and skeletal musculus. Mycetoma is characterized past the presence of draining sinus tracts from which small-scale but grossly visible pigmented grains or granules are extruded. These grains are microcolonies of fungi causing the infection.

Chromoblastomycosis and mycetoma are caused by only certain fungi. The nearly common causes of chromoblastomycosis are Fonsecaea pedrosoi, Fonsecaea compacta, Cladosporium carionii, and Phialophora verrucosa. The causes of mycetoma are more various but tin be classified every bit eumycotic and actinomycotic mycetoma. Inside the United states of america, the virtually common agent of eumycotic mycetoma is Pseudallescheria boydii and the most common cause of actinomycotic mycetoma is Nocardia brasiliensis. Many of the fungi causing mycetoma are pigmented chocolate-brown to black. These organisms are known as dematiaceous (melanized) fungi. The melanin pigment is deposited in the prison cell walls of these organisms. These fungi may produce a range of infections from superficial to subcutaneous to deep (visceral) infection characterized by the presence of dematiaceous hyphal and/or yeast-like cells in tissue. Such deep infections due to dematiaceous fungi are termed phaeohyphomycosis.

Sporotrichosis is the third full general class of subcutaneous mycoses. This infection is due to Sporothrix schenckii and involves the subcutaneous tissue at the point of traumatic inoculation. The infection usually spreads along cutaneous lymphatic channels of the extremity involved.

Deep Mycoses

General Concepts

Primary versus opportunistic mycoses

Deep mycoses are caused by primary pathogenic and opportunistic fungal pathogens. The primary pathogenic fungi are able to institute infection in a normal host; whereas, opportunistic pathogens require a compromised host in lodge to establish infection (e.grand., cancer, organ transplantation, surgery, and AIDS). The primary deep pathogens usually proceeds access to the host via the respiratory tract. Opportunistic fungi causing deep mycosis invade via the respiratory tract, alimentary tract, or intravascular devices.

The master systemic fungal pathogens include Coccidioides immitis, Histoplasma capsulatum, Blastomyces dermatitidis, and Paracoccidioides brasiliensis. The opportunistic fungal pathogens include Cryptococcus neoformans, Candida spp., Aspergillus spp., Penicillium marneffei, the Zygomycetes, Trichosporon beigelii, and Fusarium spp.

Dimorphism in the Pathogenic Fungi

Fungal dimorphism is the morphological and physiological conversion of sure fungi from one phenotype to another when such fungi change from one environment to another. Dimorphic fungi include C immitis, H capsulatum, B dermatitidis, P brasiliensis, P marneffei, and S schenckii, and sure opportunistic fungi such as Candida albicans and Penicillium marneffei. Various environmental host factors command fungal dimorphism. These factors include amino acids, temperature, carbohydrates, and trace elements (east.g. zinc). Amidst the principal pathogens and South schenckii, the morphological transformation is from a hyphal course to a yeast-like form (or spherule in the instance of C immitis) in tissue (Fig. 75-3). Withal, the dimorphism of Candida albicans is somewhat dissimilar in that the organism transforms from a budding yeast-like structures (blastoconidia) to filamentous structures known as germ tubes (Fig. 75-4). Other filamentous structures may later develop as pseudohyphae and hyphae. Penicillium marneffei is unique in beingness the merely Penicillium species pathogenic to humans. It undergoes dimorphic conversion in vivo to transversely dividing sausage-shaped cells.

Figure 75-iii

Diagrammatic representation of the saprophytic and invasive tissue forms of pathogenic fungi.

Primary Mycoses

Most cases of primary deep mycoses are asymptomatic or clinically mild infections occurring in normal patients living or traveling in endemic areas. However, patients exposed to a high inoculum of organisms or those with contradistinct host defenses may suffer life-threatening progression or reactivation of latent foci of infection.

The arthroconidia of C immitis are inhaled and convert in the lung to spherules. Well-nigh cases of coccidioidomycosis are clinically occult or balmy infections in patients who inhale infective arthroconidia. However, some patients take progressive pulmonary infection and also may suffer dissemination to the brain, os, and other sites. Coccidioides meningitis is a life-threatening infection requiring lifelong treatment.

Histoplasmosis is a master pulmonary infection resulting from inhalation of conidia of Histoplasma capsulatum which convert in vivo into the blastoconidial (budding yeast) form. Broadcasting to the hilar and mediastinal lymph nodes, spleen, liver, bone marrow, and brain may be life-threatening in infants and other immunocompromised patients. Histoplasmosis (like tuberculosis) is characterized by intracellular growth of the pathogen in macrophages and a granulomatous reaction in tissue. These granulomatous foci may reactivate and cause dissemination of fungi to other tissues. These patterns of primary infection and reactivation are similar to those of Mycobacterium tuberculosis (run into Affiliate 33). Histoplasmosis also may be associated with a chronic inflammatory process known as fibrosing mediastinitis, where scar tissue (formed in response to H capsulatum) encroaches on vital structures in the mediastinum.

