INTRODUCTION: CDC estimates that influenza resulted in 9-41 million illnesses, 140,000-710,000 hospitalizations, and 12,000-52,000 deaths annually during 2010-2020. Persons from some racial and ethnic minority groups have historically experienced higher rates of severe influenza and had lower influenza vaccination coverage compared with non-Hispanic White (White) persons. This report examines influenza hospitalization and vaccination rates by race and ethnicity during a 12-13-year period (through the 2021-22 influenza season). METHODS: Data from population-based surveillance for laboratory-confirmed influenza-associated hospitalizations in selected states participating in the Influenza-Associated Hospitalization Surveillance Network (FluSurv-NET) from the 2009-10 through 2021-22 influenza seasons (excluding 2020-21) and influenza vaccination coverage data from the Behavioral Risk Factor Surveillance System (BRFSS) from the 2010-11 through 2021-22 influenza seasons were analyzed by race and ethnicity. RESULTS: From 2009-10 through 2021-22, age-adjusted influenza hospitalization rates (hospitalizations per 100,000 population) were higher among non-Hispanic Black (Black) (rate ratio [RR] = 1.8), American Indian or Alaska Native (AI/AN; RR = 1.3), and Hispanic (RR = 1.2) adults, compared with the rate among White adults. During the 2021-22 season, influenza vaccination coverage was lower among Hispanic (37.9%), AI/AN (40.9%), Black (42.0%), and other/multiple race (42.6%) adults compared with that among White (53.9%) and non-Hispanic Asian (Asian) (54.2%) adults; coverage has been consistently higher among White and Asian adults compared with that among Black and Hispanic adults since the 2010-11 season. The disparity in vaccination coverage by race and ethnicity was present among those who reported having medical insurance, a personal health care provider, and a routine medical checkup in the past year. CONCLUSIONS AND IMPLICATIONS FOR PUBLIC HEALTH PRACTICE: Racial and ethnic disparities in influenza disease severity and influenza vaccination coverage persist. Health care providers should assess patient vaccination status at all medical visits and offer (or provide a referral for) all recommended vaccines. Tailored programmatic efforts to provide influenza vaccination through nontraditional settings, along with national and community-level efforts to improve awareness of the importance of influenza vaccination in preventing illness, hospitalization, and death among racial and ethnic minority communities might help address health care access barriers and improve vaccine confidence, leading to decreases in disparities in influenza vaccination coverage and disease severity.

BACKGROUND: Many health departments and private enterprises began offering SARS-CoV-2 testing to travelers at US airports in 2020. Persons with positive SARS-CoV-2 test results who have planned upcoming travel may be subject to US federal public health travel restrictions. We assessed availability of testing for SARS-CoV-2 at major US airports. We then describe the management of cases and close contacts at Denver International Airport's testing site. METHODS: We selected 100 US airports. Online surveys were conducted during November-December 2020 and assessed availability of testing for air travelers, flight crew, and airport employees. Respondents included health department (HD) staff or airport directors. We analyzed testing data and management practices for persons who tested positive and their close contacts at one airport (Denver International) from 12/21/2020 to 3/31/2021. RESULTS: Among the 100 selected airports, we received information on 77 airports; 38 (49%) had a testing site and several more planned to offer one (N=7; 9%). Most sites began testing in the fall of 2020. The most frequently offered tests were RT-PCR or other NAAT tests (N=28). Denver International Airport offered voluntary SARS-CoV-2 testing. Fifty-four people had positive results among 5724 tests conducted from 12/21/2020 to 3/31/2021 for a total positivity of <1%. Of these, 15 were travelers with imminent flights. The Denver HD issued an order requiring the testing site to immediately report cases and notify airlines to cancel upcoming flight itineraries for infected travelers and their traveling close contacts, minimizing the use of federal travel restrictions. CONCLUSIONS: As of December 2020, nearly half of surveyed US airports had SARS-CoV-2 testing sites. Such large-scale adoption of airport testing for a communicable disease is unprecedented and presents new challenges for travelers, airlines, airports, and public health authorities. This assessment was completed before the US and other countries began enforcing entry testing requirements; testing at airports will likely increase as travel demand returns and test requirements for travel evolve. Lessons from Denver demonstrate how HDs can play a key role in engaging airport testing sites to ensure people who test positive for SARS-CoV-2 immediately before travel do not travel on commercial aircraft.

