MMWR: Notes From the Field - Characteristics and Monitoring of the 2026 Outbreak of Ebola Disease . . . (DRC)

Figure 1. Distribution of cumulative confirmed cases

of Bundibugyo virus disease in the Democratic Republic

of the Congo, as of 26 August

#19,321

On May 15th Africa's CDC Convened an  Emergency Meeting After Reports of a Large Outbreak of Non-Zaire Ebola In the DRC, which was later confirmed to be Ebola Bundibugyo.  On May 20th the U.S. CDC issued a HAN (#00530) and 2 days later the ECDC released a Threat Assessment Brief. 

In June the CDC's MMWR released Modeled Scenario Projections for the Ebola Disease Outbreak Caused by Bundibugyo Virus, 2026 which warned that:

`Large-scale, rapid public health action is needed to control the current outbreak, already the largest known BVD outbreak, from becoming one of the largest Ebola epidemics in history.'

The most recent (Aug 28th) update from the WHO reports:

As of 26 August 2026, a total of 5794 confirmed cases, including 2786 deaths, have been reported, corresponding to a crude case fatality ratio (CFR) of 48.1%. These figures demonstrate a substantial increase in the scale and geographic extent of the outbreak over the past three months.

The crude case fatality ratio of 48% underscores the severity of the disease and ongoing challenges related to timely case detection, access to and quality of clinical care, and effective interruption of viral transmission. Delays in recognizing cases increase the likelihood of onward transmission within households, communities and healthcare facilities. The outbreak remains a public health emergency of international concern, following the advice of Emergency Committee meeting convened on 18 August.

This week, the CDC's MMWR has published a new assessment which finds that this Ebola outbreak is now the second largest on record, and it continues to expand rapidly. 

Despite concerted efforts, too many cases are being identified belatedly - many being treated or dying at home or outside of treatment centers - which prevents timely contact tracing and helps to enable community spread. 

 They report that `Nearly all operational indicators remain below identified targets (Table)'. 

While this MMWR report outlines areas where improvements are needed, efforts in that regard are complicated by an ongoing humanitarian emergency in the eastern part of the DRC which includes armed conflicts, limited healthcare infrastructure and availability, population displacement, and difficulty accessing affected communities.

Notes from the Field: Characteristics and Monitoring of the 2026 Outbreak of Ebola Disease Caused by Bundibugyo Virus — Democratic Republic of the Congo, August 2026

Early Release / September 1, 2026 / 75
Please note: This report has been corrected.
Dumazedier Kabasele1; Erika Meyer1; Issaka Kabore1; Amber Dismer1; Joelle K. Kabamba1; Anna Bratcher1; Constantin Kabwe Kola1; Carrie Eggers1; Delayo Zomahoun1; Noemi Hall1; Mutshiene Deogratias Ekwanzala1; Natalie Peters1; Amy Schuh1,2; Tara Sealy1; Philip Ricks1; Billy Mpianga Mutombo1; Michael Kinzer1; Benjamin A. Dahl1; Hyacinte Kabore1; Mary J. Choi1,2; John Rossow1,2; Sascha Ellington1; CDC 2026 Ebola Response International Epidemiology and Laboratory Task Force (VIEW AUTHOR AFFILIATIONS)View suggested citation

Summary

What is already known about this topic?

In May 2026, an outbreak of Ebola disease caused by Bundibugyo virus was identified in the Democratic Republic of the Congo.

What is added by this report?

This ongoing outbreak is now the second largest Ebola outbreak in history. The targets for five critical public health response indicators (case detection alerts, contact tracing, laboratory testing, isolation of infected persons, and safe and dignified burials) have not yet been met, and the outbreak continues to expand rapidly.

What are the implications for public health practice?

Substantial improvements in established outbreak control measures are crucial to rapidly detect and diagnose cases and isolate and provide treatment for infected persons, prevent funeral-associated transmission to prevent additional spread, and control this rapidly expanding outbreak.

The Democratic Republic of the Congo (DRC) Ministry of Public Health declared an Ebola outbreak on May 15, 2026 (1). Two days later, CDC activated its Emergency Operations Center as part of the U.S. government response to this rapidly growing outbreak (2). This report describes the epidemiologic characteristics and monitoring of the ongoing outbreak in DRC.

