13 results on '"Fadda, Giovanni"'
Search Results
2. Genome-wide expression profiling of the response to short-term exposure to fluconazole in Cryptococcus neoformans serotype A.
- Author
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Florio AR, Ferrari S, De Carolis E, Torelli R, Fadda G, Sanguinetti M, Sanglard D, and Posteraro B
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- Cryptococcus neoformans physiology, Gene Expression Profiling, Humans, Stress, Physiological, Antifungal Agents pharmacology, Cryptococcus neoformans drug effects, Cryptococcus neoformans genetics, Fluconazole pharmacology, Gene Expression Regulation, Fungal
- Abstract
Background: Fluconazole (FLC), a triazole antifungal drug, is widely used for the maintenance therapy of cryptococcal meningoencephalitis, the most common opportunistic infection in AIDS patients. In this study, we examined changes in the gene expression profile of the C. neoformans reference strain H99 (serotype A) following FLC treatment in order to investigate the adaptive cellular responses to drug stress., Results: Simultaneous analysis of over 6823 transcripts revealed that 476 genes were responsive to FLC. As expected up-regulation of genes involved in ergosterol biosynthesis was observed, including the azole target gene ERG11 and ERG13, ERG1, ERG7, ERG25, ERG2, ERG3 and ERG5. In addition, SRE1 which is a gene encoding a well-known regulator of sterol homeostasis in C. neoformans was up-regulated. Several other genes such as those involved in a variety of important cellular processes (i.e. lipid and fatty acid metabolism, cell wall maintenance, stress and virulence) were found to be up-regulated in response to FLC treatment. Conversely, expression of AFR1, the major transporter of azoles in C. neoformans, was not regulated by FLC., Conclusions: Short-term exposure of C. neoformans to FLC resulted in a complex altered gene expression profile. Some of the observed changes could represent specific adaptive responses to the antifungal agent in this pathogenic yeast.
- Published
- 2011
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3. Synthesis of new antifungal peptides selective against Cryptococcus neoformans.
- Author
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Grimaldi M, De Rosa M, Di Marino S, Scrima M, Posteraro B, Sanguinetti M, Fadda G, Soriente A, and D'Ursi AM
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- Amino Acid Sequence, Antifungal Agents chemistry, Antifungal Agents pharmacology, Antimicrobial Cationic Peptides chemistry, Antimicrobial Cationic Peptides pharmacology, Circular Dichroism, Cryptococcus neoformans enzymology, Enzyme Inhibitors chemistry, Enzyme Inhibitors pharmacology, Fungal Proteins metabolism, Microbial Sensitivity Tests, Protein Structure, Secondary, Antifungal Agents chemical synthesis, Antimicrobial Cationic Peptides chemical synthesis, Cryptococcus neoformans drug effects, Enzyme Inhibitors chemical synthesis, Fungal Proteins antagonists & inhibitors
- Abstract
Many drugs are available for the treatment of systemic or superficial mycoses, but only a limited number of them are effective antifungal drugs, devoid of toxic and undesirable side effects. Furthermore, resistance development and fungistatic rather than fungicidal activities represent limitations of current antifungal therapy. Therefore there remains an urgent need for a new generation of antifungal agents. According to a polypharmacological approach, the present work concerns the synthesis and antifungal activity of a set of peptides designed to simultaneously target the fungal cell surface and lanosterol demethylase, a key enzyme involved in ergosterol synthesis. Our peptides include amino acid sequences characteristic of membrane-active antimicrobial peptides (AMP), and due to the presence of His residues, they carry the imidazole ring characteristic of azole compounds. The peptides synthesized by us, were tested against different yeast species, and displayed general antifungal activity, with a therapeutically promising antifungal specificity against Cryptococcus neoformans., (Copyright © 2010 Elsevier Ltd. All rights reserved.)
- Published
- 2010
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4. Early mannan detection in bronchoalveolar lavage fluid with preemptive treatment reduces the incidence of invasive Candida infections in preterm infants.
