Evolving technologies available to clinical laboratories and laboratory-related updates to clinical guidelines both drive the need for clinical laboratories to keep their test menu updated and in line with current technological and clinical developments. Our laboratory has developed a targeted Illumina-based amplicon next-generation sequencing (NGS) assay to interrogate the hsp65 and erm(41) genes of Mycobacterium spp. for the purposes of providing species-level ± subspecies-level identification of Mycobacterium spp. organisms in clinical samples and genotypic predictions for inducible macrolide resistance (in the case of M. abscessus complex members). The developed assay demonstrated 100% sensitivity and specificity for M. tuberculosis and M. abscessus complex cultured organisms, 98% ID overall concordance relative to the available reference identification, and a nearly 60% “rescue” rate for primary samples that could not be identified using our previous method. There was 94.6% concordance between genotypic and phenotypic results for inducible macrolide resistance. The developed assay was successfully implemented in our clinical laboratory and has been accredited for clinical use.

Treatment of Mycobacterium tuberculosis requires multi-drug regimens, and resistance to any individual antibiotic can compromise outcomes. For slow-growing organisms like M. tuberculosis, rapid detection of resistance-conferring mutations enables timely initiation of effective therapy. Conversely, confirming wild-type status in resistance-associated genes supports confidence in standard regimens. We developed an amplicon-based next generation sequencing (amplicon tNGS) assay on the Illumina platform targeting eight genes linked to resistance to isoniazid, rifampin, ethambutol, pyrazinamide, and fluoroquinolones. Sequencing results were analyzed using a custom bioinformatics pipeline. Forty-seven samples were used for assay development, and 37 additional samples underwent post-implementation clinical validation. Compared to whole genome sequencing (WGS), amplicon tNGS demonstrated 97.7% sensitivity, 98.9% specificity, and 98.7% overall accuracy for variant detection in targeted regions. Resistance prediction showed 79.3% concordance with WGS; discrepancies were primarily due to mutations outside of target regions. Among post-implementation samples, 27/37 passed quality metrics for all targets, with 95.7% concordance between amplicon tNGS results and final susceptibility results. This assay is now in use in our laboratory and offers significantly faster turnaround than both WGS and phenotypic methods on cultured isolates, enabling more rapid, informed treatment decisions for tuberculosis patients.

Motivation: The multinational outbreak of human mpox virus (MPOXV) in the summer of 2022 highlighted the need for improved tools to assist public health officials in tracking and responding to new local outbreak clusters. Phylogenetic characterization of MPOXV can support local case investigations by shedding light on whether the virus may have been acquired locally, belongs to endemically circulating strains, or represents a new introduction. In this work, we adapt clustering tools developed for SARS-CoV-2 surveillance to track local MPOXV outbreaks. Results: We present an adapted version of cov2clusters, originally developed for monitoring SARS-CoV-2 cases in British Columbia. The tool offers stable cluster codes between trees and has been improved with optimizations in execution time and memory management. We also demonstrate the advantages of adapting previously developed tools, validated against the pathogen they were originally designed for, to monitor a new pathogen. This approach can conserve resources that would otherwise be spent on developing new tools and facilitate faster deployment in public health settings.

