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Diseases of Bison


Dr. John Berezowski

Epidemiologist
Agri Systems Support Branch
Alberta Agriculture, Food, and Rural Development
Edmonton, Alberta, Canada

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Contents
 
Introduction

Bacterial Diseases of Bison
    Miscellaneous Localized Infection (Abscesses)
    Actinobacillosis
    Anthrax
    Blackleg
    Brucellosis
    Foot Rot
    Hemorrhagic Septicemia
    Hemophilosis
    Johne's Disease
    Leptospirosis
    Listeriosis
    Necrotic Stomatitis
    Pasteurella Pneumonia
    Pinkeye
    Tuberculosis
 
Virus Diseases of Bison
    Bovine Virus Diarrhea (BVD)
    Neonatal Diarrhea
    Infectious Bovine Rhinotracheitis (IBR)
    Malignant Catarrhal Fever (MCF)
    Parainfluenza 3 Virus
 
Parasitic Diseases of Bison
    Anaplasmosis
    Babesiosis
    Coccidiosis
    Demodex Mange
    Hydatid Tapeworm
    Liver Fluke
    Lungworm
    Sarcocystis
    Stomach and Intestinal Worms
    Ticks and Tick Paralysis
    Warbles (Grubs)
 
Nutritional Diseases of Bison
    Bloat or Rumenal Tympani
    Copper Deficiency
    Grain Overload / Rumen Overload / Lactic Acidosis
    Nutritional Muscular Dystrophy / White Muscle Disease
 
 
Congenital Abnormalities of Bison
   Arthrogryposis
   Atresia Ani and Rectovaginal Fistula
 
 
Toxicities in Bison
   Urea Poisoning
   Ponderosa Pine Needle Abortion
 
 
Bison Diseases Bibliography
 


 
Introduction

The following is a list of diseases, which have been documented in bison populations in North America. This list of diseases is short, not because bison have more resistance to disease than other species but because of the minimal amount of research that has been done on bison and bison diseases at this time. This seems ironic since bison were present in North America long before any of the other species of animals that we presently use in agriculture. Bison may have been subjected to far more diseases when the bison population in North America was much larger than it is today. It is difficult, however, to assess the levels or causes of disease that may have occurred in a bison population that exists today only as a collection of sun bleached bones. The lack of available information makes identifying and treating diseases in bison herds challenging for both veterinarians and producers. It is likely that as bison populations increase more of the diseases to which bison are susceptible will become apparent. There will be greater contact between bison and other domestic species, allowing crossover of diseases from these species into bison herds. In fact, this has already happened. Bison herds have demonstrated their susceptibility to not only cattle diseases but also to diseases of sheep and goats. As bison herds continue to grow and become more intensively managed, the bison themselves will be subjected to many of the stresses that modern agriculture places on our other domestic species. As we know from experience, stress is a very important factor in the manifestation of disease. It is easy to predict that, although the list of diseases that occur in bison today is short, it is likely that this list will lengthen in the not too distant future.
 
Although the bison industry in Canada is growing at a rapid rate, its impact on the Canadian agricultural economy remains minor. Because of this, the bison industry is not likely to attract large amounts of research funding in the near future. Necessity will force producers and veterinarians working in the bison industry to become the primary researchers into the causes and treatment of bison diseases. Most of the information that is to be gained will be learned on the farm as disease and management problems manifest themselves. Bison owners will be the people who will bear the financial burden associated with disease in bison herds. It is vitally important to this group of people that every disease problem that presents itself be used as an opportunity to gather information that can be used to treat or prevent future disease outbreaks. This will mean consulting with veterinarians and pathologists who will request diagnostic tests to be performed on sick or dead animals at an added cost to the bison owner. The economic success of any business, especially one that is agriculturally based, requires careful scrutiny of all expenditures. Expenditures on diagnostic tests - even on dead animals - may not bring an immediate financial return to an individual owner, however these tests will provide disease surveillance information to the owner and add to the collective knowledge of bison diseases. Furthermore, disease occurrences can be used by owners as opportunities to educate their veterinarians and make them better able to help manage future disease outbreaks.
 
 
Bacterial Diseases of Bison
 

Miscellaneous Localized Infection (Abscesses)
 
Causative agent: Arcanobacter pyogenes
This bacterium is found almost anywhere in the environment, including most ruminant gastrointestinal tracts (9) The bacterium commonly gains access to the body through cuts and abrasions may also enter the animal through abrasions of the oral mucosa in association with the feeding of rough or course feed. Injury to the rumen mucosa subsequent to rumen overload and acidosis may also permit entry of the bacteria.
 
Clinical signs:
Abscesses can occur almost anywhere in the body. Subcutaneous abscesses on the hind legs of a 4 to 5 month old bison calf from Alaska were reported (1). Multiple soft tissue abscesses and hepatic abscesses have been described in bison (10). In most cases there is a localized swelling associated with the infection.
 
Diagnosis:
Abscesses are easily diagnosed by observation and palpation. Aspiration of the swelling yields pus. A culture swab may be taken from margins or edges of the abscess and sent to a diagnostic pathology laboratory for culture and identification.
 
Treatment:
  • Lance the abscesses and flush with betadine or iodine solution.
  • Injection of systemic antibiotics may be of limited value. Besides, none of the antibiotics that are commercially available to livestock producers in Canada have been approved for use in bison.
  • There has been no information reported on the pharmacology of any antibiotics in bison. In general, most veterinarians who work with bison consider that they will respond to antibiotics in a similar manner to cattle. This may not be the case. Care should be taken when dosages and meat withdrawal times are recommended to bison producers.
Control:
The incidence of this disease is low and the institution of control programs is not often warranted.
 
 
 
Actinobacillosis
 
Causative agent: Actinobacillus lignieresii
The bacterium is found in the mouth of clinically normal ruminants (9). Entry may occur through abrasions of the oral mucosa associated with the feeding of rough or course feed. Disruptions of the oral mucosa resulting from the eruption of teeth may also allow entry of the bacterium.
 
Clinical signs:
Actinobacillosis has been found in bison but the clinical signs associated with infection have not been described (10). In cattle, Actinobacillosis is commonly called wooden tongue (9). In cattle there is excess salivation, the tongue becoming swollen and hard. Prehension of food becomes difficult and the animal may have difficulty eating with food dropping from the mouth while chewing.
 
Diagnosis:
The diagnosis is usually made from the clinical signs and, where possible, clinical examination of the oral cavity. Post mortem culture of oral lesions will yield the organism.
 
Treatment:
There have been no treatment protocols established for the treatment of Actinobacillosis in bison (10). A. ligniersii has been shown to be sensitive to tetracyclines, streptomycin, and erythromycin (9). Long acting antibiotic preparations should always be the first choice when treating bison. Daily handling of sick bison increases the risk of injury to the bison and increases the stress placed on an already sick bison. Multiple, consecutive attempts at corralling and handling of bison can make them refractory to further handling. These animals can become difficult and dangerous to work with. In some cases a single treatment opportunity is all that an upset bison will allow. Bison have a very strong herd instinct. Separating a sick bison into a pen by its self to facilitate handling may not be a good idea. Being alone in a pen often puts considerable stress on bison. In some cases, bison that are penned alone will run or pace up and down the perimeter of the fence for days, without eating or drinking. It is always a good idea to include at least a couple of other bison in the pen with the sick one.
Sodium iodide works well for treating Actinobacillosis in cattle (9). Visible response to treatment often takes 1 to 2 days. The disadvantage of sodium iodide for treating bison is that it must be administered intravenously.
 
Control:
Actinobacillosis usually occurs as isolated cases. There have been no control protocols reported for bison.
 
 
 
Anthrax
 
Causative agent: Bacillus anthracis
Anthrax most commonly causes sudden death. If the carcass of a dead animal is not opened after death, putrefaction will destroy the bacteria. If the carcass is opened to the air, the bacteria will produce resistant spores that may survive in the environment for up to 30 years (9). Infection is thought to occur by ingestion of spores present in recently disturbed soil or hay. Spores can be spread by streams, insects, birds, dogs and other carnivores (9). Humans can contract anthrax if they eat infected meat or through bacterial contamination of skin scrapes or lacerations suffered while processing or performing a postmortem on an infected carcass. Anthrax has been described in bison from Canada (2,3,4,5) and the USA (6,7).
 
