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Malignant Catarrhal Fever in Bison


Murray Woodbury DVM, MSc.

Specialized Livestock Health and Production
Department of Large Animal Clinical Sciences
Western College of Veterinary Medicine
University of Saskatchewn, Saskatoon, Saskatchewan  S7N 5B4
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Contents

Introduction
Cause
Geographic distribution
Transmission
Clinical signs
Post mortem findings
Diagnosis
Differential diagnosis
Treatment
Prevention
Significance
References

Introduction

Malignant Catarrhal Fever (MCF) is an infectious disease of cattle, bison, deer and other ruminants. (2) Relatively little is known about MCF in bison.
 

Cause

MCF is caused by viruses in the herpes virus family. In North American bison the disease is associated with a virus that has never actually been isolated, but named Ovine herpes virus-2 (OHV-2) (2,5). It can be found in most sheep and possibly goats, but does not cause clinical disease in these hosts (3,5). MCF caused by OHV-2 is therefore known as sheep-associated MCF (SA-MCF).

In Africa, a closely related virus called Alcelaphine herpes virus-1 (AHV-1) is responsible for most cases. In 1960, the virus was isolated and identified from the principal host and carrier of the virus, the wildebeest (10). MCF caused by AHV-1 is known as wildebeest-associated MCF (WA-MCF).

A more recent discovery using DNA technology for typing disease causing organisms is a herpes virus isolated from cases of MCF in white-tailed deer (11). The virus has not yet been named because the reservoir or carrier species has not been recognized. Whether or not this virus also causes disease in cattle, bison or other ruminants is not known but researchers have observed that there are no official reports of MCF in cattle or bison where either OHV-2 or AHV-1 has not been detected (12).
 

Geographic distribution

MCF has a worldwide distribution (5). However most of the world's bison, and therefore bison related cases of MCF, are found in North America.

The incidence of clinical MCF in wild bison is unknown. A serosurvey for antibodies against OHV-2 in ranched bison from Montana and Washington showed positive titers in 2% of animals tested (3). Other researchers have placed this figure much higher at between 15 to 20% for the general bison population (9). Levels of serological evidence for MCF infection in Canadian bison have never been established. The high antibody prevalence rates and relatively low clinical disease rates suggest that many infections are unapparent and non lethal. Seropositive animals and clinical MCF are most common in those regions farming bison under intensive management (12).
 

Transmission

There is strong evidence that sheep carrying OHV-2 virus are the primary source of MCF. However, the mechanism of transmission of the virus from sheep to bison is unknown (5). In some outbreaks there has been no immediate history of previous contact with sheep (9). This raises the possibility of latent infection of bison with OHV-2 virus.

In sheep infection occurs early in life with most lambs being infected via horizontal transmission from the mother or members of the flock by the time they are six months of age. Since the virus is shed in nasal secretions of infected animals, bison are infected through contact with infected sheep and transfer of the virus from saliva or nasal secretions. Hay feeders, common water sources, birds and care givers may facilitate virus transmission (16). Direct contact with sheep may not be necessary, as cattle and bison have apparently been infected by sheep held some distance away. This suggests windborne transfer of aerosolized virus, although this has never been proven (13).

Bison-to-bison transmission has not been demonstrated. It is not known if bison calves can become infected from seropositive mothers and herd mates soon after birth as do sheep. OHV-2 is a cell-associated virus and bison and cattle have been infected experimentally by injection of either whole blood or white blood cells from a calf with MCF (1).

At one time bison and other species like deer were considered "dead end" hosts, meaning that they were susceptible to infection but were unable to pass the infection to other individuals. The existence of MCF in feedlot cattle (14,15) and more recent outbreaks of MCF in feedlot bison (13) with no history of exposure to sheep have challenged this assumption.

Although OHV-2 has been associated or linked with MCF in bison there are likely to be other factors involved in the development of MCF in a bison. PCR testing (DNA test) for the presence of OHV-2 has shown that not all persistently infected animals become diseased and die (12). Other viruses have been isolated from cases of MCF using PCR, although none consistently. Their role, if any, in the development of clinical disease is unknown (17). The incidence of MCF increases in winter and under intensive management conditions. This suggests that stress or other factors that suppress the immune function may be necessary to develop clinical MCF (6).
 

Clinical signs

General clinical signs of MCF are depression, separation from the herd, anorexia (not eating), incoordination, and persistent fever (40-410 C). There may be excessive salivation and nasal discharge due to erosions on the tongue and palate. Ocular discharge, conjunctivitis, and corneal opacity are often observed. Affected animals may have diarrhea (occasionally with blood), or hematuria (bloody urine) (1,2,4). These signs can occur in any combination, lasting from 1 to 4 days prior to death. Most commonly, bison infected with MCF are simply found dead. However, while the clinical course in bison is usually very rapid, there are reports of survival for months (2,9).
 

Post mortem findings

Post mortem lesions vary considerably, depending on the severity and course of the disease. Animals dying from per acute (rapid onset, sudden death) MCF have few lesions other than hemorrhagic enterocolitis (2). In cases of acute and subacute disease there are ulcerations throughout the alimentary tract and trachea, corneal opacity, conjunctivitis, enlarged lymph nodes, and ulcerations or hemmorhage in the urinary bladder wall (1,2,4,5).

Microscopic findings reflect the lymphoproliferative nature of the disease. Immune cells called lymphocytes infiltrate the tissue around blood vessels due to vasculitis (inflammation of blood vessels) and cause destructive changes in organs such as the kidney and liver. These lymphoid cells infiltrate the liver and kidneys of most cases (2). Blocked blood vessels result in local cell necrosis (death) and inflammation leading to the ulcerations in the upper respiratory, urinary and gastrointestinal tracts (2).
 

