• View in gallery

    Distribution of all Sporothrix schenckii human Australian isolates reported in Australia. Blue circles represent outbreaks attributed to moldy hay.14,19 Case numbers are attributed to State or Territory if no specific geographic location was recorded.

  • View in gallery

    (A) Lesion overlying index finger knuckle. (B) Lesion ascending the forearm. (C) Cord like appearance of lymphatic channel in upper arm.

  • View in gallery

    Case 2. Hand lesion with sporotrichoid spread ascending the forearm.

  • View in gallery

    Case 3. Shin lesion shown after regression on treatment.

  • View in gallery

    (A) Sabaroud's agar at 25°C, colonies are slow growing, with a wrinkled and folded surface, forming shapes suggestive of inverted cones or volcanoes. (B) Conidiophores and conidia of S. schenckii. Conidia are ovoid, one-celled, and smooth-walled. Conidiophores (black arrow) arise at right angles from the thin septate hyphae and are usually solitary. Conidia are formed in clusters on small denticles by proliferation of the conidiophore, their arrangement often suggestive of a flower.

  • 1.

    Rivitti EA, Aoki V, 1999. Deep fungal infections in tropical countries. Clin dermatol 17: 171190; discussion 105–106.

  • 2.

    Tobin EH, Jih WW, 2001. Sporotrichoid lymphocutaneous infections: etiology, diagnosis and therapy. Am Fam Physician 63: 326332.

  • 3.

    Barros MB, de Almeida Paes R, Schubach AO, 2011. Sporothrix schenckii and sporotrichosis. Clin Microbiol Rev 24: 633654.

  • 4.

    Sivagnanam S, Bannan AM, Chen SC, Ralph AP, 2012. Sporotrichosis (Sporothrix schenckii infection) in the New South Wales mid-north coast, 2000–2010. Med J Aust 196: 588590.

    • Search Google Scholar
    • Export Citation
  • 5.

    Robinson CF, Orban TD, 1951. A case of regional lymphatic sporotrichosis. Aust J Dermatol 1: 142144.

  • 6.

    Barrack BB, Powell RE, 1952. Sporotrichosis. Med J Aust 2: 624626.

  • 7.

    Minty CC, Mead M, McCaffrey MF, 1956. Sporotrichosis: a case report from Queensland. Med J Aust 43: 704705.

  • 8.

    Mead M, Ridley MF, 1957. Sporotrichosis and chromoblastomycosis in Queensland. Med J Aust 44: 192197.

  • 9.

    Durie EB, Frey D, Becke RF, 1961. Sporotrichosis: report of a case from Sydney, Australia. Aust J Dermatol 6: 7172.

  • 10.

    O'Donnell JM, 1962. A case of sporotrichosis. Med J Aust 49: 517518.

  • 11.

    Muir DB, Pritchard RC, 1984. Sporothrix schenckii–incidence in the Sydney region. Australas J Dermatol 25: 2728.

  • 12.

    Robertson D, 1967. Report of two cases of sporotrichosis of the face. Australas J Dermatol 9: 7682.

  • 13.

    Black RB, McAleer R, 1975. A case of sporotrichosis in Western Australia. Australas J Dermatol 16: 3238.

  • 14.

    Auld JC, Beardmore GL, 1979. Sporotrichosis in Queensland: a review of 37 cases at the Royal Brisbane Hospital. Australas J Dermatol 20: 1422.

    • Search Google Scholar
    • Export Citation
  • 15.

    Beardmore GL, 1979. Recalcitrant sporotrichosis: a report of a patient treated with various therapies including oral miconazole and 5-fluorocytosine. Australas J Dermatol 20: 1013.

    • Search Google Scholar
    • Export Citation
  • 16.

    Bullpitt P, Weedon D, 1978. Sporotrichosis: a review of 39 cases. Pathology 10: 249256.

  • 17.