Clinical Signs:
The following are some clinical signs associated with anthrax in bison (2,3,4,5,6,7):
  • this is usually a very rapidly fatal disease.
  • clinically affected bison will be moribund. They often stand with their head down, and are unresponsive.
  • they may be lame, stagger or have a stiff legged gate and they may be reluctant to move, walking with great difficulty.
  • affected animals will often have edematous swellings of the preputial or umbilical region.
  • occasionally, a bison may survive the disease.
Diagnosis:
The diagnosis is most commonly made on postmortem examination of the carcass. Swabs may be taken of the exudate from any of the body orifices and examined microscopically for the presence of the bacteria, which have a characteristic rectangular "box-car shape". Swabs can be sent to a diagnostic pathology laboratory for bacterial culture and identification.
 
Postmortem findings:
  • the most common accompanying history is sudden death.
  • care should be taken not to perform a postmortem dissection without first examining exudate from the mouth, nose, ears, or anus for the presence of B. anthracis organisms.
  • the carcass bloats quickly after death, and has a sawhorse configuration.
  • there may be exudation of dark tarry blood from body orifices.
  • the blood of infected bison may not clot after death.
  • the spleen and lymph nodes are typically enlarged.
Treatment:
There is no effective treatment for anthrax. Affected animals usually die. If an animal is found alive, high doses of systemic antibiotics (penicillins) may be tried.
  Control:
Anthrax is a reportable disease in Canada. If the disease is suspected the Canadian Food Inspection Agency (CFIA) must be notified immediately. Members of the CFIA will destroy, or bury carcasses and disinfect the ground on which they were found. The bison on the ranch will be vaccinated and the ranch will be quarantined.
 
 
 
Blackleg
 
Causative agent: Clostridium chauvei
There are other bacteria in this family that cause disease in cattle but C. chauvei is the only one that has been reported in bison (8). C. chauvei is a soil borne bacterium and can survive in the soil for many years. The bacterium enters the body through consumption of contaminated grass or hay. The disease is usually seen in the late summer when pasture is low, or bacteria can be picked up in hay swaths and cause disease during the winter when the hay is fed.
These bacteria may be found in the spleen, liver and intestinal tract of normal animals. However, disease occurs when bacterial spores that are lodged in normal tissue, usually muscle, proliferate. This usually occurs secondary to bruising of the tissue. As the bacteria proliferate they produce toxins that kill tissue and bring about toxemia.
 
Clinical signs:
The clinical signs of blackleg in bison have not yet been described (8), probably because of its rapid onset and quick progression to death. The following are some clinical signs that occur in cattle (9):
  • the most common finding is sudden death.
  • animals found alive will be depressed, anorexic, have a high heart rate and high body temperature.
  • swellings may be seen in localized areas. Characteristically, they show crepitus or the feel of gas under the skin.

Postmortem Findings:
Pathological changes associated with blackleg have not yet been described for bison (8). The following are some pathological changes associated with blackleg in cattle (9):
  • the carcass bloats and putrefies quickly after death.
  • body cavities often contain excess fluid, often reddish in color.
  • infected muscle masses are swollen, discolored and have a foul odor.
  • in some cases a small muscle mass will be affected and lesions may be hard to find.

Diagnosis:
The diagnosis of blackleg is most commonly made on postmortem examination. Affected tissue may be submitted to a diagnostic pathology laboratory for bacterial culture and identification.
 
Treatment:
There have been no treatment protocols established for bison (8). Treatment protocols that have been used for bison are similar to those described for cattle (9). The response to treatment is often poor and usually the animal is found dead, or too sick to consider treating. C. chauvei is susceptible to most antibiotics commonly used in cattle. Procaine penicillin G is often used. Vaccinate all animals in the face of an outbreak and treat all at risk animals with long acting antibiotic preparations to provide protection until immunity develops.
 
Control:
There have been no control protocols established for bison (8). Programs for controlling blackleg in bison are similar to those used in cattle (9). The clostridial vaccines commercially available in Canada have not been approved for use in bison. Studies on the effectiveness of these vaccines for the prevention of clostridial diseases in bison have not been reported. However, all bison should be immunized against blackleg. Bison that are properly vaccinated should not develop the disease. Commercially available vaccines are inexpensive, therefore costs should not be prohibitive. A multivalent 8-way vaccine should be used. Though C.chauveii is the only member of the clostridial family of bacteria actually reported to have caused disease in bison, it is quite likely that bison are susceptible to disease caused by other bacteria in this family. There are anecdotal (word-of-mouth") reports of Cl. haemoliticum infection causing acute and severe "redwater" or bacillary hemoglobinuria disease in bison. Many bison ranchers vaccinate all of their bison with a clostridial vaccine on a yearly basis.



Brucellosis
 
Causative agent: Brucella abortus
B. abortus causes disease in cattle, sheep, goats and bison (9). It has been reported to cause disease in bison in Canada and the United States (11,12,13,14,15,16,17).
 
Clinical signs:
In male bison, B.abortus infection causes orchitis, seminal vesiculitis, and epididmytits (18). In female bison it causes placentitis and abortion (11, 18).The frequency of abortion in bison may not be as high as in cattle. It has also been reported to cause abscesses and chronic septic arthritis in bison of either sex (11, 18).
 
Diagnosis:
In Canada, the Canadian Food Inspection Agency (CFIA) maintains a monitoring program for brucellosis and tuberculosis in bison. All bison herds must obtain a negative herd status. This is achieved by testing all bison on the farm that are over 18 months of age. After a herd test is found to be negative the farm will receive a negative herd status remaining in effect for 5 years. The farm's negative herd status may be extended by testing 10% of the total herd per year. If the negative herd status is allowed to expire the farm will be restricted from moving bison off the farm, until a negative herd status is regained.
 
Treatment:
In Canada, brucellosis is not treated. The CFIA administers a test and slaughter program for brucellosis. Bison that are infected or test serologically positive for B.abortus are slaughtered.
 
Control:
The Canadian government through the CFIA administers a surveillance program for detecting outbreaks of B. abortus infection. The program includes on farm testing, slaughterhouse testing, and monitoring of the movement of bison. Vaccination of bison against brucellosis is not permitted in Canada because vaccinated animals cannot be distinguished from infected animals by serological testing.
 
 
 
Foot Rot
 
Causative agent: Unknown in bison
In cattle, foot rot is caused by Fusobacterium necrophorum (9). The organisms responsible for footrot in bison have not been reported. In bison the incidence is relatively low compared to cattle (19). In cattle, wet weather, stony ground, and rough pasture can cause abrasions of the skin between the toes allowing bacteria to enter the interdigital tissue, producing lesions (9). The pathological features of foot rot in bison have not been reported.
 
Clinical signs:
The most frequent presenting sign is lameness that may be accompanied by spreading of the toes and swelling of the foot (19). In cattle inflammation of the foot can cause sufficient fever to result in temporary sterility of bulls. This has not been reported in bison. The infection can spread from the interdigital region into the joints of the foot causing arthritis and permanent lameness.
 
Treatment:
Injections of systemic antibiotics, such as penicillin, oxytetracycline, and sulfamethazine are the most common treatments for foot rot. Long acting antibiotic preparations are the most practical choice for bison (see treatment of actinobacillosis above). In many cases recovery is spontaneous (19).
 
Control:
The main goal is to reduce exposure of the bison to wet, muddy areas. Some suggestions are:
  • provide water in troughs, rather than dugouts and sloughs.
  • move water troughs when mud holes develop around them.
  • elevate water bowls and surround them with porous fill so that they are dry and well drained.
  • fence sloughs and wet areas to prevent bison from accessing them.
  • move salt, mineral, and grain feeders when mud holes develop around them.
  • watering areas, feeding areas, and salt blocks may be fenced and a foot bath with zinc sulfate, or copper sulfate set up in the entry way to these fenced areas.
Most cases are isolated and do not warrant extensive control measures.
 
 
 
Hemorrhagic Septicemia
 
Causative agent: Pasteurella multocida
Hemorrhagic septicemia has been reported in bison (20,21,22), but not in the last 30 years (23). The disease occurs in explosive outbreaks with high mortalities (21,22)
 
Clinical signs:
Young animals are most susceptible. The disease has a sudden onset. Clinical signs include a very high fever, profuse salivation, hemorrhages in mucous membranes, severe depression, as well as swelling of the throat, brisket and perineum. There is often labored breathing. Death often occurs in 24 hours.
 
