Blastomycosis.

Blastomycosis is the fungal disease caused by thermally dimorphic fungi in the genus Blastomyces, with B dermatitidis complex causing most cases. It is considered hyperendemic in areas adjacent to the Great Lakes and along the St. Lawrence, Mississippi, and Ohio rivers, but definitive geographic distribution of blastomycoses remains obscure. Clinical presentation is variable. Disseminated blastomycosis with extrapulmonary manifestations is more common in immunosuppressed individuals. Culture positivity is required for definitive diagnosis, but compatible histology is often sufficient for presumptive diagnosis and initiation of treatment. Treatment should be provided to all symptomatic cases to prevent progression or recurrence.

Blastomycosis.

Blastomycosis is a serious fungal disease of humans and other mammals caused by environmentally acquired infection with geographically restricted, thermally dimorphic fungi belonging to the genus Blastomyces. The genetic and geographic diversity of these pathogens is greater than previously appreciated. In addition to Blastomyces dermatitidis and the cryptic species Blastomyces gilchristii, which cause blastomycosis in mid-western and various eastern areas of North America, atypical blastomycosis is occasionally caused by Blastomyces helicus in western parts of North America and Blastomyces percursus in Africa. Blastomycosis is acquired by inhalation of the conidia that are produced in the mold phase; in the lungs, temperature-dependent transformation occurs to the yeast phase. In this form, the organism is phagocytized by macrophages and can spread hematogenously to various organs causing disseminated infection. Pulmonary disease is most common and varies from mild, self-limited infection to severe, potentially fatal adult respiratory distress syndrome. Disseminated infection is manifested primarily by skin lesions, but many other organs can be involved. Diagnosis is established by growth of the organism in culture; however, a tentative diagnosis can be made quickly by histopathological identification of the classic yeast form in tissues or by finding Blastomyces antigen in urine or serum. Blastomycosis is treated initially with amphotericin B when the disease is severe, involves the central nervous system, or the host is immunosuppressed. Itraconazole is recommended for primary therapy in mild-to-moderate infection and for step-down therapy after initial amphotericin B treatment. Voriconazole and posaconazole can be used for patients in whom itraconazole is not tolerated.

Disseminated Blastomycosis in a Teenager Presenting with Pleural Effusion and Splenomegaly.

BACKGROUND: Blastomycosis is caused by a fungus endemic to states and providences bordering the Lawrence Rivers and the Great Lakes. It can lead to significant pathology in both immunocompetent and immunocompromised hosts. This case report describes disseminated blastomycosis in an otherwise healthy 16-year-old patient. CASE REPORT: A 16-year-old male presented with a chief complaint of flank pain. In the Emergency Department he described additional symptoms of emesis, cough, and weight loss. His vitals were appropriate; however, he had absent lung sounds in the left lower lung field, splenomegaly, a left thigh abscess, and lower-extremity edema. Imaging studies showed a left pleural effusion, mediastinal shift to the right, splenomegaly, a left psoas abscess, and undifferentiated bony involvement of L1 transverse process and the left 12th rib. Abscess cultures grew Blastomyces dermatitides. He was treated with amphotericin B, demonstrated clinical improvement, and was discharged on itraconazole. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: The case fatality rate of blastomycosis is estimated at between 4.3% and 6.4%. Patients with solid organ transplant and associated immune suppression had a mortality of 33-38%. Given the nonspecific nature of this condition, a high level of suspicion is required for diagnosis, and early diagnosis is essential, as end organ damage in disseminated disease can include high-severity illness, including acute respiratory distress syndrome and central nervous system dysfunction. If any patient presents with symptomatology involving both skin and pulmonary systems, blastomycosis must be entertained as a possible diagnosis. Prompt diagnosis and treatment will significantly improve morbidity and mortality.

Turning on virulence: Mechanisms that underpin the morphologic transition and pathogenicity of Blastomyces.

