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Abstract

Since 2020, the emergence and global dissemination of high pathogenicity avian influenza (HPAI) H5Nx clade 2.3.4.4b infection has had devastating effects in wild and domestic bird populations, and resulted in spillover events in many terrestrial and marine mammalian species, including susceptible captive big cat collections, and feral and domestic feline species. The recent outbreaks in dairy herds in the USA following proposed exposure to infection from wild birds, with subsequent spread to in-contact mammals, demonstrates successful interspecies transmission of this virus and warrants close monitoring. In this literature review, we provide an overview of HPAI H5N1 infection in feline species to date, focusing on domestic but also captive wild cats, looking at the epidemiology, clinical and pathological presentations and management, and a current perspective on risk, testing and strategies to prevent infection.

Plain language summary

Understanding H5N1 bird flu in cats: what we know now and what we have learned from the past

Since 2020, H5N1 bird flu has spread widely around the world, severely affecting both wild and domestic birds. This virus has also been found in mammals, particularly marine mammals, captive wild cats, and pet and stray cats. Recently, the virus was detected in dairy cows in the USA, most likely after contact with wild birds carrying the virus. The fact that it can spread between different kinds of animals shows how adaptable this virus is and why it is necessary to monitor it. In this article, we review what is currently known about H5N1 infections in cats. We look at how cats are infected, the signs they show and what happens internally. We also discuss how the illness is diagnosed and managed, and what can be done to reduce the risk of infection. Our aim is to give a clearer picture of the threat this virus poses to both domestic and wild cats, and what steps can be taken to protect public health.

Keywords

H5N1 review avian influenza presentation pathology prevention risk

Introduction

Since the emergence of high pathogenicity avian influenza (HPAI) H5N1 in Asia in 1996, it has caused multiple epizootics resulting in significant wild and domestic avian losses as the virus has spread worldwide. HPAI viruses continue to pose an ongoing threat to wild birds and poultry globally and are of particular concern because of their frequent spillover into mammals, including humans.¹ Over the past two decades, sporadic reports and outbreaks of severe, fatal disease have been documented in wild, captive and domestic cats in parallel with infections in wild and domestic birds, with an increased incidence after the emergence of HPAI H5N1 clade 2.3.4.4b at the end of 2021 in Europe.² Although cats appear to be dead-end hosts,³ and cat-to-human transmission has not been reported, domestic cats are an integral part of households worldwide and surveillance remains prudent.

Avian influenza (AI) is caused by infection with avian influenza virus (AIV) of the Orthomyxoviridae family, genus Alphainfluenzavirus.⁴ The virus is an enveloped, negative-sense, single-stranded RNA virus and has a genome of eight segments. These encode for at least 11 different viral proteins, including the two major surface glycoproteins, haemagglutinin (HA) and neuraminidase (NA), on which AIVs are categorised into 16 antigenically distinct HA subtypes (H1–H16) and nine NA subtypes (N1–N9).⁵ Changes in the HA or NA can occur after coinfection with two different subtypes, with exchange of genetic material, termed genetic shift, leading to novel subtype emergence that may have a profound effect on replication dynamics, species susceptibility and antigenicity. Furthermore, antigenic variation and individual segment evolution can occur through the error-prone nature of the viral polymerase complex, termed genetic drift, where mutations accumulate over time. This has led to diversification of HA subtypes into lineages (groups of viruses sharing evolutionary history), clades and subclades (groups of viruses with similar HA gene sequences defined by genetic drift in HA), and genotypes (groups of viruses from the same clade that have different internal genes but the same HA).⁶ AIVs are also classified based on their pathogenicity in chickens into HPAI viruses and low pathogenicity avian influenza (LPAI) viruses.⁷

