Public health response to outbreaks of Avian Influenza A(H5N2) and (H5N1) among poultry - British Columbia, December 2014-February 2015.

In December 2014, the first detection in Canada of a highly pathogenic avian influenza A (HPAI) virus was reported in poultry within the Fraser Health Authority of British Columbia. It was the second outbreak of HPAI from Eurasian H5 reassortment viruses in North America. The Fraser Health Authority provided the lead public health coordination for this response as well as consultation and support to the occupational health response. The public health response focused on contact tracing, monitoring and follow-up for household, farm worker and other community contacts exposed on the affected farms. A total of 50 contacts were identified. Contacts received daily active monitoring by public health nurses for seven days from their last exposure and were advised to self-monitor until day 10. All contacts and other household members were recommended seasonal influenza vaccination to protect against further possible reassortment with human influenza viruses circulating within the community at the time. A total of 26 (52%) contacts were recommended chemoprophylaxis for ongoing exposure to the affected barns and flocks, of whom only 11 (42%) initiated this. During the seven-day active surveillance period, four contacts developed acute respiratory symptoms and influenza B was identified in one individual. Local area health care providers and acute care facilities were alerted to the outbreak and public messaging was provided regarding the human health risks from avian influenza. Collaboration between health and agriculture at the local, regional, provincial and federal levels was key to a rapid response to this outbreak.

Anthrax among heroin users in Europe possibly caused by same Bacillus anthracis strain since 2000.

Injection anthrax was described first in 2000 in a heroin-injecting drug user in Norway. New anthrax cases among heroin consumers were detected in the United Kingdom (52 cases) and Germany (3 cases) in 2009-10. In June 2012, a fatal case occurred in Regensburg, Bavaria. As of December 2012, 13 cases had been reported in this new outbreak from Germany, Denmark, France and the United Kingdom. We analysed isolates from 2009-10 and 2012 as well as from the first injection anthrax case in Norway in 2000 by comparative molecular typing using a high resolution 31 marker multilocus variable-number tandem repeat analysis (MLVA) and a broad single nucleotide polymorphism (SNP) analysis. Our results show that all cases may be traced back to the same outbreak strain. They also indicate the probability of a single source contaminating heroin and that the outbreak could have lasted for at least a decade. However, an additional serological pilot study in two German regions conducted in 2011 failed to discover additional anthrax cases among 288 heroin users.

Immunodetection of inactivated Francisella tularensis bacteria by using a quartz crystal microbalance with dissipation monitoring.

Francisella tularensis are very small, gram-negative bacteria which are capable of infecting a number of mammals. As a highly pathogenic species, it is a potential bioterrorism agent. In this work we demonstrate a fast immunological detection system for whole F. tularensis bacteria. The technique is based on a quartz crystal microbalance with dissipation monitoring (QCMD), which uses sensor chips modified by a specific antibody. This antibody is useful as a capture molecule to capture the lipopolysaccharide structure on the surface of the bacterial cell wall. The QCMD technique is combined with a microfluidic system and allows the label-free online detection of the binding of whole bacteria to the sensor surface in a wide dynamic concentration range. A detection limit of about 4 × 10(3) colony-forming units per milliliter can be obtained. Furthermore, a rather short analysis time and a clear discrimination against other bacteria can be achieved. Additionally, we demonstrate two possibilities for specific and significant signal enhancement by using antibody-functionalized gold nanoparticles or an enzymatic precipitation reaction. These additional steps can be seen as further proof of the specificity and validity.

Glycogen synthase kinase-3ß is a crucial mediator of signal-induced RelB degradation.

The immediate early transcription factor nuclear factor (IκBs) kappa B (NF-κB) is crucially involved in the regulation of numerous physiological or pathophysiological processes such as inflammation and tumourigenesis. Therefore, the control of NF-κB activity, which is mainly regulated by signal-induced degradation of cytoplasmic inhibitors of NF-κB (IκBs), is of high relevance. One known alternative pathway of NF-κB regulation is the stimulus-induced proteasomal degradation of RelB, a component of the NF-κB dimer. Here, we identified the serine/threonine protein kinase glycogen synthase kinase-3ß (GSK-3ß) as a critical signalling component leading to RelB degradation. In Jurkat leukaemic T cells as well as in primary human T cells, tetradecanoylphorbolacetate/ionomycin- and CD3/CD28-induced RelB degradation were impaired by a GSK-3ß-specific pharmacological inhibitor, an ectopically expressed dominant-negative GSK-3ß mutant and by small-interfering RNA-mediated silencing of GSK-3ß expression. Furthermore, a physical interaction between RelB and GSK-3ß was shown by co-immunoprecipitation, which was already notable in unstimulated cells. Most importantly, as demonstrated by in vitro kinase assays, human RelB is inducibly phosphorylated by GSK-3ß, indicating a direct substrate-enzyme relationship. The serine residue 552 is a target of GSK-3ß-mediated phosphorylation in vitro and in vivo. We conclude that GSK-3ß is a crucial regulator of RelB degradation, stressing the relevant linkage between the NF-κB system and GSK-3ß.

Diagnostic challenges of hepatitis C virus infections.

In less than 10 years, tremendous progress has been made in our understanding of the biology of hepatitis C virus. Since it was defined as the causal agent of most hepatitis non-A, non-B infections in 1989, clinical laboratories now have access to powerful new techniques for the diagnosis of infection and control of therapy. Identification of the specific virus strain in the patients as well as measurement of the individual viral load and the prediction of a possible therapeutic success have become routine procedures. This effort is warranted because the treatment options are still limited, with alpha-interferon being the only approved drug. No new treatment regimens have emerged yet from the wealth of data from subtyping and quantitating.