Nature Sci Rpts: Detection of H5N1 HPAI virus RNA in filth flies collected from California farms in 2024

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Even after more than 2 decades of outbreaks linked to farms, live markets, and wild birds, there remains a good deal we don't know about how HPAI H5 (and other novel flu types) spread; often defeating ramped up biosecurity measures. 

While many were quick to blame contaminated milking equipment for the spread of H5N1 among dairy herds in 2024, four months ago, in Preprint: Surveillance on California Dairy Farms Reveals Multiple Sources of H5N1 Transmission, we saw evidence that Bird flu is ‘everywhere’ on dairy farms.

Following that report, UNMC's Global Center for Health Security - quoting Dr. Richard Webby as saying “It’s a ridiculously contaminated environment” - published Bird Flu on Dairy Farms May Be Airborne After All.

These airborne concerns go far beyond just`exhaled' breath from infected cattle in milking parlors, or `milk spray', as massive quantities of contaminated milk and manure  must be safely handled and disposed of (along with farm wastewater); none of which are trivial tasks. 

We've seen numerous environmental persistence studies showing that - under the right conditions - HPAI H5 can survive for days, weeks, or even months outside of a living host.

• In 2012's EID Journal: Persistence Of H5N1 In Soil, we looked at several studies that found H5N1 could remain viable on various surfaces, and in different types of soil, for up to 13 days (depending upon temperature, relative humidity, and UV exposure).

• In 2017, researchers showed that - when refrigerated - H5N1 infected poultry could remain infectious for months (see Appl Environ Microbiol: Survival of HPAI H5N1 In Infected Poultry Tissues).

• In 2020 we looked at a study from researchers at the USGS (see Proc. Royal Society B: Influenza A Viruses Remain Viable For Months In Northern Wetlands - USGS), which found long-term (up to 7 months) survival of influenza A viruses in wetlands in both Alaska and Minnesota.

How long avian flu viruses may remain viable, and how far they might be carried (by personnel, vehicles, peridomestic mammals, birds, flies, or even the wind), continues to be poorly understood.

Very early on in this blog (2007) - in Cats and Dogs and Flies, Oh My! - we looked at a 2006 study by Kyoko Sawabe et al. that found that at least 2 types of flies could carry the H5N1 virus.

While flies weren't shown to be infected with the virus, they could ingest (and subsequently regurgitate or defecate) infected material, or potentially spread it mechanically by their feet or body, thereby spreading the disease.

We've revisited this idea a number of times since, including 2023's preprint (later published in Sci Repts: Blowflies As Potential Vectors Of Avian Influenza) that tested blowflies for HPAI at the national wildlife reserve in Izumi City, Kagoshima Prefecture, which is the overwintering home for thousands of endangered Hooded Cranes.

The authors wrote:

In December 2022, 648 Calliphora nigribarbis were collected. Influenza virus RT-PCR testing identified 14 virus-positive samples (2.2% prevalence), with the highest occurrence observed near the crane colony (14.9%). Subtyping revealed the presence of H5N1 and HxN1 in some samples. Subsequent collections in December 2023 identified one HPAI virus-positive specimen from 608 collected flies in total, underscoring the potential involvement of blowflies in HPAI transmission.

Our observations suggest C. nigribarbis may acquire the HPAI virus from deceased wild birds directly or from fecal materials from infected birds, highlighting the need to add blowflies as a target of HPAI vector control.

And last July, in H5N1 in California: The Return of the Fly, after Raj Rajnarayanan @RajlabN - Associate Dean of Research and Associate Professor, NYITCOM at Arkansas State University - uploaded to X/Twitter a quick analysis of H5N1 sequences sampled from a HouseFly uploaded to @GISAID from California (2.3.4.4b B3.13 Collected Oct 2024).

Today we've a report, published this week in Scientific Reports, which documents the detection of HPAI H5N1 RNA in flies collected from several California dairy farms in 2024. 

While they state that `. . . infectious virus was not detected in this study', based on the following, it appears they did not attempt to isolate or culture the virus. 

The successful amplification and sequencing of full-length HPAI H5N1 genomic DNA from fly samples collected from positive dairy operations, along with the incidence of relatively low Ct values in some pools, together suggest the presence of intact viral genomes at the time of fly collection. 