Blastomycosis, similar to histoplasmosis, is a chief pulmonary infection resulting from inhalation of conidia from the mycelial stage of Blastomyces dermatitidis which convert in vivo to the parasitic yeast phase. Blastomycosis (due to B dermatitidis) in the blastoconidial phase also causes a chief pulmonary infection. The organism elicits a granulomatous reaction oft associated with a marked fibrotic reaction. The clinical blueprint of pulmonary blastomycosis is 1 of chronic pneumonia. Dissemination occurs most commonly to the skin, bone, and, in males, prostate.

Opportunistic Mycoses

Candidiasis

Candidiasis (due to C albicans and other Candida spp.) is the virtually common opportunistic fungal infection. Candida albicans is the most common crusade of candidiasis. Candidiasis may exist classified as superficial or deep. Superficial candidiasis may involve the epidermal and mucosal surfaces, including those of the oral crenel, pharynx, esophagus, intestines, urinary bladder, and vagina. The alimentary tract and intravascular catheters are the major portals of entry for deep (or visceral) candidiasis. The kidneys, liver, spleen, brain, optics, centre, and other tissues are the major organ sites involved in deep or visceral candidiasis. The principal risk factors predisposing to securely invasive candidiasis are protracted courses of wide spectrum antibiotics, cytotoxic chemotherapy, corticosteroids, and vascular catheters.

Aspergillosis

Invasive aspergillosis most ofttimes involves the lungs and paranasal sinuses. This fungus may disseminate from the lungs to involve the brain, kidneys, liver, middle, and bones. The primary portal of entry for aspergillosis is the respiratory tract, however, injuries to the skin may as well introduce the organism into susceptible hosts. Quantitative and functional defects in circulating neutrophils are key risk factors for development of invasive aspergillosis. For example, neutropenia due to cytotoxic chemotherapy and systemic corticosteroids are common predisposing factors for invasive aspergillosis.

Zygomycosis

Zygomycosis due to Rhizopus, Rhizomucor, Absidia, Mucor species, or other members of the class of Zygomycetes, too causes invasive sinopulmonary infections. An especially life-threatening course of zygomycosis (as well known as mucormycosis), is known as the rhinocerebral syndrome, which occurs in diabetics with ketoacidosis. In addition to diabetic ketoacidosis, neutropenia and corticosteroids are other major hazard factors for zygomycosis. Aspergillus spp and the Zygomycetes have a potent propensity for invading blood vessels.

Cryptococcosis

Cryptococcosis is virtually typically an opportunistic fungal infection that most oft causes pneumonia and/or meningitis. Defective cellular immunity, especially that associated with the caused immune deficiency syndrome, is the most mutual gamble factor for developing cryptococcosis.

Phaeohyphomycosis

Phaeohyphomycosis is an infection by chocolate-brown to black pigmented fungi of the cutaneous, superficial, and deep tissues, peculiarly brain. These infections are uncommon, life-threatening, and occur in various immunocompromised states.

Hyalohyphomycosis

Hyalohyphomycosis is an opportunistic fungal infection caused by any of a diversity of normally saprophytic fungi with hyaline hyphal elements. For example, Fusarium spp. infect neutropenic patients to cause pneumonia, fungemia, and disseminated infection with cutaneous lesions.

Basic Concepts of Ecology Epidemiology

The epidemiology of dimorphic primary pathogens may be contrasted with that of the opportunistic fungal pathogens. The primary pathogens accept a relatively well-defined geographic range of endemic infection in immunocompromised hosts. Past comparison, the opportunistic fungi (due east.chiliad. Aspergillus spp.) are ubiquitously distributed with the frequency of infection existence dependent upon a population of immunocompromised hosts. Penicillium marneffei, an opportunistic pathogen, appears to be geographically restricted to the Eastern asia, particularly Thailand and China.

Control and Handling

Hospital-acquired fungal infections may be reduced by maintaining the everyman possible concentration of fungal spores in the ambient air of the establishment. Ideally, a "spore-free" environment should be sought. Antifungal therapy, which is reviewed in depth elsewhere, is an area of intense investigation (Meet Chapter 76). New antifungal compounds volition hopefully meliorate the efficacy and reduce toxicity of treatment of invasive fungal infections.

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Source: https://www.ncbi.nlm.nih.gov/books/NBK7902/

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