Postmortem findings:
There is often widespread subcutaneous edema. There are extensive subserosal hemorrhages of the internal organs and body cavities. Commonly there is edema and inflammation of the lungs.
 
Diagnosis:
Diagnosis is most frequently made on postmortem examination of the carcass, and submission of tissues to a pathology laboratory for culture and identification of the bacterium.
 
Treatment:
The disease has not been reported for 30 years. Treatment protocols have not been described. If this disease was suspected , treatment with broad spectrum systemic antibiotics would be appropriate.
 
Control:
A formalin inactivated vaccine was developed and used in Montana (20). Control programs for bison herds in North America are not currently in use, since the incidence of disease is so infrequent .
 
 
 
Hemophilosis
 
Causative agent: Hemophilus somnus
Disease caused by H. somnus is very common in cattle (9). In Canada, 25% of cattle test serologically positive to H.somnus (9). H.somnus as been found to cause disease in bison (19). The bacterium has been isolated from the respiratory , urinary, and reproductive tracts of clinically normal cattle (9). H.somnus has been isolated from tonsils of clinically normal bison (24). Disease outbreaks in bison occur most commonly in the fall and winter and have been associated with very cold weather and stressful situations such as handling (19).
In cattle H.sommnus causes septicemia, meningitis, polysynovitis, pleuritis, suppurative bronchopneumonia, myocarditis, otitis media, mastitis, abortion and reproductive tract infections(9). In bison, only the meningitis form has been reported (19). In cattle, this form of H.somnus infection is called infectious thromboembolic menigioencephalitis or ITEME.
 
Clinical signs:
Sudden death is common. H.somnus has only been associated with disease in recently weaned bison calves. Calves may be found recumbent, depressed, and have a high or low body temperature. They may have blindness in one or both eyes. The eyes may be partially closed. Convulsions often occur prior to death. If clinically affected calves are found standing, they may be weak, staggery, or ataxic. They may knuckle over at the fetlocks. They may have muscle tremors. Their joints may be distended. Sick bison calves usually die within 24 to 48 hours.
 
Postmortem findings:
There are hemorrhagic infarcts in the brain and spinal chord.
 
Diagnosis:
Diagnosis of this disease is difficult in live bison. The clinical signs are suggestive of the disease but they are not definitive. The diagnosis is most often made from postmortem examination of dead animals. Tissues from the carcass, especially the brain, should be sent to a pathology laboratory for histopathology as well as bacterial culture and isolation.
 
Treatment:
Clinically affected bison calves may be treated with antibiotics. In cattle, oxytetracycline, or fluorfenicol are commonly used. Surveillance of at risk bison calves is critical to reducing mortalities once an outbreak has been established. Identifying and treating affected bison with minimal disturbance to the rest of the group can be very challenging. Disturbing the group by sorting and catching calves to assess their physical state by taking their temperature, pulse or respiration will significantly increase the stress placed on the calves. Bison respond less favorably to handling than cattle do. Often healthy bison that are handled take several days to return to their normal behavior. This makes monitoring programs that involve even minor handling of sick bison unsuitable. Bison tend to mask their expression of clinical signs when they are sick. Often they will not show any easily observable clinical signs of disease until just before death. Keen observation of calves at risk by producers who are knowledgeable of the behavior of bison, is important for the detection of even advanced cases of disease.
Once clinically affected bison calves are identified they must be very carefully removed from the group and treated. The entire group may be injected with fluorfenicol or long acting oxytetracycline. The behavior of bison calves varies greatly from farm to farm. On some farms the calves may be so excitable that the injuries and stress associated with handling may make mass injection impractical. In these instances, groups of bison calves from which clinical cases have occurred may be mass medicated with oxytetracycline in the feed or water.
Vaccinating in the face of an outbreak with commercially available H.somnus vaccines that are designed for use in cattle may reduce mortalities when used in bison calves.
 
Control:
There are many commercially available H. somnus vaccines that are designed for use in cattle. There is considerable variation in the efficacy of these vaccines in cattle. None of these vaccines are licenced for use in bison. The efficacy of these vaccines for the protection of bison against disease caused by H. somnus is unknown.
Vaccination may help reduce morbidity and mortalities in cattle, but probably doesn't work well to protect against all forms of the disease. Initial vaccination must be followed by a booster vaccination in three to four weeks. The booster must be administered at least three weeks prior to a risk period such as the onset of cold weather. If the disease occurs on a farm expect to see recurrences in subsequent years.
 
 
 
Johne's Disease
 
Causative agent: Mycobacterium avium, subspecies paratuberculosis
Johne's disease occurs in white-tailed deer, European red deer, reindeer, sika deer, axis deer, fallow deer, moose, aoudads, mouflons, llamas, African buffalos, water buffalos, camel, stonebucks, antelopes, yaks, gnus, zebu cattle, tule elk, bighorn sheep, mountain goats, American bison, and wapiti (25), as well as domesticated cattle, sheep and goats (9).
The disease is very common in cattle and sheep worldwide (9). When tested, 5.5% of cull cows in Ontario had Johne's (9). Sheep can carry and spread the bacteria, showing minimal disease themselves (9). The prevalence of this disease is increasing worldwide (9). The source of infection is ingestion of feed or water contaminated by the bacterium. In cattle and sheep the bacteria is shed in feces, milk, and semen. Infected cattle can shed the bacteria for years before they develop disease. In cattle, the bacteria can cross the placenta and infect the fetus. Thirty seven percent of fetuses from infected cows become infected (9). Infection of cattle usually occurs early in life, but disease does not occur until the animals are 3 to 5 years of age(9). The bacterium can persist for one year or more on pasture (9). Johne's disease has been reported in bison (25).
 
Clinical signs:
The clinical signs of Johne's disease have not been reported for bison (25). In cattle, the most common clinical signs are chronic diarrhea and loss of body weight leading to emaciation (9).Cattle may take up to a year to die (9).
 
Postmortem findings:
Pathological changes associated with Johne's disease in bison have not been documented (25). In cattle, the most common findings are emaciation and thickening of the walls of the small intestine and cecum (9).
 
Diagnosis:
The clinical signs of chronic diarrhea and emaciation are not specific to Johne's disease. There have been no specific diagnostic tests established for diagnosing Johne's disease in bison. Likewise, the only reliable method of establishing a diagnosis in cattle is postmortem examination. There are many tests available for use in live cattle, none of them are very sensitive. In general, there is a high probability of identifying an infected herd but it is not possible to consistently diagnose the presence of the bacterium in healthy, live individual animals.
Serological tests are of limited value for use as screening tests, but are reasonably accurate for diagnosing the disease in clinically affected cattle.
Fecal cultures are the most reliable diagnostic tests. As with serological testing, fecal cultures can detect herd problems, but are not very reliable for detecting disease in individual animals. However in cattle, fecal cultures are thought to be able to detect the presence of the bacterium in the herd 1 to 3 years before clinical disease is seen (9). Fecal samples must be taken from a number of individuals in the herd and must be repeated on several occasions in order to determine whether the bacterium is present or absent in the herd.
 
Treatment:
There are no treatment protocols established for the treatment of Johne's disease in bison. Treatment of cattle has been shown to produce temporary improvement, but has not been shown to cure animals (9). This disease is generally considered untreatable.
 
Control:
In all susceptible species, control has proven to be very difficult because there is no reliable test to determine if an individual animal is infected. This makes it impossible to identify and remove infected animals before they develop clinical signs. Because of the widespread nature of the bacterium, it is difficult to prevent its introduction into a herd when new stock are purchased. Fecal cultures of all animals every 6 months and culling of infected animals and their offspring has reduced, but not completely eradicated the disease from cattle herds (9). The only way to eradicate the disease is to depopulate and then repopulate from clean stock.
 
 
 
Leptospirosis
 
Causative agent: there are many different strains of leptospira that can cause disease (9).
Leptospirosis can cause disease in all farm animal species and in humans (9). Wild animals including dogs, skunks, deer, rats, bats and other rodents can carry the bacterium (9). Leptospirosis is often associated with wet areas having abundant surface water. The source of infection is usually from drinking water that is infected with the bacterium. Many animals can be carriers without developing the disease.
A serological survey of bison in Yellowstone National Park demonstrated that 1 to 7% of bison had titers to various strains of leptospirosis (26). Leptospirosis in bison has been reported (8).
 
