drawing of deer

Chronic Wasting Disease Management Plan

Texas Parks and Wildlife Department
Texas Animal Health Commission
August 2020

The following management plan will guide Texas Parks and Wildlife Department (TPWD) and Texas Animal Health Commission (TAHC) in addressing risks, developing management strategies, and protecting big game resources from chronic wasting disease (CWD) in captive and free-ranging cervid populations in the state of Texas. Both agencies recognize the need for full cooperation and partnership among government agencies, conservation organizations, private landowners, hunters, and the general public in managing CWD in Texas. CWD is a reportable disease and TAHC has authority to require reporting of this disease in exotic livestock including elk, red deer, sika deer and their hybrids, and for overseeing a voluntary herd certification program for interstate movement of CWD susceptible species. TPWD has regulatory authority for free-ranging white-tailed deer and mule deer, and both agencies have regulatory authority regarding certain disease surveillance and movement qualification standards.

This management plan is intended to be dynamic; management strategies described within are likely to change as both the epidemiology and management of this disease become better understood through time. Thus, more specific, science-based responses may be developed and incorporated into this plan following further discoveries of CWD or more impactful management techniques. Three major goals of this CWD management plan are:

  • Manage for healthy free-ranging and captive white-tailed deer, mule deer, and other susceptible species in Texas.
  • Establish and maintain stakeholder support for CWD management through effective outreach and communication.
  • Minimize direct and indirect impacts of CWD to hunting, hunting related economies, and conservation in Texas.

Background

Chronic wasting disease is a transmissible neurological disease in the family of diseases known as transmissible spongiform encephalopathies (TSEs). Other TSE diseases include bovine spongiform encephalopathy (BSE) in cattle (“mad cow” disease), scrapie in sheep, feline spongiform encephalopathy (FSE) in cats, and Creutzfeldt-Jakob disease (CJD) and variant (vCJD) in humans, as well as others. CWD, like the other diseases in the TSE family, has no cure and is invariably fatal. Research suggests that TSEs are caused by a misfolded protein (“prion”) that replicates and infects other normal proteins (Prusiner 1998, Fryer and McLean 2011). Experts on prion diseases believe that these malformed proteins accumulate in lymphoid and nervous tissues of susceptible cervids and eventually cause severe degradation (e.g., significant holes in the brain). While other theories as to the cause have been proposed (Bastian at al. 2017), the preponderance of scientific evidence available supports prions as the causative agent of TSEs.

Other cofactors cannot be ruled out but have not been substantiated. CWD is aptly named for the symptoms of the disease: appetite loss, weight loss (hence the name “wasting disease”), listlessness, excessive drooling, blank stares, decreased awareness, and behavioral changes (Williams 2005).

The origins of CWD are unknown, but it was first recognized in 1967 in captive mule deer in a Colorado Parks and Wildlife captive wildlife research facility in Fort Collins, Colorado. This disease received relatively little national attention until it was discovered over 900 miles away in free-ranging white-tailed deer in southern Wisconsin in early 2002. To date, CWD has been detected in free-ranging and/or captive cervids in 26 states and 3 Canadian provinces (Figure 1). This disease was first detected in Texas in July 2012 in the Hueco Mountains of northern El Paso and Hudspeth counties in far west Texas. In this case, two free-ranging mule deer tested positive during a targeted surveillance effort. CWD has since been detected in 4 white-tailed deer breeding facilities and associated release sites in Medina County, free ranging white-tailed deer in the same immediate area of Medina County, a captive white-tailed deer breeding facility in Lavaca County that received deer from the index captive facility, a captive white- tailed deer breeding facility in Kimble County, free ranging white-tailed deer, mule deer and elk in the northwestern Panhandle, and free ranging white-tailed deer in Val Verde County. Up to date information on CWD detections in Texas can be found at www.tpwd.texas.gov/cwd.

distribution of CWD in North America map, 2019
Figure 1. Distribution of CWD in North America, 2019.

Immunohistochemistry (IHC) is the confirmatory test to diagnose CWD by detecting CWD- associated prion protein (PrPCWD) in brain tissues (specifically in the obex of the medulla oblongata) or medial retropharyngeal lymph nodes (MRLN). Enzyme Linked Immunosorbent Assay (ELISA) is a more rapid test using the same tissues but is considered by USDA to be a screening test. TPWD and TAHC have incorporated live animal (ante-mortem) testing by IHC using tonsil biopsies, rectal biopsies and MRLN biopsies, in addition to required post-mortem testing to increase surveillance in permitted deer breeding facilities. Utilizing both types of testing provides more confidence that the disease would be detected if present. Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL) performs diagnostic testing on tissues collected from live animals since 2016 under an agreement authorized by the National Animal Health Laboratory Network (NAHLN). The current USDA CWD program standards reference the utilization of testing of rectoanal mucosa-associated lymphoid tissue (RAMALT) by IHC in CWD- exposed captive herds or epidemiologically linked herds as prescribed to allow qualified herds to be removed from quarantine. Research to validate ante-mortem tissues as valid indicators of disease when tested by IHC is ongoing as well as other novel test methods.