Investigation and Outcomes

The 2026 Ebola DRC outbreak caused by Bundibugyo virus is now the second largest Ebola outbreak ever recorded. As of August 21, 2026, DRC reported 5,458 confirmed cases and 2,606 (48%) confirmed deaths. Compared with previous Ebola outbreaks, the increase in cases in DRC is unprecedented, with approximately 5,000 cases in 100 days (Ebola Outbreak: Current Situation | CDC).

Cases have been reported from six of the 26 DRC provinces (Bas-Uélé, Haut-Uélé, Ituri, North Kivu, South Kivu, and Tshop), affecting 57 of 151 health zones in the affected provinces. Ituri province remains the outbreak epicenter, accounting for 84% of reported cases. Strategies known to control Ebola outbreaks include community-based surveillance, case detection alert notifications,* rapid and in-depth case investigations, identification and monitoring of contacts, infection control measures (e.g., prompt isolation of persons with suspected or confirmed Bundibugyo virus disease [BVD]), rapid diagnostic testing, mortality surveillance, and safe and dignified burials (SDBs).†

Data Source

Operational indicators for five domains have been generated based on experience with previous Ebola outbreaks, including DRC’s 2018 outbreak (3) (Table). Targets reflect the levels necessary to end the outbreak. The DRC Ministry of Public Health prepares publicly available daily situation reports, and CDC abstracts data from these reports to evaluate the established indicators each day. Indicator data are monitored over time to assess the outbreak trajectory. This activity was reviewed by CDC, deemed not research, and conducted consistent with applicable federal law and CDC policy.§

Operational Indicator Analysis

Nearly all operational indicators remain below identified targets (Table). Operational indicator values were calculated for the 21-day period of July 31–August 21. The average percentage of alerts investigated within 24 hours (last reported August 5, 2026) was 83% (target = >90%). An average of 10.6 contacts were identified per confirmed case (target = ≥20), suggesting underreporting and underascertainment of case contacts. The percentage of confirmed new cases previously identified as known contacts (last reported July 12, 2026) was 15%–20% (target = >90%); this suggests that most cases are occurring outside known transmission chains. In addition, more than one half (59%) of confirmed Ebola deaths are occurring outside an Ebola treatment unit (ETU) (target = 0%), suggesting insufficient ETU capacity, fear of ETUs, and ongoing spread through unidentified transmission chains. Laboratory testing was performed for 72% of validated alerts (target = >90%), indicating that a substantial number of suspected cases remain untested. Test positivity was 24%, with a target of 0%. Although the national ETU bed occupancy was 64%, meeting the target of <80%, occupancy varied substantially by health zone, with some facilities unable to isolate all infected persons and reporting occupancies as high as 140%. Fewer than one half (49%) of affected health zones had at least one SDB team (target = 100%). Current data were not available for several response indicators, such as percentage of persons with confirmed BVD receiving prompt isolation (target = >90%) and percentage of deaths with SDBs (target = 100%), underscoring ongoing data gaps in this complex public health response.

Preliminary Conclusions and Actions

As of August 21, 2026, most operational indicator measures remained below established response targets, and data for others were unavailable, indicating gaps in surveillance, contact tracing, laboratory testing, health care–seeking, isolation, and SDB capacity that limit control of the ongoing outbreak. These missing data and operational gaps, together with continued geographic expansion of the outbreak, a high percentage of deaths occurring outside ETUs, and a low percentage of cases among persons previously identified as contacts, indicate uncontrolled expansion of the outbreak. Public health response activities are complicated by a protracted complex humanitarian emergency in the eastern part of DRC, including armed conflict, limited health infrastructure, population displacement and mobility, and constraints on access to affected communities.

Containment and control of the 2026 Ebola disease outbreak requires integration and coordination of at least five response areas: 1) expansion of community-based surveillance systems ensuring rapid investigation of alerts; 2) improvements in contact tracing completeness and timeliness; 3) expansion of treatment and isolation capacity in affected health zones; 4) increased laboratory testing capacity, enabling prompt case identification; and 5) ensuring SDBs in affected health zones.

In addition, collecting robust, high-quality data regarding these operational actions is essential at the health zone level; CDC’s continued support to the DRC Ministry of Public Health and partners with improving data collection is critical. Collecting data at the level of the health zone facilitates timely local outbreak response decisions. Rapidly enhancing international humanitarian coordination and mobilizing global technical, operational, and other needed support are critical for accelerating the response and controlling the outbreak.

