West Nile Virus Infection in American Singer Canaries: An Experimental Model in a Highly Susceptible Avian Species.

This study investigated the susceptibility of American singer canaries ( Serinus canaria) to West Nile virus (WNV) infection. Adult canaries were inoculated with 105, 102, and 101 plaque forming units (PFU) of WNV. All birds became infected and mortality occurred by 5 days postinoculation. The load of viral RNA as determined by RT-qPCR was dose dependent, and was higher at all doses than the level of viral RNA detected in American crows ( Corvus brachyrhynchos) challenged with 105 PFU of WNV. In a subset of birds, viremia was detected by virus isolation; canaries inoculated with 101 PFU of WNV developed viremia exceeding 1010 PFU/mL serum, a log higher than American crows inoculated with 105 PFU of virus. In canaries euthanized at 3 days postinoculation, WNV was isolated at >107 PFU of virus/100 mg of lung, liver, heart, spleen, and kidney tissues. Pallor of the liver and splenomegaly were the most common macroscopic observations and histologic lesions were most severe in liver, spleen, and kidney, particularly in canaries challenged with 102 and 101 PFU. Immunoreactivity to WNV was pronounced in the liver and spleen. IgG antibodies to WNV were detected in serum by enzyme immunoassay in 11 of 21 (52%) challenged canaries and, in 4 of 5 (20%) of these sera, neutralization antibodies were detected at a titer ≥ 1:20. American singer canaries provide a useful model as this bird species is highly susceptible to WNV infection.

Acute oral toxicity and tissue residues of saxitoxin in the mallard (Anas platyrhynchos).

Since 2014, widespread, annual mortality events involving multiple species of seabirds have occurred in the Gulf of Alaska, Bering Sea, and Chukchi Sea. Among these die-offs, emaciation was a common finding with starvation often identified as the cause of death. However, saxitoxin (STX) was detected in many carcasses, indicating exposure of these seabirds to STX in the marine environment. Few data are available that describe the effects of STX in birds, thus presenting challenges for determining its contributions to specific mortality events. To address these knowledge gaps, we conducted an acute oral toxicity trial in mallards (Anas platyrhynchos), a common laboratory avian model, using an up-and-down method to estimate the median lethal dose (LD50) for STX. Using an enzyme-linked immunosorbent assay (ELISA), we tested select tissues from all birds and feces from those individuals that survived initial dosing. Samples with an ELISA result that exceeded approximately 10 µg 100 g-1 STX and randomly selected ELISA negative samples were further tested by high-performance liquid chromatography (HPLC). Tissues collected from mallards were also examined grossly at necropsy and then later by microscopy to identify lesions attributable to STX. The estimated LD50 was 167 µg kg-1 (95% CI = 69-275 µg kg-1). Saxitoxin was detected in fecal samples of all mallards tested for up to 48 h after dosing and at the end of the sampling period (7 d) in three birds. In those individuals that died or were euthanized <2 h after dosing, STX was readily detected throughout the gastrointestinal tract but only infrequently in heart, kidney, liver, lung, and breast muscle. No gross or microscopic lesions were observed that could be attributable to STX exposure. Given its acute toxicity, limited detectability, and frequent occurrence in the Alaska marine environment, additional research on STX in seabirds is warranted.

Elodontoma in captive southern red-backed voles (Myodes gapperi).

Five southern red-backed voles (Myodes gapperi) of the first generation of a wild-caught breeding colony were presented with lesions at the maxillary incisors consistent with elodontoma. The affected animals had a history of chronic weight loss, were >16 months of age, and were siblings. Radiographs of the head showed multiglobular to irregularly outlined mineral opacity masses at the apices of the maxillary incisors. On necropsy, maxillary incisor teeth were not grossly visible, and a gingival ulceration was observed at the expected site of eruption. Microscopically, the apical region of the maxillary incisors was thickened or replaced by irregular dental tissue masses consistent with elodontoma. This is the first report to describe elodontoma in red-backed voles.