One characteristic of CWD is the extended preclinical stage where the animal looks and acts normally without demonstrating clinical signs. The diagnosis of the disease cannot be made by symptoms, since other diseases or afflictions can cause the animal to exhibit similar symptoms. Incubation periods, the time from exposure to development of clinical symptoms, in naturally exposed free-ranging deer are difficult to determine, but the average incubation period is thought to be in the range of two to four years (Williams 2005). The incubation period and the time it takes an animal to succumb to CWD likely varies based on method of exposure, intensity of prion exposure, genetics, and other factors. Death often occurs within months of clinical symptoms being exhibited (Williams and Miller 2002). Captive-deer research has recorded deaths of mule deer and white-tailed deer infected with CWD at 41 and 59 months, respectively (Miller and Wild 2004).

Despite considerable research on CWD during the past several decades, there are still knowledge gaps about the disease. CWD is known to occur via natural transmission in white- tailed deer, mule deer, black-tailed deer, red deer, sika deer, elk, reindeer, and moose, and experimentally in muntjac (Sohn et al. 2011, CWD Alliance 2012, Saunders et al. 2012). The discovery of multiple strains of CWD suggests potential for interspecies transmission (Belay et al. 2004, Barria et al. 2011). Therefore, several studies have simulated artificial transmission via intracerebral inoculation to other species including fallow deer, cattle, sheep, goats, mink, ferrets, squirrel monkeys, voles, and mice (Saunders et al. 2012). However, previous research indicates that CWD infection of livestock through natural transmission pathways is unlikely (Sigurdson 2008).

TSEs are usually acquired through exposure to infectious material, but some TSE prions appear spontaneously and sporadically. Some suspect that recent cases of CWD occurring in moose in Norway and Finland may be spontaneous (Pirisinu 2018), but data are lacking to suggest that any CWD in detections in North America are spontaneous occurrences (Chesebro 2004, Greenlee and Greenlee 2015).

The lack of interspecies transmission has been described as the species barrier phenomenon and ongoing research in this area is critical to truly understand this mechanism in order to assess the risk of spreading any TSE to other species (Greenlee and Greenlee, 2015). Currently, there is no indication of a documented transmission of CWD to a human (Sandberg et al. 2010, Apostol et al. 2011). Humans have been infected with BSE by consuming meat contaminated with specified risk materials; therefore, any potential risk to humans needs to be explored further (Bradley et al. 2006). Recognizing the fact that while the risk of human susceptibility to CWD is considered very low but not zero, the Center for Disease Control (CDC) modified their recommendations regarding (1) testing susceptible species harvested within a CWD endemic area, and (2) avoiding the consumption of venison from CWD-positive animals. The CDC’s recommendations can be found at www.cdc.gov/prions/cwd/prevention.html.

Transmission

There are two primary sources of exposure to CWD for uninfected deer: 1) CWD infected deer, and 2) a CWD contaminated environment (Williams et al. 2002, Miller et al. 2004, Mathiason et al. 2009). Prions are shed from infected animals in saliva, urine, blood, soft-antler material, and/or feces (Gough et al. 2010, Mathiason et al. 2009, Saunders et al. 2012, Tamguney et al. 2009). Infected individuals on the landscape serve as a reservoir for prions, which are continuously shed into the environment. Once shed, prions potentially can be maintained in soil and waterways for extended periods of time and can be taken up by plants (Rasmussen et al. 2014, Pritzkow et al. 2015) or infect cervids that occur in that same environment (Plummer et al. 2018). Research also indicates that tissues from infected carcasses can serve as a source of infection and contribute to environmental contamination (Miller et al. 2004). Intuitively, the presence of infected deer in one area over time would increase contact with infected animals and increase the number of infectious prions in that environment, thereby increasing the risk of disease transmission.

As CWD becomes established, prions occurring on the landscape may become the primary source of exposure for uninfected deer. Conversely, in areas where CWD is not established, and where the environment is relatively uncontaminated, direct animal contact is considered the most likely source of transmission of CWD to uninfected deer. In early stages of infection, the reduction of infected individuals may offer some control in limiting disease prevalence and distribution (Wasserberg et al. 2009, Almberg et al. 2011).

Decontamination of prion-contaminated surfaces and environments is challenging since these agents are resistant to standard sterilization methods as well as formalin, alcohol, heat, ultraviolet radiation, microwave irradiation, and ionizing radiation. Prions can also bind to stainless steel and plastic without losing infectivity (CFSPH, 2016). To date, there are no proven effective methods for cleaning and disinfecting facilities (Travis and Miller 2003). However, Kuznetsova et al. (2018) reported that high concentrations of the soil organic matter compound, humic acid, may reduce CWD infectivity. Also, Williams et al. (2019) reported that CWD prions on instruments and tools with limited organic material can be deactivated by exposure to strong bleach (NaClO) solution. The practical implications of this recent research may provide potential future mitigation strategies. Nonetheless, there are currently no known management strategies to successfully mitigate the risk of indirect transmission once an environment has been contaminated with infectious prions, and eradication of CWD is extremely unlikely in areas where CWD has been established for a long period of time.