However, the detection of intact genomes does not necessarily equate to the presence of infectious virus, which is a limitation of our approach that could be improved if virus culture precedes molecular characterization.

As this report points out:

Prior bioassays determined that infectious HPAI H5N1 survives in the digestive tract (including crop) of house flies for up to 72 h [18] and blow flies for up to 24 h [24], although viral RNA can be detected for much longer (for example, up to 4 days in house flies and 14 days in blow flies).

Due to its length, I've only posted the abstract and a brief excerpt.  Follow the link to read it in its entirety.  I'll have a brief postscript after you return.

Detection of H5N1 highly pathogenic avian influenza virus RNA in filth flies collected from California farms in 2024
Dana Nayduch, Stacey L.P. Scroggs, Phillip Shults, Luke A. Brendel, Lindsey M. Reister-Hendricks, Caitlin Taylor, Edward Bird, Brina Lopez & Edith S. Marshall

Scientific Reports , Article number: (2025) Cite this article

Abstract


The emergence of highly pathogenic avian influenza (HPAI) H5N1 clade 2.3.4.4b in U.S. dairy cattle highlights the urgent need to understand transmission dynamics within and among farms. House flies (Musca domestica) and blow flies (Calliphoridae), ubiquitous in agricultural settings, are suspected mechanical vectors of numerous pathogens, including viruses. 

We investigated the presence of H5N1 viral RNA in filth flies collected opportunistically from four H5N1-positive farms (three dairy and one poultry) in California during the 2024 outbreak. H5N1 RNA was detected via qRT-PCR in fly pools from all four locations, with the lowest Ct values (highest viral RNA) in house flies collected near milking parlors and dead animals. Whole-genome sequencing confirmed H5N1 viral genomes in flies from dairy farms, demonstrating high similarity (99.92–99.95%) to the B3.13 lineage circulating in the region and grouping closely with farm-associated viral sequences from milk.

Although infectious virus was not detected in this study, our findings suggest that filth flies acquire HPAI H5N1 RNA from their environment, supporting their potential role as sentinels and/or mechanical vectors. These results underscore the critical importance of fly control, targeted surveillance, and integrated pest management strategies in agricultural settings to enhance biosecurity and potentially mitigate HPAI H5N1 transmission.

       (SNIP)

Our data suggest that both the milking parlor and dead animals may be potentially potent sources of virus for flies on the two dairy operations for which we had these metadata, as indicated by low Ct values (i.e., high viral RNA template), a high prevalence of positive fly pools collected from these locations, and the close relatedness of genomes of fly-associated and milk-associated virus from the same farm and nearby farms in the same  county (e.g., Fig. 1).

Together, these findings support local acquisition of HPAI H5N1 by house flies from both milk and dead animals (carcasses, aborted fetus), which concurs with the trophic behaviors of filth flies.

Female filth flies readily seek out and feed on proteinaceous substances like milk (e.g., house flies; [15]) and both species visit dead or decaying materials for oviposition [28,29], often ingesting the substrate during this process. Interestingly, milk seems to extend the stability of HPAI H5N1 in wastewater and on structural surfaces [30,31]. Milk also has been shown to increase persistence, perhaps by decreasing degradation rates, of SARS CoV-2 ingested by house flies [32].

       (Continue . . . )

While there are probably multiple pathways that HPAI utilizes to spread within and between farms, it seems increasingly likely that flies are at least part of the equation. 

In addition to flies, over the years we've looked at a number of other `less obvious' ways the virus may be spreading.

• There is growing evidence that HPAI may be spread via `contaminated dust particles' - carried by the wind - from one farm to the next (see Preprint: Genetic & Meteorological Data Supporting Windborne Transmission of HPAI H5N1).

• The role of peridomestic mammals - particularly in and around farms - in the spread of HPAI is only partially understood, and remains under-researched (see Emer. Microbe & Inf.: HPAI Virus H5N1 clade 2.3.4.4b in Wild Rats in Egypt during 2023).

• While contaminated milking machines have been blamed for the cow-to-cow spread of HPAI, a recent preprint (Dairy Cows Infected with Influenza A(H5N1) Reveals Low Infectious Dose and Transmission Barriers) was unable to duplicate transmission in a controlled lab setting, leading researchers to warn `. . . Other agent, host, and environmental cofactors that might contribute to transmission cannot be ruled out and must be explored . . . ).