    Conias S, Wilson P, 1998. Epidemic cutaneous sporotrichosis: report of 16 cases in Queensland due to moldy hay. Australas J Dermatol 39: 3437.

    • Search Google Scholar
    • Export Citation
  • 18.

    Moaven LD, Altman SA, Newnham AR, 1999. Sporotrichosis mimicking necrotising arachnidism. Med J Aust 171: 685686.

  • 19.

    Feeney KT, Arthur IH, Whittle AJ, Altman SA, Speers DJ, 2007. Outbreak of sporotrichosis, Western Australia. Emerg Infect Dis 13: 12281231.

  • 20.

    Dooley DP, Bostic PS, Beckius ML, 1997. Spook house sporotrichosis. A point-source outbreak of sporotrichosis associated with hay bale props in a Halloween haunted-house. Arch Intern Med 157: 18851887.

    • Search Google Scholar
    • Export Citation
  • 21.

    Pappas PG, Tellez I, Deep AE, Nolasco D, Holgado W, Bustamante B, 2000. Sporotrichosis in Peru: description of an area of hyperendemicity. Clin Infect Dis 30: 6570.

    • Search Google Scholar
    • Export Citation
  • 22.

    Currie BJ, Carapetis JR, 2000. Skin infections and infestations in Aboriginal communities in northern Australia. Australas J Dermatol 41: 139143, quiz 44–45.

    • Search Google Scholar
    • Export Citation
  • 23.

    Fisher D, Burrow J, Lo D, Currie BJ, 1993. Cryptococcus neoformans in tropical northern Australia: predominantly variant gattii with good outcomes. Aust N Z J Med 23: 678682.

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    Clinical and Laboratory Standards Institute, 2008. CLSI Reference Method for Broth Dilution Antifungal Susceptibility Testing of Filamentous Fungi: Approved Standard. Second edition. 2005. Available at: http://shopping.netsuite.com/c.1253739/site/Sample_pdf/M38A2_sample.pdf.

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    Ellis DH, Davis S, Alexiou H, Handke R, Bartley R, 2007. Descriptions of Medical Fungi. Second edition. ISBN: 9780959851267. Available at: http://www.mycology.adelaide.edu.au/downloads/Mycology-BookWEB.pdf.

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    Tambini R, Farina C, Fiocchi R, Dupont B, Guého E, Delvecchio G, Mamprin F, Gavazzeni G, 1996. Possible pathogenic role for Sporothrix cyanescens isolated from a lung lesion in a heart transplant patient. J Med Vet Mycol 34: 195198.

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    Sigler L, Harris JL, Dixon DM, Flis AL, Salkin IF, Kemna M, Duncan RA, 1990. Microbiology and potential virulence of Sporothrix cyanescens, a fungus rarely isolated from blood and skin. J Clin Microbiol 28: 10091015.

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    Jackson L, Klotz SA, Normand RE, 1990. A pseudoepidemic of Sporothrix cyanescens pneumonia occurring during renovation of a bronchoscopy suite. J Med Vet Mycol 28: 455459.

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    Pegg GS, Dwyer CO, Carnegie AJ, Burgess TI, Wingfield MJ, Drenth A, 2008. Quambalaria species associated with plantation and native eucalypts in Australia. Plant Pathol 57: 702714.

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    Sutton DA, Fothergill AW, Rinaldi MG, 1998. Guide to the Clinically Significant Fungi. First edition. Baltimore, MD: Williams and Wilkins.

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    de Beer ZW, Harrington TC, Vismer HF, Wingfield BD, Wingfield MJ, 2003. Phylogeny of the Ophiostoma stenoceras-Sporothrix schenckii complex. Mycologia 95: 434441.

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    Paap T, Burgess TI, McComb JA, Shearer BL, St J Hardy GE, 2008. Quambalaria species, including Q. coyrecup sp. nov., implicated in canker and shoot blight diseases causing decline of Corymbia species in the southwest of Western Australia. Mycol Res 112: 5769.