Potential Implications of CWD

The number of states and provinces in which CWD has been discovered has steadily increased in the past decade, forcing many wildlife agencies, hunters, and stakeholders to confront the myriad of consequences and implications this disease presents. Implications of CWD are often centered on the potential impacts to wild cervid populations, most notably concerns for population impacts in infected herds. However, other possible direct and indirect impacts include:

  • economic losses related to CWD,
  • property devaluation,
  • hunter retention and recruitment,
  • hunter participation,
  • potential or perceived human health and safety concerns.

Disease eradication is expected to be nearly unattainable once established in a population, so surveillance and rapid response plans are critical. Disease prevention is the best approach to protecting cervid populations and avoiding the negative social and economic impacts of CWD (Sleeman & Gillin 2012).

Mortality rates of CWD infected deer are considerably higher than those of uninfected deer (Miller et al. 2008). The prevalence of CWD exceeds 20% and even 50% in some deer populations in Wisconsin, Colorado, and Wyoming (Saunders et al. 2012). Prevalence rates documented in mule deer near Boulder, CO were 41% for adult males and 20% for adult females. CWD is believed to have existed in that herd since at least 1985 and has coincided with a 45% decline in mule deer abundance over the following two decades, despite adequate habitat and no hunting (Miller et al. 2008). The South Converse Game Unit in Wyoming has prevalence rates exceeding 50% and has seen an approximate 50% decline in mule deer populations (Wyoming Game and Fish Department 2012). Because CWD is believed to spread relatively slowly when disease prevalence is low (Conner et al. 2007), long-term implications on population stability and productivity are likely of greater concern than short-term population impacts. Research conducted by Edmunds et al. (2016) suggests that CWD likely contributes to additive mortality in white-tailed deer populations. Other work suggest that population dynamics of this nature can be seen in populations of mule deer (Foley et al. 2016) and elk (Galloway et al. 2017, Monello et al. 2014).

Under many scenarios where CWD occurs at relatively low prevalence rates in relatively localized areas, hunter retention or displacement has not been a great concern for those state agencies (Petchenik 2003, Gigliotti 2004, Miller 2004, Needham et al. 2007, Zimmer et al. 2012). However, hunters are known to make decisions based on the balance of perceived risks and rewards associated with hunting (Vaske 2004, Needham et al. 2017). An increase in prevalence rate or disease distribution, or research indicating that CWD may be a human health risk, is expected to alter hunter behavior significantly, as these factors increase the risks (actual or perceived) involved with hunting (Needham et al. 2007, Vaske 2009, Zimmer 2012). Needham et al. (2007) found that this effect would be greatest among casual hunters, those who are new to hunting, or those who hunt occasionally. A significant decline of this population of hunters would have serious implications for future recruitment and retention, which would ultimately impact license sales and the hunting heritage of the state of Texas. Reduced license sales of a large magnitude would be detrimental for all state wildlife conservation programming, as this is a major source of funding for TPWD. A decline in hunters is also likely to impact rural towns and communities that derive economic benefits from big game hunting. Shifts in hunting locations could lead to reapportioning revenue to other areas of the state where CWD prevalence is not as high or where CWD has not been detected (Bishop 2004, Zimmer 2012). The risk of CWD is also likely to reduce economic stimulation from out-of-state hunters.

Active Disease Management

Since the recognition of CWD in the 1960’s there has been extensive research on different facets of the disease. However, effective management techniques for this unique disease are not well understood (Uehlinger et al. 2016). Many different strategies to combat CWD have been employed around the country with varying levels of success. For any hope of disease eradication, early detection of CWD infected animals is paramount. The time between introduction and detection of the disease is the most critical factor impacting an agency’s ability to control and possibly eradicate the disease. Once the landscape becomes a reservoir for CWD prions, mitigating the spread of the disease is likely the only possible course of action.

Population reductions may help reduce the dispersion of infected deer to non-infected areas. Severe population reductions proximate to the index case would likely be most effective in scenarios where CWD appears to have been recently introduced and has not likely become established in the environment (Brown et al. 2005). However, culling efforts have been less popular in areas where CWD is well established, as hunters and the general public eventually grow weary from intensive culling practices that continue indefinitely.

Eradication Attempts

There have been three recorded cases where CWD may have been eliminated from, or prevented from becoming established in a locality. In 2005, New York discovered CWD in two different captive herds during routine CWD surveillance efforts. They promptly initiated an intensive surveillance effort within 10 miles of the infected premises and detected CWD in two free-ranging deer. It appears that removal of those two deer at least temporarily prevented further spread of CWD, as the disease has not been detected in any additional deer despite intensive sampling through severe population reductions in subsequent years (Saunders et al. 2012, Minnesota DNR 2019). CWD surveillance continues in that area of the state and without any disease detections. Similarly, Minnesota Department of Natural Resources has yet to detect additional CWD-positive animals through aggressive surveillance actions in the years following their index case in Olmsted County in 2010, which was found in close association to a CWD-positive captive-elk facility (Minnesota DNR 2019). Lastly, CWD was detected in a single doe in Washburn County in northwestern Wisconsin in 2011, hundreds of miles from known endemic areas. No additional positives have been detected out of almost 3,000 additional deer that were sampled in that county from 2012-2017 (Minnesota DNR 2019). These three cases demonstrate that early detection may allow for appropriate management actions to prevent the disease from becoming established in the environment.

