Sporotrichosis: an update on epidemiology, etiopathogenesis, laboratory and clinical therapeutics

Abstract

In the late 90's there was a change in both the route of transmission and the people at risk for sporotrichosis. This zoonotic cat-man alternative transmission route elicited changes in strategies to control the epidemic. There was a progressive increase in the number of cases involving especially children and the elderly. In addition to becoming hyperendemic, uncommon clinical pictures like immunoreactive clinical presentations or severe systemic cases have emerged. New species were identified and classified through molecular tools using more virulent clinical isolates, like S. brasiliensis, compared to the environmental isolates. Likewise, different species of Sporothrix have been associated with different geographic regions. The serological and molecular techniques are used as an auxiliary tool for the diagnosis and/or for species identification, although the isolation and the identification of Sporothrix spp. in clinical specimen is still the gold standard. Currently sporotrichosis epidemics requires the knowledge of the epidemiological-molecular profile to control the disease and the specific treatment. Itraconazole, potassium iodide, terfinafine, and amphotericin B are the available drugs in Brazil to treat sporotrichosis. The drug of choice, its posology, and treatment duration vary according to the clinical presentation, the Sporothrix species, and host immune status. New treatment choices, including a vaccine, are being developed; nevertheless, more clinical trials are required to confirm its efficacy.

Figure 1

Ulcerated lesions on the hands of three members of the same family, at the beginning of the zoonotic transmission sporotrichosis epidemics in Rio de Janeiro, in 1997, treated at Hospital Universitário Pedro Ernesto

Figure 2

Phylogenetic relations between the clinical and environmental clade members in Sporothrix, based on calmodulin sequences (exon 3-5). Available at GenBank (https://www.ncbi.nlm.nih.gov/genbank/). Method: Maximum likelihood The numbers close to the branches refer to resample percentages (1000 bootstrap)

Figure 3

A. Lymphocutaneous form in adults (ascending lymphangitis); B. lymphocutaneous form in a child's face (descending lymphangitis); C. fixed cutaneous form on the back of the hand; D, E, F. systemic form with disseminated skin lesions in an AIDS patient

Figure 4

A. Granulomatous lesion at the upper eyelid ocular conjunctiva; B. primary lymphocutaneous lesion on the finger; and C. pseudovesicular lesions over an erythematous plaque on the back of the same patient - Sweet's syndrome (immunoreactive form)

Figure 5

A. Macromorphology of Sporothrix brasiliensis; B. Micromorphology reveals delicate, hyaline septate hyphae, conidiophore that originates primary hyaline conidia in a bouquet arrangement (cotton blue, x400); C. Asteroid body (Grocott, X400)

Figure 6

Flowchart for laboratory diagnosis of sporotrichosis. GMS (Gomori methenamine silver); CMA (corn meal agar); 'C' - carbon; ITS (Internal Transcript Spacer); PCR (Polymerase Chain Reaction)

Figure 7

Algorithm for the treatment of sporotrichosis. LC - lym phocutaneous; CF - fixed cutaneous; KI - potassium iodide; ITZ - itraconazole; TBF - terbinafine; AmB - amphotericin B ¹Hyperkeratotic or refractory cutaneous lesions: heat, cryosurgery, electrosurgery, exci sion/drainage, Kl + ITZ or Kl + TBF ²Children, elderly, immunoreactive forms: Kl Pregnant women: Heat, cryosurgery, AmB Modified from: Orofino-Costa, et al. 2015