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    Chen SC, Currie BJ, Campbell HM, Fisher DA, Pfeiffer TJ, Ellis DH, Sorrell TC, 1997. Cryptococcus neoformans var. gattii infection in northern Australia: existence of an environmental source other than known host eucalypts. Trans R Soc Trop Med Hyg 91: 547550.

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    Tang MM, Tang JJ, Gill P, Chang CC, Baba R, 2012. Cutaneous sporotrichosis: a six-year review of 19 cases in a tertiary referral center in Malaysia. Int J Dermatol 51: 702708.

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Sporotrichosis from the Northern Territory of Australia

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  • National Mycology Reference Center, SA Pathology, Adelaide, South Australia; Royal Darwin Hospital, Microbiology, Darwin, Northern Territory, Australia; Royal Darwin Hospital, Department of Medicine, Royal Darwin Hospital, Northern Territory, Australia; Global Tropical Health Division, Menzies School of Health Research, Darwin, Northern Territory, Australia

We report three cases of lymphocutaneous infection caused by the thermally dimorphic fungus, Sporothrix schenckii from Australia's tropical Northern Territory. Two cases were acquired locally, making them the first to be reported from this region. All three cases presented with ulceration in the limb; however, the classical sporotrichoid spread was present only in the first two cases. Their occurrence within several weeks of each other was suggestive of a common source of environmental contamination such as hay used as garden mulch. Diagnoses were delayed in each case, with each patient having substantial exposure to ineffective antibiotics before the correct diagnosis was made. These cases bring the total number of reported sporotrichosis cases in Australia since 1951 to 199. Lessons from these cases are to consider the diagnosis of sporotrichosis in lesions of typical appearance, even in geographical settings from where this pathogen has not previously been reported.

Introduction

Sporotrichosis is a cutaneous infection caused by Sporothrix schenckii, a widely distributed dimorphic ascomycete fungus found in decaying vegetation, soil, and contaminated organic matter.1 The classical clinical appearance of lesions spreading along lymphatic channels gives rise to the term “sporotrichoid” spread, which can also be caused by Nocardia species, Mycobacterium marium and Leishmania brasilienses.2 Infection usually occurs by traumatic inoculation of soil, plant, or organic materials contaminated with the fungus. The lesions are usually restricted to skin and subcutaneous tissues, although depending on inoculum load and host immune responses, systemic dissemination can occur.3

Sporothrix schenckii is recognized to have a near-global distribution, except for latitudes further from the equator than 50° north or south.1 In Australia, cases tend to cluster in temperate or sub-tropical settings.4 Numbers are sparse, with 196 cases having been reported since 1951, mostly from the states of Queensland and New South Wales (Table 1 and Figure 1). Australian cases occur either as outbreaks, attributed to a contaminated source such as moldy hay,19,20 or may be endemic to certain areas,4 although at far lower rates than hyperendemic foci such as that in Peru.21 Zoonotic transmission of this fungus can occur from scratches or bites of animals such as armadillos, squirrels, dogs, and cats,18,21 and a spider bite has also been implicated as a potential inoculating culprit.18 There has been a suggestion of clustering of cases during higher rainfall periods.4 The Northern Territory of Australia is a tropical setting at 12°S with an annual monsoon season and no previous reported cases of sporotrichosis.

Table 1

Human cases of Sporothrix schenckii reported in Australia

ReferenceYearLocationNumber of cases
Robinson51951New South Wales1
Barrack and Powell61952New South Wales1
Minty and others71956Queensland1
Mead and Ridley81957Queensland2
Durie and others91961New South Wales1
O'Donnell101962Western Australia1
Muir and Pritchard111963–1981 (published 1984)New South Wales12
Robertson121967Queensland2
Black and McAleer131975Western Australia1
Auld and Beardmore141965–1977 (published 1979)Queensland37
Beardmore151979Queensland1
Bullpitt and Weedon161978Queensland39
Conias and Wilson171998Queensland16
Moaven181999Western Australia1
Feeny and others192003–2004 (published 2007)Busselton-Margaret River Region, Western Australia49
Sivagnanam and others42000–2010 (published 2012)New South Wales mid-north coast31
Subedi and others (current report)2013Northern Territory2
  Queensland1
Total  199
Figure 1.
Figure 1.

