Enhancing pnemonia surveillance in acute care facilities in post SARS era : a Canadian hospital surveillance study, 2003-2004 influenza season

A retrospective study of patients hospitalized with influenza and/or pneumonia in a Niagara area community hospital for the influenza season 2003-04 was designed with the main goal of enhancing pneumonia surveillance in acute care facilities and the following specific objectives: 1) identify etiologies, factors, and clinical presentation associated with pneumonia; 2) assess the ODIN score on ICU patients to predict outcomes of severe pneumonia; 3) identify the frequency of pneumonia and influenza in a hospital setting; and 4) develop a hospital pneumonia electronic surveillance tool. A total of 172 patients' charts (50% females) were reviewed and classified into two groups: those with diagnosis of pneumonia (n=132) and those without pneumonia (n=40). The latter group consisted mainly of patients with influenza (85%). Most patients were young (<10yrs) or elderly (>71yrs). Presenting body temperature <38°C, cough symptoms, respiratory and cardiac precomorbidities were common in both groups. Pneumonia was more frequent in males (p= .032) and more likely community-acquired (98%) than nosocomial (2%). No evidence of ventilator-associated pneumonia was found. Microbiology testing in 72% of cases detected 19 different pathogens. In pneumonia patients the most common organisms were Streptococcus pneumoniae (3%), Respiratory syncytial virus (4%), and Influenza A virus (2%). Conversely, Influenza A virus was identified in 73% of non-pneumonia patients. Community-acquired influenza was more common (80%) than nosocomial influenza (20%). The ODIN score was a good predictor of mortality and the new electronic surveillance tool was an effective prototype to monitor patients in acute care, especially during influenza season. The results of this study provided baseline data on respiratory illness surveillance and demonstrated that future research, including prospective studies, is warranted in acute care facilities.

The Molecular Consequences of CK2-mediated Phosphorylation of the TGA2 Transcription Factor within Systemic Acquired Resistance of Arabidopsis thaliana

During infection, the model plant Arabidopsis thaliana is capable of activating long lasting defence responses both in tissue directly affected by the pathogen and in more distal tissue. Systemic acquired resistance (SAR) is a type of systemic defence response deployed against biotrophic pathogens resulting in altered plant gene expression and production of antimicrobial compounds. One such gene involved in plant defence is called pathogenesis-related 1 (PR1) and is under the control of several protein regulators. TGA II-clade transcription factors (namely TGA2) repress PR1 activity prior to infection by forming large oligomeric complexes effectively blocking gene transcription. After pathogen detection, these complexes are dispersed by a mechanism unknown until now and free TGA molecules interact with the non-expressor of pathogenesis-related gene 1 (NPR1) protein forming an activating complex enabling PR1 transcription. This study elucidates the TGA2 dissociation mechanism by introducing protein kinase CK2 into this process. This enzyme efficiently phosphorylates TGA2 resulting in two crucial events. Firstly, the DNA-binding ability of this transcription factor is completely abolished explaining how the large TGA2 complexes are quickly evicted from the PR1 promoter. Secondly, a portion of TGA2 molecules dissociate from the complexes after phosphorylation which likely makes them available for the formation of the TGA2-NPR1 activating complex. We also show that phosphorylation of a multiserine motif found within TGA2’s N terminus is responsible for the change of affinity to DNA, while modification of a single threonine in the leucine zipper domain seems to be responsible for deoligomerization. Despite the substantial changes caused by phosphorylation, TGA2 is still capable of interacting with NPR1 and these proteins together form a complex on DNA promoting PR1 transcription. Therefore, we propose a change in the current model of how PR1 is regulated by adding CK2 which targets TGA2 displacing it’s complexes from the promoter and providing solitary TGA2 molecules for assembly of the activating complex. Amino acid sequences of regions targeted by CK2 in Arabidopsis TGA2 are similar to those found in TGA2 homologs in rice and tobacco. Therefore, the molecular mechanism that we have identified may be conserved among various plants, including important crop species, adding to the significance of our findings.