There are two forms of piedra—white and black—which are both superficial infections of the hair shaft. White piedra, which is common in temperate climates, is primarily caused by Trichosporon asahii, formerly known as Trichosporon beigelii. White piedra presents as asymptomatic, soft, white or cream colored nodules that are loosely adherent to hair shafts. While this is primarily a self-limited infection, T. asahii has been known to cause a systemic infection called trichosporonosis in immunosuppressed patients [9]. This is a multisystem disease that includes fevers, renal failure, pulmonary infiltrates, and skin lesions that range from papules to necrotic nodules.

The differential of piedra includes pediculosis (lice), hair casts, trichomycosis axillaris, eczema, and psoriasis.

Tinea versicolor is caused by lipophilic yeasts in the Malassezia genus, including M. furfur and M. globosa. These are present in small numbers on normal skin, and they cause skin disease only when they proliferate and form hyphae. This is usually stimulated by excessive heat and perspiration, but a number of other factors have been implicated [10]. Tinea versicolor occurs worldwide, with a higher incidence in hot, humid climates.

Clinically, tinea versicolor presents as numerous ovoid patches with fine scale that may coalesce. They can range in color from hypopigmented to red to hyperpigmented, depending on the host. Common areas of involvement are the back, chest, and shoulders (Fig. 17.10). Pruritus is usually absent or minimal. The differential diagnosis includes vitiligo, pityriasis alba, postinflammatory pigment alteration, seborrheic dermatitis, pityriasis rosea, guttate psoriasis, tinea corporis, and secondary syphilis.

M. furfur and M. globosa can also invade hair follicles, leading to pityrosporum folliculitis. Common in young men and women, this presents as monomorphic red papules and pustules on the upper trunk and shoulders. It can be pruritic. Pityrosporum folliculitis has also been known to arise in the immunosuppressed and those on chronic antibiotics. The differential commonly includes acne, bacterial folliculitis, and eosinophilic folliculitis.

Chromoblastomycosis is caused by a number of dematiaceous fungi that are naturally found in soil and decaying plant matter. Fonsecaea pedrosoi is the most common agent, but others in the genera Fonsecaea, Phialophora, Cladophialophora, and Rhinocladiella have been identified [11]. These are most often found in tropical and subtropical climates, but they are occasionally seen in the United States. The most common route of infection is local inoculation via trauma. The first lesion is often a small verrucous papule which can slowly grow and spread locally. Over time, large, fungating tumors may develop. These can be complicated by superinfection, regional lymphadenopathy, and loss of function of the affected limb, but they rarely spread distally or to internal organs.

The differential diagnosis for chromoblastomycosis includes other subcutaneous fungal infections such as sporotrichosis and mycetoma, blastomycosis, cutaneous tuberculosis or other atypical mycobacterium, leishmaniasis, tertiary syphilis, warts, and mycosis fungoides.

Sporotrichosis is caused by the dimorphic fungus Sporothrix schenckii. It is present in soil and on vegetation such as rose bushes and sphagnum moss. It has a broad geographic distribution which includes portions of the southeastern United States. The organism is introduced to humans almost exclusively through puncture injuries, which are usually occupation related. Sporotrichosis begins as a small red papule or nodule at the site of injury. Within weeks it will exhibit lymphangitic, or “sporotrichoid,” spread. This includes the development of erythematous nodules along the course of lymphatic drainage which may ulcerate (Fig. 17.11). Other forms of sporotrichosis exist, such as a fixed cutaneous form without lymphangitic spread, rosacea-like lesions, and disseminated disease [12]. However, these are the exception to the rule.

The differential diagnosis of sporotrichosis, especially with lymphangitic spread, includes the following: leishmaniasis, atypical mycobacteria, tuberculosis, nocardia, tularemia, lepromatous leprosy, and other deep and subcutaneous fungal infections.

Mycetoma, or Madura foot, is a phenotype that is caused by two different classes of organisms: true fungi and filamentous bacteria. Eumycetomas, those caused by true fungi, include members of the Madurella, Pseudallescheria, Acremonium, and several other genera [13]. Actinomycetomas are caused by Nocardia, Actinomadura, Actinomyces, and Streptomyces species of bacteria. Both kinds of mycetoma are acquired through direct penetration of the organism into the foot or leg from soil. They are also found in similar environments—arid climates near the equator.

Mycetomas, both eumycotic and actinomycotic, are characterized by their draining sinus tracts and profound local edema. The lesions begin as asymptomatic nodules at the site of inoculation, before undergoing a period of steady swelling and growth. They can involve underlying structures such as fascia, muscle, and even bone, while generally remaining painless. The material that drains from the sinuses is composed of characteristic, tightly packed clumps of organisms. While the appearance of mycetoma is fairly characteristic, other subcutaneous and deep infections can be in the differential.

