Survival,Movements, and Reproduction of Translocated Greater Sage-Grouse in Strawberry Valley,Utah

Abstract Translocations of greater sage-grouse (Centrocercus urophasianus) have been attempted in 7 states and one Canadian province with very little success. To recover a small remnant population and test the efficacy of sage-grouse translocations, we captured and transported 137 adult female sage-grouse from 2 source populations to a release site in Strawberry Valley, Utah, USA, during March-April 2003–2005. The resident population of sage-grouse in Strawberry Valley was approximately 150 breeding birds prior to the release. We radiomarked each female and documented survival, movements, reproductive effort, flocking with resident grouse, and lek attendance. We used Program MARK to calculate annual survival of translocated females in the first year after release, which averaged 0.60 (95% CI = 0.515-0.681). Movements of translocated females were within current and historic sage-grouse habitat in Strawberry Valley, and we detected no grouse outside of the study area. Nesting propensity for first (newly translocated) and second (surviving) year females was 39% and 73%, respectively. Observed nest success of all translocated females during the study was 67%. By the end of their first year in Strawberry Valley, 100% of the living translocated sage-grouse were in flocks with resident sage-grouse. The translocated grouse attended the same lek as the birds with which they were grouped. In 2006, the peak male count for the only remaining active lek in Strawberry Valley was almost 4 times (135 M) the 6-year pretranslocation (1998–2003) average peak attendance of 36 males (range 24–50 M). Translocations can be an effective management tool to increase small populations of greater sage-grouse when conducted during the breeding season and before target populations have been extirpated.     

Natural and experimental West Nile virus infection in five raptor species

We studied the effects of natural and/or experimental infections of West Nile virus (WNV) in five raptor species from July 2002 to March 2004, including American kestrels (Falco sparverius), golden eagles (Aquila chrysaetos), red-tailed hawks (Buteo jamaicensis), barn owls (Tyto alba), and great horned owls (Bubo virginianus). Birds were infected per mosquito bite, per os, or percutaneously by needle. Many experimentally infected birds developed mosquito-infectious levels of viremia (>10(5) WNV plaque forming units per ml serum) within 5 days postinoculation (DPI), and/ or shed virus per os or per cloaca. Infection of organs 15-27 days postinoculation was infrequently detected by virus isolation from spleen, kidney, skin, heart, brain, and eye in convalescent birds. Histopathologic findings varied among species and by method of infection. The most common histopathologic lesions were subacute myocarditis and encephalitis. Several birds had a more acute, severe disease condition represented by arteritis and associated with tissue degeneration and necrosis. This study demonstrates that raptor species vary in their response to WNV infection and that several modes of exposure (e.g., oral) may result in infection. Wildlife managers should recognize that, although many WNV infections are sublethal to raptors, subacute lesions could potentially reduce viability of populations. We recommend that raptor handlers consider raptors as a potential source of WNV contamination due to oral and cloacal shedding.     

Nest Predation of Greater Sage-Grouse in Relation to Microhabitat Factors and Predators

ABSTRACT Nest predation is a natural component of greater sage-grouse (Centrocercus urophasianus) reproduction, but changes in nesting habitat and predator communities may adversely affect grouse populations. We used a 2-part approach to investigate sage-grouse nest predation. First, we used information criteria to compare nest survival models that included indices of common raven (Corvus corax) abundance with other survival models that consisted of day of incubation, grouse age, and nest microhabitat covariates using measurements from 77 of 87 sage-grouse nests. Second, we used video monitoring at a subsample of 55 of 87 nests to identify predators of depredated nests (n = 16) and evaluated the influence of microhabitat factors on the probability of predation by each predator species. The most parsimonious model for nest survival consisted of an interaction between day of incubation and abundance of common ravens (w_{ravenXincubation day} = 0.67). An estimated increase in one raven per 10-km transect survey was associated with a 7.4% increase in the odds of nest failure. Nest survival was relatively lower in early stages of incubation, and this effect was strengthened with increased raven numbers. Using video monitoring, we found the probability of raven predation increased with reduced shrub canopy cover. Also, we found differences in shrub canopy cover and understory visual obstruction between nests depredated by ravens and nests depredated by American badgers (Taxidea taxus). Increased raven numbers have negative effects on sage-grouse nest survival, especially in areas with relatively low shrub canopy cover. We encourage wildlife managers to reduce interactions between ravens and nesting sage-grouse by managing raven populations and restoring and maintaining shrub canopy cover in sage-grouse nesting areas.     

