Biomedical subjects

Joseph K Gaydos

Publications and source records attributed to Joseph K Gaydos.

9 recordsLinked to original sources

PubMed2006

Collaborative science, policy development and program implementation in the transboundary Georgia Basin/Puget Sound ecosystem.

The transboundary Georgia Basin Puget Sound ecosystem is situated in the southwest corner of British Columbia and northwest comer of Washington State. While bountiful and beautiful, this international region is facing significant threats to its marine and freshwater resources, air quality, habitats and species. These environmental challenges are compounded by rapid population growth and attendant uiban sprawl. As ecosystem stresses amplified and partnerships formed around possible solutions, it became increasingly clear that the shared sustainability challenges in the Georgia Basin and Puget Sound required shared solutions. Federal, state and provincial institutional arrangements were made between jurisdictions, which formalized small scale interest in transboundary management of this ecosystem. Formal agreements, however, can only do so much to further management of an ecosystem that spans international boarders. A transboundary regional research meeting, the 2003 GB/PS Research Conference, opened the doors for large-scale informal cross-boarder cooperation and management. In addition to cooperation, continued efforts to stem toxic pollution, contain urban growth, and protect and restore ecosystems, require a commitment from scientists, educators and policy makers to better integrate research and science with decision-making.

Animals↗

PubMed2006

Avian vacuolar myelinopathy outbreaks at a southeastern reservoir.

Avian vacuolar myelinopathy (AVM) is a neurologic disease of unknown etiology that affects bald eagles (Haliaeetus leucocephalus), American coots (Fulica americana), and several species of waterfowl. An unidentified neurotoxin is suspected as the cause of AVM, which has been documented at several reservoirs in the southeastern United States. We conducted diagnostic and epidemiologic studies annually during October-March from 1998-2004 at Clarks Hill/Strom Thurmond Lake on the Georgia/South Carolina border to better understand the disease. Avian vacuolar myelinopathy was confirmed or suspected as the cause of morbidity and mortality of 28 bald eagles, 16 Canada geese (Branta canadensis), six American coots, two great-horned owls (Bubo virginianus), and one killdeer (Charadrius vociferus). Active surveillance during the outbreaks yielded annual average prevalence of vacuolar lesions in 17-94% of coots, but not in 10 beavers (Castor canadensis), four raccoons (Procyon lotor), and one gray fox (Urocyon cinereoargenteus) collected for the study. Brain lesions were not apparent in 30 Canada geese collected and examined in June 2002. The outbreaks at this location from 1998-2004 represent the most significant AVM-related bald eagle mortality since the Arkansas epornitics of 1994-95 and 1996-97, as well as the first confirmation of the disease in members of Strigiformes and Charadriiformes.

Animals↗

PubMed2005

Detection of Ehrlichia spp. in raccoons (Procyon lotor) from Georgia.

Raccoons (Procyonis lotor) and opossums (Didelphis virginianus) acquired from six contiguous counties in the Piedmont physiographic region of Georgia were investigated for their potential role in the epidemiology of ehrlichial and anaplasmal species. Serum was tested by indirect fluorescent antibody (IFA) assay for the presence of antibodies reactive to Ehrlichia chaffeensis, E. canis, and Anaplasma phagocytophilum (HGA agent). Nested polymerase chain reaction (PCR) assay was used to test whole blood or white blood cell preparations for the presence of Ehrlichia and Anaplasma spp. 16S rRNA (rDNA) gene fragments. In addition, ticks were collected from these animals and identified. Twenty-three of 60 raccoons (38.3%) had E. chaffeensis-reactive antibodies (>1:64), 13 of 60 raccoons (21.7%) had E. canis-reactive antibodies, and one of 60 raccoons (1.7%) had A. phagocytophilum- reactive antibodies. A sequence confirmed E. canis product was obtained from one of 60 raccoons and a novel Ehrlichia-like 16S rDNA sequence was detected in 32 of 60 raccoons. This novel sequence was most closely related to an Ehrlichia-like organism identified from Ixodes ticks and rodents in Asia and Europe. Raccoons were PCR negative for E. chaffeensis and E. ewingii DNA. Five tick species, including Dermacentor variabilis, Amblyomma americanum, Ixodes texanus, I. cookei, and I. scapularis, were identified from raccoons and represent potential vectors for the ehrlichiae detected. Opossums (n = 17) were free of ticks and negative on all IFA and PCR assays. This study suggests that raccoons are potentially involved in the epidemiology of multiple ehrlichial organisms with known or potential public health and veterinary implications.

