Spatial epidemiology of chronic wasting disease in Wisconsin white-tailed deer

Chronic wasting disease (CWD) is a fatal, emerging disease of cervids associated with transmissible protease-resistant prion proteins. The potential for CWD to cause dramatic declines in deer and elk populations and perceived human health risks associated with consuming CWD-contaminated venison have led wildlife agencies to embark on extensive CWD control programs, typically involving culling to reduce deer populations. We characterized the spatial distribution of CWD in white-tailed deer (Odocoileus virginianus) in Wisconsin to facilitate CWD management. We found that CWD prevalence declined with distance from a central location, was locally correlated at a scale of 3.6 km, and was correlated with deer habitat abundance. The latter result is consistent with patterns expected for a positive relationship between density and prevalence of CWD. We recommend management activities focused on culling in geographic areas with high prevalence to have the greatest probability of removing infected individuals. Further research is needed to elucidate the factors involved in CWD spread and infection rates, especially the role of density-dependent transmission.     

Prevalence of chronic wasting disease and bovine tuberculosis in free-ranging deer and elk in South Dakota

Heads of hunter-harvested deer and elk were collected throughout South Dakota (USA) and within established chronic wasting disease (CWD) surveillance areas from 1997-2002 to determine infection with CWD and bovine tuberculosis (TB). We used immunohistochemistry to detect CWD-infected individuals among 1,672 deer and elk sampled via geographically targeted surveillance. A total of 537 elk (Cervus elaphus nelsoni), 813 white-tailed deer (Odocoileus virginianus), and 322 mule deer (O. hemionus) was sampled for CWD. Estimated overall prevalence and associated confidence intervals (95%) in white-tailed deer was 0.001% (0-0.007%). Similarly, estimated overall prevalence in elk and mule deer was 0.0% (0-0.004%) and 0.0% (0-0.011%), respectively. A total of 401 elk, 1,638 white-tailed deer, and 207 mule deer was sampled for TB. Estimated overall prevalence of infection with TB in elk harvested in South Dakota was 0.0% (0-0.009%). Similarly, estimated overall prevalence of TB in white-tailed deer and mule deer harvested throughout South Dakota was 0.0% (0-0.002%) and 0.0% (0-0.018%), respectively.     

Epidemiology of chronic wasting disease in captive white-tailed and mule deer

The natural occurrence of chronic wasting disease (CWD) in a 1993 cohort of captive white-tailed deer (Odocoileus virginianus) afforded the opportunity to describe epidemic dynamics in this species and to compare dynamics with those seen in contemporary cohorts of captive mule deer (O. hemionus) also infected with CWD. The overall incidence of clinical CWD in white-tailed deer was 82% (nine of 11) among individuals that survived >15 mo. Affected white-tailed deer died or were killed because of terminal CWD at age 49-76 mo (x = 59.6 mo, SE = 3.9 mo). Epidemic dynamics of CWD in captive white-tailed deer were similar to dynamics in mule deer cohorts. Incidence of clinical CWD was 57% (4/7) among hand-raised (HR) and 67% (4/6) among dam-raised (DR) mule deer; affected HR mule deer succumbed at 64-86 mo of age (x = 72 mo; SE = 5 mo), and affected DR mule deer died at age 31-58 mo (x = 41.3 mo; SE = 6.1 mo). Sustained horizontal transmission of CWD most plausibly explained epidemic dynamics, but the original source of exposures could not be determined. Apparent differences in mean age at CWD-caused death among these cohorts may be attributable to differences in the timing or intensity of exposure to CWD, and these factors appear to be more likely to influence epidemic dynamics than species differences. It follows that CWD epidemic dynamics in sympatric, free-ranging white-tailed and mule deer sharing habitats in western North American ranges also may be similar.     

Landscape genetics and the spatial distribution of chronic wasting disease

Predicting the spread of wildlife disease is critical for identifying populations at risk, targeting surveillance and designing proactive management programmes. We used a landscape genetics approach to identify landscape features that influenced gene flow and the distribution of chronic wasting disease (CWD) in Wisconsin white-tailed deer. CWD prevalence was negatively correlated with genetic differentiation of study area deer from deer in the area of disease origin (core-area). Genetic differentiation was greatest, and CWD prevalence lowest, in areas separated from the core-area by the Wisconsin River, indicating that this river reduced deer gene flow and probably disease spread. Features of the landscape that influence host dispersal and spatial patterns of disease can be identified based on host spatial genetic structure. Landscape genetics may be used to predict high-risk populations based on their genetic connection to infected populations and to target disease surveillance, control and preventative activities.     