J. Raptor Research: Rapid Decline of Nesting Peregrine Falcons in the San Francisco Bay Region of California Synchronous with an Outbreak of H5N1 HPAI

 
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Twice last month (see here, and here) we looked at the enormous impact of HPAI H5 on raptors and other scavenger birds around the globe. Previously - over 2023-2024 - we followed attempts to protect endangered California Condors against the avian flu threat. 

For those like me - born in the 1950s - this has an oddly familiar ring to it, as we witnessed a similar steep decline in raptors and songbirds due to the overuse of DDT and other chlorinated hydrocarbons, famously exposed by Rachel Carson in her 1962 book Silent Spring. 

While demonized by many, that book eventually led to the banning of DDT in 1972, followed by the slow recovery of condors, eagles, and falcons. But it was a close thing, as by 1980 the California Condor was all but extinct.

Today we are witnessing the loss of tens, perhaps hundreds, of millions of wild birds due to HPAI. The USDA's list of (known) H5N1 wild bird infections lists more than 600 bald eagles, more than 500 hawks, more than 400 owls, and scores of falcons affected by the virus, most of which were fatal. 

These are just what has been reported in the U.S., and represent only a tiny fraction of the actual losses. While we lack good numbers, the impact of H5Nx on avian and mammalian wildlife around the globe has been staggering (see Nature Reviews: The Threat of Avian Influenza H5N1 Looms Over Global Biodiversity).

First a link to, and the abstract from, the study; followed by an excerpt from a press release. Follow the links to read both in their entirety.  I'll have a bit more after the break. 

Rapid Decline of Nesting Peregrine Falcons in the San Francisco Bay Region of California Synchronous with an Outbreak of H5N1 Highly Pathogenic Avian Influenza 

Authors: Glucs, Zeka E., Hunt, W. Grainger, Kilpatrick, A. Marm, Ambrosini, Jan, Armstrong, Daniel J., et al.
Source: Journal of Raptor Research, 60(3) : 1-11 Published By: Raptor Research Foundation
URL: https://doi.org/10.3356/jrr26022

Abstract

After rebounding from near extirpation during the organochlorine era, breeding Peregrine Falcons (Falco peregrinus, hereafter peregrines) in California are again facing adversity, this time consistent with an outbreak of a highly pathogenic avian influenza (HPAI; Alphainfluenzavirus influenzae).

Following the first detection of the H5N1 variant clade 2.3.4.4b of HPAI in California wild birds in July 2022, we assembled data from long-term monitoring (2000–2025) of peregrine breeding territory occupancy in the broad vicinity of San Francisco Bay to examine possible impacts on falcon populations. Prior to the outbreak, 47 focal breeding territories had shown nearly complete occupancy by pairs (98.5% of 390 territory-years), with very few vacancies, single birds in attendance, or subadult pair members.

Within 8 mo of the outbreak, occupancy had dropped to 65.1%, and 2 yr later (2025), only 36.2% of territories remained occupied. Territories were increasingly occupied by single birds after the outbreak, but it is unclear whether these were survivors or floaters attempting to fill vacant territories where both pair members had perished. The high vacancy rates also signaled an impact upon floaters (nonbreeding adults) that normally buffer breeding territory occupancy in healthy peregrine populations. From October 2022 through November 2025, 17 peregrine fatalities were diagnosed with H5N1 within our study area.

Evidence that H5N1 caused these territory vacancies includes (1) the temporal coincidence of occupancy loss with the outbreak and (2) the lethality of the virus to peregrines and its confirmed presence in their prey in our study area. Our study reaffirms the value of long-term territory occupancy monitoring in this sentinel species.

       (Continue . . . )

First DDT now the flu: Peregrine falcons in San Francisco Bay area hit hard by H5N1 variant 

Raptor Research Foundation

Highly Pathogenic Avian Influenza (HPAI) featured prominently in the news during 2020 as it took the lives of millions of birds across the globe. While the worst seems to be behind us, population-level effects are just now emerging. A new study published in the Journal of Raptor Research, titled “Rapid Decline of Nesting Peregrine Falcons in the San Francisco Bay Region of California Synchronous with an Outbreak of H5N1 Highly Pathogenic Avian Influenza,” reports an alarming decrease in the number of occupied territories for a population of Peregrine Falcons (Falco peregrinus) that has maintained a longstanding presence in coastal California. As top predators, peregrines show warning signs when the health of their food web is jeopardized. They indicated the threat of DDT to wildlife in the 1960’s, and they are once again sounding the alarm to those who know where to look.

