We studied 23 clinical and environmental strains of Sporothrix schenckii sensu lato collected from 1984 to 2017 in Argentina. The molecular identification (partial sequencing of a fragment of the calmodulin gene) of the strains was performed. For the yeast and mycelial phases, the in vitro susceptibility testing by a microdilution reference method was determined against eight antifungal drugs. Strains studied were identified as S. schenckii sensu stricto 13 (56.5%), S. brasiliensis 8 (34.7%) and S. globosa 2 (8.7%). The most active antifungal drugs tested for the yeast and mycelial phases expressed as geometric mean (GM) value of the minimal inhibitory concentration (MIC) (μg mL ) were terbinafine (0.07 and 0.24), posaconazole (0.13 and 0.58), itraconazole (0.38 and 1.10) and ketoconazole (0.22 and 0.89), while fluconazole (110.10 and 131.92) and flucytosine (2.96 and 79.03) were the less active. For voriconazole and amphotericin B the GM-MIC values were acceptably low for the yeast phase (0.39 and 0.72 μg mL ), while the mycelial phase showed values ≥2-fold higher (8.76 and 1.88 μg mL ), P < .05. Here, we described S. schenckii sensu stricto, S. brasiliensis and S. globosa, these species were isolated from humans, animals and soil and are circulating in Argentina since at least 1984.

Trichosporon species are emerging causative agents of mycoses; most are documented in immunocompromised patients. Species identification is important for epidemiological purposes in order to better define species clinical associations and to improve antifungal treatment. Here, we studied a collection of 41 Trichosporon strains recovered from hospitalized patients in Argentina. All strains were identified by sequencing the D1/D2 domain of 26S, internal transcribed spacer (ITS) regions, and intergenic spacer 1 (IGS1) region. In addition, we determined the IGS1 region genotypes of the suspected T. asahii strains. Antifungal susceptibility of all strains was investigated. Thirty-eight of the 41 strains in this study were identified as follows: 29 T. asahii, 3 T. inkin, 3 T. montevideense, 2 T. faecale, and 1 T. dermatis. The identity of the three remaining strains could not be confirmed. Strain DMic 114126 (Culture collection of the Mycology Department (DMic), National Institute of Infectious Diseases "Dr. Carlos G. Malbrán".) may represent a T. asahii subspecies or a new Trichosporon species, strain DMic 94750 was identified as T. cf. guehoae and strain DMic 114132 as T. cf. akiyoshidainum. The distribution of T. asahii genotypes was as follows: 12 genotype 3, 9 genotype 1, 4 genotype 4, 2 genotype 5, and 2 genotype 7. Amphotericin B minimal inhibitory concentrations (MICs) were ≤1 mg/l for 78% (32/41) of the strains. Fluconazole MICs were ≥2 mg/l for 90% of the strains. However, itraconazole, voriconazole, ketoconazole, and posaconazole MICs were ≤1 mg/l for 100% of the strains. Terbinafine MICs were ≤1 mg/l for 98% 40/41 of the strains.

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We report the first case of blood infection due to Pseudozyma aphidis in Latin America. We contribute evidence showing this organism to be a potential human pathogen, and we provide new data about its identification, drug susceptibility, and treatment outcome. CASE REPORTA 6-year-old female from Córdoba, Argentina, was diagnosed with osteosarcoma of the left tibia and lung metastasis and started chemotherapy administered through a long-term indwelling central line (a central venous catheter [CVC]) on 2 September 2013 at the Hospital de niños de la Santísima Trinidad. On 2 October, she presented with febrile neutropenia and was empirically treated with ceftazidime, vancomycin, and amikacin; blood and urine samples were submitted for laboratory testing, and both cultures were negative. On 4 October, she received clindamycin due to facial edema. From 6 October to 13 November, she was transfused with platelets and red blood cells several times due to thrombocytopenia and anemia. On 5 November, she developed severe mucositis and erythroderma and was treated with ceftazidime, nystatin, amikacin, vancomycin, and fluconazole. On 13 November, she received a 1-week treatment with meropenem and liposomal amphotericin B. On 18 November, she developed conjunctival hyperemia and was treated with tobramycin. On 28 November, she underwent supracondylar amputation of the left lower limb. On 20 December, the patient presented with febrile neutropenia (white blood cells [WBCs], 1,030/mm 3 ) and was admitted to the intensive care unit (ICU) in the same hospital. Table 1 summarizes the clinical data and evolution of the case since admission. A blood sample (BS1) obtained by venipuncture and a hub blood sample (drawn through the catheter hub) (HBS1) were taken and sent to the microbiology laboratory. Yeast cells (Pseudozyma aphidis; isolate Y1) were detected in the hub blood sample after 2.6 days of incubation in a Bact/ALERT PF (bioMérieux Inc., Durham, NC). However, the patient did not show clinical signs of illness on day 3 after admission; therefore, the isolate was considered not significant and she was discharged. Four days later, the patient presented with vomiting, dehydration, and febrile neutropenia (WBCs, 200/mm 3 ) and was admitted once again at the ICU in the same institution. At that point, an empirical antibiotic treatment with ceftazidime and amikacin was initiated and a new blood sample and hub blood sample (BS2 and HBS2) were taken and processed. After 18 h of incubation, both cultures were positive for Pseudomonas aeruginosa. Four days after readmission, the patient presented with fever and severe neutropenia (WBCs, 80/ mm 3 ) and showed high (233 mg/liter) C-reactive protein levels. A blood sample and a hub blood sample (BS3 and HBS3) were taken and processed. After 12 h of incubation, the blood sample culture was positive for Escherichia coli, and 2 h later, the hub blood sample culture was positive for yeast (Y2). This isolate (Y2) had the same phenotypic features as the first yeast isolate (Y1). Six days after...

The molecular basis of fluconazole resistance in Cryptococcus neoformans has been poorly studied. A common azole resistance mechanism in Candida species is the acquisition of point mutations in the ERG11 gene encoding the enzyme lanosterol 14-α-demethylase, target of the azole class of drugs. In C. neoformans only two mutations were described in this gene. In order to evaluate other mutations that could be implicated in fluconazole resistance in C. neoformans we studied the genomic sequence of the ERG11 gene in 11 clinical isolates with minimal inhibitory concentration (MIC) values to fluconazole of ≥16μg/ml. The sequencing revealed the G1855A mutation in 3 isolates, resulting in the enzyme amino acid substitution G484S. These strains were isolated from two fluconazole-treated patients. This mutation would not intervene in the susceptibility to itraconazole and voriconazole.