Transmission of elk and deer prions to transgenic mice

Chronic wasting disease (CWD) is a fatal prion disease in deer and elk. Unique among the prion diseases, it is transmitted among captive and free-ranging animals. To facilitate studies of the biology of CWD prions, we generated five lines of transgenic (Tg) mice expressing prion protein (PrP) from Rocky Mountain elk (Cervus elaphus nelsoni), denoted Tg(ElkPrP), and two lines of Tg mice expressing PrP common to white-tailed deer (Odocoileus virginianus) and mule deer (Odocoileus hemionus), denoted Tg(DePrP). None of the Tg(ElkPrP) or Tg(DePrP) mice exhibited spontaneous neurologic dysfunction at more than 600 days of age. Brain samples from CWD-positive elk, white-tailed deer, and mule deer produced disease in Tg(ElkPrP) mice between 180 and 200 days after inoculation and in Tg(DePrP) mice between 300 and 400 days. One of eight cervid brain inocula transmitted disease to Tg(MoPrP)4053 mice overexpressing wild-type mouse PrP-A in approximately 540 days. Neuropathologic analysis revealed abundant PrP amyloid plaques in the brains of ill mice. Brain homogenates from symptomatic Tg(ElkPrP) mice produced disease in 120 to 190 days in Tg(ElkPrP) mice. In contrast to the Tg(ElkPrP) and Tg(DePrP) mice, Tg mice overexpressing human, bovine, or ovine PrP did not develop prion disease after inoculation with CWD prions from among nine different isolates after >500 days. These findings suggest that CWD prions from elk, mule deer, and white-tailed deer can be readily transmitted among these three cervid species.     

Wasting and neurologic signs in a white-tailed deer (Odocoileus virginianus) not associated with abnormal prion protein

A captive adult male white-tailed deer (Odocoileus virginianus) with wasting and neurologic signs similar to chronic wasting disease (CWD) was evaluated by histopathology, histochemistry, and immunohistochemistry (IHC) for disease-associated prion protein (PrP(d)). On histologic examination, the brainstem had areas of vacuolation in neuropil and extensive multifocal mineralization of blood vessels with occasional occlusion of the lumen. Some of the clinical and pathologic features of this case were similar to the CWD of white-tailed deer. However, the tissues were negative for PrP(d) by IHC. Because the lesions were more prominent in the obex region of the brainstem, it is speculated that this would have resulted in clinical signs similar to CWD in white-tailed deer. To our knowledge, neither cerebrovascular mineralization nor clinicopathologic changes resembling CWD have previously been described in white-tailed deer without the presence of PrP(d). Such a case should be considered in a differential diagnosis of CWD of white-tailed deer.     

Population genetic structure of white-tailed deer: Understanding risk of chronic wasting disease spread

Understanding factors that influence the spread of wildlife diseases can assist in designing effective surveillance programs and appropriate management strategies. Chronic wasting disease (CWD), a fatal prion disease of cervids, was detected in south-central Wisconsin in 2002 and over time has been identified increasingly farther west in the state leading to concerns about CWD spreading to Iowa. Our objective was to characterize genetic connectivity between white-tailed deer (Odocoileus virginianus) populations in eastern Iowa and western Wisconsin to assess the risk of CWD-infected deer dispersing to Iowa. We hypothesized that the Mississippi River, which separates the states, may restrict the movement of deer and thus disease. We genotyped hunter-harvested female deer collected from both states at 12 nuclear microsatellite loci (n = 249) and sequenced a portion of the mitochondrial DNA (mtDNA) control region (n = 173). Microsatellite data indicated there was low genetic differentiation (Φ_PT = 0.005) between states and weak spatial genetic structure across the study area as a whole. Verifying expectations that dispersal in deer is male-biased, maternally inherited mtDNA data showed stronger spatial structuring across the study area and greater genetic differentiation between the states (Φ_PT = 0.052) such that clustering analysis grouped the majority of deer from Iowa and Wisconsin into separate clusters. The low level of genetic differentiation between deer in northeast Iowa and southwest Wisconsin, primarily the result of dispersing males who have greater CWD prevalence than females, indicates that the Mississippi River is unlikely to prohibit the westward spread of CWD, and underscores the importance of continued CWD surveillance in Iowa. © 2011 The Wildlife Society.     