Unless and until we get a better handle on how HPAI is spreading in the wild - and among and between farms - our ability to slow or contain these outbreaks will remain limited. 

Referral : Science - Avian-origin influenza A viruses tolerate elevated pyrexic temperatures in mammals

 

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While I try to focus primarily on open-access studies that allow me to read them in their entirety, and hopefully lift an excerpt or two, every once in awhile I'll find a paywalled or copyright restricted paper that seems worthy of referral.

Today we've a study, published behind a paywall in Science, which shows that that avian-origin PB1 segments make human-adapted influenza A viruses more tolerant of febrile temperatures (~40–41 °C) in vitro and in a mouse model with artificially elevated body temperature. 

We've often talked about the fact that birds run `hotter’ than mammals, with a normal body temperature that hovers at or above 40°C, which would be considered a `fever level' in humans. 

These viruses replicate primarily in the avian gut - which is several degrees warmer than the human airway - and it means that an avian virus must adapt to replicate at a lower temperature in order to become a bigger human threat.

One of the mutations we look for is (PB2-E627K); the swapping out of the amino acid Glutamic acid (E) at position 627 for Lysine (K) - which allows an influenza virus to replicate at the lower temperatures (roughly 33°C) normally found in the upper human respiratory tract (see Eurosurveillance: Genetic Analysis Of Novel H7N9 Virus).

Today's study looks at the impact of a different Avian-origin gene segment (PB1) and focuses on `two amino acid substitutions' (which, disappointingly are not specified in the abstract) that allow avian viruses to tolerate (and even thrive) at higher temperatures. 

The human immune system's most obvious response to any infection is to mount a fever, which often slows or inhibits the replication of the invading pathogen. This is why many doctors suggest allowing a mild or moderate fever to run its course. 

But an influenza virus that is both tolerant of higher temperatures and replicates at the lower temperatures in the human airway would complicate matters considerably. 

As the authors point out, the pandemic viruses of 1918, 1957, and 1968 all acquired an avian-origin PB1, which may help explain why they were more virulent than seasonal flu.

While I'm more than a little hobbled by my lack of access to the full paper, the Editor’s summary and graphical and text abstracts are interesting enough for me to recommend that you might want to take a deeper look. 

Avian-origin influenza A viruses tolerate elevated pyrexic temperatures in mammals
Matthew L. Turnbull , Yingxue Wang, Simon Clare, Gauthier Lieber , Stephanie L. Williams , Marko Noerenberg , Akira J. T. Alexander , Sara Clohisey Hendry , Douglas G. Stewart, [...] , and Sam J. Wilson +22 authors Authors Info & Affiliations
Science 27 Nov 2025
Vol 390, Issue 6776
DOI: 10.1126/science.adq4691

J.I.D.: Avian influenza virus A(H5N1) genotype D1.1 is better adapted to human nasal and airway organoids than genotype B3.13

 
Flu Virus binding to Receptor Cells – Credit CDC

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While there has been no shortage of (understandable) relief over the relatively mild presentation of the `Bovine' B3.13 genotype of HPAI H5N1 in humans (0 Severe/Fatal cases), the same cannot be said for the D1.1 genotype, which emerged in North America in October of 2024.

• In November of 2024, we learned of a severe case involving a teenage girl in British Columbia (see NEJM: Critical Illness in an Adolescent with Influenza A(H5N1) Virus Infection)
• The following January the Louisiana Department of Health Announced the 1st U.S. H5N1-related Fatality
• And a Fatal case was reported in Mexico (see WHO DON Update On Mexico's Fatal H5N1 Infection) in April.

The exact number of human infections with the D1.1 genotype is unknown, since not all of the (now, roughly 6 dozen) North American human cases have been fully characterized. Today's study describes this ambiguity as:

A total of 53 strains were identified, of which 6 strains had 2 sequences deposited. These 53 strains were collected from patients between March 28, 2024 and February 12, 2025 (Supplementary Table S3). Of these 53 strains, 22 (41.5%) were assigned to genotype B3.13, 8 (15.1%) were assigned to D1.1, 1 (1.9%) was assigned to D1.3, and 22 (41.5%) could not be assigned to any genotypes according to GenoFLU version 1.06 (https://github.com/USDA-VS/GenoFLU). 

