Sporotrichosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Alison Leibowitz [2]

Sporotrichosis (also known as “rose gardener’s disease”^[1]) is a disease caused by an infection of the fungus Sporothrix schenckii.^[2] This fungal disease usually affects the skin, although other less common forms can affect the lungs, joints, bones, and even the brain. Because roses can spread the disease, it is one of a few diseases referred to as rose-thorn or rose-gardeners’ disease.^[3]

Because S. schenckii is naturally found in soil, hay, sphagnum moss, and plants, it usually impacts farmers, gardeners, and agricultural workers.^[2] Typically, infection manifests following the interruption of the epidermal integrity, as this allows the fungus to enter the host. In cases where sporotrichosis impacts the lungs, known as pulmonary sporotrichosis, the fungal spores enter through the respiratory pathways upon inhalation. Zoonotic transmission of sporotrichosis occurs most frequently from handling infected cats, making this an occupational hazard for veterinarians.^[4]

Sporotrichosis progresses slowly – the first symptoms may appear 1 to 12 weeks (average 3 weeks) following initial exposure to S. schenckii, and the patient may not recall the injury that led to infection. Serious complications can also arise in patients with compromised immune systems. As systemic forms of sporotrichosis, also known as extracutaneous sporotrichosis, are opportunistic infections, immunocompromised patients are much more susceptible to these more severe subtypes.

The first definitive case of sporotrichosis was described by Benjamin Schenck, an American medical student, in 1896.

Sporotrichosis may be classified, according to the location of the lesions, into particular subtypes: fixed cutaneous, lymphocutaneous, disseminated cutaneous, and extracutaneous/systemic. These subtypes may be further separated into increasingly specific forms based upon clinical manifestations.

S. schenckii is usually transmitted via posttraumatic inoculation to the human host, however, infrequently sporotrichosis may also develop as a result of spore inhalation. The pathophysiology of sporotrichosis depends on the histological subtype and the frequently nonspecific histopathology may mimic other granulomatous diseases.^[5] S. schenckii is capable of modulating the immune response to promote its own survival by blocking cytokine production by macrophages.^[6]

Sporothrix schenckii is a fungus that can be found throughout the world. Areas characterized by warm, humid climates, are ideal for the fungus to thrive. The species is present in soil as well as in and on living and decomposing plant material such as peat moss. It can infect humans as well as animals and is the causative agent of sporotrichosis, commonly known as “rose handler’s disease”.

As sporotrichosis manifests in a variety of clinical forms, differentiation must be established in accordance with the particular subtype. Forms of cutaneous sporotrichosis must be differentiated from other diseases that cause lesions, such as cutaneous leishmaniasis and mycobacteriosis, while the various forms of extracutaneous sporotrichosis must be differentiated from other diseases with similar clinical manifestations. For example, pulmonary sporotrichosis must be differentiated from other diseases that attack the lungs, such as coccidioidomycosis and histoplasmosis, whereas osteoarticular sporotrichosis must be distinguished from diseases that affect the bones and joints, such as chronic bacterial osteomyelitis.

Sporothrix schenckii can be found throughout the world in soil and plant matter. Peru is suspected to be an area where S. schenckii is extremely common in the environment. Outbreaks of sporotrichosis have been documented in both developing and developed countries.

The most potent risk factor in the development of sporotrichosis is handling thorny plants, sphagnum moss, bales of hay, or any plant or plant product that can cause skin trauma. These risk factors either lead to direct inoculation or merely enable the entry of the fungus. Other risk factors include a weakened immune system, a history of alcoholism, and the handling of infected animals. ^[7]

The incubation period of sporotrichosis varies from a few days to multiple months. ^[8] Complicatiaons of sporotrichosis include bacterial superinfection and sepsis. Depending on the progression of the sporotrichosis at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as good. The presence of disseminated sporotrichosis is associated with a particularly poor prognosis among immunodeficient patients and these patients are prone to relapse.

Symptoms of cutaneous sporotrichosis include nodular lesions on the skin, at the point of inoculation, as well as along lymph nodes and vessels. The lesion is initially small and painless, and ranges in color from pink to purple. Left untreated, the lesion becomes larger, ulcerates, and oozes. Typically, cutaneous sporotrichosis lesions manifest in the upper extremities. Extracutaneous forms of sporotrichosis typically manifest with a broad range of unspecific clinical symptoms, frequently resulting in delayed diagnosis.