Distribution of all Sporothrix schenckii human Australian isolates reported in Australia. Blue circles represent outbreaks attributed to moldy hay.14,19 Case numbers are attributed to State or Territory if no specific geographic location was recorded.

Citation: The American Society of Tropical Medicine and Hygiene 91, 6; 10.4269/ajtmh.14-0456

Important differential diagnoses exist locally that can also cause chronic ulceration with or without sporotrichoid spread. These include nocardiosis, cutaneous melioidosis (Burkholderia pseudomallei), chromoblastomycosis, and group A streptococcal pyoderma.22 Another plant-associated fungal pathogen of particular importance in the Northern Territory, also implicated in occasional skin lesions, is Cryptococcus gattii.23

Here, we report three cases of sporotrichoid lymphocutaneous infection diagnosed in Australia's Northern Territory. Additionally, Quambalaria cyanescens was isolated from one biopsy sample, although that was not likely to be contributing to the clinical presentation.

Case Reports

Case 1.

A 47-year-old caucasian male used as a Groundsman was referred to the Infectious Diseases Outpatient Clinic at the Royal Darwin Hospital with an 8-week history of ulceration of the dorsum of the knuckle of his right index finger (Figure 2A). There was sporotrichoid spread ascending the forearm (Figure 2B) and a tight cord-like appearance of the upper arm lymphatic channel (Figure 2C). He described multiple potential inoculating events before the onset of the lesion, which had been in May (the end of the monsoon season). These included lifting wet hay bales using twine encompassing the bales, using his hand to remove leaves from a blocked gutter, and fixing an irrigation pipe that involved submerging his hands in muddy water. He had been treated with several courses of cephalexin and amoxicillin-clavulanic acid by his general practitioner without improvement in the lesions.

Figure 2.
Figure 2.

(A) Lesion overlying index finger knuckle. (B) Lesion ascending the forearm. (C) Cord like appearance of lymphatic channel in upper arm.

Citation: The American Society of Tropical Medicine and Hygiene 91, 6; 10.4269/ajtmh.14-0456

His past medical history included squamous cell carcinoma (SCC) of the tongue diagnosed in 2007, treated with chemoradiotherapy with no evidence of recurrence seen on a positron emission tomography scan in 2009. He did not take any regular medications and has no known drug allergies. He had a history of moderate alcohol intake of six standard drinks daily.

Punch biospies were obtained for microbiological and histopathological processing. Despite the provisional diagnosis of “sporotrichosis” being written on the pathology request form, the pathologist concluded that the sample showed inflammatory SCC. Features included intense, acute dermal inflammation and necrosis. Implantation of squamous epithelial cell elements caused by penetrating trauma was listed as a differential diagnosis and a more extensive repeat biopsy was suggested, which was arranged while fungal cultures remained in progress. Bacterial cultures including for B. pseudomallei were negative, and B. pseudomallei serology was also negative. A further biopsy was arranged, given the unexpected report of inflammatory SCC, which was disturbing given the patient's history of SCC. The ulcerated lesion overlying the knuckle and the one forearm lesion were then biopsied. The follow-up histopthology again reported SCC, which was withdrawn on review, in light of the emerging fungal culture results. The first fungal culture report to be received was that of Quambalaria cyanescens in the forearm lesion, identified by DNA sequencing (internal transcribed spacer region) at the National Mycology Reference Center (NMRC). Subsequently, fungal cultures both from the original biopsy and the later finger and forearm biopsies all yielded S. schenckii. The patient was commenced on itraconazole 200 mg daily. The lesions regressed substantially, and treatment was continued for a total of 3 months at which stage the lesions were healed.