Oral and parenteral immunization of chickens (Gallus gallus) against West Nile virus with recombinant envelope protein.

West Nile virus (WNV) causes morbidity and mortality in humans, horses, and in more than 315 bird species in North America. Currently approved WNV vaccines are designed for parenteral administration and, as yet, no effectiveoral WNV vaccines have been developed. WNV envelope (E) protein is a highly antigenic protein that elicits the majority ofvirus-neutralizing antibodies during a WNV immune response. Leghorn chickens were given three vaccinations (each 2 wk apart) of E proteinorally (20 microg or 100 microg/dose), of E protein intramuscularly (IM, 20 microg/dose), or of adjuvant only (control group) followed by a WNV challenge. Viremias were measured post-WNV infection, and three new enzyme-linked immunosorbent assays were developed for quantifying IgM, IgY, and IgA-mediated immune response of birds following WNV infection. WNV viremia levelswere significantly lower in the IM group than in both oral groups and the control group. Total WNV E protein-specific IgY production w assignificantly greater, and WNV nonstructural 1-specific IgY w as significantly less, in the IM group compared to all other treatment groups.The results of this study indicate that IM vaccination of chickens with E protein is protective against WNV infection and results in a significantly different antibody production profile as compared to both orally vaccinated and nonvaccinated birds.

Experimental infection of Hawai'i 'Amakihi (hemignathus virens) with West Nile virus and competence of a co-occurring vector, culex quinquefasciatus: potential impacts on endemic Hawaiian avifauna.

Introduced mosquito-borne avian disease is a major limiting factor in the recovery and restoration of native Hawaiian forest birds. Annual epizootics of avian pox (Avipoxvirus) and avian malaria (Plasmodium relictum) likely led to the extinction of some species and continue to impact populations of susceptible Hawaiian honeycreepers (Drepanidinae). The introduction of a novel pathogen, such as West Nile virus (WNV), could result in further population declines and extinctions. During September and October 2004, we infected Hawai'i' Amakihi (Hemignathus virens) with a North American isolate of WNV by needle inoculation and mosquito bite to observe susceptibility, mortality, and illness in this endemic passerine, and to determine the vector competence of the co-occurring, introduced mosquito Culex quinquefasciatus. All experimentally infected Hawai'i ;Amakihi became viremic, with a mean titer >10(5) plaque-forming units (PFU)/ml, and they experienced clinical signs ranging from anorexia and lethargy to ataxia. The fatality rate among needle-inoculated Hawai'i' Amakihi (n=16) was 31.3%, but mortality in free-ranging birds is likely to increase due to predation, starvation, thermal stress, and concomitant infections of avian malaria and pox. Surviving Hawai'i' Amakihi seem to clear WNV from the peripheral blood by 7-10 days postinfection (DPI), and neutralizing antibodies were detected from 9 to 46 DPI. In transmission trials, Hawaiian Cx. quinquefasciatus proved to be a competent vector and Hawai'i Amakihi an adequate amplification host of WNV, suggesting that epizootic WNV could readily become an additional limiting factor of some native Hawaiian bird populations.

Population Differences in Susceptibility to Plasmodium relictum in Zebra Finches Taeniopygia guttata.

Domesticated Australian and Timor zebra finches (Taeniopygia guttata castanotis and Taeniopygia guttata guttata, respectively) were inoculated with canary (Serinus canaria) blood containing a Hawaiian isolate of Plasmodium relictum (lineage GRW04), a hemoparasite that causes avian malaria. In two experimental trials, TZFs but not AZFs developed parasitemia that was detected by microscopic examination of blood smears. In the second trial, in which molecular detection methods were used, a single AZF and five of six challenged TZFs were positive for the parasite. Additionally, P. relictum DNA was detected in multiple blood samples obtained from TZFs over the 28 days following challenge. TZFs may provide a useful, easily maintained, laboratory model for the study of Plasmodium interactions in passerines but are still inferior to canaries, the traditionally used model of avian malaria infection, in terms of supporting high-parasitemia infections.