Control Attempts

Eradication is an unrealistic management option in areas of Wyoming, Colorado, and Wisconsin, where CWD has been established for many years. In these situations, major population reductions might not prevent animals from contracting CWD from the contaminated environment. Although, strategies to restrict or reduce the movements of free- ranging or captive cervids and carcass parts from CWD endemic areas may effectively reduce the spread of CWD. Strategic localized culling, in addition to traditional hunting, has been shown to stabilize CWD prevalence in Illinois white-tailed deer populations. Similar results were observed in Wisconsin until a severe reduction of their localized culling program occurred in 2007 (Manjerovic et al. 2014). Several states also employ other disease management strategies such as differential harvest strategies, prohibiting unnatural (i.e., man-induced) movements of deer or carcasses, a ban on baiting/feeding and urine-based attractants, and general education efforts to encourage responsible actions by hunters and other stakeholders (Gillin and Mawdsley 2018, CWD Alliance website 2019 and Michigan DNR, unpublished data), but the effectiveness of those management strategies is varied and in some cases speculative. Since baiting deer could improve harvest efficiency and aid population control efforts, this practice could be an effective disease management strategy.

Outreach and Education

A well-designed outreach and education plan is a critical component of this CWD management plan to keep Texas hunters and citizens informed on the most current information about CWD. Ensuring that accurate information is provided to hunters and other constituents is essential to facilitate understanding and compliance with management strategies designed to curtail disease expansion. Strategies designed to increase public awareness of CWD and the implications of CWD include:

  • Networking with natural resource professionals and encourage them to schedule CWD presentations with wildlife, hunting, or other conservation organizations as well as local civic groups.
  • Developing and distributing information to relevant businesses (e.g., taxidermists, processors, feed stores) and local radio, newspaper, and television media. Information may be designed to focus on specific issues of importance to landowners, hunters, meat processors, taxidermists, veterinarians, rehabilitators, feed companies, feeder manufacturers, and operators of captive deer and elk facilities. This information includes:
    • basic history and understanding of CWD;
    • CWD distribution, and status of knowledge of the disease (e.g., epidemiology, transmission, clinical signs, population effects);
    • other CWD related issues and cautions (e.g., carcass handling and proper carcass disposal, meat preparation and consumption, deer feeding); and
    • potential research and management actions.
  • Maintaining the TPWD and TAHC CWD webpages to provide the public with up-to-date disease information, research findings, management strategies, and other pertinent information.

The dissemination of accurate, factual information is important for establishing an understanding of the magnitude of risks posed by CWD. Spreading this information is also critical for gaining and maintaining support for active CWD management efforts (Stafford et al. 2006). False information may result in apathy toward CWD management among hunters, landowners, and other stakeholders, and possibly unnecessary panic among others. With the extent of private lands in Texas (~95%), landowners and hunters play a key role in helping TPWD and TAHC manage CWD. Uninformed constituents could unintentionally hasten the spread of CWD, for example, through transportation of live animals or their carcasses. Failure to keep these groups and others informed with relevant facts could influence the effective implementation and enforcement of disease management strategies (Vaske et al. 2006).

CWD in Texas

The first case of CWD in Texas was discovered in 2012 in free-ranging mule deer in the Hueco Mountains of far West Texas. CWD has since been detected in free-ranging mule deer, white- tailed deer, and elk in Dallam and Hartley counties, located in the northwest Panhandle. The first case of CWD in Texas white-tailed deer was found in a Medina County deer-breeding facility in 2015 as a result of routine disease monitoring. TPWD and TAHC have been working in collaboration to actively monitor this disease and minimize or mitigate its harmful effects. Each of the elements of this management plan will assist in achieving the goals of:

  • Manage for healthy free-ranging and captive white-tailed deer, mule deer, and other susceptible cervid species in Texas.
  • Establishing and maintaining stakeholder support for CWD management through effective outreach and communication.
  • Minimizing direct and indirect impacts of CWD to hunting, hunting related economies, and conservation in Texas.

This plan has included a rigorous, statewide surveillance program, as well as a protocol for action in the instance of a detection. The following section will outline the results of this surveillance effort, as well as standard responses to positive cases of CWD in free-ranging and captive deer herds. This section will also detail management options that other states have put into place and may merit consideration by the TPW Commission or the TAHC.