Case 2.

A 54-year-old Caucasian male presented to the Royal Darwin Hospital with a 6-week history of ulcerated lesion on the dorsum of his left hand with sporotrichoid spread ascending the left forearm. He was treated in the community with several courses of amoxicillin-clavulanic acid with no improvement. There was no history of specific inoculating injury, although he was a keen gardener. Hay is often used as a garden mulch locally but it is unclear whether he was directly exposed to hay as was Case 1. He has no significant past medical history and did not take regular medications. There was no history of overseas or interstate travel. On examination, there was a 5 × 4 cm ulcerated lesion on the dorsum of his left hand with nodular lymphangitis (Figure 3).

Figure 3.
Figure 3.

Case 2. Hand lesion with sporotrichoid spread ascending the forearm.

Citation: The American Society of Tropical Medicine and Hygiene 91, 6; 10.4269/ajtmh.14-0456

Several punch biopsies were taken from the ulcerated area and submitted for histopathology, microscopy, and culture including for fungi and mycobacteria. He was commenced on empirical treatment of Nocardia with trimethoprim-suphamethoxazole two double strength tablets twice daily while awaiting further results.

He was reviewed in the Infectious Diseases Outpatient clinic 3 weeks later when he was noted to have new lesions in the anterior forearm. Histopathology from the punch biopsy showed skin with intense acute and chronic inflammation. Focally, at the margin of the biopsy there were several multinucleated giant cells present. Culture from the tissue eventually yielded a yeast-like organism which was identified as S. schenckii at the NMRC ∼3 weeks after the biopsy had been performed. The patient was commenced on itraconazole 100 mg daily, increased to 200 mg daily with an acidic soft drink after a trough itraconazole level of 423 μg/L was noted. His lesions regressed within weeks of commencing the itraconazole and were deemed to have been cured when treatment was ceased after 3 months of therapy.

Case 3.

A 47-year-old Caucasian male was seen at the Infectious Diseases Outpatient Clinic at the Royal Darwin Hospital on the same date as Case 1, with a 9-week history of a progressive ulcer with associated nodules of his right shin. The lesion developed after he went bushwalking in the Airlie Beach region in Queensland (latitude 20°S). He had been systemically well with no fevers. He has no significant past medical history. Cultures from a swab of the lesion had yielded Pseudomonas aeruginosa, hence he had been treated with ciprofloxacin 750 mg twice daily for 2 weeks with some improvement.

On examination, there was a lesion of the right shin with central ulceration. Several satellite lesions were near the area of ulceration but there was no sporotrichoid spread (Figure 4, shown after partial response to treatment). Punch biopsy was performed. While awaiting biopsy results, ciprofloxacin was continued but after 3 weeks, S. schenckii was reported from the biopsy sample. Hence, ciprofloxacin was ceased and fluconazole 400 mg daily commenced, changed to itraconazole 200 mg daily when the antifungal susceptibilities became available. The MIC of fluconazole was 32 μg/mL and itraconazole 0.5 μg/mL as determined by the Clinical and Laboratory Standards Institute (CLSI) M38-A2 standard,24 fairly typical of S. schenckii.25 His lesion was slow to resolve, and itraconazole was continued for 6 months. On review 2 months after completion of therapy, scarring was evident but there was apparent cure of active infection.

Figure 4.
Figure 4.

Case 3. Shin lesion shown after regression on treatment.