This review article focuses on the mechanisms underlying temperature adaptation and virulence of the etiologic agents of blastomycosis, Blastomyces dermatitidis, Blastomyces gilchristii, and Blastomyces percursus. In response to temperature, Blastomyces undergoes a reversible morphologic switch between hyphae and yeast known as the phase transition. The conversion to yeast for Blastomyces and related thermally dimorphic fungi is essential for virulence. In the yeast phase, Blastomyces upregulates the essential virulence factor, BAD1, which promotes attachment to host cells, impairs activation of immune cells, and blunts cytokine release. Blastomyces yeast also secrete dipeptidyl-peptidase IVA (DPPIVA), a serine protease that blunts the action of cytokines released from host immune cells. In vivo transcriptional profiling of Blastomyces yeast has uncovered genes such as PRA1 and ZRT1 involved in zinc scavenging that contribute to virulence during murine pulmonary infection. The discovery and characterization of genes important for virulence has led to advances at the bedside regarding novel diagnostics, vaccine development, and new targets for drug discovery.

Chronic Pulmonary Blastomycosis Mimicking Pulmonary Tuberculosis.

Introduction: Blastomyces dermatitidis is a dimorphic fungus endemic to the Mississippi River valley. We describe a rare case of chronic pulmonary blastomycosis complicated by large pulmonary cavitation in a young service member who was misdiagnosed with active pulmonary tuberculosis. Case Presentation: A 25-year-old active duty male presented to his primary care provider with complaints of hemoptysis, fatigue, weight loss, and fever. Computed tomography chest with contrast identified a large cavitary lesion in the right upper lobe (RUL). The patient was admitted to an outside hospital and he underwent bronchoscopy with transbronchial biopsies and bronchoalveolar lavage of the RUL. Histology and cultures were unremarkable however; Histoplasma serum antigen was positive. The patient was empirically treated for active pulmonary tuberculosis and soon discharged. He returned for medical evaluation 3 mo later with continued hemoptysis. Repeat bronchoscopy with transbronchial biopsies of the RUL cavity grew Blastomyces dermatitidis. The patient's symptoms resolved and chest imaging significantly improved with initiation of itraconazole. Discussion: Chronic pulmonary blastomycosis can present with a constellation of symptoms that may be indistinguishable from chronic pulmonary histoplasmosis, pulmonary tuberculosis, or lung cancer. Knowledge of endemic diseases and a thorough travel history should be an integral part of a military physician's infectious disease evaluation.

Urinary tract blastomycosis diagnosed by urine cytology.

Urinary tract blastomycosis is an uncommon manifestation of disseminated Blastomyces infection. Here, we report a 50-year-old male with common variable immunodeficiency who presented with urinary symptoms and a renal mass concerning for a kidney neoplasm. Urine cytology revealed typical broad-based budding yeasts with thick-walled refractile capsules, leading to diagnosis of urinary tract blastomycosis. In this case, urine cultures were negative, and urine cytology was the main method of diagnosis of blastomycosis. Thus, urine cytology represents a rapid and reliable method of diagnosing blastomycosis, which in the current case led to prompt treatment of this potentially life threatening infection.

Phylogeographic Analysis of Blastomyces dermatitidis and Blastomyces gilchristii Reveals an Association with North American Freshwater Drainage Basins.

Blastomyces dermatitidis and Blastomyces gilchristii are dimorphic fungal pathogens that cause serious pulmonary and systemic infections in humans. Although their natural habitat is in the environment, little is known about their specific ecologic niche(s). Here, we analyzed 25 microsatellite loci from 169 strains collected from various regions throughout their known endemic range in North America, representing the largest and most geographically diverse collection of isolates studied to date. Genetic analysis of multilocus microsatellite data divided the strains into four populations of B. dermatitidis and four populations of B. gilchristii. B. dermatitidis isolates were recovered from areas throughout North America, while the B. gilchristii strains were restricted to Canada and some northern US states. Furthermore, the populations of both species were associated with major freshwater drainage basins. The four B. dermatitidis populations were partitioned among (1) the Nelson River drainage basin, (2) the St. Lawrence River and northeast Atlantic Ocean Seaboard drainage basins, (3) the Mississippi River System drainage basin, and (4) the Gulf of Mexico Seaboard and southeast Atlantic Ocean Seaboard drainage basins. A similar partitioning of the B. gilchristii populations was observed among the more northerly drainage basins only. These associations suggest that the ecologic niche where the sexual reproduction, growth, and dispersal of B. dermatitidis and B. gilchristii occur is intimately linked to freshwater systems. For most populations, sexual reproduction was rare enough to produce significant linkage disequilibrium among loci but frequent enough that mating-type idiomorphic ratios were not skewed from 1:1. Furthermore, the evolutionary divergence of B. dermatitidis and B. gilchristii was estimated at 1.9 MYA during the Pleistocene epoch. We suggest that repeated glaciations during the Pleistocene period and resulting biotic refugia may have provided the impetus for speciation as theorized for other species associated with temperate freshwater systems.

