Fungi as Human Pathogens

 Chapter -6 

Fungi as Human Pathogens

Primary Mycoses

• Primary systemic mycoses include histoplasmosis (Histoplasma capsulatum), North American blastomycosis (Blastomyces dermatitidis), coccidioidomycosis (Coccidioides immitis), and South American blastomycosis (Paracoccidioides Brasiliense). The natural habitat of these pathogens is the soil. Their spores are inhaled with dust, get into the lungs, and cause a primary pulmonary mycosis. Starting from foci in the lungs, the organisms can then be transported, hematogenous or lymphopenias, to other organs including the skin, where they cause granulomatous, purulent infection foci. Laboratory diagnostics aim at direct detection of the pathogens under the microscope and in cultures as well as identification of antibodies. The therapeutics used to treat these infections are amphotericin B and azoles. All of the primary systemic mycoses are endemic to certain geographic areas, in some cases quite limited in extent. Central Europe is not affected by these diseases. They are not communicable among humans.

Histoplasma capsulatum (Histoplasmosis)

Histoplasma capsulatum is the pathogen responsible for histoplasmosis, an intracellular mycosis of the reticuloendothelial system. The sexual stage or form of this fungus is called Emmonsiella capsulata.

• Morphology and culture. H. capsulatum is a dimorphic fungus. As an infectious pathogen in human tissues it always forms yeast cells (Fig. 6.1). The small individual cells are often localized inside macrophages and have a diameter of 2–3 m.

• Giemsa and gram staining do not “take” on the cell walls of H. capsulatum, for which reason the cells often appear to be surrounded by an empty areola, which was incorrectly taken to be a capsule, resulting in the designation H. capsulatum. This species can be grown on the nutrient mediums normally used for fungal cultures. H. capsulatum grows as a mycelium in two to three weeks on Sabour Aud agar at a temperature of 20–30 8C.

• Pathogenesis and clinical picture. The natural habitat of H. capsulatum is the soil. Spores (conidia) are inhaled into the respiratory tract, are taken up by alveolar macrophages, and become yeast cells that reproduce by budding. Small granulomatous inflammatory foci develop. The pathogens can disseminate hematogenously from these primary infection foci. The reticuloendothelial system (RES) is hit particularly hard. Lymphadenopathies develop and the spleen and liver are affected. Over 90% of infections remain clinically silent. The clinical picture depends heavily on any predisposing host factors and the infective dose. A histoplasmosis can also run its course as a respiratory infection only. Disseminated histoplasmoses are also observed in AIDS patients.

• Diagnosis. Suitable material for diagnostic analysis is provided by bronchial secretion, urine, or scrapings from infection foci. For microscopic examination, Giemsa or Wright staining is applied and yeast cells are looked for inside the macrophages and polymorphonuclear leukocytes. Cultures on blood or Sabour Aud agar must be incubated for several weeks. Antibodies are detected using the complement fixation test and agar gel precipitation. The diagnostic value of positive or negative findings in a histoplasmin scratch test is doubtful.

• Therapy. Treatment with amphotericin B is only indicated in severe infections, especially the disseminated form.

• Epidemiology and prevention. Histoplasmosis is endemic to the midwestern USA, Central and South America, Indonesia, and Africa. With few exceptions, Western Europe is free of the disease. The pathogen is not communicable among humans. No special prophylactic measures are taken.

Coccidioides immitis (Coccidioidomycosis)

• Morphology and culture. C. immitis is an atypical dimorphic fungus. In cultures, this fungus always grows in the mycelial form; in body tissues, however, it neither buds nor produces mycelia. What is found in vivo are spherical structures (spherules) with thick walls and a diameter of 15–60 lm, each filled with up to 100 spherical-to-oval endospores

• C. immitis is readily cultivated on the usual fungus nutrient mediums. After five days of incubation, a white, wooly (fuzzy) mycelial colony is observed. One of the morphological characteristics of the mycelium is the asexual arthrospores seen as separate entities among the hyphae.

• Pathogenesis and clinical picture. The infection results from inhalation of dust containing arthrospores. Primary coccidioidomycosis is always localized in the lungs, whereby the level of manifestation varies from silent infections (60% of infected persons) to severe pneumonia. Five percent of those infected develop a chronic cavernous lung condition. In fewer than 1%, hematogenous dissemination produces granulomatous lesions in skin, bones, joints, and meninges.

