Version May 2024
INTRODUCTION — Sporotrichosis is a subacute to chronic infection caused by the dimorphic fungi belonging to the genus Sporothrix. Sporothrix schenckii is the most common organism to cause human disease, but there are several other species that also are pathogenic for humans and animals [1]. Infection usually involves cutaneous and subcutaneous tissues but can occasionally occur in other sites, primarily in immunocompromised patients. Activities that are usually associated with the development of sporotrichosis include landscaping, rose gardening, and other activities that involve inoculation of soil through the skin.
The basic biology of S. schenckii and the epidemiology of sporotrichosis will be reviewed here. The clinical features, diagnosis, and treatment of this infection are discussed separately. (See "Clinical features and diagnosis of sporotrichosis" and "Treatment of sporotrichosis".)
MYCOLOGY — S. schenckii is the primary pathogen in the genus Sporothrix, and most laboratories still identify isolates as S. schenckii. However, molecular studies have found that this species actually consists of a complex of at least six phylogenetically different species that cluster in different geographic regions [2-7].
S. schenckii sensu stricto occurs worldwide and remains the most common human pathogen, but Sporothrix brasiliensis appears to be equally or perhaps more virulent and causes most infections in Brazil, including the large zoonotic outbreak related to cats in Rio de Janeiro. (See 'Virulence factors' below and 'Epidemiology' below.)
Sporothrix globosa is found worldwide but causes fewer infections than S. schenckii and S. brasiliensis [4]. Sporothrix mexicana, present in Mexico and other Latin American countries, Sporothrix luriei, and Sporothrix pallida are less common causes of infection in humans [5].
Dimorphism — S. schenckii exhibits thermal dimorphism. It produces hyphae in the environment at temperatures that are lower than normal human body temperatures (picture 1) and exists as a yeast form at 37ºC in vitro and in human tissues. Some strains are less thermotolerant than others, growing poorly at temperatures above 35ºC; these strains tend to be found in fixed dermal lesions and do not have the propensity to spread along lymphatics into subcutaneous tissues as do most strains of S. schenckii [8].
Growth in vitro — At 25 to 27ºC, the filamentous form of S. schenckii grows readily on standard media, such as Sabouraud dextrose agar. Within one to two weeks, growth begins as a white- to cream-colored mold and then assumes a brown, gray, or black color with further incubation (picture 2). With age, the colonies become wrinkled and, with repeated subculturing, may lose their dark color and turn off-white. The conidia may be dark colored or hyaline and arrange themselves along the hyphae in "bouquet-like" arrangements. The hyphae are thin, septate, and branched.
Growth of the yeast phase in vitro requires incubation at 37ºC on enriched media, such as brain heart infusion agar. During yeast phase growth, the colonies are usually off-white and wrinkled.
Growth in vivo — In human or animal tissues at 37ºC, S. schenckii assumes a yeast-like form and reproduces by budding. The yeasts are usually 4 to 6 microns in diameter and variable in their shape; cigar-shaped yeast cells are classically described, but round and oval shaped yeast cells are also common.
Antigenic structure — The cell wall of S. schenckii, as with most other pathogenic fungi, contains chitin, glucans, and mannans. However, unique to S. schenckii is the presence of L-rhamnose, in addition to mannose and glucose, as a major constituent of the glycopeptides in the cell wall [9].
VIRULENCE AND IMMUNE RESPONSE — S. schenckii is generally not considered a highly virulent fungus. Disease in humans is usually localized to cutaneous and subcutaneous tissues and has a subacute to chronic course.
Experimental animal infection — Laboratory rodents, including rats, mice, hamsters, and guinea pigs, can be infected with S. schenckii. Experimental infection mimics natural infection, usually causing localized infection [9].
Those organisms that are isolated from fixed cutaneous lesions and that grow poorly at 37ºC will multiply in colder areas, such as the testes, but rarely cause disseminated infection. Those strains that grow well at 37ºC and have caused either extracutaneous or cutaneous lesions in humans spread and multiply in multiple internal organs as well as the testes [8].