OBJECTIVES: Widespread global transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus causing coronavirus disease 2019 (COVID-19), continues. Many questions remain about asymptomatic or atypical infections and transmission dynamics. We used comprehensive contact tracing of the first 2 confirmed patients in Illinois with COVID-19 and serologic SARS-CoV-2 antibody testing to determine whether contacts had evidence of undetected COVID-19. METHODS: Contacts were eligible for serologic follow-up if previously tested for COVID-19 during an initial investigation or had greater-risk exposures. Contacts completed a standardized questionnaire during the initial investigation. We classified exposure risk as high, medium, or low based on interactions with 2 index patients and use of personal protective equipment (PPE). Serologic testing used a SARS-CoV-2 spike enzyme-linked immunosorbent assay on serum specimens collected from participants approximately 6 weeks after initial exposure to either index patient. The 2 index patients provided serum specimens throughout their illness. We collected data on demographic, exposure, and epidemiologic characteristics. RESULTS: Of 347 contacts, 110 were eligible for serologic follow-up; 59 (17% of all contacts) enrolled. Of these, 53 (90%) were health care personnel and 6 (10%) were community contacts. Seventeen (29%) reported high-risk exposures, 15 (25%) medium-risk, and 27 (46%) low-risk. No participant had evidence of SARS-CoV-2 antibodies. The 2 index patients had antibodies detected at dilutions >1:6400 within 4 weeks after symptom onset. CONCLUSIONS: In serologic follow-up of the first 2 known patients in Illinois with COVID-19, we found no secondary transmission among tested contacts. Lack of seroconversion among these contacts adds to our understanding of conditions (ie, use of PPE) under which SARS-CoV-2 infections might not result in transmission and demonstrates that SARS-CoV-2 antibody testing is a useful tool to verify epidemiologic findings.

Gulf War illness (GWI) is a chronic and multi-symptomatic disorder with persistent neuroimmune symptomatology. Chemokine receptor 6 (CCR6) has been shown to be involved in several inflammation disorders in humans. However, the causative relationship between CCR6 and neuroinflammation in GWI has not yet been investigated. By using RNA-seq data of prefrontal cortex (PFC) from 31 C57BL/6J X DBA/2J (BXD) recombinant inbred (RI) mouse strains and their parental strains under three chemical treatment groups – saline control (CTL), diisopropylfluorophosphate (DFP), and corticosterone combined with diisopropylfluorophosphate (CORT+DFP), we identified Ccr6 as a candidate gene underlying individual differences in susceptibility to GWI. The Ccr6 gene is cis-regulated and its expression is significantly correlated with CORT+DFP treatment. Its mean transcript abundance in PFC of BXD mice decreased 1.6-fold (p < 0.0001) in the CORT+DFP group. The response of Ccr6 to CORT+DFP is also significantly different (p < 0.0001) between the parental strains, suggesting Ccr6 is affected by both host genetic background and chemical treatments. Pearson product-moment correlation analysis revealed 1473 Ccr6-correlated genes (p < 0.05). Enrichment of these genes was seen in the immune, inflammation, cytokine, and neurological related categories. In addition, we also found five central nervous system-related phenotypes and fecal corticosterone concentration have significant correlation (p < 0.05) with expression of Ccr6 in the PFC. We further established a protein-protein interaction subnetwork for the Ccr6-correlated genes, which provides an insight on the interaction of G protein-coupled receptors, kallikrein-kinin system and neuroactive ligand-receptors. This analysis likely defines the heterogeneity and complexity of GWI. Therefore, our results suggest that Ccr6 is one of promising GWI biomarkers.

Gulf War Illness (GWI) is thought to be a chronic neuroimmune disorder caused by in-theater exposure during the 1990-1991 Gulf War. There is a consensus that the illness is caused by exposure to insecticides and nerve agent toxicants. However, the heterogeneity in both development of disease and clinical outcomes strongly suggests a genetic contribution. Here, we modeled GWI in 30 BXD recombinant inbred strains with a combined treatment of corticosterone (CORT) and diisopropyl fluorophosphate (DFP). We quantified transcriptomes from 409 prefrontal cortex samples. Compared to the untreated and DFP treated controls. The combined treatment significantly activated pathways such as cytokine-cytokine receptor interaction and TNF signaling pathway. Protein-protein interaction analysis defined 6 subnetworks for CORT+DFP, with the key regulators being Cxcl1, Il6, Ccnb1, Tnf, Agt, and Itgam. We also identified 21 differentially expressed genes having significant QTLs related to CORT+DFP, but without evidence for untreated and DFP treated controls, suggesting regions of the genome specifically involved in the response to CORT+DFP. We identified Adamts9 as a potential contributor to response to CORT+DFP and found links to symptoms of GWI. Furthermore, we observed a significant effect of CORT+DFP treatment on the relative proportion of myelinating oligodendrocytes, with a QTL on Chr5. We highlight three candidates, Magi2, Sema3c, and Gnai1, based on their high expression in the brain and oligodendrocyte. In summary, our results show significant genetic effects of the CORT+DFP treatment, which mirrors gene and protein expression changes seen in GWI sufferers, providing insight into the disease and a testbed for future interventions.

