Clinical features, fungal load, coinfections, histological skin changes, and itraconazole treatment response of cats with sporotrichosis caused by Sporothrix brasiliensis

Abstract

Zoonotic sporotrichosis caused by the fungus Sporothrix brasiliensis is usually severe in cats. This study investigated the associations between clinical features, fungal load, coinfections, histological skin changes, and response to itraconazole in cats with sporotrichosis caused by S. brasiliensis. Fifty-two cats with skin lesions and a definitive diagnosis of sporotrichosis were treated with itraconazole for a maximum period of 36 weeks. The animals were submitted to clinical examination and two subsequent collections of samples from the same skin lesion for fungal diagnosis and histopathology, as well as serology for feline immunodeficiency (FIV) and leukaemia (FeLV) viruses. Thirty-seven (71%) cats were clinically cured. Nasal mucosa lesions and respiratory signs were associated with treatment failure. Cats coinfected with FIV/FeLV (n = 12) had a lower neutrophil count in the lesion. A high fungal load in skin lesions was linked to young age and treatment failure, as well as to a longer time of wound healing, poorly formed granulomas and fewer neutrophils, macrophages and lymphocytes in these lesions. These results indicate that itraconazole is effective, but nasal mucosal involvement, respiratory signs and high fungal loads in skin lesions are predictors of treatment failure that will assist in the development of better treatment protocols for cats.

Figure 1

(A–C) Female cat, 5 years, with sporotrichosis and negative serology for FIV and FeLV. (A) Multiple ulcers on the flank and thigh in the first appointment before treatment with itraconazole. One of the lesions of the flank (arrow) was submitted to the first biopsy. (B) Time of the second biopsy of the same lesion (arrow) after 7 weeks of treatment. Remarkable regression of size and partial healing of the ulcer on the right flank submitted to the first biopsy, as well as of the other initial lesions. (C) Clinical cure after 16 weeks of treatment with itraconazole. (D–F) Female cat, 3 years, with sporotrichosis and negative serology for FIV and FeLV. (D) Ulcer on the tail before treatment with itraconazole submitted to the first biopsy. (E) Time of the second biopsy of the same lesion after 9 weeks of treatment. Note the stagnation of the ulcer on the tail. (F) Therapeutic failure after 36 weeks of itraconazole treatment. Persistence of the ulcer on the tail.

Figure 2

Histological changes in the skin lesion of a cat with sporotrichosis (the same as in Fig. 1A–C) whose outcome was clinical cure after 16 weeks of treatment with itraconazole. (A,B) Skin lesion sample at the time of the first biopsy before treatment. (A) Marked and diffuse pyogranulomatous dermatitis exhibiting multiple well-formed granulomas. H&E. (B) Note the black-stained single, round, budding yeast cell, demonstrating low fungal load. GMS. (C,D) Sample of the same skin lesion at the time of the second biopsy after 7 weeks of treatment. (C) Dermal fibrosis. H&E. (D) Absence of yeasts. GMS.

Figure 3

Histological changes in the skin lesion of a cat with sporotrichosis and seropositive for FIV whose outcome was therapeutic failure after 36 weeks of itraconazole treatment. (A,B) Skin lesion sample at the time of the first biopsy before treatment. (A) Fungus-rich granuloma containing abundant yeasts inside macrophages and few neutrophils, lymphocytes and plasma cells. H&E. (B) Abundant black-stained round yeasts, some with narrow-base single buds, or cigar-shaped cells. GMS. (C,D) Sample of the same skin lesion at the time of the second biopsy after 7 weeks of treatment. (C) Pyogranulomatous dermatitis exhibiting a poorly formed granuloma characterised by marked and diffuse infiltration of macrophages, neutrophils, plasma cells, and lymphocytes. Note also the dermal fibrosis. H&E. (D) Reduction in the initial fungal load showing the presence of black-stained round yeasts, some with narrow-base single buds, or cigar-shaped cells, and hyphae. GMS.