The COVID-19 pandemic, caused by SARS-CoV-2, highlighted the need for accurate and timely data on virus spread and immune responses at a population level. Serological surveys offer a comprehensive view of population-level immune response to SARS-CoV-2 post- infection and/or vaccination. Here, we performed a serial cross-sectional study from residual serum samples collected from pregnant individuals in British Columbia during their first trimester antenatal screening. A total of 28,050 samples were collected between November 2021 and March 2024. We tracked changes in antibody levels over time and examined differences in antibody responses based on age and vaccination status during different phases of the pandemic. Antenatal serum samples enabled tracking of SARS-CoV-2 serostatus within the population and waves of major SARS-CoV-2 infections, such as the Omicron surge in 2021-2022 and increases in infection during the 2023-2024 respiratory season. During the 2023-2024 season, we observed a significant rise in Nucleocapsid (N) seropositivity compared to the previous year, reaching 64.3 % in the vaccinated group and 67.05 % in the unvaccinated group. This suggests a high infection rate, likely driven by the latest Omicron variants. Additionally, we differentiated between infection-induced and vaccine-induced seroprevalence. By March 2024, Spike (S) seroprevalence was 94 % in the unvaccinated group and 100 % in the vaccinated group. We assessed the longevity of vaccine-induced antibody within the population. A significant negative correlation was observed between S seropositivity (indicative of vaccination without infection, S+/N-) and time since the last vaccine dose. In contrast, anti-N levels began to rise above the cut-off value of seropositivity 15 months post-vaccination, indicating increased infection rates and N seroprevalence as time post-vaccination increased. This serosurveillance approach provide critical insights for public health strategies for the future, emphasizing the importance of ongoing serosurveillance to help understand corelates of seroprotection at a population level and to support ongoing evidence-based vaccine policy.

BACKGROUND:Since introduction of conjugate vaccines against serotype b Haemophilus influenzae (Hib), invasive Hib disease in British Columbia (BC), Canada has been rare (average 2.8 cases per year). However, between 2021 and 2024, 62 cases of culture confirmed cases were documented. This study examined Hib isolates from BC between January 1, 2010 to December 31, 2024. METHODS:Hib were characterized by whole genome sequencing. Demographics of Hib cases as well as clinical presentation inferred from bacteriological isolation sites were obtained from BC Centre for Disease Control. RESULTS:Ninety-eight case isolates of Hib (9.3 %) were identified from all invasive H. influenzae disease (n = 1047). The most common Hib sequence type (ST) was ST-231 (68 isolates or 69.4 %). SNVPhyl analysis clustered ST-231 Hib as uniquely different from all other Hib isolates, and also grouped them into an early E1 (from 2011 to 2008), a late L2 (from 2022 to 2023) and a late L3 (from 2017 to 2023) clusters. Core-genome multi-locus sequence typing (cgMLST) and Life Identification Numbers (LIN) assigned by PubMLST showed that the ST-231 Hib were highly similar (with five or fewer core gene differences). Only four non-Canadian Hib isolates identified by LIN and cgMLST to cluster distantly with ST-231 Hib were showing 110 core gene differences. Most (91.2 %) ST-231 Hib cases occurred in adults aged ≥ 30 years, and no case in children ≤ five years old. Most (94.1 %) cases showed positive blood culture. Temporal and geographical variations of Hib STs were found by linking Hib cases to their Health Regions. CONCLUSION:This study documented an increase of Hib cases in adults due to an uncommon ST, which was very different from other Hib found in the PubMLST databsae. ST-231 Hib cases were initially found in only two Health Regions, subsequent cases spread to cover four Health Regions suggesting community spread and endemicity in the province.

We characterized highly pathogenic avian influenza A(H5N1) clade 2.3.4.4b genotype D1.1 in wild birds and a human in British Columbia, Canada, during 2024. D1.1, the predominant genotype circulating in fall 2024, is a reassortment between Eurasian A3 lineage viruses, introduced to North America in 2022, and North American lineage viruses.

