Louisiana DOH Reports Naegleria fowleri infection in Louisiana resident

 Credit CDC

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Nearly every year we see a handful of rare - mostly fatal - brain infections caused by free living amoebas (Naegleria fowleri) that inhabit warm, fresh water (see A Reminder About Naegleria Season - 2019).

Dubbed the `brain eating amoeba' by the press - this infection is called PAM (Primary amebic meningoencephalitis) - and occurs when the amoeba enters the brain through the nasal passages, usually due to the forceful aspiration of contaminated water into the nose.

Not every PAM case is due to Naegleria, as Balamuthia mandrillaris and Acanthamoeba - and other non-Naegleria amoebic infections - can cause similar pathologies.

Last year the CDC's MMWR carried a report on a fatal 2024 case from Texas, which involved a previously healthy 71-year old woman who used unsterilized water to perform nasal irrigation.  

This is a common way that people around the world have become infected (see 2011's Neti Pots & Naegleria Fowleri).  The CDC and state health departments have long warned on the dangers of using tap water to perform nasal irrigation, and offer advice on safer alternatives. 

But most U.S. cases occur while swimming, often in warm stagnant freshwater lakes, rivers, canals, and ponds.  Less commonly, we've  seen infections attributed to water parks, private swimming pools, and even the public water supply. 

• In 2013, in Louisiana: St. Bernard Parish Water Supply Tests Positive For Naegleria Fowleri, we saw the tragic story of a 4-year-old Mississippi child visiting a St. Bernard Parish home, who (according to this NOLA.COM report) appears to have contracted the amoeba while playing with a water hose and a slip-and-slide.

• Five years ago we looked at an MMWR: Epidemiological Investigation Into A Case Of Primary Amebic Meningoencephalitis in California which suggested a poorly chlorinated spring-fed swimming pool was the likely source of infection and death of a 21 year old woman.

•  In 2013, in Arkansas: Naegleria fowleri Shuts Water Park, we saw the second suspected case in 3 years from the same recreational venue.

Only 3 or 4 cases are reported in the United States each summer, but in 2017 a research letter written by epidemiologists at the CDC (see EID Journal: Estimation of Undiagnosed Naegleria fowleri (PAM), United States) estimated the yearly number PAM cases in the United States probably averages closer to 16 (8 males, 8 females).

Meaning that 70%-80% likely go unrecognized. But even so, your odds of contracting PAM are exceedingly low.

 Louisiana Health Department report follows:

LDH reports Naegleria fowleri infection in Louisiana resident 

Rare infection most likely acquired while swimming in Lake Claiborne

Baton Rouge, Louisiana, Aug 19, 2026 - The Louisiana Department of Health is reporting a confirmed Naegleria fowleri infection in a Louisiana resident. The resident most likely acquired the infection while swimming in Lake Claiborne, located in Claiborne Parish, shortly before illness.

Naegleria fowleri, often referred to as a brain-eating amoeba, is commonly found in warm freshwater lakes, rivers, canals, and ponds throughout the United States. It can cause primary amebic meningoencephalitis (PAM), a brain infection that may result when water containing the amoeba rushes up the nose and reaches the brain. The infection is extremely rare, but nearly always fatal.

Naegleria fowleri cannot infect people if swallowed and is not spread from person to person. The amoeba is not found in salt water or in properly maintained and chlorinated pools. Symptoms of Naegleria fowleri infection typically start with severe headache, fever, nausea and vomiting and progress to stiff neck, seizures, and coma that can lead to death. Symptoms usually begin about five days after infection but can start within one to 12 days.

Naegleria fowleri thrives in warm, fresh water and grows best at higher temperatures up to 115°F. The amoeba is naturally occurring, and there is no routine environmental test for Naegleria fowleri in bodies of water.

A Health Alert Network (HAN) was shared to all state providers from Louisiana Department of Health on August 18, 2026, advising on symptoms and reporting.