• Diagnosis. The available tools are pathogen detection in sputum, pus, cerebrospinal fluid or biopsies, and antibody identification. The spherules can be seen under the microscope in fresh material. The fungus can be readily cultured on Sabouraud agar at 25 8C. The resulting arthrospores are highly infectious and must be handled very carefully. Antibodies can be detected using the complement fixation test, gel precipitation or latex agglutination. A coccidioidin skin test measuring any cellular allergy to components of the fungus is used as an initial orientation test if an infection is suspected.

• Therapy. Amphotericin B can be used to treat the disseminated forms. An oral azole derivative will serve as an alternative, or for use, in clinically less severe forms.

• Epidemiology and prevention. Coccidioidomycosis is endemic to desert areas of California, Arizona, Texas, New Mexico, and Utah and is only rarely observed elsewhere. The source of infection is the fungus-rich soil. Animals can also be infected. This disease is not transmitted among humans or from animals to humans.

Blastomyces dermatitidis (North American Blastomycosis)

• Blastomyces dermatitidis is a dimorphic fungus that causes a chronic granulomatous infection. The pathogens occur naturally in the soil and are transmitted to humans by inhalation.

• The primary blastomycosis infection is pulmonary. Secondary hematogenous spread can lead to involvement of other organs including the skin. Laboratory diagnostic methods include microscopy and culturing to identify the fungus in sputum, skin lesion pus, or biopsy material. Antibody detection using the complement fixation test or agar gel precipitation is of limited diagnostic value. Amphotericin B is the therapeutic agent of choice. Untreated blastomycoses almost always have a lethal outcome.

• Blastomycosis occurs mainly in the Mississippi Valley as well as in the eastern and northern USA. Infections are also relatively frequent in animals, especially dogs. Susceptible persons cannot, however, be infected by infected animals or humans. There are no prophylactic measures.

Paracoccidioides brasiliensis (South American Blastomycosis)

• Paracoccidioides brasiliensis (syn. Blastomyces brasiliensis) is a dimorphic fungus that, in living tissues, produces thick-walled yeast cells of 10–30 lm in diameter, most of which have several buds. When cultivated (25 8C), the fungus grows in the mycelial form.

• The natural habitat of P. brasiliensis is probably the soil. Human infections are caused by inhalation of spore-laden dust. Primary purulent and/or granulomatous infection foci are found in the lung. Starting from these foci, the fungus can disseminate hematogenously or lymphopenias into the skin, mucosa, or lymphoid organs. A disseminated paracoccidioidomycosis progresses gradually and ends lethally unless treated. The therapeutic agents of choice are azole derivatives (e.g., itraconazole), amphotericin B, and sulfonamides. Therapy can prevent the disease from progressing, although no cases are known in which the disease is eliminated over the longer term. Laboratory diagnostics are based on detection of the pathogen under the microscope and in cultures as well as on antibody detection with the complement fixation test or gel precipitation.

Para coccidioidomycosis is observed mainly among farmers in rural parts of South America.

Opportunistic Mycoses (OM)

• Opportunistic mycoses (OM) that affect skin and mucosa as well as internal organs are caused by both yeast and molds. A precondition for development of such infections is a pronounced weakness in the host’s immune defenses. Candidiasis is an endogenous infection. Other OMs are exogenous infections caused by fungi that naturally inhabit the soil or plants. These environmental fungi usually invade via the respiratory tract. The most important are aspergillosis, cryptococcosis, and the Mucor mycoses. Besides Candida and other yeasts, phaeohyphomycotic and hyalohyphomycotic, which are only very mildly pathogenic, can also cause systemic infections. All OMs have a primary infection focus, usually in the upper or lower respiratory tract. From this focus, the pathogens can disseminate hematogenously and/or lymphopenias to infect additional organs. Infection foci should be removed surgically if feasible. Antimycotic agents are used in chemotherapy. In infected immunocompromised patients, the prognosis is usually poor.

Candida (Soor)

• At least 70% of all human Candida infections are caused by C. albicans, the rest by C. parapsilosis, C. tropicalis, C. Guillermo, C. Kruize, and a few other rare Candida species.

• Morphology and culture. Gram staining of primary preparations reveals C. albicans to be a Gram-positive, budding, oval yeast with a diameter of approximately 5 lm. Gram-positive pseudo hyphae are observed frequently and septate mycelia occasionally

• C. albicans can be grown on the usual culture mediums. After 48 hours of incubation on agar mediums, round, whitish, somewhat rough-surfaced colonies form. They are differentiated from other yeasts based on morphological and biochemical characteristics.