Movements of white-tailed deer in riparian habitat: Implications for infectious diseases

Movements of male white-tailed deer (Odocoileus virginianus) are of great concern with respect to spread of chronic wasting disease (CWD) across landscapes because most yearlings males disperse and adult males have higher prevalence of CWD than do females and younger deer. We radiocollared and monitored 85 male white-tailed deer in the middle Missouri River Valley of eastern Nebraska and western Iowa, USA from 2004 to 2008. Average size (±SE) of fixed-kernel annual home ranges (95%) and core areas (50%) for resident deer were 449 (±32) ha and 99 (±7) ha, respectively. Resident deer exhibited a high-degree of fidelity to their home ranges. Mean overlap between consecutive annual home ranges and core areas was 81% and 74%, respectively. Average dispersal distance was 17.7 ± 4.5 km (range = 3–121 km) for 22 radio-marked and 6 ear-tagged yearlings. Mean spring dispersal distance (25 km) was 150% greater than fall (10 km). Dispersal direction from Desoto National Wildlife Refuge (DNWR) was bimodal on a northwest to southeast axis that followed the Missouri River corridor. Of 22 yearlings that dispersed, 18 (82%) established adult home ranges within the river valley. Dispersal movements of yearling males represent the greatest risk for rapid spread of diseases from infected source populations. Disease management efforts in riparian habitats should target male fawns and yearling males for removal in areas within or immediately adjacent to river corridors. © 2011 The Wildlife Society.     

Prion sequence polymorphisms and chronic wasting disease resistance in Illinois white-tailed deer (Odocoileus virginianus)

Nucleic acid sequences of the prion gene (PRNP) were examined and genotypes compiled for 76 white-tailed deer from northern Illinois, which previously tested positive for chronic wasting disease (CWD), and 120 negative animals selected to control for geographic location and age. Nine nucleotide polymorphisms, seven silent and two coding, were found in the sampled population. All observed polymorphisms except two of very low frequency were observed in both negative and positive animals, although five polymorphic loci had significantly different distributions of alleles between infected and non-infected individuals. Nucleotide base changes 60C/T, 285A/C, 286G/A, and 555C/T were observed with higher than expected frequencies in CWD negative animals suggesting disease resistance, while 153C/T was observed more than expected in positive animals, suggesting susceptibility. The two coding polymorphisms, 285A/C (Q95H) and 286G/A (G96S), have been described in white-tailed deer populations sampled in Colorado and Wisconsin. Frequency distributions of coding polymorphisms in Wisconsin and Illinois deer populations were different, an unexpected result considering the sampled areas are less than 150 km apart. The total number of polymorphisms per animal, silent or coding, was negatively correlated to disease status. The potential importance of silent polymorphisms (60C/T, 153C/T, 555C/T), either individually or cumulatively, in CWD disease status has not been previously reported.     

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.     

Prion sequence polymorphisms and chronic wasting disease resistance in Illinois white-tailed deer (Odocoileus virginianus)

Nucleic acid sequences of the prion gene (PRNP) were examined and genotypes compiled for 76 white-tailed deer from northern Illinois, which previously tested positive for chronic wasting disease (CWD), and 120 negative animals selected to control for geographic location and age. Nine nucleotide polymorphisms, seven silent and two coding, were found in the sampled population. All observed polymorphisms except two of very low frequency were observed in both negative and positive animals, although five polymorphic loci had significantly different distributions of alleles between infected and non-infected individuals. Nucleotide base changes 60C/T, 285A/C, 286G/A and 555C/T were observed with higher than expected frequencies in CWD negative animals suggesting disease resistance, while 153C/T was observed more than expected in positive animals, suggesting susceptibility. The two coding polymorphisms, 285A/C (Q95H) and 286G/A (G96S), have been described in white-tailed deer populations sampled in Colorado and Wisconsin. Frequency distributions of coding polymorphisms in Wisconsin and Illinois deer populations were different, an unexpected result considering the sampled areas are less than 150 km apart. The total number of polymorphisms per animal, silent or coding, was negatively correlated to disease status. The potential importance of silent polymorphisms (60C/T, 153C/T, 555C/T), either individually or cumulatively, in CWD disease status has not been previously reported.Key words: CWD, PRNP, synonymous polymorphism, cumulative polymorphisms, haplotype     

Genetic assessment of environmental features that influence deer dispersal: implications for prion-infected populations