Highly Pathogenic Avian Influenza (HPAI) is an infectious disease that typically remains at low levels in wild bird populations. However, in 2020, the variant H5N1 emerged and ran amuck in what is now considered one of the most severe disease outbreaks to affect large animal populations ever recorded. Infections were documented in 400 bird species and at least 50 mammal species that year. Waterbirds are particularly susceptible to becoming carriers of HPAI, so predators and scavengers that feed on them are at a higher risk of exposure. Peregrines are master bird hunters and therefore primed to encounter this bird-born illness. However, it can be challenging to verify cause-of-death for raptors because of their low densities and the challenge of finding their carcasses, so raptor biologists must employ other tools to investigate population-level responses.

Lead author on the study Zeka Glucs, Director or the Predatory Bird Research Group at the University of California Santa Cruz, worked with a team of researchers to compare the presence of Peregrine Falcons on known territories in the Bay Area before and after the H5N1 outbreak, which was first detected in the state in 2022. They accessed a long-term dataset from 2000-2025 to examine trends in peregrine presence, underscoring the importance of maintaining research that spans decades.

The team found that prior to the H5N1 outbreak, 47 peregrine territories in the Bay Area were consistently occupied with stable breeding pairs. Following the outbreak, peregrine presence on these same territories dropped by 65% in three years, and the decline continues.

        (Continue . . . )
 

Three years ago, in Avian Flu's New Normal: When the Extraordinary Becomes Ordinary, I wrote about the numbing effect that comes with the constant barrage of disturbing HPAI H5 reports from around the world.

Events that were nearly unthinkable five years ago (e.g. Repeated trans-Atlantic introduction of avian flu from Europe, the spread of HPAI H5 across the length of South America, numerous spillovers of H5 into mammalian species, the arrival of HPAI H5 to Antarctica, and most recently to Australia ) have now become `the new normal'.

Even if HPAI H5 never sparks a pandemic in humans, it is already a panzootic affecting the entire globe. One that already manifests itself in higher food costs, increased food insecurity, and growing public health and surveillance costs. 

How the loss of millions of wild birds and mammals will ultimately affect humanity is a matter of debate, but it is hard to envision a good outcome. 

Meanwhile, H5N1 marches on. 

Nature Comms: Acute viral infection accelerates neurodegeneration in a mouse model of ALS

 

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One of the great - yet unanswered - questions about acute viral illnesses is what role (if any) do they play in the development of neurodegenerative diseases, perhaps years or even decades later? 

A hundred years ago the world was embroiled in a global epidemic of Encephalitis Lethargica (EL) following the 1918 influenza pandemic, which appears to have affected millions of people.  

While a viral cause is suspected, it isn't clear whether it was sequelae from the  H1N1 influenza virus, or from some other viral agent (see Evidence for an enterovirus as the cause of encephalitis lethargica).

Throughout history, there have been other reports of neurological outbreaks following severe epidemics, including febris comatosa which sparked a severe outbreak in London between 1673 and 1675, and following the 1889–1890 influenza (?) pandemic, a severe wave of somnolent illnesses (nicknamed the "Nona") was described in Italy

Among those who survived, Parkinsonism and other neurological sequelae was common. 

Over the past 6 years, we've seen numerous reports of memory and neurological problems associated with COVID infection, including 2025's BMC Neurology: Long-term Neurological and Cognitive Impact of COVID-19: A Systematic Review and Meta-analysis in over 4 Million Patients. 

While this is an extensive review - and its 16-page PDF deserves careful review - briefly, they report fatigue affecting over 40% of patients and memory disorders affecting nearly 30%, at least 6 months post infection.

More broadly, in 2023 we looked at a study (see Neuron: Virus Exposure and Neurodegenerative Disease Risk Across National Biobanks), which found statistical linkage between viral illnesses and developing neurodegenerative diseases in the future.

With the very strong caveat that the exact cause of Alzheimer's, Parkinson's, and other neurodegenerative diseases are not yet known - and all are likely the result of multiple genetic and environmental factors - the role of infectious diseases is a hypothesis under serious investigation.

All of which brings us to a report in Nature Communications which reports that  a single, nonfatal respiratory virus infection appears to hasten ALS-like disease in genetically susceptible mice (SOD1-G93A mutation). 

ALS-susceptible mice were infected before they showed motor symptoms with either influenza A (H1N1) or SARS-CoV-2 and compared with uninfected (SOD1-G93A) mice. 