• Pathogenesis and clinical pictures. Candida is a normal inhabitant of human and animal mucosa (commensal). Candida infections must therefore be considered endogenous.Candodoses usually develop in persons whose immunity is compromised, most frequently in the presence of disturbed cellular immunity. The mucosa are affected most often, less frequently the outer skin and inner organs (deep candidiasis). In oral cavity infections, a white, stubbornly adherent coating is seen on the cheek mucosa and tongue. Pathomorphological Ly similar to oral soor is vulvovaginitis. Diabetes, pregnancy, progesterone therapy, and intensive antibiotic treatment that eliminate the normal bacterial flora are among the predisposing factors. Skin is mainly infected on the moist, warm parts of the body. Candida can spread to cause secondary infections of the lungs, kidneys, and other organs. Conidial endocarditis and endophthalmitis are observed in drug addicts. Chronic mucocutaneous candidiasis is observed as a sequel to damage of the cellular immune system

• Diagnosis. This involves microscopic examination of preparations of different materials, both native and Gram-stained. Candida grows on many standard nutrient mediums, particularly well on Sabouraud agar. Typical yeast colonies are identified under the microscope and based on specific metabolic evidence

• Detection of Candida-specific antigens in serum (e.g., free mannan) is possible using an agglutination reaction with latex particles to which monoclonal antibodies are bound. Various methods are used to identify antibodies in deep candidiasis (agglutination, gel precipitation, enzymatic immunoassays, immunoelectrophoretic).

• Therapy. Nystatin and azoles can be used in topical therapy. In cases of deep candidiasis, amphotericin B is still the agent of choice, often administered together with 5-fluorocytosine. Echinocandins (e.g., spongin) can be used in severe oropharyngeal and esophageal candidiasis.

• Epidemiology and prevention. Candida infections are, with the exception of candidiasis in newborn children, endogenous infections.

Aspergillus (Aspergillosis)

• Aspergilloses are most frequently caused by Aspergillus fumigatus and A. flavus. A. nicer, A. nodulin's, and A. Terius are found less often. Aspergilli are ubiquitous in nature. They are found in large numbers on rotting plants.

• Morphology and culture. Aspergillus is recognized in tissue preparations, exudates and sputum by the filamentous, septate hyphae, which are approximately 3–4 lm wide with Y-shaped branching

• Aspergillus grows rapidly, in mycelial form, on many of the mediums commonly used in clinical microbiology. Sabouraud agar is suitable for selective culturing.

• Pathogenesis and clinical pictures. The main portal of entry for this pathogen is the bronchial system, but the organism can also invade the body through injuries in the skin or mucosa. The following localizations are known for aspergilloses:

• Aspergillosis of the respiratory tract. An aspergilloma is a circumscribed “fungus ball” that usually grows in a certain space (e.g., a cavern). Another pulmonary aspergillosis is a chronic, necrotizing pneumonia. Acute, invasive pulmonary aspergillosis is seen in patients suffering from neutropenia or AIDS or following organ transplants and has a poor prognosis. Another aspergillosis of the respiratory tract is tracheobronchitis. Of all fungi, aspergilli are most frequently responsible for various forms of sinusitis. In persons with atopic allergies, asthma may be caused by an allergic aspergillus alveolitis.

• Other aspergilloses. Endophthalmitis can develop two to three weeks after surgery, or an eye injury and the usual outcome is loss of the eye. Cerebral aspergillosis develops after hematogenous dissemination. Less often, Aspergillus spp. cause endocarditis, myocarditis, and ostomies.

• Diagnosis. Since Aspergillus is a frequent contaminant of diagnostic materials, diagnosis based on direct pathogen detection is difficult. Finding the typically branched hyphae in the primary preparation and repeated culture growth of Aspergillus make the diagnosis probable. If the branched hyphae are found in tissue biopsies stained with methenamine silver stain, the diagnosis can be considered confirmed

• Therapy. High-dose amphotericin B, administered in time, is the agent of choice. Azoles can also be used. The echinocandin caspofungin has been approved in the treatment of refractory aspergillosis as salvage therapy. Surgical removal of local infection foci (e.g., aspergilloma) is appropriate.

Cryptococcus neoformans (Cryptococcosis)

• Morphology and culture. C. neoformans is an encapsulated yeast. The individual cell has a diameter of 3–5 lm and is surrounded by a polysaccharide capsule several micrometers wide. C. neoformans can be cultured on Sabouraud agar at 30–35 8C with an incubation period of three to four days.

