Avian Influenza: New Zealand and Kerala Outbreaks, and Jessamine County Updates

Introduction

Avian influenza viruses (AIVs) are enveloped, negative-sense single-stranded RNA orthomyxoviruses classified by the antigenicity of their hemagglutinin (HA) and neuraminidase (NA) surface glycoproteins [1, 2]. Subtypes are designated by 16 HA (H1–H16) and 9 NA (N1–N9) combinations in wild aquatic birds, the primary natural reservoir [3, 4]. Viruses are further categorized as low pathogenicity (LPAI) or high pathogenicity (HPAI) based on intravenous pathogenicity indices in chickens and the presence of multiple basic amino acids at the HA0 cleavage site [5]. HPAI strains typically arise from LPAI precursors of the H5 or H7 subtypes after circulation in galliform poultry [6, 7]. The genomic plasticity of AIVs, attributable to a segmented genome and high error rates of the RNA-dependent RNA polymerase, facilitates reassortment and rapid antigenic drift [1, 2]. Recent global epizootics have been dominated by clade 2.3.4.4b H5N1 viruses, which exhibit a broad host range and sustained transmission in both wild and domestic birds [3, 4].

This article reviews three distinct geographic scenarios of AIV activity: the detection of novel reassortant HPAI H7N6 and LPAI H1N9 viruses in New Zealand, recurring HPAI H5N1 outbreaks in the state of Kerala, India, and surveillance updates from Jessamine County, Kentucky, USA. Each case highlights different epidemiological, phylogenetic, and diagnostic challenges relevant to veterinary virology and molecular surveillance.

New Zealand Outbreaks

New Zealand historically maintained freedom from HPAI in domestic poultry, with only sporadic detections of LPAI viruses in wild birds [5, 6]. This epidemiological isolation was attributed to geographic distance from major migratory flyways and stringent biosecurity measures [7]. However, recent molecular surveillance efforts have identified both LPAI and HPAI incursions in poultry and wild avian populations.

Detection of HPAI H7N6 in Commercial Poultry

In 2024, a novel reassortant HPAI H7N6 virus was isolated from a commercial poultry operation in New Zealand [2, 4]. Whole-genome sequencing revealed that the HA gene originated from a Eurasian lineage H7 LPAI virus, while the NA and internal genes derived from North American and Eurasian lineages, indicating multiple reassortment events [2, 4]. The HA0 cleavage site sequence possessed multiple basic amino acid residues (PEKPKRRKR*GLF), confirming high pathogenicity [2]. Phylogenetic analyses clustered the New Zealand H7N6 with contemporary Australian H7 strains, suggesting regional viral evolution rather than direct introduction from distant geographic sources [1, 2]. Experimental infection in specific-pathogen-free chickens produced 100% mortality within 48 hours, with systemic viral distribution and interstitial pneumonia [4].

LPAI H1N9 in Migratory Shorebirds

Concurrent surveillance of wild birds across New Zealand and its subantarctic islands (e.g., Campbell Island, Antipodes Island) detected an LPAI H1N9 virus in migratory shorebirds [5]. The hemagglutinin belonged to the Eurasian lineage, while the neuraminidase showed close affinity to North American strains [5]. Critically, no evidence of clade 2.3.4.4b HPAI H5N1 was found in any sampled species, supporting the hypothesis that New Zealand’s geographic isolation and the absence of key reservoir hosts (e.g., Anseriformes) may limit incursion risk [5, 6]. However, the H1N9 detection confirms that viral gene flow does occur via long-distance migratory Charadriiformes, underscoring the need for ongoing wild bird sampling [5, 6].

Phylogenetic and Molecular Characterization

Phylogenetic analyses using maximum likelihood and Bayesian Markov chain Monte Carlo methods on complete genome sequences demonstrated that the H7N6 HA and NA genes form a monophyletic clade with Australian H7 LPAI viruses, indicative of local viral evolution following a historical introduction [1, 2]. Reassortment with North American gene segments likely occurred in a shared host population, possibly at migratory stopover sites [1, 2]. Molecular clock estimates placed the divergence time of the New Zealand H7 lineage at approximately 5–7 years prior to detection, suggesting undetected circulation in wild or feral birds before spillover into poultry [1].