• Influenza-infected mice developed declining motor performance earlier and reached severe ALS-related endpoints sooner. 

• SARS-CoV-2 infected mice saw similar declines in motor ability, but their endpoint was not significantly shortened.  

While this isn't proof that flu or COVID-19 causes ALS or accelerates neurodegenerative disease in humans, it is another datapoint to consider. Although peer-reviewed, the final version will be uploaded when completed. 

Due to its length and technical nature, I've only posted the Abstract. Follow the link to read it in its entirety.  I'll have a postscript after the break. 

Acute viral infection accelerates neurodegeneration in a mouse model of ALS

Art Marzok, Jonathan P. Mapletoft, Imran Ahmed, Braeden Cowbrough, Daniel B. Celeste, Michael R. D’Agostino, Jann C. Ang, Andrew T. Chen, Vithushan Surendran, Yona Tugg, Hahn Li, Karena Wong, Anna Dvorkin-Gheva, Ali Zhang,
Hannah D. Stacey, Mannie Lam, Yasmine Kollar, Kevin R. Milnes, Sam Afkhami & Matthew S. Miller

Nature Communications (2026) Cite this article
 
PDF

We’re sharing this article early to provide faster access to peer-reviewed, accepted research. It is citable and carries a permanent DOI. This version is subject to further edits and will be replaced automatically by the final Version of Record. All legal disclaimers apply.

Abstract

While several viral infections have been associated with amyotrophic lateral sclerosis (ALS), the mechanism(s) through which they promote disease remains elusive. Here we investigate the impact of common, acute viral infections on ALS disease onset and progression in the SOD1G93A mouse model. 

A single sublethal infection prior to onset of ALS clinical signs is associated with markedly accelerated ALS disease progression characterized by rapid loss of hindlimb function. Prior infection results in gliosis in the lumbar spine and upregulation of transcriptional pathways involved in inflammatory responses, metabolic dysregulation, and muscular dysfunction. Therapeutic suppression of gliosis with an anti-inflammatory small molecule, or administration of a direct-acting antiviral, is associated with significantly improved ALS clinical signs, akin to what is observed in uninfected animals. 

Our study provides causal and mechanistic evidence that the immune response elicited by acute viral infections may be an important etiological factor that alters ALS disease trajectory.

        (Continue . . .) 

Although the link between COVID/Flu infection and neurodegenerative diseases later in life is far from established, over the past 15 years we've seen numerous studies that have linked heart attacks and strokes to acute influenza and respiratory infections.

At the same time, we've seen growing evidence that the uptake of the seasonal flu vaccine may reduce the incidence of heart attack and stroke, even if the vaccine doesn't prevent influenza infection. 

Eurosurveillance: Influenza Vaccination Attenuates Acute Myocardial Infarction and Stroke Risk Following Influenza Infection

Conclusions

Our findings add to the evidence that influenza vaccination confers cardiovascular protection. In this study, prior vaccination halved the excess risk of acute myocardial infarction or stroke following breakthrough influenza infection.   

Which is why I'll be rolling up my sleeve again for my 21st consecutive yearly flu shot later this month, and why I'll be getting the updated COVID shot when it becomes available. 

If they turn out to be neuroprotective as well, I'll consider it a welcome bonus. 

WHO WPRO Reports 2 Recent H9N2 Cases From Chinese Mainland

 

#19,318

While case reports remain widely scattered, and there are no signs of human-to-human spread, Mainland China's summer uptick of H9N2 continues, with 2 more cases reported over the past 2 weeks. 

This follows 3 cases in June and 5 in July (see chart below), which I reported on 2 weeks ago. 

Last week, the WHO WPRO Avian Influenza Weekly Update # 1058: 21 August 2026 reported:

Human infection with avian influenza A(H9N2) virus

From 14 to 20 August 2026, one new case of human infection with avian influenza A(H9N2) virus was reported to WHO in the Western Pacific Region. The case is a male child under 5 years of age from Anhui Province, China, with symptom onset on 3 August 2026. The case was hospitalised and subsequently discharged. The case had exposure to live poultry market, and no additional cases were reported from close contacts.

Since 2015, a total of 179 cases of human infection with avian influenza A(H9N2), including two deaths(both with underlying conditions), have been reported to WHO in the Western Pacific Region. Of these, 176 were reported from China, two were from Cambodia, and one was from Viet Nam.

