<i>In vitro</i> activity of 4 antifungal drugs against planktonic cells of 54 clinical isolates of <i>Trichosporon</i> spp. according to the isolation site.

<p>MIC₅₀: Minimal inhibitory concentration capable of inhibiting growth of 50% of isolates.</p><p>MIC₉₀: Minimal inhibitory concentration capable of inhibiting growth of 90% of isolates.</p><p>GM: Geometric Mean.</p><p><i>In vitro</i> activity of 4 antifungal drugs against planktonic cells of 54 clinical isolates of <i>Trichosporon</i> spp. according to the isolation site.</p

Scanning electron microscopy of 4 <i>Trichosporon</i> spp. strains grown on catheter surfaces.

<p><b>A</b> and <b>B</b>: Low biofilm producer <i>T. asahii</i> 05-001 (CV-A₅₇₀  =  0.287); <b>C</b> and <b>D</b>: Medium biofilm producer <i>T. asahii</i> 18-001 (CV-A₅₇₀  =  1.557); <b>E</b> and <b>F</b>: High biofilm producer <i>T. asahii</i> 07-001A (CV-A₅₇₀  =  3.337); and <b>G</b> and <b>H</b>: High biofilm producer <i>T. asteroides</i> 13-001 (CV-A₅₇₀  =  2.755).</p

Species distribution of 54 <i>Trichosporon</i> spp. clinical isolates according to the site of infection or colonization identifiyed by IGS1 rDNA sequencing.

<p>Species distribution of 54 <i>Trichosporon</i> spp. clinical isolates according to the site of infection or colonization identifiyed by IGS1 rDNA sequencing.</p

Inter and intra species variation in the biofilm production of 54 <i>Trichosporon</i> spp. clinical isolates and 7 reference strains.

<p><b>A-</b> 19 isolates from blood identified as <i>T. asahii, T. asteroides, T. coremiiforme</i> and <i>T. dermatis</i>. <b>B-</b> 20 isolates from urine identified as <i>T. asahii</i>. <b>C-</b> 15 isolates from superficial mycosis/skin colonization identified as <i>T. asahii, T. dermatis, T. faecale</i> and <i>T. inkin</i>. <b>D-</b> 7 reference strains from CBS obtained from different sources.</p

Comparative analysis of MIC values obtained against planktonic cells of <i>T. asahii</i> (36 isolates) <i>versus</i> non-<i>T. asahii</i> (18) isolates for all antifungals tested.

<p><b>A-</b> Fluconazole; <b>B-</b> Itraconazole<b>; C-</b> Voriconazole and D- Amphotericin B.</p

<i>In vitro</i> activity of 4 antifungal drugs against biofilm forming cells of 54 clinical isolates of <i>Trichosporon</i> spp.

<p>MIC₅₀: Minimal inhibitory concentration capable of inhibiting growth of 50% of isolates.</p><p>MIC₉₀: Minimal inhibitory concentration capable of inhibiting growth of 90% of isolates.</p><p><i>In vitro</i> activity of 4 antifungal drugs against biofilm forming cells of 54 clinical isolates of <i>Trichosporon</i> spp.</p

<i>In vitro</i> susceptibility of 47 <i>Candida</i> spp. strains against 4 antifungal agents.

<p><i>In vitro</i> susceptibility of 47 <i>Candida</i> spp. strains against 4 antifungal agents.</p

Demographics and clinical characteristics of the 137 patients with <i>Candida</i> spp. monomicrobial nosocomial bloodstream infections.

<p>Demographics and clinical characteristics of the 137 patients with <i>Candida</i> spp. monomicrobial nosocomial bloodstream infections.</p

Crude mortality of patients with candidemia stratified by venue.

<p>Crude mortality of patients with candidemia stratified by venue.</p

Brazilian guidelines for the clinical management of paracoccidioidomycosis

<div><p>Abstract Paracoccidioidomycosis is a systemic fungal disease occurring in Latin America that is associated with rural environments and agricultural activities. However, the incidence and prevalence of paracoccidiodomycosis is underestimated because of the lack of compulsory notification. If paracoccidiodomycosis is not diagnosed and treated early and adequately, the endemic fungal infection could result in serious sequelae. While the Paracoccidioides brasiliensis ( P. brasiliensis ) complex has been known to be the causal agent of paracoccidiodomycosis, a new species, Paracoccidioides lutzii ( P. lutzii ), has been reported in Rondônia, where the disease has reached epidemic levels, and in the Central West and Pará. Accurate diagnoses and availability of antigens that are reactive with the patients’ sera remain significant challenges. Therefore, the present guidelines aims to update the first Brazilian consensus on paracoccidioidomycosis by providing evidence-based recommendations for bedside patient management. This consensus summarizes etiological, ecoepidemiological, molecular epidemiological, and immunopathological data, with emphasis on clinical, microbiological, and serological diagnosis and management of clinical forms and sequelae, as well as in patients with comorbidities and immunosuppression. The consensus also includes discussion of outpatient treatments, severe disease forms, disease prevalence among special populations and resource-poor settings, a brief review of prevention and control measures, current challenges and recommendations.</p></div