- Author
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Posteraro B, Sanguinetti M, Boccia S, De Feo E, La Sorda M, Tana M, Tirone C, Aurilia C, Vendettuoli V, Fadda G, Romagnoli C, and Vento G
- Subjects
- Candida isolation & purification, Female, Humans, Incidence, Infant, Male, Premature Birth, Antifungal Agents therapeutic use, Bronchoalveolar Lavage Fluid chemistry, Candidiasis diagnosis, Candidiasis drug therapy, Mannans analysis
- Abstract
Background: Candida colonization is an important predictor for development of invasive fungal infection (IFI). We investigated whether early detection of Candida mannan (Mn) in bronchoalveolar lavage fluid (BALF) reduces IFI among preterm infants., Methods: We conducted an observational study of infants with gestational age of < or =28 weeks, where a group undergoing Candida surveillance cultures (pre-Mn detection group) was compared with a group defined after the initiation of routine use of Candida Mn detection in BALF (Mn detection group). Antifungal treatment was started based on positive microbiologic (surveillance culture or Mn-antigen assay) results., Results: No significant differences were detected when the groups were compared for several predictors of IFI. IFI was observed for 12 (23%) of 51 infants in the pre-Mn detection group, and for 0 (0%) of 29 infants in the Mn detection group (P = 0.003). Surveillance cultures in the pre-Mn detection group became positive at 15.0 +/- 7.2 days after birth, whereas the mean age at time of positive Mn antigen results in the Mn detection group was 4.3 +/- 3.1 days (P < 0.0001). Among 16 infants positive for surveillance cultures, 12 (75%) developed IFI (P < 0.0001)., Conclusions: This study suggests that Candida Mn detection in BALF may be useful for earlier identification and preemptive therapy targeting preterm infants at high risk of IFI.
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- 2010
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5. Reliability of the Vitek 2 yeast susceptibility test for detection of in vitro resistance to fluconazole and voriconazole in clinical isolates of Candida albicans and Candida glabrata.
- Author
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Posteraro B, Martucci R, La Sorda M, Fiori B, Sanglard D, De Carolis E, Florio AR, Fadda G, and Sanguinetti M
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- Candida albicans isolation & purification, Candida glabrata isolation & purification, Candidiasis microbiology, Drug Resistance, Fungal, Humans, Microbial Sensitivity Tests methods, Sensitivity and Specificity, Voriconazole, Antifungal Agents pharmacology, Candida albicans drug effects, Candida glabrata drug effects, Fluconazole pharmacology, Pyrimidines pharmacology, Triazoles pharmacology
- Abstract
The Vitek 2 yeast susceptibility test was evaluated by testing 122 Candida isolates against fluconazole and voriconazole. Excellent categorical agreement with the CLSI broth microdilution method was observed (97.5% for both the azoles). Moreover, the Vitek 2 system was able to identify all but 2 of 59 investigated fluconazole-resistant organisms.
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- 2009
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6. Fungaemia caused by Candida glabrata with reduced susceptibility to fluconazole due to altered gene expression: risk factors, antifungal treatment and outcome.
- Author
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Tumbarello M, Sanguinetti M, Trecarichi EM, La Sorda M, Rossi M, de Carolis E, de Gaetano Donati K, Fadda G, Cauda R, and Posteraro B
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- Aged, Antifungal Agents pharmacology, Candida glabrata isolation & purification, Candidiasis epidemiology, Candidiasis mortality, Case-Control Studies, Female, Fluconazole pharmacology, Fungal Proteins biosynthesis, Fungemia epidemiology, Fungemia mortality, Gene Expression Profiling, Humans, Male, Membrane Transport Proteins biosynthesis, Middle Aged, Multivariate Analysis, Reverse Transcriptase Polymerase Chain Reaction, Risk Factors, Treatment Outcome, Antifungal Agents therapeutic use, Candida glabrata drug effects, Candidiasis drug therapy, Candidiasis microbiology, Drug Resistance, Fungal, Fluconazole therapeutic use, Fungemia drug therapy, Fungemia microbiology
- Abstract