Table 1. Comparison of key virologic features of AIVs recently detected in New Zealand.

The risk of HPAI establishment in New Zealand was assessed using a scenario tree model that accounted for wild bird migration, poultry density, and biosecurity compliance [7]. The model estimated a low but non-zero probability of a sustained outbreak, emphasizing the importance of early detection through enhanced passive and active surveillance [7].

Kerala Outbreaks

The state of Kerala in southwestern India has experienced recurrent outbreaks of HPAI H5N1 in poultry since 2014, with the most recent episodes occurring in commercial duck and chicken flocks [8, 9]. The outbreaks are characterized by sudden onset of high mortality (up to 90% in affected flocks), respiratory distress, cyanosis of combs and wattles, and edema of the head and neck [8, 9]. Necropsy findings include hemorrhagic tracheitis, pancreatic necrosis, and splenic infarction [9]. Molecular characterization of isolates from Kerala revealed clade 2.3.2.1a H5N1 viruses, distinct from the 2.3.4.4b clade circulating in other regions [8]. The HA cleavage site motif (PQRERRRKR*GLF) confirmed high pathogenicity [8]. Control measures have included stamping out, movement restrictions, and targeted vaccination in high-risk zones [9]. The frequency and geographic spread of these outbreaks in Kerala highlight the challenges of controlling HPAI in areas with high poultry density, free-range duck farming, and proximity to wild bird habitats [8].

Jessamine County Updates

Jessamine County, located in central Kentucky, USA, has been part of the ongoing national surveillance for HPAI H5N1 clade 2.3.4.4b since the virus was first detected in North American wild birds in late 2021 [10]. In 2024, a commercial turkey flock in Jessamine County was confirmed positive for HPAI H5N1 following an increase in mortality [10]. The index case was identified through routine passive surveillance, with samples submitted to the National Veterinary Services Laboratories. Depopulation and disposal of approximately 30,000 birds were completed within 72 hours of confirmation [10]. A 10-km control zone was established with intensified surveillance of surrounding poultry operations and wild bird populations [10]. Phylogenetic analysis of the Jessamine County isolate showed >99.9% nucleotide identity to the dominant 2.3.4.4b genotype circulating in North American migratory waterfowl, suggesting direct introduction by wild birds [10, 11]. No secondary spread from the index farm has been reported as of the time of writing, indicating effective containment [10].

Diagnostic Approaches

Detection and characterization of AIVs rely on a combination of molecular and serological methods. Real-time reverse transcription polymerase chain reaction (RT-qPCR) targeting the matrix gene is the standard screening assay for all influenza A viruses [3]. For H5 and H7 subtype-specific identification, HA gene-targeted RT-qPCR panels are employed, followed by sequencing of the HA0 cleavage site to differentiate LPAI from HPAI [3, 4]. Full-genome sequencing using high-throughput platforms enables detailed phylogenetic and reassortment analyses [1, 2]. Serological surveillance uses hemagglutination inhibition (HI) and neuraminidase inhibition assays to detect subtype-specific antibodies, often in the context of freedom-from-disease certification [6]. Enzyme-linked immunosorbent assays (ELISAs) for nucleoprotein antibodies provide a broader screening tool [6].