Common physical examination findings of cutaneous sporotrichosis include painless pink to purple nodular lesions or erythematous plaque on the skin, which may begin to grow, ulcerate, and drain. These lesions characteristically manifest on upper extremities. Non-cutaneous forms of sporotrichosis are not generally associated with distinctive physical findings.

Laboratory findings consistent with the diagnosis of sporotrichosis include isolation of S. schenckii upon culture, molecular detection, a positive sporotrichin skin test, and techniques involving antibody detection. Definitive diagnosis of sporotrichosis occurs upon the isolation and identification of S. schenckii in culture.

Findings suggestive of sporotrichosis on chest x-ray include the presence of cavitations, tracheobronchial lymph node enlargement, and presence of nodular lesions.

Because spontaneous resolution in cases of sporotrichosis is a rarity, the majority of patients require treatment. The recommended treatment regimens are largely empirical and predominantly based upon retrospective evaluations, case study reports, and nonrandomized control trials. The predominant therapy for sporotrichosis is itraconazole, which is used as the primary treatment in immunocompetent patients, and as a suppressive therapy in immunocompromised patients. The primary line of treatment for immunocompromised patients is amphotericin B.

Surgery is not the first­ line treatment option for patients with cutaneous sporotrichosis. Surgical therapy is usually reserved for patients with either osteoarticular sporotrichosis or pulmonary sporotrichosis.

There are no available vaccines against sporotrichosis. Primary prevention strategies include wearing protective clothing while engaging in high risk activities, such as handling thorny plants, sphagnum moss, bales of hay, or any plant or plant product that may potentially cause skin trauma, limiting handling of sphagnum moss, and avoiding physical contact with infected animals, namely felines.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Alison Leibowitz [2]

The first definitive case of sporotrichosis was described by Benjamin Schenck, an American medical student, in 1896.

• The first definitive case of sporotrichosis was described by Benjamin Schenck, an American medical student, in Baltimore, Maryland in 1896. Schenck isolated Sporothrix schenckii from lesions manifesting on the right arm and index finger of a 36-year-old male patient. Schenck sent the fungus sample to Dr. Erwin Smith, a mycologist at the United States Department of Agriculture, for further study. Smith erroneously determined that the fungus sample belonged to the genus Sporotrichum.^[1]
• Linck, in 1809, and Lutz, in 1889, discussed potential cases of sporotrichosis. Though their descriptions were similar to Schneck’s, definite diagnosis was not possible, as neither author was able to isolate the fungal organism.^[2]
• In 1900 in Chicago, Illinois, Ludvig Hektoen, M.D. and C. F. Perkins, M.D. described the second definitive case of sporotrichosis, after isolating the fungus from a lesion on a young male patient’s finger. Hektoen and Perkins established the current denomination, Sporothrix schenckii, for the sporotrichosis agent.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Alison Leibowitz [2]

Sporotrichosis may be classified, according to the location of the lesions, into particular subtypes: fixed cutaneous, lymphocutaneous, disseminated cutaneous, and extracutaneous/systemic. These subtypes may be further separated into increasingly specific forms based upon clinical manifestations.

• Presentations vary based upon numerous factors, such as the patient’s immunological status, the severity and depth of the inoculum, and the particular strain’s thermal zone of tolerance and pathogenicity.

Cutaneous forms of Sporotrichosis typically manifest following minor epidermal trauma. Patients may present with multiple forms of cutaneous lesions.

Fixed form:

• Staying localized within the subcutaneous tissue, the fungus transforms into its yeast form.
• Manifests at the site of inoculation with at least one, frequently ulcerated, lesion
• The lesions are characterized by red edges due to capillary dilation and congestion.
• Fixed form sporotrichosis may spontaneously regress ^[1]
• Fixed form sporotrichosis is the main clinical presentation in child patients.
• Initially manifests as painless nodules, which then become palpable, purulent, and ulcerated

Lymphocutaneous form:

• The yeast form of S. schenckii extends through the nearby lymphatic vessels.^[2]
• Approximately 70% of the cases of sporotrichosis may be classified as lymphocutaneous sporotrichosis.^[3]
• The primary lesion frequently manifests on the upper extremities and is initially painless.
• Initially a patient will present with a papule or pustule, which later expands into a subcutaneous nodule.^[3]
• Subepidermal pressure results in ischemia, and the lesion evolves into a palpable, purulent, and ulcerated nodule.
• Secondary lesions manifest along the adjacent lymphatic pathway.^[4]
• The presence of systemic symptoms is rare.

