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Feline-transmitted Sporotrichosis: A case study from California

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Feline-transmitted Sporotrichosis: A case study from California
Rachel K Rees MPH MT(ASCP)1, John E Swartzberg MD2
Dermatology Online Journal 17 (6): 2

1. School of Public Health, University of California, Berkeley, Berkeley, California. rkrees@calmail.berkeley.edu
2. School of Public Health, University of California, Berkeley, Berkeley, California


Abstract

We report a case of cat-associated sporotrichosis in an adult female in California. A retrospectively diagnosed cutaneous sporotrichosis infection in the patient’s cat and the unusual site of the primary lesion in the patient contributed to delayed diagnosis and treatment. Here, we also review the English literature regarding the epidemiology of Sporothrix schenkii as a cat-associated zoonosis.



Introduction

Sporothrix schenkii, a dimorphic fungus, is the etiologic agent of sporotrichosis, commonly known as rose gardener’s disease. Dimorphic fungi exist as molds in the environment. However, once the conidia are introduced into the body by inhalation or traumatic injury, the organisms convert to the yeast phase. Thus, dimorphic fungi are typically infectious when in the mold form. Sporothrix schenkii is unusual amongst the dimorphic fungi in that zoonotic transmission of both the mold and the yeast phases occurs. Zoonotic transmission has been reported from a variety of domestic and wild animals, but is most commonly associated with felines [1].


Case report


Figure 1Figure 2
Figure 1. Chest wall lesion approximately 9 weeks after initial presentation. Ruler units are in inches.

Figure 2. Sporotrichoid distribution of lesions.

In the spring of 2008, an otherwise healthy 41-year-old woman presented to the university student health clinic with a skin ulcer on the left chest wall. The patient reported that the lesion began as a single painless, erythematous papule approximately three weeks prior, followed by the appearance of additional papules and subsequent ulceration (Figure 1). She was afebrile and reported no trauma to the site. A course of doxycycline was prescribed and a swab of the lesion was obtained for routine bacteriological culture. No pathogens were isolated. During the doxycycline course, new papules and tender subcutaneous nodules developed in a linear pattern on the lateral side of the left breast (Figure 2). Examination by a dermatologist resulted in no recommendation for further work-up and no treatment was advised.

Because some of these masses were associated with the left breast, consultation with an oncology surgeon was advised. Approximately two months after the original papule was noticed, two core biopsies were obtained, one from the chest wall mass and one from a breast mass. The biopsies were preserved in formalin and submitted for pathological examination. No cultures were performed. Results of the two biopsies were similar, showing suppurative granulomatous infiltrates comprised of lymphocytes, eosinophils, neutrophils, and scattered plasma cells. No malignancy was identified. Stains for acid-fast bacilli (AFB) and fungal elements (Gomori methenamine silver (GMS)) were negative. The patient refused a course of clindamycin and requested an infectious disease consultation, which occurred the following week.


Patient History

The patient was raised in the San Joaquin Valley in central California and was employed as a clinical microbiologist. Medications for the patient’s asthma included a corticosteroid inhaler and a leukotriene receptor inhibitor. She reported no recent travel history. She lived in Guatemala from 1991-1993 and in Saudi Arabia from 2000-2003. During the time in Saudi Arabia, she traveled to Costa Rica, Australia, Egypt, and Europe. She also lived in Michigan during 2004-2005. She had two healthy four-year old indoor-outdoor cats that were spayed and neutered. Outside, the cats occasionally fought with local stray felines. When inside, the cats often engaged in kneading type activity, that consists of repetitive clawing, while, on the patient’s lap or in the bed with her.

Blood samples were submitted for complete blood count and coccidioides serology. The CBC was normal and her coccidioides serology was negative by enzyme immunoassay, immunodiffusion, and complement fixation. A chest x-ray was normal.


Figure 3
Figure 3. Microscopic morphology of the mold form of Sporothrix schenkii

Ten weeks after the first papule was noticed, complete excision of a chest wall lesion and biopsy of a subcutaneous nodule of the breast were performed. The specimens were submitted for aerobic, anaerobic, AFB, mycology, and viral cultures. The AFB stains were negative and the pathology specimens showed no granulomas. No fungal elements were seen, but five days later a mold grew from both the chest wall lesion and the subcutaneous nodule specimens. The mold grew at 30°C on both potato flake agar (PFA) and inhibitory mold agar (IMA). A slide culture (incubated at 30°C in ambient air) and a brain heart infusion slant with added broth (incubated at 35°C in CO2) of the mold were prepared for further analyses. Conversion of the mold to the yeast form occurred within two days. At 6 days, definitive identification as Sporothrix schenkii was made from demonstration of typical microscopic mold morphology upon staining the slide culture with lactophenol cotton blue and examining under light microscopy (Figure 3).