This week, in Avian Influenza Weekly Update # 1059: 28 August 2026 they report:

Human infection with avian influenza A(H9N2) virus

From 21 to 27 August 2026, one new case of human infection with avian influenza A(H9N2) virus was reported to WHO in the Western Pacific Region. The case is a pediatric patient from Beijing Province, China,with symptom onset on 15 August 2026. The case has since recovered. The case had exposure to live poultry market, and no additional cases were reported from close contacts.

Since 2015, a total of 179 cases of human infection with avian influenza A(H9N2), including two deaths (both with underlying conditions), have been reported to WHO in the Western Pacific Region. Of these,176 were reported from China, two were from Cambodia, and one was from Viet Nam.

I'm not sure why the case counts are not being incremented, but I assume it is just an oversight. Given the limits of surveillance and testing, these reported cases are assumed to represent a subset of the actual number of spillovers into humans.

Notably, both cases reportedly had exposure at a live poultry market, which has long been recognised as a risk factor. 

While H9N2 is rarely thought of as being in the same league as H5N1, the CDC lists two lineages (A(H9N2) G1 and A(H9N2) Y280) as having at least some pandemic potential, and several candidate vaccines have been developed.

In terms of risk of emergence, the H9N2 Y280 lineage is ranked higher than H5N1 

And as we've discussed often, most recently in EM&I: Genetic evolution, phylodynamics, geographic spread of H9N2 avian influenza viruses in China from 2014 to 2025: an increasing potential zoonotic risk, LPAI H9N2 appears to be evolving towards a more mammalian-adapted virus.  

Whether H9N2 has true pandemic potential is unknown, but this is definitely a virus worth keeping our eye on.

September Is National Preparedness Month (#NPM26)

 

#19,317

For more than 20 years September has been designated National Preparedness Month here in the U.S., and while we cover emergency preparedness issues year-round (recent examples include here, here, here, here, and here), over the next 30 days I'll be uploading a number of new, or updated, preparedness blogs. 

So far we've been lucky with a suppressed Atlantic Hurricane Season this summer, but we are about to experience a strong - perhaps record breaking - El Nino Fall and Winter. One which could produce extreme weather events (floods, ice storms, severe weather) in some parts of the country.

Other threats, ranging from earthquakes and tsunamis to cyber attacks and power failures know no season, and can strike without warning. Even aging infrastructure poses a risk.

In 2025 the U.S. Department of Energy published a 73-page report that warned that if current schedules for retirement of reliable power generation (especially baseload) continue, without enough firm replacement, the risk of blackouts by 2030 could increase dramatically.

And as we saw last week in UK National Risk Register 2026 - Urges Citizen Preparedness, many countries continue to put the emergence of a `Disease X' pandemic at the top of their threats list. 

How well you and your family will fare during any of these emergencies depends largely upon how well prepared you were when they started.  Our first stop today is the 2026 message from Ready.gov, which reads in part:

National Preparedness Month

Last Updated: 08/28/2026

FEMA’s Ready Campaign has observed National Preparedness Month since 2004 to encourage Americans to prepare for emergencies. The month is a great time to take small steps to make a big difference in being prepared.

Preparedness Starts at Home, the 2025 theme, focuses on getting back to the essentials of preparedness. In addition to sharing the tips, messages and graphics you can find on Ready.gov, there are four key actions you can take to prepare for any disaster you may face:

Know your risk

• Know what could happen where you and your family live. This helps you figure out what you need to do to stay safe. You can explore various disasters and emergencies on Ready.gov. 

Make a family emergency plan

• Making a plan early helps you reduce stress and save time and money. Follow four easy steps and create a free Family Emergency Plan quickly and easily with our fillable form.
• Disasters are costly but preparing for them doesn’t have to be. Taking time to prepare now can help save you thousands of dollars and give you peace of mind when the next disaster or emergency occurs. Visit Ready.gov’s low and no-cost tip page to see how you can be better prepared without spending a lot of money.

Build an emergency supply kit

• Having enough food, water and medicine can help you stay safe and comfortable until help arrives. Having what you need can also prevent injury and damage to your home.
• Build a go-bag with all the essentials you might need, so you don’t need to scramble in an evacuation situation. Find a list of supplies at Build A Kit.