Diagnosis

A definitive diagnosis is made only by microscopic examination of tissues on post mortem. In live animals clinical signs and a detailed history can be used to form a presumptive diagnosis which needs to be supported by laboratory tests. An OHV-2 specific test using DNA technology called PCR (Polymerase Chain Reaction) for the presence of virus can be done on an unclotted blood sample. A recently developed but less reliable serological test for the presence of antibodies against OHV-2, called a competitive-inhibition ELISA test, can also be performed on blood serum. Interpretation of the test results is not always straight forward. Positive ELISA or PCR tests in otherwise healthy animals do not seem to be indicators of impending clinical disease and their significance is presently not well understood (3,17).

In dead animals the diagnosis depends upon an autopsy performed by a veterinarian or a pathologist at a veterinary diagnostic laboratory. In addition to the autopsy examination, tissue samples are taken for PCR testing and microscopic evaluation. The microscopic tissue changes in cases of MCF are unmistakable. The typical lesions of MCF in addition to positive diagnostic tests form the diagnosis for MCF.
 

Differential diagnosis

There are many diseases that cause sudden death, including rabies (8), bloat, and anthrax. If the disease is more protracted, infectious bovine rhinotracheitis (IBR), bovine virus diarrhea (BVD), vesicular stomatitis, or foot and mouth disease might be confused with MCF unless appropriate laboratory tests are performed.
 

Treatment

There is no effective treatment known for MCF. There is evidence that supportive care with antibiotics and corticosteroids may prolong the course of disease (9) but the case fatality rate remains at or near 100%.
 

Prevention

There is no vaccine against MCF. Prevention is aimed at minimizing risk factors associated with the occurrence of MCF. It is good practice to avoid any contact with sheep and goats including wild varieties. Minimize the stress caused by inadequate diets and excessive handling or inappropriate handling techniques. There is evidence that bison can be infected with OHV-2 for long periods of time, perhaps years, before developing clinical MCF (9). However, it may be wise to quarantine or segregate newly acquired animals from the main herd for at least one or two months.
 

Significance

MCF poses an economic threat to the bison producer. Although outbreaks of clinical MCF are uncommon and sporadic, the morbidity rate (percentage of animals that become sick) in infected herds is reported to be from 3 to 53 % (5) but can go as high as 100%. The mortality rate is almost 100%.
 

References

  1. Liggit HD. Experimental transmission of bovine malignant catarrhal fever to a bison (Bison bison). J Wild Dis 1987; 16(2):299-304
  2. Schultheiss PC, Collins JK, Austgen LE, DeMartini JC. Malignant catarrhal fever in bison, acute and chronic cases. J Vet Diagn Invest 1998; 10:255-262.
  3. Li, H, Shen DT et al Prevalence of antibody to malignant catarrhal fever virus in wild and domesticated ruminants by competitive-inhibition Elisa. J Wild Dis 1996; 32(3):437-443.
  4. Ruth GR, Reed DE, Daley CA et al. Malignant catarrhal fever in bison. J Am Vet Med Assoc 1977; 171:913-917.
  5. Radostits, OM. Blood, DC., Gay, CC. Veterinary Medicine, 8th ed. London: Bailliere Tindall, 1994, 1081-1085.
  6. Lahijani-R-R et al, The use of PCR to assist in the diagnosis of malignant catarrhal fever, Erkrankungen der Zootiere 1994; 36:225-230.
  7. Junge, Randall E. [Ed]. Joint conference AAZV / WDA / AAWV, Michigan, August 1995, 137-143.
  8. Stoltenow, C. et al. Rabies in an American bison from North Dakota. J Wild Dis 2000; 36(1):169-171.
  9. O'Toole D, Li H, Crawford T. Malignant catarrhal fever in bison. Smoke Signals 2000; 11(2):18-25.
  10. Plowright W, Ferris RD, Scott GR. Blue Wildebeest and the etiological agent of bovine malignant catarrhal fever. Nature 1960; 188:1167-1169.
  11. Li H, Dyer N, Keller J, Crawford TB. Newly recognized herpes virus causing malignant catarrhal fever in white-tailed deer (Odocoileus virginianus). J Clin Microbiol 2000; 38(4):1313-1318.
  12. O'Toole D, Li H, Montgomery DL, Sourk C, Crawford, TB. A prospective and retrospective study on ovine herpes virus-2 malignant catarrhal fever in feedlot bison. Abstract. Proc Amer Assoc Vet Diag Lab. October 2000. Birmingham, Alabama.
  13. Schultheiss PC, Collins JK, Spraker TR, DeMartini JC. Epizootic malignant catarrhal fever in three bison herds: Differences from cattle and association with ovine herpes virus-2.J Vet Diag Invest 2000;12:
  14. O'Toole D, Li H, Roberts S, et al Chronic generalized obliterative artieriopathy in cattle: a sequel to sheep associated malignant catarrhal fever. J Vet Diagn Invest 1995; 7:108-121.
  15. Pierson RE, Thake D, McChesney AE, Storz J. An epizootic of malignant catarrhal fever in feedlot cattle J Am Vet Med Assn 1973; 163:349-350.
  16. Crawford TB, O'Toole D, Li H. Malignant Catarrhal Fever in Current Veterinary Therapy IV, JL Howard, RA Smith eds. 1994 WB Saunders, Toronto.
  17. Collins JK, Bruns C, Vermedahl TL, Scheibel AL et al. Malignant catarrhal fever; PCR survey for ovine herpes virus-2 and other persistent herpes virus and retro virus infections of dairy cattle and bison. J Vet Diagn Invest 12;406-411.
  18. Liggit HD, Demartini JC, McChesney AE, et al. Experimental transmission of malignant catharral fever in cattle: gross and histopathologic changes. Am J. Vet. Res. 1978; 39:1249-1257.