Tuberculosis in Cervids

Tuberculosis is a chronic, granulomatous disease of wild and domestic ruminants that poses zoonotic risk.  Eradication of the disease in cattle has been a federal goal since the early 20^th century; however, complete eradication of tuberculosis has been thwarted by the presence of tuberculosis in wild populations of cervids in specific regions in the United States.  With the increase in farming of deer and elk, tuberculosis is an important contemporary issue for farmers who raise cervids or domestic ruminants.

  Tuberculosis in ruminants is caused by Mycobacterium bovis.  Mycobacterium bovis is a gram positive, small, slightly curved rod.  These bacteria are aerobic and acid-fast; thus, bacteria can only be visualized with stains such as Ziehl-Neelson.  Mycobacterium bovis has a thick cell wall that contains a high content of waxes and glycolipids.  The composition of the cell wall offers excellent protection against humoral defense mechanisms and disinfectants, and is responsible for the granulomatous response and long-term survival of organisms within macrophages.  Mycobacterium bovis can remain active on a fomite in cooler climates up to 112 days.

  The spread of Mycobacterium bovis organisms is primarily through respiratory secretions and saliva.  Therefore, exchange of these secretions on feedstuffs is likely occurring between wild deer and cattle and/or captive cervids in Michigan.  This proposed mode of exchange is further complicated by the fact that Mycobacterium bovis can live for an extended length of time in cooler climates; therefore, direct wild deer to cattle or captive cervid contact is not needed to spread the disease.   The route of infection is usually indicated by the distribution of the lesions.  In deer, infection is by inhalation or ingestion, with the bulk of the lesions found in retropharyngeal lymph nodes.  One of the main risk factors for tuberculosis infection is overcrowding.  Overcrowding increases the opportunity that a single infected animal can infect multiple animals.  Supplemental feeding and baiting of wild deer, which brings large populations of animals into smaller areas, may also promote spread of the disease.

  The typical clinical signs of tuberculosis in deer are quite variable.  The type of clinical signs that are observed are due to the route of infection.  The most consistent clinical sign is swelling of lymph nodes, particularly the medial retropharyngeal lymph node, which drains the nasal passage and mouth.  Respiratory distress and lung lesions occur after inhalation of the bacteria.  Emaciation can also occur commonly with chronic Mycobacterium bovis infection.

  Grossly, lesions in deer are different from those observed in cattle.  The main lesion seen in a deer is purulent lymphadenitis of the medial retropharyngeal lymph node.  The abscess is filled with a pale white to tan, purulent material.  In cattle, affected lymph nodes nodes contain caseous granulomas that can be surrounded by fibrosis.  Cervids can exhibit granulomatous lymphadenitis, but at a much lower frequency than in cattle.

  Lung lesions are concentrated in the dorsocaudal half of caudal lung lobes.  The lung lesions appear as pale yellow to tan nodules that are seen throughout the lung parenchyma and pleural surface.  These nodules can range from small miliary foci of 1mm in diameter to large abscesses greater than 30cm in diameter.  When these lesions are cut, a pale white to tan purulent exudates is exuded.  The abscesses in deer are indistinguishable grossly from abscesses caused by other bacteria such as Staphylococcus sp., Streptococcus sp., Actinobacillus sp., or Actinomyces sp.

  Histopathologically, the lymph node contains a round, central area of caseous necrosis with a narrow mantle of mixed inflammatory cells.  The leukocytes consist of neutrophils, epithelioid macrophages, lymphocytes, and plasma cells.  The lung lesions usually have more neutrophils than the lymph nodes.  In cattle, tuberculous lesions consist mainly of a central, irregular, coalescing area of caseous necrosis.  The center is mineralized and is surrounded by macrophages, lymphocytes, plasma cells, and Langhans giant cells.  In the cervid, mineralization is centrally and peripherally located, with foci of mineralization located in the cellular infiltrate.  Acid-fast bacilli are difficult to detect in the lesions from cattle, as compared to lesions in cervids.

  The standard protocol for identification of possible infected animals in the field is tuberculin testing.  A single cervical skin test is used in most herds as a preliminary test.  The single cervical skin test is done on cervids one year of age or older and any cervid younger than one year that was not born into the herd.  The tuberculin test is performed in the neck as opposed to the caudal fold, as in cattle, due to the increased sensitivity of the cervical test in cervids.  The test is performed by injecting 0.1 ml of tuberculin intradermally in the mid-cervical region.  The test is then read 72 hours later.  A positive reaction includes visualization and palpation of a mass of 2 mm in size or greater.  The animals that are positive to a single cervical skin test are subjected to the comparative cervical skin test.  The comparative cervical tuberculin test is administered by an approved state or federal veterinarian within 10 days of a positive single cervical skin test.  In this test, an injection of bovine tuberculin will be injected intradermally along with a separate injection of avian tuberculin in two separate areas of the cervical neck region.  These two injections will be evaluated to determine whether the cervid is infected with Myco-bacterium bovis or another species of Mycobacterium.

