Severity of influenza A 2009 (H1N1) pneumonia is underestimated by routine prediction rules. Results from a prospective, population-based study.

Characteristics of patients with community-acquired pneumonia (CAP) due to pandemic influenza A 2009 (H1N1) have been inadequately compared to CAP caused by other respiratory pathogens. The performance of prediction rules for CAP during an epidemic with a new infectious agent are unknown. Prospective, population-based study from November 2008-November 2009, in centers representing 70% of hospital beds in Iceland. Patients admitted with CAP underwent evaluation and etiologic testing, including polymerase chain reaction (PCR) for influenza. Data on influenza-like illness in the community and overall hospital admissions were collected. Clinical and laboratory data, including pneumonia severity index (PSI) and CURB-65 of patients with CAP due to H1N1 were compared to those caused by other agents. Of 338 consecutive and eligible patients 313 (93%) were enrolled. During the pandemic peak, influenza A 2009 (H1N1) patients constituted 38% of admissions due to CAP. These patients were younger, more dyspnoeic and more frequently reported hemoptysis. They had significantly lower severity scores than other patients with CAP (1.23 vs. 1.61, P= .02 for CURB-65, 2.05 vs. 2.87 for PSI, P<.001) and were more likely to require intensive care admission (41% vs. 5%, P<.001) and receive mechanical ventilation (14% vs. 2%, P= .01). Bacterial co-infection was detected in 23% of influenza A 2009 (H1N1) patients with CAP. Clinical characteristics of CAP caused by influenza A 2009 (H1N1) differ markedly from CAP caused by other etiologic agents. Commonly used CAP prediction rules often failed to predict admissions to intensive care or need for assisted ventilation in CAP caused by the influenza A 2009 (H1N1) virus, underscoring the importance of clinical acumen under these circumstances.Icelandic Center for Research, Rannis 100436021 Landspitali University Hospital Science Fun

Physical and cognitive impact following SARS-CoV-2 infection in a large population-based case-control study

© 2023. The Author(s).BACKGROUND: Persistent symptoms are common after SARS-CoV-2 infection but correlation with objective measures is unclear. METHODS: We invited all 3098 adults who tested SARS-CoV-2 positive in Iceland before October 2020 to the deCODE Health Study. We compared multiple symptoms and physical measures between 1706 Icelanders with confirmed prior infection (cases) who participated, and 619 contemporary and 13,779 historical controls. Cases participated in the study 5-18 months after infection. RESULTS: Here we report that 41 of 88 symptoms are associated with prior infection, most significantly disturbed smell and taste, memory disturbance, and dyspnea. Measured objectively, cases had poorer smell and taste results, less grip strength, and poorer memory recall. Differences in grip strength and memory recall were small. No other objective measure associated with prior infection including heart rate, blood pressure, postural orthostatic tachycardia, oxygen saturation, exercise tolerance, hearing, and traditional inflammatory, cardiac, liver, and kidney blood biomarkers. There was no evidence of more anxiety or depression among cases. We estimate the prevalence of long Covid to be 7% at a median of 8 months after infection. CONCLUSIONS: We confirm that diverse symptoms are common months after SARS-CoV-2 infection but find few differences between cases and controls in objective parameters measured. These discrepancies between symptoms and physical measures suggest a more complicated contribution to symptoms related to prior infection than is captured with conventional tests. Traditional clinical assessment is not expected to be particularly informative in relating symptoms to a past SARS-CoV-2 infection.Peer reviewe

Etiologic causes of community acquired pneumonia (CAP) identified during the 12-month study, by quarters.

<p>The proportion of total pneumonia admissions accounted for by each etiology for each quartile is shown. Influenza during the first and second quartiles was caused by seasonal influenza H3N2 whereas all influenza cases during the third and fourth quartiles were pandemic influenza (H1N1). Less frequently encountered pathogens listed as “other” included <i>M. catarrhalis</i>, <i>S. aureus</i>, <i>C. pneumoniae</i>, <i>Legionella</i> species, <i>P. aeruginosa</i> as well as various streptococcal species.</p

Comparison of CAP Patients by Etiology – Treatment and Outcome.