Surveillance Results

Effective CWD management is extremely dependent on accurate monitoring and surveillance. Thus, CWD sampling in Texas is based on a rigorous stratified survey design to account for the estimated disease risk in each Deer Management Unit (DMU). This design was informed by a risk assessment that considered the following factors:

  • the number of CWD samples collected in previous years;
  • the number of deer breeding facilities;
  • the number of Class III release sites (i.e., direct trace-outs from CWD positive facilities);
  • the proximity of a county to a known CWD site; and
  • the distance to the Texas border.

The data for each DMU were converted to a Z-score and scores for each risk category were then ranked. The sampling priorities were ranked independently within each ecoregion.

Surveillance efforts focused on white-tailed deer and mule deer (“deer” for the remainder of this sub-section), given that these are the most commonly hunted cervids in the state. Figure 2 illustrates the sampling goal for each DMU based on that risk assessment.

annual CWD sampling goals for each Deer Management Unit map
Figure 2. Annual CWD sampling goals for each Deer Management Unit.

TPWD received an average of approximately 2,300 “Not Detected” test results annually for free-ranging white-tailed deer and mule deer populations throughout the state from 2002 through the 2014-15 hunting season. Sampling intensity increased significantly following the June 2015 detection of CWD in a permitted deer breeding facility. This facility was known to have transferred deer extensively to and from other facilities and to release sites across the state. Since then, “Not Detected” test results have increased to an average of >13,000 free- ranging deer for each year from 2015-2019. Most of the free-ranging samples were collected from hunter-harvested deer, while the remaining samples were collected from various permitted activities, deer killed by vehicles, or collected from those exhibiting clinical symptoms.

CWD surveillance for permitted deer breeding facilities has also increased significantly since the index case was confirmed in June of 2015. Prior to that detection, deer breeding facilities were required to test only 20% of reported eligible-aged mortalities (i.e., deer ≥16 months of age) to maintain Movement Qualified (MQ) status. This resulted in an average of almost 1,700 "Not Detected" test results annually from May 2006 to August 2015. Surveillance requirements increased in 2016, to include at least 80% of reported eligible-aged mortalities and at least 3.6% of the eligible-aged herd size (which may involve ante-mortem sampling within herds that reported zero mortalities) to maintain MQ status. “Not Detected” test results were submitted for an annual average of ~4,500 postmortem samples for the following 4 years. The 2016-17 hunting season marked the first season in which CWD testing was required of any breeder-deer release sites, and that testing was required only of release sites considered to be of moderate or high relative risk, based on the CWD surveillance history of their source facilities. Release site testing ceased to exist for all compliant release sites on March 1, 2019. Additionally, almost 34,000 ante-mortem samples were collected through September 2019 either to 1) substitute for missed postmortem samples, or 2) achieve a TC 1 status, which could result in no required testing of deer harvested on recipient release sites.

Response Plans

Response Plan – Free-Ranging Populations

Implementation of the following disease-management strategies may be effective in CWD prevention as well as containment in CWD-positive areas where the disease has yet to be detected:

  • limiting unnatural movement of live CWD susceptible species; and
  • limiting the movement of carcass parts to prevent the possibility of spreading infectious CWD material.

Upon detection of CWD in a free-ranging animal, TPWD and TAHC will create geographically distinct surveillance and containment zones based on:

  • known current geographic extent of the disease;
  • home-range and movement patterns of the species affected;
  • past sampling in the area; and
  • population distribution.

In most cases, the boundaries for these zones will be delineated by physical landmarks that are easily recognized by landowners and hunters (i.e., roads, rivers, etc.). Management strategies within these zones will be designed to reduce the risk of spreading the disease to areas outside of the zones by:

  • further limiting unnatural movement of live CWD susceptible species;
  • further limiting the movement of carcass parts to prevent the possibility of spreading infectious CWD material;
  • managing cervid populations at or below carrying capacity of the habitat; and
  • increasing surveillance to determine the extent and prevalence of the disease.

Containment Zone: A geographic area in this state within which CWD has been detected or the TPWD and TAHC have determined, using the best available science and data, CWD detection is probable, and where the following management practices will be conducted:

  • mandatory testing of harvested CWD susceptible species as necessary to determine disease prevalence in the area;
  • mandatory restrictions on removing from the zone those carcass parts that are known to concentrate infectious material, primarily brain, spinal cord and viscera; and
  • restrictions on susceptible species movements out of and within the zone.

Surveillance Zone: A geographic area in this state that is in close proximity to a known CWD area and where TPWD and TAHC have determined, using the best available science and data, that the presence of CWD could reasonably be expected, and where the following management practices will be conducted:

  • mandatory testing of CWD susceptible species harvested in the zone to achieve early detection and containment if the disease is present;
  • mandatory restrictions on removing from the zone those carcass parts that are known to concentrate infectious material, primarily brain, spinal cord and viscera; and
  • restrictions on susceptible species movements involving practices and facilities that pose a high risk of moving the disease.

The delineations and rules pertaining to these zones will be reviewed as needed by TPWD and TAHC, with stakeholder input, and changes made accordingly from information gained through surveillance and new scientific knowledge.

