Sporotrichosis

Etiology

Sporothrix schenckii was first isolated in 1896 by Benjamin Schenx, a medical student at Johns Hopkins Hospital. Sporotrichosis was first thought to be caused by a single organism, but is now known to contain several species, including S. brasilienis, S. globosa, and S. Mexicana. Therefore, sporotrichosis has been renamed S. schenckii complex or S. schenckii senu lato.[3] Sporotrichosis has been reported in most mammals, including cats, dogs, swine, horses, rats, and armadillos.

Epidemiology

Sporotrichosis is found worldwide, with the majority of cases reported in the tropical and subtropical regions of the Americas. In North America, sporotrichosis occurs most often in southern coastal regions and river valleys. Rose gardeners, farmers, miners, horticulturists, and armadillo hunters have an increased risk of infection.[4] Therefore, patients with suggestive syndromes should be asked about occupational and recreational activities. Sporothrix schenckii can be isolated from soil, plants, or plant products.

Infection may also occur during animal and zoonotic transmission, which is associated with scratches or bites from infected cats. Over the last 2 decades, Brazil has experienced an outbreak of cat-transmitted sporotrichosis in Rio de Janeiro, with 4,669 cases being reported.[5] Sporotrichosis can affect anyone regardless of age or gender, depending on occupational exposure. In Uruguay, sporotrichosis is found more commonly in males and armadillo hunters; whereas, in India, this infection is more prevalent in females due to their greater involvement in agricultural work.[6]

Pathophysiology

Sporothrix schenckii is a dimorphic fungus existing in hyphal form at temperatures less than 98.6 °F (37 °C) and as a yeast at temperatures greater than 98.6 °F (37 °C). S. schenckii is found on soil, marine animals, moss, wood, and decaying vegetation. A virulence factor is a feature of the organism that enhances microbial growth. Some virulence factors of S. schenckii include thermotolerance, ergosterol peroxide, and melanin.[7] The ergosterol peroxide found in the fungus is formed to evade reactive oxygen species during phagocytosis.[8]

Histopathology

Sporothrix schenckii is evident as budding yeasts, which may be round to oval in both human and animal tissues. The transition from mold to yeast form can be observed by culturing mycelia at 98.6 °F (37 °C). This transition in sporotrichosis cases is regulated by calcium, which induces RNA and protein synthesis in the yeast cell. Microscopically, the yeast form is cigar-shaped and exhibits narrow-based budding.[7] In some cases, yeasts are surrounded by Splendore-Hoeppli material or asteroid bodies; however, this is not pathognomonic for sporotrichosis, as asteroid bodies can be seen with other organisms.

History and Physical

Sporotrichosis has an incubation period of several days to 3 months after exposure. Infections can be divided into several syndromes: cutaneous, pulmonary, and disseminated.

Cutaneous Sporotrichosis

Cutaneous syndrome arises from the fungus into the skin, which is most common in rose gardeners. The initial lesions are erythematous papulonodular lesions that may be smooth or verrucous and involve lymphatic channels.[7] Lesions are typically painless, even after ulceration. With cutaneous sporotrichosis, the patient will not have systemic symptoms, and laboratory exams will be normal.

Pulmonary Sporotrichosis

Pulmonary sporotrichosis symptoms include a cough, low-grade fever, or weight loss. Risk factors for pulmonary sporotrichosis include middle-aged men who have chronic pulmonary issues, abuse alcohol or have a history of steroid use, diabetes mellitus, sarcoidosis, and an immunocompromised state.[7] Chest radiograph reveals unilateral or bilateral cavitary lesions, and if left untreated, the cavities gradually enlarge, causing pulmonary dysfunction. Differential diagnoses for this form of sporotrichosis include histoplasmosis, coccidiomycosis, and mycobacteria. 

Disseminated Sporotrichosis

Disseminated infections typically occur in immunocompromised patients. Widespread visceral dissemination occurs with lung abscess, liver and spleen involvement, and fungemia with spread to the esophagus, colon, bone marrow, and lymph nodes.[9]

Ocular Sporotrichosis

Sporotrichosis may also involve the eye in the form of ocular sporotrichosis. Ocular sporotrichosis usually presents as chronic granulomatous lesions of the eyelid, manifesting as erythematous, indurated nodules or ulcers that may mimic chalazion, hordeolum, or neoplastic conditions.[10] Conjunctival involvement can appear as granulomatous conjunctivitis with nodular masses, hyperemia, or chemosis, often misdiagnosed as allergic or bacterial conjunctivitis. The lacrimal system may be less frequently involved, presenting as dacryocystitis with persistent swelling and purulent discharge. In rare cases, especially in immunocompromised patients, intraocular involvement, eg, uveitis or choroiditis, may occur, potentially leading to visual impairment.[11] Cases have been reported of ocular sporotrichosis transmitted by dogs.[12]