Nota de investigación- Diferencias poblacionales en la susceptibilidad a Plasmodium relictum en diamantes cebra Taeniopygia guttata. Se inocularon diamantes cebra de Australia y de Timor (Taeniopygia guttata castanotis y Taeniopygia guttata guttata, respectivamente) con sangre de canario silvestre (Serinus canaria) que contenía un aislado hawaiano de Plasmodium relictum (linaje GRW04), que es un hemoparásito que causa la malaria aviar. En dos ensayos experimentales, los diamantes cebra de Timor desarrollaron una parasitemia detectada mediante un examen microscópico de frotis de sangre, pero los diamantes cebra australianos no desarrollaron dicha parasitemia. En el segundo ensayo, en el que se utilizaron métodos de detección molecular, un solo pinzón australiano y cinco de las seis aves de Timor desafiadas resultaron positivas para el parásito. Además, se detectó el ADN de P. relictum en múltiples muestras de sangre obtenidas de las aves de Timor durante 28 días posteriores al desafío. Los diamantes cebra de Timor pueden proporcionar un modelo de laboratorio útil y de fácil mantenimiento para el estudio de las interacciones de Plasmodium en passeriformes, pero áun son inferiores en comparación con los canarios, que son utilizados como modelo de infección por malaria aviar tradicionalmente usado en términos de apoyo a las infecciones con alta parasitemia.

An examination of the effect of aerosolized Permanone insecticide on zebra finch susceptibility to West Nile virus.

West Nile virus (WNV) is maintained cryptically primarily in avian (passerine) populations, where it is transmitted by Culex spp. mosquitoes. Mosquito-control measures currently include physical activities to reduce mosquito-breeding sites and the application of mosquito larvicides or aerosolized insecticides to kill adults (adulticides) when arboviral diseases such as WNV or Zika virus are detected in mosquito populations. Organochlorine, organophosphorus, carbamate, and pyrethroid insecticides are often used. Previous work suggests an effect of pyrethroids on the immune system in a variety of vertebrates. We examined the effects of exposure to aerosolized Permanone® 30:30 insecticide (permethrin and piperonyl butoxide in soy oil vehicle) at approximately 103 to 106 times potential environmental concentrations on the response of captive zebra finches (Taeniopygia guttata) to experimental challenge with WNV. Compared to vehicle control birds, WNV outcome was unchanged (65% of birds produced a viremia) in the "low" exposure (9.52 ± 3.13 mg/m3 standard deviation [SD] permethrin) group but reduced in the "high" exposure (mean 376.5 ± 27.9 mg/m3 SD permethrin) group (30% were viremic; p < 0.05). After clearing WNV infection, birds treated with Permanone regained less body mass than vehicle-treated birds (p < 0.001). The present study suggests that exposure to aerosolized Permanone insecticide at levels exceeding typical application rates has the potential to not change or to mildly enhance a bird's resistance to WNV. Environ Toxicol Chem 2017;36:3376-3386. Published 2017 Wiley Periodicals Inc. on behalf of SETAC. This article is a US government work and, as such, is in the public domain in the United States of America.

Transcriptional response to West Nile virus infection in the zebra finch (Taeniopygia guttata).

West Nile virus (WNV) is a widespread arbovirus that imposes a significant cost to both human and wildlife health. WNV exists in a bird-mosquito transmission cycle in which passerine birds act as the primary reservoir host. As a public health concern, the mammalian immune response to WNV has been studied in detail. Little, however, is known about the avian immune response to WNV. Avian taxa show variable susceptibility to WNV and what drives this variation is unknown. Thus, to study the immune response to WNV in birds, we experimentally infected captive zebra finches (Taeniopygia guttata). Zebra finches provide a useful model, as like many natural avian hosts they are moderately susceptible to WNV and thus provide sufficient viremia to infect mosquitoes. We performed RNAseq in spleen tissue during peak viremia to provide an overview of the transcriptional response. In general, we find strong parallels with the mammalian immune response to WNV, including upregulation of five genes in the Rig-I-like receptor signalling pathway, and offer insights into avian-specific responses. Together with complementary immunological assays, we provide a model of the avian immune response to WNV and set the stage for future comparative studies among variably susceptible populations and species.