Many bird species are susceptible to AIV infection, although the outcome of infection can be hard to predict. Typically, infection of poultry with H5 or H7 subtypes can lead to severe (HPAI) or mild but occasionally invasive (LPAI) disease. However, infection of wild birds, even with viruses deemed HPAI for poultry, can have a range of outcomes from high morbidity and mortality to mild clinical disease with survival. Conversely, LPAI infections are generally subclinical in wild birds and poultry, although invasive infection of poultry can occur.⁸ However, evolution and adaptation of LPAI viruses can result in naturally occurring high pathogenicity H5 and H7 influenza A virus infection, leading to acute, often severe, clinical disease in poultry⁹ with the potential for spillover into susceptible mammalian hosts. Over 25 years ago, the HPAI H5 A/Goose/Guangdong/1/96 (GsGd) lineage first emerged in domestic birds in southern regions of Asia.¹⁰ Since that emergence, GsGd lineage HPAI H5Nx strains have spread globally via migratory wild birds. Genetic drift in the HA gene has led to the creation of multiple clades.¹¹ HPAI H5N1 clade 2.3.4.4 viruses were first detected in China between 2010 and 2011, and by 2014 had been detected in the USA.¹² The 2.3.4.4b subclade was detected in Eurasia, the Middle East and Africa in 2020, and had become the dominant clade in Asia, Africa and Europe by 2021.¹³ By the end of 2021, HPAI H5N1 clade 2.3.4.4b had reached North America and continued to expand its geographic range into Central and South America, with recent detection in several avian and mammalian species in the Antarctic and subantarctic regions.¹⁴ The host range of species affected by the clade 2.3.4.4b H5N1 viruses greatly exceeds previous H5N1 clades, and includes over 90 species of wild and domestic birds and more than 21 mammalian species, such as cats, cattle and humans.¹⁵ The HPAI A H5N1 clade 2.3.4.4b virus isolates from the epizootic in dairy herds in the USA have been designated as genotype B3.13 or D1.1;¹⁶ at the time of writing, this genotype or any other Eurasian–North American reassortants have not been detected in any species in Europe or the UK.¹⁷

History of HPAI H5N1 in cats

For the purposes of this review, all feline cases referenced in this paper as positive for HPAI H5N1 infection were confirmed through a combination of clinical history, RT-PCR, virus isolation, whole-genome sequencing and pathological investigation. The first reports of HPAI H5N1 infection in cats were after large outbreaks in poultry in Thailand in 2004, where domestic cats,¹⁸ along with captive tigers and leopards, were reported to have died after ingestion of infected poultry meat.^19,20 An experimental study performed in the Netherlands in 2004, investigated the outcome of infection, where cats were infected either intratracheally or through the ingestion of infected day-old chicks and by direct contact between naive and infected cats. Successful infection occurred in all routes, resulting in severe disease and euthanasia.^21,22 In 2006, natural infection was documented in a domestic cat in Thailand, after ingestion of a dead pigeon,²³ and confirmed in two domestic cats in a household in Iraq during an investigation into high mortality in a group of chickens.²⁴ In Germany in 2007, three unrelated domestic shorthair cats were all found dead within a mile of known wild bird detections,²⁵ and although coinfected with Aelurostrongylus species, all three tested positive for the virus using real-time RT-PCR. In the same year, 40 cats were sampled in a shelter in Austria after possible exposure to HPAI H5N1-positive poultry in mutual housing, three of which were virus positive but subclinical. Of these three, two seroconverted and an additional initially virus negative cat also seroconverted, but none showed clinical signs; this was the only documentation at that time of the existence of subclinical infection in cats.²⁶

Little was reported until the height of the 2021–2022 pandemic, when in France in 2022, a domestic cat living on a property bordering a duck-breeding farm developed severe HPAI H5N1 clade 2.3.4.4b infection and was euthanased.²⁷ In 2023, case reports of three cats in Nebraska²⁸ and one in Wyoming²⁹ in the USA were described, and serological evidence suggestive of HPAI H5N1 infection in a clinically healthy cat from a backyard poultry farm in northern Italy was reported.³⁰ This was followed by a larger outbreak of 33 cases in Poland in June and July 2023.^31,32 In Seoul, South Korea, also in June and July 2023, a further outbreak occurred in two cat shelters. Out of 40 cats, 38 died within 1 month in one shelter, of which five were confirmed positive for HPAI H5N1 infection. In the second shelter, infection was confirmed in four cats that had died,^33,34 and infected raw cat food of avian origin was confirmed in shelter 2 and presumed in shelter 1 to be the source.³⁵ After the detection of HPAI H5N1 in dairy cattle in multiple states in the USA in March 2024, fatal systemic infection was reported in a cluster of domestic cats fed unpasteurised milk from infected cattle on a north Texas dairy farm.³⁶ Since then, infections in free-roaming and domestic cats have been detected in multiple states, including two farm cats in New Mexico resident on a dairy farm with infected cattle and two indoor cats in Minnesota in contact only with workers from an affected dairy farm.³⁷ At the time of writing, the first report of feline HPAI H5N1 in Belgium was announced on 4 March 2025. Two cats living on infected premises developed severe signs and were euthanased; they are thought to have been infected by ingesting contaminated eggs or drinking infected water, but the route of transmission is yet to be confirmed.³⁸

In addition to infections in domestic cats, HPAI H5N1 infections in wild and captive cats have been reported sporadically since 2004, with the most recent being in Vietnam in October 2024³⁹ and in big cat species in zoos across the USA.⁴⁰ Ongoing detection in free-roaming wild cats around the world⁴¹ highlights the impact on wildlife and raises concerns in the species of conservational importance. Currently, no cases of HPAI H5N1 infection have been reported in captive or domestic cats in the UK.