It appears, however, that Bovine B3.13 human infections have likely outnumbered D1.1 infections by a factor of 2:1, making the difference in virulence even more pronounced. 

Today's report, from researchers at the University of Hong Kong, provides some insight on why D1.1 human infections appear to be more severe than B3.13.  

They demonstrate that the D1.1 genotype replicates better in lab-grown nasal and lung tissues than the bovine B3.13 strain, and it binds more tightly to human‑type (α2,6-linked SA) receptors.  

I've reproduced the abstract, and a brief excerpt, below. Follow the link to read the full report.  I'll have a bit more after the break. 

Avian influenza virus A(H5N1) genotype D1.1 is better adapted to human nasal and airway organoids than genotype B3.13

 Xiaojuan Zhang, Stephanie Joy-Ann Lam, Lin-Lei Chen, Carol Ho-Yan Fong, Wan-Mui Chan, Jonathan Daniel Ip, Shaofeng Deng, Siwen Liu, Rachel Chun-Yee Tam, Pui Wang

The Journal of Infectious Diseases, jiaf598, https://doi.org/10.1093/infdis/jiaf598
Published:24 November 2025 Article history

PDF

Abstract

Three critically ill or fatal avian influenza A(H5N1) human infections have been reported in North America since November 2024. Notably, all were infected with genotype D1.1 instead of B3.13, the dominant genotype before November 2024. Here, we demonstrated that D1.1 could replicate to higher titers in human nasal and airway organoid-derived transwell monolayers from 6 donors.

D1.1 exhibited a better binding to α2,3- and α2,6-linked SA than B3.13. No significant differences in most inflammatory or antiviral cytokines/chemokines was observed. These observations suggest that D1.1 is better adapted to both the upper and lower human respiratory tract epithelium than B3.13.

(SNIP)

Our observations suggest that D1.1 genotype may be better adapted to humans than B3.13. Further studies are required to determine if there are differences in the replication of different strains within the same clade. As D1.1 is now widespread among dairy cows in the United States, there is an increasing risk of further adaptation of D1.1 with higher transmissibility or virulence among mammals. Continuous phenotypic monitoring using human organoids and other in vivo models will provide critical information for assessing the risk of D1.1 or other novel genotypes in humans.

       (Continue. . . )

Almost 13 years ago, in  Differences In Virulence Between Closely Related H5N1 Strains, we looked at the varying impact of HPAI H5N1 viruses around the globe.  Some countries saw CFRs (Case Fatality Rates) of 50%-80%, while others reported relatively few deaths (see chart below). 

While we're thankfully not seeing the kind of high CFR H5N1 in North America and Europe that once was far too common in Indonesia, Vietnam, and Egypt, the events over the past 3 years in Cambodia remind us that severe H5N1 still exists. 

And recent offshoots of H5N1 - like the H5N5 case in Washington State and the Novel Reassortant H5N2 case in Mexico - demonstrate that these HPAI viruses continue to reinvent themselves at a rapid pace. 

Whether this ultimately leads to another pandemic is anyone's guess, but right now HPAI H5 appears to be on a roll, and should give all of us pause. 

Reminder: Thanksgiving Is National Family History Day

 

Free Online Tool From HHS to Collect Family HX

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One of the perils of blogging for two decades is that over time embedded links to outside sources no longer function. The past couple of years have been particularly bad following major upgrades/revamping of both the CDC and WHO websites, where even some of their internal links go nowhere.

Normally, the day before Thanksgiving I repost my annual `Thanksgiving Is National Family History Day' blog, with links and quotes from the CDC, the HHS, and the Office of the Surgeon General. 

Since 2023, some of those links (here & here) have gone missing, although the CDC retains an abbreviated version at https://www.cdc.gov/family-health-history/

So, starting over . . . 

Every year since 2004 the Surgeon General of the United States has declared Thanksgiving – a day when families traditionally gather together - as National Family History Day, since it provides an excellent opportunity to ask about and document the medical history of relatives.

As a former paramedic, I am keenly aware of how important it is for everyone to know and have access to their personal and family medical history.

During routine visits with your doctor, knowing your family history can provide important information regarding your care. Under more urgent conditions, emergency room doctors are often faced with patients unable to remember or relay their health history, current medications, or even drug allergies during a medical crisis.