Though the risk of infection is low, recreational water users should always assume there is a risk when they enter warm fresh water. You can reduce your risk of infection by limiting the amount of water that goes up the nose. Recommended precautions include:

• Use caution when engaging in water-related activities in warm freshwater during periods of extended extreme heat. Naegleria fowleri usually occurs when temperatures increase for prolonged periods, resulting in higher water temperatures and lower water levels.
• Swimmers can reduce their risk by keeping their heads out of the water and using nose clips or plugging their noses when going underwater.
• Avoid submersing your head in hot springs and other untreated fresh thermal water.
• Avoid digging in or stirring up the sediment while taking part in water-related activities in shallow, warm freshwater areas.

​Naegleria fowleri infections are rare, with only 180 known cases of PAM in the U.S. (between zero and eight cases annually) from 1937 through 2025. Louisiana had three Naegleria fowleri cases during that time period.

For more information regarding Naegleria fowleri, please visit Naegleria fowleri Infections | Naegleria fowleri Infection | CDC.

For more information on the Naegleria parasite, you can also visit the CDC’s Naegleria webpage.

Australia: Media Reports of Multiple Mass Mortality Events in Birds (H5N1 Suspected)

 
Data as of 4pm AEST, 19 August 2026

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While HPAI H5N1 reporting from governmental sources have slowed in recent days, overnight the Australian press reported on multiple mass mortality events involving birds in South Australia and Tasmania (see ABC News Bird flu suspected after more than 1,000 birds found dead in SA, more deaths in Tasmania).

According to multiple news sources (see here and here), South Australian Premier Peter Malinauskas addressed the SA parliament (Aug 20th) to announce that more than 1,000 crested terns had died across three mass mortality events on several remote offshore islands. 

Additionally there are reports of > 2 dozen dead penguins in Tasmania.  While H5N1 has not been confirmed, HPAI is strongly suspected.  For now, there are no reports of H5N1 in non-avian wildlife, poultry, or livestock. 

While we await further details (and/or confirmation) we've two other sources of background information; an expert commentary from Australia's National Testing laboratory CSIRO, and a series of academic analyses from The Conversation.

First this analysis from CSIRO (h/t Pathfinder on FluTrackers):

Expert Commentary: What do we know about H5 bird flu?

18 AUGUST 2026 4 MIN READ

In June 2026, Australia recorded its first cases of the highly contagious H5 bird flu.

As Australia's national reference laboratory for animal diseases, CSIRO's Australian Centre for Disease Preparedness (ACDP) plays a critical role in protecting Australia's valuable livestock and aquaculture industries and the wider community from infectious diseases such as bird flu.

Scientists at ACDP have been conducting testing and genetic analysis to learn more about exactly which strain of the virus has arrived on our shores, and how it is spreading.

All quotes below are available for use by media. Spokespeople quoted:

• Dr Frank Wong, Senior Research Scientist at CSIRO's Australian Centre for Disease Preparedness. Dr Wong is also a World Organization for Animal Health-designated reference expert on avian influenza
• Dr Matt Neave, Team Leader of Sequencing and Agent Characterisation at CSIRO's ACDP
• Dr Debbie Eagles, Director of CSIRO's ACDP.

What is H5N1 and why is it a concern?

Dr Frank Wong:

For the past 5 or 6 years the world has been affected by a bird flu panzootic. This is what we call a pandemic in animals. In this case, because the virus is an avian virus, it has mostly impacted birds around the world.

The clade 2.3.4.4b lineage of H5N1 is a highly pathogenic bird flu virus that emerged around 2020-2021, first spreading across Europe and then moving on to other continents, including Asia and North America.

Along the way it has caused mass mortalities in both domestic poultry as well as many species of wild bird.

H5N1 has been able to spread rapidly across different continents largely due its ability to be sustained in migratory wild birds, like waterfowl such as ducks and geese.

The genotype that we're talking about for Australia, known as genotype B3.2, arose from reassortment in North America and then spread to South America and the sub-Antarctic islands.

It had a great impact on South American poultry industries as well as wild bird life and marine mammals, so that's why we're concerned about the introduction of the virus to Australia.

What does ACDP's genetic testing show us?

Dr Matt Neave:

Sequencing the virus genome has become really important in disease outbreaks like this one. We're now able to do it much quicker than in the past and can get a whole influenza genome in around 15 to 26 hours.

From the viral genome we are able to determine several important things, including the exact strain of the virus. Another thing we can do is compare that viral genome to other reference sequences in our database or public databases online. This allows us to determine how closely related our Australian cases are to the sub-Antarctic ones, for example.

