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At least 145 records · Page 8Linked to original sources
PubMed2005

Characterization of a new species of adenovirus in falcons.

In 1996, a disease outbreak occurred at a captive breeding facility in Idaho, causing anorexia, dehydration, and diarrhea or sudden death in 72 of 110 Northern aplomado falcons (Falco femoralis septentrionalis) from 9 to 35 days of age and in 6 of 102 peregrine falcons (Falco peregrinus) from 14 to 25 days of age. Sixty-two Northern aplomado and six peregrine falcons died. Epidemiologic analyses indicated a point source epizootic, horizontal transmission, and increased relative risk associated with cross-species brooding of eggs. Primary lesions in affected birds were inclusion body hepatitis, splenomegaly, and enteritis. The etiology in all mortalities was determined by molecular analyses to be a new species of adenovirus distantly related to the group I avian viruses, serotypes 1 and 4, Aviadenovirus. In situ hybridization and PCR demonstrated that the virus was epitheliotropic and lymphotropic and that infection was systemic in the majority of animals. Adeno-associated virus was also detected by PCR in most affected falcons, but no other infectious agents or predisposing factors were found in any birds. Subsequent to the 1996 epizootic, a similar disease caused by the same adenovirus was found over a 5-year period in orange-breasted falcons (Falco deiroleucus), teita falcons (Falco fasciinucha), a merlin (Falco columbarius), a Vanuatu peregrine falcon (Falco peregrinus nesiotes), and gyrfalcon x peregrine falcon hybrids (Falco rusticolus/peregrinus) that died in Wyoming, Oklahoma, Minnesota, and California. These findings indicate that this newly recognized adenovirus is widespread in western and midwestern North America and can be a primary pathogen in different falcon species.

Adenoviridae Infections↗
PubMed2005

Isolation and epidemiology of falcon adenovirus.

An adenovirus was detected by electron microscopy in tissues from falcons that died during an outbreak of inclusion body hepatitis and enteritis that affected neonatal Northern aplomado (Falco femoralis septentrionalis) and peregrine (Falco peregrinus anatum) falcons. Molecular characterization has identified the falcon virus as a new member of the aviadenovirus group (M. Schrenzel, J. L. Oaks, D. Rotstein, G. Maalouf, E. Snook, C. Sandfort, and B. Rideout, J. Clin. Microbiol. 43:3402-3413, 2005). In this study, the virus was successfully isolated and propagated in peregrine falcon embryo fibroblasts, in which it caused visible and reproducible cytopathology. Testing for serum neutralizing antibodies found that infection with this virus was limited almost exclusively to falcons. Serology also found that wild and captive peregrine falcons had high seropositivity rates of 80% and 100%, respectively, although clinical disease was rarely reported in this species. These data implicate peregrine falcons as the natural host and primary reservoir for the virus. Other species of North American falcons, including aplomado falcons, had lower seropositivity rates of 43 to 57%. Falcon species of tropical and/or island origin were uniformly seronegative, although deaths among adults of these species have been described, suggesting they are highly susceptible. Chickens and quail were uniformly seronegative and not susceptible to infection, indicating that fowl were not the source of infection. Based on the information from this study, the primary control of falcon adenovirus infections should be based on segregation of carrier and susceptible falcon species.

Adenoviridae Infections↗
PubMed2005

Field trial of a Caryospora species vaccine for controlling clinical coccidiosis in falcons.

A Caryospora species vaccine was prepared and used in an attempt to prevent infection and associated morbidity in falcons. A blind field trial was conducted, involving a vaccinated group of 20 birds and two control groups of seven and four birds, which were subsequently challenged with a live mixed-species vaccine. There was a statistically significant reduction in morbidity and shedding of oocysts in the vaccinated group compared with the control groups.

Animals↗
PubMed2006

Assessment of a commercial sandwich ELISA in the diagnosis of aspergillosis in falcons.

A commercial sandwich elisa (Platelia Aspergillus EIA; Bio-Rad) developed for the detection of galactomannan, a major cell wall constituent of Aspergillus species, was tested for its efficacy in the diagnosis of aspergillosis in falcons. Ninety serum samples from 50 aspergillosis-positive falcons and 182 samples from 142 aspergillosis-negative falcons were tested. The sensitivity of the test was only 12 per cent and its specificity was 95 percent. The test was therefore unsatisfactory for detecting galactomannan in the serum samples and cannot be used as a screening test for aspergillosis in falcons.