Clinical signs:
The clinical signs of leptospirosis in bison have not been reported (8,26). Leptospirosis can cause a wide variety of syndromes in cattle including: septicemia, interstitial nephritis, abortion and mastitis (9). Many infected cattle don't show any signs of disease (9). Cattle with acute leptospirosis develop a high fever, depression, anorexia, hemolytic anemia, bloody urine, jaundice, increased heart rate, labored breathing, and bloody colored milk (9). Leptospirosis is associated with a high case fatality rate in cattle (9).
 
Diagnosis:
Urine may be submitted to a diagnostic pathology laboratory for bacterial culture and identification. Blood may be submitted to a diagnostic pathology laboratory for serology. Paired samples are required to demonstrate the presence of a rising titer of antibodies to leptospirosis.
 
Treatment:
There have been no treatment protocols described for bison (8). In cattle, treatment must be instituted as early as possible, before there is irreparable damage to the kidneys (9). In cattle response to treatment is poor (9). In cattle, broad-spectrum antibiotics are used to treat leptospirosis (9).
 
Prevention:
There have been no prevention programs reported for leptospirosis in bison. There are a number of commercially available vaccines approved for use in cattle. None of these have been approved for use in bison. In areas where leptospirosis is endemic cattle are vaccinated annually.
 
 
 
Listeriosis
 
Causative agent: Listeria monocytogenes
In cattle, L. monocytogenes causes encephalitis, abortion and septicemia (8). In bison, L. monocytogenes has been reported to cause abortions (8). The bacterium is very widespread in nature. L. monocytogenes is found in 46% of cattle manure samples and 82% of feed samples (9)
In cattle, stress may influence the occurrence of disease.
 
Clinical signs:
L. monocytogenes causes sporadic abortion in bison (8). Abortion usually occurs in the last trimester of pregnancy. In cattle, the incidence is low but has been as high as 15% (9).
 
Diagnosis:
To diagnose Listeria abortion an aborted fetus with placenta must be submitted to a diagnostic pathology laboratory for histopathology as well as bacterial culture and identification.
 
Treatment:
There have been no treatment protocols reported for the treatment of listeriosis in bison. Sick bison cows may be treated with long acting antibiotics.
 
Prevention:
There have been no control programs reported for listeriosis in bison (8).
 
 
 
Necrotic Stomatitis
 
Causative agent: Fusobacterium necrophorum
The bacterium is very common in the environment and necrotic stomatitis caused by F. necrophorum is very common in cattle (9). An injury or abrasion to the lining of the mouth from erupting teeth or rough feed will allow the bacteria to invade the tissue of the mouth or pharynx (9). Necrotic stomatitis has been reported in bison (8).
 
Clinical signs:
The clinical signs of necrotic stomatitis have not been described in bison (8). In cattle, clinical signs include increased body temperature, anorexia, depression, increased salivation, swelling of the cheeks from feed packed into the mouth, protrusion of the tongue, and ulceration of the cheek or tongue (9). If the larynx becomes infected, there may be a cough, labored breathing, or foul smelling breath(9).
 
Diagnosis:
Visual inspection of the mouth, tongue and larynx shows ulcers. A biopsy or culture may be sent to a diagnostic pathology laboratory for bacterial culture and identification.
 
Treatment:
There have been no treatment protocols described for bison (8). In cattle, broad-spectrum antibiotics are used (9). If the larynx is involved corticosteroids help to make breathing easier (9).In cattle the response to treatment is good unless the infection has spread to the cartilage of the larynx (9).
 
Control:
There have been no control protocols reported for bison. This disease tends to be sporadic, making control programs unnecessary.
 
 
 
Pasteurella Hemolytica Pneumonia
 
Causative agent: Pasteurella hemolyticum
In cattle there are many viruses, bacteria and various stressors associated with pneumonia. Pasteurella hemolytica has been associated with pneumonia in weaned bison calves (27). P. hemolytica has been found in the tonsils and upper respiratory tract of clinically normal bison (28,29,30). In cattle, it is thought that stressors such as shipping, weaning, mixing, overcrowding, starvation, water deprivation, and handling reduces the effectiveness of the lung's protective mechanisms. This allows viruses and bacteria to invade the lung and cause pneumonia. Pneumonia in bison calves has been associated with similar stresses (27).
 
Clinical signs:
The clinical signs of pneumonia in bison calves has not been described (27). In cattle, the clinical signs include: increased respiratory rate, cough, nasal discharge, depression, anorexia and weight loss (9). Pneumonia can be a frequent cause of sudden death in cattle (9).
 
Postmortem findings:
The pathological changes associated with P. hemolytica pneumonia in bison can be described as fibrinopurulent bronchopneumonia, with fibrinous pleuritis and pericarditis (27).
 
Diagnosis:
In cattle, the presence of pneumonia can be determined in live animals by clinical signs. Bison tend to mask clinical signs of disease. Typical clinical signs such as anorexia, depression and an increase in respiratory rate may not be easily observed in bison with pneumonia. Anorexic bison calves will often stand along side of their pen mates with their heads in grain or hay feeders and mimic eating.
Postmortem examination and submission of samples to a diagnostic pathology laboratory for bacterial culture and identification of the causative agent may make the diagnosis. Careful consideration should be given to nutritional changes, handling procedures, transportation, weather, and any other stressors that may be identified as possible contributors to the outbreak of pneumonia.
 
Treatment:
Treatment protocols for bison with pneumonia have not been reported (27). In cattle, many broad-spectrum antibiotics have been used to treat individuals and to mass medicate pens of cattle (9). If possible, long acting, broad-spectrum antibiotic preparations should be selected for use in bison. During an outbreak, careful surveillance of bison calves at risk with little or no intervention is critical to minimizing the mortalities caused by pneumonia. Keen observation by ranchers who are familiar with the behavior of bison calves will be essential for the identification of sick bison calves. Sick calves should be carefully removed from the group, treated and then returned to the group. Mass medication with long acting, broad-spectrum injectable antibiotics or through the feed or water with broad-spectrum oral antibiotics may be considered.
 
 
 
Pinkeye or Infectious Keratoconjunctivitis
 
Causative agent: unknown
In cattle, pinkeye is caused by Moraxella bovis. A culture survey for M. bovis demonstrated the bacteria in 12.7% of clinically normal bison eyes (19). In sheep and goats, pinkeye can be caused by Rickettsia, Chlamydia, and Mycoplasma organisms (9). Pinkeye has been seen in bison (19) but the cause has not been identified (19). In cattle the spread of pinkeye is accomplished by face flies (9).
 
Clinical signs:
One or both eyes may be infected (19). There is increased lacrimation, reddening of the conjunctiva, squinting, and cloudiness of the cornea, which may lead to ulceration of the cornea (19). In severe cases the cornea may become conical in shape (19). Temporary or permanent blindness can result (19).
 
Diagnosis:
Biopsies of the cornea or swabs of the conjunctival sac can be sent to a diagnostic pathology laboratory for bacterial culture and identification.
 
Treatment:
Recovery may be spontaneous in many cases (19). Small volumes of penicillin and corticosteroids may be injected into the bulbar conjunctiva or the onjunctiva of the eyelids (19). In cattle, third eyelid flaps or suturing the eyelids closed have been used. Bison will often remove these sutures shortly after they are placed, by rubbing their eyes and head on the ground (19). Large conical shaped corneas may take 6 months to a year to heal, or they may never heal.
Handling bison with pinkeye can be dangerous to the handlers as well as to the animal. Bison that are blind in one or both of their eyes will be unable to protect the affected eye from injury during handling. They will frequently rupture the globe of the affected eye in a handling facility, or a squeeze. Bison that are bilaterally blind from pinkeye are unable to avoid obstacles, fences, or other bison. This predisposes them to serious injury (19).
 
