Sporotrichosis can be classified clinically into five forms, namely skin, mucous membrane, systemic, immunoreactive and spontaneous regression. Systemic sporotrichosis is further classified into pulmonary, cutaneous disseminated, osteoarticular, and neurological [6]. Systemic sporotrichosis in an immunocompetent individual is rare. It has been reported in literatures, however these cases involved cutaneous disseminated alone, or involved non-pulmonary sites such as osteoarticular, neurological and ocular [1-4]. To our knowledge, this is the first case reported of systemic sporotrichosis with cutaneous and pulmonary involvement in immunocompetent individual. Such systemic presentation more commonly occurs in the setting of immunosuppressive state such as uncontrolled diabetes mellitus, immunosuppressant use, HIV infection, malignancy and connective tissue disease [5].

Sporotrichosis is caused by thermodimorphic fungi of the genus Sporothrix. Sporothrix comprises of 51 taxons, in which only four taxons are known to be pathogenic in human, namely S. Brasiliensis, S. Schenckii, S. globose and S. luriei [6]. S. Schenckii, which is the organism identified in our patient, is the most common causative agent for sporotrichosis in Malaysia [4]. It is usually found in contaminated plants or in the mouth, nasal cavity, nails and feces of infected cats [4]. Cutaneous sporotrichosis is usually caused by direct inoculation of organism into the skin by trauma. Unfortunately, only 10-62% of patients were able to recall this information [7]. Systemic sporotrichosis is believed to be transmitted either via inhalation of Sporothrix propagules or via hematogenous spread and the latter mode of spread typically occurs in immunosuppressed patients [6]. We postulated that our patient may have contracted the infection through a missed trauma during gardening or via inhalation of the fungal propagules during contact with cats’ feces.

Cutaneous lesions typically present as papules or nodules which may ulcerate or fistulize draining a purulent discharge. 80% of cutaneous cases present as lymphocutaneous form, in which the lesions were distributed along the lymphatic drainage [6]. However, in disseminated cutaneous sporotrichosis, the lesions may be generalized with no specific distribution as seen in our patient. Pulmonary sporotrichosis typically presents with cough, hemoptysis, anorexia and fever [5-7]. Nevertheless, 14.1% may not have any respiratory symptoms (Aung K et al) as demonstrated in our case [5].

Cutaneous manifestation of sporotrichosis can mimic other infectious diseases namely tuberculosis and non-tuberculous mycobacterium, nocardiasis, chromomycosis and leishmaniasis. It may also imitate non-infectious diseases such as pyoderma gangrenosum, primary cutaneous tumors and even cutaneous metastases [6]. Skin biopsy is warranted to rule out these differential diagnoses. Typical histopathological findings are diffuse chronic granulomatous inflammation with a central abscess. The fungal structures, which are highlighted by PAS and GMS, is seen in 18 to 35.3% of cases [6]. Pulmonary involvement can display two different patterns on radiology, depending on the transmission route. Hematogenous route leads to predominantly diffuse or bibasal reticulonodular infiltrate pattern. On the contrary, inhalation route frequently results in upper lobe involvement. Chronic inflammatory response is then ensued, leading to breakdown of necrotic lung tissue and upper lobe cavity formation. These group of patients may be asymptomatic initially until large cavities are formed [5]. These findings further supported the hypothesis that our patient might have contracted the fungal agent through inhalation based on the upper lobe radiological findings and relatively free of pulmonary symptoms. Culture and isolation of S. schenckii from biopsy samples remains the gold standard to diagnose sporotrichosis [5-7]. Depending on the species of Sporothrix, it usually takes 4 to 6 days to isolate Sporothrix spp. for samples collected from skin lesions, and 10-19 days from extracutaneous lesions [6].

Treatment of sporotrichosis depends on the clinical presentation. In lymphocutaneous or osteoarticular manifestation, oral itraconazole 200mg per day is the preferred treatment [6,8]. However, for systemic sporotrichosis, recommended treatment is amphotericin B, given as a lipid formulation at 3-5 mg/kg daily or amphotericin B deoxycholate, administered at 0.7-1.0 mg/kg daily. Treatment is continued until a favorable response has been achieved, after which the therapy is changed to oral itraconazole 200mg BD for at least 1 year [8]. Other than the commonly reported side effects such as nephrotoxicity, amphotericin B can also cause hepatotoxicity. The incidence of increased transaminases and bilirubin due to amphotericin B had been reported at approximately 20% [9]. We hypothesize that our patient’s underlying hepatic disease might have predisposed him to develop raised transaminases upon exposure to amphotericin B.

The response of patients to treatment varies. Uncomplicated skin or mucosal manifestation in immunocompetent patients, usually heal with fibrous scar. However, untreated sporotrichosis can disseminate to other organ systems and may be fatal [6].