Which is why I always keep an EMERGENCY MEDICAL HISTORY CARD – filled out and frequently updated – in my wallet, and have urged (and have helped) others in my family to do the same.

I addressed this issue at some length in a 2009 blog called Those Who Forget Their History . . . . A few excerpts (but follow the link to read the whole thing):

Since you can’t always know, in advance when you might need medical care it is important to carry with you some kind of medical history at all times. It can tell doctors important information about your history, medications, and allergies when you can’t.

Many hospitals and pharmacies provide – either free, or for a very nominal sum – folding wallet medical history forms with a plastic sleeve to protect them. Alternatively, there are templates available online.

I’ve scanned the one offered by one of our local hospitals below. It is rudimentary, but covers the basics.

Since family gatherings are common over the holidays, Thanksgiving can be an ideal time to ask family members about their medical history. The HHS even provides a free, online tool, for organizing and storing this information.

The CDC's website contains additional information, including:

Family Health History and Adults

Key points

• If you have a family health history of a chronic disease such as cancer, heart disease, or diabetes, you are more likely to get that disease yourself.
• Knowing your family health history risk can help you—if you act on it.
• Share your family health history with your healthcare provider, who can help you take steps to prevent disease and catch it early if it develops.
• Finding disease early can often mean better health in the long run.

And lastly, a couple of other items that - while not exactly a medical history - may merit discussion in your family as it has in mine (see 2012's His Bags Are Packed, He’s Ready To Go).

• First, all adults should consider having a Living Will that specifies what types of medical treatment you would desire should you become incapacitated, and unable to communicate your wishes.  
• While not a `legal document' the CDC also provides a `Complete Care Plan' PDF tool  for managing day-to-day care. 

• You may also wish to consider assigning someone as your Health Care Proxy, who can make decisions regarding your treatment should you be unable to do so for yourself. 

• Elderly family members with chronic health problems, or those with terminal illnesses, may even desire a home DNR (Do Not Resuscitate) Order. 
• Without legal documentation, verbal instructions by family members – even if the patient is in the last stages of an incurable illness – are likely to be ignored by emergency personnel.

While admittedly, not the cheeriest topic of conversation in the world, a few minutes spent during this Thanksgiving holiday putting together concise written medical histories could spare you and your family a great deal of anguish down the road.

Preprint: Emergence of a Novel Reassorted HPAI A(H5N2) Virus Associated with Severe Pneumonia in a Young Adult

 

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Roughly 6 weeks ago we saw the brief mention in an Oct 15th PAHO H5N1 Epidemiological Report of an H5 case in Mexico City, although details on the virus were limited. 

On 2 October 2025, Mexico's International Health Regulations (IHR) National Focal Point (NFP)notified PAHO/WHO of a laboratory-confirmed human infection caused by avian influenza A(H5) virus in Mexico City, the second confirmed human case in the country in 2025 (6, 7).

The patient - a woman in her 20's - developed symptoms on September 14th, and after two weeks of increasing respiratory distress was finally hospitalized and a bronchoalveolar lavage sample was obtained, which tested positive for an unsubtypable influenza A on Sept 29th.

As of that initial announcement, the NA type remained undetermined.

This was the third H5 case reported from Mexico since 2024, and the source of all three remain undetermined.

• The first occurred in April of 2024 (see Mexico announced the death of a 58-year-old man) when a patient - who also suffered from serious comorbidities - tested positive for LPAI H5N2, becoming the first laboratory-confirmed human case of influenza A(H5N2) infection reported globally.

• A year later (April 2025), a 3-year old girl from Durango State died following an H5N1 infection (see WHO DON Update On Mexico's Fatal H5N1 Infection).

On October 18th, in the ECDC Summary: Human Infection with Avian Influenza A(H5) virus - Mexico - 2025, a few more details emerged, but it still wasn't clear whether this was H5N1, H5N2, or some other subtype.

About a week ago, the WHO published their latest Influenza at the human-animal interface summary and assessment report, which identified the full subtype as H5N2, but further characterization of the virus was reportedly still underway.