ABSTRACT The Burkholderia cepacia complex (BCC) is a group of Gram-negative bacteria that cause opportunistic infections, most notably in people with cystic fibrosis (CF), and have been associated with outbreaks caused by contaminated medical products. Antimicrobial susceptibility testing (AST) is often used to guide treatment for BCC infections, perhaps most importantly in people with CF who are being considered for lung transplant. However, recent studies have highlighted problems with AST methods. Here, we address limitations from previous studies to further evaluate BCC AST methods. We assessed the performance of reference broth microdilution (BMD), disk diffusion (DD) using Mueller-Hinton agar (MHA) from three manufacturers, agar dilution (AD), and gradient diffusion (ETEST) for ceftazidime (CAZ), levofloxacin (LVX), meropenem (MEM), minocycline (MIN), and trimethoprim-sulfamethoxazole (TMP-SMX) on a set of 205 BCC isolates. The isolate set included 100 isolates from people with CF and 105 isolates from people without CF from a variety of sources, which enabled us to systematically evaluate whether specimen source impacts AST performance. For all BCC isolates, BMD reproducibility was 93%, 98%, 99%, 98%, and 96% for CAZ, LVX, MEM, MIN, and TMP-SMX, respectively. Using BMD as the comparator method, we show that DD, AD, and ETEST perform poorly, with neither MHA manufacturer nor specimen source significantly impacting method performance. Based on our data, we recommend that routine AST should not be performed for BCC isolates. If a provider requests AST, clinical microbiology laboratories should perform Clinical and Laboratory Standards Institute reference methodology for BMD (stored frozen) and report MIC only. IMPORTANCE Antimicrobial susceptibility testing for the Burkholderia cepacia complex (BCC) is often used to determine eligibility for lung transplant in people with cystic fibrosis. However, problems with method performance have been reported. Here, we systematically evaluate the performance of reference broth microdilution, disk diffusion, agar dilution, and gradient diffusion (ETEST) for BCC organisms isolated from people with and without cystic fibrosis. We show that broth microdilution reproducibility is acceptable for levofloxacin, meropenem, minocycline, and trimethoprim-sulfamethoxazole, while ceftazidime was just below the acceptability cut-off. Regardless of specimen source, the results from disk diffusion, agar dilution, and ETEST do not correlate with broth microdilution. Based on these findings, we recommend that antimicrobial susceptibility testing should not be routinely performed for BCC, and if requested by the provider, only broth microdilution following Clinical and Laboratory Standards Institute guidelines should be used. Providers should be aware of the significant limitations of antimicrobial susceptibility testing methods for BCC.

This procedure provides instructions on how to generate amplicons and NGS data for the near whole genome of Mpox. Illumina, Oxford Nanopore or other NGS sequencing platforms can all be utilized if amplicon specific library preparations and platform specific bioinformatic analysis pipelines are available. We detail specific use of a modified Illumina DNA prep library preparation and the analysis pipelines using the generated data in this protocol. The BCCDC / ARTIC V2.3.4 Mpox WGS 2500bp primer scheme was optimized to match and efficiently generate data from the global 2022 West African clade outbreak. The MPV_3000_1_Left to MPV_3000_79_Right primers tile the near whole genome of the Mpox virus. Since the first and last ~6500bp of the Mpox genome (ITR) are usually identical, the last ~6500bp of the genome is masked out on the reference genome to simplify analysis using short read Illumina data. The resulting ITR regions thus represent a consensus ITR combining the amplification products from the dual ITR primer binding sites. For specific ITR region sequence information the use of unique external primer binding sites is required along with removal of all but one common internal ITR binding site to generate specific region spanning PCR products. These products can then be sequenced using Nanopore long read sequencing, see here for some candidate primer combinations (MPV_3000_4_RIGHT, MPV_3000_80_LEFT, and MPV_3000_1_LEFT), to provide specific ITR region sequences. This approach was used to generate the BCCDCmpx2 sequence (available on GISAID, EPI_ISL_13351002) which used both Oxford Nanopore and Illumina data to fully sequence the individual ITR regions and repeat regions refractory to short read technologies alone. The sample PCRs are performed in two pools before being combined for library preparation in order to minimize primer interactions and allow near complete coverage tiling of the Mpox genome. Sequences for the primers and locations on reference genomes can be found in the Materials section tables as well as linked file locations and here. Effort were made to increase sequencing efficiency / genome coverage for a given amount of generated sequence data by performing a number of rounds of primer pair concentration re-balancing in the PCR primer pools (Figure 1.). The primer amounts for V2.3.4 are detailed in this protocol and Materials section.

