#19,338
In 2024 - just over 2 months after the discovery of HPAI H5N1 in U.S. dairy cattle - the USDA reported that HPAI H5N1 had been Detected In Alpacas from a premises (in Idaho) where HPAI-affected poultry had recently been depopulated.
Alpacas belong the the family Camelidae, which includes 3 types of camels ( dromedary camels, Bactrian camels, wild Bactrian camels), and 4 lamoids (llama, alpaca, guanaco, and vicuña).
In an attempt to determine how vulnerable Alpaca are to the virus, and their ability to carry, and shed the virus, researchers at Germany's FLI (Friedrich-Loeffler-Institut) experimentally infected 6 alpaca with the HPAI H5N1 genotype B3.13 (`bovine') virus.
That said, there would seem to be enough here to warrant inclusion of camelids in farm biosecurity and surveillance plans.
Research
Experimental Highly Pathogenic Avian Influenza A(H5N1) Clade 2.3.4.4b Virus Infection in Alpacas, 2026
Jacob Schön , Angele Breithaupt, Nico Joel Halwe, Maxi Hertel, Ann Kathrin Ahrens, Andrea Aebischer, Donata Hoffmann, and Martin Beer
Abstract
Highly pathogenic avian influenza (HPAI) A(H5N1) clade 2.3.4.4b virus continues to spread globally and sporadically transmits from avian reservoirs to mammalian hosts. In May 2024, H5N1 infections in young goats and alpacas in the United States were reported. Nevertheless, the overall susceptibility of camelids to clade 2.3.4.4b virus remains unclear.We conducted a controlled experimental infection study in 6 alpacas, assessing clinical signs, viral shedding, tissue distribution, and serologic responses after intranasal inoculation with HPAI H5N1 genotype B3.13 virus.Observed illness was generally mild; body temperature increased slightly and food intake reduced for up to 3 days postinfection. We detected viral RNA in nasal swab samples and confirmed infectious HPAI H5N1 virus. Immunohistochemistry and RNA in situ hybridization detected virus only in the nasopharyngeal tonsil and nasal conchae at 4 days postinfection.
Our findings suggest alpacas are susceptible to productive H5N1 infection, highlighting implications for livestock surveillance and biosecurity in regions with ongoing circulation.
We experimentally confirmed that alpacas can be intranasally infected with a bovine HPAIV H5N1 B3.13 isolate, leading to subsequent nasal shedding of infectious virus. IHC and ISH confirmed H5N1 virus replication in the nasopharyngeal tonsil and the nasal conchae. Productive infection was corroborated by seroconversion at 20 dpi. We detected individual variation of neutralizing antibody levels, but the small number of animals does not enable general conclusions. The infection did not cause fever, but alpacas reduced feed intake. Whether the viral load shed by the alpacas would be sufficient to cause transmission to contact animals remains undetermined. Intermittent viral RNA detection and low viral titer at 3 dpi might reflect technical variability of the sampling procedure rather than reduced shedding.
Our data did not suggest that alpacas replicate H5N1 clade 2.3.4.4b genotype B3.13 virus with exceptionally high efficiency. However, nasal replication occurred, and infectious virus was detectable in nasal swab samples for up to 6 dpi, but sequencing did not indicate accumulation of mutation to that timepoint. Nevertheless, viral adaptation after infection or shedding to naive contact animals or humans cannot be excluded. A follow-up study should include direct-contact animals to assess the biologic relevance of low-level shedding and to clarify the potential role of alpacas in H5N1 transmission. In addition, future studies should include experimental intramammary inoculation of female alpacas to evaluate susceptibility via that route.
In conclusion, H5N1 clade 2.3.4.4b virus will likely continue to drive substantial mortality rates in wild birds and marine mammals across North and South America. Risk for virus spillover into domestic animals, including poultry and potentially camelids, will continue considering their large populations on the continents. The demonstrated capacity of H5N1 clade 2.3.4.4b virus to acquire mammalian-adaptive mutations heightens concern about cross-species transmission and possible establishment in new mammalian hosts, which could intensify wildlife losses, disrupt livestock production, and generate new zoonotic risks. Sustained surveillance, strengthened biosecurity, and rapid response measures will be essential to limit those impacts.