Epidemiology

In all reports of HPAI H5N1 in domestic cats to date, there has been no specific breed, age or sex predilection identified. Until recently, the source of the infection was generally considered to be infected wild birds and domestic poultry, with transmission occurring through contact with infected birds (inhalation or ingestion) or ingestion of raw poultry meat.⁴² However, raw (unpasteurised) milk and colostrum from infected cattle³⁶ is now a recognised source of the virus for cats in the USA. The virus is shed in mucous, saliva and faeces from the respiratory tract and digestive tracts of infected animals, and in cats, shedding is most reliably detected from the oropharyngeal and upper respiratory tracts but is variable in faeces.^22,43,44 Based on previous experimental evidence, virus shedding begins 1–3 days after infection and persists for up to 7 days.

Transmission

In most cases, transmission has been through direct contact with or ingestion of infected birds. In the recent outbreak in Poland, many affected cats were outdoor cats with potential access to infected material. However, some were entirely indoor, and in one case, infection through feeding of raw poultry meat was documented.⁴⁵ To date, raw poultry meat has been further implicated as a source of infection after reports of infections occurring after consumption of a raw pet food diet in the USA.⁴⁶ Although exposure to infected wild birds cannot be entirely ruled out in the cats involved, likely cattle-to-cat transmission through known ingestion of raw unpasteurised milk or colostrum from infected cows after recent outbreaks in dairy herds in the USA was reported for the first time in 2024.³⁶

Cat-to-cat transmission through direct contact with clinically infected cats has been demonstrated experimentally²¹ and proposed previously²⁰ in earlier reports; however, it has not been specifically studied or definitively confirmed since. In these cases, cats were exposed to high infectious doses, which suggests that transmission may depend on the level of virus shedding,⁴⁷ as well as route of exposure and host response. Generally, as a result of social organisation, direct cat-to-cat contact is often limited in free-living cat populations; therefore, the virus is unlikely to spread efficiently by this route.⁴² However, in multi-cat households or in colonies (unowned and owned), zoo collections and shelters, where cats have more contact with each other, precautions should be considered.

Indirect transmission through fomites is suspected in two cases where indoor cats in Minnesota were in contact with farm workers on an affected dairy farm with no other obvious sources of infection.³⁷ Contact with fomites was also proposed in a recent epidemiological investigation of two affected multi-cat households in Michigan, undertaken in February 2025. This was not definitively confirmed because of difficulty obtaining information and appropriate timely samples, and possible cat-to-cat transmission could not be ruled out.⁴⁸

So far, no cat-to-human transmission or cat-to-other species transmission of HPAI H5N1 has been confirmed or reported, possibly because of limited shedding. Currently, without any evidence to the contrary, cats are therefore considered dead-end hosts, and the risk to humans is considered low. However, with the presumed cat-to-human transmission of low pathogenic avian influenza A(H7N2) virus in a New York animal shelter in 2016,⁴⁹ the well-demonstrated ability of the virus to mutate and adapt to enhance its ability to transmit, and where close contact with household pets occurs, the risk cannot be dismissed.

Pathogenesis of HPAI H5N1 infection in domestic cats has been described experimentally as having a short incubation period of 1–2 days.²¹ Depending on the route of transmission, replication most likely begins with attachment of the virus to specific receptors on host cells in the lower respiratory tract and/or gastrointestinal tract,²² with subsequent viraemia and dissemination to the liver, brain, kidney, adrenal cortex and other organs. This leads to widespread systemic necrosis and inflammation, bronchointerstitial pneumonia and neurological disease.⁵⁰