The landscape can influence host dispersal and density, which in turn, affect infectious disease transmission, spread, and persistence. Understanding how the landscape influences wildlife dispersal and pathogen epidemiology can enhance the efficacy of disease management in natural populations. We applied landscape genetics to examine relationships among landscape variables, dispersal of white-tailed deer hosts and transmission/spread of chronic wasting disease (CWD), a fatal prion encephalopathy. Our focus was on quantifying movements and population structure of host deer in infected areas as a means of predicting the spread of this pathology and promoting its adaptive management. We analyzed microsatellite genotypes of CWD-infected and uninfected deer from two disease foci (Southern Wisconsin, Northern Illinois). We quantified gene flow and population structure using F _ST, assignment tests, and spatial autocorrelation analyses. Gene flow estimates were then contrasted against a suite of landscape variables that potentially mediate deer dispersal. Forest fragmentation and grassland connectivity promoted deer movements while rivers, agricultural fields and large urbanized areas impeded movement. Landscape variables, deer dispersal, and disease transmission covaried significantly and positively in our analyses. Habitats with elevated host gene flow supported the concept of dispersal-mediated CWD transmission by reflecting a concomitant, rapid CWD expansion. Large, interrelated social groups isolated by movement barriers overlapped disease foci, suggesting that philopatry exacerbated CWD transmission. Our results promote adaptive management of CWD by predicting patterns of its spread and identifying habitats at risk for invasion. Further, our landscape genetics approach underscores the significance of topography and host behavior in wildlife disease transmission.     

Sarcocystis of deer in South Dakota

The prevalence of Sarcocystis in white-tailed deer (Odocoileus virginianus) and mule deer (O. hemionus) in South Dakota was determined through microscopic examination of tongue samples. The percentage of Sarcocystis infection for both species of deer was determined for prairies east of the Missouri River, west of the Missouri River, and Black Hills of western South Dakota. Sixteen percent (N = 62) of the white-tailed deer tongues from East River, 69% (N = 42) from West River, and 74% (N = 23) from the Black Hills were infected. Prevalence for mule deer was 88% (N = 24), 78% (N = 63), and 75% (N = 12) from East River, West River, and the Black Hills, respectively. Of 50 tongue samples obtained from both species of deer during a special antlerless deer hunt in the Black Hills in 1978, 66% were infected. Coyotes (Canis latrans), dogs (Canis familiaris), red foxes (Vulpes vulpes), a gray fox (Urocyon cinereoargenteus), bobcat (Felis rufus), and raccoon (Procyon lotor) were fed muscle from white-tailed deer and mule deer naturally infected with Sarcocystis to determine their role as definitive hosts. All coyotes, dogs, and the gray fox shed sporocysts, while none were recovered from the other animals. Sporocysts shed by coyotes were counted and concentrated into an inoculum and administered to a white-tailed deer fawn, which was necropsied 85 days after inoculation. Sections of heart, tongue, esophagus, diaphragm, and skeletal muscle were found to be heavily infected with sarcocysts, while sarcocysts were not detected in a control fawn.     

Relative vulnerability of chronic wasting disease infected mule deer to vehicle collisions

We estimated chronic wasting disease (CWD) prevalence among vehicle-killed mule deer (Odocoileus hemionus) in select data analysis units (DAUs) in northern Colorado, USA, and compared these with estimated CWD prevalence among mule deer of the same sex sampled in the vicinity of collision sites to assess relative vulnerability of CWD-infected individuals to vehicle collisions. Twenty-five of 171 vehicle-killed mule deer tested positive for CWD (overall prevalence=0.146, 95% confidence interval [CI]=0.097-0.208); 173 of 2,317 deer sampled in the vicinity of these vehicle-killed deer tested positive (overall prevalence=0.075, 95% CI=0.064-0.085). In nine of ten DAU x sex comparisons, relative risk of CWD infection tended to be higher among vehicle-killed deer (range of estimated relative risks=1.6-15.9). Spongiform encephalopathy was detected in 12 of 20 (60%; 95% CI=39-81%) CWD-positive deer killed by vehicles and in 79 of 180 (44%; 95% CI=37-52%) CWD-positive deer detected via random sampling (relative risk=1.37; 95% CI=0.92-2.03), suggesting that infected deer killed by vehicles tended to be in later stages of disease than those killed by hunters. Our data offer evidence that CWD-infected mule deer may be relatively vulnerable to vehicle collisions. It follows that sampling of vehicle-killed mule deer may be exploited to increase efficiency of surveillance programs designed to detect new foci of CWD infection; moreover, evidence of increased susceptibility to vehicle collisions may aid in understanding vulnerability of CWD-infected individuals to other forms of death, particularly predation.     