In a small study that involved the inoculation of mice with S. schenckii isolates from patients who had either disseminated or lymphocutaneous infection, differences in virulence depended on the type of infection in humans; only the isolates causing disseminated infection in humans were able to cause systemic infection and death in the mice [10]. (See "Clinical features and diagnosis of sporotrichosis".)
Virulence factors — There are several virulence factors of S. schenckii are [11]. Components of the cell wall of S. schenckii, especially a 70 kDa glycoprotein (GP70), mediate adhesion to extracellular matrix and endothelial cell surface proteins, initiating invasion [5]. Several extracellular proteinases are capable of hydrolyzing collagen and elastin and are likely important for pathogenicity [9]. Melanin, found in Sporothrix species, is a known virulence factor for many fungi [12,13].
The large outbreak of zoonotic S. brasiliensis infection in Rio de Janeiro has led to the observation that S. brasiliensis appears to be more virulent than S. schenckii. Results obtained using an experimental murine model have verified this clinical observation [14]. It seems likely that increased virulence is related to differences in cell wall composition between S. schenckii and S. brasiliensis [15].
Immune response — The immune response to S. schenckii has not been completely elucidated; most data are derived from experimental murine models of sporotrichosis and in vitro studies. The innate immune system is important in phagocytosis and killing of the organism [16]. Both antibody and cell-mediated immunity appear to have a role in the specific immune response to infection [9,17,18].
A role for T cells in containing infection is suggested by the observations that sporotrichosis is more severe in nude mice and that protection can be transferred by CD4 lymphocytes from immune mice [19]. In addition, the infection tends to disseminate widely in patients with HIV and CD4 cells less than 200/microL [20,21], a characteristic seen rarely in normal hosts. Disseminated disease has also been reported in patients with hairy cell leukemia [22].
A role for cytokines, such as tumor necrosis factor (TNF)-alpha and interferon-gamma, has been noted in an experimental murine model of sporotrichosis and in several patients treated with TNF-alpha antagonists [9,23,24].
EPIDEMIOLOGY — S. schenckii is found worldwide in climates ranging from temperate to tropical [25,26]. Sporotrichosis is endemic in at least one remote area of Peru with a mean annual incidence of 73 cases per 100,000 adults and 156 cases per 100,000 children <15 years of age [27-29]. Sporotrichosis is also common in certain provinces of China, where young children account for approximately 20 percent of cases [30]. In Brazil, the incidence is rising due to the emergence of S. brasiliensis and zoonotic transmission from cats [31].
Sources of infection — S. schenckii exists in a variety of environmental niches that include sphagnum moss, decaying wood and other vegetation, hay, and soil. Thus, infection is most frequent in persons whose vocation or avocation brings them into contact with the environment.
Activities associated with the development of sporotrichosis include landscaping, Christmas tree farming, rose gardening, topiary production, baling and using hay for packing materials or displays, and motor vehicle accidents that involve inoculation of soil into wounds [12,32-34]. In some cases, a discrete cutaneous inoculation site is not obvious, but the patient may recall exposure to soil, wood, or plant material.
Inhalation of S. schenckii from soil is the presumed route of transmission for pulmonary sporotrichosis. Most patients have been involved in an occupation that exposes them to aerosols from soil, but specific sources are rarely identified.
In the United States, an outbreak involving 84 patients in 15 states was traced back to conifer seedlings that had been packed in sphagnum moss obtained from Wisconsin [12,13]. Other outbreaks in the United States also have been traced back to Wisconsin sphagnum moss [32,33]. A large outbreak of sporotrichosis involved contaminated timber in gold mines in Witwatersrand, South Africa [35]. Over a three-year period, nearly 3000 workers developed sporotrichosis, presumably after direct inoculation of the organism from wood splinters.