Clinical presentation

Since it was first reported in cats in 2004, HPAI H5N1 infection manifests as respiratory and/or neurological signs, or sudden death. Occasionally, gastrointestinal signs are observed.⁵¹ In contrast to LPAI infections, where upper respiratory clinical signs are more common,⁴² cats infected with HPAI H5N1 may present with anorexia, lethargy, pyrexia and dyspnoea, with increased effort 1–3 days after infection.^{19,20,22,27,28,32,34} The H5N1 virus has been shown to attach to type II pneumocytes, alveolar macrophages and non-ciliated cuboidal epithelial cells in terminal bronchioles in humans, ferrets and cats, making the lower respiratory tract its primary target.⁵² Upper respiratory signs have also been recognised, such as conjunctivitis, oculonasal discharge and third eyelid protrusion,^20,22,28,32 but this could be related to reactivation or active infection with other potential respiratory pathogens, such as feline herpesvirus, feline calicivirus or feline coronavirus.⁵³ Neurological signs may occur after respiratory signs or, more commonly, can be the only presentation. Signs may vary as the virus can affect any part of the brain, but those reported include somnolence, ataxia, anisocoria, nystagmus, tremors, hyperaesthesia and eventually seizures and death. Blindness has also recently been reported.^{21,23,27
–29,31,32,36,37,42,53} The time course is generally rapid, with affected cats surviving up to 7 days. However, in one report, one cat survived for up to 10 days, presenting only with neurological signs,²⁸ while in other reports, cats have been found obtunded or dead.^36,⁵⁴

These descriptions highlight the variable clinical presentation after infection and underlines the current limited understanding of the spectrum of disease. At one end, it is apparent that HPAI H5N1 infected cats often develop severe neurological signs and that sudden death can be the only presentation. However, at the other end, acute upper respiratory tract infection is a common condition in clinical practice and is infrequently investigated. Thorough investigation of clinical cases is further hampered by the less frequent presentation of cats to veterinary practice in general, while those high-risk cats, such as farm cats, are even less likely to be presented.⁵¹ Suspicion of infection should therefore be based not only on the clinical presentation but also in the light of the clinical history and the presence of risk factors, such as access to outdoors in an area where infection in birds or dairy cattle has been detected, or suspected ingestion of unpasteurised milk or raw poultry meat (via diet or hunting).^33,36 Although infection appears to be progressively severe and most often fatal, confirmed infection with clinical signs followed by full recovery has also been documented.^37,43 Although definitive evidence is lacking, theoretically, onset and progression of neurological signs is likely to be associated with a poor outcome.

Clinical investigations in live animals have only recently been described in detail. In one case, clinical pathology findings included a mild neutrophilia, hyperglycaemia, and increased liver enzymes and bilirubin.³² In other cases, hyperproteinaemia, hyperglobulinaemia, hyperglycaemia, hyperbilirubinaemia and hyperlipasaemia have been documented.²⁸ Imaging was performed in one case, where bilateral parenchymal densities were identified in the anterior and middle lung lobes on thoracic radiographs, alongside subpleural densities visible on thoracic ultrasound.³²

Diagnosis is generally through RT-quantitative PCR assay (RT-qPCR) on oropharyngeal swabs or blood collected in the first 4 days of infection. Results are then confirmed through virus isolation and/or further supported by pathological investigation, including immunohistochemistry using an anti-influenza A antibody targeting viral proteins on post-mortem tissues (lung and brain). Point-of-care influenza antigen tests are not validated in cats. In high-risk situations where they are used as a screening test, their sensitivity and specificity is generally lower than RT-PCR; reliability can be affected by specimen type, quality of the specimen and timing of collection.⁷ They should therefore be interpreted with caution in the context of the whole clinical picture.^42,55 In addition to RT-PCR, in epidemiological research or in surveillance settings, trends in serology may be used in survivors or subclinically infected cats to document exposure, through detection of antibodies using the haemagglutination inhibition test or neutralisation assays. A four-fold or greater increase in influenza virus strain-specific antibodies within 14–21 days indicates recent influenza A virus infection.⁴²

Pathology

Where pathology investigations were carried out (n = 11), gross pathology findings from previous reports included mild to marked pulmonary congestion and oedema, and multifocal red to purple discolourations of the lung lobes, sometimes accompanied by pleural effusion.^{19,20,21,23,25,28,32,43} Gross examination of the brain, when performed, was unremarkable or revealed discolouration of the meninges or surface of the cerebral cortex or, rarely, malacia.28,36 Other abnormalities included multifocal haemorrhages in multiple organs.

On histological examination, in all 11 reports of natural and experimental infection, the lungs were affected in all cases, with multifocal moderate to severe inflammation and necrosis of the bronchioles and alveoli, and pulmonary congestion and oedema.^{15,19,20,22,23,25,28,32,36,37,43,56} Interstitial pneumonia was more commonly observed but not exclusively identified in later cases,^28,37 with occasional evidence of vascular compromise (vasculitis, thrombosis and fibrin exudation).²⁸ The brain was also commonly affected (9/11 reports), where acute to subacute multifocal moderate to severe meningoencephalitis – characterised by gliosis, neuronal necrosis, lymphocytic perivascular infiltrates and occasionally spongiosis – was seen.^{15,19,20,22,23,28,32,37,44} An example of the neuropathological changes in the brain of a cat naturally infected by HPAI H5N1 is depicted in Figure 1.