Use of Implanted Radiotransmitters to Estimate Survival of Greater Sage-Grouse Chicks

ABSTRACT Reduced chick survival has been implicated in declines of greater sage-grouse (Centrocercus urophasianus) populations. Because monitoring survival of unmarked sage-grouse chicks is difficult, radiotelemetry may be an effective technique to estimate survival rates, identify causes of mortality, and collect ecological data. Previous studies have used subcutaneous implants to attach radiotransmitters to hatchlings of several species of birds with precocial young. Previous researchers who used subcutaneous implants in free-ranging populations removed chicks from the capture location and implanted transmitters at an alternate site. Because logistics precluded removing newly hatched greater sage-grouse chicks from the field, we evaluated a method for implanting transmitters at capture locations. We captured 288 chicks from 52 broods and monitored 286 radiomarked chicks daily for 28 days following capture during May and June 2001–2002. Two (>1%) chicks died during surgery and we did not radiomark them. At the end of the monitoring period, 26 chicks were alive and 212 were dead. Most (98%, 207/212) radiomarked chick mortality occurred < 21 days posthatch and predation (82%, 174/212) was the primary cause of death. Necropsies of 22 radiomarked chicks did not indicate inflammation or infection from implants, and they were not implicated in the death of any chicks. Fate of 48 chicks was unknown because of transmitter loss (n = 16), radio failure (n = 29), and brood mixing (n = 3). Overall, the 28-day chick survival rate was 0.220 (SE = 0.028). We found that mortalities related to the implant procedure and transmitter loss were similar to rates reported by previous researchers who removed chicks from capture sites and implanted transmitters at an alternate location. Subcutaneous implants may be a useful method for attaching transmitters to newly hatched sage-grouse chicks to estimate survival rates, identify causes of mortality, and collect ecological data.     

Gamma interferon plays a crucial early antiviral role in protection against West Nile virus infection

West Nile virus (WNV) causes a severe central nervous system (CNS) infection in humans, primarily in the elderly and immunocompromised. Prior studies have established an essential protective role of several innate immune response elements, including alpha/beta interferon (IFN-alpha/beta), immunoglobulin M, gammadelta T cells, and complement against WNV infection. In this study, we demonstrate that a lack of IFN-gamma production or signaling results in increased vulnerability to lethal WNV infection by a subcutaneous route in mice, with a rise in mortality from 30% (wild-type mice) to 90% (IFN-gamma(-/-) or IFN-gammaR(-/-) mice) and a decrease in the average survival time. This survival pattern in IFN-gamma(-/-) and IFN-gammaR(-/-) mice correlated with higher viremia and greater viral replication in lymphoid tissues. The increase in peripheral infection led to early CNS seeding since infectious WNV was detected several days earlier in the brains and spinal cords of IFN-gamma(-/-) or IFN-gammaR(-/-) mice. Bone marrow reconstitution experiments showed that gammadelta T cells require IFN-gamma to limit dissemination by WNV. Moreover, treatment of primary dendritic cells with IFN-gamma reduced WNV production by 130-fold. Collectively, our experiments suggest that the dominant protective role of IFN-gamma against WNV is antiviral in nature, occurs in peripheral lymphoid tissues, and prevents viral dissemination to the CNS.     

West Nile Virus Infection in American Robins: New Insights on Dose Response

West Nile virus (WNV) is a vector-borne pathogen that was first detected in the United States in 1999. The natural transmission cycle of WNV involves mosquito vectors and avian hosts, which vary in their competency to transmit the virus. American robins are an abundant backyard species in the United States and appear to have an important role in the amplification and dissemination of WNV. In this study we examine the response of American robins to infection with various WNV doses within the range of those administered by some natural mosquito vectors. Thirty American robins were assigned a WNV dosage treatment and needle inoculated with 10^0.95 PFU, 10^1.26 PFU, 10^2.15 PFU, or 10^3.15 PFU. Serum samples were tested for the presence of infectious WNV and/or antibodies, while oral swabs were tested for the presence of WNV RNA. Five of the 30 (17%) robins had neutralizing antibodies to WNV prior to the experiment and none developed viremia or shed WNV RNA. The proportion of WNV-seronegative birds that became viremic after WNV inoculation increased in a dose dependent manner. At the lowest dose, only 40% (2/5) of the inoculated birds developed productive infections while at the highest dose, 100% (7/7) of the birds became viremic. Oral shedding of WNV RNA followed a similar trend where robins inoculated with the lower two doses were less likely to shed viral RNA (25%) than robins inoculated with one of the higher doses (92%). Viremia titers and morbidity did not increase in a dose dependent manner; only two birds succumbed to infection and, interestingly, both were inoculated with the lowest dose of WNV. It is clear that the disease ecology of WNV is a complex interplay of hosts, vectors, and viral dose delivered.     