• Pathogenesis and clinical picture. The normal habitat of this pathogen is soil rich in organic substances. The fungus is very frequently found in bird droppings. The portal of entry in humans is the respiratory tract. The organism is inhaled and enter the lungs, resulting in a pulmonary cryptococcosis that usually runs an inapparent clinical course. From the primary pulmonary foci, the pathogens spread hematogenously to other organs, above all into the central nervous system (CNS), for which compartment C. neoformans shows a pronounced affinity. A dangerous meningoencephalitis is the result. Good preconditions for dissemination from the lung foci are provided especially by primary diseases that weaken the immune defenses. Malignancies and steroid therapy are other frequent predisposing factors. AIDS patients also frequently develop cryptococcoses.

• Diagnosis. This is particularly important in meningitis. The pathogens can be detected in cerebrospinal fluid sediment using phase contrast microscopy. An ink preparation results in a negative image of the capsule. Culturing is most successful on Sabouraud agar. C. neoformans can be differentiated from other yeasts and identified based on special metabolic properties (e.g., breakdown of urea). A latex agglutination test is available for detection of capsule polysaccharide in cerebrospinal fluid and serum (anticapsular antibodies coupled to latex particles). Identification of antibodies to the capsular polysaccharide is achieved by means of an agglutination test or an enzymatic immunosorbence test.

• Therapy. Amphotericin B is the agent of choice in CNS cryptococcosis, often used in combination with 5-fluorocytosine.

• Epidemiology and prevention. No precise figures are available on the frequency of pulmonary cryptococcosis. The incidence of the attendant meningoencephalitis is one case per million inhabitants per year. There are no specific prophylactic measure.

Mucor, Absidia, Rhizopus (Mucor mycoses)

• Mucormycoses are caused mainly by various species in the genera Mucor, Absidia, and Rhizopus. More rarely, this type of opportunistic mycosis is caused by species in the genera Cunningham'll, Rhizomorph, and others. All of these fungal genera are in the order Mucorales and occur ubiquitously. They are found especially often on disintegrating organic plant materials.

• Morphology and culture. Mucorales are molds that produce broad, nonstate hyphae with thick walls that branch off nearly at right angles (Fig. 6.6). Mucorales are readily cultured. They grow on all standard mediums, forming high, whitish gray to brown, “fuzzy” aerial mycelium. Culturing is best done on Sabouraud agar.

• Pathogenesis and clinical pictures. Mucorales are typical opportunists that only cause infections in patients with immune deficiencies or metabolic disorders (diabetes). The pathogens penetrate into the target organic system with dust. They show a high affinity to vascular structures, in which they reproduce, potentially resulting in thrombosis and infarction. The infections are classified as follows according to their manifestations.

Rhino cerebral Mucor mycosis, spreads from the nose or sinuses and may affect the brain. Most often observed as a sequel to diabetic acidosis.

Phaeohyphomycetes, Hyalohyphomycotic, Opportunistic Yeasts, Penicillium Minefee

• The list of clinically relevant fungi previously not categorized as classic opportunists has lengthened appreciably in recent years. These organisms are now being found in pathogenic roles in patients with malignancies, in AIDS patients, in patients undergoing cytostatic and immunosuppressive therapies, massive corticosteroid therapy, or long-term treatment with broad spectrum antibiotics. The terms phaeohyphomycotic, hyalohyphomycotic, and opportunistic yeasts have been created with the aim of simplifying the nomenclature.

• Phaeohyphomycoses. These are subcutaneous and paranasal sinus infections caused by “Demarious” molds or “black fungi.” To date, numerous genera and species have been described as pathogenic agents. Common to all is the formation of hyphae, which appear as a brownish black color due to integration of melanin in the hyphal walls. Examples of the genera include Uvularia, Bipolarism, Xestobium, Wangele, Dactyl aria, Ramichloridium, Chaetomium, and Alternaria. The natural habitat of these fungi is the soil. They occur worldwide. Phaeohyphomycetes invade the body through injuries in the skin or inhalation of spores. Starting from primary foci (see above), the pathogens can disseminate hematogenously to affect other organs including the CNS. The clinical pictures of such infections most closely resemble the Mucor mycoses and aspergillosis. If feasible, surgical removal of infected tissues and administration of antimycotic agents is indicated. The prognosis is poor.