BACKGROUND: On April 29, 2015, the Florida Department of Health in Miami-Dade County (DOH-Miami-Dade) was notified by a local dermatologist of three patients with suspect nontuberculous mycobacterial (NTM) infection after receiving tattoos at a local tattoo studio. METHODS: DOH-Miami-Dade conducted interviews and offered testing, described below, to tattoo studio clients reporting rashes. Culture of clinical isolates and identification were performed at the Florida Bureau of Public Health Laboratories (BPHL). Characterization of NTM was performed by the Centers for Disease Control and Prevention (CDC) and the United States Food and Drug Administration (FDA), respectively. Whole-genome sequencing (WGS) and single-nucleotide polymorphism (SNP) analyses were used to construct a phylogeny among 21 Mycobacterium isolates at FDA. RESULTS: Thirty-eight of 226 interviewed clients were identified as outbreak-associated cases. Multivariate logistic regression revealed individuals who reported grey tattoo ink in their tattoos were 8.2 times as likely to report a rash [95% CI: 3.07-22.13]. Multiple NTM species were identified in clinical and environmental specimens. Phylogenetic results from environmental samples and skin biopsies indicated that two M. fortuitum isolates (greywash ink and a skin biopsy) and 11 M. abscessus isolates (five from the implicated bottle of greywash tattoo ink, two from tap water, and four from skin biopsies) were indistinguishable. In addition, M. chelonae was isolated from five unopened bottles of greywash ink provided by two other tattoo studios in Miami-Dade County. CONCLUSIONS: WGS and SNP analyses identified the tap water and the bottle of greywash tattoo ink as the sources of the NTM infections.

Intended Use: Field-deployed use for analysis of | aerosol collection filters and/or liquids | 1 Applicability | Detection of Burkholderia pseudomallei in collection buffers | from aerosol collection devices. Field-deployable assays are | preferred. | 2 Analytical Technique | Molecular detection of nucleic acid. | 3  Definitions | Acceptable minimum detection level (AMDL).— | Predetermined minimum level of an analyte, as specified by | an expert committee which must be detected by the candidate | method at a specified probability of detection (POD). | Exclusivity.—Study involving pure nontarget strains, which | are potentially cross-reactive, that shall not be detected or | enumerated by the candidate method. | Inclusivity.—Study involving pure target strains that shall be | detected or enumerated by the candidate method. | Maximum time-to-result.—Maximum time to complete an | analysis starting from the collection buffer to assay result. | Probability of detection (POD).—Proportion of positive | analytical outcomes for a qualitative method for a given matrix | at a specified analyte level or concentration with a ≥0.95 | confidence interval. | System false-negative rate.—Proportion of test results that | are negative contained within a population of known positives. | System false-positive rate.—Proportion of test results that are | positive contained within a population of known negatives. | 4  Method Performance Requirements | See Table 1. | 5  System Suitability Tests and/or Analytical Quality Control | The controls listed in Table 2 shall be embedded in assays as | appropriate. Manufacturer must provide written justification if | controls are not embedded in the assay.

In May of 2011, an enteroaggregative Escherichia coli O104:H4 strain that had acquired a Shiga toxin 2-converting phage caused a large outbreak of bloody diarrhea in Europe which was notable for its high prevalence of hemolytic uremic syndrome cases. Several studies have described the genomic inventory and phylogenies of strains associated with the outbreak and a collection of historical E. coli O104:H4 isolates using draft genome assemblies. We present the complete, closed genome sequences of an isolate from the 2011 outbreak (2011C-3493) and two isolates from cases of bloody diarrhea that occurred in the Republic of Georgia in 2009 (2009EL-2050 and 2009EL-2071). Comparative genome analysis indicates that, while the Georgian strains are the nearest neighbors to the 2011 outbreak isolates sequenced to date, structural and nucleotide-level differences are evident in the Stx2 phage genomes, the mer/tet antibiotic resistance island, and in the prophage and plasmid profiles of the strains, including a previously undescribed plasmid with homology to the pMT virulence plasmid of Yersinia pestis. In addition, multiphenotype analysis showed that 2009EL-2071 possessed higher resistance to polymyxin and membrane-disrupting agents. Finally, we show evidence by electron microscopy of the presence of a common phage morphotype among the European and Georgian strains and a second phage morphotype among the Georgian strains. The presence of at least two stx2 phage genotypes in host genetic backgrounds that may derive from a recent common ancestor of the 2011 outbreak isolates indicates that the emergence of stx2 phage-containing E. coli O104:H4 strains probably occurred more than once, or that the current outbreak isolates may be the result of a recent transfer of a new stx2 phage element into a pre-existing stx2-positive genetic background.