Fungal Mimicry of a Mammalian Aminopeptidase Disables Innate Immunity and Promotes Pathogenicity.

Systemic fungal infections trigger marked immune-regulatory disturbances, but the mechanisms are poorly understood. We report that the pathogenic yeast of Blastomyces dermatitidis elaborates dipeptidyl-peptidase IVA (DppIVA), a close mimic of the mammalian ectopeptidase CD26, which modulates critical aspects of hematopoiesis. We show that, like the mammalian enzyme, fungal DppIVA cleaved C-C chemokines and GM-CSF. Yeast producing DppIVA crippled the recruitment and differentiation of monocytes and prevented phagocyte activation and ROS production. Silencing fungal DppIVA gene expression curtailed virulence and restored recruitment of CCR2(+) monocytes, generation of TipDC, and phagocyte killing of yeast. Pharmacological blockade of DppIVA restored leukocyte effector functions and stemmed infection, while addition of recombinant DppIVA to gene-silenced yeast enabled them to evade leukocyte defense. Thus, fungal DppIVA mediates immune-regulatory disturbances that underlie invasive fungal disease. These findings reveal a form of molecular piracy by a broadly conserved aminopeptidase during disease pathogenesis.

The Dynamic Genome and Transcriptome of the Human Fungal Pathogen Blastomyces and Close Relative Emmonsia.

Three closely related thermally dimorphic pathogens are causal agents of major fungal diseases affecting humans in the Americas: blastomycosis, histoplasmosis and paracoccidioidomycosis. Here we report the genome sequence and analysis of four strains of the etiological agent of blastomycosis, Blastomyces, and two species of the related genus Emmonsia, typically pathogens of small mammals. Compared to related species, Blastomyces genomes are highly expanded, with long, often sharply demarcated tracts of low GC-content sequence. These GC-poor isochore-like regions are enriched for gypsy elements, are variable in total size between isolates, and are least expanded in the avirulent B. dermatitidis strain ER-3 as compared with the virulent B. gilchristii strain SLH14081. The lack of similar regions in related species suggests these isochore-like regions originated recently in the ancestor of the Blastomyces lineage. While gene content is highly conserved between Blastomyces and related fungi, we identified changes in copy number of genes potentially involved in host interaction, including proteases and characterized antigens. In addition, we studied gene expression changes of B. dermatitidis during the interaction of the infectious yeast form with macrophages and in a mouse model. Both experiments highlight a strong antioxidant defense response in Blastomyces, and upregulation of dioxygenases in vivo suggests that dioxide produced by antioxidants may be further utilized for amino acid metabolism. We identify a number of functional categories upregulated exclusively in vivo, such as secreted proteins, zinc acquisition proteins, and cysteine and tryptophan metabolism, which may include critical virulence factors missed before in in vitro studies. Across the dimorphic fungi, loss of certain zinc acquisition genes and differences in amino acid metabolism suggest unique adaptations of Blastomyces to its host environment. These results reveal the dynamics of genome evolution and of factors contributing to virulence in Blastomyces.

Could Histoplasma capsulatum Be Related to Healthcare-Associated Infections?

Healthcare-associated infections (HAI) are described in diverse settings. The main etiologic agents of HAI are bacteria (85%) and fungi (13%). Some factors increase the risk for HAI, particularly the use of medical devices; patients with severe cuts, wounds, and burns; stays in the intensive care unit, surgery, and hospital reconstruction works. Several fungal HAI are caused by Candida spp., usually from an endogenous source; however, cross-transmission via the hands of healthcare workers or contaminated devices can occur. Although other medically important fungi, such as Blastomyces dermatitidis, Paracoccidioides brasiliensis, and Histoplasma capsulatum, have never been considered nosocomial pathogens, there are some factors that point out the pros and cons for this possibility. Among these fungi, H. capsulatum infection has been linked to different medical devices and surgery implants. The filamentous form of H. capsulatum may be present in hospital settings, as this fungus adapts to different types of climates and has great dispersion ability. Although conventional pathogen identification techniques have never identified H. capsulatum in the hospital environment, molecular biology procedures could be useful in this setting. More research on H. capsulatum as a HAI etiologic agent is needed, since it causes a severe and often fatal disease in immunocompromised patients.