Susceptibility and Antibody Response of the Laboratory Model Zebra Finch (Taeniopygia guttata) to West Nile Virus.

Since the introduction of West Nile virus (WNV) into North America in 1999 a number of passerine bird species have been found to play a role in the amplification of the virus. Arbovirus surveillance, observational studies and experimental studies have implicated passerine birds (songbirds, e.g., crows, American robins, house sparrows, and house finches) as significant reservoirs of WNV in North America, yet we lack a tractable passerine animal model for controlled studies of the virus. The zebra finch (Taeniopygia guttata) serves as a model system across a diversity of fields, and here we develop the zebra finch a songbird model for WNV. Like many natural hosts of WNV, we found that zebra finches developed sufficient viremia to serve as a competent host, yet in general resisted mortality from infection. In the Australian zebra finch (AZF) T. g. castanotis, we detected WNV in the majority of sampled tissues by 4 days post injection (dpi). However, WNV was not detected in tissues of sacrificed birds at 14 dpi, shortly after the development of detectable anti-WNV antibodies in the majority of birds indicating successful viral clearance. We compared susceptibility between the two zebra finch subspecies AZF and Timor zebra finch (TZF) T. g. guttata. Compared to AZF, WNV RNA was detected in a larger proportion of challenged TZF and molecular detection of virus in the serum of TZF was significantly higher than in AZF. Given the observed moderate host competence and disease susceptibility, we suggest that zebra finches are appropriate as models for the study of WNV and although underutilized in this respect, may be ideal models for the study of the many diseases carried and transmitted by songbirds.

SURVEY FOR WEST NILE VIRUS ANTIBODIES IN WILD DUCKS, 2004-06, USA.

Detection of West Nile virus (WNV) in ducks has been reported in North America in isolated cases of mortality in wild waterbirds and following outbreaks in farmed ducks. Although the virus has been noted as an apparent incidental finding in several species of ducks, little is known about the prevalence of exposure or the outcome of infection with WNV in wild ducks in North America. From 2004-06, we collected sera from 1,406 wild-caught American Wigeon ( Anas americana ), Mallard ( Anas platyrhynchos ), and Northern Pintail ( Anas acuta ) ducks at national wildlife refuges (NWRs) in North Dakota and Wood Ducks ( Aix sponsa ) at NWRs in South Carolina and Tennessee. We measured the prevalence of previous exposure to WNV in these ducks by measuring WNV antibodies and evaluated variation in exposure among species, age, and year. Additionally, we evaluated the performance of a commercial antibody to wild bird immunoglobulin in duck species that varied in their phylogenetic relatedness to the bird species the antibody was directed against. As determined by a screening immunoassay and a confirmatory plaque reduction neutralization assay, the prevalence of WNV antibody was 10%. In light of experimental studies that show ducks to be relatively resistant to mortality caused by WNV, the antibody prevalence we detected suggests that wild ducks may be less-frequently exposed to WNV than expected for birds inhabiting wetlands where they may acquire infection from mosquitoes.

SUSCEPTIBILITY AND ANTIBODY RESPONSE OF VESPER SPARROWS (POOECETES GRAMINEUS) TO WEST NILE VIRUS: A POTENTIAL AMPLIFICATION HOST IN SAGEBRUSH-GRASSLAND HABITAT.