Evaluation

Sporotrichosis is definitively diagnosed by culture that demonstrates the dimorphism of the fungus. Cutaneous sporotrichosis can be diagnosed through direct examination of the specimen, eg, tissue biopsy or pus from lesions, while sputum culture aids in diagnosing pulmonary sporotrichosis. Disseminated sporotrichosis can be diagnosed from urine, blood, and synovial fluid analysis.

Observation of yeast cells with potassium hydroxide may show the characteristic cigar-shaped buds or asteroid bodies. Other methods, eg, polymerase chain reaction (PCR) detection, enzyme-linked immunosorbent assay (ELISA) testing, antibody detection, and the sporotrichin skin test, have been employed with no strong standardization in testing.

Treatment / Management

Before the introduction of azole compounds in the 1990s, potassium iodide was the treatment of choice.[13] However, due to the adverse effects of potassium iodide, itraconazole is currently the treatment of choice.[7] The dosage varies from 100 to 200 mg/day orally for cutaneous forms, while 400 mg/day should be used for pulmonary forms.(B3)

For children weighing up to 20 kg, itraconazole 5 to 10 mg/kg/day is recommended. Itraconazole cannot be used in pregnant patients; amphotericin B may be used after 12 weeks of pregnancy. However, amphotericin B is reserved for disseminated and pulmonary forms, particularly in those patients with an immunocompromised state. Prevention and control measures include wearing gloves, long sleeves, and heavy boots to prevent puncture wounds.[14]

Differential Diagnosis

Differential diagnoses resembling cutaneous sporotrichosis include nocardiosis due to Nocardia. Nocardia is a gram-positive, rod-shaped bacterium that can cause cutaneous, pulmonary, and disseminated forms of nocardiosis. Other differentials to look for include cutaneous leishmaniasis, Francisella tularensis, Fusarium, and mycobacterial infections, including Mycobacterium marinum, Mycobacterium kansai, and Mycobacterium tuberculosis. Lesions resembling plaque sporotrichosis include blastomycosis, paracocidomycosis, chromoblastomycosis, lobomycosis, psoriasis, and pyoderma gangrenosum.

Prognosis

The prognosis of sporotrichosis is generally favorable in immunocompetent individuals, particularly when recognized early and treated appropriately with itraconazole, which remains the first-line antifungal agent. Lymphocutaneous and fixed cutaneous forms typically respond well to prolonged oral therapy, with complete clinical resolution in the majority of cases. However, therapeutic response may be delayed, often requiring treatment durations of 3 to 6 months or longer, depending on lesion chronicity and depth.

In contrast, disseminated, osteoarticular, and extracutaneous forms carry a more guarded prognosis, particularly in patients with underlying immunosuppression such as advanced HIV infection, malignancy, or chronic alcoholism. These forms may necessitate prolonged or combination antifungal therapy, including amphotericin B, and are associated with higher relapse rates. Prognosis also varies by geographic region and infecting Sporothrix species, with emerging zoonotic transmission, especially from S. brasiliensis, being linked to more aggressive and treatment-refractory disease. Prompt diagnosis, appropriate systemic therapy, and host immune status remain key prognostic determinants.

Complications

While the lymphocutaneous form remains the most common and typically indolent manifestation, sporotrichosis can lead to significant complications, particularly in immunocompromised hosts. In such individuals, hematogenous dissemination may result in extracutaneous involvement, including osteoarticular sporotrichosis, manifesting as monoarthritis or tenosynovitis, and, more rarely, pulmonary or meningeal forms. Chronicity and delayed diagnosis can result in extensive local tissue destruction, sinus tract formation, secondary bacterial infection, and scarring.

Fixed cutaneous lesions may ulcerate or mimic neoplastic or other granulomatous diseases, leading to misdiagnosis and inappropriate interventions. Zoonotic transmission, particularly from felines in hyperendemic regions, is associated with more aggressive and atypical presentations, including multifocal skin lesions and regional lymphadenitis. Additionally, therapeutic failure or relapse is more likely in cases with delayed initiation of antifungal therapy, poor compliance, or underlying immunosuppression, eg, HIV/AIDS [15], alcoholism, or diabetes mellitus.[16]