Background: The role of Candida glabrata in fungaemia is attributed in part to its reduced susceptibility to azoles, usually due to altered expression of genes encoding drug efflux pumps. The aims of this study were to identify risk factors for fungaemia due to C. glabrata isolates with decreased susceptibility to fluconazole and to analyse the response to antifungal treatment and the clinical outcome of C. glabrata infections in hospitalized patients., Methods: A retrospective case-case-control study was conducted at a university hospital from 2000 to 2006. Three patient groups were studied: 14 patients infected by a fluconazole-less-susceptible isolate [susceptible-dose-dependent (SDD) or resistant]; 21 patients infected by a fluconazole-susceptible (FS) isolate; and 70 uninfected controls. We measured expression of the drug efflux pump-encoding CgCDR1 and CgCDR2 genes in isolates of the two infected groups using quantitative real-time PCR., Results: Multivariable analysis found that patients with prior fluconazole use [odds ratio (OR) 12.24, 95% confidence intervals (CIs) 1.77-84.39, P = 0.01], diabetes (OR 10.47, 95% CI 1.96-55.96, P = 0.006) and a central venous catheter (CVC) (OR 8.48, 95% CI 1.82-39.36, P = 0.006) were more likely to develop fungaemia due to a less-susceptible isolate. Previous surgery (OR 7.73, 95% CI 2.18-27.41, P = 0.002) was an independent risk factor for fungaemia due to a susceptible isolate, in addition to the presence of a CVC (OR 5.48, 95% CI 1.69-17.72, P = 0.004). The crude 30 day mortality rate was high for both case groups. Seven patients received inadequate antifungal treatment, including five infected by a fluconazole-resistant isolate but empirically treated with fluconazole; six of these seven patients died. Expression of the CgCDR genes was up-regulated in all fluconazole-resistant and, to a lesser extent, SDD isolates, but not in the FS isolates., Conclusions: Our data suggest that when candidaemia is suspected or detected, a more broad-spectrum antifungal drug (i.e. echinocandins or amphotericin B) should be considered as initial treatment for patients with prior azole exposure.
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- 2008
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7. The role of Candida surveillance cultures for identification of a preterm subpopulation at highest risk for invasive fungal infection.
- Author
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Vendettuoli V, Tana M, Tirone C, Posteraro B, La Sorda M, Fadda G, Romagnoli C, and Vento G
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- Candidiasis drug therapy, Candidiasis mortality, Case-Control Studies, Humans, Infant, Infant, Newborn, Infant, Premature, Infant, Premature, Diseases drug therapy, Infant, Premature, Diseases mortality, Infant, Very Low Birth Weight, Intensive Care Units, Neonatal, Neonatal Screening, Risk Factors, Statistics, Nonparametric, Antifungal Agents therapeutic use, Candida isolation & purification, Candidiasis diagnosis, Infant, Premature, Diseases diagnosis
- Abstract
Candida surveillance cultures were obtained from 51 neonatal intensive care unit patients. Sixteen infants showing positive cultures developed subsequent Candida infection, whereas it did not occur for the 35 infants with negative cultures. Fifteen of 16 infants (<1000 g) had <27 weeks of gestational age. Antifungal treatment was started at the time colonization was detected; only 1 infant died of Candida infection.
- Published
- 2008
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8. Caspofungin activity against clinical isolates of azole cross-resistant Candida glabrata overexpressing efflux pump genes.
- Author
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Posteraro B, Sanguinetti M, Fiori B, La Sorda M, Spanu T, Sanglard D, and Fadda G
- Subjects
- Biological Transport, Active genetics, Candida glabrata genetics, Candida glabrata metabolism, Caspofungin, Echinocandins, Gene Expression, Humans, Lipopeptides, Microbial Sensitivity Tests, RNA, Fungal analysis, Reverse Transcriptase Polymerase Chain Reaction, Antifungal Agents pharmacology, Azoles pharmacology, Candida glabrata drug effects, Drug Resistance, Fungal genetics, Peptides, Cyclic pharmacology
- Abstract
Objectives: Several studies have documented the potent in vitro activity of caspofungin against Candida spp. This is of special concern for Candida glabrata infections that are often resistant to many azole antifungal agents and, consequently, difficult to treat. The aim of the present study was to expand the data on the in vitro activity of caspofungin against azole-resistant isolates of C. glabrata., Methods: A total of 50 clinical isolates of C. glabrata were tested for susceptibility to caspofungin. The isolates were cross-resistant to multiple azoles, including fluconazole, itraconazole, ketoconazole and voriconazole. Expression of the resistance-related CgCDR1 and CgCDR2 genes was evaluated by quantitative RT-PCR analysis. The MICs of caspofungin were determined by using the National Committee for Clinical Laboratory Standards M27-A2 reference method., Results: C. glabrata isolates exhibited increased expression of the CDR efflux pump(s), and this was in accordance with their high-level azole resistance. In contrast, all the isolates were highly susceptible to caspofungin (100% of isolates were inhibited at
- Published
- 2006
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9. Role of AFR1, an ABC transporter-encoding gene, in the in vivo response to fluconazole and virulence of Cryptococcus neoformans.
