Unraveling the Mysteries of Chronic Wasting Disease

During 2001 and 2002, the Animal Disease Surveillance Unit (ADSU) participated in a number of on-farm investigations for Chronic Wasting Disease (CWD) in farmed elk. Our Unit’s involvement has been triggered by two circumstances, namely:

  1. where it is suspected that a premise will be designated as highly contaminated, or
  2. where the apparent source of the disease remains unexplained.

In both instances, a team comprising the CFIA district and regional veterinarian, a provincial wildlife or veterinary official, and an epidemiologist from the ADSU conducts an on-site visit to review the relevant history and tour the farm.

When a premise is rated as highly contaminated, particular emphasis is placed on:

  1. assessing the disease transmission risk posed by each site or object that came into contact with the animals. High risk sites or objects include watering and feeding troughs, mineral feeding sites, and heavily used winter bedding or calving areas. Contaminated ground is excavated and buried, porous feeders and tubs are buried or burned, and
  2. large metal objects (squeeze chutes) are disinfected with a 2% chlorine solution for a minimum of one hour. Certain small objects that come into intimate contact with animals, such as velveting equipment, balling guns, and tagging equipment are disposed of by deep burial. A detailed farm decontamination plan outlines all of the measures to be completed.

Of the 41 farms that have been depopulated to date, four have been designated as highly contaminated. Three of the four have already completed the decontamination and the remaining one is in the process of doing so.

The second reason for ADSU involvement is to review cases where the source of the disease is unexplained. There have been four instances of this sort. These investigations focus on reviewing the history of animal movement, the acquisitions and sales, how animals were grouped and managed on the farm, cow-calf relationships, and spatio-temporal relationships between positive animals. Unexplained or suspicious deaths in preceding years are closely reexamined. Much of this work is like searching for the proverbial needle in a haystack, and therefore all possible methods of introducing disease, no matter how extraordinary they might appear, are considered. These include the risk:

  • of introduction by wildlife, or risk of spread to wildlife
  • posed by animals that temporarily escape
  • posed by nearby infected farms
  • posed by sharing equipment
  • posed by boarding or commingling animals from other farms
  • posed by unrecorded animal movements, and
  • posed by previously unrecognized cases that contaminated the environment.

These investigations are time consuming, often occupying 1-2 days of site visits and interviews with the owner, followed by 4-5 days of record analysis. Nevertheless, they offer golden opportunities to learn more about CWD transmission.

The single most helpful advance in this process over the last year has been the assessment of brain lesions to determine the stage of disease at depopulation (courtesy Dr Aru Balachandran, Nepean). Using this information, we can determine approximately how long an animal was infected before it was killed, and then construct a time line of disease infection, incubation, and expression for each positive case. In many instances, these time lines have illustrated that the period of infection coincides with another event, such as the death of an animal ascribed to other, but suspicious, circumstances.

Any unusual deaths in animals more than 18 months of age should be investigated. CWD causes central nervous system damage and elk will often shun or drive out animals that are not exhibiting normal behaviour. Our investigations particularly investigate deaths due to unusual circumstances, such as:

  • a fractured neck from running into a fence
  • fractured ribs from fighting
  • pneumonia from aspiration and inability to swallow
  • grain overload in a single animal, or
  • a single animal that is thin, when the rest are in good body condition.

In many of these cases, we do not have the benefit of a necropsy examination for CWD. Until testing programs are universally applied, it will be difficult to rule out CWD as a differential diagnosis.

Although we cannot conclusively prove the source of the infection on each and every farm, CFIA’s investigation success rate has been quite good. In all but two of the 41 depopulated farms, the source of infection has been linked, more or less, to animals from other infected premises. In the two remaining situations, wildlife vectors and recrudescent environmental contamination have been proposed as possible sources. In one case, the producer postulated that his animals became infected when ravens fed on infective material from nearby farms and then defecated in his grain feeders. In the other, an animal that died suspiciously a decade earlier could have contaminated a small water hole. While perhaps unlikely, these suggestions cannot be discounted out of hand and must remain on the list of possible explanations.

The principles of investigating a chronic, slowly progressive disease such as CWD are the same as those involving other infectious agents. Similar to diseases that cause acute epidemics, transmissible spongiform encephalopathies exhibit a disease outbreak pattern and an epidemic curve, but these are measured in months and years, rather than in days or weeks. And because clinical signs are often seen in only a handful of animals (often expressed in the single digit percentages), following up on each and every suspicious case is necessary.

Much remains to be learned about CWD. However, thorough investigation of field outbreaks has given us additional insight into the dynamics of disease transmission and has launched a formal survey of affected farms.

Source: Wayne Lees, DVM, Epidemiologist, Animal Disease Surveillance Unit, Canadian Food Inspection Agency, Oak Lake, Manitoba.