Anaplasma↗

PubMed2004

Epizootiology of an epizootic hemorrhagic disease outbreak in West Virginia.

An outbreak of epizootic hemorrhagic disease virus, serotype 2 (EHDV-2) was responsible for localized white-tailed deer (Odocoileus virginianus) mortality in Hardy and Hampshire counties, West Virginia (USA), in the summer and fall of 1993. Using available historical data on regional herd immunity, data opportunistically collected during the epizootic, and postepizootic sampling of hunter-harvested deer, we grossly estimate certain epidemiologic parameters and compare findings to a hypothesis about hemorrhagic disease outbreaks in the Appalachian Mountains. During the epizootic, 57.9 km(2) were actively searched and 228 dead deer were found. Epizootic hemorrhagic disease virus, serotype 2 was isolated from seven of nine deer sampled in Hardy and Hampshire counties. Preepizootic exposure of deer to EHD viruses was unknown, but available data suggest that it was negligible. The geographic distribution of the outbreak was defined by plotting the locations of dead deer found during the outbreak, as well as the locations of deer harvested by hunters after the outbreak that had antibodies to EHDV-2 on a map sectioned into 16.65 km(2) rectangular sections. Sections that included one or more dead deer or hunter-harvested deer with antibodies to EHDV-2 were included in the defined outbreak area. Postoutbreak sampling revealed monospecific EHDV-2 antibodies in 12% of deer harvested by hunters within the defined outbreak area. Based on the available data and accepting certain assumptions, gross calculations suggest that this outbreak appears to have been isolated and probably killed a high percentage of the deer that were infected. This is consistent with the hypothesis that sporadic hemorrhagic disease outbreaks in the Appalachian Mountains are usually localized and severe.

Animals↗

PubMed2002

Oral and fecal shedding of epizootic hemorrhagic disease virus, serotype 1 from experimentally infected white-tailed deer.

Epizootic hemorrhagic disease (EHD), one of the most important infectious diseases of white-tailed deer (Odocoileus virginianus), is vectored by species of midges in the genus Culicoides. Although vector borne, fecal shedding of EHD virus, serotype 2 has been reported from infected deer in a previous study. To evaluate the potential for fecal and oral shedding, oral and rectal swabs were obtained on day 8 post-inoculation from white-tailed deer fawns experimentally infected with EHD virus, serotype 1 (EHDV-1). Eight deer were viremic for EHDV-1; virus was detected in oral swabs from three (38%) and in rectal swabs from four (50%). The ability to isolate EHDV-1 in oral secretions or feces was not dependent on being able to detect clinical disease. These results indicate that in a relatively large proportion of EHDV-1 infected deer, virus can be detected in feces and oral secretions. Although more work is necessary, such shedding may be important in experimental studies or pen situations where deer-to-deer contact is prevalent and intense.

Animals↗

PubMed2002

Dynamics of maternal antibodies to hemorrhagic disease viruses (Reoviridae: Orbivirus) in white-tailed deer.

Enzootic stability, potentially associated with acquired resistance and subsequent transfer of maternal antibodies, innate resistance, or both, has been hypothesized to explain the lack of reports of hemorrhagic disease (HD) in white-tailed deer (Odocoileus virginianus) from Texas. The objectives of this research were to determine the following: how long maternal antibodies to epizootic hemorrhagic disease (EHD) and bluetongue (BT) viruses persist; whether fawns from an enzootic site are naturally exposed to EHD and BT viruses while maternal antibodies are present; and whether field-challenged fawns develop clinical disease. Twelve of 52 fawns from Texas were moved to an indoor facility. All 12 (100%) were positive for maternal antibodies to EHD or BT viruses by agar gel immunodiffusion (AGID) and serum neutralization (SN) tests. Weekly monitoring demonstrated that precipitating antibodies disappeared by 23 wk of age and serum neutralizing antibodies disappeared by 17-18 wk of age. Fawns that remained outdoors in Texas were not observed with signs of HD. At 14-21 wk of age (October), 39 of 40 (98%) fawns that had remained outdoors were positive for EHD and/or BT virus antibodies by AGID and 32 (80%) had SN antibody titers to one or more of five viruses (EHDV-1, EHDV-2, BTV-10, BTV-11, BTV-17). Antibody titers to EHDV-1, EHDV-2, and BTV-11 all exceeded titers of same-age indoor fawns, suggesting recent exposure. Epizootic hemorrhagic disease viruses were isolated from seven (18%) of the outdoor fawns and all 40 remained clinically normal. Natural exposure of deer to EHD and BT viruses occurred at this site in the presence of maternal antibodies without causing disease. This may be due to acquired immunity and the subsequent transfer of maternal antibodies, but it does not exclude innate resistance as a possible factor in the enzootic stability of EHD and BT viruses at this location.