- Author
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Sanguinetti M, Posteraro B, La Sorda M, Torelli R, Fiori B, Santangelo R, Delogu G, and Fadda G
- Subjects
- ATP-Binding Cassette Transporters genetics, Animals, Antifungal Agents pharmacology, Cryptococcosis microbiology, Cryptococcus neoformans drug effects, Cryptococcus neoformans growth & development, Fluconazole pharmacology, Fungal Proteins genetics, Fungal Proteins metabolism, Macrophages microbiology, Mice, Mice, Inbred C57BL, Microbial Sensitivity Tests, Mutation, Virulence, ATP-Binding Cassette Transporters metabolism, Antifungal Agents therapeutic use, Cryptococcosis drug therapy, Cryptococcus neoformans pathogenicity, Fluconazole therapeutic use
- Abstract
We have recently demonstrated that upregulation of the ATP binding cassette (ABC) transporter-encoding gene AFR1 in Cryptococcus neoformans is involved in the in vitro resistance to fluconazole of this yeast. In the present study, we investigated the role of AFR1 in the in vivo response to fluconazole in a mouse model of systemic cryptococcosis. Mice were infected with a wild-type fluconazole-susceptible strain of C. neoformans, strain BPY22; an afr1 mutant, BPY444, which displayed hypersusceptibility to fluconazole in vitro; or an AFR1-overexpressing strain, BPY445, which exhibited in vitro resistance to the drug. In each of the three groups, infected animals were randomly assigned to fluconazole treatment or untreated-control subgroups. As expected, fluconazole prolonged survival and reduced fungal tissue burdens (compared with no treatment) in BPY22- and BPY444-infected mice, whereas it had no significant effects in mice infected with BPY445. When the pathogenicities of these strains in mice were investigated, strain BPY445 was significantly more virulent than BPY22 following inhalational or intravenous inoculation, but mice infected with BPY444 survived significantly longer than BPY22-infected animals only when infection was acquired via the respiratory tract. In in vitro macrophage infection studies, strain BPY445 also displayed enhanced intracellular survival compared with strains BPY22 and BPY444, suggesting that its increased virulence may be due to its reduced vulnerability to the antimicrobial factors produced by phagocytic cells. These findings indicate that the upregulation of the AFR1 gene is an important factor in either determining the in vivo resistance to fluconazole or influencing the virulence of C. neoformans.
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- 2006
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10. Mechanisms of azole resistance in clinical isolates of Candida glabrata collected during a hospital survey of antifungal resistance.
- Author
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Sanguinetti M, Posteraro B, Fiori B, Ranno S, Torelli R, and Fadda G
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- ATP-Binding Cassette Transporters antagonists & inhibitors, Candida glabrata classification, Candida glabrata genetics, Cloning, Molecular, Data Collection, Dose-Response Relationship, Drug, Drug Resistance, Fungal, Fluconazole pharmacology, Gene Expression Regulation, Fungal drug effects, Genes, Fungal genetics, Humans, Microbial Sensitivity Tests, Phenotype, RNA, Fungal genetics, Reverse Transcriptase Polymerase Chain Reaction, Up-Regulation, Antifungal Agents pharmacology, Azoles pharmacology, Candida glabrata drug effects, Candidiasis microbiology, Cross Infection microbiology
- Abstract
The increasing use of azole antifungals for the treatment of mucosal and systemic Candida glabrata infections has resulted in the selection and/or emergence of resistant strains. The main mechanisms of azole resistance include alterations in the C. glabrata ERG11 gene (CgERG11), which encodes the azole target enzyme, and upregulation of the CgCDR1 and CgCDR2 genes, which encode efflux pumps. In the present study, we evaluated these molecular mechanisms in 29 unmatched clinical isolates of C. glabrata, of which 20 isolates were resistant and 9 were susceptible dose dependent (S-DD) to fluconazole. These isolates were recovered from separate patients during a 3-year hospital survey for antifungal resistance. Four of the 20 fluconazole-resistant isolates were analyzed together with matched susceptible isolates previously taken from the same patients. Twenty other azole-susceptible clinical C. glabrata isolates were included as controls. MIC data for all