Zoonotic transmission and epidemic S. brasiliensis infection — Zoonotic transmission of sporotrichosis has been traced to a variety of animals [36-44]. Most cases of transmission from animals to humans have been associated with cats [28,36,38,39], and sporotrichosis is a known occupational hazard for veterinarians treating infected cats [38]. In a highly endemic area in Peru, risk factors for infection among children were playing in fields, living in houses with dirt floors, and owning a cat [28].
An ongoing outbreak that began in Rio de Janeiro, Brazil, in 1997 is related primarily to domestic and feral cats [36,39,44-46]. Over 4000 people and many thousands of cats with sporotrichosis were reported from one referral center in Rio de Janeiro; however, the disease is now widespread, and it is very likely that cases are under-reported in humans and are assuredly under-reported in cats. The disease has spread from the epicenter in Rio de Janeiro, and cases are now reported from other areas of Brazil, as well as in Paraguay, Chile, Argentina, and Panama [45,47,48].
Most infections have been reported from poor neighborhoods and have been seen predominantly in women and children, who were most likely to care for and play with cats [36]. Disseminated infection with this species, including pulmonary involvement, has been noted in patients with advanced HIV [49]. Most cats have cutaneous lesions on the head and face with frequent mucosal involvement [39]. Dogs also have been infected during this outbreak and have a predominance of facial and nasal mucous membrane lesions [40]. The strains in this outbreak have been identified as S. brasiliensis and appear to have originated from a single source [50,51].
In Uruguay, a common history is that of a patient who describes hunting armadillos, receives scratches from the animal, and later develops skin lesions. In these cases, the armadillo is not infected but inoculates S. schenckii, which is present in nesting materials and the soil, into the skin [37]. Other cases have been ascribed to inoculation of the organism by insect stings, bird pecks, rodent bites, and by handling fish [36,38,41-43].
Laboratory-acquired sporotrichosis — Several cases of sporotrichosis have been described in laboratory workers handling experimentally infected animals or culture materials [52]. Most cases involved cutaneous inoculation of infectious material, but ocular involvement occurred in several cases after infectious material was splashed into the eye.
SUMMARY
●General – Sporotrichosis is a subacute to chronic infection caused by the dimorphic fungus Sporothrix schenckii. Infection usually involves cutaneous and subcutaneous tissues but can occasionally occur in other sites, primarily in immunocompromised patients. Activities associated with the development of sporotrichosis include landscaping, rose gardening, and other activities that involve inoculation of soil through the skin. (See 'Introduction' above.)
●Mycology
•Most laboratories still identify isolates as S. schenckii, but molecular studies have found that this species is actually made up of a complex of at least six phylogenetically different species that cluster in different geographic regions. (See 'Mycology' above.)
•S. schenckii exhibits thermal dimorphism since it produces hyphae in the environment at temperatures that are lower than normal human body temperatures (picture 1) and exists as a yeast form when at 37ºC in vitro and in human tissues. (See 'Dimorphism' above.)
●Epidemiology – S. schenckii is found worldwide in climates ranging from temperate to tropical. In Brazil, the incidence is rising due to the emergence of S. brasiliensis and zoonotic transmission from cats. (See 'Epidemiology' above.)
•Sources of infection – S. schenckii exists in a variety of environmental niches that include sphagnum moss, decaying wood and other vegetation, hay, and soil. Thus, infection is most frequent in persons whose vocation or avocation brings them into contact with the environment. In some cases, a discrete cutaneous inoculation site is not obvious, but the patient may recall exposure to soil, wood, or plant material. Inhalation of S. schenckii from soil is the presumed route of transmission for pulmonary sporotrichosis. (See 'Sources of infection' above.)
•Zoonotic transmission – Zoonotic transmission of sporotrichosis has been traced back to a variety of animals. Most cases of transmission from animals to humans have been associated with cats. (See 'Zoonotic transmission and epidemic S. brasiliensis infection' above.)
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