Our testing shows us that the sequences from the first two cases in Australia were closely related to ones from Heard Island. From the data we have at hand, it appears Heard Island is the most likely source of the Australian infections.

By comparing genetic sequences from virus samples, scientists can trace the relationships between the first Australian H5 bird flu cases and those detected on Heard Island. Credit: Matthew J. Neave et al. Show image description 

        (Follow link to read the full report). 

Although there are now roughly 2 dozen entries, going back to H5N1's arrival in Australia in mid-June, over the past few days these 4 essays have been published.

Published: August 20, 2026
The first wave of bird flu is the worst: what Australia can learn from overseas
Bethany J Hoye, University of Wollongong
The rest of the world has already had to grapple with bird flu – and there are lessons for Australia.

Published: August 18, 2026
More than 5,000 little penguins will be vaxxed against bird flu. How will this protect them?
Julie Old, Western Sydney University
Little penguins are flightless and return at night to the same burrow, making it easier to capture and vaccinate them.

Published: August 17, 2026
From the coasts to the plains, bird flu could threaten not just birds – but their homes
Penny Olsen, Australian National University
From raucous honeyeaters to top predators, Australia’s birds are vital to nature.

Published: August 16, 2026
Is bird flu infecting humans? How would we know?
Allen Cheng, Monash University
Even with bird flu circulating in Australia, the risk to humans is low. But some groups are still at increased risk.

 

WHO Influenza at the human-animal interface (Aug 7th) - Uptick in H9N2 Cases in China

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The WHO has released an update (dated Aug 7th, but posted overnight) of human novel flu infections reported between July 8th and Aug 7th. Included are 8 H9N2 cases from Mainland China, and 1 H5N1 case from Cambodia (all previously reported).

This report also confirms the H5 case reported from Bangladesh in July has been confirmed as H5N1. 

For reasons well above my pay grade, reporting from Hong Kong's CHP on H9N2 cases has been a bit chaotic this month (reporting the same 4 recent cases as `new' for the past 3 weeks running), and the WHO's weekly WPRO avian flu report hasn't been updated since Aug 7th. 

What we can say, however, is that China (along with a recent case in Hong Kong) has seen an uptick in reported H9N2 cases this summer. Whether this is due to more frequent spillovers, or better surveillance, isn't known. 

Despite being clearly zoonotic - LPAI H9N2 is considered a `non-reportable' disease in poultry or wild birds by WOAH (see Terrestrial Animal Code). Complicating matters, China's attempts to control LPAI H9N2 through vaccines have been less than successful. 

In 2025's NPJ Vaccines: Impact of Inactivated Vaccine on Transmission and Evolution of H9N2 Avian Influenza Virus in Chickens, we saw evidence that inactivated vaccines failed to prevent - or even reduce - H9N2 in China's poultry, and may have driven viral evolution (including mammalian adaptations).

Several recent Chinese studies have found signs that LPAI H9N2 is becoming better adapted to mammals, warning of its pandemic potential; including:

• Two weeks ago, in EM&I: Genetic evolution, phylodynamics, geographic spread of H9N2 avian influenza viruses in China from 2014 to 2025: an increasing potential zoonotic risk, we saw yet another Chinese study warning that H9N2 was accruing mammalian adaptations which increases its zoonotic risk.
• Two months ago, in Viruses: Epidemiological and Virological Characteristics of H9N2 Avian Influenza Virus in Jiangsu Province, China, 2024, researchers warned that that Jiangsu’s circulating H9N2 viruses have acquired human receptor preference and mammalian adaptation, posing silent infection and pandemic risks

• Last October, in China CDC Weekly: Epidemiological and Genetic Characterization of Three H9N2 Viruses Causing Human Infections, investigators reported a number of indicators of increased mammalian adaptation within the virus, including an enhanced ability to infect upper respiratory (α2,6-sialic acid) tract receptors, and a number of HA protein mutations, including; H191N, A198V, Q226L, and Q234L.

• The Asian Y280/G57 lineages have shown increasing signs of mammalian adaptation (see EM&I: Enhanced Replication of a Contemporary Avian Influenza A H9N2 Virus in Human Respiratory Organoids)), while the African and Middle Eastern Lineages (mostly European G1-like) are older and less evolved.