West Nile virus (WNV) spread to the US western plains states in 2003, when a significant mortality event attributed to WNV occurred in Greater Sage-grouse ( Centrocercus urophasianus ). The role of avian species inhabiting sagebrush in the amplification of WNV in arid and semiarid regions of the North America is unknown. We conducted an experimental WNV challenge study in Vesper Sparrows ( Pooecetes gramineus ), a species common to sagebrush and grassland habitats found throughout much of North America. We found Vesper Sparrows to be moderately susceptible to WNV, developing viremia considered sufficient to transmit WNV to feeding mosquitoes, but the majority of birds were capable of surviving infection and developing a humoral immune response to the WNV nonstructural 1 and envelope proteins. Despite clearance of viremia, after 6 mo, WNV was detected molecularly in three birds and cultured from one bird. Surviving Vesper Sparrows were resistant to reinfection 6 mo after the initial challenge. Vesper sparrows could play a role in the amplification of WNV in sagebrush habitat and other areas of their range, but rapid clearance of WNV may limit their importance as competent amplification hosts of WNV.

Immunoglobulin detection in wild birds: effectiveness of three secondary anti-avian IgY antibodies in direct ELISAs in 41 avian species.

Immunological reagents for wild, non-model species are limited or often non-existent for many species.In this study, we compare the reactivity of a new anti-passerine IgY secondary antibody with existing secondary antibodies developed for use with birds. Samples from 41 species from the following six avian orders were analysed: Anseriformes (1 family, 1 species), Columbiformes (1 family, 2 species), Galliformes (1 family, 1 species), Passeriformes (16 families, 34 species), Piciformes (1 family, 2 species) and Suliformes (1 family, 1 species). Direct ELISAs were performed to detect total IgY using goat anti-passerine IgY, goat anti-chicken IgY or goat anti-bird IgY secondary antibodies.The anti-passerine antibody exhibited significantly higher IgY reactivity compared to the anti-chicken and/or anti-bird antibodies in 80% of the passerine families tested. Birds in the order Piciformes (woodpeckers) and order Suliformes (cormorants) were poorly detected by all three secondary antibodies. A comparison of serum and plasma IgY levels was made within the same individuals for two passerine species (house finch and white-crowned sparrow), and serum exhibited significantly more IgY than the plasma for all three secondary antibodies. This result indicates that serum may be preferred to plasma when measuring total antibody levels in blood.This study indicates that the anti-passerine IgY secondary antibody can effectively be used in immunological assays to detect passerine IgY for species in most passerine families and is preferred over anti-chicken and anti-bird secondary antibodies for the majority of passerine species. This anti-passerine antibody will allow for more accurate detection and quantification of IgY in more wild bird species than was possible with previously available secondary antibodies.

Surveillance Potential of Non-Native Hawaiian Birds for Detection of West Nile Virus.

West Nile virus (WNV) was first detected in North America in 1999. Alaska and Hawaii (HI) remain the only U.S. states in which transmission of WNV has not been detected. Dead bird surveillance has played an important role in the detection of the virus geographically, as well as temporally. In North America, corvids have played a major role in WNV surveillance; however, the only corvid in HI is the endangered Hawaiian crow that exists only in captivity, thus precluding the use of this species for WNV surveillance in HI. To evaluate the suitability of alternate avian species for WNV surveillance, we experimentally challenged seven abundant non-native bird species present in HI with WNV and compared mortality, viremia, oral shedding of virus, and seroconversion. For detection of WNV in oral swabs, we compared viral culture, reverse-transcriptase polymerase chain reaction, and the RAMP(®) test. For detection of antibodies to WNV, we compared an indirect and a competitive enzyme-linked immunoassay. We found four species (house sparrow, house finch, Japanese white-eye, and Java sparrow) that may be useful in dead bird surveillance for WNV; while common myna, zebra dove, and spotted dove survived infection and may be useful in serosurveillance.

Relatively high prevalence of pox-like lesions in Henslow's sparrow (Ammodrammus henslowii) among nine species of migratory grassland passerines in Wisconsin, USA.