Collection of samples from road kills and clinical animals shall remain a high priority throughout the state. Protocols and regulations to allow for collection of samples from clinical animals by staff, landowners and hunters will be developed. TPWD and TAHC may request assistance from local and state law enforcement agencies, local government entities, TXDOT, Texas Agri-Life Extension, local landowners, hunters, and CWD certified sample collectors in gathering samples from road kills or clinical animals.

Response Plan – Captive Cervid Facilities

Upon detection of CWD in a captive cervid facility, TPWD and TAHC will:

  • Immediately place the affected facility under TAHC quarantine and change the facility’s official status to Not Movement Qualified (NMQ).
  • Initiate an epidemiological investigation to trace the translocation of captive cervids that may have come into contact with CWD-positive individuals or were in the CWD-positive facility. This includes determining herds that have received animals from or contributed animals to the CWD-positive herd within the past five years. These herds will then be placed under a TAHC hold order with TPWD NMQ status, as applicable.
  • TAHC and TPWD will work with the facility owners to develop testing plans and herd plans to outline subsequent steps to minimize the risk to other captive and free-ranging cervid populations. While a facility is under quarantine, elements of a testing plan or herd plan will be provided and will include the following key components as the best course to reduce the risk to other captive and free-ranging populations:
    • depopulation and post-mortem testing of animals in positive facilities;
    • euthanasia and testing of exposed animals in trace facilities; and
    • potential population reduction on associated properties and mandatory testing of hunter-harvested susceptible species.
  • For the length of the quarantine in a breeding facility and in situations where depopulation is delayed, the following components shall be incorporated:
    • increased surveillance including the mandatory submission of samples from all mortalities in a breeding facility;
    • increased biosecurity measures;
    • cleaning and disinfection protocols based on the most recent science;
    • proper carcass disposal;
    • fencing maintenance to prevent the ingress or egress of susceptible species; and
    • additional CWD mitigation efforts as determined by an epidemiological assessment.
  • Containment and Surveillance Zones may be created based on the criteria for free- ranging detection. In some instances, the herd plan may suffice for a Containment Zone based on the epidemiological assessment.

Potential Future Management Strategies

As previously stated, this plan is meant to be dynamic and evolving as we gain knowledge of the epidemiology and management of this disease. Management practices should be based on science. However, due to the length of time required to evaluate effects of management decisions with this disease, strategies may need to be implemented based on conventional disease models until new research findings provide alternative management strategies. Basic disease management practices to reduce the anthropogenic spread of the disease should be considered. The responsible agencies and the wildlife community would be negligent to not consider any management recommendation that might mitigate the spread of this disease in the long term.

Current management goals are to continue to implement strategies outlined in this plan to contain CWD where it currently exists in Texas. Commitment to sustained surveillance efforts outside of known CWD areas will also be critical for early detection, which may provide greater management options. TPWD and TAHC will continue to work together to limit the effects of this disease using science-based approaches and input from stakeholders. This plan will be continuously evaluated and revised as changes in the epidemiological situation and scientific information evolve.