Thermally Dimorphic Human Fungal Pathogens--Polyphyletic Pathogens with a Convergent Pathogenicity Trait.

Fungi are adept at changing their cell shape and developmental program in response to signals in their surroundings. Here we focus on a group of evolutionarily related fungal pathogens of humans known as the thermally dimorphic fungi. These organisms grow in a hyphal form in the environment but shift their morphology drastically within a mammalian host. Temperature is one of the main host signals that initiates their conversion to the "host" form and is sufficient in the laboratory to trigger establishment of this host-adapted developmental program. Here we discuss the major human pathogens in this group, which are Blastomyces dermatiditis, Coccidioides immitis/posadasii, Histoplasma capsulatum, Paracoccidioides brasiliensis/lutzii, Sporothrix schenckii, and Talaromyces marneffei (formerly known as Penicillium marneffei). The majority of these organisms are primary pathogens, with the ability to cause disease in healthy humans who encounter them in endemic areas.

Uncontrolled pneumonia in a 49-year-old white man.

PATIENT: A 49-year-old white man. CHIEF COMPLAINT: Shortness of breath, fever, and ongoing unintended weight loss. HISTORY OF PRESENT ILLNESS: The patient had arrived at the emergency department of a hospital in St. Augustine, Florida with coughing and progressive shortness of breath. He reported that he had been experiencing these symptoms for the past 6 weeks. He was examined by his primary physician, who had prescribed him a course of antibiotics and treated him on an outpatient basis. The patient reported no improvement in his symptoms at present, despite the antibiotics. He mentioned that he had traveled to St. Augustine, Florida approximately 10 days previously. Medical personnel in the emergency department subsequently performed a chest x-ray on the patient, as well as computed tomography (CT) scanning of his lymphadenopathy. MEDICAL AND FAMILY HISTORY: Positive for hypertension, diabetes mellitus, and osteoporosis. He reported that he has chewed 2 packs of chewing tobacco per day for the past 30 years, occasionally drinks alcohol, and is a nonsmoker with no known allergies. FAMILY HISTORY: Noncontributory. SOCIAL HISTORY: Noncontributory. PHYSICAL EXAMINATION RESULTS: The patient exhibited mild respiratory distress; however, he was awake, alert, and oriented, with a temperature of 37.3°C. He also exhibited poor respiratory effort with diffuse expiratory rhonchi. His heart rate and heart rhythm were regular, with no murmurs, gallops, or rubs. His bowel sounds were positive; he exhibited no organomegaly and no cyanosis, clubbing, or edema of his extremities.

N-acetylglucosamine (GlcNAc) triggers a rapid, temperature-responsive morphogenetic program in thermally dimorphic fungi.

The monosaccharide N-acetylglucosamine (GlcNAc) is a major component of microbial cell walls and is ubiquitous in the environment. GlcNAc stimulates developmental pathways in the fungal pathogen Candida albicans, which is a commensal organism that colonizes the mammalian gut and causes disease in the setting of host immunodeficiency. Here we investigate GlcNAc signaling in thermally dimorphic human fungal pathogens, a group of fungi that are highly evolutionarily diverged from C. albicans and cause disease even in healthy individuals. These soil organisms grow as polarized, multicellular hyphal filaments that transition into a unicellular, pathogenic yeast form when inhaled by a human host. Temperature is the primary environmental cue that promotes reversible cellular differentiation into either yeast or filaments; however, a shift to a lower temperature in vitro induces filamentous growth in an inefficient and asynchronous manner. We found GlcNAc to be a potent and specific inducer of the yeast-to-filament transition in two thermally dimorphic fungi, Histoplasma capsulatum and Blastomyces dermatitidis. In addition to increasing the rate of filamentous growth, micromolar concentrations of GlcNAc induced a robust morphological transition of H. capsulatum after temperature shift that was independent of GlcNAc catabolism, indicating that fungal cells sense GlcNAc to promote filamentation. Whole-genome expression profiling to identify candidate genes involved in establishing the filamentous growth program uncovered two genes encoding GlcNAc transporters, NGT1 and NGT2, that were necessary for H. capsulatum cells to robustly filament in response to GlcNAc. Unexpectedly, NGT1 and NGT2 were important for efficient H. capsulatum yeast-to-filament conversion in standard glucose medium, suggesting that Ngt1 and Ngt2 monitor endogenous levels of GlcNAc to control multicellular filamentous growth in response to temperature. Overall, our work indicates that GlcNAc functions as a highly conserved cue of morphogenesis in fungi, which further enhances the significance of this ubiquitous sugar in cellular signaling in eukaryotes.