<p>CAP, community acquired pneumonia; CI, confidence interval; IV, intravenous; abx, antibiotic; UAT, urine antigen test;; ICU, intensive care unit; BAL, bronchoalveolar lavage.</p>a<p>P-values<.05 shown in bold.</p>b<p>Atypical coverage denotes empiric antimicrobial treatment including coverage for “atypical” bacterial organisms.</p

Epidemiology of influenza in Iceland, December 2008-December 2009, showing the number of reported cases of influenza-like illness (ILI) and confirmed influenza A 2009 (H1N1) (left y-axis) and weekly ILI incidence per 100 000 population (right y-axis).

<p>In Iceland approximately 62% of all virologically confirmed cases and ILI were in Reykjavik <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0046816#pone.0046816-Sigmundsdottir1" target="_blank">[21]</a>. (Ref: <a href="http://www.influensa.is/pages/1505" target="_blank">http://www.influensa.is/pages/1505</a>).</p

Comparison of CAP Patients by Etiology – Symptoms, Test Results and Severity Scores.

<p>CAP, community acquired pneumonia; CI, confidence interval; BP, blood pressure; MAP, mean arterial pressure; RR, respiratory rate; SpO2, pulse-oximetry; WBC, white blood cell; CRP, C-reactive protein; PSI, pneumonia severity index.</p>a<p>P-values<.05 shown in bold.</p>b<p>Worst value denotes the worst noted value during the first 24 hours of admission.</p

Comparison of CAP Patients by Etiology – Characteristics and Underlying Conditions.

<p>CAP, community acquired pneumonia; CI, confidence interval; PPI, proton pump inhibitor; COPD, chronic obstructive pulmonary disease; DM, diabetes mellitus.</p>a<p><i>P</i> values<.05 shown in bold.</p>b<p>Immune suppression due to medications or malignancy.</p>c<p>Any chronic disease is a composite of the conditions listed above.</p

Humoral Immune Response to SARS-CoV-2 in Iceland.

To access publisher's full text version of this article click on the hyperlink belowBackground: Little is known about the nature and durability of the humoral immune response to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Methods: We measured antibodies in serum samples from 30,576 persons in Iceland, using six assays (including two pan-immunoglobulin [pan-Ig] assays), and we determined that the appropriate measure of seropositivity was a positive result with both pan-Ig assays. We tested 2102 samples collected from 1237 persons up to 4 months after diagnosis by a quantitative polymerase-chain-reaction (qPCR) assay. We measured antibodies in 4222 quarantined persons who had been exposed to SARS-CoV-2 and in 23,452 persons not known to have been exposed. Results: Of the 1797 persons who had recovered from SARS-CoV-2 infection, 1107 of the 1215 who were tested (91.1%) were seropositive; antiviral antibody titers assayed by two pan-Ig assays increased during 2 months after diagnosis by qPCR and remained on a plateau for the remainder of the study. Of quarantined persons, 2.3% were seropositive; of those with unknown exposure, 0.3% were positive. We estimate that 0.9% of Icelanders were infected with SARS-CoV-2 and that the infection was fatal in 0.3%. We also estimate that 56% of all SARS-CoV-2 infections in Iceland had been diagnosed with qPCR, 14% had occurred in quarantined persons who had not been tested with qPCR (or who had not received a positive result, if tested), and 30% had occurred in persons outside quarantine and not tested with qPCR. Conclusions: Our results indicate that antiviral antibodies against SARS-CoV-2 did not decline within 4 months after diagnosis. We estimate that the risk of death from infection was 0.3% and that 44% of persons infected with SARS-CoV-2 in Iceland were not diagnosed by qPCR