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The activity of biocides against Aspergillus fumigatus is unknown. In the European guidelines to evaluate the fungicidal activity of a biocide, the critical step concerning the preparation of conidial suspensions is cumbersome and time-consuming. The aims of this study were to evaluate a simplified procedure to prepare conidial suspensions to test a biocide in comparison with the recommended one and to investigate the in vitro activity of seven biocides by the suspension neutralization method against A. fumigatus clinical isolates. The proposed simplified procedure proved reproducible, gave the same results and was quicker than that described in the European guidelines. Benzalkonium chloride (0.25 %), glutaraldehyde (1.6 %), polyvinylpyrrolidone iodine (1 % available iodine) and polyester glycol iodine (0.18 % available iodine) showed biocidal activity in

Two-hundred sequential Aspergillus fumigatus isolates recovered from 26 immunocompromised patients with invasive aspergillosis or bronchial colonization were tested for their in vitro susceptibility to posaconazole, itraconazole, voriconazole, terbinafine and amphotericin B. Twenty-one patients were treated with amphotericin B and/or itraconazole. Antifungal susceptibilities of the isolates recovered before treatment were not significantly different from those of isolates recovered after the onset of antifungal therapy. The highest MICs were 0.125, 0.5, 0.5, 1 and 1 microg ml(-1) for posaconazole, itraconazole, voriconazole, terbinafine and amphotericin B, respectively. It is concluded that the emergence of resistance in A. fumigatus during antifungal therapy with amphotericin B or itraconazole is an uncommon phenomenon.

This study investigated the source of infection and strain relatedness of Aspergillus fumigatus isolates from bronchial colonisation and invasive aspergillosis (IA) in four transplant patients. Environmental isolates from the patient's home and from the hospital and infecting isolates were obtained for patient A who developed IA. Clinic environmental and colonising isolates were obtained for patient B. Sequential isolates were obtained from various organs from patient C who developed IA and also from patient D who had a bronchitic aspergillosis that developed into IA. Ninety-one A. fumigatus isolates were analysed by three typing methods: multi-locus enzyme electrophoresis (MLEE), random amplified polymorphic DNA (RAPD) and sequence-specific DNA primers (SSDP). The three combined typing methods demonstrated a greater differentiation of isolates than the typing methods used separately or in pairs. This demonstrated the genotypic variability of A. fumigatus and facilitated better epidemiological analysis. Large polymorphisms were demonstrated for each patient isolate between and colonies within various samples. The relatedness of the isolates suggested nosocomially acquired aspergillosis for patient B, but the source of infection for patient A remained unclear. The results suggested at least three multiple infections among the four patients. This study enabled the identification of the source of infection and strain relatedness, which in turn facilitates the development of preventive measures for patient management in the future.

The diversity in virulence of different Aspergillus fumigatus strains was studied in an experimental murine model of invasive pulmonary aspergillosis (IPA) and the results were correlated with possession of a putative molecular marker of virulence. Seven strains from different patients with non-invasive or invasive aspergillosis and four environmental strains were typed by PCR with specific primers and scored as positive or negative, according to whether or not a 0.95-kb DNA fragment was amplified. Immunosuppressed mice were inoculated intranasally with A. fumigatus conidia from these different strains. The mortality curves revealed differences in virulence between the strains. The environmental strains produced a weaker infection than the strains from patients and the 0.95-kb-positive patient strains caused significantly higher mortality rates in mice than the 0.95-kb-negative patient strains. These findings support the hypothesis that certain isolates of A. fumigatus are more virulent than others and that their virulence appears to be associated with the 0.95-kb molecular marker.

A possible relationship between the ability of Aspergillus fumigatus strains to invade tissues and genetic polymorphism was studied by random amplified polymorphic DNA (RAPD) analysis. One hundred randomly designed oligonucleotide decamers were examined with DNA of three reference strains, eight environmental isolates and 21 isolates from two distinct clinical situations: non-invasive aspergillosis (predominantly aspergilloma) and invasive aspergillosis. One primer (OPQ 6) was found to generate a reproducible amplification product that enabled distinction between the two groups according to the presence or absence of a 0.95-kb fragment that correlated with the nature of the infection (non-invasive or invasive) and immune status of the patient. The results indicated that the pathogenicity of A. fumigatus was related not only to the host's immune status but also to the virulence of the strain of A. fumigatus.