Structure and function of a fungal adhesin that binds heparin and mimics thrombospondin-1 by blocking T cell activation and effector function.

Blastomyces adhesin-1 (BAD-1) is a 120-kD surface protein on B. dermatitidis yeast. We show here that BAD-1 contains 41 tandem repeats and that deleting even half of them impairs fungal pathogenicity. According to NMR, the repeats form tightly folded 17-amino acid loops constrained by a disulfide bond linking conserved cysteines. Each loop contains a highly conserved WxxWxxW motif found in thrombospondin-1 (TSP-1) type 1 heparin-binding repeats. BAD-1 binds heparin specifically and saturably, and is competitively inhibited by soluble heparin, but not related glycosaminoglycans. According to SPR analysis, the affinity of BAD-1 for heparin is 33 nM±14 nM. Putative heparin-binding motifs are found both at the N-terminus and within each tandem repeat loop. Like TSP-1, BAD-1 blocks activation of T cells in a manner requiring the heparan sulfate-modified surface molecule CD47, and impairs effector functions. The tandem repeats of BAD-1 thus confer pathogenicity, harbor motifs that bind heparin, and suppress T-cell activation via a CD47-dependent mechanism, mimicking mammalian TSP-1.

Tc17 cells mediate vaccine immunity against lethal fungal pneumonia in immune deficient hosts lacking CD4+ T cells.

Vaccines may help reduce the growing incidence of fungal infections in immune-suppressed patients. We have found that, even in the absence of CD4(+) T-cell help, vaccine-induced CD8(+) T cells persist and confer resistance against Blastomyces dermatitidis and Histoplasma capsulatum. Type 1 cytokines contribute to that resistance, but they also are dispensable. Although the role of T helper 17 cells in immunity to fungi is debated, IL-17 producing CD8(+) T cells (Tc17 cells) have not been investigated. Here, we show that Tc17 cells are indispensable in antifungal vaccine immunity in hosts lacking CD4(+) T cells. Tc17 cells are induced upon vaccination, recruited to the lung on pulmonary infection, and act non-redundantly in mediating protection in a manner that requires neutrophils. Tc17 cells did not influence type I immunity, nor did the lack of IL-12 signaling augment Tc17 cells, indicating a distinct lineage and function. IL-6 was required for Tc17 differentiation and immunity, but IL-1R1 and Dectin-1 signaling was unexpectedly dispensable. Tc17 cells expressed surface CXCR3 and CCR6, but only the latter was essential in recruitment to the lung. Although IL-17 producing T cells are believed to be short-lived, effector Tc17 cells expressed low levels of KLRG1 and high levels of the transcription factor TCF-1, predicting their long-term survival and stem-cell like behavior. Our work has implications for designing vaccines against fungal infections in immune suppressed patients.

Blastomycosis presenting as a nonhealing wound.

A 41-year-old man was referred to the wound clinic for an enlarging 9.5 x 14-cm ulceration of the right upper arm of 8 months' duration. A biopsy was obtained, and fungal stains showed broad-based budding spores typical of blastomycosis. He was treated with oral itraconazole, and the ulcer healed in 2 months. Blastomycosis is a systemic fungal infection acquired by inhalation of the spores of the fungus Blastomyces dermatitidis. Initially a pulmonary infection, the skin is the most common secondary site of involvement. More typically presenting as hyperkeratotic nodules, it may occur as ulcerations. Blastomycosis has significant morbidity and mortality, and in unsuspected or asymptomatic cases, the skin lesions may be the key to successful diagnosis and treatment.

Pulmonary blastomycosis.