Migrating Birds as Dispersal Vehicles for West Nile Virus

Whereas migrating birds have been implicated in the spread of West Nile virus (WNV), there is no direct evidence of birds actively migrating while infectious. The role of birds in WNV dispersal is difficult to assess in the field. However, this role can be evaluated experimentally because birds in migratory disposition display increased locomotor activity or restlessness under captive conditions. We tested the following hypotheses: (1) migrating passerine birds continue to exhibit migratory activity while infectious with WNV and (2) the migratory state of the individual affects the magnitude of viremia. We examined the migratory activity of two neoarctic-neotropical passerine migrants, Swainson’s thrush (Catharus ustulatus) and gray catbird (Dumetella carolinensis), during acute WNV infection. All gray catbirds and six of nine Swainson’s thrushes exhibited migratory activity while infectious. Moreover, migratory status did not appear to influence viremia titers, as might be expected if individuals were immunosuppressed during migration. Therefore, we demonstrate that migrating passerine birds are potential dispersal vehicles for WNV.     

Blood parasites in sage-grouse from Nevada and Oregon

Peripheral blood smears from 196 adult and yearling female greater sage-grouse (Centrocercus urophasianus) were examined for blood parasites (167 from the breeding and 29 from the brood-rearing season) to determine prevalence of blood parasites, to attempt to correlate infection with chick survival, and to establish base-line values of prevalence in sage-grouse from Nevada and Oregon (USA). Birds were captured and released on two study areas during 1999-2001; Sheldon National Wildlife Refuge (SNWR) in northwestern Nevada, and Hart Mountain National Antelope Refuge (HMNAR) in southeastern Oregon. Birds from a third study area, Beaty's Butte grazing allotment (BB) in southeastern Oregon, were sampled in 2000 and 2001. Overall, 19 birds (10%) were positive for Leucocytozoon lovati (= L. bonasae), 1 (0.5%) for Plasmodium pedioecetii, and 2 (1%) for microfilariae. Although prevalence of L. lovati on HMNAR was 39% during the breeding season in 1999 and 100% during the brood-rearing season in 2000, statistically, prevalence of L. lovati among study areas and years was not different. However, there were statistical differences between capture periods. Overall, 31% of the hens were positive for L. lovati during the brood-rearing season compared to 6% during the breeding season. There was no difference in packed cell volume between infected and non-infected birds and no difference between age-classes. However, mean sage-grouse productivity on HMNAR was higher (1.6 chicks/hen) for non-infected (n = 10) compared to infected hens (0.7 chicks/hen; n = 7), during 1999. Based on these limited observations on HMNAR in 1999, the possible effects that L. lovati may have on young sage-grouse could be detrimental to sage-grouse populations in Nevada and Oregon.     

Mosquito saliva causes enhancement of West Nile virus infection in mice

West Nile virus (WNV) is transmitted to vertebrate hosts primarily by infected Culex mosquitoes. Transmission of arboviruses by the bite of infected mosquitoes can potentiate infection in hosts compared to viral infection by needle inoculation. Here we examined the effect of mosquito transmission on WNV infection and systematically investigated multiple factors that differ between mosquito infection and needle inoculation of WNV. We found that mice infected with WNV through the bite of a single infected Culex tarsalis mosquito exhibited 5- to 10-fold-higher viremia and tissue titers at 24 and 48 h postinoculation and faster neuroinvasion than mice given a median mosquito-inoculated dose of WNV (10(5) PFU) by needle. Mosquito-induced enhancement was not due to differences in inoculation location, because additional intravenous inoculation of WNV did not enhance viremia or tissue titers. Inoculation of WNV into a location where uninfected mosquitoes had fed resulted in enhanced viremia and tissue titers in mice similar to those in mice infected by a single infected mosquito bite, suggesting that differences in where virus is deposited in the skin and in the virus particle itself were not responsible for the enhanced early infection in mosquito-infected mice. In addition, inoculation of mice with WNV mixed with salivary gland extract (SGE) led to higher viremia, demonstrating that mosquito saliva is the major cause of mosquito-induced enhancement. Enhanced viremia was not observed when SGE was inoculated at a distal site, suggesting that SGE enhances WNV replication by exerting a local effect. Furthermore, enhancement of WNV infection still occurred in mice with antibodies against mosquito saliva. In conclusion, saliva from C. tarsalis is responsible for enhancement of early WNV infection in vertebrate hosts.     