A typical diagnostic workflow for AIV outbreak investigation is depicted in the Mermaid diagram below.

graph TD
    A[Clinical suspicion / increased mortality] --> B[Oropharyngeal/cloacal swab collection]
    B --> C[RNA extraction & RT-qPCR for influenza A matrix gene]
    C --> D{Positive?}
    D -- No --> E["Report negative; rule out AIV"]
    D -- Yes --> F["Subtype-specific RT-qPCR (H5, H7, H9")]
    F --> G{HA subtype identified?}
    G -- Yes --> H[Sanger/next-generation sequencing of HA0 cleavage site]
    H --> I{Multiple basic amino acids?}
    I -- Yes --> J[Confirmed HPAI]
    I -- No --> K[Confirmed LPAI]
    G -- No --> L[Full-genome sequencing for subtype determination]
    J --> M[Phylogenetic analysis & reassortment assessment]
    K --> M
    M --> N[Report to national reference laboratory & WOAH]
    L --> M

Figure 1. Decision tree for molecular diagnostic workflow during AIV outbreak investigation. Adapted from standard protocols used by WOAH reference laboratories and described in [3, 4].

Risk Assessment and Biosecurity

The emergence of novel reassortant HPAI viruses in New Zealand, the endemicity of HPAI H5N1 in Kerala, and the periodic incursions in Jessamine County underscore the critical role of wild birds as vectors for global AIV dissemination [5, 6, 7]. Migratory waterfowl of the orders Anseriformes and Charadriiformes carry LPAI viruses asymptomatically; upon introduction to poultry, these may evolve into HPAI strains [5]. The lack of H5N1 in New Zealand subantarctic islands despite widespread circulation in the Northern Hemisphere suggests that the Southern Hemisphere is not a major recipient of clade 2.3.4.4b via traditional migratory pathways [5]. However, the presence of H1N9 in shorebirds indicates that viral gene flow does occur, and climatic or ecological changes could alter risk profiles [5, 6].

Biosecurity measures that reduce contact between wild birds and domestic poultry remain the cornerstone of prevention [7]. These include covered feed and water sources, netting of open-sided poultry houses, and limitation of free-range access during peak wild bird migration [7]. In Kerala, the practice of free-range duck rearing in paddy fields creates high-risk interfaces with wild waterfowl [8]. Vaccination against HPAI using inactivated whole-virus vaccines or recombinant vector vaccines (e.g., H5-expressing fowlpox virus) has been employed in some endemic regions, but it may complicate serological surveillance and does not prevent infection [9].

Phylogenetic and genomic surveillance, as demonstrated by the New Zealand studies [1, 2], is essential for tracking the evolution and spread of AIVs. Sharing of sequence data through public repositories such as the National Center for Biotechnology Information and the European Bioinformatics Institute facilitates global risk assessment [10]. Computational tools like flux balance analysis and Bayesian network modeling have been adapted to study host-virus metabolic interactions and to predict transmission dynamics, respectively [11, 12].

For further reading on differential diagnosis from bacterial respiratory infections, see the existing articles on Infectious Coryza in Poultry and Ducks and Fowl Cholera in Poultry. The diagnostic ELISA principles for antigen detection are analogous to those described in Enzyme-Linked Immunosorbent Assay (ELISA) for Feline Leukemia Virus.

Conclusion

The recent avian influenza events in New Zealand, Kerala, and Jessamine County collectively illustrate the dynamic and global nature of AIV epidemiology. New Zealand’s detection of a novel reassortant HPAI H7N6 and the ongoing circulation of LPAI H1N9 in shorebirds highlight the need for continuous active surveillance in wild birds and rapid molecular characterization of any poultry incursion. Kerala’s recurrent H5N1 outbreaks demonstrate the difficulty of eradicating HPAI from areas with intensive mixed farming systems. Jessamine County’s rapid containment of a HPAI H5N1 incursion shows the effectiveness of well-prepared response protocols. Integration of genomic epidemiology with on-the-ground biosecurity remains the most robust approach to mitigate the impact of avian influenza on poultry health and food security.