• Last summer, in Nature: Genetic diversity of H9N2 avian influenza viruses in poultry across China and implications for zoonotic transmission, researchers reported rising prevalence of key mutations associated with increased infectivity and pathogenicity in mammals.

While H9N2 doesn't garner the kind of headlines that H5N1 gets, our own 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

Which is why any uptick in activity is worthy of our attention. 

Australia H5N1 Update

 

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It's been a week since Australia Changed How They Report H5N1 - reporting `events' rather than individual detections in wildlife - and while the numbers have continued to rise (see below), we seem to be getting fewer (and less detailed) updates. 

In the first 10 days of August, Australia's Chief Veterinary Officer released 11 bird flu updates/statements, but has only released one in the past 9 days. Similarly, Victoria's last update was August 15th.  

Up until a week ago, DAFF was reporting both the number of positive and negative test results, along with number hotline reports (see below). This gave us some idea of the percentage of hotline reports being investigated (roughly 1 in 13).

(Aug 13th DAFF)

With the move towards only tracking `events', that metric is no longer provided.

While I'd certainly like more data, there is only so much that any country can reasonably do when they are faced with a highly aggressive pathogen like avian H5N1. 

For now, South Australia continues to post detailed daily updates, but added the following notice this week:

Thus far, H5N1 has not been detected in poultry, livestock, or non-avian wildlife. But how long that reassuring status quo can last is unknown.  

Preprint: Enhanced Pathogenicity and Contact Transmissibility of Human-origin Avian Influenza H5N1 Clade 2.3.4.4b Genotype B3.13 Compared to D1.1 in Ferrets

 

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The two main H5N1 genotypes (out of > 100) we are watching in the United States are the B3.13 `Bovine' strain which emerged in Texas Cattle in early 2024, and the D1.1 avian strain that appeared in Canada the following fall and quickly spread through wild birds and poultry across the continent. 

From a distance, it appears that the B3.13 strain produces mainly mild illness in humans (ie. conjunctivitis), while the D1.1 strain has been linked to a number of severe illnesses and several deaths.  

But appearances, particularly when surveillance and testing are limited, can be deceiving. 

• Bovine B3.13 H5N1 infections are probably easier to track because they occur on dairy farms, are more likely to be treated with antivirals, and may be more likely due to `splash' events where infection occurs through the ocular route. 

• While many D1.1 infections occur on poultry farms, it may also be encountered by the general public through contact with wild birds and/or backyard poultry, which makes it more difficult to track. 

Complicating matters, we've seen a number of head-to-head comparison studies (see here, here, and here) that have provided differing assessments of the transmissibility and virulence of these two genotypes. 

In one study using human nasal and airway organoids, D1.1 appeared to be better adapted to human physiology, while in another (see IJID study)  B3.13 caused severe disease, extra-respiratory spread, and lethality in ferrets while D1.1 caused milder disease with no lethality.

To be fair, differences in methods and materials used in these studies can make a huge difference in their outcomes.  

• Some studies have used laboratory-propagated, clinical-origin H5N1 isolates, while others have used full-genome reverse-genetics reconstructions, or engineered PR8 reassortants carrying the relevant H5 and N1 genes from each genotype.

• Some studies used co-housed ferrets, or adjacently-housed ferrets (for airborne transmission), while others used organoids or other in vitro proxies to study replication or receptor binding.

And in all of these studies, researchers have relied on one or two isolates from each genotype, which may ignore a much larger and diverse pool of circulating viruses.  None of which invalidates their findings, but it does make direct comparisons between genotypes more difficult. 

All of which serves as prelude to a new preprint (not yet peer reviewed) which tested transmission and pathogenicity of D1.1 and B3.13 genotypes in co-housed ferrets. 

Using primarily full-genome reverse-genetics viruses, these researchers found that - out of the box - the B3.13 genotype appeared to be better adapted to mammalian hosts than D1.1.

They cite:

HPhTX B3.13 infection resulted in more severe clinical disease and enhanced viral shedding, with evidence of increased transmission relative to HPhLA D1.1. 

But 

. . . HPhLA D1.1 showed rapid acquisition of the mammalian-adaptive mutation E627K in infected ferrets and both E627K and Q194K in the only fatal contact animal. 