Animals↗
PubMed2006

Plasma chemistry reference values in hybrid falcons in relation to their species of origin.

Twenty-one blood chemistry parameters were determined in 127 peregrine falcons (Falco peregrinus), 79 gyr-peregrine hybrids and 166 gyr-saker hybrids. These parameters, together with those previously established in 53 gyr falcons (Falco rusticolus) and 234 saker falcons (Falco cherrug), were compared. There were statistically significant differences in 15 of the parameters between the saker and peregrine falcons; the saker and gyr falcons; the saker and gyr-saker hybrids; the peregrine and gyr falcons; and the peregrine and gyr-peregrine hybrids, but not between the gyr falcons and the gyr-saker falcon hybrids.

Animals↗
PubMed2006

Susceptibility of fungi isolated from the respiratory tract of falcons to amphotericin B, itraconazole and voriconazole.

The minimum inhibitory concentrations (mics) of fungi isolated from the air sacs of falcons before (group 1), and during antifungal treatment with amphotericin B nebulisation and oral itraconazole or voriconazole (group 2), or with itraconazole alone (group 3) or voriconazole alone (group 4) were determined. Before treatment, 95 per cent of the isolates, including Aspergillus fumigatus, Aspergillus flavus, Aspergillus niger and Aspergillus terreus, were susceptible to voriconazole at mics up to 0.38 microg/ml, and all the isolates were susceptible at mics up to 1 microg/ml. Before treatment, 21 per cent of the isolates, including A fumigatus (27.6 per cent), A flavus (16.6 per cent), A niger (100 per cent) and A terreus (23 per cent), were resistant (mic > or =1 microg/ml) to itraconazole; 51 per cent of the isolates, including A fumigatus (31 per cent), A flavus (78 per cent), A niger (14 per cent) and A terreus (77 per cent), had mics of over 1 microg/ml to amphotericin B, and after treatment their mics increased significantly. In contrast, there were no significant differences between the mics of voriconazole and itraconazole for the different Aspergillus species before and during treatment with these antifungal agents.

Air Sacs↗
PubMed2026

Genomic and Clinicopathological Characterization of a Reassortant HPAI H5N1 (Clade 2.3.4.4b) in an Endangered Cinereous Vulture (Aegypius monachus) in South Korea, 2026.

Clade 2.3.4.4b highly pathogenic avian influenza viruses (HPAIVs) continue to circulate widely in East Asia and undergo frequent reassortment in wild birds. Raptors are regarded as spillover hosts that may be exposed through predation or scavenging, yet integrated clinicopathologic and genomic investigations in cinereous vultures remain limited. Here, we describe a fatal H5N1 HPAIV infection in a cinereous vulture (Aegypius monachus) found in South Korea on January 17, 2026. On presentation, the cinereous vulture showed severe neurologic dysfunction, including inability to stand, right-sided head tilt with pathologic nystagmus, reduced oculocephalic and palpebral reflexes, and intermittent bilateral leg tremors. The cinereous vulture died within 2 days after rescue, and a complete necropsy was performed. Hematologic and biochemical testing revealed marked heterophil predominance, severe lymphopenia, mild monocytosis, and globulin values near the upper end of the reference interval. An oropharyngeal swab tested positive for influenza A virus, and a virus isolate, designated A/Cinereous_Vulture/Korea/26-JBN47/2026(H5N1), was recovered in embryonated chicken eggs. Histopathology showed nonsuppurative encephalitis and necrotizing myocarditis, and influenza A nucleoprotein was detected immunohistochemically in neurons and cardiomyocytes. Tissue real-time RT-PCR showed the lowest cycle threshold value in the brain. Whole-genome sequencing demonstrated that 26-JBN47 belonged to clade 2.3.4.4b and contained a polybasic HA cleavage site (PLREKRRKR/GLF). Segment-level phylogenetic analysis revealed a reassortant genome constellation comprising a maintained H5N1 backbone in HA, NA, and M; low PAIV (LPAIV)-associated but H5N1-incorporated PA and NP segments; flyway-associated PB2 and NS segments; and a PB1 segment phylogenetically linked to regional LPAIV lineages. Molecular marker analysis identified multiple substitutions previously reported to be associated with receptor-binding properties, polymerase-related fitness, virulence, and host-response modulation, whereas canonical PB2 mammalian-adaptive markers were absent. These findings show that 26-JBN47 was a reassortant clade 2.3.4.4b H5N1 HPAIV associated with systemic disease and clinicopathological findings consistent with neurotropic and cardiotropic infection in a cinereous vulture. They also support the potential value of scavenging raptors as sentinels of local or regional HPAIV circulation involving reassortant viruses in East Asia.

