A case of #H10N3 avian #influenza in a young woman

 

Context and significance

The avian influenza A virus subtype H10N3 is a possible candidate for causing a fatal flu and may present a serious public health threat. Research increasingly shows that the avian influenza virus H10N3 can be transmitted from birds to humans, causing severe viral pneumonia and potentially leading to acute respiratory distress syndrome and respiratory failure. Researchers at the Fourth People’s Hospital of Nanning (China) provide evidence supporting the cross-species transmission of the avian influenza virus H10N3 to humans, which can give rise to severe pneumonia. The authors report that a female patient with avian influenza virus H10N3 infection, who was suffering from severe pneumonia, respiratory failure, pneumothorax, and numbness and dysesthesia in her feet, recovered after receiving appropriate therapy and was discharged from the hospital.

Highlights

• A young woman contracted the avian influenza virus H10N3

• Secondary infections, pneumothorax, and foot numbness developed consecutively

• Baloxavir marboxil and oseltamivir were administered

Summary

Background

Avian influenza viruses, frequently identified in wild waterfowl and poultry, have occasionally been transmitted to humans, causing severe respiratory diseases. This report covers the fourth case of a human contracting the H10N3 subtype of avian influenza virus.

Methods

A case of novel avian influenza virus subtype H10N3 was detected in a female patient hospitalized in Nanning, China, in December 2024. Blood, feces, urine, and bronchoalveolar lavage fluid were collected from the patient for medical analysis during the hospitalization.

Findings

A case of novel avian influenza virus subtype H10N3 was detected in a female patient hospitalized in Nanning, China, in December 2024. She also had a history of exposure to live poultry. This case represents the fourth documented instance of H10N3 infection in humans. She was treated with a combination of baloxavir marboxil and oseltamivir. She exhibited extensive lung lesions. Additionally, she presented complicating factors, including secondary infection, pneumothorax, and numbness in her feet. She recovered and was discharged on March 27, 2025, amid comprehensive supportive care, which included therapy with baloxavir marboxil, oseltamivir, fluconazole, tigecycline, amikacin, extracorporeal membrane oxygenation, and rehabilitation therapy.

Conclusions

The virus was effectively cleared by the combination therapies. The internal genes of the H10N3 virus in this patient were highly homologous to the corresponding genes from the A/Yunnan/2024 virus (GenBank accession numbers, hemagglutinin [HA] [GenBank: PP555669] and PB-2 [GenBank: PP555666]).

Funding

This work was funded by the Fourth People’s Hospital of Nanning - Human Immunodeficiency Virus/Acquired Immune Deficiency Syndrome (HIV/AIDS) Clinical Treatment Center of Guangxi (Nanning).

Source: Med., https://www.cell.com/med/abstract/S2666-6340(25)00272-7

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In-hospital #outcomes and 6-month follow-up results of #patients supported with #ECMO for #COVID19 from the 2nd wave to end of pandemic (EuroECMO-COVID)...

Summary

Background

Extracorporeal membrane oxygenation (ECMO) for COVID-19 was thoroughly assessed during the first pandemic wave, but data on subsequent waves are limited. We aimed to investigate in-hospital and 6-month survival of patients with COVID-19 supported with ECMO from the second pandemic wave (Sept 15, 2020) until the end of the pandemic (March 21, 2023, announced by WHO).

Methods

EuroECMO-COVID is a prospective, observational study including adults (aged ≥16 years) requiring ECMO respiratory support for COVID-19 from 98 centres in 21 countries. We compared patient characteristics and outcomes between in-hospital survivors and non-survivors. Mixed-effects multivariable logistic regressions were used to investigate factors linked to in-hospital mortality. 6-month survival and overall patient status were determined via patient contact or chart review. This study is registered with ClinicalTrials.gov, NCT04366921, and is complete.