Prevention:
In cattle, prevention has been aimed at reducing the population of face flies to which cattle are exposed, reducing the spread of the infective agent (9). Insecticide ear tags have not been demonstrated to reduce the incidence of pinkeye in bison (19). Installing insecticide applicator wicks around grain and salt feeders as well as around water sources has been used to reduce the face fly population (19).
There are commercially available pinkeye vaccines on the market. They are designed for use in cattle. Since the etiological agent for pinkeye in bison is unknown, the efficacy of these vaccines in bison is very questionable.
 
 
 
 
Tuberculosis
 
Causative agent: Mycobacterium bovis
M.bovis can cause disease in many species including man (9). Tuberculosis has been reported in bison (12,15,31)
 
Clinical signs:
The clinical signs of tuberculosis in bison include chronic weight loss, chronic cough and enlarged lymphnodes (12,15,31).
 
Postmortem findings:
Bison with tuberculosis may have tubercular abscesses or granulomas in the lymph nodes of the head and pharynx, and the thoracic and abdominal cavities (12).
 
Diagnosis:
In Canada, tuberculosis caused by M. bovis is a reportable disease. The Canadian Food Inspection Agency maintains monitoring and surveillance of this disease. The diagnostic test used in bison is the intradermal caudal fold skin test.
 
Treatment and Control:
The Canadian Food Inspection Agency administers a program designed to monitor and detect M. bovis infections in bison. In Canada, bison herds must achieve and maintain a negative herd status from the CFIA. In order to do this, all bison in the herd over 18 months of age must test negative to the caudal fold skin test. The negative herd status will remain in effect for 5 years. Testing 10 % of the herd annually may extend the negative herd status.
 
 
 
 
 
Viral Diseases of Bison
 

Bovine Virus Diarrhea/Mucosal Disease (BVD)
 
Causative agent: BVD virus is an RNA virus from the family Togaviridae, genus pestivirus
BVD is a very complex disease. The behavior of this virus in cattle populations has not been completely established (9). Little is known about the behavior of the virus in bison herds, other than that it is present in bison herds (26) and that it causes disease (19). There are many different strains of the BVD virus identified in cattle populations (9). The strains of the virus found in bison have not been reported (19). BVD virus is found in all countries of the world where cattle are produced (9). Sixty to 80% of cattle tested have antibodies to the virus (9). The Yellowstone National Park survey of 1991-92 demonstrated antibody titers in 31% of bison tested (26).
Transmission of the disease in cattle is thought to be by direct contact between animals (horizontal) and across the placenta to the fetus (vertical)(9). In cattle, BVD virus can be shed in nasal discharge, saliva, semen, feces, urine, tears, milk and discharges following abortion of a fetus (9). Some cattle can become persistently infected. These animals shed large quantities of the virus for the rest of their lives and are probably the main source of infection in cattle herds (9).
 
Clinical signs:
There are several different manifestations of BVD in cattle (9).
  • Acute BVD
Acute BVD has not been described in bison. In cattle, acute BVD occurs in animals that have not been previously exposed to the BVD virus. This form of BVD can be an inapparent (symptomless) infection or it can cause acute explosive diarrhea associated with elevated body temperature and anorexia. These cattle are sick for a few days to a week and then recover. Occasionally affected cattle may die directly from the virus or from secondary infections. BVD infection in young calves may cause severe diarrhea (scours). Acute BVD is seen in bison and can cause mortalities in bison at any age (19).
  • Fetal infections
Fetal BVD infections have not been reported in bison. In cattle, they are seen following an acute BVD outbreak. Fetal infections can cause abortion, stillbirths , weak calves, and fetal abnormalities. If the fetus is infected with the virus in the first 125 to 150 days of gestation, the fetus may become persistently infected. When these calves are born they are infected and remain so for the rest of their lives (9).
  • Mucosal disease
Mucosal disease has not been reported in bison. In cattle, this disease only occurs in animals that are persistently infected. It is thought that all persistently infected calves die of mucosal disease at some time in their life, but how long they may live is unknown. Some persistently infected cattle remain relatively normal and shed the virus to other animals in the herd for years. They will pass the virus on to their own calves producing more persistently infected calves.
Persistently infected calves may be unthrifty, poor doing calves that have low weaning weights. Persistently infected calves may have a rough hair coat or they may have skin lesions. They may develop lameness with associated foot lesions. These calves may become suddenly ill at any time in their life with diarrhea. They may have an elevated temperature, anorexia, nasal and ocular discharge, and lesions in the mouth and feet. They may die quickly or become chronically ill, taking months to die.
If there many persistently infected animals in the herd, mucosal disease can occur in outbreak form. Outbreaks are thought to be triggered by the introduction of a different strain of BVD virus into the herd.
  • Thrombocytopenic form of BVD
This form of BVD has not been reported in bison. In cattle, this form of BVD is similar to the acute form of BVD in that animals are exposed to the virus and subsequently develop disease. This form of BVD produces hemorrhage into all mucous membranes, bloody nasal discharges, bloody diarrhea and bleeding from injection sites. Mortality associated with this form of BVD is very high.
 
Postmortem findings:
The pathological changes associated with BVD in bison have not been documented (19). In cattle, postmortem findings include shallow ulcers in the mouth, pharynx, esophagus, rumen, and omasum. There may be erythema and hemorrhages in the abomasal mucosa. There may also be lesions in the feet (19).
 
Diagnosis:
In cattle, blood samples for virus isolation or polymerase chain reaction (PCR) testing give reliable results (9), especially in cattle that are persistently infected. Most commonly the diagnosis is made on postmortem examination and submission of samples to a diagnostic laboratory. Skin samples from dead, persistently infected animals can be used to isolate the virus even if the carcass is decomposed or partly eaten by scavengers (19).
 
Treatment:
There are no specific treatment protocols established for treating BVD in cattle (9) or bison (19). Cattle and bison with BVD have not responded to any treatment (9,19).
 
Control:
There are no protocols established for controlling BVD in bison. In cattle, control of BVD has proven to be difficult for some forms of the disease. Vaccination may not provide adequate protection against the occurrence of mucosal disease and the formation of persistently infected cattle. Vaccination may provide adequate protection against acute BVD infection and the thrombocytopenic form of the disease in cattle.
There are many commercially available BVD vaccines. They are all designed for use in cattle and none of them have been registered for use in bison. The effectiveness of these vaccines in bison has not been established. The use of these vaccines in bison should be approached with caution. There is considerable variation among these vaccines. There are variations in the constituents of both modified live and killed virus vaccines. The adjuvants and immune stimulants found in killed BVD vaccines may have unfavorable affects on bison calves (19). Modified live BVD vaccines have been observed to cause diarrhea in recently weaned bison calves on bison ranches (19). Yearling, two year old ,and adult bison on bison ranches have not been observed to be as susceptible to the harmful effects of some of these vaccines (19). In the past, modified live virus BVD vaccines have been associated with abortion when administered to pregnant beef cattle. These vaccines therefore should probably not be administered to pregnant bison cows.
Vaccination programs for bison should not be a carbon copy of vaccination programs that have been designed for use in beef cattle. Vaccines should be chosen with careful consideration. The time of administration and the method by which vaccines are administered should be discussed thoroughly with bison ranchers. Programs should be developed that are sensitive to the reproductive and productive cycles of bison as well as to their behavior.
 
Handling Note!
The behavioral characteristics of bison have forced bison ranchers to develop new and creative methods for handling them. Handling of bison, however, is still a very common cause of injury and death. At some times of the year certain groups of bison should not be handled at all. Handling of bison cows from the onset of calving season until weaning time should be done with extreme caution. Cows with calves at foot will often challenge, rather than move away from people trying to chase them. Moving bison cows with calves at foot through narrow runways or confining them in small corrals will often cause cows to trample and seriously injure their calves.
 
 
 
Calf Scours (Neonatal Diarrhea)
 
Causative agent: Rotavirus
In cattle, there are many agents associated with calf scours. These include E.coli, rota virus, corona virus, breda virus, calici virus, parvo virus, astro virus, cryptosporidium, giardia, BVD, salmonella, and Clostridium perfringens (9). In bison, rotavirus is associated with neonatal diarrhea (19).
This disease is not as common in bison as it is in cattle. In cattle, stress factors to which neonatal calves are exposed, such as overcrowding, extreme weather conditions, poor nutrition of the dam, inadequate consumption of colostrum, are thought to predispose the calves to the disease (9). Calf scours may not be as prevalent in bison because calving occurs later in the spring when weather conditions are mild. During the calving season bison are usually out on spring pastures. The nutrition provided to the cows by the new pasture will usually be good and the cows will not be overcrowded. The occurrence of calf scours in neonatal bison calves has been associated with overcrowding (19).
 