The B3.13 used in this experiment was better adapted, but more stable. D1.1 appears to be more of a wildcard.  While neither have acquired the ability to spread efficiently among humans, both require continued monitoring for further changes.  

This is a lengthy (66 pages) and at times technical paper, so I've only posted the abstract and some excerpts from the conclusion.  Those desiring a deeper dive will want to follow the link to read it in its entirety.  

I'll have a bit more after the break.

Enhanced Pathogenicity and Contact Transmissibility of Human-origin Avian Influenza H5N1 Clade 2.3.4.4b Genotype B3.13 Compared to D1.1 in Ferrets
 Ahmed M. Elsayed, Ramya S. Barre, Mahmoud Bayoumi, Alvaro Padron, Hossein Batebi, Vinay Shivanna, Roy N. Platt, Fiona Burmeister, Joshua Castro, Arash Rahmani,  Juliane Lang,  Chengjin Ye,  Timothy J.C. Anderson, Roland Netz, Aitor Nogales,  Robert P. de Vries, Geert-Jan Boons, Adolfo Garcia-Sastre,  Elsayed M. Abdelwhab,  Gregory C Ippolito, Luis Martinez-Sobrido
doi: https://doi.org/10.64898/2026.08.10.744032
This article is a preprint and has not been certified by peer review 
 
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Abstract

Since its emergence in 2020, multiple genotypes of the H5N1 clade 2.3.4.4b have been identified, with B3.13 and D1.1 emerging in the USA as two major and concerning genotypes. However, their relative pathogenicity and transmissibility in mammals have not been fully elucidated. 

We compared the pathogenicity and transmissibility of the first two human H5N1 clade 2.3.4.4b cases caused by B3.13 in Texas (A/Texas/37/2024; HPhTX B3.13) and D1.1 in Louisiana (A/Louisiana/12/2024; HPhLA D1.1) in a ferret model of infection and transmission. 

HPhTX B3.13 infection resulted in more severe clinical disease and enhanced viral shedding, with evidence of increased transmission relative to HPhLA D1.1. 

Histopathological analysis revealed more extensive lung pathology in animals infected with HPhTX B3.13, consistent with increased viral loads and inflammatory responses. Importantly, both genotypes showed no significant differences in reactivity to ferret sera raised against candidate vaccine virus (CVV) strains, receptor binding properties, or neuraminidase (NA) activity and thermostability. 

Whole-genome sequencing revealed no adaptive mutations in HPhTX B3.13 following infection or transmission. In contrast, HPhLA D1.1 showed rapid acquisition of the mammalian-adaptive mutation E627K in infected ferrets and both E627K and Q194K in the only fatal contact animal. 

Both mutations were associated with enhanced polymerase activity and computational analyses suggested that they enhance interactions with the mammalian host factors ANP32A and B. 

Our findings indicate that B3.13 is already well adapted for mammalian infection and transmission whereas D1.1 retains evolutionary potential through the rapid acquisition of adaptive mutations, highlighting important genotype-specific differences relevant to zoonotic risk assessment and pandemic preparedness.

(SNIP)

 Overall, our study supports a model in which mammalian adaptation of contemporary HPAIV H5N1 is driven predominantly by optimization of viral polymerase function rather  than by changes in receptor specificity. The genetic stability of HPhTX B3.13, together with its high polymerase activity, efficient transmission, and increased pathogenicity, suggest that this genotype is already well adapted for mammalian replication.

In contrast,  HPhLA D1.1 remains incompletely adapted but rapidly acquires mammalian-adaptive PB2 mutations during replication in ferrets. The identification of PB2 Q194K as a cooperative mutation that enhances the activity of PB2 E627K expands our understanding of influenza polymerase adaptation and identifies a potential molecular marker for the surveillance of emerging H5N1 viruses with increased zoonotic potential.

Finally, this study has some limitations. 

First, transmission was assessed in a single  mammalian model with a relatively small sample size under controlled laboratory conditions, which may not fully recapitulate natural exposure settings or host diversity. 

Second, only one isolate per genotype was evaluated. Third, the potential contribution of sex to pathogenicity or transmission was not assessed since only female ferrets were used in this study and because some previous studies used male ferrets 17,72 . 