Get involved in your community by taking action to prepare for emergencies

• Emergencies can happen fast, and emergency responders aren’t always nearby. You may be able to save a life by taking simple actions immediately. You can learn these steps when you take a first aid class through many organizations in your community..
• Join a Community Emergency Response Team program and get trained on basic disaster response skills, such as fire safety, light search and rescue, team organization and disaster medical operations.
• Take a free online independent study course through FEMA’s Emergency Management Institute or a CPR course through the American Red Cross to learn more about how to help your community become more prepared.

(Continue . . . )

Although I'm a huge proponent of having a good first aid kit (or three), emergency power options, and a full pantry, I can think of no prep more valuable than having one or more `disaster or flu'  buddies on whom you can rely in an emergency. 

While I first wrote about it 16 years ago, in In An Emergency, Who Has Your Back?, you find a more recent (2025) update at With A Potentially Severe Flu Season Ahead: Time to Line Up A `Flu Buddy'.

While I've no idea what challenges we as a nation will face in the coming year, I do know that individual preparedness is relatively cheap insurance.  So I hope you'll find some useful information in this year's crop of preparedness blogs. 

Transb. & Emerg. Dis.: A Multi-Reassortant H3N8 Avian Influenza Virus Derived From Migratory Birds in Eastern China Exhibits Cross-Species Transmission Potential

Credit ECDC

#19,316

While our knowledge of the subtypes of influenza pandemic viruses prior to 1918 is admittedly murky - historical and serological reconstructions (as depicted in the above pandemic timeline produced by ECDC) - suggest that an H3 virus, possibly H3N8, circulated globally around 1900. 

What is certain is that roughly seventy years later an avian H3 virus ressorted with seasonal H2N2 and produced another pandemic in 1968, and its descendents have remained in circulation for nearly 6 decades.

This fits nicely into the H1, H2, H3 pattern of known influenza pandemic viruses going back nearly 140 years (see Are Influenza Pandemic Viruses Members Of An Exclusive Club?) 

Since then we've also seen:

• An equine H3N8 virus jump to dogs in 2004, followed three years later by an avian H3N2 virus in South Korea, with both reassorting with other subtypes (see J. Virology: Zoonotic Risk, Pathogenesis, and Transmission of Canine H3N2).

• An avian H3N8 virus was found in marine mammals (harbor seals) in 2011, and 2012’s mBio: A Mammalian Adapted H3N8 In Seals, provided evidence that this virus had recently adapted to bind to alpha 2,6 receptor cells, the type found in the human upper respiratory tract.

• In 2015's J.Virol.: Experimental Infectivity Of H3N8 In Swine, we saw a study that found that avian (but not canine or equine) H3N8 could easily infect pigs.

All worrisome signals, but it was the 2022 emergence of a zoonotic H3N8 virus in China - first infecting 2 children 400 km apart in Henan and Hunan Provinces in April and May of 2022 - and more recently a fatal infection of a 56 year old woman in Guangdong Province, that really set off alarm bells.

This led to 2023's EID Journal: Evolution of Avian Influenza Virus (H3) with Spillover into Humans, China, where researchers described finding 4 sub-lineages and an astonishing 126 genotypes of avian H3 viruses circulating in China.

The authors also described a recent reassortment event where H3N8 acquired the internal genes from LPAI H9N2, a promiscuous virus which had previously contributed genes to both H5N1 and H7N9 (see PNAS: Evolution Of H9N2 And It’s Effect On The Genesis Of H7N9).

Since then, we've seen an increasing number of cautionary reports on H3 viruses from China, including:

J. of Infection: Global Spread of H3 Subtype Avian Influenza Viruses With an Accelerated Evolution After Interspecies Transmission

Vet. Research: Emergence of a Novel Reassortant H3N3 Avian Influenza Virus with Enhanced Pathogenicity and Transmissibility in Chickens in China

Transboundary & Emerg. Dis.: H3 Avian Influenza Virus Isolated from China in 2021–2022 Showed the Emerging H3N8 Posed a Threat to Human Health

Eurosurveillance: Analysis of Avian Influenza A (H3N8) Viruses in Poultry and their Zoonotic Potential

All of which serves as prelude to the following report - again from China - describing another migratory-bird-origin H3N8 subtype AIV - isolated and identified in Jiangsu Province in 2024 - that has also acquired a number of mammalian–adaptive mutations, exhibits dual receptor–binding capacity, and has cross-species transmission potential.

Due to its length, and technical nature, I've only posted the link, abstract, and some excerpts from the discussion. Follow the link to read it in its entirety.  I'll have a bit more after the break.