Literature Cited

  • Almberg, E. S., P. C. Cross, C. J. Johnson, D. M. Heisey, and B. J. Richards. 2011. Modeling routes of chronic wasting disease transmission: environmental prion persistence promotes deer population decline and extinction. PLoS ONE. 6(5):e19896.
  • Barria, M. A., G. C. Telling, P. Gambetti, J. Mastrianni, C. Soto. 2011. Generation of a new form of human PrPSc in vitro by interspecies transmission from cervid prions. Journal of Biological Chemistry. 286:7490–5.
  • Bastian, F. O., J. Lynch, S. Hagius, X. Wu, G. McCormick, D. Luther, P. Elzner. 2017. Novel Spiroplasma Spp. Cultured From Brains and Lymph Nodes From Ruminants Affected With Transmissible Spongiform Encephalopathy. Journal of Neuropathology & Experimental Neurology. 77(1):64–73.
  • Belay, E. D., R. A. Maddox, E. S. Williams, M. W. Miller, P. Gambetti, and L. B. Schonberger. 2004.
  • Chronic wasting disease and potential transmission to humans. Emerging Infectious Disease Journal. 10(6). . Accessed 10 Apr 2012.
  • Bishop, R. C. 2004. The economic impacts of chronic wasting disease (CWD) in Wisconsin. Human Dimensions of Wildlife. 9(3):181-92.
  • Bradley, R.J., G.Collee, P.P.Liberski. 2006. Variant CJD (vCJD) and Bovine Spongiform (BSE): 10 and 20 years on: part 1. Folia Neuropathol 44(2): 93-101.
  • Brown, T. L., J. Shanahan, D. Decker, W. Siemer, P. Curtis, and J. Major. 2005. Response of hunters and the general public to the discovery of chronic wasting disease in deer in Oneida County, New York. Human Dimensions Research Unit, Department of Natural Resource Cornell University. Series 5-08.
  • Centers for Disease Control and Prevention. 2019 Chronic Wasting Disease (CWD) prevention webpage. https://www.cdc.gov/prions/cwd/prevention.html . Accessed 8 Apr 2019.
  • Chronic Wasting Disease Factsheet. 2016. The Center for Food Security and Public Health (CFSPH). webpage. http://www.cfsph.iastate.edu/Factsheets/pdfs/chronic_wasting_disease.pdf .Accessed 16 April 2020.
  • Chesebro, Bruce. 2004. A fresh look at BSE. Science. 305:1918-1921.
  • Chronic Wasting Disease Alliance. 2012. Homepage. . Accessed 4 Apr 2012.
  • Edmunds, D. R., M. J. Kauffman, B. A. Schumaker, F. G. Lindzey, W. E. Cook, T. J. Kreeger, R. G. Googan, and T. E. Cornish. (2016) Chronic Wasting Disease Drives Population Decline of White-Tailed Deer. PLoS ONE 11(8): e0161127.
  • Foley, A. M., D. G. Hewitt, C. A. DeYoung, R. W. DeYoung, and M. J. Schnupp. 2016. Modeled Impacts of Chronic Wasting Disease on White-Tailed Deer in a Semi-Arid Environment. PLoS ONE 11(10): e0163592
  • Fryer, H. R., and A. R. McLean. 2011. There is no safe dose of prions. PLoS ONE. 6(8):e23664.
  • Galloway, N. L., R. J. Monello, D. Brimeyer, E. Cole, and N. T. Hobbs. 2017. Model forecasting of the impacts of chronic wasting disease on the Jackson Hole elk herd. National Elk Refuge Final Report. National Park Service. 32 Pp.
  • Gigliotti, L. M. 2004. Hunters’ concerns about chronic wasting disease in South Dakota. Human Dimensions of Wildlife. 9:233-235.
  • Gillin, Colin M., and Mawdsley, Jonathan R. (eds.). 2018. AFWA Technical Report on Best Management Practices for Surveillance, Management and Control of Chronic Wasting Disease. Association of Fish and Wildlife Agencies, Washington, D. C. 111 pp.
  • Greenlee, J. J., and M. H. West Greenlee. 2015. The Transmissible Spongiform Encephalopathies of Livestock. ILAR Journal. 56(1): 7-25.
  • Gough, K.C., and B.C. Maddison. 2010. Prion transmission: Prion excretion and occurrence in the environment. Landes Bioscience Journal: Prion. 4:275–82.
  • Kuznetsova, A., C. Cullingham, D. McKenzie, and J. M. Aiken. (2018). Soil humic acids degrade CWD prions and reduce infectivity. PLoS Pathog 14(11): e1007414. https://doi.org/10.1371/journal.ppat.1007414
  • Mathiason, C. K., S. A. Hays, J. Powers, J. Hayes-Klug, J. Langenberg, et al. 2009. Infectious prions in pre- clinical deer and transmission of chronic wasting disease solely by environmental exposure. PLoS ONE. 4(6):e5916.
  • Manjerovic, M.B., M. L. Green, N. Mateus-Pinilla, J. Novakofski. 2014. The importance of localized culling in stabilizing chronic wasting disease prevalence in white-tailed deer populations. PREVET- 3436. . 113(1):139-45.
  • Miller, M. M., H. M. Swanson, L. L. Wolfe, F. G. Quartarone, S. L. Huwer, C. H. Southwick, P. M. Lukacs. 2008. Lions and Prions and Deer Demise. PLoS ONE. 3(12):e4019.
  • Miller, W., E. S. Williams, N. T. Hobbs, L. L. Wolfe. 2004. Environmental sources of prion transmission in mule deer. Emerging Infectious Disease Journal. 10(6). . Accessed 10 Apr 2012.
  • Monello, R., J. Powers, N. T. Hobbs, T. Spraker, M. Watry, and M. Wild. 2014. Survival and Population Growth of a Free-Ranging Elk Population with a Long History of Exposure to Chronic Wasting Disease. Journal of Wildlife Management. 78. 214-223. 10.1002/jwmg.665.
  • Needham, M. D., J. Vaske, M. P. Donnelly and M. J. Manfredo. 2007. Hunting specialization and its relationship to participation in response to chronic wasting disease. Journal of Leisure Research. 39(3):413-437.