• Hyalohyphomycoses. This collective term is used for mycoses caused by hyaline (melanin-free) molds. Examples of some of the genera are Fusarium, Scapularies, Paecilomyces, Trichoderma, Acremonium, and Pseudopodium. These fungi are also found all over the world. Pathogenesis, clinical pictures, therapy, and prognosis are the same as for the phaeohyphomycoses

• Opportunistic yeast mycoses. Other yeasts besides the most frequent genus by far, Candida, are also capable of causing mycoses in immunosuppressed patients. They include Torulosis glabrata, Trichopterans bigoli, and species of the genera Rotorua, Malassezia, Saccharomyces, Hannula, and others. These “new” mycoses are not endogenous, but rather exogenous infections. Inimical and therapeutic terms, they are the same as candidiasis. Malassezia furfur occasionally causes catheter sepsis in premature neonates and persons who have to be fed lipids parenterally. Lipids encourage growth of this yeast.

• Penicilloic. This fungal infection is caused by the dimorphic fungus Penicillium marneffei, which probably inhabits the soil. P. marneffei infections are one of the most opportunistic infections most frequently seen in AIDS patients who either live in Southeast Asia or have stayed in that area for a while. The infection foci are located primarily in the lungs, from where dissemination to other organs can take place. The therapeutic of choice in the acute phase is amphotericin B, this treatment must be followed by long-term prophylactic azoles (itraconazole) to prevent remission.

Pneumocystis carinii (Pneumocystis)

• Pneumocystis carinii is a single-celled, eukaryotic microorganism that was originally classified as a protozoan, but is now considered a fungus. This pathogen can cause pneumonia in persons with defective cellular immune systems, in particular those showing AIDS. Extrapulmonary manifestations are also recorded in a small number of cases. Laboratory diagnostic methods include direct detection of the microbes under the microscope, by means of direct immunofluorescence or PCR. Appropriate anti-infective agents for therapy include cotrimoxazole, pentamidine, or a combination of the two.

• Pneumocystis carinii is a single-celled, eukaryotic microorganism that was, until recently, classified with the protozoans. Molecular DNA analysis has revealed that it resembles fungi more than it does protozoans, although some of the characteristic properties of fungi, such as membrane ergosterol, are missing in Pneumocystis carinii. This microbe occurs in the lungs of many mammalian species including humans without causing disease in the carriers. Clinically manifest infections emerge in the presence of severe underlying defects in cellular immunity, as in AIDS.

• Morphology and developmental cycle. Three developmental stages are known for P. carinii. The trophozoites are elliptical cells with a diameter of 1.5–5 lm. Presumably, the trophic form reproduces by means of binary transverse fission, i.e., asexually. Sexual reproduction does not begin until two haploid trophozoites fuse to make one diploid sporozoite (or precyst), which are considered to be an intermediate stage in sexual reproduction. After further nuclear divisions, the sporozoites possess eight nuclei at the end of their development. The nuclei then compartmentalize to form eight spores with a diameter of 1–2 lm each, resulting in the third stage of development, the cyst. The cysts then release the spores, which in turn develop into trophozoites.

• Culture. P. carinii cannot be grown in nutrient mediums. It can go through a maximum of 10 developmental cycles in cell cultures. Sufficient propagation is only possible in experimental animals, e.g., rats. This makes it difficult to study the pathogen’s biology and the pathogenic process and explains why all aspects of these infections have not yet been clarified.

• Pathogenesis and clinical pictures. Humans show considerable resistance to P. carinii infections, which explains why about two-thirds of the populace are either carriers or have a history of contact with the organism. Disease only becomes manifest in the presence of defects in the cellular immune system. Of primary concern among the clinical manifestations is the interstitial pneumonia. Profuse proliferation of the pathogen in the alveoli damages the alveolar epithelium. The pathogens then penetrate into the interstitium, where they cause the pneumonia. Starting from the primary infection foci, the fungi spread to other organs in 1–2% of cases, causing extrapulmonary P. carinii infections (of the middle ear, eye, CNS, liver, pancreas, etc.).

• Diagnosis. Suitable types of diagnostic material include pulmonary biopsies or bronchoalveolar lavage (BAL) specimens from the affected lung segments. Grocott silver staining can be used to reveal cysts and Giemsa staining shows up trophozoites and sporozoites. Direct immunofluorescence, with labeled monoclonal antibodies to a surface antigen of the cysts, facilitates detection (see Fig. 6.7c). Amplification of specific DNA sequences using the PCR has recently come to the fore as a useful molecular detection method.

• Therapy. Acute pneumocystis is treated with cotrimoxazole (oral or parenteral) or pentamidine (parenteral) or a combination of both of these anti-infective agents. Pentamidine can also be applied in aerosol form to reduce the side effects.

