Successful treatment of a previously healthy woman with Pseudomonas aeruginosa community-acquired pneumonia with plasmapheresis.

A previously healthy 39-year-old woman with severe chest pain presented at our hospital. She was diagnosed with bacterial pneumonia by chest X-ray and computed tomography. Despite adequate antimicrobial treatment, she had to undergo intubation for respiratory distress and was treated with mechanical ventilation 42 hours after admission. However, her condition improved markedly after plasmapheresis. Bacterial culture specimens from the sputum, blood, and pleural fluid were positive for Pseudomonas aeruginosa (P. aeruginosa). Pseudomonas aeruginosa community-acquired pneumonia (CAP) in previously healthy individuals is very rare, rapidly progressive, and often fatal. This is the first report of the successful treatment of this life-threatening pneumonia with plasmapheresis.

Intrahepatic splenosis with severe iron deposition presenting with atypical magnetic resonance images.

An intrahepatic mass was incidentally found in a 41-year-old man with a history of a traffic accident injury which resulted in removal of a ruptured spleen. Hepatic splenosis was considered in the differential diagnosis but magnetic resonance imaging showed hypointensity on T2-weighted images, atypical for normal spleen. Histologically, the mass showed sinusoidal structures and lymphoid follicular aggregates. Immunohistochemical study showed that the phenotype of the vascular lining cells was CD8-positive, CD31-positive, and CD34 negative, the pattern diagnostic for ectopic spleen. In addition, severe iron deposition was histologically demonstrated, which was considered as the cause of the hypointense T2-weighted images.

Arrangement and regulation of the genes for meta-pathway enzymes required for degradation of phenol in Comamonas testosteroni TA441.

Comamonas testosteroni TA441 degrades phenol by a meta-cleavage pathway after the occurrence of a spontaneous mutation that derepresses the aphKLMNOPQB operon encoding phenol hydroxylase and catechol 2,3-dioxygenase, the enzymes for the initial two steps of the degradation pathway. A gene cluster, aphCEFGHJI, encoding the meta-pathway enzymes for degradation of 2-hydroxymuconic semialdehyde (HMS) to TCA cycle intermediates was found downstream of the aphK operon. The upstream operon and the downstream gene cluster were found to be separated by two open reading frames of unknown function and an oppositely oriented aphT gene, which is similar to regulatory genes for ortho-cleavage of catechol or chlorinated catechols. A promoter assay using an aphC::lacZ transcriptional fusion plasmid revealed that the aphC promoter activity is induced by both phenol and HMS. The phenol-dependent induction was mediated by AphR and the HMS-dependent induction was mediated by AphT. The aphC promoter in strain TA441 was not silenced, unlike the cases of the aphK and aphR promoters, and was highly induced by HMS.

Adaptation of Comamonas testosteroni TA441 to utilize phenol: organization and regulation of the genes involved in phenol degradation.

Comamonas testosteroni TA441 was not able to grow on phenol as a sole carbon and energy source, but it gained the ability to utilize phenol after a 2-3-week incubation in a medium containing phenol. Phenol hydroxylase (PH) and catechol 2,3-dioxygenase (C230) were highly induced by phenol in the adapted strain designated as strain P1, suggesting that phenol was degraded via the meta-pathway. Gene clusters for phenol degradation were isolated from both strains TA441 and P1. The structural genes encoding multi-component PH and C230 (aphKLMNOPQB), and a regulatory gene of the NtrC family (aphR), were located in a divergent transcriptional organization. The cloned aphKLMNOPQB genes from either strain TA441 or strain P1 produced active PH and C230 enzymes in strain TA441. No difference was found between the strains in the sequences of aphR and the intergenic promoter region of aphK and aphR. However, the transcriptional activities of the aphK and aphR promoters were higher in strain P1 than in strain TA441. The aphK-promoter activity was not observed in aphR mutant strains and these strains could not grow on phenol. The aphR mutant of strain P1 was able to grow on phenol after transformation with a recombinant aphR gene but strain TA441 was not, suggesting that the expression of the aph genes is silenced by an unidentified repressor in strain TA441 and that this repressor is modified in strain P1.