Findings

We included 3860 patients (2687 [69·7%] were male and 1169 [30·3%] were female; median age 51 years [SD 11]) from 98 centres in 21 countries. In-hospital mortality was 55·9% (n=2158), with 81·2% (n=1752) deaths occurring during ECMO support. More non-survivors had diabetes, hypertension, cardiovascular disease, and renal failure, and required more pre-ECMO inotropes and vasopressors compared with survivors. Median support duration was 18 days (IQR 10–31) for both groups. Factors linked to in-hospital mortality included older age, pre-ECMO renal failure, pre-ECMO vasopressors use, longer time from intubation to ECMO initiation, and complications, including neurological events, sepsis, bowel ischaemia, renal failure, and bleeding. Of the 1702 (44·1%) in-hospital survivors, 99·7% (n=1697) were alive at 6 months follow-up. Many patients at 6 months follow-up had dyspnoea (501 [32·0%] of 1568 patients), cardiac (122 [7·8%] of 1568 patients), or neurocognitive (168 [10·7%] of 1567 patients) symptoms.

Interpretation

Our data for patients undergoing ECMO support for respiratory distress from the second COVID-19 wave onwards confirmed most findings from the first wave regarding patient characteristics and factors correlated to in-hospital mortality. Nevertheless, in-hospital mortality was higher than during the initial pandemic wave while 6-month post-discharge survival remained favourable (99·7%). Persisting post-discharge symptoms confirmed the need for post-ECMO patient follow-up programmes.

Source: Lancet Respiratory Medicine, https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(24)00369-2/abstract?rss=yes

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#Critical #Illness in an #Adolescent with #Influenza A(#H5N1) Virus #Infection

To the Editor:

Highly pathogenic avian influenza A(H5N1) viruses are circulating among wild birds and poultry in British Columbia, Canada.1 These viruses are also recognized to cause illness in humans. Here, we report a case of critical illness caused by influenza A(H5N1) virus infection in British Columbia.

On November 4, 2024, a 13-year-old girl with a history of mild asthma and an elevated body-mass index (the weight in kilograms divided by the square of the height in meters) of greater than 35 presented to an emergency department in British Columbia with a 2-day history of conjunctivitis in both eyes and a 1-day history of fever. She was discharged home without treatment, but cough, vomiting, and diarrhea then developed, and she returned to the emergency department on November 7 in respiratory distress with hemodynamic instability. On November 8, she was transferred, while receiving bilevel positive airway pressure, to the pediatric intensive care unit at British Columbia Children’s Hospital with respiratory failure, pneumonia in the left lower lobe, acute kidney injury, thrombocytopenia, and leukopenia (...). A nasopharyngeal swab obtained at admission was positive for influenza A but negative for A(H1) and A(H3) by the BioFire Respiratory Panel 2.1 assay (BioFire Diagnostics). Reflex testing of the specimen with the Xpert Xpress CoV-2/Flu/RSV plus assay (Cepheid) revealed an influenza A cycle threshold (Ct) value of 27.1. This finding indicates a relatively high viral load for which subtyping would be expected; the lack of subtype identification suggested infection with a novel influenza A virus. Oseltamivir treatment was started on November 8 (Table S2), and the use of eye protection, N95 respirators, and other precautions against droplet, contact, and airborne transmission were implemented.

A reverse-transcriptase–polymerase-chain-reaction (RT-PCR) test specific for influenza A(H5)2 was positive on the day of admission. The patient had signs of respiratory deterioration — chest radiographs were consistent with progression to acute respiratory distress syndrome (...) — which prompted tracheal intubation and initiation of venovenous extracorporeal membrane oxygenation (ECMO) on November 9. Continuous renal replacement therapy was initiated on November 10. Combination antiviral treatment with amantadine (initiated on November 9) and baloxavir (initiated on November 11) was added to ongoing treatment with oseltamivir. Bacterial cultures of blood (samples obtained at admission) and endotracheal aspirate (obtained after intubation) yielded no growth.