Epizootiology of chronic wasting disease in free-ranging cervids in Colorado and Wyoming

Surveillance and epidemic modeling were used to study chronic wasting disease (CWD), a transmissible spongiform encephalopathy that occurs naturally among sympatric, free-ranging deer (Odocoileus spp.) and Rocky Mountain elk (Cervus elaphus nelsoni) populations in contiguous portions of northeastern Colorado and southeastern Wyoming (USA). We used clinical case submissions to identify endemic areas, then used immunohistochemistry to detect CWD-infected individuals among 5,513 deer and elk sampled via geographically-focused random surveys. Estimated overall prevalence (prevalence, 95% confidence interval) in mule deer (4.9%, 4.1 to 5.7%) was higher than in white-tailed deer (2.1%, 0.5 to 3.4%) or elk (0.5%, 0.001 to 1%) in endemic areas; CWD was not detected in outlying portions of either state. Within species, CWD prevalence varied widely among biologically- or geographically-segregated subpopulations within the 38,137 km2 endemic area but appeared stable over a 3-yr period. The number of clinical CWD cases submitted from an area was a poor predictor of local CWD prevalence, and prevalence was typically > or =1% before clinical cases were first detected in most areas. Under plausible transmission assumptions that mimicked field data, prevalence in epidemic models reached about 1% in 15 to 20 yr and about 15% in 37 to 50 yr. Models forecast population declines once prevalence exceeded about 5%. Both field and model data supported the importance of lateral transmission in CWD dynamics. Based on prevalence, spatial distribution, and modeling, we suggest CWD has been occurring in northeastern Colorado and southeastern Wyoming for >30 yr, and may be best represented as an epizootic with a protracted time-scale.     

Prion protein gene sequence and chronic wasting disease susceptibility in white-tailed deer (Odocoileus virginianus)

ABSTRACT

The sequence of the prion protein gene (PRNP) affects susceptibility to spongiform encephalopathies, or prion diseases in many species. In white-tailed deer, both coding and non-coding single nucleotide polymorphisms have been identified in this gene that correlate to chronic wasting disease (CWD) susceptibility. Previous studies examined individual nucleotide or amino acid mutations; here we examine all nucleotide polymorphisms and their combined effects on CWD. A 626 bp region of PRNP was examined from 703 free-ranging white-tailed deer. Deer were sampled between 2002 and 2010 by hunter harvest or government culling in Illinois and Wisconsin. Fourteen variable nucleotide positions were identified (4 new and 10 previously reported). We identified 68 diplotypes comprised of 24 predicted haplotypes, with the most common diplotype occurring in 123 individuals. Diplotypes that were found exclusively among positive or negative animals were rare, each occurring in less than 1% of the deer studied. Only one haplotype (C, odds ratio 0.240) and 2 diplotypes (AC and BC, odds ratios of 0.161 and 0.108 respectively) has significant associations with CWD resistance. Each contains mutations (one synonymous nucleotide 555C/T and one nonsynonymous nucleotide 286G/A) at positions reported to be significantly associated with reduced CWD susceptibility. Results suggest that deer populations with higher frequencies of haplotype C or diplotypes AC and BC might have a reduced risk for CWD infection – while populations with lower frequencies may have higher risk for infection. Understanding the genetic basis of CWD has improved our ability to assess herd susceptibility and direct management efforts within CWD infected areas.     

Evaluation of the influence of supplemental feeding of white-tailed deer (Odocoileus virginianus) on the prevalence of bovine tuberculosis in the Michigan wild deer population

A retrospective study was conducted to test the hypothesis that supplemental feeding of white-tailed deer (Odocoileus virginianus) from 1995 to 1997 was associated with the prevalence of bovine tuberculosis (TB) in free-ranging deer in northeastern Michigan.Bovine TB prevalence data were obtained from an ongoing surveillance program, while data relating to supplemental feeding and other risk factors were collected via in-person interviews. A multivariable Poisson regression modeling approach was used to test the stated hypothesis while controlling for other risk factors. Of the 389 potential participants, 59% agreed to participate in the study. Results showed that supplemental feeding of deer was associated with bovine TB in white-tailed deer. Specific risk factors associated with increasing risk for bovine TB were locating feed sites in areas with high levels of hardwood forests (O.R. = 1.8, 95% C.I. = 1.3-2.4), other large-scale feeding sites in the area (O.R. = 1.1, 95% C.I. = 1.0-1.2), the number of deer fed per year (O.R. = 3.9, 95% C.I. = 1.4-11.4), the numbers of feed sites spreading grain (O.R. = 14.7, 95% C.I. = 2.2-98.9), the quantity of grains provided at the site (O.R. = 1.4, 95% C.I. = 1.1-1.7), and the quantity of fruits and vegetables provided (O.R. = 1.4, 95% C.I. = 1.2-1.7). Conversely, factors associated with decreasing risk of bovine TB were locating feed sites in areas with high levels of hardwood forests (O.R. = 0.1, 95% C.I. = 0.02-0.4), locating feed sites in forests (O.R. = 0.05, 95% C.I. = 0.01-0.4), and the level of sites providing grain (O.R. = 0.1, 95% C.I. = 0.01-0.3). The results of this study suggest that banning the practice of supplemental feeding is a valid policy for control of bovine tuberculosis in free-ranging white-tailed deer.     