In immunocompromised patients, such as recipients of renal transplants, candidal infections represent the most common systemic fungal infection. The most common pathogen is C. albicans, while C. tropicalis may be more common in patients with hematologic malignancy. The portal of entry is thought to be the gastrointestinal tract, and long-term IV catheterization is a strong risk factor. The mortality associated with disseminated candidiasis is between 30 and 40 %, so early recognition and initiation of treatment is paramount [14].

Disseminated candidiasis usually presents as fever that is unresponsive to antimicrobials, proximal muscle tenderness, and skin lesions that can range from red macules and papules with a pale center, to purpura, to vesicles and necrotic ulcers. Septic shock and failure of virtually any end organ can occur. Unfortunately blood cultures will not always be positive for yeast, so a high index of suspicion is required. Items in the differential diagnosis include bacterial sepsis or septic shock, as well as other opportunistic infections such as aspergillosis, fusariosis, cryptococcosis, and phaeohyphomycosis.

Aspergillosis is an opportunistic fungal infection caused by two Aspergillus species, flavus and fumigatus. Specific risk factors for aspergillosis include neutropenia, burn patients, and high-dose corticosteroids [15]. There are two main ways in which this infection occurs. In the first, the fungus gains entry to the skin and subcutaneous tissue through a burn site, long-standing IV catheter, or compromised wound under occlusion. In an immunocompromised host, it can then invade the local vasculature and become disseminated. The second pathway is via inhalation, which leads to pulmonary infection and dissemination from there.

Cutaneous lesions in aspergillosis usually include purpura, necrotic papules, and ulcers. Disseminated aspergillosis is rapidly fatal, with spread to the lungs, kidneys, heart, and central nervous system (CNS). Septic shock and hemoptysis are frequently present.

Zygomycosis is an opportunistic, angioinvasive infection caused by multiple organisms including Rhizopus and Mucor species. These fungi are ubiquitous in soil and vegetation but rarely cause disease in immunocompetent hosts. However, they are known to cause rapidly fatal infections in those with leukopenia and acidosis, particularly uncontrolled diabetes [16]. Other predisposing conditions include hematologic malignancy, pharmacologic immunosuppression, solid organ or bone marrow transplantation, burns, trauma, malnutrition, and IV drug use. Of particular interest are infections in patients with iron or aluminum overload, patients undergoing hemodialysis, and those receiving the chelating agent deferoxamine [17]. The classic and most common form of zygomycosis is rhinocerebral, which usually occurs in patients with diabetic ketoacidosis (DKA). Patients may complain of fever and unilateral facial pain, including pain with eye movements. Diffuse erythema and induration will progress to necrotic ulcers with characteristic black centers. A less common form of cutaneous zygomycosis follows trauma and direct inoculation into the skin. This can occur anywhere and usually presents as a sharply demarcated necrotic ulcer with a dark black center (Fig. 17.12). Occasionally these lesions can also occur in various locations on the skin secondary to disseminated disease. Disseminated zygomycosis is a rapidly progressive infection that usually begins in the lungs and spreads to the brain. Patients begin with fever and headaches and soon develop confusion, obtundation, and death. They may or may not have cutaneous findings. In 2008, Reyes et al. [17] reported such a case in a patient with secondary iron overload treated with deferoxamine.

The term phaeohyphomycosis encompasses a large group of dematiaceous fungi with this in common—the production of dark brown or black hyphae in tissue. Most of these organisms are found in soil and plant material, and they are introduced into human hosts via trauma. Phaeohyphomycosis can range from asymptomatic superficial infection, such as tinea nigra, to onychomycosis, to rapidly progressive and fatal systemic infection [18]. Infected puncture wounds can lead to cutaneous papules, subcutaneous cysts, or nodules (Fig. 17.13). In a normal host these lesions typically become walled off but do not spread further. In immunocompromised hosts, these fungi can gain access to the bloodstream and disseminate from there. Common targets of dissemination include the heart valves and central nervous system (CNS), and when present, skin lesions appear as necrotic, dry ulcers and eschars with red borders.

Hyalohyphomycosis includes nondematiaceous fungi that produce tan or white hyphae in tissue. The most important organisms in this group include species of three genera: Fusarium, Penicillium, and Paecilomyces. These organisms are ubiquitous in nature but rarely cause disease in competent hosts. One exception is that Fusarium spp. can cause onychomycosis, which is thought to be a possible source of disseminated disease [19]. Fusarium spp. are known to affect patients with profound neutropenia, hematologic malignancy, and severe burns. While Penicillium species are mostly found in southeast Asia, they have been seen in the United States, primarily in HIV patients [20].

Clinically, patients with disseminated fusariosis will have fevers, severe myalgias, and diffuse targetoid lesions that become necrotic and ulcerated (Figs. 17.14 and 17.15). Skin findings associated with penicilliosis include papules on the forehead and cheeks that resemble acne or molluscum. The differential diagnosis of fusariosis includes other angioinvasive infections like aspergillosis and candidiasis. For penicilliosis, the list is similar but also includes dimorphic fungi like cryptococcosis, blastomycosis, histoplasmosis, and coccidioidomycosis, which can all form molluscum-type lesions in immunocompromised hosts.