Aspergillosis is a serious pathologic condition caused by Aspergillus organisms and is frequently seen in immunocompromised patients. At computed tomography (CT), saprophytic aspergillosis (aspergilloma) is characterized by a mass with soft-tissue attenuation within a lung cavity. The mass is typically separated from the cavity wall by an airspace ("air crescent" sign) and is often associated with thickening of the wall and adjacent pleura. CT findings in allergic bronchopulmonary aspergillosis consist primarily of mucoid impaction and bronchiectasis involving predominantly the segmental and subsegmental bronchi of the upper lobes. Aspergillus necrotizing bronchitis may manifest as an endobronchial mass, obstructive pneumonitis or collapse, or a hilar mass. Bronchiolitis is characterized by centrilobular nodules and branching linear or nodular areas of increased attenuation ("tree-in-bud" pattern). Obstructing bronchopulmonary aspergillosis mimics allergic bronchopulmonary aspergillosis at CT and manifests as bilateral bronchial and bronchiolar dilatation, large mucoid impactions, and diffuse lower lobe consolidation caused by postobstructive atelectasis. Characteristic CT findings in angioinvasive aspergillosis consist of nodules surrounded by a halo of ground-glass attenuation ("halo sign") or pleura-based, wedge-shaped areas of consolidation. Although imaging findings in pulmonary aspergillosis may be nonspecific, in the appropriate clinical setting, familiarity with the CT findings may suggest or even help establish the diagnosis.
Pseudomonas putida KT2440 is a chloramphenicol-resistant bacterium that is able to grow in the presence of this antibiotic at a concentration of up to 25 g/ml. Transcriptomic analyses revealed that the expression profile of 102 genes changed in response to this concentration of chloramphenicol in the culture medium. The genes that showed altered expression include those involved in general metabolism, cellular stress response, gene regulation, efflux pump transporters, and protein biosynthesis. Analysis of a genome-wide collection of mutants showed that survival of a knockout mutant in the TtgABC resistance-nodulation-division (RND) efflux pump and mutants in the biosynthesis of pyrroloquinoline (PQQ) were compromised in the presence of chloramphenicol. The analysis also revealed that an ABC extrusion system (PP2669/PP2668/PP2667) and the AgmR regulator (PP2665) were needed for full resistance toward chloramphenicol. Transcriptional arrays revealed that AgmR controls the expression of the pqq genes and the operon encoding the ABC extrusion pump from the promoter upstream of open reading frame (ORF) PP2669.
Environmental microbes harbor an enormous pool of antibiotic and biocide resistance genes that can impact the resistance profiles of animal and human pathogens via horizontal gene transfer. Pseudomonas putida strains are ubiquitous in soil and water but have been seldom isolated from humans. We have established a collection of P. putida strains isolated from in-patients in different hospitals in France. One of the isolated strains (HB3267) kills insects and is resistant to the majority of the antibiotics used in laboratories and hospitals, including aminoglycosides, ß-lactams, cationic peptides, chromoprotein enediyne antibiotics, dihydrofolate reductase inhibitors, fluoroquinolones and quinolones, glycopeptide antibiotics, macrolides, polyketides and sulfonamides. Similar to other P. putida clinical isolates the strain was sensitive to amikacin. To shed light on the broad pattern of antibiotic resistance, which is rarely found in clinical isolates of this species, the genome of this strain was sequenced and analysed. The study revealed that the determinants of multiple resistance are both chromosomally-borne as well as located on the pPC9 plasmid. Further analysis indicated that pPC9 has recruited antibiotic and biocide resistance genes from environmental microorganisms as well as from opportunistic and true human pathogens. The pPC9 plasmid is not self-transmissible, but can be mobilized by other bacterial plasmids making it capable of spreading antibiotic resistant determinants to new hosts.
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