Somewhat intriguingly, that report did disclose:

Respiratory samples collected from close contacts including hospital contacts, tested negative for influenza viruses. During the epidemiologic investigation, several animals (including birds) and bird droppings were found in the building where the case resides, in an area the case passes frequently. A dog was identified as a pet at the case’s residence. Samples collected from the animals tested positive for influenza A(H5). Information on whether this virus was a high or low pathogenicity avian influenza virus (HPAI or LPAI) is pending further testing

Overnight, a fascinating new preprint has appeared on the medRxiv server, which provides additional - and somewhat concerning - details on this latest case.  It turns out this H5N2 virus was a new reassortment between the local, long-endemic, LPAI H5N2 virus in Mexico and the clade 2.3.4.4b H5N1 virus circulating globally. 

While numerous H5N1 reassortments have occurred in the past, producing scores of new H5N1 genotypes (e.g. A3, B3.13, D1.1, D1.2, D1.3, etc.), this introduces a novel subtype - HPAI H5N2 - to an already crowded field. 

First the abstract, and a few excerpts from this preprint, but you'll want to read it in its entirety. I'll have a bit more after the break.

Emergence of a novel reassorted high pathogenicity avian influenza A(H5N2) virus associated with severe pneumonia in a young adult

Joel Armando Vazquez-Perez, Eduardo Becerril-Vargas, Jose Ernesto Ramirez-Gonzalez, Mario Solis-Hernandez, Charles Todd Davis, Pamela Garciadiego-Fossas, Marco Villanueva-Reza, Hansel Hugo Chavez-Morales, Enrique Mendoza-Ramirez, Christian Diego Olivares-Flores, America Citlai Vera-Jimenez, Uriel Rumbo-Nava, Cristobal Guadarrama-Perez, Elio German Recinos-Carrera, Joaquin Zuniga, Irma Lopez-Martinez, Lucia Hernandez-Rivas, Gisela Barrera-Badillo, Nohemi Colin-Soto, Laura Flores-Cisneros, Guillermo Carbajal-Sandoval, Diana Vidal-Aguirre, Dayanira Sarith Arellano-Suarez, Rodrigo Aparicio-Antonio, Ramiro Lopez-Elizalde, Carlos Javier Alcazar-Ramiro, Armando Garcia-Lopez, Han Di, Marie Kirby, Yunho Jang, Miguel Angel Lezana-Fernandez, Carmen Margarita Hernandez-Cardenas

doi: https://doi.org/10.1101/2025.11.21.25340167

        PDF 

Abstract

Background Infection of backyard and poultry with low pathogenicity avian influenza LPAI A(H5N2) viruses has occurred in Mexico since 1994, and the first human infection caused by this influenza virus was detected in 2024. Since its emergence in the Americas, frequent reassortments between high pathogenicity avian influenza HPAI A(H5N1) and LPAI viruses has occurred.

In September 2025, the Instituto Nacional de Enfermedades Respiratorias of Mexico City identified an unsubtypeable influenza A virus infection in a young adult patient later determined to be a reassortant HPAI (H5N2) virus with a clade 2.3.4.4b HA.

Methods We analyzed clinical and epidemiologic data from this patient. Respiratory samples were tested for influenza RT-qPCR assays. Genomic sequence and phylogenetics analyses were performed to provisionally assign a new genotype to the novel HPAI A(H5N2) reassortant virus.

Results The patient presented with fever and tachypnea, later developed hemoptysis and thoracic pain, with oxygen saturation decreasing to 70%. CT scan showed bilateral ground-glass opacities consistent with diffuse alveolar hemorrhage and zones consistent with consolidation. Clinical improvement was observed and the patient was discharged.

Through viral complete genome analysis, we identified an HPAI A(H5N2) virus with genes from both clade 2.3.4.4b A(H5N1) viruses similar to those detected in North America during 2022-2023 and genes from the LPAI A(H5N2) viruses detected in Mexico during 2024.

Conclusions This is the first ever laboratory-confirmed human infection caused by an HPAI A(H5N2) virus infection, suggesting a new genotype provisionally classified as B3.14. The relationship of the virus with the severity of illness remains unknown.

       (SNIP)      

Further studies are required to determine the predicted pathogenicity and the transmissibility of the virus and its potential threat to human health. Although obesity was the sole comorbidity, the patient exhibited unusually extensive pulmonary damage, underscoring the need for further characterization of their pathogenic potential of this or related viruses. Since no cases of this reassorted A(H5N2) influenza virus in humans have been previously reported, we are unaware of the clinical outcomes that this HPAI virus subtype may have in humans.

