U.S. Department of the Interior

U.S. Geological Survey

Fact Sheet 2007–3070

August 2007

Chronic Wasting Disease

Introduction

Chronic wasting disease (CWD) 

is an always-fatal, neurological illness 

occurring in North American cervids 

(members of the deer family), including 

white-tailed deer, mule deer, elk and 

moose. Since its discovery in 1967, 

CWD has spread geographically and 

increased in prevalence locally. CWD 

is contagious; it can be transmitted 

freely within and among free-ranging 

populations. It is likely that diseased 

animals can transmit CWD to healthy 

animals long before they become 

clinically ill. Managing CWD in 

free-ranging populations is extremely 

difficult, therefore preventative 

measures designed to reduce the 

chance for disease spread are critically 

important.

History

Chronic wasting disease was 

first documented in a Colorado 

research facility in 1967. During 

the next decade, additional cases 

were documented in Colorado and 

Wyoming research facilities. In 1978, 

Dr. Elizabeth Williams determined that 

CWD was a transmissible spongiform 

encephalopathy (TSE), a family of 

diseases that includes scrapie in sheep, 

bovine spongiform encephalopathy 

(BSE, mad-cow disease) in cattle, and 

kuru and Creutzfeldt-Jakob disease 

(CJD) in humans. The first detection of 

CWD in a free-ranging population was 

in 1981 in an elk in Rocky Mountain 

National Park (Colorado). Prior to 

2000, CWD had been documented 

in only a handful of counties in 

southeastern Wyoming and adjacent 

northeastern Colorado. Since 2000, 

CWD has been detected in many 

additional locations (Fig. 1).

Causative Agent

Although debate still occurs, the 

vast majority of research indicates that 

the causative agent of TSEs (including 

CWD) is a misfolded protein called a 

prion. All mammals produce normal 

prions (abbreviated PrP) that are used 

by cells, then degraded and eliminated, 

or recycled, within the body. When 

disease-associated prions (PrPCWD) 

contact normal prions, they cause them 

CWD in free-ranging

populations

Known distribution

prior to 2000

CWD in captive

facilities

to refold into the abnormal shape. 

These disease-associated prions are 

not readily broken down and tend to 

accumulate in lymphatic and neural 

tissues. Tissue damage associated 

with PrPCWD accumulation in the brain 

results in a sponge-like appearance, 

microscopically.

Clinical Signs

CWD has an extended incubation 

period averaging 18–24 months 

between infection and the onset of 

clinical signs. The most obvious 

clinical sign of CWD is progressive 

weight loss, thus, the name (Fig. 

2). Numerous behavioral changes 

also have been reported, including 

decreased social interaction, loss of 

awareness, and loss of fear of humans. 

Clinically diseased animals also may 

exhibit increased drinking, urination, 

and excessive salivation.

Figure 1. Distribution of chronic wasting disease in North America.

CWD has been 

documented in captive 

and/or free-ranging 

populations in 

14 U.S. States and 

2 Canadian Provinces.
Diagnosis

CWD is typically diagnosed by 

examination of brain or lymphoid 

tissue from a dead animal. A 

variety of assays (tests), including 

immunohistochemistry (IHC), 

immuno-blotting, and enzyme-linked 

immunosorbent assay (ELISA) 

techniques are currently in use. These 

same techniques have been successfully 

used to test surgical biopsies of tonsil 

tissue collected from live animals. 

Many researchers are working to 

develop additional live-animal tests. 

However, live-animal tests are difficult 

to apply in free-ranging populations 

due to the complexity of capturing live 

animals.

Transmission

It has long been hypothesized that 

CWD is transmitted via direct (nose-tonose) contact between animals. It has 

now been demonstrated that CWD also 

can be transmitted indirectly. Diseased 

animals shed infectious prions into the 

environment where they persist and can 

be ingested by healthy animals at a later 

date. Saliva collected from clinically 

affected deer has been recently shown 

to be infectious, helping to elucidate a 

potential mechanism for both direct and 

indirect transmission. In areas where 

CWD has been established the longest, 

prevalence has continued to increase 

over time (greater than 30% prevalence 

has been reported in localized areas). 

Demographic data show higher rates 

of disease in adults than juveniles, and 

2–4 times higher rates in adult males 

than adult females. It is theorized that 

adult male breeding behaviors result in 

higher disease exposure.

Preventative Measures

Because CWD is difficult to 

successfully manage in free-ranging 

populations, disease prevention is 

critical. Many states have restricted 

or banned importing live cervids and 

are requiring whole-herd disease 

monitoring within game farms. Some 

states have banned hunters from 

bringing whole carcasses into their 

home states. Others have banned 

feeding and baiting of cervids to reduce 

artificial congregations of animals that 

can increase chances for disease spread.

Surveillance

Disease surveillance can be 

simply defined as looking for disease. 

Nearly every state is currently 

conducting some level of surveillance 

for CWD. In areas where CWD has 

been detected, surveillance is used to 

monitor changes in disease distribution 

and severity. In areas where CWD 

has not been detected, surveillance 

is used to look for the disease and to 

determine the likelihood that CWD is 

not present. Surveillance efforts include 

examination of hunter-killed animals, 

animals killed in collisions with 

vehicles, and live animals displaying 

clinical signs compatible with this 

disease. In a few specialized situations, 

wildlife researchers capture and test 

live animals using tonsil biopsies.

Management

Disease management objectives 

include limiting geographic spread, 

reducing disease prevalence, and 

eliminating disease. Methods to 

manage CWD in free-ranging 

populations are extremely limited. 

Several states have attempted to greatly 

Printed on recycled paper

reduce deer populations, primarily 

through extended opportunities for 

hunters, in an effort to reduce disease 

transmission. Agency sharpshooters 

have also been used to cull deer in 

disease “hotspots.” To be successful, 

CWD management efforts will likely 

need to be intensive and sustained 

over many years. Management efforts 

for CWD are difficult and expensive 

for states to undertake. However, the 

economic and social values associated 

with deer, elk, and moose in North 

America dictate that we continue 

efforts to detect and successfully 

manage CWD.

Human Risk

While the increasing volume of 

scientific research continues to suggest 

that the risk of CWD transmission to 

humans is remote, scientists cannot 

rule out the possibility. Simple 

precautionary measures may help 

reduce the risk even further. Do not 

consume meat from obviously sick 

animals. If you hunt in areas where 

CWD is known to occur, you may 

choose to have a CWD test run on 

your animal. Avoid consuming internal 

organs, spinal cord and lymph nodes 

from harvested animals. Wearing 

disposable gloves while field-dressing 

animals helps reduce exposure risk, 

not only for CWD, but for many other 

diseases as well.

Additional Information

For additional information on 

chronic wasting disease, please contact: 

Bryan Richards, CWD Project Leader

USGS National Wildlife Health 

Center

6006 Schroeder Road

Madison, WI 53711

(608) 270-2485 

Visit the USGS National Wildlife Health 

Center at http://www.nwhc.usgs.gov/ and 

the Wildlife Disease Information Node 

of the National Biological Information 

Infrastructure at http://wildlifedisease.

nbii.gov

Figure 2. White-tailed deer with chronic 

wasting disease. Photograph courtesy 

of the Wisconsin Department of Natural 

Resources.