Blastomyces dermatitidis is acquired in almost all cases via inhalation, and pulmonary disease is the most frequent clinical manifestation of blastomycosis. Pulmonary disease can range from asymptomatic infection to rapidly severe and fatal disease. Most cases will present as pneumonia, either acute or chronic, or as a lung mass. In rare cases pulmonary blastomycosis is associated with the acute respiratory distress syndrome. Blastomycosis can present as isolated pulmonary disease or along with coexisting extrapulmonary disease that usually will involve the skin, bony structures, genitourinary tract, or central nervous system. Diagnosis is largely based on isolation of the organism via culture or visualization of the organism in clinical specimens. Detection of urinary Blastomyces antigen is a recent addition to diagnostic options. Itraconazole is the drug of choice for most forms of the disease; amphotericin B is reserved for the more severe forms. Newer azoles such as voriconazole and posaconazole have a limited role in the treatment of pulmonary blastomycosis.

Blastomycosis in man after kinkajou bite.

We report transmission of Blastomyces dermatitidis fungal infection from a pet kinkajou to a man. When treating a patient with a recalcitrant infection and a history of an animal bite, early and complete animal necropsy and consideration of nonbacterial etiologies are needed.

Blastomicosis: presentación de un caso importado en México, con lesiones exclusivamente cutáneas / Blastomycosis: report of an imported case in Mexico, with only cutaneous lesions

Antecedentes. La blastomicosis es una enfermedad infecciosa granulomatosa, causada por el hongo dimorfo Blastomyces dermatitidis. Predomina en Estados Unidos de América, y en México solo se han reportado 2 casos sistémicos importados. La forma primaria cutánea es la presentación clínica menos frecuente de la enfermedad y ocurre después de la inoculación del hongo por traumatismo. Objetivos. Se presenta el caso de un hombre de 54 años de edad, originario de Guadalajara, México, y residente en Chicago, Estados Unidos. Presentaba en la región frontal y surco nasogeniano derecho 2 nódulos verrugosos de 8mm de diámetro de 4 semanas de evolución. Métodos. Se realizó un estudio histopatológico (tinciones de hematoxilina-eosina, Gomori-Grocott y ácido peryódico de Schiff), además, estudio micológico (directo con KOH y cultivos en agar Sabouraud y micobiótico). Además, se realizaron otros estudios que descartaron afección sistémica. Resultados. La biopsia mostró una dermis con infiltrado inflamatorio compuesto por linfocitos, neutrófilos, histiocitos y células gigantes multinucleadas, y escasas levaduras monogemantes con base ancha y rodeadas por un halo. Al examen directo con KOH, se observaron levaduras monogemantes de 8 a 10mm de diámetro de B. dermatitidis. En el cultivo a 35°C creció una colonia blanca, plegada que, con el tiempo, se tornó amarillenta y cerebriforme. Resultados. Se indicó tratamiento con itraconazol a dosis de 200mg/d durante 2 meses con curación clínica y micológica. Conclusiones. El caso presentado podría ser el primero importado en México donde la blastomicosis se presenta solo con lesiones cutáneas y sin compromiso sistémico(AU)

Background. Blastomycosis is a granulomatous infectious disease. It is caused by the dimorphus fungus Blastomyces dermatitidis. It predominates in the United States of America, but in Mexico two systemic imported cases have been reported. Cutaneous primary blastomycosis is a rare clinical presentation, which occurs after traumatic inoculation of the fungus. Objectives. We present a case of a 54 year old male, born in Guadalajara, Mexico, and living in Chicago, USA, who had two verrucous nodules (8mm in diameter) on the forehead and right nasogenian fold, of 4 weeks progression. Methods. We made a histopathological study (hematoxylin and eosin, Gomori Groccot and periodic acid-Schiff stains) and mycology studies (direct microscopic examination, Sabouraud and mycobiotic agar cultures). Multiple studies were made with no evidence of systemic spread. Results. Biopsy showed a dermal inflammatory infiltrate made up of lymphocytes, neutrophils, histiocytes and multinucleated giant cells. A few large, haloed, broad-based budding yeasts were also observed. Direct examination with KOH revealed broad-based budding yeasts, 10ìm in diameter. Culture at 35°C yielded a white, pleated colony, which changed into a yellowish cerebriform. Multiple studies were made with no evidence of systemic spread. Results. Itraconazole 200mg qd PO was given over a 2 month period, with a complete clinical and mycological response. Conclusions. This is the first imported case in Mexico of blastomycosis with cutaneous lesions without systemic involvement(AU)