The patient began a three month course of itraconazole (200 mg bid). The lesions healed over approximately an 8-10 week time frame. Two years post-surgery, there were no signs of infection.

The patient later recalled an infection of the front right paw of her male cat. Upon review of the veterinary records, it was noted that the cat’s infection occurred just prior to the patient’s illness onset. Thinking it was an abscess, the patient treated the cat with ampicillin. However, the infection did not resolve and the cat was examined by a veterinarian. The veterinarian initially had a high clinical suspicion for sporotrichosis. A biopsy was submitted for pathological examination, but no culture was submitted. Results of the hematoxilin and eosin stain (H&E) examination, although negative for pathogens, showed severe chronic suppurative inflammation. The cat was treated for bacterial infection with enrofloxacin in conjunction with twice daily 2-minute betadine soaks, and the infection healed completely.

After the definitive diagnosis was obtained, the patient contacted her veterinarian to request a re-examination of the cat’s biopsy specimen. Re-examination of the original H&E stain showed low numbers of organisms that resembled inflammatory debris. Subsequent examination of tissue sections with periodic acid-schiff (PAS) stain confirmed small numbers of yeast forms consistent with Sporothrix schenkii.


Discussion

Sporothrix schenkii, a dimorphic fungus, is the etiologic agent of sporotrichosis, commonly known as rose gardener’s disease. Schenck first described the fungus in the United States in 1896 [2]. Sporotrichosis occurs globally, although it tends to occur more frequently in tropical and subtropical regions. In the United States, sporotrichosis is considered to be endemic to the Mississippi and Missouri River valleys [3, 4], whereas cases have been reported infrequently in California and the southwestern United States [3, 5-10]. It is difficult to estimate the incidence of sporotrichosis because it is not a reportable disease either in California or nationally.

Historically, sporotrichosis has been associated with gardeners and agricultural workers. Dimorphic fungi such as S. schenkii exist as a mold in the environment. Once the conidia are introduced into the body by inhalation or traumatic injury, the organisms convert to the yeast phase. Thus, dimorphic fungi are typically infectious while in the mold form. S. schenkii is present in soil, hay, sphagnum moss, and decaying vegetation. Inoculation usually occurs via penetration of the skin on the extremities while manipulating plant and soil materials. Rarely, the organisms may be inhaled, resulting in pulmonary sporotrichosis. Compared to other dimorphic fungi, Sporothrix schenkii is unusual in that zoonotic transmission occurs, particularly from felines [1].

Sporadic cases of zoonotic transmission from various animals have been reported throughout the decades, some of which indicate the possibility of transmission in the absence of wounds [1, 5, 11-18]. In 2005, Brazilian researchers initially reported on the first known epidemic of cat-associated sporotrichosis [19]. As of 2008, this on-going epidemic has affected 759 people, 64 canines, and 1503 felines. Of the people affected, 83.4 percent reported contact with cats with sporotrichosis, 55.8 percent of whom reported a cat scratch or bite [18]. The same research group conducted a study in 2001 that isolated Sporothrix schenkii from the nails of affected cats [20]. A case-control study in Peru identified cat ownership as a risk factor for lymphocutaneous sporotrichosis [21]. A subsequent Peruvian study of 84 cats showed a 2.38 percent prevalence of Sporothrix schenkii isolated from the nails of apparently healthy cats, suggesting that unaffected cats may serve as a reservoir for human infections [22]. Outdoor cats are at highest risk for contracting sporotrichosis. Like humans, cats acquire the disease via penetrating injury by foreign body or by fighting other cats [12]. We could find no instances of sporotrichosis occurring in indoor cats in the literature. However, Smilack reported a case in which both humans and felines exposed to sphagnum moss applied outdoors developed sporotrichosis [11]. Thus, there is potential risk for indoor cats to acquire the infection from sphagnum moss used for houseplants.

In the United States, sporotrichosis is an uncommon feline disease. Veterinarians and cat owners are at increased risk of contracting the disease because of the high level of transmissibility from felines to humans as compared with other animal species [12, 23]. The high level of contagiousness of cats with sporotrichosis is thought to arise from the typically high numbers of organisms present in the lesions. High numbers of yeast-phase organisms in cat lesions coupled with the fact that humans often recall no injury suggests that the yeast phase of S. schenkii may be acquired through intact skin. However, microscopic tears in the skin may occur without knowledge, permitting inoculation of the yeast phase organism.