Citation: The American Society of Tropical Medicine and Hygiene 91, 6; 10.4269/ajtmh.14-0456

Discussion

The cases of sporotrichosis we report are notable for their occurrence in a new location (Australia's tropical Northern Territory, Cases 1 and 2), the somewhat atypical appearance without classical sporotrichoid spread and slow treatment response in Case 3, the concurrent isolation of Q. cyanescens with S. schenckii from one patient's lesion, and the unexpected histopathology report of SCC. These cases bring the total number of reported sporotrichosis cases in Australia to 199 (Table 1). This is likely to be a substantial underestimate of true national case numbers, because the infection is not notifiable. Because sporotrichosis remains relatively uncommon, the lack of recognition of this infection in general practice, leading to ineffective antibiotic treatment often for weeks to months before correct diagnosis, is likely to be an ongoing problem. Local recognition of the possibility of this disease occurring in the Northern Territory is therefore of major importance. We acknowledge it is possible that the two apparently local cases were acquired after contact with contaminated material such as hay, which might have been imported from interstate, meaning that the organism did not originate in the Northern Territory.

The identification of Q. cyanescens in Case 1 was of great interest because it was the only isolate from the initial biopsy, causing us to wonder whether it might be the pathogen responsible for the sporotrichoid lesions. However, the subsequent isolation of S. schenckii from a repeat biopsy of the same lesion, and a forearm lesion, make it far more likely that Q. cyanescens was not implicated in the pathogenesis of the lesions, in keeping with the existing understanding of this organism.2628

Quambalaria cyanescens is a basidiomycetous plant pathogen,29 which has undergone a number of taxonomic reassignments including, previously, Sporothrix cyanescens and Fugomyces cyanescens.30,31 There are no human case reports of the isolation of Q. cyanescens from human specimens or as a cause of human pathology. However, when previously known as S. cyanescens, this organism was postulated to have had a pathogenic role in one immunosuppressed patient with pulmonary nodules.26 Sporothrix cyanescens features in just two other human reports as a potential pathogen27 or an environmental contaminant appearing in bronchial washings.28 Quambalaria species cause pathology such as canker and shoot blight in Australian native trees of the Eucalyptus and Corymbia genera (red flowering gums)32 different trees from those with which Cryptococcus gattii is associated.33

We hypothesise that Q. cyanescens was inoculated at the same time as S. schenckii, given its similar ecological niche, and colonized the wound. The national reference laboratory in South Australia had also identified Q. cyanescens several months prior, in another Royal Darwin Hospital (Northern Territory) patient who had a staphylococcal abscess of the shin. A sample from the shin yielded both Staphylococcus aureus and Q. cyanescens, with the latter being considered non-pathogenic. The patient responded to conventional antibiotics. Quambalaria cyanescens has the potential to be misidentified as Sporothrix species in the laboratory, hence the importance of accurate laboratory workup. In Case 1 and in the additional case seen at the NMRC, identification was by macroscopic and microscopic appearance of colonies grown on a variety of media and DNA sequencing.

Sporothrix schenckii is a thermally dimorphic fungus that assumes a filamentous form when cultured at 25°C. Colonies may be slow growing, glabrous, with a leathery to velvety texture, and pigmentation varies from white to dark grey-brown with age; microscopically, septate hyphae bear perpendicular conidiophores with sympodial clusters of denticulate conidia at the apex, and with age, ovoidal conidia may be borne directly on the sides of the conidiophore and hyphae (Figure 5). In human and animal tissues and on brain heart infusion agar at 37°C, S. schenckii has a yeast-like morphology with smooth cream to beige colonies; microscopically budding ovoidal to cigar-shaped budding yeast cells. Dimorphism must be shown to morphologically identify the isolate as S. schenckii. Molecular diagnostics are particularly helpful in situations of slow growth.3 Quambalaria cyanescens is distinguishable from S. schenckii by its velvety to powdery colony texture, production of an intense purple diffusible pigment on potato dextrose agar after several weeks incubation, and a lack of a yeast phase.

Figure 5.
Figure 5.

(A) Sabaroud's agar at 25°C, colonies are slow growing, with a wrinkled and folded surface, forming shapes suggestive of inverted cones or volcanoes. (B) Conidiophores and conidia of S. schenckii. Conidia are ovoid, one-celled, and smooth-walled. Conidiophores (black arrow) arise at right angles from the thin septate hyphae and are usually solitary. Conidia are formed in clusters on small denticles by proliferation of the conidiophore, their arrangement often suggestive of a flower.