Alpha/beta interferon protects against lethal West Nile virus infection by restricting cellular tropism and enhancing neuronal survival

West Nile virus (WNV) is a mosquito-borne flavivirus that is neurotropic in humans, birds, and other animals. While adaptive immunity plays an important role in preventing WNV spread to the central nervous system (CNS), little is known about how alpha/beta interferon (IFN-alpha/beta) protects against peripheral and CNS infection. In this study, we examine the virulence and tropism of WNV in IFN-alpha/beta receptor-deficient (IFN- alpha/betaR-/-) mice and primary neuronal cultures. IFN-alpha/betaR-/- mice were acutely susceptible to WNV infection through subcutaneous inoculation, with 100% mortality and a mean time to death (MTD) of 4.6 +/- 0.7 and 3.8+/- 0.5 days after infection with 10(0) and 10(2) PFU, respectively. In contrast, congenic wild-type 129Sv/Ev mice infected with 10(2) PFU showed 62% mortality and a MTD of 11.9 +/- 1.9 days. IFN-alpha/betaR-/- mice developed high viral loads by day 3 after infection in nearly all tissues assayed, including many that were not infected in wild-type mice. IFN-alpha/betaR-/- mice also demonstrated altered cellular tropism, with increased infection in macrophages, B cells, and T cells in the spleen. Additionally, treatment of primary wild-type neurons in vitro with IFN-beta either before or after infection increased neuronal survival independent of its effect on WNV replication. Collectively, our data suggest that IFN-alpha/beta controls WNV infection by restricting tropism and viral burden and by preventing death of infected neurons.     

Vγ4+ T cells regulate host immune response to West Nile virus infection

The Vγ4(+) cells, a subpopulation of peripheral γδ T cells, are involved in West Nile virus (WNV) pathogenesis, but the underlying mechanism remains unclear. In this study, we found that WNV-infected Vγ4(+) cell-depleted mice had lower viremia and a reduced inflammatory response in the brain. The Vγ4(+) cells produced IL-17 during WNV infection, but blocking IL-17 signaling did not affect host susceptibility to WNV encephalitis. We also noted that there was an enhanced magnitude of protective splenic Vγ1(+) cell expansion in Vγ4(+) cell-depleted mice compared to that in controls during WNV infection. In addition, Vγ4(+) cells of WNV-infected mice had a higher potential for producing TGF-β. The γδ T cells of WNV-infected Vγ4(+) cell-depleted mice had a higher proliferation rate than those of WNV-infected controls upon ex vivo stimulation with anti-CD3, and this difference was diminished in the presence of TGF-β inhibitor. Finally, Vγ4(+) cells of infected mice contributed directly and indirectly to the higher level of IL-10, which is known to play a negative role in immunity against WNV infection. In summary, Vγ4(+) cells suppress Vγ1(+) cell expansion via TGF-β and increase IL-10 level during WNV infection, which together may lead to higher viremia and enhanced brain inflammation.     

Survival of resident and translocated greater sage-grouse in Strawberry Valley,Utah: A 13-year study

Survival of greater sage-grouse (Centrocercus urophasianus) has been well described in large populations across the species range. Very little published information exists, however, on survival rates of translocated sage-grouse or grouse from a long-term (>10 yr) study. Our objectives were to estimate seasonal and annual survival rates; assess differences in survival between resident and translocated, adult and yearling, and male and female sage-grouse; identify environmental and behavioral factors associated with survival; and assess the influence of mammalian predator control on survival rates of radio-marked sage-grouse in Strawberry Valley, Utah from 1998 to 2010. We used a 2-stage model selection approach using Akaike's Information Criterion corrected for sample size (AIC_c) with known-fate models in Program MARK to evaluate the influences of seasonal, annual, demographic, and behavioral effects on survival rates of sage-grouse. We captured and fitted 535 individual sage-grouse (male and female, resident and translocated) with radio transmitters over a 13-year period and monitored them weekly. The top model of survival, which accounted for 22% of the AIC_c weight, included 3 seasons that varied by year where rates were influenced by residency, sex, and whether a female initiated a nest. A group-level covariate for the number of canids killed each year received some support as this variable improved model fit compared to identical models without it, although confidence intervals around β estimates overlapped zero slightly. All other demographic or environmental variables showed little or no support. Annual estimates of survival for females ranged between 28% and 84% depending on year and translocation source. Survival was consistently highest during the fall–winter months with a mean monthly survival rate of 0.97 (95% CI = 0.96–0.98). The lack of a control site and other potential confounding factors limit the extent of our inference with respect to predator control. Nonetheless, we suggest managers consider enhancing nesting habitat, translocating sage-grouse, and possibly controlling predators to improve survival rates of sage-grouse. © The Wildlife Society, 2013     