Subcutaneous Mycoses

• Fungi that cause classic subcutaneous mycoses grow in the soil and on dying plants. They penetrate through skin injuries into the subcutaneous connective tissue, where they cause local, chronic, granulomatous infections. These infections are seen mainly in the tropics and subtropics.

• Sporotrichosis is caused by Sporothrix schenckii, a dimorphic fungus that grows as yeast cells in host tissues. Sporotrichosis is characterized by an ulcerous primary lesion, usually on an extremity, and multiple nodules and abscesses along the lymphatic vessels.

• Chromomycosis (also chromoblastomycosis) can be caused by a number of species of black molds. The nomenclature of these pathogens is not firmly established. Weeks or months after the spores penetrate into a host, wartlike, ulcerating, granulomatous lesions develop, usually on the lower extremities.

• Madura foot or mycetoma can be caused by a wide variety of fungi as well as by filamentous bacteria (Nocardia sp., Actinomadura madurae, Streptomyces somaliensis). Potential fungal contributors include Madurella sp., Pseudoallescheria boydii, and Aspergillus sp. The clinical picture is characterized by subcutaneous abscesses, usually on the feet or hands. The abscesses can spread into the musculature and even into the bones. Fistulae are often formed.

Cutaneous Mycoses

• Classification. Dermatophytes are classified in three genera: Trichophyton (with the important species T. mentagrophytes, T. rubrum, T. Schoenlein Ii, T. tonsurans); Micros Porum (M. Arduini, M. Canis, M. gypsum); and Epidermophyton (E. Flocco sum). Some dermatophyte species are anthropophilic, others zoophilic. The natural habitat of the geophilic species M. gypsum is the soil.

• Morphology and culture. The dermatophytes are filamentous fungi. They grow readily on fungal nutrient mediums at 25–30 8C. After 5–14 days, cultures with a woolly appearance, in different colors, usually.

• Pathogenesis and clinical pictures. Dermatomycoses are infections that are transmitted directly by human contact, animal-human contact or indirectly on inanimate objects (clothes, carpets, moisture, and dust in showers, swimming pools, wardrobes, gyms). The localization of the primary foci corresponds to the contact site. Thus feet, uncovered skin (hair, head, facial skin) are affected most frequently. Different species can cause the same clinical picture. Frequent dermatomycoses include:

• Tinea corporis (ringworm): Microsporum canis and Trichophyton mentagrophytes. Affects hairless skin.

• Tinea pedis (athlete’s foot): T. rubrum, T. mentagrophytes, and Epidermophyton floccosum. Affects mainly the lower legs.

• Tinea capitis: T. tonsurans and M. canis. Affects scalp hair.

• Tinea barbae: T. rubrum and T. mentagrophytes. Beard ringworm.

• Tinea unguium: T. rubrum, T. mentagrophytes, and E. floccosum.

• Onychomycosis (nail mycosis): Various dermatophytes and Candida spp.

Diagnosis. Material suitable for diagnostic analysis include skin and nail scrapings and infected hair. The fungi are observed under the microscope in a KOH preparation. Identification is based on the morphology of the hyphae as well as on the macroconidia and microconidia in the fungal cultures.

Therapy. Dermatomycoses can be treated with locally applied antimycotic agents. In cases of massive infections of the hair, and above all of the nails, the oral allylamine terbinafine or azoles can be used. Griseofulvin is rarely used today.

Epidemiology and prevention. Dermatophytes occur naturally all over the world. The geophilic dermatophyte, M. gypsum, can cause infections in persons in constant, intensive contact with the soil (e.g., gardeners). Prophylactic measures for all dermatomycoses consist in avoiding direct contact with the pathogen. Regular disinfection of showers and wardrobes can contribute to prevention of athlete’s foot, a very frequent infection.

Other Cutaneous Mycoses

Pityriasis (or tinea) versicolor is a surface infection of the skin caused by Malassezia furfur. This infection is observed mainly in the tropics but is known all over the world. It causes hypopigmentations. M. furfur is dependent for its metabolic needs on a source of long-chain fatty acids. This fungus is actually a component of the skin’s normal flora. The pathogenesis of the infections has not yet been clarified.

Tinea nigra, which occurs mainly in the tropics, is caused by Exophiala werneckii. Infection results in brown to black, maculous efflorescences on the skin.

White and black piedras is an infection of the hair caused by Trichosporon beigelii or Piedraia hortae.