Disseminated cutaneous form:

• Manifests upon the hematogenous dissemination of the yeast form of S. schenckii
• Not associated with extracutaneous involvement
• Characterized by greater than or equal to three epidermal lesions, which form on at least two noncontiguous sites on the body

Mucosal Form:

• Typically manifests with enlargement of the submandibular and preauricular (anterior to ear tragus) lymph nodes
• Nasal mucosa is a variant of mucosal form sporotrichosis, which frequently involves septum lesions characterized by bloody discharge and crustal detachment.^[4]

The extracutaneous forms of sporotrichosis are more likely to manifest following the onset of AIDS. These forms are uncommon and difficult to diagnose, but are almost always associated with immunological impairment^[4]

• Most common extracutaneous form of sporotrichosis
• Cutaneous lesions rarely manifest in cases of osteoarticular sporotrichosis.
• Usually starts as monoarticular disease without systemic illness
• May manifest by contiguity or hematogenous spread^[4]
• Characterized by the involvement of bones and joints
• Usually affects joints in the knee, wrist, elbow, and ankle
• May manifest with tenosynovitis or bursitis^[5]
• Frequently associated with arthritis
  • In these cases of coexisting diagnoses, lesions typically manifest along bones adjacent to affected joints. ^[6]

• Patients present with primary pulmonary sporotrichosis following the inhalation of S. schenckii.
• Typically associated with alcoholism, chronic obstructive pulmonary disease, chronic corticosteroid use, and immunosuppressive diseases^[4]
• High risk of delayed diagnosis as a result of the rarity of pulmonary involvement in sporotrichosis manifestation and nonspecific symptoms

• Characterized by the involvement of at least two sites in the body
• Manifests as a result of hematogenic dissemination of S. schenckii, resulting in multifocal or widespread infection
• May initially manifest as another form of extracutaneous sporotrichosis
• Strongly associated with immunodeficiency

Other rare forms of sporotrichosis:

• endophthalmitis
• chorioretinitis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Alison Leibowitz [2]

S. schenckii is usually transmitted via posttraumatic inoculation to the human host, however, infrequently sporotrichosis may also develop as a result of spore inhalation. The pathophysiology of sporotrichosis depends on the histological subtype and the frequently nonspecific histopathology may mimic other granulomatous diseases.^[1] S. schenckii is capable of modulating the immune response to promote its own survival by blocking cytokine production by macrophages.^[2]

• S. schenckii is usually transmitted to the human host via posttraumatic inoculation. However, sporotrichosis may also develop as a result of spore inhalation, although this mode of transmission is infrequent.
• Modes of transmission either lead to direct inoculation or enable the entry of the fungus.

• Actions, such as handling thorny plants, sphagnum moss, bales of hay, or any plant or plant product that can cause skin trauma, may enable S. schenckii entry.

• The pathophysiology of sporotrichosis depends on the histological subtype and the frequently nonspecific histopathology may mimic other granulomatous diseases.^[1]
• S. schenckii is capable of modulating the immune response to promote its own survival by blocking cytokine production by macrophages.^[2]

• S. schecknii accesses the subcutaneous tissue following minor epidermal trauma.
• S. schecknii, a thermo-dependent fungus, converts into its yeast form upon entering the tissue.

• Fixed form
  • The yeast form of S. schenckii remains localized in subcutaneous tissue
• Lymphocutaneous form
  • The yeast form of S. schenckii extends through the nearby lymphatic vessels
• Disseminated cutaneous form
  • Manifests upon the hematogenous dissemination of the yeast form of S. schenckii

• Osteoarticular form
  • May manifest upon contiguity or hematogenous spread
• Pulmonary form
  • Manifests following inhalation of S. schenckii spores
• Disseminated form
  • Manifests upon the hematogenous dissemination of the yeast form of S. schenckii^[3]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief: Alison Leibowitz [3]