the fluconazole-resistant isolates revealed extensive cross-resistance to the other azoles tested, i.e., itraconazole, ketoconazole, and voriconazole. Quantitative real-time PCR analyses showed that CgCDR1 and CgCDR2, alone or in combination, were upregulated at high levels in all but two fluconazole-resistant isolates and, to a lesser extent, in the fluconazole-S-DD isolates. In addition, slight increases in the relative level of expression of CgSNQ2 (which encodes an ATP-binding cassette [ABC] transporter and which has not yet been shown to be associated with azole resistance) were seen in some of the 29 isolates studied. Interestingly, the two fluconazole-resistant isolates expressing normal levels of CgCDR1 and CgCDR2 exhibited increased levels of expression of CgSNQ2. Conversely, sequencing of CgERG11 and analysis of its expression showed no mutation or upregulation in any C. glabrata isolate, suggesting that CgERG11 is not involved in azole resistance. When the isolates were grown in the presence of fluconazole, the profiles of expression of all genes, including CgERG11, were not changed or were only minimally changed in the resistant isolates, whereas marked increases in the levels of gene expression, particularly for CgCDR1 and CgCDR2, were observed in either the fluconazole-susceptible or the fluconazole-S-DD isolates. Finally, known ABC transporter inhibitors, such as FK506, were able to reverse the azole resistance of all the isolates. Together, these results provide evidence that the upregulation of the CgCDR1-, CgCDR2-, and CgSNQ2-encoded efflux pumps might explain the azole resistance in our set of isolates.
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- 2005
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11. Identification and characterization of a Cryptococcus neoformans ATP binding cassette (ABC) transporter-encoding gene, CnAFR1, involved in the resistance to fluconazole.
- Author
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Posteraro B, Sanguinetti M, Sanglard D, La Sorda M, Boccia S, Romano L, Morace G, and Fadda G
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- Amino Acid Sequence, Cloning, Molecular, Cryptococcus neoformans genetics, Cryptococcus neoformans growth & development, Fungal Proteins chemistry, Fungal Proteins genetics, Fungal Proteins metabolism, Gene Deletion, Gene Library, Humans, Microbial Sensitivity Tests, Molecular Sequence Data, Nucleic Acid Hybridization methods, Sequence Alignment, ATP-Binding Cassette Transporters chemistry, ATP-Binding Cassette Transporters genetics, ATP-Binding Cassette Transporters metabolism, Antifungal Agents pharmacology, Cryptococcus neoformans drug effects, Drug Resistance, Fungal genetics, Fluconazole pharmacology
- Abstract
Resistance to fluconazole is a possible event during prolonged suppressive drug therapy for cryptococ-cal meningitis, the most frequently encountered life-threatening manifestation of cryptococcosis. The knowledge of this resistance at the molecular level is important for management of cryptococcosis. In order to identify genes involved in azole resistance in Cryptococcus neoformans, a cDNA subtraction library technique was chosen as a strategy. First, a fluconazole-resistant mutant BPY22.17 was obtained from a susceptible clinical isolate BPY22 by in vitro exposure to the drug. Then, a subtractive hybridization procedure was used to compare gene expression between the obtained strains. We identified a cDNA overexpressed in the fluconazole-resistant strain BPY22.17 that was used as a probe to isolate the entire gene in a C. neoformans genomic library. Sequence analysis of this gene identified an ATP Binding Cassette (ABC) transporter-encoding gene called C. neoformans AntiFungal Resistance 1 (CnAFR1). Disruption of CnAFR1 gene in the resistant isolate (BPY22.17) resulted in an enhanced susceptibility of the knock-out mutant cnafr1 against fluconazole, whereas reintroduction of the gene in cnafr1 resulted in restoration of the resistance phenotype, thus confirming that CnAFR1 is involved in fluconazole resistance of C. neoformans. Our findings therefore reveal that an active drug efflux mechanism can be involved in the development of azole resistance in this important human pathogen.
- Published
- 2003
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12. Azole susceptibility patterns and genetic relationship among oral Candida strains isolated in the era of highly active antiretroviral therapy.