Effects of post-release movements on survival of translocated sage-grouse

Translocation is a vital tool in conservation and recovery programs, and knowledge of factors that determine demographic rates of translocated organisms is important for assessing the efficacy of translocations. Greater sage-grouse (Centrocercus urophasianus) have been the subject of recent translocation efforts because of their declining range and their usefulness as an umbrella species for conservation. Using a long-term data set on sage-grouse in central Washington, USA, we compared movement and demographic rates of translocated and resident birds. Because newly translocated birds experience physiological stress during translocation and are released in unfamiliar habitat, we hypothesized their demographic rates would differ from residents. We analyzed 18 years of radio-tracking data acquired from resident, newly translocated (<1 yr post-translocation; T1), and previously translocated (>1 yr post-translocation; T2) sage-grouse between 1989 and 2017 to estimate movement rates, survival, and productivity. Newly translocated sage-grouse exhibited farther daily movements (0.58 km/day) and smaller 95% home ranges (89 km²) than residents and previously translocated birds. Daily movements and sex influenced survival, but survival did not differ according to residency status. Furthermore, birds that survived to a second year after translocation exhibited shorter daily movements compared to their first year ( = −0.727 ± 0.157 [SE]), which corresponded with increased survival the second year (T1 = 0.526, T2 = 0.610). This decrease in movements and increase in survival the second year was not apparent in the control group of resident birds, indicating a possible behavioral link to survival of newly translocated sage-grouse. Most productivity metrics were similar for translocated and resident birds, except for nest propensity (i.e., nest initiation rate), which was lower for newly translocated birds (35%) compared to residents and previously translocated birds. Our results reveal that translocated sage-grouse exhibit temporary differences in some demographic parameters in their first year, which later align with those of resident birds in subsequent years. Similarities in adult and nest survival according to residency status further suggest that translocation may prove to be a viable tool for restoring and conserving this species. Continued declines in sage-grouse populations in Washington, however, indicate that habitat conversion and fragmentation may be reducing demographic rates of residents and translocated birds, which warrants further study. © 2019 The Wildlife Society.     

Induction of neutralizing antibodies in reindeer (Rangifer tarandus) after administration of a killed West Nile virus vaccine

In 2002, West Nile virus (WNV) infection with clinical neurologic disease and encephalomyelitis was described in reindeer (Rangifer tarandus). The susceptibility of reindeer to WNV prompted questions concerning vaccination of reindeer to prevent WNV infection. Between January and April 2003, eleven 2-4-yr-old, castrated male reindeer, some of which had antibody titers suggestive of prior exposure to WNV, were vaccinated three times at 4-wk intervals with a commercially available vaccine approved for use in horses. No adverse reactions to vaccination were noted. All vaccinated reindeer developed high neutralizing antibody titers to WNV, as determined by the plaque reduction neutralization test. Reindeer without antibody titers from previous natural exposure to WNV required a primary vaccination and one or two booster vaccinations for development of neutralizing antibody to WNV. Protective efficacy of vaccination was not evaluated. Vaccination of reindeer for WNV may be warranted in certain circumstances combined with management practices to limit exposure to potential vectors.     