Figure 1

(a,c,e) Histopathological and (b,d,f) immunohistochemical features of high pathogenicity avian influenza H5N1 virus infection in the cerebrum of a naturally infected cat. This was a young adult, intact male domestic shorthair cat that lived near a dairy herd. Over the course of approximately 3 days, it was observed that the cat developed conjunctivitis and nasal discharge, followed by severe neurological signs and death. Other cats on the premises were also reported to display similar signs. The sections displayed represent mid-thalamic level. (c–f) Homologous areas stained with haematoxylin and eosin and immunolabelled for influenza A virus M (IA-M) protein (visualised in red). (a) Although the neurodegenerative and inflammatory changes are not readily evident at low magnification, there is multifocal distribution of (b) IA-M antigen, involving multiple cortical grey matter and subcortical white matter, thalamic and hypothalamic regions, and the third ventricle lining elements. (c) Neuronal degeneration, necrosis and loss, satellitosis and mild gliosis at mid-layer of the fissure splenialis can be seen. (d) Abundant local IA-M-antigen is primarily seen in neurons and, to a lesser degree, in astrocytes. (e) Focal gliosis, mainly astrocytosis/astrogliosis, with neuronal degeneration in the deep cortical neuronal layer at the coronalis posterior. (f) IA-M-antigen is largely seen in neurons and, to a lesser degree, in astrocytes

Multifocal moderate to marked hepatic necrosis was also frequently observed in 9/11 reports,^{15,20,22,23,25,28,32,37,43} while inflammation, haemorrhage and necrosis were seen sporadically in the heart in 5/11 reports^{15,22,25,28,37} and in the adrenal glands in 4/11 reports;^15,22,28,37 however, it was rarely identified in the pancreas.^15,28 In addition, inflammation was detected in the neuronal plexuses of the gastrointestinal tract in both experimental²² and natural^15,32 infection. Furthermore, severe segmental to diffuse chorioretinitis and moderate multifocal sialadenitis were described for the first time.³⁷ Histopathological findings are summarised in Tables 1 and 2.

Table 1

Histopathological lesion distribution in cats naturally infected by high pathogenicity avian influenza H5N1 virus

Paper/report	Route of infection	Brain	Lung	Liver	GIT	Heart	Other tissues/comments
Keawcharoen et al¹⁹	Ingestion (n = 4)	+	+	–	–	–	Zoo animals (two tigers, two leopards)
Thanawongnuwech et al²⁰	Ingestion (n = 3)	+	+	+	–	–	Tigers
Songserm et al²³	Ingestion (n = 1)	+	+	+	–	–	Kidney, spleen (lymphoid depletion), vasculitis (brain)
Klopfleisch et al²⁵	Unknown, ingestion suspected (n = 3)	–	+	+	–	+	Aelurostronglyus species seen in lungs
Sillman et al²⁸	Unknown, cat 1	+	+	+	–	–	Adrenal gland, pancreas, kidney, lymphoid depletion; vasculitis and degenerative vascular changes in many tissues associated with necrosis
	Cat 2	+	+	–	–	+	Pulmonary thrombosis
	Cat 3	+	+	–	–	–	Vasculitis (brain), pulmonary thrombosis
Szalus-Jordanow et al³²	Unknown (n = 1)	+	+	+	+	–	Necrosis in myenteric complex
Mainenti et al^{37 }	Ingestion: Texas (n = 2)	+ (2/2)	+ (2/2)	–	–	+ (2/2)	Vasculitis (brain); eye (1/2)
Mainenti et al^{37 }	New Mexico (n = 2)	+ (2/2)	+ (2/2)	+ (1/2)	–	+ (1/2)	Eye (1/2), adrenal gland (1/2), epithelium of glands incl. submandibular gland (2/2), tonsils (1/2), nasal cavity (1/2)
Chothe et al¹⁵	Unknown: South Dakota (n = 2)	+ (2/2)	+ (2/2)	+ (1/2)	+ (2/2)	+ (1/2)	Pancreas (1/2), thyroid gland (1/2), spleen (lymphoid depletion) (1/2)

Eight reports of natural infection are included. Where information is available for each tissue sampled, the number of cats affected out of the number of cats submitted for necropsy are in brackets

