SPOROTRICHOSIS - pediagenosis
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Wednesday, February 17, 2021

SPOROTRICHOSIS

SPOROTRICHOSIS

Sporothrix schenckii is an environmental fungus that is capable of causing human disease after direct inoculation into the skin. Inoculation is the cause of cutaneous sporotrichosis, which is considered to be a subcutaneous mycosis. Unusual cases of inhalation sporotrichosis have been described in the literature, as have cases of central nervous system disease. These cases occur almost exclusively in immunosuppressed hosts. Sporotrichosis has classically been associated with inoculation after the prick from a rose plant. This is well reported; the fungus can be isolated from rose plants but is also found on many other plants and in soil environments. Clinical Findings: Gardeners, florists, and outdoor enthusiasts are at highest risk for infection from S. schenckii. These activities and occupations increase the likelihood of contact with the soil fungus. The fungus lives in the environment, and humans become infected by direct implantation of the fungus into the skin. Common methods of inoculation are the prick of a thorn or an injury contaminated with soil or plant mate- rial. Within a few days after entry into the skin, a papule and then a pustule form at the site of inoculation. Patients may initially be given an antibiotic in the belief that they have a bacterial infection. Often, it is not until the pustule ulcerates and develops into a larger plaque that the diagnosis is suspected or considered. Once this has occurred, the fungus enters the local lymphatics and proceeds to migrate proximally. As the fungus travels through the lymphatic system, it periodically causes draining sinus tracts to the surface, which appear as papules or nodules. This characteristic lymphangitic spread, also called sporotrichoid spread, is seen in most cases of cutaneous sporotrichosis.

Although a few other infections can manifest with lymphangitic spread, its presence along with a history of trauma suggests an infection with sporotrichosis. If lymphangitic spread is present, a skin biopsy and fungal, bacterial, and atypical mycobacterium cultures should be performed. Less commonly, solitary plaques of sporotrichosis occur without any evidence of sporotrichoid spread. The disease manifests as solitary, nonhealing, slowly enlarging plaques with various amounts of ulceration and drainage.

SPOROTRICHOSIS
Plate 6-24


Pathogenesis: S. schenckii is a dimorphic soil fungus found throughout the environment. S. schenckii causes human infection by direct implantation of the mold form of the fungus into the skin. Once the fungus has entered the human body, it transforms into its yeast form in response to the stable temperature. Most infections stay localized in the skin. In rare cases of severe immunosuppression, S. schenckii becomes disseminated; this occurs most frequently in association with human immunodeficiency virus infection.

Histology: Findings from skin biopsy specimens of sporotrichosis are not diagnostic in many cases. The presence of a granulomatous infiltrate is often the main histological feature. The periodic acid–Schiff (PAS) stain and Gomori’s methenamine silver (GMS) stain are two excellent stains that highlight the fungus and allow the pathologist to more readily appreciate the few cigar- shaped fungal elements that are present within the dense inflammation. Multiple fungal organisms are rarely seen; they are observed most frequently in patients with an underlying immunodeficiency.

S. schenckii is best cultured on Sabouraud’s media at room temperature. In these conditions, a white to brown colony of mold forms readily. As time elapses, the fungus forms a brown pigment that turns the entire colony brown to black. Because of its dimorphic nature, S. schenckii can be grown at 37°C, although it grows much more slowly at that temperature.

Treatment: Saturated solution of potassium iodide (SSKI) has been used for decades to treat cutaneous infections with S. schenckii. This medication has an unknown mechanism of action in treating fungal infections, but it is believed to interrupt protein synthesis of the fungus and to boost local host immune function. The treatment of choice is one of the azole antifungal medications. Itraconazole has been the most widely studied and used antifungal and is the preferred agent. All the azole antifungal agents inhibit the fungal cytochrome P450 enzyme 14-α-sterol-demethylase (CYP51A1). This inhibition prevents the fungus from producing ergosterol, a vital cell membrane component. Patients with pulmonary or central nervous system involvement or disseminated disease should be treated with amphotericin B.


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