Globally, Avipoxvirus species affect over 230 species of wild birds and can significantly impair survival. During banding of nine grassland songbird species (n=346 individuals) in southwestern Wisconsin, USA, we noted species with a 2-6% prevalence of pox-like lesions (possible evidence of current infection) and 4-10% missing digits (potential evidence of past infection). These prevalences approach those recorded among island endemic birds (4-9% and 9-20% for the Galapagos and Hawaii, respectively) for which Avipoxvirus species have been implicated as contributing to dramatic population declines. Henslow's Sparrow Ammodramus henslowii (n=165 individuals) had the highest prevalence of lesions (6.1%) and missing digits (9.7%). Among a subset of 26 Henslow's Sparrows from which blood samples were obtained, none had detectable antibody reactive to fowlpox virus antigen. However, four samples (18%) had antibody to canarypox virus antigen with test sample and negative control ratios (P/N values) ranging from 2.4 to 6.5 (median 4.3). Of four antibody-positive birds, two had lesions recorded (one was also missing a digit), one had digits missing, and one had no signs. Additionally, the birds with lesions or missing digits had higher P/N values than did the antibody-positive bird without missing digits or recorded lesions. This study represents an impetus for considering the impacts and dynamics of disease caused by Avipoxvirus among North American grassland bird species.

West Nile virus in American White Pelican chicks: transmission, immunity, and survival.

West Nile virus (WNV) causes significant mortality of American White Pelican chicks at northern plains colonies. We tested oropharyngeal/cloacal swabs from moribund chicks for shed WNV. Such shedding could enable chick-to-chick transmission and help explain why WNV spreads rapidly in colonies. WNV was detected on swabs from 11% of chicks in 2006 and 52% of chicks in 2007; however, viral titers were low. Before onset of WNV mortality, we tested blood from < 3-week-old chicks for antibodies to WNV; 5% of chicks were seropositive, suggesting passive transfer of maternal antibodies. Among near-fledged chicks, 41% tested positive for anti-WNV antibodies, indicating that they survived infection. Among years and colonies, cumulative incidence of WNV in chicks varied from 28% to 81%, whereas the proportion of chicks surviving WNV (i.e., seropositive) was 64-75%. Our data revealed that WNV kills chicks that likely would fledge in the absence of WNV, that infection of chicks is pervasive, and that significant numbers of chicks survive infection.

West Nile virus: North American experience.

West Nile virus, a mosquito-vectored flavivirus of the Japanese encephalitis serogroup, was first detected in North America following an epizootic in the New York City area in 1999. In the intervening 11 years since the arrival of the virus in North America, it has crossed the contiguous USA, entered the Canadian provinces bordering the USA, and has been reported in the Caribbean islands, Mexico, Central America and, more recently, South America. West Nile virus has been reported in over 300 species of birds in the USA and has caused the deaths of thousands of birds, local population declines of some avian species, the clinical illness and deaths of thousands of domestic horses, and the clinical disease in over 30 000 Americans and the deaths of over 1000. Prior to the emergence of West Nile virus in North America, St. Louis encephalitis virus and Dengue virus were the only other known mosquito-transmitted flaviviruses in North America capable of causing human disease. This review will discuss the North American experience with mosquito-borne flavivirus prior to the arrival of West Nile virus, the entry and spread of West Nile virus in North America, effects on wild bird populations, genetic changes in the virus, and the current state of West Nile virus transmission.

Seroprevalence of West Nile virus in feral horses on Sheldon National Wildlife Refuge, Nevada, United States.

We screened 1,397 feral horses (Equus caballus) on Sheldon National Wildlife Refuge, Nevada, United States, for IgM and IgG against flavivirus during 2004-2006, 2008, and 2009. Positive serum samples were tested for neutralizing antibodies to West Nile virus (WNV) and St. Louis encephalitis virus (SLEV). One animal was positive for antibody against WNV in 2004, but all others tested in 2004-2006 were negative. In 2008 and 2009, we found evidence of increasing seropositive horses with age, whereas seroprevalence of WNV decreased from 19% in 2008 to 7.2% in 2009. No horses were positive for antibody against SLEV. Being unvaccinated, feral horses can be useful for WNV surveillance.

Occurrence of west nile virus infection in raptors at the Salton Sea, California.