Where reported findings have been previously described and included in a later publication, they have been grouped

= inflammation and necrosis; − = no lesions; GIT = gastrointestinal tract

Table 2

Histopathological lesion distribution in cats experimentally infected by high pathogenicity avian influenza H5N1 virus

Paper/report	Route of infection	Brain	Lung	Liver	GIT	Heart	Other tissues/comments
Rimmelzwaan et al²²	Intratracheal (n = 3)	+ (3/3)	+ (3/3)	+ (1/3)	–	+ (2/3)	Kidney (1/3), adrenal glands (3/3), vasculitis
	Ingestion(n = 3)	+ (3/3)	+ (3/3)	+ (3/3)	+ (2/3)	+ (2/3)	Adrenal glands (2/3), vasculitis
	In contact (n = 2)	n/d	+ (2/2)	+ (2/2)	–	–	Adrenal glands (1/2)
Vahlenkamp et al⁴³	Ocular and nasopharyngeal; high dose only(n = 3)	–	+ (2/3)	+ (2/3)	–	–	Third cat recovered; no lesions in medium/low dose
Kim et al⁴⁴	Intranasal(n = 10)	+	+	–	–	–	Description grouped for all 10 cats

Three reports are detailed. Where available for each tissue, the number of cats affected out of the number of cats submitted for necropsy are in brackets

= inflammation and necrosis; − = no lesions; GIT = gastrointestinal tract

Immunohistochemistry (see Table 3) was performed in eight investigations, with viral antigen detected mainly in bronchiolar epithelial cells, type I and type II pneumocytes, and alveolar macrophages. In the brain (representative case in Figure 1), immunolabelling was seen mostly within neurons and glial cells, while in the liver, antigen was observed within hepatocytes. Positive cardiomyocytes and endocardial epithelium were seen in the heart, and antigen was detected in the glandular epithelium in the adrenal gland, pancreas, submandibular gland and minor salivary glands of the tongue. Immunolabelling was occasionally seen in macrophages and reticular cells of the periarteriolar sheath in the spleen and rarely observed in the medullary tubular epithelium and glomerular endothelium in the kidney. Notably, viral antigen was detected in all layers of the retina in the eye and neurons of the myenteric plexus in the intestine, but also within vasculature, particularly in the brain and lung, as observed in other carnivore species.⁵⁷

Table 3

Summary of immunohistochemistry (IHC) findings in eight reports of feline high pathogenicity avian influenza H5N1 infection, where anti-influenza A antibody against viral proteins is used to detect viral antigen

Tissue	IHC positive cell types	Report
Lung	Bronchial and bronchiolar epithelial cells, type I and type II pneumocytes, alveolar macrophages, endothelial cells, vascular smooth muscle (rare)	Keawcharoen et al¹⁹ Thanawongnuwech et al²⁰ Rimmelzwaan et al²² Songserm et al²³ Klopfleisch et al²⁵ Vahlenkamp et al⁴³ Mainenti et al³⁷
Brain	Neurons, glial cells, leptomeningeal cells, choroid epithelium, ependymal cells	Thanawongnuwech et al²⁰ Rimmelzwaan et al²² Songserm et al²³ Mainenti et al³⁷ Sillman et al²⁸
Liver	Hepatocytes	Thanawongnuwech et al²⁰ Rimmelzwaan et al²² Klopfleisch et al²⁵ Vahlenkamp et al⁴³
Adrenal gland	Adrenocortical epithelium and pheochromocytes	Rimmelzwaan et al²² Klopfleisch et al²⁵ Sillman et al²⁸
Heart	Cardiomyocytes, endocardial epithelium	Rimmelzwaan et al²² Songserm et al²³ Mainenti et al³⁷ Sillman et al²⁸
Kidney	Visceral epithelial/mesangial cells, medullary tubular epithelium	Rimmelzwaan et al²² Songserm et al²³ Sillman et al²⁸
Eye	All cell layers of the retina	Mainenti et al³⁷
Gastrointestinal tract	Neurons of myenteric plexus	Rimmelzwaan et al²² Sillman et al²⁸
Lymphoid system	Macrophages (spleen, lymph nodes), reticular cells periarteriolar sheath (spleen)	Klopfleisch et al²⁵ Mainenti et al³⁷
Glandular epithelium	Submandibular salivary and minor salivary gland epitheliumPancreatic exocrine and ductal epithelium	Mainenti et al³⁷ Sillman et al²⁸