A Multi-Reassortant H3N8 Avian Influenza Virus Derived From Migratory Birds in Eastern China Exhibits Cross-Species Transmission Potential

Yunfei Guo, Zhonglong Yang, Hui Yang, Xinyu Miao, Tao Qing, Daxin Peng, Sujuan Chen
First published: 30 August 2026
https://doi.org/10.1155/tbed/9889145Digital Object Identifier (DOI)
  
PDF 

Abstract

Migratory birds are one of the main reservoirs and long-distance transmission vectors of avian influenza viruses (AIVs). A migratory-bird-origin H3N8 subtype AIV (A/wild bird/Huadong/sy17/2024, hereafter named as WD/HDsy17/24) was isolated and identified in Jiangsu Province, Eastern China, in 2024. However, few studies have been conducted on the cross-species transmission potential of H3N8 AIVs from migratory birds. 

Phylogenetic analysis indicated that the eight gene segments of WD/HDsy17/24 originated from different subtypes of AIV such as H3N8, H1, H5N1, H5N2, and H7N7 and was a multirecombinant virus. WD/HDsy17/24 virus showed a binding affinity to both SAα-2, 3-galactose (Gal) and SA α-2, 6 Gal receptors, relatively weak thermal stability and pH stability.

The SPF chicken pathogenicity indicated that the virus only causes mild respiratory symptoms and leads to lung hemorrhage and congestion. The mice pathogenicity indicated that the body weight of infected mice drops to the lowest value on the third day after infection, the lung-to-body ratio significantly increases, and inflammatory or edema lesions appear in the lungs. 

Moreover, this virus can infect guinea pigs through contact transmission and aerosol transmission routes from infected SPF chickens. After infection, obvious secretions can be seen in the eyes of guinea pigs. In the contact transmission group, viral shedding was detected in the nasal wash of one guinea pig at 6 days postinfection (dpi). In the aerosol transmission group, viral shedding was detected in the nasal washes of one guinea pig at both 10 and 12 dpi and in another guinea pig at 14 dpi. After 21 days, the seroconversion rate of serum antibodies in both groups is 100%. 

These findings underscore the need for continued surveillance of H3N8 viruses to identify circulating strains that may potentially threaten human health.

        (SNIP)

Discussion

As a natural reservoir, wild birds facilitate transregional and cross-national transmission [28]. H3N8 AIVs, a dominant subtype in wild birds, have a broad host range, infecting poultry [29] and crossing species barriers to infect horses, dogs, pigs, and humans [30–33]. Therefore, long-term surveillance in wild bird migration areas is urgently needed.

Recent reports have documented novel reassortant H3N8 variants isolated a reassortant H3N8 from a wild bird in Jiangxi has become widespread in Chinese chicken flocks, forming a triple-reassortant genotype [5, 10]. The isolate WD/HDsy17/24 also displayed multi-reassortant characteristics, with eight gene segments derived from reassortment of H1, H3N8, H5N1, H5N2, and H7N7 influenza viruses. This is consistent with a broader analysis showing that wild-bird-origin H3N8 in China evolved into at least 126 genotypes from 2009 to 2022, with genotype G25 (reassorted with H9N2) capable of infecting chicken and crossing to humans [34]. The close genetic relationship of our isolate’s M and NS genes to H9N2 AIVs suggests enhanced host adaptability via reassortment.

(SNIP)

In summary, through analysis of the genetic evolutionary characteristics and pathogenicity of a wild-bird-origin H3N8 AIV from eastern China in 2024, this study confirmed that the strain carries multiple mammalian–adaptive mutations and exhibits dual receptor–binding capacity and cross-species transmission potential. 

The findings provide important experimental data for the early warning, surveillance, risk assessment, and control strategy development of H3N8 AIVs and are of great significance for mitigating their potential public health risks.

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While this latest H3N8 paper doesn't identify a new pandemic strain, it does add to what has become difficult to ignore; that the panoply avian H3 viruses in China have become increasingly diverse, they continue to evolve rapidly, and some have already displayed worrisome mammalian adaptations.  

As any kid with an erector set can tell you, the more interchangeable parts you have, the more neat stuff you can build. The same holds true for influenza reassortment - the more gene segments available for swapping - the more novel subtypes/genotypes that are possible.

While that doesn't guarantee an untoward outcome, this trend has obviously captured the attention of Chinese researchers, and should be on our radar as well.