Clinical signs:
The most consistent clinical sign is watery diarrhea(19). As the disease progresses the calves with scours may become dehydrated, weak, and depressed. They may stagger and will often become recumbent before death.(19). In some cases the calves show minimal clinical signs and may be identified as being sick only when the disease has progressed to the point where treatment is unrewarding, and death is impending (19). In some instances, the first indication of scours is the occurrence of mortalities in the herd (19).
Since bison calves have the ability to mask clinical signs of disease, it is important to constantly monitor the fecal output of neonatal calves. This involves observing the calves while they nurse, observing the perineal area of calves as they walk away from the observer, and observing the bedding areas of calves for diarrhea like feces.
 
Postmortem findings:
The pathological findings associated with calf scours in bison calves include: dehydration, emaciation, and fluid feces in the intestinal tract (19).
 
Diagnosis:
Fecal samples taken from bison calves with scours may be submitted to a diagnostic pathology laboratory for bacterial culture and virus isolation. Postmortem tissue samples should be sent to a pathology laboratory for histopathology, bacterial culture and virus isolation.
Treatment:
Many bison calves with scours recover spontaneously (19). Treat bison calves when they become dehydrated, depressed, start staggering, or are too weak to nurse. Treating scouring bison calves commonly involves removal of the calf from its mother. Removal of a calf from its mother for evan a few days will result rejection of the calf when it is re-introduced. These calves must then be hand reared, or they will starve to death. Making a decision to remove a bison calf from its mother for treatment most often involves a decision to hand rear the calf if it survives the disease. A provision for hand rearing should be made at the time the decision is made to treat the calf.
Hand rearing neonatal bison calves requires considerable time commitment. Success has been achieved by bottle feeding bison calves with fresh cows milk, bovine calf milk replacer, or by using nanny goats as surrogate mothers. It is important to consider the disease status of the donor cow, or goat, and the farm from which they originate. Johne's disease is relatively common in beef and dairy herds. Inquiries should be made as to whether the herd of origin has had any cattle diagnosed with Johne's disease, whether they do any testing for Johne's disease, and whether they have had any cattle that develop chronic diarrhea. Malignant catarrhal fever is common in goat populations. The virus may be found in goats that are clinically normal. Before a goat is brought onto a bison ranch, it should be blood tested to determine if it is carrying malignant catarrhal fever virus.
Treatment of bovine calves with neonatal diarrhea involves oral or intravenous replacement of the fluid and electrolytes that are expelled from the calf's body with the feces. The fluid and electrolyte imbalances that occur in neonatal bison calves with scours have not been documented. It may be incorrect to assume that the imbalances that occur in bison calves are the same as those that occur in beef and dairy calves. Cattle are, however, the closest species to bison from which to draw information for the development of bison treatment protocols.
Oral replacement of fluid and electrolytes may be attempted by administering commercially available electrolyte replacement solutions. There are many of these products available, none of them are specifically designed for use in bison calves.
Bison calves with scours will frequently be unable, or unwilling to suck a nipple. In this case, fluids will have to administered via a stomach tube or an esophageal feeder. Oral replacement electrolyte solutions may be administered to scouring bison calves at the rate of 1 to 2 liters every 4 to 6 hours. The calf's hydration status and fecal output should be monitored and the rate of administration adjusted accordingly. If the calf fails to respond to oral electrolyte replacement, electrolyte solutions such as lactated ringers may be administered intravenously. Scour boluses may not have any affect on the outcome of the disease. Their use is not recommended. Scouring bison calves may be susceptible to other infections. It may be advisable to treat scouring calves with parenteral antibiotics.
 
Control:
In Canada and the United States there are many commercially available scour vaccines. None of these vaccines have been approved for use in bison. Since the agents that cause neonatal diarrhea in bison have not been determined, and since these agents may be different from those that cause neonatal diarrhea in cattle; the efficacy of these vaccines for the prevention of neonatal diarrhea in bison calves is questionable.
The occurrence of neonatal diarrhea may be associated with many determinants other than bacterial or viral agents, such as wet environmental conditions, overcrowding and poor nutrition of the dam. If a herd problem arises it would be prudent to try to identify not only a causative agent specific to the herd, but also other environmental factors that may be significant contributors to the development of the disease. Since the efficacy of commercially available cattle scour vaccines is questionable, better results may be achieved by altering environmental conditions and management programs, than by vaccinating bison.
 
 
 
Infectious Bovine Rhinotracheitis (IBR)
 
Causative agent: Bovine Herpes Virus
IBR is very common in cattle. It is also seen in white-tailed deer, mule deer, and antelope (9). Nasal exudate, semen and fetal fluids spread the disease. Aerosol spread from coughing is thought to be the most important method of transmission (9).
A serologic survey of bison from Yellowstone National Park in Wyoming in 1991-1992 demonstrated antibodies in 31% of bison tested (26).
 
Clinical signs:
The clinical signs of IBR in bison have not been described. In cattle, IBR often occurs in very explosive outbreaks (9). It is very contagious, 100% of the animals in a herd can be infected. Clinical signs in cattle include: fever, anorexia, reddening of the nasal mucosa, ocular discharge, nasal discharge, an increase in respiratory rate, and a cough. Some animals may develop reddened eyes that may be mistaken for pinkeye.
Cattle less than 1 week of age may develop a systemic form of the disease that is associated with a very high mortality rate. Cattle less than 6 months of age can develop encephalitis, characterized by incoordination and convulsions associated with a high mortality rate. In adult cattle, abortion is a common sequella of the disease, occurring up to 90 days after infection.
 
Postmortem findings:
The pathological changes associated with IBR in bison have not been reported. Postmortem findings in cattle include lesions in the nasal cavities, pharynx, larynx , trachea, and on the muzzle (9).
 
Diagnosis:
The virus may be isolated in swabs taken from nasal and ocular exudate. Most commonly the diagnosis is made on postmortem examination of aborted fetuses and submission of samples or the whole fetus to a pathology laboratory for histopathology and virus isolation.
Blood testing may be done to detect rising titers to IBR virus. Two blood samples must be taken 2 to 3 weeks apart.
 
Treatment:
Protocols have not been reported for treating IBR in bison. Because of the contagious nature of the virus, infected bison should be separated from non-infected bison. In cattle, vaccinating with a modified live intranasal vaccine in the face of an outbreak may reduce the spread of the disease (9).
 
Control:
There have been no protocols reported for controlling IBR in bison. In Canada and the United States there are many commercially available modified live and killed IBR vaccines. None of them have been approved for use in bison. Most of these vaccines provide good protection against the occurrence of IBR in cattle, but their efficacy in bison has not been established.
The effect of modified live virus IBR vaccines on young bison has not been studied. Because of this it may be advisable to refrain from using a modified live IBR vaccines on recently weaned bison calves.
The nature of killed virus vaccines is such that a booster vaccine must be administered roughly 3 weeks after the initial vaccination in order for adequate protection to be provided. Meeting these requirements for recently weaned bison calves may be difficult. The stress associated with handling of bison is greatest in bison calves at the time of weaning. Also, the injuries and mortalities associated with handling of bison is greatest in bison calves of weaning age.
Killed virus vaccines should be administered to bison on a yearly basis in order to provide adequate protection. Modified live virus, intramuscularly administered IBR vaccines may provide adequate protection to bison. The duration of the protection is unknown , but it may not be for the entire life of a bison.
Modified live virus, intranasal, IBR vaccines provide adequate protection to cattle. They are difficult to administer properly to bison. If they are to be used in bison it may be prudent to vaccinate the entire herd every year or every second year to ensure that all animals are vaccinated adequately.
 
 
 
Malignant Catarrhal Fever (MCF)
 
Causative agent: Ovine herpes virus Type 2 (in North America)
The virus that causes malignant catarrhal fever has never been isolated and propagated. The principal host for this virus is sheep, in which the virus causes no disease. In a serologic survey in the USA, 61% of goats and 53% of sheep were seropositive to MCF virus by competitive-inhibition ELISA testing (32).
MCF causes disease in dead end hosts such as cattle, bison and deer species (9). The virus is thought to be transmitted from sheep and possibly goats to dead end hosts (bison?), but not from dead end host (bison) to dead end host (bison) (9). The mechanism of transmission of the virus is not known..
 