Given the virus's propensity for rapid genetic reassortment, genomic surveillance is essential, particularly for emerging strains. Such surveillance forms a critical component of global preparedness and rapid response strategies, enabling countries to strengthen viral diagnostics, vaccine development and therapeutic strategies to prevent widespread outbreaks.

In summary, our findings support the emergence of a new clade 2.3.4.4b reassortant virus provisionally classified as genotype B3.14 and the first ever global human case of an HPAI A(H5N2) virus infection.

       (Continue . . . )
 

While the public health implications of a one-off infection such as this are hard to assess, this is the second human infection with a novel subtype reported in North America in a matter of a few weeks (see Washington State DOH: H5N5 Avian influenza confirmed in Grays Harbor County resident). 

Both cases may well end up being flukes, but they remind us that influenza A's superpower is its ability to continually reinvent itself through reassortment.  

Admittedly, most reassortants end up as evolutionary failures - unable to compete against the panoply of existing flu strains - but on rare occasions an overachiever is generated.   

And should that overachiever also have (or develop) an affinity for infecting humans, then our world may face yet another global health threat. 

EFSA: Unprecedented High Level of HPAI in Wild Birds in Europe During the 2025 Autumn Migration

The Uncertain Picture in October

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A month ago, in A Robust Start To Avian Flu Season In Europe & North America, we looked at worrying signs that the recent trend in declining European HPAI outbreaks (see chart above) might be over, and that we could be on the verge of seeing a significant uptick in bird flu activity. 

As early as August the UK reported an unexpected summer surge in H5N1 outbreaks in poultry farms, and by mid-September we were seeing similar trends reported in North America (see Canada & U.S. Report Early Fall Uptick In H5N1 Outbreaks In Poultry).

Replacing the ? in my graphic of a month ago, we now have the first EFSA (European Food Safety Authority) assessment, which confirms that an `unprecedented'  high level of HPAI has occurred in Europe in recent weeks.

  

The above graphic comes from the following 9-page report, published yesterday by the EFSA, which characterizes this as the fastest start to the fall HPAI season since at least 2016.  

As we discussed last August, in H5Nx: Reassort & Repeat, the emergence of new genotypes of HPAI H5 is often associated with increased virulence and/or transmission of avian flu viruses.  

Not surprisingly, today's announcement contains confirmation that the bulk of the detections this fall in Europe are due to a new genotype DI.2.1 While we've yet to see a detailed phenotypic characterization of this variant, it appears to be the driving force behind this surge. 

First, the abstract and some excerpts, followed by a statement from the EFSA. I'll have a bit more after the break.

Unprecedented high level of highly pathogenic avian influenza in wild birds in Europe during the 2025 autumn migration

Published: 24 November 2025
Documents
EFSA statement_HPAI_6 Sep-14 Nov
QUESTION NUMBER
EFSA-Q-2025-00661
CONTACT biohaw@efsa.europa.eu

Abstract

Between 6 September and 14 November 2025, 1,443 highly pathogenic avian influenza (HPAI) A(H5) virus detections were reported in wild birds across 26 countries in Europe. This number was four times higher than in the same period in 2024 and the highest overall for those weeks since at least 2016.

Almost all the detections (99%) were due to HPAI A(H5N1) viruses, and most of them belonged to EA-2024-DI.2.1, a new sub-lineage of the EA-2024-DI.2 genotype.

These HPAI virus detections in wild birds involved increasing numbers of waterfowl species (ducks, geese and swans) that were found positive in large parts of Europe. In addition, high numbers of common cranes were affected across a wide band stretching from northeast to southwest Europe.

Given the unprecedented high circulation of HPAI virus in the wild bird population compared to previous years, and the associated high environmental contamination, strict biosecurity measures and early detection of infected poultry establishments are urgently needed to prevent introductions from wild to domestic birds and further spread among poultry establishments. Prompt removal of wild bird carcasses is indicated to reduce the risk of infection for other wild and domestic birds and mammals.

© European Food Safety Authority        

3. Results

During the current reporting period from 6 September to 14 November 2025, a total of1,443 HPAI virus detections in wild birds (with an HPAI virus detection potentially including more than one wild bird species) were reported in Europe. Compared to the same dates in previous years, this number was four times higher than in 2024, ten times higher than in 2023, twice as high as in 2022, and four times higher than in 2021 (Figure 1).