Once the organism gains entry, the typical incubation period is 1 week to 2 months in humans, with most cases manifesting within the first three weeks of exposure. The clinical forms of sporotrichosis are categorized as localized (or fixed) cutaneous, lymphocutaneous, disseminated (systemic), and pulmonary. The lymphocutaneous form is the most common clinical presentation, with a primary ulcerative lesion and subcutaneous nodules extending in a linear pattern along the lymphatic channels (sporotrichoid distribution). As Kwon-Chung and Bennett note [24], the organisms forming the subcutaneous nodules rarely infect the lymph tissues themselves. Disseminated disease may arise from cutaneous inoculation or hematogenous spread from the lungs and most often occurs in immunocompromised patients [6, 25].

Because of the high burden of organisms in feline lesions, diagnosis of sporotrichosis in cats is often possible by histological examination, but the definitive diagnosis of sporotrichosis in both humans and cats requires recovery of the organism from culture [25, 26]. Demonstration of the mold form at 25°C and the yeast form at 37°C is required for definitive identification. The microscopic morphology of Sporothrix schenkii is distinctive. In the mold form the conidia are arranged in a bouquet-like fashion at the ends of the conidiophores. Serological [27-31] and molecular [32] assays are being developed by researchers as an aid to diagnosis.

In conclusion, we presume the patient contracted sporotrichosis from her male cat. The patient had no exposure to environmental risk factors such as gardening or other activities that entail contact with vegetation. The only known exposure she had was from her cat, which was retrospectively diagnosed with cutaneous sporotrichosis. No known cat-associated trauma occurred at the site of infection, but close contact with both cats was frequent, suggesting that transmission of the yeast phase organism via unbroken skin may be possible. A more likely mode of transmission is microscopic tearing of the skin from the typical kneading type of activity by a cat, allowing introduction of the organism. Maintaining clipped claws in domestic cats’ and restricting access to the outdoors may help prevent the transmission of sporotrichosis. The type of intimate contact that may occur with domestic felines may lead to infection of sites other than the extremities and complicate the diagnosis. Because the definitive diagnosis is contingent upon culture of the organism, it is important to submit samples for cultures early in the disease course to avoid adverse patient outcomes such as multiple invasive procedures and the risk of disseminated disease.

References

1. Reed KD, Moore FM, Geiger GE, Stemper ME. Zoonotic transmission of sporotrichosis: case report and review. Clin Infect Dis. 1993 Mar;16(3):384-7. [PubMed]

2. Schenck B. Refractory subcutaneous abscesses caused by a fungus possibly related to the sporotrichosis. Bull Johns Hopkins Hosp. 1898;9:286-90.

3. Epstein E. Sporotrichosis in California. Calif Med. 1965 Aug;103:130-1. [PubMed]

4. Duran RJ, Coventry MB, Weed LA, Kierland RR. Sporotrichosis; a report of twenty-three cases in the upper extremity. J Bone Joint Surg Am. 1957 Dec;39-A(6):1330-42. [PubMed]

5. Caravalho J, Jr., Caldwell JB, Radford BL, Feldman AR. Feline-transmitted sporotrichosis in the southwestern United States. West J Med. 1991 Apr;154(4):462-5. [PubMed]

6. Zhou CH, Asuncion A, Love GL. Laryngeal and respiratory tract sporotrichosis and steroid inhaler use. Arch Pathol Lab Med. 2003 Jul;127(7):893-4. [PubMed]

7. Wang JP, Granlund KF, Bozzette SA, Botte MJ, Fierer J. Bursal sporotrichosis: case report and review. Clin Infect Dis. 2000 Aug;31(2):615-6. [PubMed]

8. Gelber A. Sporotrichosis - Report of a Case of Its Occurrence in California. Archives of Dermatology and Syphilology. 1946;54(2):208-9. ISI:A1946UP39500011

9. Greenburg W. Sporotrichosis - Report of a case in California. Archives of Dermatology and Syphilology. 1937 Aug;36(2):355-7. ISI:000200436800018

10. Sinski JT, Miller OB, Jacoby WD. Sporotrichosis in southern Arizona. Case report. Ariz Med. 1976 Aug;38(8):628-9. [PubMed]

11. Smilack JD. Zoonotic transmission of sporotrichosis. Clin Infect Dis. 1993 Dec;17(6):1075. [PubMed]

12. Welsh RD. Sporotrichosis. J Am Vet Med Assoc. 2003 Oct 15;223(8):1123-6. [PubMed]

13. Dunstan RW, Langham RF, Reimann KA, Wakenell PS. Feline sporotrichosis: a report of five cases with transmission to humans. J Am Acad Dermatol. 1986 Jul;15(1):37-45. [PubMed]