  • Needham, M. D., J. J. Vaske, and J. D. Petit. 2017. Risk Sensitivity and Hunter Perceptions of Chronic Wasting Disease Risk and Other Hunting, Wildlife, and Health Risks. Human Dimensions of Wildlife. 22(3):197-216. DOI: 10.1080/10871209.2017.1298011.
  • Petchenik, J. B. 2003. Chronic wasting disease in Wisconsin and the 2002 hunting season: gun deer hunters’ first response. Wisconsin Department of Natural Resources, Bureau of Integrated Science Services, Madison, Wisconsin, USA.
  • Pirisinu L., L. Tran, B. Chiappini, I. Vanni, M. A. Di Bari, G. Vaccari, et al. 2018. Novel type of chronic wasting disease detected in moose (Alces alces), Norway. Emerging Infectious Disease Journal. 24(12). https://doi.org/10.3201/eid2412.180702
  • Plummer, I.H., Johnson, C.J., Chesney, A.R., Pedersen, J.A. and Samuel, M.D., 2018. Mineral licks as environmental reservoirs of chronic wasting disease prions. PloS one, 13(5), p.e0196745.
  • Pritzkow, S., R. Morales, F. Moda, U. Khan, G. Telling, E. Hoover, C. Soto. 2015. Grass plants bind, retain, uptake, and transport infectious prions. Cell Reports. 11:1168–1175.
  • Prusiner, S. B. 1998. Prions. Proceedings of the National Academy of Sciences of the United States of America. 95(23):13363-13383.
  • Rasmussen, J., B. H. Gilroyed, T. Reuter, S. Dudas, N. F. Neumann, A. Balachandran, N. N. V. Kav, C. Graham, S. Czub, and T. A. McAllister. 2014. Can plants serve as a vector for prions causing chronic wasting disease? Prion Vol. 8, Iss. 1.
  • Sandberg, M. K., H. Al-Doujaily, C. J. Sigurdson, M. Glatzel, C. O’Malley, C. Powell, E. A. Asante, J. M. Linehan, S. Brandner, J. D. F. Wadsworth, and J. Collinge. 2010. Chronic wasting disease prions are not transmissible to transgenic mice overexpressing human prion protein. Journal of General Virology. 91:2651-2657.
  • Saunders, S. E., S. L. Bartelt-Hunt, J. C. Bartz. 2012. Occurrence, transmission, and zoonotic potential of chronic wasting disease. Emerging Infectious Disease Journal. 18(3). http://dx.doi.org/10.3201/eid1803.110685. Accessed 4 April 2012.
  • Sigurdson, C. J. 2008. A prion disease of cervids: chronic wasting disease. Veterinary Research. 39(4):41.
  • Sleeman, J., C. Gillin. 2012. Ills in the pipeline: emerging infectious diseases and wildlife. The Wildlife Professional. 6(1):28-32.
  • Sohn, H., Y. Lee, M. Kim, E. Yun, H. Kim, W. Lee, D. Tark, and I. Cho. 2011. Chronic wasting disease (CWD) outbreaks and surveillance program in the Republic of Korea. Page 3 in Proceedings of the Prion 2011, Pre-congress Workshop: Transmissible Spongiform Encephalopathies in animals and their environment, 16 May 2011, Montreal, Quebec, Canada.
  • Tamgüney, G., M. W. Miller, L. L. Wolfe, T. M. Sirochman, D. V. Glidden, C. Palmer, A. Lemus, S. J. DeArmond, and S. B. Prusiner. 2009. Asymptomatic deer excrete infectious prions in feces. Nature 461, 529–532.
  • Travis, D. and M. W. Miller. 2003. A short review of transmissible spongiform encephalopathies, and guidelines for managing risks associated with chronic wasting disease in captive cervids in zoos Journal of Zoo and Wildlife Medicine 34:125–133
  • Uehlinger, F. D., A. C. Johnston, T. K. Bollinger, and C. L. Waldner. 2016. Systematic review of management strategies to control chronic wasting disease in wild deer populations in North America. BMC Veterinary Research 12:173.
  • Vaske, J., L. Shelby, M. Needham. 2009. Preparing for the next disease: the human-wildlife connection. Pages 244-261 in M. J. Manfredo, J. J. Vaske, P. J. Brown, D. J. Decker, and E. A. Duke, editors, Wildlife and Society: The Science of Human Dimensions. Island Press, Washington D.C., USA.
  • Vaske, J.J., Timmons, N.R., Beaman, J. and Petchenik, J., 2004. Chronic wasting disease in Wisconsin: hunter behavior, perceived risk, and agency trust. Human Dimensions of Wildlife, 9(3), pp.193-209.
  • Wasserber, G., E. E. Osnas, R. E. Rolley, and M.D. Samuel. 2009 Host culling as an adaptive management tool for chronic wasting disease in white-tailed deer: a modeling study. Journal of Applied Ecology. 46:457-466.
  • Wyoming Game and Fish Department. 2012. Hunting season justification for the South Converse mule deer herd unit. http://gf.state.wy.us/web2011/wildlife-1000287.aspx Accessed 17 April 2012.
  • Williams, E. S. 2005. Chronic wasting disease. Veterinary Pathology. 42:530-549.
  • Williams, K., A. G. Hughson, B. Chesebro, and B. Race. 2019. Inactivation of chronic wasting disease prions using sodium hypochlorite. PLoS ONE. 14(10): e0223659.
  • World Health Organization [WHO]. 2000. Proceedings of the meeting of World Health Organization consultation on public health and animal transmissible spongiform encephalopathies: Epidemiology, risk, and research requirements. Geneva, Switzerland.
  • Zimmer, N. P., P. C. Boxall, and W. L. Adamowicz. 2012. The impacts of chronic wasting disease and its management on recreational hunters. Canadian Journal of Agricultural Economics. 60:71-92.