An Adenovirus Outbreak in Captive Aplomado Falcons (Falco femoralis septentrionalis) Causing High Morbidity and Mortality
American Association of Zoo Veterinarians Conference 1997
Bruce A. Rideout1,4, DVM, PhD; Dave Rotstein2, DVM; J. Lindsay Oaks3, DVM; Cal Sandfort4; Christi Hall4; Laura Richman5,6, DVM; Dana P. Scott5, DVM; Richard Garber7, PhD; Ilse Stalis1, DVM; J. Peter Jenny4
1Department of Pathology, Center for Reproduction of Endangered Species, Zoological Society of San Diego, San Diego, CA, USA; 2Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA, USA; 3Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, WA, USA; 4The Peregrine Fund, World Center for Birds of Prey, Boise, ID, USA; 5The Armed Forces Institute of Pathology, Washington, DC, USA; 6National Zoological Park, Washington, DC, USA; 7Pathogenesis Corporation, Seattle, WA, USA


The Northern aplomado falcon (Falco femoralis septentrionalis) was extirpated from the United States in the 1950s, with reduced populations surviving only in Mexico. In 1986 a recovery program began to reestablish the U.S. population of this endangered species through captive propagation and release of hatch-year juveniles. More than 100 falcons have now been hatched and released in Southern Texas. The first nesting of this species in the United States since 1952 occurred in 1995. In 1996 the captive propagation effort yielded an unprecedented 110 hatchlings (85% hatchability). However, the 22nd chick to hatch died on 6 June 1996 at nine days of age, beginning a viral outbreak which ultimately resulted in 57 mortalities. Affected birds ranged in age from 9–35 days and were either found dead without premonitory signs, or exhibited various combinations of lethargy, anorexia, diarrhea, and green mutes (feces). All 57 aplomado falcons received complete necropsies. The most consistent gross lesions were moderate to marked hepatomegaly and/or splenomegaly. Five birds also exhibited either intraluminal hemorrhage or fibrinonecrotic cast formation in the small or large intestine. The primary histopathologic findings included multifocal necrotizing hepatitis and splenitis with variably rare to abundant intranuclear viral inclusions. In cases with rare inclusions, the biliary epithelium was more prominently affected than hepatocytes. Most inclusions were large and basophilic, but smaller eosinophilic herpesvirus-like inclusions were also seen. Intranuclear inclusions were also seen in intestinal epithelial cells of the birds with enteritis. Polymerase chain reaction studies utilizing a nested set of consensus primers for herpesviruses were negative on samples of frozen liver, spleen, kidney, lung, and large intestine from four affected aplomado falcons (not all organs were tested from each falcon). Transmission electron microscopy on liver from three cases revealed 58–70 nm nonenveloped, hexagonal virions in the nucleus of hepatocytes, forming paracrystalline arrays in one case. These findings are compatible with an adenovirus infection. Virus isolation attempts using pooled falcon liver and spleen homogenates inoculated onto chicken embryo hepatocytes and embryonated eggs were negative but limited cytopathic effect and viral replication were observed on a primary culture of quail fibroblasts. Scanning electron microscopy of sediment from the tissue culture supernatant revealed virions morphologically compatible with an adenovirus. Attempts to transmit the virus to day-old and adult coturnix quail using falcon liver and spleen homogenates were also negative. The inoculated quail remained clinically normal and seronegative for group I or II adenoviruses by agar gel precipitation. Epidemiologic investigations revealed a point-source epidemic with two clusters of cases resulting from horizontal transmission. The two clusters followed the index case by eight and 14 days, respectively. The median incubation period was 10 days, assuming two days of viral shedding prior to death. Supportive therapy was ineffective, serving only to prolong the period of viral shedding by 0.5 day.

Management of the outbreak included strict isolation of birds showing clinical signs, segregation of caretakers to certain areas, utilization of foot baths, immediate disinfection of contaminated areas, and a change in diet from fresh ground coturnix quail (Coturnix coturnix, reared on-site) to chickens and rodents. The last mortality occurred 5 July 1996. Chicks hatching on 21 June 1996 or later were not affected. Adult aplomado falcons were not affected during the outbreak, but six peregrine falcons (Falco peregrinus) ranging in age from two weeks to five years died during the period of the outbreak. All had gross and microscopic lesions indistinguishable from the affected aplomado falcons. The epidemiologic pattern suggests that the peregrines were secondarily infected through fomites. Serologic testing of 16 remaining aplomado and six peregrine falcons for type I and type II adenoviruses by agar gel precipitation was negative. Negative-stain electron microscopic examination of feces from 10 surviving aplomado falcons was also negative for viral particles.


An unidentified adenovirus is capable of causing explosive outbreaks with high mortality in young aplomado falcons and can cause fatal infections in peregrine falcons. Adenoviral infections in raptors are rare, with only two other reports in the literature.1,2 The source of this virus is unknown, but epidemiologic and experimental evidence suggests that the feeder coturnix quail were not the source. Because the median incubation period is 10 days, rapid postmortem diagnostics on early cases can provide a window of time for intervention to prevent propagation of an outbreak. The morphology of the viral inclusions by light microscopy is variable; therefore, additional diagnostics may be required to distinguish this adenovirus from falcon herpesvirus, which can cause similar lesions.3 Strict hygiene and quarantine of breeding facilities may be the best preventive strategy, and when combined with isolation and segregation procedures, may be able to arrest an outbreak in progress. Because treatment is ineffective and mortality approaches 100%, euthanasia of any birds showing clinical signs during an outbreak may be warranted.

Literature Cited

1.  Schelling SH, Garlick DS, Alroy J. Adenoviral hepatitis in a merlin (Falco columbarius). Vet Pathol. 1989;26(6):529–530.

2.  Sileo L, Franson JC, Graham DL, Domermuth CH, Rattner BA, Pattee OH. Hemorrhagic enteritis in captive American kestrels (Falco sparverius). J Wildl Dis. 1983;19(3):244–247.

3.  Wheler CL. Herpesvirus disease in raptors: a review of the literature. In: Redig PT, ed. Raptor Biomedicine. Cooper JE, Remple JD, Hunter DB, eds. Minneapolis, MN: University of Minnesota Press; 1993:103–107.


Speaker Information
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Bruce A. Rideout, DVM, PhD
Center for Reproduction of Endangered Species
Department of Pathology
Zoological Society of San Diego
San Diego, CA, USA

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