Highly pathogenic avian influenza (HPAI) is a viral disease that causes significant rates of morbidity and mortality in domestic poultry and wild birds, with occasional spillover into mammals, including humans. Beginning in November 2021, Canada experienced its longest and largest outbreak of HPAI in history. A portion of this outbreak (H5N1, clade 2.3.4.4b) occurred in western Canada, specifically in British Columbia (B.C.) and the Yukon, between April 12 and September 11, 2022, which was classified as the "first wave" in this region. Wild birds and mammals identified through passive surveillance and suspect domestic poultry flocks were screened for avian influenza virus (AIV), typed H5 by qPCR, and positive cases were whole genome sequenced. Descriptive epidemiological and phylodynamic analyses were performed to: (1) understand the taxonomic and geographic extent of wild species involved; and (2) examine the origins and probable transmission networks of HPAI viruses introduced into B.C./Yukon by comparing local viruses with those circulating elsewhere in North America. This outbreak included 21 species of wild birds, 2 species of wild mammals, 4 commercial, and 12 domestic small flock infected premises. Canada geese (Branta canadensis) and bald eagles (Haliaeetus leucocephalus) were the most common wild species detected. We demonstrate that north-south avian migration via the Pacific Flyway is the probable route of multiple incursions into this region. Phylogenetic analysis of the hemagglutinin (HA) segment revealed that the B.C./Yukon viruses detected formed five distinct genetic clusters which were maintained across the whole genome. Although, the genome segments were predominantly Eurasian in origin, NP and PB2 segments from all samples, as well as NS and PB1 segments from Cluster 3, had North American origins. Overall, we demonstrate the utility of genomic epidemiology to inform HPAI transmission dynamics across Western Canada and discuss potential knowledge gaps that exist in passive surveillance strategies for HPAI.

Surveillance data from wildlife and poultry was used to describe the spread of highly pathogenic avian influenza (HPAI) H5N1 clade 2.3.4.4b in British Columbia (B.C.) and the Yukon, Canada from September 2022 - June 2023 compared to the first "wave" of the outbreak in this region, which occurred April - August 2022, after the initial viral introduction. Although the number of HPAI-positive poultry farms and wildlife samples was greater in "Wave 2", cases were more tightly clustered in southwestern B.C. and the most commonly affected species differed, likely due to an influx of overwintering waterfowl in the area. Eight HPAI genetic clusters, representing seven genotypes and two inter-continental viral incursions, were detected, with significant variation in the relative abundance of each cluster between the waves. Phylogenetic data suggests multiple spillover events from wild birds to poultry and mammals but could not rule out transmission among farms and among mammals.

To evaluate immune responses to COVID-19 vaccines in adults aged 50 years and older, spike protein (S)-specific antibody concentration, avidity, and function (via angiotensin-converting enzyme 2 (ACE2) inhibition surrogate neutralization and antibody dependent cellular phagocytosis (ADCP)), as well as S-specific T cells were quantified via activation induced marker (AIM) assay in response to two-dose series. Eighty-four adults were vaccinated with either: mRNA/mRNA (mRNA-1273 and/or BNT162b2); ChAdOx1-S/mRNA; or ChAdOx1-S/ChAdOx1-S. Anti-S IgG concentrations, ADCP scores and ACE2 inhibiting antibody concentrations were highest at one-month post-second dose and declined by four-months post-second dose for all groups. mRNA/mRNA and ChAdOx1-S/mRNA schedules had significantly higher antibody responses than ChAdOx1-S/ChAdOx1-S. CD8+ T-cell responses one-month post-second dose were associated with increased ACE2 surrogate neutralization. Antibody avidity (total relative avidity index) did not change between one-month and four-months post-second dose and did not significantly differ between groups by four-months post-second dose. In determining COVID-19 correlates of protection, a measure that considers both antibody concentration and avidity should be considered.