Environmental risk factors associated with West Nile virus clinical disease in Florida horses

The objective of this study was to examine the extrinsic risk factors of West Nile virus (WNV) clinical disease in Florida horses as established from confirmed and negative horses tested within the state from 2001 to 2003. An Arboviral Case Information Form (ACF) was submitted by a referring veterinarian at the time of testing to the Florida Department of Agriculture and Consumer Services on every horse suspected of a viral encephalitis in Florida. A follow‐up survey that focused on arbovirus prevention and farm ecology was created and mailed to the owner of each tested horse. Data from the follow‐up survey indicated peak WNV prevalence in the late summer months in Florida. Quarter horses were the most commonly affected breed. The WNV vaccine was highly protective and natural water on the property also had a protective association. Factors that increased the risk of WNV to horses were the use of fans and a stable construction of solid wood or cement. Some risk indicators were dead birds on the property and other ill animals on the property. Data from this retrospective study have helped identify factors associated with WNV transmission in equines in Florida. Horses that have not been vaccinated and show clinical signs of arboviral infection from June to November should be tested for WNV. Horses that have been vaccinated and show clinical signs should be tested when the vaccination was administered within 1 month or greater than 6 months prior to the onset of clinical symptoms associated with WN infection.     

Infection and injury of neurons by West Nile encephalitis virus

West Nile virus (WNV) infects neurons and leads to encephalitis, paralysis, and death in humans, animals, and birds. We investigated the mechanism by which neuronal injury occurs after WNV infection. Neurons in the anterior horn of the spinal cords of paralyzed mice exhibited a high degree of WNV infection, leukocyte infiltration, and degeneration. Because it was difficult to distinguish whether neuronal injury was caused by viral infection or by the immune system response, a novel tissue culture model for WNV infection was established in neurons derived from embryonic stem (ES) cells. Undifferentiated ES cells were relatively resistant to WNV infection. After differentiation, ES cells expressed neural antigens, acquired a neuronal phenotype, and became permissive for WNV infection. Within 48 h of exposure to an exceedingly low multiplicity of infection (5 x 10(-4)), 50% of ES cell-derived neurons became infected, producing nearly 10(7) PFU of infectious virus per ml, and began to die by an apoptotic mechanism. The establishment of a tractable virus infection model in ES cell-derived neurons facilitates the study of the molecular basis of neurotropism and the mechanisms of viral and immune-mediated neuronal injury after infection by WNV or other neurotropic pathogens.     

West Nile Virus and California Breeding Bird Declines

Since it was first detected in 1999, West Nile virus (WNV) quickly spread, becoming the dominant vector-borne disease in North America. Sometimes fatal to humans, WNV is even more widespread among birds, with hundreds of species known to be susceptible to WNV infection in North America alone. However, despite considerable mortality and local declines observed in American crows (Corvus brachyrhynchos), there has been little evidence of a large regional association between WNV susceptibility and population declines of any species. Here we demonstrate a correlation between susceptibility to WNV measured by large-scale testing of dead birds and two indices of overall population change among bird species following the spread of WNV throughout California. This result was due primarily to declines in four species of Corvidae, including all species in this family except common ravens (Corvus corax). Our results support the hypothesis that susceptibility to WNV may have negative population consequences to most corvids on regional levels. They also provide confirmation that dead animal surveillance programs can provide important data indicating populations most likely to suffer detrimental impacts due to WNV.     

Using Human-Imprinted Chicks to Evaluate the Importance of Forbs to Sage-Grouse

Abstract Although several studies have indicated the importance of forbs in brood habitats, no studies have quantified direct effects of the amount of forb cover on sage-grouse (Centrocercus urophasianus) chicks. In 2002 and 2003, we conducted field experiments in Middle Park and Moffat County, Colorado, USA, respectively. Our objective was to quantify effects of 3 levels of forb cover in brood habitat on mass gain and feather growth of human-imprinted sage-grouse chicks. The results indicate that increasing forb cover in brood areas with <20% forb cover may lead to increased chick survival and grouse productivity.     

Territorial status and survival in red grouse Lagopus lagopus scoticus: hope for the doomed surplus?

A previous study of survival in territorial and non-territorial red grouse Lagopus lagopus scoticus conducted between 1957 and 1967 found that territorial status in the autumn pre-determined over-winter survival. A very high proportion of territorial birds survived and virtually all non-territorial birds died or emigrated. We tested the hypothesis that over-winter survival was dependent on territorial status within four grouse populations in Scotland between 1986 and 1993. In contrast to the previous study, 66% of non-territorial birds survived over winter compared to approximately 70% of territorial birds. There was no significant effect of territorial status on the survival estimates. Moreover, some of the birds considered to be non-territorial during autumn went on to successfully raise a brood. We suggest that on our study sites, territory ownership in autumn did not greatly influence over-winter survival, and territorial behaviour did not determine breeding density as previously supposed. We postulate differences with other studies may reflect variations in scale and predation pressure.