Sporothrix schenckii is a fungus that can be found throughout the world. Areas characterized by warm, humid climates, are ideal for the fungus to thrive. The species is present in soil as well as in and on living and decomposing plant material such as peat moss. It can infect humans as well as animals and is the causative agent of sporotrichosis, commonly known as “rose handler’s disease”.^[1] Posttraumatic inoculation of S. schenckii is the typical method of infection. However, sporotrichosis may also develop as a result of spore inhalation, although this mode of transmission is infrequent. Infection commonly occurs in otherwise healthy individuals but is rarely life-threatening and can be treated with antifungals. In the environment, Sporothrix schenckii exists as a filamentous hyphae. In host tissue, S. schenckii thrives as a yeast. The transition from its hyphal form to yeast form is temperature dependent, making S. schenckii a thermally dimorphic fungus.^[2]

Sporothrix schenckii can be found in one of two morphologies, mold or yeast, making it a dimorphic fungus. The saprophytic form is found in the environment on plants and decaying matter. When the fungus infects a host, the yeast form predominates as a result of its temperature dependent morphology.^[3]

• At 25 °C (77 °F), in the environment or grown in the laboratory (in malt extract agar or potato dextrose agar), S. schenckii assumes its saprophytic stage.^[4]
• Macroscopically, colonies are characterized by apparent filaments, a smooth to leathery texture, and a finely wrinkled surface. Initially appearing off-white to creamy, the color may later become dark brown to black (“dirty candle-wax” color).^[2] Some strains are capable of growing darkly colored colonies from initial formation.
• Microscopically, composed of hyaline, hyphae are septate and approximately 1 to 2μm in diameter. Arising from undifferentiated hyphae, conidiogenous cells form clusters of conidia on denticles. Conidia, which do not generate chains, are tear to clavate shaped and glass-like in appearance. They may be colorless or darkly colored. Conidia are sometimes referred to as resembling a flower.^[5]
  • Frequently, dark thick-walled conidia form adjacent to hyphae, and serve as a tool to distinguish S. schenckii from alternative, nonpathogenic species of Sporothrix.

• At 37 °C (98.6 °F) either in a laboratory or in host tissue, S. schenckii assumes its yeast form.
• Macroscopically, the yeast form grows as smooth, white to tan colonies.
• Microscopically, yeast cells are 2 to 6μm in diameter and have a round to oval shape. Typically, the cells appear to have elongated cigar-shaped buds stemming from a narrow origin.^{[2] [3]}

Virulence factors of S. schenckii are the microbial characteristics that catalyze or augment microbial growth in host tissue.

• S. schenckii synthesizes melanin both in vitro and in vivo,^[4] meaning that both morphologies, yeast and mold, have the capacity to produce melanin.
• Melanin production is a virulence factor found in many pathogenic fungi^[6] and its production in S. schenckii protects the fungus from oxidative stress as well as ultraviolet light and macrophage killing.
• Melanin has been shown to be synthesized using the 1,8-DHN pentaketide pathway.^[4]
• Melanization in S. schenckii is dependent on environmental factors such as, pH, temperature, and nutrient availability. Conidial menanization helps to enable the first stage of host infection, as it increases microbial resistance to macrophage phagocytosis.^[7]

• Primary adhesion to extracellular matrix components and to epithelial and endothelial cells are necessary steps to effective pathogenesis.
• Both the yeast and conidia cells of S. schenckii display an increased ability to recognize and subsequently bind^[2] to extracellular matrix glycoproteins, fibronectin, type II collagen, and laminin, using separate receptors that are specific for these proteins^[8].

• The fibronectin adhesions, which are found on the surface of yeast cells, are directly connected to virulence.^[9]

• S. schenckii is capable of crossing intercellular space, enabling hematogenous dissemination.^[10]

• S. schenckii breaks down proteins by producing two separate proteases, a serine protease and an aspartic protease.^[11]
• These proteases appear to be essential for fungal growth, however, they have some functional overlap. The inactivation of either protein does not affect growth, but inactivation of both inhibits the fungus.^[12]
• Protease activity has been shown to be important in in vivo infection of mice.^[11] Substrates for these proteases include the skin proteins type-I collagen, stratum corneum, and elastin.^[11]

• Growing at host body temperature (37 °C (98.6 °F)) is an important requirement for pathogenesis.
• Strains of S. schenckii that are capable of growth at 35 °C (95 °F), but not 37 °C (98.6 °F), are only capable of causing the fixed cutaneous form of Sporotrichosis, as this form manifests with epidermal lesions (the skin is cooler than the body’s interior).
• Strains that are able to thrive at 37 °C (98.6 °F) are responsible for lymphatic, disseminated, and extracutaneous/systematic forms of Sporotrichosis.^{[3] [11]}