Abstract Background Multiple combinations of COVID-19 vaccine regimens have been used in Canada throughout the SARS-CoV-2 immunization campaign. Studies evaluating the humoral immune response following COVID-19 vaccination in community dwelling older adults remain limited. This study assessed COVID-19 vaccine elicited antibody responses in older adult populations, alongside factors that influence antibody responses. Methods Community dwelling adults aged 50 to 87 years (mean=65) were enrolled (n=612). Detection of index SARS-CoV-2 anti-spike IgG (anti-S-IgG) concentration and surrogate neutralization were performed on dried blood spot samples via two multiplex assays (Meso Scale Diagnostics). Anti-S-IgG concentration and surrogate neutralization were quantified following mRNA (mRNA-1273 [m-1273], BNT162b2 [BNT]) or viral vector (ChAdOx1-S [ChAd]) vaccination. Vaccine groups were compared using one-way ANOVA and Tukey-Kramer multiple comparisons tests. Multivariable regression analyses evaluated influences of demographic and clinical factors on humoral immune responses. Results Three doses of m-1273 resulted in significantly higher anti-S-IgG compared with three BNT doses at four months (geometric mean concentration; 10167 AU/mL vs. 5412 AU/mL, P=0.009) post dose three. Three dose mixed vaccination with ChAd, m-1273 and BNT resulted in comparable anti-S-IgG concentration to three dose m-1273 at four months post dose three. Three doses of either m-1273 or mixed mRNA containing vaccines was associated with significantly higher surrogate neutralization compared with three BNT doses at four months (46% & 43% vs. 34%, P=0.002) post dose three. No significant difference in anti-S-IgG concentration was observed in four dose vaccination regimens. SARS-CoV-2 infection, health status of excellent or very good, and m-1273 containing vaccine regimens positively influenced the antibody response. Conclusion Immunization schedules including a minimum of one m-1273 dose elicited the strongest and most durable antibody responses compared with BNT only containing regimens. There is no established correlate of protection for COVID-19, and as such this data should be interpreted alongside vaccine effectiveness studies. Omicron and XBB specific antibody responses will be compared. Disclosures Sofia R. Bartlett, PhD, Abbvie: Advisor/Consultant|Abbvie: Grant/Research Support|Cepheid: Advisor/Consultant|Gilead: Advisor/Consultant|Gilead: Grant/Research Support Theodore Steiner, MD, FRCPC, Edesa: Grant/Research Support|Ferring: Advisor/Consultant|Ferring: Grant/Research Support|Qu Biologics: Advisor/Consultant|Qu Biologics: Stocks/Bonds|Seres: Grant/Research Support Manish Sadarangani, BM BCh, FRCPC, DPhil, GlaxoSmithKline: Grant/Research Support|Merck: Grant/Research Support|Moderna: Grant/Research Support|Pfizer: Grant/Research Support|Sanofi Pasteur: Grant/Research Support|Seqirus: Grant/Research Support|Symvivo: Grant/Research Support|VBI Vaccines: Grant/Research Support

OBJECTIVES:Clustering pathogen sequence data is a common practice in epidemiology to gain insights into the genetic diversity and evolutionary relationships among pathogens. We can find groups of cases with a shared transmission history and common origin, as well as identifying transmission hotspots. Motivated by the experience of clustering SARS-CoV-2 cases using whole genome sequence data during the COVID-19 pandemic to aid with public health investigation, we investigated how differences in epidemiology and sampling can influence the composition of clusters that are identified.METHODS:We performed genomic clustering on simulated SARS-CoV-2 outbreaks produced with different transmission rates and levels of genomic diversity, along with varying the proportion of cases sampled.RESULTS:In single outbreaks with a low transmission rate, decreasing the sampling fraction resulted in multiple, separate clusters being identified where intermediate cases in transmission chains are missed. Outbreaks simulated with a high transmission rate were more robust to changes in the sampling fraction and largely resulted in a single cluster that included all sampled outbreak cases. When considering multiple outbreaks in a sampled jurisdiction seeded by different introductions, low genomic diversity between introduced cases caused outbreaks to be merged into large clusters. If the transmission and sampling fraction, and diversity between introductions was low, a combination of the spurious break-up of outbreaks and the linking of closely related cases in different outbreaks resulted in clusters that may appear informative, but these did not reflect the true underlying population structure. Conversely, genomic clusters matched the true population structure when there was relatively high diversity between introductions and a high transmission rate.CONCLUSION:Differences in epidemiology and sampling can impact our ability to identify genomic clusters that describe the underlying population structure. These findings can help to guide recommendations for the use of pathogen clustering in public health investigations.