Prion protein gene heterogeneity in free-ranging white-tailed deer within the chronic wasting disease affected region of Wisconsin

Chronic wasting disease (CWD) was first identified in Wisconsin (USA) in whitetailed deer (Odocoileus virginianus) in February 2002. To determine if prion protein gene (Prnp) allelic variability was associated with CWD in white-tailed deer from Wisconsin, we sequenced Prnp from 26 CWD-positive and 100 CWD-negative deer. Sequence analysis of Prnp suggests that at least 86-96% of the white-tailed deer in this region have Prnp allelic combinations that will support CWD infection. Four Prnp alleles were identified in the deer population, one of which, resulting in a glutamine to histidine change at codon 95, has not been previously reported. The predominant allele in the population encodes for glutamine at codon 95, glycine at codon 96, and serine at codon 138 (QGS). Less abundant alleles encoded QSS, QGN, and HGS at the three variable positions. Comparison of CWD-positive with CWD-negative deer suggested a trend towards an over-representation of the QGS allele and an under-representation of the QSS allele.     

Intracranial abscessation in white-tailed deer of North America.

From January 1996 through April 1997, the geographic distribution, etiology, demographics, seasonality, and prevalence of an intracranial abscessation/suppurative meningoencephalitits syndrome in white-tailed deer (Odocoileus virginianus) were evaluated by surveying wildlife disease diagnostic laboratories and by examining both natural mortality and hunter-harvested deer skulls from North America. Intracranial abscesses were diagnosed as the cause of death or illness in 97 of nearly 4,500 (2.2%) white-tailed deer examined from 12 states and four Canadian provinces by the diagnostic laboratories. The bacterium Arcanobacterium pyogenes was isolated from 61% of cases; 18 other genera of bacteria also were isolated. The disease was strongly gender-biased (P < 0.01) with 87% of cases occurring in males, and the overall prevalence among males was 4.9%. Cases were most common among antlered males (> or = 1 yr) with few cases among male fawns. Among antlered males, cases were seasonal, primarily occurring from September through April. Four hundred eighteen skulls from deer found dead in the field were examined from southeastern USA, and of the 119 used for further evaluation, 9% had characteristic lesions. Skulls from hunter-harvested males in the southeastern USA had a lesion prevalence of 1.4%. The similarity of disease prevalence among male deer found dead in the field (9.0%) and deer examined as southeastern diagnostic laboratory cases (8.4%) suggests that this disease accounts for slightly < 10% of the natural mortality for yearling and adult male white-tailed deer in the southeastern region. The strong bias for occurrence among males suggests this disease may affect quality deer management strategies.     

Effectiveness of Spayvac for reducing white-tailed deer fertility

Overabundant white-tailed deer (Odocoileus virginianus) populations have been reported in many urban and suburban communities across the United States. Large populations of deer can potentially increase the risk of human-wildlife conflicts, such as deer-vehicle collisions, transmission of disease to humans, and vegetation damage. In 2003, efforts to control white-tailed deer numbers were initiated at the National Aeronautical and Space Agency's (NASA) Lyndon B. Johnson Space Center (JSC) in Houston, Texas, using the long-lasting, single-dose contraceptive SpayVac. Our objectives were to evaluate the effectiveness of SpayVac for reducing white-tailed deer fertility and determine the partial cost for treatment. Between 2003 and 2004, we monitored 45 adult female deer (34 treated with SpayVac, 11 controls treated with a placebo). Fawning rate over 2 yr for deer treated with SpayVac >30 days prior to the rut was 0% (n=31), whereas the fawning rate for control deer was 78% (n=11). Inoculation 1 mo prior to the breeding season was sufficient time to achieve fertility control. We conclude that SpayVac can effectively reduce the fertility of urban white-tailed deer.