Because of concern for cytokine-mediated hemodynamic instability, plasma exchange was performed daily from November 14 through November 16. Serial influenza A–specific RT-PCR tests showed increasing Ct values, which suggested a decline in the viral RNA load in serum and a decline in viral RNA in upper- and lower-respiratory specimens shortly after the initiation of antiviral treatment, with the first negative RT-PCR result for serum obtained on November 16 (...). It is notable that lower-respiratory specimens consistently yielded lower Ct values than upper-respiratory specimens, a finding that suggested higher viral levels in the lower-respiratory tract (...).

Influenza A(H5N1) virus was cultured from respiratory specimens obtained between November 8 and November 12 but not from subsequent respiratory specimens or from any serum specimens (...). No evidence of reduced susceptibility to any of the three antiviral agents used in treatment was observed in serial respiratory specimens by either genomic analysis or phenotypic testing with the NA-Star influenza neuraminidase inhibitor resistance detection kit (ThermoFisher Scientific) (...). The patient’s respiratory status improved, ECMO was discontinued on November 22, and the patient’s trachea was extubated on November 28.

The viral genome sequence obtained from a tracheal-aspirate specimen collected on November 9 (8 days after the onset of symptoms) was reconstructed as described previously.3 The virus was typed as clade 2.3.4.4b, genotype D1.1,4 most closely related to viruses detected in wild birds in British Columbia around the same time (...). Markers of adaptation to humans were detected in the tracheal-aspirate specimen collected on November 9: the E627K mutation was detected (52% allele frequency) in the polymerase basic 2 (PB2) gene product, and analysis of the H5 hemagglutinin (HA) gene yielded ambiguous calls in the codons for amino acid residues E186 (E190 according to H3 mature HA numbering) — 28% allele frequency for E186D — and Q222 (Q226 according to H3 mature HA numbering) — 35% allele frequency for Q222H. The mutations in the H5 HA gene have previously been shown to increase binding to α2-6–linked sialic acids, which act as receptors that facilitate viral entry into cells in the human respiratory tract and enable viral replication.5

Highly pathogenic avian influenza A(H5N1) virus infection acquired in North America can cause severe human illness. Evidence for changes to HA that may increase binding to human airway receptors is worrisome.

Agatha N. Jassem, Ph.D., British Columbia Centre for Disease Control, Vancouver, BC, Canada; Ashley Roberts, M.D., British Columbia Children’s Hospital, Vancouver, BC, Canada; John Tyson, Ph.D., James E.A. Zlosnik, Ph.D., Shannon L. Russell, Ph.D., British Columbia Centre for Disease Control, Vancouver, BC, Canada; Jessica M. Caleta, M.Sc., Public Health Agency of Canada, Winnipeg, MB, Canada; Eric J. Eckbo, M.D., British Columbia Centre for Disease Control, Vancouver, BC, Canada; Ruimin Gao, Ph.D., Taeyo Chestley, Ph.D., Public Health Agency of Canada, Winnipeg, MB, Canada; Jennifer Grant, M.D., British Columbia Centre for Disease Control, Vancouver, BC, Canada; Timothy M. Uyeki, M.D., M.P.H., Centers for Disease Control and Prevention, Atlanta, GA; Natalie A. Prystajecky, Ph.D., British Columbia Centre for Disease Control, Vancouver, BC, Canada; Chelsea G. Himsworth, D.V.M., Ph.D., British Columbia Ministry of Agriculture and Food, Abbotsford, BC, Canada; Elspeth MacBain, M.D., British Columbia Children’s Hospital, Vancouver, BC, Canada; Charlene Ranadheera, Ph.D., Public Health Agency of Canada, Winnipeg, MB, Canada; Lynne Li, M.D., British Columbia Children’s Hospital, Vancouver, BC, Canada; Linda M.N. Hoang, M.D., British Columbia Centre for Disease Control, Vancouver, BC, Canada; Nathalie Bastien, Ph.D., Public Health Agency of Canada, Winnipeg, MB, Canada; David M. Goldfarb, M.D., British Columbia Children’s Hospital, Vancouver, BC, Canada.

Source: New England Journal of Medicine, https://www.nejm.org/doi/full/10.1056/NEJMc2415890

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