Finally, our in silico computational analysis suggested that the PB2 mutations 194K and 627K affect  PB2-ANP32 binding in a host-dependent manner, with APN32A maintaining a more stable association than ANP32B and showing reduced binding stability. However, future studies are needed to confirm this hypothesis. 

       (Continue . . . )

The caveat to all of this is that while neither genotype appears ready for prime time - both were collected back in 2024 - and evolution never stops. Existing genotypes evolve slowly through antigenic drift or adaptation, while new genotypes can emerge via reassortment (antigenic shift). 

We've even seen new subtypes emerge (see J. Virology: Risk assessment of avian influenza A(H5N5) virus from the first human case using the ferret model) during this epizootic. 

There are no guarantees how long B3.13 - or D1.1 - will remain the primary HPAI threats going forward.  

Right now, as the days grow shorter in the Northern Hemisphere, migratory birds that spent their summer in their high latitude roosting spots are starting to move south (see Sci Repts.: Southward Autumn Migration Of Waterfowl Facilitates Transmission Of HPAI H5N1).

As we discussed a year ago, in H5Nx: Reassort & Repeat, the fall can often bring abrupt changes.  

While it is always possible the next wave will be less virulent, last year South Korea's MAFRA reported 3 different subtypes of HPAI (H5N1, H5N6, H5N9) in wild birds, and significantly increased infectivity. 

Which makes now a good time for poultry producers - from commercial operations to back-yard hobby farms - to review their biosecurity procedures, and to make necessary adjustments before the fall wave arrives. 

Preprint: Clinical outcomes of early aspirin versus non-aspirin NSAID use in adults hospitalized with influenza: A retrospective study

Photo Credit –CDC PHIL

Note: Nothing in this blog post should be construed as specific medical advice - as individual needs may vary - and everyone should consult their own doctor. The following is presented for educational uses only.

 

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Sixteen years ago, in A Hot Topic For Further Research, we saw a retrospective analysis in the Journal of the Royal Society of Medicine showing the risk of mortality increased by roughly 33% when antipyretics (aspirin, paracetamol, and diclofenac) were used in influenza-infected (non-human) animals.

While the mechanism behind this reported increased mortality wasn't established, it was suggested that the reduction of the natural host response to infection - fever - may have been a contributing factor.

There were a lot of limitations to that study, not the least of which is that research on mice, chickens, and even ferrets isn’t always applicable to humans. Over the next few years, we saw several other studies emerge, including:

• In 2011, in A Feverish Debate, the well respected Wellington based Medical Research Institute of New Zealand, published a paper (Antipyretic therapy for influenza infection—benefit or harm?) in the New Zealand Medical Journal that questioned the conventional wisdom of using these antipyretic drugs with influenza.

• Also from 2011 - the American Academy of Pediatrics (AAP) released a report on the use of antipyretics in children, suggesting that we ought not over-treat fevers (Clinical Report—Fever and Antipyretic Use in Children)

• And in 2013, in Adding To A Feverish Debate, we looked at a study in the Journal of Pediatrics on another possible (albeit, rare) adverse effect seen in a small number of young children with fever and dehydration at a hospital in Indiana who received treatment with NSAIDs - AKI or Acute Kidney Injury.

Somewhat related to all of this have been studies suggesting that the concurrent use of antipyretics may inhibit the immune response when receiving vaccines (see Anti-Inflammatory Meds And Vaccines and Common Pain Relievers May Dampen Vaccination Benefits).

While none of these studies provided definitive proof of harm, they (and others) have raised some interesting questions.

We revisited the topic in 2015's JJID: Evaluating The Mortality Risks Of Taking NSAIDs & ASA With Influenza, which - while subject to a number of limitations - provided some reassurance on the use of antipyretic drugs with influenza, finding that:

We found no compelling evidence that NSAID or ASA use influenced mortality in severe pH1N1.

A 2020 Danish study, published in JAMA (Association of Nonsteroidal Anti-inflammatory Drug Use and Adverse Outcomes Among Patients Hospitalized With Influenza) was similarly unable to find a link between NSAID use and increased mortality with influenza.