Infection by S. schenckii is generally self-limiting in immunocompetent hosts. The immune response prevents fungal dissemination and is the reason that most Sporothrix infections are cutaneous.^[13]

The yeast form of S. schenckii is effectively phagocytosed by cells of the innate immune system^[13] and are recognized based on the sugars displayed on their surface^[14] or lipids in the yeast cell membrane.^[13] Although they are taken up, they are not efficiently killed. It is hypothesized that ergosterol peroxide reacts with and detoxifies reactive oxygen species generated by the respiratory burst used by phagocytes to kill cells they have ingested.^[13] S. schenckii is also capable of modulating the immune response to promote its own survival by blocking cytokine production by macrophages.^[13]

The specific immune response becomes active at later stages of infection and involves both B cells and T cells. Severe sporotrichosis is rare in endemic areas where humans are in near constant contact with S. schenckii spores. This fact, combined with the increased severity of disease in immunocompromised patients, suggests an important role for specific immunity in S. schenckii infection.^[13] Patients with sporotrichosis have been shown to produce antibodies specific to S. schenckii^[15] and these antibodies may actually be protective against the disease.^[2]

• Fungus Page: Sporothrix schenckii, cause of Rose-picker’s Disease
• EMedicine: Sporotrichosis
• Adelaide University: Sporothrix schenckii
• American Society for Microbiology: Sporothrix schenckii and Sporotrichosis
• Microbe wiki: Sporothrix schenckii

Template:Mycoses

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Alison Leibowitz [2]

As sporotrichosis manifests in a variety of clinical forms, differentiation must be established in accordance with the particular subtype. Forms of cutaneous sporotrichosis must be differentiated from other diseases that cause lesions, such as cutaneous leishmaniasis and mycobacteriosis, while the various forms of extracutaneous sporotrichosis must be differentiated from other diseases with similar clinical manifestations. For example, pulmonary sporotrichosis must be differentiated from other diseases that attack the lungs, such as coccidioidomycosis and histoplasmosis, whereas osteoarticular sporotrichosis must be distinguished from diseases that affect the bones and joints, such as chronic bacterial osteomyelitis.

Sporotrichosis manifests through a broad range of clinical symptoms shared with multiple different diseases, causing misdiagnosis to be common.^[1] Sporotrichosis must be differentiated from:

• Atypical mycobacteriosis
• Bacterial and fungal pneumonia
• Blastomycosis
• Candidiasis
• Chromoblastomycosis
• Chronic bacterial osteomyelitis
• Coccidioidomycosis    
• Cutaneous leishmaniasis^[2]
• Cutaneous tuberculosis
• Erythema nodosum
• Foreign body granulomas
• Histoplasmosis
• Leishmaniasis
• Leprosy
• Mycobacterium avium-intracellulare complex infection^[3]    
• Mycobacterium marinum
• Nocardiosis
• Paracoccidioidomycosis
• Pinta
• Rheumatoid arthritis
• Sarcoidosis
• Staphylococcal infections
• Syphilis
• Tuberculosis
• Tularemia
• Yaws^[1]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Alison Leibowitz [2]

Sporothrix schenckii can be found throughout the world in soil and plant matter. Peru is suspected to be an area where S. schenckii is extremely common in the environment. Outbreaks of sporotrichosis have been documented in both developing and developed countries.

• The global incidence of sporotrichosis is unknown, with significant variation in occurrence rates between countries.
• The incidence of sporotrichosis is approximately 0.1-0.2 per 100,000 individuals within the United States, with roughly 200-250 cases reported every year. ^[1]

• While patients of all age groups may develop sporotrichosis, the association between age and and occurrence largely depends on region.
• Within developed countries, the incidence of sporotrichosis is highest among adults.
• Conversely, within tropical areas and nations in which the disease is more prevalent, sporotrichosis may be more prevalent in adolescents and children. ^[2]
• The fixed cutaneous form of sporotrichosis is more common in children than in adults.^[3]

• As a result of increased exposure risk, particularly in developing countries, males are more commonly affected by sporotrichosis than females. The exact ratio between the sexes is unknown.