  After a cervid is confirmed as a positive reactor, the whole herd is quarantined until the reactor is slaughtered or necropsied.   At necropsy, if the reactor deer is found to have lesions consistent with tuberculosis, histopathology and isolation of Mycobacterium bovis is performed.  If Mycobacterium bovis is isolated from the lesion, the herd is considered an affected herd.  The affected herd is quarantined until the herd has tested negative on three whole herd tests.  These tests should be given 90 days, 270 days, and 360 days after the reactor tested positive.  If the herd tests negative those three times, the quarantine is lifted and the herd is considered an unclassified herd.  The herd must then undergo five consecutive annual tests to be a classified herd.  An alternative to testing of an affected herd is depopulation of a herd.

  Prevention of the spread of tuberculosis is an active endeavor, especially with the concern of spread to cattle and interstate commerce.  Nowhere is this more evident than in Michigan, where there is an active tuberculosis infection in the wild cervid population.  The proposed methods of prevention of the spread of tuberculosis have met great opposition in Michigan.  Cattle farmers have pushed for the complete eradication of deer to rid the area of tuberculosis.  The hunters do not want to see the complete eradication of deer as that will rid the area of hunting, which is considered economically important in Michigan.  So, Michigan has decided to decrease the population through increases in deer hunting permits in an attempt to lower the number of infected deer.  This policy has resulted in a reduction in the prevalence of the disease to a constant level of 1-2% infection.  Michigan has also banned the use of deer baiting in the area of tuberculosis positive deer.  Some ways to prevent the spread of tuberculosis to cattle and captive cervids is feeding cattle and cervids away from wooded areas.  Feeding them in open areas where deer would not have cover will theoretically keep deer from congregating in an area where cattle and cervids would be eating.  Also, excluding deer from stored feed sources can help prevent the spread of tuberculosis through contaminated feed.  Ultimately, the education of hunters, farmers, and veterinarians about clinical signs and whom to contact is the only way to prevent an outbreak in cervids and cattle.

-by Seth McDevitt, PUSVM Class of 2010

-edited by Dr. Grant Burcham, ADDL Graduate Student

References:

1. Animal and Plant Health Inspection Service. 2008.  Tuberculosis (9CFR part 77).  Washington, DC: USDA

2. Cook RA: 1999.  Mycobacterium bovis Infection of Cervids: Diagnosis, Treatment, and Control. In: Zoo and Wild Animal Medicine, Current Therapy. Fowler ME, Miller RE, eds. Vol. 4, Saunders, Philadelphia PA. Pp 650-657.

3. Fitzgerald SD, Kaneene JB, Butler KL, Clarke KR, Fierke JS, Schmitt SM, Bruning-Fann CS, Mitchell RR, Berry DE, Payeur JB: 2000.  Comparison of postmortem techniques for the detection of Mycobacterium bovis in white-tailed deer (Odocoileus virginanus).  Journal of Veterinary Diagnostic Investigation 12:322-27.

4. Flach E: 2003. Ceridae and Tragulidae. In: Zoo and Wild Animal Medicine, Current Therapy. Fowler ME, Miller RE, eds. Vol.5. Saunders Elsevier, St. Louis, MO. Pp 634-49.

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6. Palmer MV, Whipple DL: 2006. Survival of Mycobacterium bovis on Feedstuffs Commonly Used as Supplemental Feed for White-tailed Deer (Odocoileus virginianus). Journal of Wildlife Diseases 42(4):853-58.

7. Rhyan JC, Saari DA: 1995.  A Comparative Study of the Histopathologic Features of Bovine Tuberculosis in Cattle, Fallow Deer (Dama dama), Sitka Deer (Cervus nippon), and Red Deer and Elk (Cervus elaphus). Veterinary Pathology 32:215-20.

8. Rhyan JC, Saari DA, Williams ES, Miller MW, Davis AJ, Wilson AJ: 1992. Gross and microscopic lesions of naturally occurring tuberculosis in a captive herd of wapiti (Cervus elaphus nelson) in Colorado.

9. Sikarskie JG: 2008. Tuberculosis in Michigan Deer. In: Zoo and Wild Animal Medicine, Current Therapy. Fowler ME, Miller RE, eds. Vol. 6, Saunders Elsevier, St. Louis, MO. Pp 423-29.