        (SNIP)

Based on genetic data available so far, most of the HPAI A(H5N1) viruses identified were a variant of the previously circulating EA-2024-DI.2 genotype, which has mutated sufficiently to form a new sub-lineage, namely EA-2024.DI.2.1. Phylogenetic analysis indicates that this sub-lineage was probably newly introduced into Europe during autumn migration from the east and rapidly spread westward. 

        (Continue . . . )

Avian influenza in Europe: enhanced surveillance and strict biosecurity needed as detections surge

Published: 24 November 2025
Last reviewed date: 25 November 2025
  


Between 6 September and 14 November 2025, 1,443 detections of highly pathogenic avian influenza (HPAI) A(H5) viruses were reported in wild birds across 26 European countries – four times higher than the same period in 2024 and the highest since at least 2016.

Waterfowl in various parts of Europe were heavily affected by HPAI during this period, including detections in apparently healthy wild birds, resulting in widespread environmental contamination. There were also high-mortality outbreaks in common cranes in Germany, France and Spain.

The vast majority of HPAI virus detections (99%) were reported as A(H5N1), and most were of a new variant of a previously circulating strain that was introduced into Europe from the east before rapidly spreading westward.

Among other measures, enhanced surveillance for early detection and robust biosecurity on farms are urgently required to prevent the introduction of HPAI in domestic birds and onward spread among poultry establishments.

Recommended measures

Depending on their role, EFSA advises national, regional and local authorities, those involved in domestic poultry production and wild bird management, and those responsible for mammals at risk of avian influenza, to implement the following actions.

• Maintain high biosecurity in establishments keeping domestic birds, during both normal production and culling operations.
• Issue housing orders for domestic birds in areas with confirmed HPAI in wild birds or mass mortality events.
• Enhance surveillance in domestic birds to ensure early detection of infection in poultry establishments.
• Focus wild bird surveillance on wetland areas and migratory stopover sites within and outside Europe.
• Include wildlife rescue or rehabilitation centres in surveillance and ensure adequate biosecurity.
• Avoid artificial feeding of wild birds – especially cranes and swans – during high‑risk periods to reduce crowding and transmission risk.
• Remove wild bird carcasses promptly to reduce contamination of the environment with HPAI and prevent infection of other wild or domestic birds and mammals.
• Minimise disturbance of wild bird populations (e.g. hunting, leisure activities, drones) to limit further dispersal of the virus.
• Monitoring and awareness-raising tools EFSA’s Bird Flu Radar can be used to monitor the probability of the introduction of HPAI virus in wild bird populations in Europe over space and time.

Access the Bird Flu Radar here. 

In September 2025, EFSA and the European Commission published the #NoBirdFlu communication toolkit – practical, ready‑to‑use materials (posters, infographic, stickers, social media posts) available in all EU languages to support farmers and veterinarians in implementing biosecurity on poultry farms.

Access the toolkit here.

Links to science
Avian influenza

Unprecedented high level of highly pathogenic avian influenza in wild birds in Europe during the 2025 autumn migration

It is striking how often the world `unprecedented' crops up in avian flu reports;

an Unprecedented `Order Shift'

`a panzootic of unprecedented scale'

Unprecedented H5N1 outbreak: a rare cross-species influenza threat

 H5N1 High pathogenicity avian influenza in wild birds -Unprecedented conservation impacts and urgent needs

H5N1 clade 2.3.4.4b caused an unprecedented number of deaths among wild birds and poultry in numerous countries

A(H5N1) clade 2.3.4.4b has resulted in unprecedented impact to animal health 

Despite these (and numerous other) clarion calls we continue to treat HPAI H5Nx as if it is the same virus that failed to spark a pandemic in 2006-2008.  

Most governments would rather ignore the threat, since its easier than dealing with it; and the public remains largely disinterested (see Two Surveys (UK & U.S.) Illustrating The Public's Lack of Concern Over Avian Flu).

While we may be able to abide the current level of damage to our economies, and to our shared ecosystems, there are no guarantees the stakes won't rise precipitously in the future.

At which point we may find our response options are far more limited than they are today.