Aspergillosis: Different Patients, Different Strains
Abstract & Commentary
Synopsis: The ability to detect genetic diversity in Aspergillus isolates depends on the number of techniques used.
Source: Bertout S, et al. Genetic polymorphism of Asper-gillus fumigatus in clinical samples from patients with invasive aspergillosis: Investigation using multiple typing methods. J Clin Microbiol. 2001;39:1731-1737.
This study set out to better understand the epidemiology of Aspergillus fumigatus involved in invasive aspergillosis. To this end, Bertout and colleagues had collected 52 isolates of the mold from the first respiratory sample obtained from 12 cases of probable invasive aspergillosis that had yielded at least 2 colonies of A fumigatus. The patients involved had been treated in 3 different geographical locations (Lyons and Grenoble, France and Milan, Italy) and had no connection with one another. Each isolate was subjected to 4 different molecular typing techniques, multilocus enzyme electrophoresis (MLEE) which yielded 8 different types, and 3 DNA typing methods: random-amplified polymorphic DNA (RAPD), sequence-specific DNS primer (SSDP), and microsatellite polymorphism analysis (MSP) which yielded 8, 9, and 14 types, respectively. Combining the 4 methods yielded 25 genotypes among the 52 isolates. As expected, no 2 patients shared the same isolate but, surprisingly, the samples from 6 patients had 2 distinct genotypes and for another 2 patients, 4 and 5 genotypes, respectively.
Comment by J. Peter Donnelly, PHD
The primary purpose of this study was to demonstrate that a combination of typing methods is useful for understanding the epidemiology of A fumigatus, and they succeeded in this regard. The number of resultant types increased proportionately with the number of techniques from 8-14 using one or another typing method to 25 using all 4 methods. With such a tool at one’s disposal it should be possible to monitor individual patients over time, identify outbreaks when they arise and locate the source, and also to establish the origin of infection in immunocompromised hosts. However, such an undertaking would prove laborious and prohibitively expensive even if only 1 strain per patient is encountered. Multiply this by the number of patients who appear to be infected anyway with 2 or more different strains of mold and the workload is at least doubled. If an outbreak is encountered, finding the source would add even more work since this mold is ubiquitous both in the hospital environment as well as in the community at large and, importantly, in the laboratory. There is little wonder then why Bertout et al are reserved about using this technique routinely. However, the real power of this type of approach would be in gaining a deeper understanding of the etiology of infection. Evidence already suggests that patients with hematological diseases tend to be infected by separate and distinct strains of the mold, ruling out a common source such as the hospital ward. Instead, it would appear that aspergilli are acquired from the community, probably in the patient’s own home environment. By contrast, lung transplant recipients would seem more likely to acquire aspergilli nosocomially. These patients may benefit from being nursed in a proper protected environment while in the hospital whereas other patients at risk may, after all, only benefit from the administration of potent, systemically available antifungal agents to arrest incipient infection and to protect them against further infection for as long as they are at risk whether they are at home or in hospital. With such powerful tools as reported here it should now be possible to provide enough insight into the epidemiology of aspergillosis to identify and evaluate effective means of bringing this wayward opportunist under control.
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