14. Barros MB, Costa DL, Schubach TM, do Valle AC, Lorenzi NP, Teixeira JL, et al. Endemic of zoonotic sporotrichosis: profile of cases in children. Pediatr Infect Dis J. 2008 Mar;27(3):246-50. [PubMed]

15. Nusbaum BP, Gulbas N, Horwitz SN. Sporotrichosis acquired from a cat. J Am Acad Dermatol. 1983 Mar;8(3):386-91. [PubMed]

16. Oliveira-Neto MP, Mattos M, Lazera M, Reis RS, Chicarino-Coelho JM. Zoonotic sporothricosis transmitted by cats in Rio de Janeiro, Brazil. A case report. Dermatol Online J. 2002 Oct;8(2):5. [PubMed]

17. Rafal ES, Rasmussen JE. An unusual presentation of fixed cutaneous sporotrichosis: a case report and review of the literature. J Am Acad Dermatol. 1991 Nov;25(5 Pt 2):928-32. [PubMed]

18. Schubach A, Barros MB, Wanke B. Epidemic sporotrichosis. Curr Opin Infect Dis. 2008 Apr;21(2):129-33. [PubMed]

19. Schubach A, Schubach TM, Barros MB, Wanke B. Cat-transmitted sporotrichosis, Rio de Janeiro, Brazil. Emerg Infect Dis. 2005 Dec;11(12):1952-4. [PubMed]

20. Schubach TM, Valle AC, Gutierrez-Galhardo MC, Monteiro PC, Reis RS, Zancope-Oliveira RM, et al. Isolation of Sporothrix schenckii from the nails of domestic cats (Felis catus). Med Mycol. 2001 Feb;39(1):147-9. [PubMed]

21. Lyon GM, Zurita S, Casquero J, Holgado W, Guevara J, Brandt ME, et al. Population-based surveillance and a case-control study of risk factors for endemic lymphocutaneous sporotrichosis in Peru. Clin Infect Dis. 2003 Jan 1;36(1):34-9. [PubMed]

22. Kovarik CL, Neyra E, Bustamante B. Evaluation of cats as the source of endemic sporotrichosis in Peru. Med Mycol. 2008 Feb;46(1):53-6. [PubMed]

23. Dunstan RW, Reimann KA, Langham RF. Feline sporotrichosis. J Am Vet Med Assoc. 1986 Oct 15;189(8):880-3. [PubMed]

24. Kwon-Chung K, Bennett JE. Sporotrichosis. Medical Mycology. 2nd ed. Philadelphia, London: Lea & Febiger; 1992. p. 866.

25. Kauffman CA. Sporotrichosis. Clin Infect Dis. 1999 Aug;29(2):231-6. [PubMed]

26. Crothers SL, White SD, Ihrke PJ, Affolter VK. Sporotrichosis: a retrospective evaluation of 23 cases seen in northern California (1987-2007). Vet Dermatol. 2009 Aug;20(4):249-59. [PubMed]

27. Lopes-Bezerra LM, Schubach A, Costa RO. Sporothrix schenckii and sporotrichosis. An Acad Bras Cienc. 2006 Jun;78(2):293-308. [PubMed]

28. Bernardes-Engemann AR, Costa RC, Miguens BR, Penha CV, Neves E, Pereira BA, et al. Development of an enzyme-linked immunosorbent assay for the serodiagnosis of several clinical forms of sporotrichosis. Med Mycol. 2005 Sep;43(6):487-93. [PubMed]

29. Costa RO, de Mesquita KC, Damasco PS, Bernardes-Engemann AR, Dias CM, Silva IC, et al. Infectious arthritis as the single manifestation of sporotrichosis: serology from serum and synovial fluid samples as an aid to diagnosis. Rev Iberoam Micol. 2008 Mar;25(1):54-6. [PubMed]

30. Toriello C, Arjona-Rosado LC, Diaz-Gomez ML, Taylor ML. Efficiency of crude and purified fungal antigens in serodiagnosis to discriminate mycotic from other respiratory diseases. Mycoses. 1991 Mar-Apr;34(3-4):133-40. [PubMed]

31. Scott EN, Muchmore HG. Immunoblot analysis of antibody responses to Sporothrix schenckii. J Clin Microbiol. 1989 Feb;27(2):300-4. [PubMed]

32. Elias Costa MR, Da Silva Lacaz C, Kawasaki M, De Camargo ZP. Conventional versus molecular diagnostic tests. Med Mycol. 2000;38 Suppl 1:139-45. [PubMed]

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