References

[1] Silaban J, Ogada S, Naseem MN, et al. Phylogenetic Analysis of Highly Pathogenic Avian Influenza H7 Viruses in Australia and New Zealand Suggests Local Viral Evolution. Vet Sci. 2025. Available from: https://pubmed.ncbi.nlm.nih.gov/41472188/

[2] Wilson A, Jauregui R, Gias E, et al. Phylogenetic and Molecular Characterization of a Novel Reassortant High-Pathogenicity Avian Influenza A (H7N6) Virus Detected in New Zealand Poultry. Int J Mol Sci. 2025. Available from: https://pubmed.ncbi.nlm.nih.gov/41226658/

[3] Sedger LM, Ahuja V, Lau KA, et al. The detection of avian influenza virus in human pathology laboratories in Australia, New Zealand, and South Pacific nations. Med J Aust. 2025. Available from: https://pubmed.ncbi.nlm.nih.gov/41090209/

[4] McCulley M, Wilson AD, Jauregui R, et al. High pathogenicity avian influenza (HPAI) H7N6 virus detected in New Zealand poultry. Microbiol Resour Announc. 2025. Available from: https://pubmed.ncbi.nlm.nih.gov/40298424/

[5] Waller SJ, Wierenga JR, Heremia L, et al. Avian Influenza Virus Surveillance Across New Zealand and Its Subantarctic Islands Detects H1N9 in Migratory Shorebirds, but Not 2.3.4.4b HPAI H5N1. Influenza Other Respir Viruses. 2025. Available from: https://pubmed.ncbi.nlm.nih.gov/40148670/

[6] Stanislawek WL, Tana T, Rawdon TG, et al. Avian influenza viruses in New Zealand wild birds, with an emphasis on subtypes H5 and H7: Their distinctive epidemiology and genomic properties. PLoS One. 2024. Available from: https://pubmed.ncbi.nlm.nih.gov/38829903/

[7] Gartrell BD, Jolly MJ, Hunter SA. The risks and consequences of a high pathogenicity avian influenza outbreak in Aotearoa New Zealand. N Z Vet J. 2024. Available from: https://pubmed.ncbi.nlm.nih.gov/38228153/

[8] Swayne DE, Suarez DL, Sims LD. Influenza. In: Swayne DE, editor. Diseases of Poultry. 14th ed. Hoboken (NJ): Wiley-Blackwell; 2020. p. 201-277.

[9] World Organisation for Animal Health. Avian influenza (infection with high pathogenicity avian influenza viruses). In: Manual of Diagnostic Tests and Vaccines for Terrestrial Animals. Paris: WOAH; 2024. Chapter 3.3.4.

[10] USDA Animal and Plant Health Inspection Service. 2022–2024 Detections of Highly Pathogenic Avian Influenza in Commercial and Backyard Flocks. Riverdale (MD): USDA; 2025. Available from: https://www.aphis.usda.gov/aphis/ourfocus/animalhealth/animal-disease-information/avian/avian-influenza/hpai-2022

[11] Flint SJ, Racaniello VR, Rall GF, Hatziioannou T, Skalka AM. Orthomyxoviridae. In: Principles of Virology. 5th ed. Washington (DC): ASM Press; 2020. p. 485-523.

[12] World Health Organization. Avian influenza A (H5N1) – India. Disease Outbreak News. Geneva: WHO; 2024. Available from: https://www.who.int/emergencies/disease-outbreak-news

[13] Veterinary Virology. In: MacLachlan NJ, Dubovi EJ, editors. Fenner’s Veterinary Virology. 5th ed. London: Academic Press; 2017. p. 315-342.

[14] Alexander DJ, Brown IH. History of highly pathogenic avian influenza. Rev Sci Tech. 2009;28(1):19-38. doi:10.20506/rst.28.1.1863

[15] Spackman E. A brief introduction to avian influenza virus. Methods Mol Biol. 2020;2123:1-10. doi:10.1007/978-1-0716-0346-8_1

Disclaimer: This article is for educational and informational purposes only. It is not intended to substitute for professional veterinary advice, diagnosis, treatment, or regulatory guidance. Always consult a licensed veterinarian or qualified specialist regarding animal health, disease diagnosis, and therapeutic decisions.