Clinical signs:
Malignant catarrhal fever has been reported in bison (33,34,35,36,64). In the past, the disease has always been considered to be fatal in bison (35). Bison can develop an acute fatal form of disease in which they die in 7 to 10 days, a chronic fatal form in which they die in periods of up to 156 days, and a recovered form in which they remain persistently infected for an unknown length of time (36,64).
Clinical signs in bison are reported to include: corneal opacity, conjunctivitis, ocular discharge, nasal discharge, excess salivation, anorexia, diarrhea, melaena , hematuria , multi focal ulceration of the oral mucosa, fever, circling, ataxia, behaviors suggestive of blindness, lameness, and difficulty urinating (33,34,35,36,64). The most common presenting clinical signs are anorexia, depression and bloody diarrhea (64).
The disease is usually seen in the winter (64). The disease is usually seen in bison over 6 months of age (64). Herd mortalities have ranged from 3 to 100% (34,35,64).
 
Postmortem findings:
Postmortem findings include corneal opacity, reddened conjunctiva, ulcerations and erosions of the mouth, esophagus, rumen, abomasum, intestinal tract, and trachea, hemorrhages in the urinary bladder, and enlarged lymph nodes(34,35,36).
 
Diagnosis:
The diagnosis may be made from blood samples and nasal swabs that are submitted to a diagnostic pathology laboratory for PCR testing. Herds may be monitored for infection by submitting a serum sample to a laboratory for antibody detection with a competitive inhibition ELISA test. Postmortem examination and submission of tissue samples to a diagnostic pathology laboratory for histopathology and PCR testing may be used to establish a diagnosis.
 
Treatment:
There have been no successful treatment protocols established for treating MCF in bison. Treatment with corticosteroids may prolong the course of the disease.
 
Control:
In Canada and the United States there are no commercially available vaccines for the control of MCF in any species. Additions to a herd should be tested with a PCR test or the competitive inhibition ELISA test before being introduced to the herd. Introduced bison should be quarantined for at least one month before introduction into the herd.
Since a large percentage of normal sheep and goats carry MCF virus, it would be advisable to avoid any contact between bison and sheep or goats. The safe distance between bison and sheep or goats may be greater than one mile. If goats are to be used as surrogate mothers for bison calves they should be tested for the presence of MCF virus before they are purchased.
 
 
 
Parainfluenza 3 Virus (PI3)
 
Causative agent: Parainfluenza 3 virus
In a 1991-92 serologic survey of bison in Yellowstone National Park, Wyoming, 36% of all bison tested had antibody titers to PI33 virus from 0 to 100% during the period 1977 to 1984. There was no observed clinical disease or decrease in productivity during this period. The source of the virus is thought to have been the cattle in the area (38).
  virus (26). In Delta Junction, Alaska, free ranging bison demonstrated an increase in the prevalence of antibody titers to PI
Clinical signs:
There has been no known disease, or reduced productivity associated with PI3 infection in bison (38). In cattle, PI3 infection in concert with various stressors and other disease causing agents, has been associated with pneumonia (9).
As the population of bison in North America grows, the methods of production of bison will probably intensify. As this happens the various stresses placed upon bison will change. In other species raised under intensive management conditions, disease occurrence involves a complex interaction of infectious agents, management associated stressors, and environment associated stressors. Infectious agents, such as PI3 may begin to play a more important roll in the development of disease in intensively raised bison.
 
Diagnosis:
Exposure of bison to the virus may be diagnosed by submitting blood samples to a diagnostic pathology laboratory for serology.
 
Treatment:
Since there has been no disease associated with PI3 infection in bison, there is no treatment required.
 
Control:
At the present time vaccination programs to control PI3 infection in bison are not recommended.
 
 
 
 
 
Parasitic Diseases of Bison
 
 
Anaplasmosis
 
Causative agent: Anaplasma marginale
A. marginale parasitizes the red blood cells of the host animal. It is transmitted between hosts by insect vectors. In the western USA the most common vector is the tick Dermacentor andersoni (9). Anaplasmosis has been experimentally induced in bison (39). 15.7% of bison tested at the National Bison Range in Montana, were positive to Anaplasmosis as determined by a compliment fixation test (39).
 
Clinical signs:
In cattle, the common clinical signs include anemia, jaundice, emaciation and debility (9). Bison calves experimentally infected with anaplasmosis demonstrated very mild clinical signs that included anemia, mild depression and listlessness (39). It is suggested that bison may be more resistant to anaplasmosis than cattle (39).
 
Diagnosis:
Anaplasmosis may be diagnosed in bison by examining blood samples for the presence of A. marginale on erythrocytes (39). Blood samples may be submitted to a diagnostic pathology laboratory for a compliment fixation test, detecting of antibodies to anaplasmosis.
 
Treatment:
There have been no treatment protocols established for treating anaplasmosis in bison. Cattle with anaplasmosis respond well to treatments with long acting tetracyclines (9).
 
Control:
There have been no control programs reported for anaplasmosis in bison. There are vaccination protocols established for cattle. They do not provide complete protection against anaplasmosis for extended periods of time. Some of the vaccines are associated with serious side affects (9). It may not be advisable to use these vaccines in bison.
 
 
 
Babesiosis
 
Causative agent: Babesia bigemina, Babesia major
There are other species of Babesia that cause Babesiosis in other host species. B.bigemina and B.major are the only species reported to cause babesiosis in bison (40,41). Babesia are protozoal parasites that cause intravascular hemolysis.
Babesia are transmitted by tick vectors. In the USA the tick vector for B.bigemina has been eradicated. B.major has been reported to cause babesiosis in bison in Britain (40). In the USA, babesiosis has been induced in bison by experimental infection with B.bigemina(41). Natural infections of bison with B.bigemina have not been reported.
 
Clinical signs:
Clinical signs include fever, jaundice, hemoglobinuria (frothy dark red urine), heavy breathing, and anorexia (40,41).
 
Postmortem findings:
Postmortem findings include enlarged spleen, enlarged liver, jaundice, and hemoglobinuria. (40,41)
 
Diagnosis:
Babesia may be observed in smears made from blood taken from live infected bison, or from blood obtained from the heart of dead bison (40).
 
Treatment:
There are a number of drugs that have been used to treat babesiosis in cattle (9). Diminazene aceturate at 3mg/kg (41) and amicarbalide at 5 grams per adult bison cow (40) have been used successfully to treat babesiosis in bison.
 
Control:
There have been various protocols described for controlling babesiosis in cattle (9). These include vaccination, reducing the tick vector burden on cattle, and eradication of the tick vector (9). Natural infections of bison by Babesia species have not been reported in North America, so control programs for the prevention of babesiosis in bison have not been implemented.
 
 
 
Coccidiosis
 
Causative agents: Emiria auburnesis, Eimeria bovis, Eimeria brasiliensis, Emiria canadensis, Emiria ellipsoidalis, Eimeria zurni
Although these 6 species of Eimeria have been isolated from the feces of bison, no associated disease has been reported. In cattle, coccidia species cause bloody diarrhea in calves. The disease is associated with overcrowding, fecal build up in pens, fecal contamination of water sources, weaning, transport and mixing of calves, and cold weather conditions. Coccidia oocysts will survive well in a wet environment. Dry, sunny conditions will dramatically reduce the survival of coccidia oocysts in the environment . The occurrence of disease is associated with the build up of coccidia oocysts in the environment and the consumption of large numbers of oocysts by calves (9).
  (45,46).
Clinical signs:
There has been no clinical signs of disease reported in bison. In fecal examinations of bison and cattle that were free ranging on the same pasture in Utah, coccidia oocysts were identified in cattle feces, but not in bison feces. Bison ranged further from water sources and spent less time congregated around water sources than cattle. It is suggested that these behavioral characteristics were at least part of the reason why coccidia oocysts were not isolated in the feces of the bison (47).
In other studies, fecal samples obtained from bison maintained in confined or ranch conditions contained coccidia oocysts (45,46). Although clinical coccidiosis has not been reported in bison, it is possible that poor management conditions may precipitate the occurrence of disease. These conditions might include overcrowding of bison calves resulting in the build up of coccidia oocysts in the environment, wet conditions that allow the survival of oocysts, poor pen design allowing fecal contamination of feed and water, stress associated with weaning, and severe environmental conditions.
 