Citation: The American Society of Tropical Medicine and Hygiene 91, 6; 10.4269/ajtmh.14-0456

Histopathology of S. schenckii-infected tissue specimens often shows mixed suppurative and granulomatous inflammatory reactions in dermis and subcutaneous tissues.34 The unexpected histopathological findings in Case 1 were reviewed and corrected to conclude that SCC was not present.

Regarding clinical features of sporotrichosis, the localized cutaneous form caused by traumatic inoculation is the commonest presentation. The fungus converts into yeast form and may remain in subcutaneous tissues or extend along adjacent lymphatic vessels, constituting the lymphocutaneous form.3 Osteoarticular is the second most common presentation, followed by pulmonary and systemic disease. Disseminated infection occurs rarely, most commonly in immunocompromised individuals, particularly those with human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS).35 Treatment of lymphocutaneous infection is usually achieved with itraconazole 200 mg daily.36,37 The recommended treatment duration is usually 3–6 months and is recommended to continue treatment of 2–4 weeks after lesions have resolved, as was used in the cases described here. Cure rates with itraconazole are over 95%.28 Fluconazole (initially commenced in Case 3) is ineffective. Alternative agents include terbinafine and amphotericin B, which also have excellent activity against the organism. Treatment duration of at least 12 months is recommended for osteoarticular infections.29

In conclusion, sporotrichosis needs to be considered as a differential diagnosis in patients from Australia's Northern Territory, alongside better known local endemic pathogens, which can cause sporotrichoid lesions (Nocardia spp.) or fixed cutaneous lesions non-responsive to conventional antibiotics (melioidosis, chromoblastomycosis, and cryptococcosis). As improved molecular diagnostics now facilitate easier distinction between similar appearing fungi such as Q. cyanescens and S. schenckii, the occurrence of Q. cyanescens from human specimens should continue to be monitored, to determine any possible indication of pathogenicity, and to distinguish it from S. schenckii, which has clearly established human pathogenicity requiring treatment.

ACKNOWLEDGMENTS

We thank Erana Gray, Nicholas Anstey, and Grace Leung for providing clinical care, Jason Lam for performing a biopsy, and Shobini Sivagnanam for providing Table 1. We are also grateful to Helen Alexiou and Steve Davis at National Mycology Reference Centre for their involvement in identifying the organisms.

  • 1.

    Rivitti EA, Aoki V, 1999. Deep fungal infections in tropical countries. Clin dermatol 17: 171190; discussion 105–106.

  • 2.

    Tobin EH, Jih WW, 2001. Sporotrichoid lymphocutaneous infections: etiology, diagnosis and therapy. Am Fam Physician 63: 326332.

  • 3.

    Barros MB, de Almeida Paes R, Schubach AO, 2011. Sporothrix schenckii and sporotrichosis. Clin Microbiol Rev 24: 633654.

  • 4.

    Sivagnanam S, Bannan AM, Chen SC, Ralph AP, 2012. Sporotrichosis (Sporothrix schenckii infection) in the New South Wales mid-north coast, 2000–2010. Med J Aust 196: 588590.

    • Search Google Scholar
    • Export Citation
  • 5.

    Robinson CF, Orban TD, 1951. A case of regional lymphatic sporotrichosis. Aust J Dermatol 1: 142144.

  • 6.

    Barrack BB, Powell RE, 1952. Sporotrichosis. Med J Aust 2: 624626.

  • 7.

    Minty CC, Mead M, McCaffrey MF, 1956. Sporotrichosis: a case report from Queensland. Med J Aust 43: 704705.

  • 8.

    Mead M, Ridley MF, 1957. Sporotrichosis and chromoblastomycosis in Queensland. Med J Aust 44: 192197.

  • 9.

    Durie EB, Frey D, Becke RF, 1961. Sporotrichosis: report of a case from Sydney, Australia. Aust J Dermatol 6: 7172.