In this study, NSAID use was not associated with a clinically significant increased risk of ICU admission or death in patients hospitalized with influenza. While studies on the association of NSAIDs with the disease course of COVID-19 are clearly needed, the currently available data, including the present study, do not seem to support strong recommendations against using NSAIDs in patients with viral pneumonia. 

That said, this study did not establish that NSAIDs are harmless in every patient or scenario, as long-term use of NSAIDs was associated with ICU admission.

While the data has been mixed, there has also been little evidence to suggest taking NSAIDs following vaccination blunts the immune response (see  No Evidence That Analgesic Use after COVID-19 Vaccination Negatively Impacts Antibody Responses), although prophylactic use remains a concern. 

All of which brings us to a new preprint (not yet peer reviewed) by researchers at the University of Minnesota, which goes as far as to suggest possible benefits from NSAIDs in treating influenza -  although their study was small, single-center, and nonrandomized - making their findings preliminary at best. 

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

Clinical outcomes of early aspirin versus non-aspirin NSAID use in adults hospitalized with influenza: A retrospective study
Suk Yin Chan-Colenbrander, Qi Wang
doi: https://doi.org/10.64898/2026.08.05.26359840
This article is a preprint and has not been peer-reviewed [what does this mean?].

Preview PDF

Abstract

Seasonal influenza remains a major cause of morbidity and mortality worldwide. Although neuraminidase inhibitors improve clinical outcomes, influenza-related deaths persist. We evaluated the associations of early aspirin and non-aspirin nonsteroidal anti-inflammatory drug (NSAID) use with clinical outcomes in adults hospitalized with influenza. This retrospective study included adults admitted to the University of Minnesota Medical Center from 2016 to 2018.

Multivariable logistic and Cox regression models adjusted for age, sex, race, smoking status, influenza vaccination status, and cardiovascular burden were used to evaluate the associations of early aspirin and NSAID use with clinical outcomes. Among 2,816 patients screened, 320 had laboratory-confirmed influenza.

Compared with unvaccinated patients, vaccinated patients had lower rates of ICU admission (11% vs. 24%; P = 0.003) and ventilatory support (6% vs. 15%; P = 0.009).

In unadjusted analyses, aspirin users had higher rates of cardiovascular complications (27% vs. 16%; P = 0.028) and lower 3-year survival (57% vs. 72%; P = 0.008).

In contrast, NSAID users had lower rates of ICU admission (7% vs. 18%; P = 0.042), cardiovascular complications (4% vs. 23%; P = 0.001), and renal complications (9% vs. 25%; P = 0.010), and higher 1-year (98% vs. 78%; P = 0.0004) and 3-year survival (89% vs. 63%; P = 0.0001).

After adjustment, aspirin use was not independently associated with any study outcome.

Early NSAID use was independently associated with lower odds of renal complications (aOR, 0.35; 95% CI, 0.13–0.97; P = 0.044) and lower hazards of 1-year (aHR, 0.11; 95% CI, 0.01–0.81; P = 0.030) and 3-year mortality (aHR, 0.33; 95% CI, 0.14–0.77; P = 0.011).

Sensitivity analyses using the Charlson Comorbidity Index yielded similar findings. Prospective studies are needed to determine whether early non-aspirin NSAID use improves clinical outcomes in adults hospitalized with influenza.

       (SNIP)

In this study, early non-aspirin NSAID use was independently associated with lower risks of renal complications and reduced 1- and 3-year mortality, whereas early aspirin use was not independently associated with clinical outcomes after multivariable adjustment. These findings emphasize the importance of distinguishing aspirin from non-aspirin NSAIDs in influenza research and raise the possibility that  earlier initiation of non-aspirin NSAIDs during influenza infection may be associated with improved clinical outcomes.

Prospective studies are warranted to determine whether these observed associations are causal and to define the optimal timing, dosage and role of non-aspirin NSAIDs as adjunctive therapy in adults hospitalized with influenza. 

        (Continue . . . ) 

While claims of potential benefits from non-aspirin NSAIDs in treating adult influenza patients may be premature, the pendulum (for now) appears to have swung away from concerns that it may be causing increased mortality.

Further research is needed, of course.

But this tortured route is a reminder why we don't cherry pick one scientific paper, and stubbornly cite it year after year. Science evolves, and our understanding of the world around us inevitably changes over time.