In summary, these findings reflect the severe and systemic nature of HPAI H5N1 infection in cats, where the virus is promiscuous and has a broad cellular tropism, affecting the epithelium, parenchyma, mesenchymal cells, neural cells and vasculature, leading to widespread necrosis, inflammation and haemorrhage. Although the lung and brain are most affected, a more pronounced neurotropism of the HPAI H5N1 clade 2.3.4.4b virus in two naturally infected cats in South Dakota has recently been described, as reported in other mammalian species,^58
–60 in comparison with infection with previous clades.^15,61 Where investigated previously, viral loads have been found to be high in the lungs and, particularly in recent cases, the brain, indicating high levels of replication in these tissues.^15,37,44 This may explain the predominance of neurological signs observed in many cases, although respiratory presentations are still seen with this clade.³⁷

Case suspicion

HPAI H5N1 infection should be considered as a differential diagnosis when a cat presenting to the veterinarian shows signs of respiratory and neurological disease, or sudden death, where other common differential diagnoses have been ruled out. As upper respiratory tract infection is such a common presentation, taking a thorough history to identify risk of exposure (eg, high numbers of wild bird mortalities nearby, proximity to confirmed infected poultry farm or dairy herd premises, consumption of raw meat or unpasteurised milk, or contact with caregivers working on affected farms and associated fomites) and vaccination history is critical to justify suspicion.⁵¹ Where history is not available, such as in shelter or rescue programmes, assessing whether shelter location and place of cat trapping/collection is near an area in which HPAI H5N1 has been documented in birds or other species may identify increased risk. Other more common infections, such as feline herpesvirus and calicivirus, feline coronavirus (feline infectious peritonitis [FIP]), bacterial infections such as Chlamydophila felis, Mycoplasma species, Bordetella bronchiseptica and others, should be excluded using anamnesis, vaccination history, appropriate testing and imaging, in cases presenting with upper or lower respiratory signs.⁵³ For neurological presentations, infectious diseases such as rabies, neurological FIP, toxoplasmosis and cryptococcosis could be considered.

Although the risk of cat-to-human transmission is low, if suspected, immediate steps should be taken to prevent the possibility of zoonotic, cat-to-cat or cross-species infection through the use of appropriate personal protective equipment (PPE; face mask, face shield/safety goggles [to prevent ocular infection], disposable gloves and gown). Careful feline-friendly handling techniques, possibly using sedation if required to reduce stress, are needed and unnecessary contact should be minimised, with strict isolation and barrier nursing of sick individuals. Care should also be taken when collecting samples, such as pharyngeal swabs, or intubating because of the generation of aerosols. Thorough cleaning to remove all organic matter followed by disinfection using a broad-spectrum virucidal agent is essential. Further advice can be sought on what appropriate validated products are recommended in each country.^53,62

Suspicion of HPAI H5N1 infection in mammals should be reported immediately to the relevant animal health and public health authorities, so that advice on safe and appropriate sampling and testing can be given.^55,62 As sample collection requirements can change, diagnostic laboratories should be contacted to ensure the correct samples are taken and to identify what tests are offered. In general, submission of oropharyngeal, nasal and rectal swabs, as well as urine in a plain sterile container, whole blood (EDTA) or serum may be advised for ante-mortem detection, and submission of tissues or the whole carcase for post-mortem investigation may be recommended.⁶³ In some countries, the handling of potentially infected post-mortem tissues is prohibited, so proactive advice must be sought. If sampling and laboratory testing or post mortem has already taken place and influenza A virus is either suspected or detected, the relevant authorities must be contacted. They will guide further actions, where steps must be taken to safeguard public health and the environment. Epidemiological investigation and whole-genome sequencing with phylogenetic analysis may be performed after diagnosis to detect the source and potential spread of the virus, to help identify and protect at-risk species, and to look for mutations consistent with adaptation allowing replication in a non-avian host, which may increase zoonotic risk.

Treatment

The only treatment available is supportive. Where respiratory effort is recognised, stress should be minimised in a quiet environment with provision of pain relief and oxygen supplementation as needed. Antipyretic agents can be used if fever is documented, alongside management of appetite and hydration. Oseltamivir, an antiviral drug that reduces replication of influenza A virus by inhibiting viral neuraminidase, has been used for the treatment of human HPAI H5N1 infection. However, when given to healthy tigers at risk from infection, no benefit was reported, although this may have been due to insufficient dosage, unknown pharmacokinetics or host factors.²⁰ Although responsible use of oseltamivir could be considered in early cases, the possible development of antiviral resistance remains a concern,⁵¹ and specialist advice should ideally be sought before use.