Animals↗
PubMed2006

Falcon adenovirus infection in breeding Taita falcons (Falco fasciinucha).

Four female and 3 male Taita falcons (Falco fasciinucha) out of a breeding colony of 14 Taita falcons (7 pairs) died during the breeding season after showing lethargy and anorexia for 1 to 2 days. All animals were submitted for necropsy. Gross lesions in the female falcons were characterized by anemia secondary to marked hemorrhage into the ovary and oviduct, serofibrinous effusion into the cardioabdominal cavity and serosal petechiae. In addition, marked necrotizing splenitis and pulmonary hemorrhage were present. Histologically, the female falcons had mild necrotizing hepatitis with numerous intranuclear inclusion bodies and necrotizing splenitis with rare inclusion bodies. There were no gross lesions in the male falcons, and the histological lesions were characterized by urate deposition and rare intranuclear inclusion bodies in the renal tubular epithelial cells. Adenoviral particles were found by electron microscopy in the cloacal contents of the female Taita falcons but not in the male falcons. DNA in situ hybridization revealed widespread aviadenoviral nucleic acid within the nuclei of hepatocytes, renal tubular epithelial cells, and adrenal cells in the female falcons but no aviadenoviral nucleic acid in 1 male falcon and only a low quantity of adenoviral nucleic acid in the liver and kidney of another male Taita falcon. PCR amplified aviadenoviral DNA in the liver and intestine of all Taita falcons. The amplicons were sequenced, and the virus was identified as falcon adenovirus. The deaths of the female and male birds were attributed to the aviadenovirus infection.

Adenoviridae Infections↗
PubMed2006

Removing the threat of diclofenac to critically endangered Asian vultures.

Veterinary use of the nonsteroidal anti-inflammatory (NSAID) drug diclofenac in South Asia has resulted in the collapse of populations of three vulture species of the genus Gyps to the most severe category of global extinction risk. Vultures are exposed to diclofenac when scavenging on livestock treated with the drug shortly before death. Diclofenac causes kidney damage, increased serum uric acid concentrations, visceral gout, and death. Concern about this issue led the Indian Government to announce its intention to ban the veterinary use of diclofenac by September 2005. Implementation of a ban is still in progress late in 2005, and to facilitate this we sought potential alternative NSAIDs by obtaining information from captive bird collections worldwide. We found that the NSAID meloxicam had been administered to 35 captive Gyps vultures with no apparent ill effects. We then undertook a phased programme of safety testing of meloxicam on the African white-backed vulture Gyps africanus, which we had previously established to be as susceptible to diclofenac poisoning as the endangered Asian Gyps vultures. We estimated the likely maximum level of exposure (MLE) of wild vultures and dosed birds by gavage (oral administration) with increasing quantities of the drug until the likely MLE was exceeded in a sample of 40 G. africanus. Subsequently, six G. africanus were fed tissues from cattle which had been treated with a higher than standard veterinary course of meloxicam prior to death. In the final phase, ten Asian vultures of two of the endangered species (Gyps bengalensis, Gyps indicus) were dosed with meloxicam by gavage; five of them at more than the likely MLE dosage. All meloxicam-treated birds survived all treatments, and none suffered any obvious clinical effects. Serum uric acid concentrations remained within the normal limits throughout, and were significantly lower than those from birds treated with diclofenac in other studies. We conclude that meloxicam is of low toxicity to Gyps vultures and that its use in place of diclofenac would reduce vulture mortality substantially in the Indian subcontinent. Meloxicam is already available for veterinary use in India.

Animal Feed↗