• Sporotrichosis commonly occurs in areas characterized by warm (15-25°C), humid (90%) climates, as this environment is ideal for saprophytic fungus to thrive. However, epidemics are not limited to these areas.^[4]

Incidences of sporotrichosis have been recorded in:

• China
• Japan
• Vietnam
• Central and South America (Mexico, Brazil, Colombia, and Peru)
• Peru: There is a particularly high occurrence rate of sporotrichosis in Peru. The incidence of sporotrichosis within the Peruvian highlands is 100 per 100,000 individuals.
• South Africa^[5]
• Uruguay
• India^[6]
• United States: The largest recorded epidemic of sporotrichosis in the United States occurred in 1988 and involved a total of 84 cases in15 states. All cases were associated with Wisconsin-grown sphagnum moss. ^[7]
• Western Australia: A cluster of sporotrichosis cases occurred in the Busselton-Margaret River region of Western Australia from 2000 to 2003. ^[8]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Alison Leibowitz [2]

The most potent risk factor in the development of sporotrichosis is handling thorny plants, sphagnum moss, bales of hay, or any plant or plant product that can cause skin trauma. These risk factors either lead to direct inoculation or merely enable the entry of the fungus. Other risk factors include a weakened immune system, a history of alcoholism, and the handling of infected animals. ^[1]

• A risk factor in the development of sporotrichosis is handling thorny plants, sphagnum moss, bales of hay, or any plant or plant product that can lead to minor skin trauma.
• Studies have established low socioeconomic status as a risk factor for sporotrichosis. ^[2]
• Agriculture-based activities or occupations, such as farming, logging, mining, hunting, wood exploitation, gardening, and landscaping, are risk factors for the development of sporotrichosis. ^[1]
• Predisposing conditions responsible for immunosuppression like diabetes mellitus, chronic alcoholism, myeloproliferative disorders, immunosuppressive therapy for organ transplant, autoimmune disorders, or cancers, prolonged treatment with systemic corticosteroids, and HIV infection have been implicated for extracutaneous sporotrichosis, an opportunistic form of infection. ^[3][4]

• Zoonotic transmission has been reported from insect bites, handling of fish, and bites from felines, birds, canines, rats, reptiles, and horses. Most commonly, incidents of zoonotic transmission result from transmission by infected cats^[5]
• Person-to-person transmission is rare. ^[6]
• In Uruguay and Brazil, cases of sporotrichosis have been associated with armadillo hunting. ^[7]
• Pulmonary sporotrichosis may result from fungal inhalation, although this form of sporotrichosis is rare.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Alison Leibowitz [2]

The incubation period of sporotrichosis varies from a few days to multiple months. ^[1] Complicatiaons of sporotrichosis include bacterial superinfection and sepsis. Depending on the progression of the sporotrichosis at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as good. The presence of disseminated sporotrichosis is associated with a particularly poor prognosis among immunodeficient patients and these patients are prone to relapse.

• The incubation period of sporotrichosis varies from a few days to multiple months. ^[1]

• Cutaneous lesions can become superinfected with bacteria, resulting in cellulitis.
• Potassium iodide has potential side effects of gastric intolerance, edema, excessive tear production, salivary gland swelling, skin rash, and erythema nodosum.
• 5-fluorocytosine therapy may result in photosensitivity^[2]
• The hematogenous spread of S. schenckii may lead to chronic meningitis, endophthalmitis, or brain abscesses.
• Treatment with amphotericin B may result in nephrocalcinosis as a complication.^[3]

• S. schenckii is an apparent opportunistic pathogen, as severe clinical forms of this disease have been linked with immunodeficient patients.
• Resistance to S. schenckii is not linked to the host’s inherent ability to fight the fungal infection, but rather results from the level of immunity that the host acquires during the initial stage, which is characterized by a large pathogen presence within the organs.^[4]
• Resultantly, depending on the host’s immune system capacity (T-cell immunity is important in limiting the disease) at the time of diagnosis, the prognosis may vary.
• In immunocompetent patients, the prognosis for cutaneous and lymphocutaneous sporotrichosis is excellent. The majority of these patients are cured with one bout of therapy and relapses only occur in a low percentage of patients.
• As a result of its frequently delayed diagnoses and association with underlying immunosuppressive diseases, forms of extracutaneous sporotrichosis generally do not respond well to therapy.
• Pulmonary sporotrichosis does not respond well to antifungal therapy and is patients are prone to relapse.^[1]
• The prognosis for disseminated sporotrichosis in immunocompromised patients is particularly poor.