There is an impending crisis in healthcare brought about by a new era of untreatable infections caused by bacteria resistant to all available antibiotics. Thus, there is an urgent need to identify novel antimicrobial agents to counter the continuing threat posed by formerly treatable infections. We previously reported that a natural mineral clay known as Kisameet clay (KC) is a potent inhibitor of the organisms responsible for acute infections. Chronic bacterial infections present another major challenge to treatment by antimicrobials, due to their prolonged nature, which results in repeated exposure to antibiotics and a constant selection for antimicrobial resistance. A prime example is bacteria belonging to the Burkholderia cepacia complex (Bcc), which particularly causes some of the most serious chronic lung infections in patients with cystic fibrosis (CF) associated with unpredictable clinical outcomes, poor prognosis, and high mortality rates. Eradication of these organisms from CF patients with limited effective antimicrobial options is a major challenge. Novel therapeutic approaches are urgently required. Here, we report the in vitro antibacterial activity of KC aqueous suspensions (1–10% w/v) and its aqueous extract (L100) against a collection of extensively and multi-drug resistant clinical isolates of Bcc, Pseudomonas aeruginosa, and Stenotrophomonas maltophilia isolated from patients with CF. These findings present a potential novel therapy for further investigation in the clinic.

Abstract Background Adults aged > 50 years are at increased risk for severe coronavirus disease 2019 (COVID-19). This study evaluated immunogenicity of COVID-19 vaccines in healthy adults aged > 50 years through quantification of antigen specific antibody concentration and function post-vaccination with two, three and four COVID-19 vaccine doses. Methods Eighty-four immunocompetent, community-dwelling adults 50 to 83 years old (median age 61 years) were enrolled. We measured index virus spike protein (S) specific antibody responses to mRNA (mRNA-1273 or BNT162b2) and/or ChAdOx1-S COVID-19 vaccines. Participants were separated into three groups: (1) mRNA/mRNA/mRNA/mRNA; (2) ChAdOx1-S/mRNA/mRNA; (3) ChAdOx1-S/ChAdOx1-S/mRNA. Responses were quantified via: anti-S IgG geometric mean concentrations (GMCs) (binding antibody units [BAU]/mL), total relative IgG avidity index (TRAI) (avidity units, AU) collected up to one, four, and seven-months after each dose. One-way ANOVA, Tukey-Kramer post-hoc compared groups and Welch’s t-test compared timepoints. Results At one month post-dose two, mRNA/mRNA (1137 BAU/mL, p = 0.0003) and ChAdOx1-S/mRNA (1388, p < 0.0001) had higher anti-S IgG GMCs compared with ChAdOx1-S/ChadOx1-S (195 BAU/mL). However, TRAI was similar amongst the three groups (all p > 0.05); mRNA/mRNA (70 AU), ChAdOx1-S/mRNA (66 AU) and ChAdOx1-S/ChAdOx1-S (58 AU). S-IgG GMCs at one month post-dose three were higher for mRNA/mRNA/mRNA than ChAdOx1-S/ChAdOx1-S/mRNA (1316 vs. 569 BAU/mL p = 0.0162). Similar to post-dose two, post-dose three there were no significant differences in TRAI between groups (all p > 0.05); mRNA/mRNA/mRNA (95 AU), ChAdOx1-S/mRNA/mRNA (98 AU), ChAdOx1-S/ChAdOx1-S/mRNA (101 AU). For mRNA/mRNA/mRNA participants, a fourth mRNA vaccine dose increased S-IgG GMCs at one-month post-dose four compared with one month post-dose two (2825 vs. 1137 BAU/mL, p = 0.0126) and maintained TRAI between timepoints (71 vs. 70 AU, p = 0.9877). Conclusion mRNA vaccines are more immunogenic compared to ChAdOx1-S with regards to S-specific antibody concentration. mRNA boosters maintained antibody avidity. Together, TRAI and anti-S IgG GMCs should be further evaluated when recommending additional booster doses and considered when determining protection against COVID-19. Disclosures Sofia R. Bartlett, PhD, Abbvie: Advisor/Consultant|Abbvie: Grant/Research Support|Cepheid: Advisor/Consultant|Gilead: Advisor/Consultant|Gilead: Grant/Research Support Manish Sadarangani, BM BCh, FRCPC, DPhil, GlaxoSmithKline: Grant/Research Support|Merck: Grant/Research Support|Moderna: Grant/Research Support|Pfizer: Grant/Research Support|Sanofi Pasteur: Grant/Research Support|Seqirus: Grant/Research Support|Symvivo: Grant/Research Support|VBI Vaccines: Grant/Research Support