- Author
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Tacconelli E, Bertagnolio S, Posteraro B, Tumbarello M, Boccia S, Fadda G, and Cauda R
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- Adult, Candida albicans classification, Candida albicans genetics, Cross-Sectional Studies, Drug Resistance, Fungal, Female, Genotype, Humans, Ketoconazole pharmacology, Male, Microbial Sensitivity Tests, Middle Aged, Risk Factors, AIDS-Related Opportunistic Infections drug therapy, Antifungal Agents pharmacology, Antiretroviral Therapy, Highly Active, Candida albicans drug effects, Candidiasis, Oral drug therapy
- Abstract
We performed a cross-sectional study to analyze patterns of azole susceptibility of oral isolates in the highly active antiretroviral therapy (HAART) era and compared current data with those obtained for isolates from 1994. We further identified patients with relapsing oral pharyngeal candidiasis (OPC) who had been included in a similar study in 1994. For these subjects, we compared the susceptibility pattern for the OPC isolates, and if a modification of azole resistance was observed, we analyzed the genotypic pattern for the 1994 and 2000 isolates to determine whether the dominant strain was closely related. We included 69 consecutive HIV-infected subjects with 137 episodes of OPC who were admitted to our ward from January to June 2000. Ninety-two strains (67%) and 21 non- strains (15%) were isolated. We identified 24 episodes of OPC caused by two different species. Compared with the pre-HAART era, the fluconazole resistance of isolates significantly decreased from 45% to 10% (p <.001). Itraconazole resistance decreased from 37% to 7% (p <.001). Ketoconazole resistance (3% in 1994) was not detected more. Nine patients whose isolate was susceptible to all azole drugs had a previous isolate resistant to all azole drugs. We observed that these isolates exhibited different fingerprint profiles. Our findings demonstrate that most cases of HIV-associated OPC observed in the HAART era are caused by azole-susceptible strains. The reversion of an isolate from azole resistant to azole susceptible is related to strain replacement.
- Published
- 2002
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13. Risk Factors and Outcomes of Candidemia Caused by Biofilm-Forming Isolates in a Tertiary Care Hospital.
- Author
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Tumbarello, Mario, Fiori, Barbara, Trecarichi, Enrico Maria, Posteraro, Patrizia, Losito, Angela, De Luca, Alessio, Sanguinetti, Maurizio, Fadda, Giovanni, Cauda, Roberto, and Posteraro, Brunella
- Subjects
CANDIDIASIS ,BIOFILMS ,BLOOD diseases ,ANTIFUNGAL agents ,DISEASE risk factors - Abstract
Background: Very few data exist on risk factors for developing biofilm-forming Candida bloodstream infection (CBSI) or on variables associated with the outcome of patients treated for this infection. Methods and Findings: We identified 207 patients with CBSI, from whom 84 biofilm-forming and 123 non biofilm-forming Candida isolates were recovered. A case-case-control study to identify risk factors and a cohort study to analyze outcomes were conducted. In addition, two sub-groups of case patients were analyzed after matching for age, sex, APACHE III score, and receipt of adequate antifungal therapy. Independent predictors of biofilm-forming CBSI were presence of central venous catheter (odds ratio [OR], 6.44; 95% confidence interval [95% CI], 3.21-12.92) or urinary catheter (OR, 2.40; 95% CI, 1.18-4.91), use of total parenteral nutrition (OR, 5.21; 95% CI, 2.59-10.48), and diabetes mellitus (OR, 4.47; 95% CI, 2.03-9.83). Hospital mortality, post-CBSI hospital length of stay (LOS) (calculated only among survivors), and costs of antifungal therapy were significantly greater among patients infected by biofilm-forming isolates than those infected by non-biofilm-forming isolates. Among biofilm-forming CBSI patients receiving adequate antifungal therapy, those treated with highly active antibiofilm (HAAB) agents (e.g., caspofungin) had significantly shorter post-CBSI hospital LOS than those treated with non-HAAB antifungal agents (e.g., fluconazole); this difference was confirmed when this analysis was conducted only among survivors. After matching, all the outcomes were still favorable for patients with non-biofilm-forming CBSI. Furthermore, the biofilmforming CBSI was significantly associated with a matched excess risk for hospital death of 1.77 compared to non-biofilmforming CBSI. Conclusions: Our data show that biofilm growth by Candida has an adverse impact on clinical and economic outcomes of CBSI. Of note, better outcomes were seen for those CBSI patients who received HAAB antifungal therapy. [ABSTRACT FROM AUTHOR]
- Published
- 2012
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