We investigated the prevalence of West Nile virus (WNV)-neutralizing antibodies and infectious virus, and the occurrence of overwinter transmission in two raptor species during January and March 2006 at the Salton Sea, Imperial County, California. We captured 208 American Kestrels (Falco sparverius) (January, n=100; March, n=108) and 116 Burrowing Owls (Athene cunicularia) (January, n=52; March, n=64). Laboratory analysis revealed that 83% of American Kestrels and 31% of Burrowing Owls were positive for WNV-neutralizing antibodies. Additionally, two seroconversions were detected in Burrowing Owls between January and March. Infectious WNV, consistent with acute infection, was not detected in any bird.

Testing independent and interactive effects of corticosterone and synergized resmethrin on the immune response to West Nile virus in chickens.

Public health agencies utilize aerial insecticides to interrupt an active West Nile virus (WNV) transmission cycle, which may expose WNV-infected birds to these agents. Although resmethrin has been considered benign to birds, no studies have evaluated whether the environmentally employed form of resmethrin with PBO synergist (synergized resmethrin (SR)) can suppress avian immunity to WNV infection and enhance a bird's host competence. Recognizing that wild birds confront toxicological stressors in the context of various physiological states, we exposed four groups (n=9-11) of 9-week-old chickens (Gallus domesticus) to drinking water with either SR (three alternate days at 50 microg/l resmethrin+150 microg/l piperonyl butoxide), CORT (10 days at 20mg/l to induce subacute stress), the combination of SR and CORT, or 0.10% ethanol vehicle coincident with WNV infection. Compared to controls, SR treatment did not magnify but extended viremia by 1 day, and depressed IgG; CORT treatment elevated (mean, 4.26 log(10)PFU/ml) and extended viremia by 2 days, enhanced IgM and IgG, and increased oral virus. The combination of SR and CORT increased the number of chickens that shed oral virus compared to those treated with CORT alone. None of the chickens developed a readily infectious viremia to mosquitoes (none >or=5 log(10)PFU/ml), but viremia in a CORT-exposed chicken was up to 4.95 log(10)PFU/ml. Given that SR is utilized during WNV outbreaks, continued work toward a complete risk assessment of the potential immunotoxic effects of SR is warranted. This would include parameterization of SR exposures with immunological consequences in wild birds using both replicating (in the laboratory) and non-replicating (in the field) antigens. As a start, this study indicates that SR can alter some immunological parameters, but with limited consequences to primary WNV infection outcome, and that elevated CORT mildly enhances SRs immunotoxicity in chickens.

In vivo characterization of colonic thermal injury caused by argon plasma coagulation.

BACKGROUND: Argon plasma coagulation has been rapidly accepted for endoscopic obliteration of vascular lesions and superficial tumors. Depth of injury is thought to be limited through preferential discharge of energy to nondesiccated tissue. However, argon plasma coagulation-induced injury has not been well characterized. The aim of this study was to characterize argon plasma coagulation-induced colonic injury by using a porcine model. METHODS: Laparotomy was performed in 6 female swine and the colon exteriorized with the subjects under general anesthesia. Lesions were made with an argon plasma coagulation probe held perpendicular and 2 mm from the mucosa. Variables studied were as follows: power (45 W, 60 W, and 75 W) and duration (1, 2, or 3 seconds; n = 11 for each power/duration combination). Injury was graded as either superficial or deep, involving the muscularis propria. RESULTS: Circular muscle layer injury correlated closely with power (p = 0.02), duration (p = 0.001), and total energy delivered (r = 0.977). Longitudinal muscle damage was associated with duration of burn (p = 0.001) and total energy delivered (r = 0.855), but correlated poorly with power (p = 0.40). No perforations occurred. Submucosal injection of saline solution had a protective effect with reductions in circular (90% to 10%, p = 0.002) and longitudinal muscle injury (50% to 0%, p = 0.1). CONCLUSIONS: Injury to the muscularis propria occurs at recommended settings for argon plasma coagulation. Injury correlates with power setting, duration of burn, and total energy delivery. Protective arcing to nondesiccated tissue does not appear to be significant in vivo. Submucosal injection of saline solution protects against deep injury.