Abdominal aortic aneurysm screening in an academic family practice: Short-term impact of guideline changes.

OBJECTIVE: To investigate abdominal aortic aneurysm (AAA) screening rates in the 6 months before and after the introduction of updated Canadian Task Force on Preventive Health Care (CTFPHC) guidelines to determine effects on practice patterns, as well as to determine whether certain patient characteristics impact AAA screening rates. DESIGN: Retrospective chart review. SETTING: Academic family health centre in London, Ont. PARTICIPANTS: Male patients between the ages of 65 and 80. MAIN OUTCOME MEASURES: Screening rates for AAA before and after the guideline update were compared using the normal approximation of the binomial distribution. Analysis of demographic characteristic effects on screening rates was completed with the Fisher exact test. Number of visits to the clinic with a primary care provider within the study period and imaging type were collected. RESULTS: Of the 266 patients included in the study, 160 patients were eligible for screening at the start of the study period, 6 months before publication of the CTFPHC AAA guideline. Individuals eligible for screening visited the clinic an average (SD) of 2.44 (1.82) times in the 6 months before and 2.66 (1.99) times in the 6 months after. Overall, 69 individuals had AAA screening completed and 9 had a discussion of AAA screening without any imaging, for a total uptake rate of 88.5% for those who had screening recommended. The overall imaging rate was 48.9%. There was no statistically significant difference in screening rates between the time periods (P=.337) among those eligible for screening. For demographic characteristics for risk stratification, 7 individuals had a documented family history, of whom 5 had imaging of their abdominal aorta performed, plus 1 additional individual who had screening recommended but not completed. This was not statistically significant relative to the total population (P=.0598). Positive smoking status (active or ex-smoker) was more common, with 135 individuals having a relevant smoking history. Approximately half of these current and former smokers (68 individuals [50.4%]) had any sort of abdominal aortic imaging performed or recommended, which was not statistically significantly different compared with non-smokers (62 of 126 imaging performed or recommended, 49.2%; P=.9016). CONCLUSION: Screening practices did not change appreciably with the introduction of the CTFPHC AAA screening guidelines. Further research is needed to improve AAA screening rates. It is worth exploring electronic medical record-based reminders, nursing staff involvement in screening, screening programs via public health, and point-of-care ultrasound screening in a primary care setting.

Performance of a new symptom checker in patient triage: Canadian cohort study.

BACKGROUND: Computerized algorithms known as symptom checkers aim to help patients decide what to do should they have a new medical concern. However, despite widespread implementation, most studies on symptom checkers have involved simulated patients. Only limited evidence currently exists about symptom checker safety or accuracy when used by real patients. We developed a new prototype symptom checker and assessed its safety and accuracy in a prospective cohort of patients presenting to primary care and emergency departments with new medical concerns. METHOD: A prospective cohort study was done to assess the prototype's performance. The cohort consisted of adult patients (≥16 years old) who presented to hospital emergency departments and family physician clinics. Primary outcomes were safety and accuracy of triage recommendations to seek hospital care, seek primary care, or manage symptoms at home. RESULTS: Data from 281 hospital patients and 300 clinic patients were collected and analyzed. Sensitivity to emergencies was 100% (10/10 encounters). Sensitivity to urgencies was 90% (73/81) and 97% (34/35) for hospital and primary care patients, respectively. The prototype was significantly more accurate than patients at triage (73% versus 58%, p<0.01). Compliance with triage recommendations in this cohort using this iteration of the symptom checker would have reduced hospital visits by 55% but cause potential harm in 2-3% from delay in care. INTERPRETATION: The prototype symptom checker was superior to patients in deciding the most appropriate treatment setting for medical issues. This symptom checker could reduce a significant number of unnecessary hospital visits, with accuracy and safety outcomes comparable to existing data on telephone triage.

Identification of a two-component Class IIb bacteriocin in Streptococcus pyogenes by recombinase-based in vivo expression technology.

Streptococcus pyogenes is a globally prominent bacterial pathogen that exhibits strict tropism for the human host, yet bacterial factors responsible for the ability of S. pyogenes to compete within this limited biological niche are not well understood. Using an engineered recombinase-based in vivo expression technology (RIVET) system, we identified an in vivo-induced promoter region upstream of a predicted Class IIb bacteriocin system in the M18 serotype S. pyogenes strain MGAS8232. This promoter element was not active under in vitro laboratory conditions, but was highly induced within the mouse nasopharynx. Recombinant expression of the predicted mature S. pyogenes bacteriocin peptides (designated SpbM and SpbN) revealed that both peptides were required for antimicrobial activity. Using a gain of function experiment in Lactococcus lactis, we further demonstrated S. pyogenes immunity function is encoded downstream of spbN. These data highlight the importance of bacterial gene regulation within appropriate environments to help understand mechanisms of niche adaptation by bacterial pathogens.

Nasopharyngeal Infection of Mice with Streptococcus pyogenes and In Vivo Detection of Superantigen Activity.

Streptococcus pyogenes is a globally prominent human-specific pathogen that is responsible for an enormous burden of infectious disease. Despite intensive experimental efforts to understand the molecular correlates that contribute to invasive infections, there has been less focus on S. pyogenes carriage and local infection of the nasopharynx. This chapter describes an acute nasopharyngeal infection model in mice that is utilized in our laboratory to study the role of superantigen toxins in the biology of S. pyogenes. We also describe a method to detect superantigen-specific T cell activation in vivo.

Bacterial superantigens promote acute nasopharyngeal infection by Streptococcus pyogenes in a human MHC Class II-dependent manner.

Establishing the genetic determinants of niche adaptation by microbial pathogens to specific hosts is important for the management and control of infectious disease. Streptococcus pyogenes is a globally prominent human-specific bacterial pathogen that secretes superantigens (SAgs) as 'trademark' virulence factors. SAgs function to force the activation of T lymphocytes through direct binding to lateral surfaces of T cell receptors and class II major histocompatibility complex (MHC-II) molecules. S. pyogenes invariably encodes multiple SAgs, often within putative mobile genetic elements, and although SAgs are documented virulence factors for diseases such as scarlet fever and the streptococcal toxic shock syndrome (STSS), how these exotoxins contribute to the fitness and evolution of S. pyogenes is unknown. Here we show that acute infection in the nasopharynx is dependent upon both bacterial SAgs and host MHC-II molecules. S. pyogenes was rapidly cleared from the nasal cavity of wild-type C57BL/6 (B6) mice, whereas infection was enhanced up to ∼10,000-fold in B6 mice that express human MHC-II. This phenotype required the SpeA superantigen, and vaccination with an MHC -II binding mutant toxoid of SpeA dramatically inhibited infection. Our findings indicate that streptococcal SAgs are critical for the establishment of nasopharyngeal infection, thus providing an explanation as to why S. pyogenes produces these potent toxins. This work also highlights that SAg redundancy exists to avoid host anti-SAg humoral immune responses and to potentially overcome host MHC-II polymorphisms.