The 2022 monkeypox outbreak: A UK military perspective.

With the emergence of SARS-CoV-2 and now monkeypox, the UK Defence Medical Services have been required to provide rapid advice in the management of patients with airborne high consequence infectious diseases (A-HCID). The Defence Public Health Network (DPHN) cadre, consisting of closely aligned uniformed and civilian public health specialists have worked at pace to provide evidence-based recommendations on the clinical management, public health response and policy for monkeypox, with military medicine and pathology clinicians (primarily infectious disease physicians and medical microbiologists). Military environments can be complicated and nuanced requiring specialist input and advice to non-specialists as well as unit commanders both in the UK and overseas. DPHN and military infection clinicians have close links with the UK National Health Service (NHS) and the UK Health Security Agency (UKHSA), allowing for a dynamic two-way relationship that encompasses patient management, public health response, research and development of both UK military and national guidelines. This is further demonstrated with the Royal Air Force (RAF) Air Transport Isolator (ATI) capability, provided by Defence to support the UK Government and UKHSA. Military infectious disease clinicians are also embedded within NHS A-HCID units. In this manuscript we provide examples of the close interdisciplinary working of the DPHN and Defence clinicians in managing military monkeypox patients, co-ordinating the public health response, advising the Command and developing monkeypox policy for Defence through cross-government partnership. We also highlight the co-operation between civilian and military medical authorities in managing the current outbreak.

Eight-year retrospective study investigating tooth survival after primary non-surgical root canal treatment in a UK military cohort.

INTRODUCTION: Root canal treatment (RCT) plays an important role in preserving the dentition by deferring other invasive treatments. Data on tooth survival and predictive factors for tooth loss after RCT in the military cohort are lacking. This investigation aimed to determine the proportion of teeth surviving in an 8-year period after RCT and identify potential predictive factors for tooth loss in a UK military cohort. METHODOLOGY: A retrospective review of an integrated electronic health record for military patients who had received RCT was performed in a random sample of 205 patients (n=219 root-filled teeth) who had received RCT between 1 January 2011 and 1 January 2012. Tooth survival was defined as tooth presence, regardless of signs or symptoms, and measured from the point of root filling until either the end of the designated study period or time of extraction. Survival was evaluated using Kaplan-Meier estimates and association with tooth loss using the χ2 test. Potentially significant predictive factors were investigated using univariate Cox regression. RESULTS: Tooth survival following RCT was 98% after 24 months; 88% after 48 months; 83% after 72 months; and 78% after 96 months. Four predictive factors were found to affect tooth loss as follows: preoperative pain (HR=3.2; p<0.001), teeth with less than two proximal contacts (HR=3.0; p=0.01), teeth with cores involving more than two surfaces (HR=2.0; p=0.03) and postoperative unscheduled dental attendances (UDA) (HR=2.7; p=0.01). CONCLUSIONS: Within the limitations of this study, the presence of preoperative pain; teeth with less than two proximal contacts or with cores involving more than two tooth surfaces; and occurrence of postoperative UDA were found to significantly increase the hazard of tooth loss.

The effect of different strains of Helicobacter pylori on platelet aggregation.

BACKGROUND AND AIMS: Helicobacter pylori is the major causative agent in peptic ulcer disease and is strongly implicated in the development of gastric cancer. It has also been linked, less strongly, to cardiovascular disease. The mechanisms by which certain strains of H pylori induce platelet aggregation through interactions with platelet glycoprotein Ib have been previously described. METHODS: In the present study, 21 different strains of H pylori, varying in their vacuolating toxin gene, cytotoxic-associated gene A status and other pathogenicity factors, were tested for their ability to induce platelet aggregation. RESULTS: Ten of the 21 strains induced platelet aggregation, a response that appeared to be independent of their vacuolating toxin gene and cytotoxic-associated gene A status. CONCLUSIONS: Platelet aggregation has been suggested to be one of the possible mechanisms involved in the effects on the cardiovascular system induced by H pylori. Our results suggest that any putative role H pylori plays in cardiovascular disease may be strain dependent. Further work to identify the H pylori factors involved in induction of platelet aggregation may allow for identification of 'higher risk' strains for cardiovascular disease.