The SARS-CoV-2 variant Omicron emerged in late 2021. In British Columbia (BC), Canada, and globally, three genetically distinct subvariants of Omicron, BA.1, BA.2, and BA.5, emerged and became dominant successively within an 8-month period. SARS-CoV-2 subvariants continue to circulate in the population, acquiring new mutations that have the potential to alter infectivity, immunity, and disease severity. Here, we report a propensity-matched severity analysis from residents of BC over the course of the Omicron wave, including 39,237 individuals infected with BA.1, BA.2, or BA.5 based on paired high-quality sequence data and linked to comprehensive clinical outcomes data between December 23, 2021 and August 31, 2022. Relative to BA.1, BA.2 cases were associated with a 15% and 28% lower risk of hospitalization and intensive care unit (ICU) admission (aHR(hospital) = 1.17; 95% confidence interval [CI] = 1.096-1.252; aHR(ICU) = 1.368; 95% CI = 1.152-1.624), whereas BA.5 infections were associated with an 18% higher risk of hospitalization (aHR(hospital) = 1.18; 95% CI = 1.133-1.224) after accounting for age, sex, comorbidities, vaccination status, geography, and social determinants of health. Phylogenetic analysis revealed no specific subclades associated with more severe clinical outcomes for any Omicron subvariant. In summary, BA.1, BA.2, and BA.5 subvariants were associated with differences in clinical severity, emphasizing how variant-specific monitoring programs remain critical components of patient and population-level public health responses as the pandemic continues.

We developed a salivary assay for the detection of naturally acquired IgA antibody against Haemophilus influenzae type a (Hia) capsular polysaccharide in healthy Indigenous children from Northwestern Ontario, Canada. Hia-specific IgA antibody was detected in the saliva of 93% of Indigenous children aged 2-7 years.

Background The COVID-19 pandemic remains a global public health concern. Advances in sequencing technologies has allowed for high numbers of SARS-CoV-2 whole genome sequence (WGS) data and rapid sharing of sequences through global repositories to enable almost real-time genomic analysis of the pathogen. WGS data has been used previously to group genetically similar viral pathogens to reveal evidence of transmission, including methods that identify distinct clusters on a phylogenetic tree. Identifying clusters of linked cases can aid in the regional surveillance and management of the disease. In this study, we present a novel method for producing stable genomic clusters of SARS-CoV-2 cases, cov2clusters, and compare the accuracy and stability of our approach to previous methods used for phylogenetic clustering using real-world SARS-CoV-2 sequence data obtained from British Columbia, Canada. Results We found that cov2clusters produced more stable clusters than previously used phylogenetic clustering methods when adding sequence data through time, mimicking an increase in sequence data through the pandemic. Our method also showed high accuracy when predicting epidemiologically informed clusters from sequence data. Conclusions Our new approach allows for the identification of stable clusters of SARS-CoV-2 from WGS data. Producing high-resolution SARS-CoV-2 clusters from sequence data alone can a challenge and, where possible, both genomic and epidemiological data should be used in combination.