Aging↗

PubMed2002

Innate resistance to epizootic hemorrhagic disease in white-tailed deer.

Differences in innate disease resistance at the sub-species level have major implications for wildlife management. Two subspecies of white-tailed deer, Odocoileus virginianus borealis and O. virginianus texanus were infected with epizootic hemorrhagic disease (EHD) viruses. These viruses are highly virulent pathogens of white-tailed deer and are endemic within the range of O. virginianus texanus but not within the range of O. virginianus borealis. Two experimental infections were performed. Five O. virginianus texanus fawns and five O. virginianus borealis fawns were infected with 10(7.1) median tissue culture infective doses (TCID50) of EHD virus, serotype 1 and five of each subspecies were infected with 10(7.1) TCID50 of EHD virus, serotype 2. Infections with both EHD virus serotypes caused severe clinical disease and mortality in O. virginianus borealis fawns, whereas disease was mild or nondetectable in O. virginianus texanus fawns. Virus titers and humoral immune response were similar in both subspecies suggesting that differences in innate disease resistance explain the differences seen in clinical disease severity. In white-tailed deer, innate disease resistance may vary at the subspecies level. Should this phenomenon occur in other species, these findings have major implications for managing wildlife populations, both endangered and non-endangered, using tools such as translocation and captive propagation.

Animals↗

PubMed2002

Cross-protection between epizootic hemorrhagic disease virus serotypes 1 and 2 in white-tailed deer.

Viruses in the epizootic hemorrhagic disease (EHD) serogroup are the most frequent cause of hemorrhagic disease in the southeastern United States, but nothing is known about cross-protection between the two EHD serotypes (EHDV-1 and EHDV-2) present in this region. We experimentally tested whether deer surviving EHDV-2 infection would be protected against subsequent infection with EHDV-1, and used field data to examine the possibility of reciprocal cross-protection. Eleven white-tailed deer fawns (Odocoileus virginianus) were experimentally infected with EHDV-2 and later challenged with EHDV-1. Two EHDV-2-naïve fawns also were infected with EHDV-1. Deer were monitored via physical examination, complete blood counts, clotting profiles, viral isolation, and serology, and each animal was assigned a quantitative clinical disease severity score based on presence of certain physical and clinical parameters. Infection of naïve controls with EHDV-1 caused severe clinical disease and death of both fawns, whereas deer previously infected with EHDV-2 exhibited no or minimal signs of disease. Thus, infection with EHDV-2 conferred protection against disease caused by subsequent EHDV-1 infection. Although prior EHDV-2 exposure protected deer from severe clinical disease, it did not prevent infection nor viremia indicating they could still act as virus amplifying hosts. These experimental infections suggest that EHDV-1 and 2 may exist in a state of mutual permissiveness.

Animals↗

PubMed2002

Paratuberculosis in key deer (Odocoileus virginianus clavium).

Paratuberculosis was diagnosed in an endangered Key deer (Odocoileus virginianus clavium) in November 1996. Between 10 April 1997 and 28 September 2000, the Key deer population was monitored for infection with Mycobacterium avium subsp. paratuberculosis by necropsy of available carcasses (n = 170), fecal cultures, and serology. One additional clinically affected Key deer was discovered in July 1998, and M. avium subsp. paratuberculosis was cultured from the feces of one live, asymptomatic deer. The results of this study provided sufficient evidence to consider the Key deer herd infected with M. avium subsp. paratuberculosis at very low prevalence.

Animals↗