Control and prevention

Risk factors include proximity to infected wild or domestic birds, access to the outdoors, hunting behaviours, ingestion of raw poultry meat or raw (unpasteurised) milk and colostrum (in areas where HPAI infection in dairy cattle is confirmed), and contact with people who work on affected premises without following biosecurity precautions to prevent fomite spread.⁶² Ideally, in areas where outbreaks of HPAI H5N1 infection in birds or dairy cattle have occurred, cats should be prevented from eating, chewing or playing with dead or sick birds, and feeding of raw meat, particularly from shot birds, and raw milk products should be avoided.^36,42 In the light of reports of pet food-associated infection in the USA and the potential for infection after ingestion of raw poultry and dairy products, owners should be educated to seek advice before feeding raw-based diets. The regulation of raw pet food production from supply of animal byproducts through to processing, transport and storage varies between countries and can range from specific regulation to general directives;⁶⁴ therefore, in all cases, food safety standards should be critically assessed. Owners should also be directly advised against feeding raw milk or any shot birds. If a raw food diet is to be fed, ingredients must be fit for human consumption and sourced from reputable suppliers that have undergone inspection. However, without additional processing, such as high-pressure pasteurisation or cooking, and controlled storage and handling, contamination with virus and other pathogens is still possible.⁵¹

Where owners, especially farm workers, have potentially been in contact with infected material, thorough hand washing and changing of clothes and shoes is advisable.⁶² If an owner suspects their cat may be infected, they should contact their veterinarian. Any contact should be minimised and the cat should be kept in a separate room, away from any immunocompromised or young individuals. Litter, bedding and bowls should be cleaned and disinfected as previously described.⁵³

After an increase in domestic feline cases in the USA, guidelines have been made available to assist shelter and rescue centres in formulating a standard operating procedure. They encourage awareness of the signs of infection, isolation of suspicious cases in a separate room, particularly those with acute neurological signs, and the use of PPE when handling such cats. Thorough history taking is essential, and testing for the virus is recommended if there is an unexplained death, neurological signs, severe respiratory disease, an increased incidence of respiratory disease or signs that resemble rabies infection. Associated staff, owners, fosterers and volunteers should receive appropriate training.⁶⁵

Unfortunately, no licensed vaccine is currently available.

Conclusions

Before 2020, HPAI H5N1 infections in cats were sporadic and thought to be associated mostly with the feeding or scavenging of infected raw poultry. The rise and global dissemination of H5N1 clade 2.3.4.4b, and its unprecedented devastation of both wild and domestic birds and spillover into mammalian species, particularly ruminants in the past 4 years, has resulted in infections in susceptible captive, wild and domestic cats. As domestic cats are in frequent contact with humans, concerns have also been raised, not only for the impact on cat populations, but also the possibility of cat-to-human transmission. There is also potential for cats to act as mixing vessels for the virus, which could enable further evolution and enhance the possibility of transmission and virulence in humans and other species. Currently, the increase in cases has mainly been concentrated in the USA after spillover into dairy cattle, and continuing analysis suggests that at this time, the risk of cat-to-human transmission remains low. At the time of writing, outside of the USA, the genotypes detected in most recent infections in dairy cattle (B3.13 and D1.1) have not been detected in Europe, Asia or the UK; therefore, the risk of feline or human infection associated with the currently circulating HPAI H5N1 clade 2.3.4.4b remains low. However, surveillance and close monitoring are paramount given the behaviour of the virus and its pandemic potential. Awareness of prevalence, risk factors, associated clinical presentation, pathology and rapid diagnosis remains critical.

Footnotes

Acknowledgements

The first author would like to thank Professor Tadeusz Frymus, Professor Séverine Tasker and fellow co-authors for their collaboration and assistance in writing this review.

Accepted: 30 July 2025

Conflict of interest

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Ethical approval

This work did not involve the use of animals and therefore ethical approval was not specifically required for publication in JFMS.

Informed consent

This work did not involve the use of animals (including cadavers) and therefore informed consent was not required. No animals or people are identifiable within this publication, and therefore additional informed consent for publication was not required.

ORCID iD

Audra-Lynne D Schlachter

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Feline high pathogenicity avian influenza H5N1 infection: past and present

Abstract

Plain language summary

Keywords

Introduction

History of HPAI H5N1 in cats

Epidemiology

Transmission

Clinical presentation

Pathology

Case suspicion

Treatment

Control and prevention

Conclusions

Footnotes

Acknowledgements

Conflict of interest

Funding

Ethical approval

Informed consent

ORCID iD

References