Abstract
Since the first description of an azole-resistant A. fumigatus strain in 1997, there has been an increasing number of papers describing the emergence of azole resistance. Firstly reported in the USA and soon after in Europe, it has now been described worldwide, challenging the management of human aspergillosis. The main mechanism of resistance is the modification of the azole target enzyme: 14-α sterol demethylase, encoded by the cyp51A gene; although recently, other resistance mechanisms have also been implicated. In addition, a shift in the epidemiology has been noted with other Aspergillus species (mostly azole resistant) increasingly being reported as causative agents of human disease. This paper reviews the current situation of Aspergillus azole resistance and its implications in the clinical setting.
Highlights
IntroductionInvasive aspergillosis (IA) is a life-threatening infection caused by ubiquitous saprophytic
Invasive aspergillosis (IA) is a life-threatening infection caused by ubiquitous saprophyticAspergillus species, which are the most common cause of invasive mold infections worldwide, especially in immunocompromised patients [1]
Azole resistance in environmental strains in Europe has been commonly detected, with TR34 /L98H and TR46 /Y121F/T289A being the most often described mechanisms (Figure 1), and their emergence has been related with the extensive use of agricultural fungicides
Summary
Invasive aspergillosis (IA) is a life-threatening infection caused by ubiquitous saprophytic. MIC (minimum inhibitory concentration) distributions in order to establish epidemiologic cutoff values (ECVs) for A. fumigatus and azoles [11,12] Based on these data and taking into account the clinical outcome, pharmacokinetics and pharmacodynamics, EUCAST defined breakpoints for A. fumigatus and azoles (ITC > 2 μg/mL, VRC > 2 μg/mL, POS > 0.25 μg/mL and ISA > 1 μg/mL), which are used to categorize A. fumigatus strains as susceptible or resistant [13]. As in vitro antifungal susceptibility testing in Aspergillus is not routinely done in non-invasive settings, the prevalence of triazole resistance strains is likely to be underestimated [6]
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