  • 10.

    O'Donnell JM, 1962. A case of sporotrichosis. Med J Aust 49: 517518.

  • 11.

    Muir DB, Pritchard RC, 1984. Sporothrix schenckii–incidence in the Sydney region. Australas J Dermatol 25: 2728.

  • 12.

    Robertson D, 1967. Report of two cases of sporotrichosis of the face. Australas J Dermatol 9: 7682.

  • 13.

    Black RB, McAleer R, 1975. A case of sporotrichosis in Western Australia. Australas J Dermatol 16: 3238.

  • 14.

    Auld JC, Beardmore GL, 1979. Sporotrichosis in Queensland: a review of 37 cases at the Royal Brisbane Hospital. Australas J Dermatol 20: 1422.

    • Search Google Scholar
    • Export Citation
  • 15.

    Beardmore GL, 1979. Recalcitrant sporotrichosis: a report of a patient treated with various therapies including oral miconazole and 5-fluorocytosine. Australas J Dermatol 20: 1013.

    • Search Google Scholar
    • Export Citation
  • 16.

    Bullpitt P, Weedon D, 1978. Sporotrichosis: a review of 39 cases. Pathology 10: 249256.

  • 17.

    Conias S, Wilson P, 1998. Epidemic cutaneous sporotrichosis: report of 16 cases in Queensland due to moldy hay. Australas J Dermatol 39: 3437.

    • Search Google Scholar
    • Export Citation
  • 18.

    Moaven LD, Altman SA, Newnham AR, 1999. Sporotrichosis mimicking necrotising arachnidism. Med J Aust 171: 685686.

  • 19.

    Feeney KT, Arthur IH, Whittle AJ, Altman SA, Speers DJ, 2007. Outbreak of sporotrichosis, Western Australia. Emerg Infect Dis 13: 12281231.

  • 20.

    Dooley DP, Bostic PS, Beckius ML, 1997. Spook house sporotrichosis. A point-source outbreak of sporotrichosis associated with hay bale props in a Halloween haunted-house. Arch Intern Med 157: 18851887.

    • Search Google Scholar
    • Export Citation
  • 21.

    Pappas PG, Tellez I, Deep AE, Nolasco D, Holgado W, Bustamante B, 2000. Sporotrichosis in Peru: description of an area of hyperendemicity. Clin Infect Dis 30: 6570.

    • Search Google Scholar
    • Export Citation
  • 22.

    Currie BJ, Carapetis JR, 2000. Skin infections and infestations in Aboriginal communities in northern Australia. Australas J Dermatol 41: 139143, quiz 44–45.

    • Search Google Scholar
    • Export Citation
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    Fisher D, Burrow J, Lo D, Currie BJ, 1993. Cryptococcus neoformans in tropical northern Australia: predominantly variant gattii with good outcomes. Aust N Z J Med 23: 678682.

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Author Notes

* Address correspondence to Shradha Subedi, 105 Rockland Drive, Tiwi, Darwin, Northern Territory, Australia 0810. E-mail: subedi_82@yahoo.com

Authors' addresses: Shradha Subedi, Department of Medicine, Royal Darwin Hospital, Tiwi, Darwin, Northern Territory, Australia, E-mail: subedi_82@yahoo.com. Sarah E. Kidd, National Mycology Reference Centre, SA Pathology, Adelaide, South Australia, Australia, E-mail: sarah.kidd@health.sa.gov.au. Robert W. Baird, Royal Darwin Hospital, Microbiology, Darwin, Northern Territory, Australia, E-mail: rob.baird@nt.gov.au. Nicholas Coatsworth, Royal Darwin Hospital, Department of Medicine, Darwin, Northern Territory, Australia, E-mail: nicholas.coatsworth@nt.gov.au. Anna P. Ralph, Global Tropical Health Division, Menzies School of Health Research, Darwin, Northern Territory, Australia, E-mail: anna.ralph@menzies.edu.au.

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