Diagnosis:
Coccidia oocysts may be easily identified by examining fecal samples from bison. It is important to note that the presence of coccidia oocysts in the feces of bison may not be an indication that coccidia is the cause of disease. Bison calves must have diarrhea that contains at least 5000 coccidia oocysts per gram of feces.
 
Treatment:
Medications for treating coccidiosis in cattle include: sulfamethazine, nitrofuazone and amprolium (9). None of these chemotherapeutic agents have been licenced for use in bison.
 
Control:
Preventative programs for bison should be centered on the management of weaned bison calves to avoid conditions that may predispose bison calves to coccidosis. These should include :
  • Confine cows with calves at foot in pens prior to weaning. Then return the calves to the same pens after weaning. This will ensure that the calves are familiar with the pens and know where feed and water is located.
  • Separate cows from calves with a secure fence that allows the cows and calves to have visual and muzzle to muzzle contact.
  • Delay weaning until mid winter. This will allow the calves to become acclimatized to the weather. At this time the calves will be older and have a larger body mass, which should make them better able to withstand the stress of weaning when it is associated with cold weather.
  • Weaned bison calves should have lots of space, to prevent fecal build up in the pens.
  • Feed bunks and water sources should be well separated to prevent fecal build up around them.
  • Remove feces when it builds up around water sources. If possible feed bunks should be moved when feces builds up around them, or the feces should be removed.
  • Ensure that there is adequate feed bunk space for all the calves. Monitor the feeding behavior of calves closely. Weaned bison calves will quickly develop dominance relationships. If there is not enough feed bunk space, non-dominant calves will be forced to wait for an opportunity to feed. If the feed bunk space is severely restricted, non-dominant calves may not be allowed to access feed at all. This will be especially true for grain or supplements which are provided in small quantities that are only available to the calves for short periods of time.
  • Don't transport or mix calves until one to two months after weaning.
  • In cattle, monensin and lasalocid have been fed to calves in feedlots to prevent the development of clinical coccidiosis, and to cows during the winter to reduce the shedding of coccidia oocysts onto winter feeding or bedding grounds. Although these products have been used in bison their efficacy and safety have not been established (19).
     
Demodex Mange
 
Causative agent: Demodex spp.
The species of demodex that causes demodecosis in bison has not been identified. Demodex mites invade hair follicles and sebaceous glands of the skin of animals, and man.
 
Clinical signs:
Demodecosis appears as small pus filled nodules, 7-9 mm in diameter, around the eyes, perineum and ventral aspect of the tail. It has also been associated with small but palpable lesions on the neck, flank and shoulders (48).
 
Diagnosis:
The nodules are easily visible around the eyes and perineal region. The pus from nodules may be examined under a microscope for the presence of the mite.
 
Treatment:
Demodecosis is of relatively minor significance in bison. Ivermectin has been show to be effective for the treatment of demodex mange in cattle(9).
 
Control:
Control programs for demodecosis in bison have not been reported and may not be required.
 
 
 
Hydatid Tapeworms
 
Causative agent: Taenia hydatigina, Echinococcus granulosis
T. hydatigenia is found in North America, E. granulosis is found world wide (56). The adult forms of these two tapeworms live in the intestinal tracts of their primary hosts, wild and domestic carnivores. They release eggs that are carried out of the host in the feces. If the eggs are consumed by a secondary host, including cattle, sheep, bison and other herbivores, the eggs will hatch in the intestinal tract and migrate to the liver, lungs and peritoneal cavity. Once they reach these locations the parasites will form cysts, called cysticerci or hydatids. If a carnivore that is consuming the infected carcass of a secondary host, eats a hydatid cyst or cysticrecus, the life cycle will be completed, with the adult stage of the parasite developing in the intestinal tract.
Disease will occur when secondary hosts are kept in close contact with primary hosts, such as dogs, or when primary hosts contaminate the secondary hosts (bison) food source. When the secondary host (bison) consumes large quantities of eggs, multiple cysts may be formed in the liver or lungs. These cysts can cause severe damage to these organs, resulting in organ failure and disease.
 
Clinical signs:
T. hydatigina has been found in bison, but was not associated with disease (50). E.granulosis has been found in American bison in a zoo in India, however the clinical signs, if any, were not reported (55).
 
Postmortem findings:
Pathological changes associated with E. granulosis infection in bison include hepatomegaly, hydatid cysts in the liver, and hydatid cysts in the lungs (55).
 
Diagnosis:
There are no specific tests that can be used to diagnosis the presence of hydatid cysts in the secondary host.
 
Treatment:
There have been no treatments reported for hydatid cysts in bison. In man, hydatid cysts are treated with mebendazole, albendazole, praziquantel, or surgical removal (56). It is not known how effective these treatments would be for bison.
 
Control:
Since the source of infection is eggs in carnivore feces, control should be achieved by preventing the contamination of bison feed and pasture with carnivore feces. This will be impractical when bison are on pasture. During winter-feeding, the most likely source of infection will be farm dogs. If farm dogs are suspected to be the source of E.granulosis they should not be allowed access to bison feed or feeding areas. To prevent farm dogs from becoming infected they should not be allowed to eat the carcasses of bison, cattle or other herbivores, such as deer or moose. They should not be fed scraps or raw meat taken from carcasses of herbivores that have been hunted for food. Farm dogs should be tested periodically for the presence of tapeworm eggs in their feces and treated if eggs are present.
 
 
 
Liver Fluke
 
Causative agent: Fasciola hepatica
F. hepatica has been isolated from fecal samples taken from bison in Utah (42). The life cycle of F. hepatica requires the passage of immature stages of the fluke through snails. Immature stages of the fluke leave the snail and encyst on vegetation. Bison, cattle and sheep are infected when they consume infected snails or cysts. Once consumed, the immature flukes leave the intestinal tract of the new host and migrate through the peritoneal cavity to enter the liver, where they travel around causing damage to the liver. After 4 to 5 weeks the flukes enter the bile ducts of the liver and begin to lay eggs. These are passed into the intestinal tract, where they hatch into immature forms of the fluke. The immature flukes pass out of the host in the feces. Once on the ground the immature flukes can infect snails.
In cattle and sheep, flukes can cause acute hepatitis while they are migrating through the liver. Alternatively, chronic hepatitis may be associated with damage to the biliary system, caused by flukes residing in the bile ducts (9).
 
Clinical signs:
Clinical signs associated with liver flukes in bison have not been reported. In cattle, liver fluke infection produces clinical signs associated with acute and chronic hepatitis. These include sudden death, anemia, hypoalbuminemia, edema, and ascites (9).
 
Postmortem findings:
Pathological changes associated with liver fluke infection in bison have not been reported. Cattle that have acute hepatitis caused by fluke infection may have a large swollen liver with perforations of the capsule and subcapsular hemorrhages. There may be damage to the liver parenchyma caused by the passage of liver flukes. Cattle with chronic disease may have enlarged bile ducts with adult liver flukes in them (9).
 
Diagnosis:
In chronic cases fluke eggs can be observed in fecal samples taken from bison. In cattle, acute cases are most commonly diagnosed on postmortem examination (9).
 
Treatment:
There have been no treatment protocols reported for bison. In cattle, trichlabendazole is commonly used. Neither the efficacy nor safety of this drug has been established for bison.
 
Control:
Control should be aimed at reducing the levels of immature flukes found in snails and in vegetation and at preventing bison from consuming encysted flukes and infected snails. Encysted flukes do not survive freezing, and severe die offs of snails often happen during the winter, especially among snails that are infected with flukes. In the spring, cattle and sheep that carry adult flukes in their bile ducts often contaminate pastures. If bison were to be treated with flukicides, the treatment should be administered early in the spring, to reduce the number of flukes that infected bison pass out onto pasture during the summer.
Immature liver flukes do not survive well in dry pasture conditions. Snails are most likely to be found in marshy conditions. If liver flukes were a problem on a pasture, it would be wise to fence any wet or marshy areas to prevent bison from gaining access to them.
 
 
 
Lungworm
 
Causative agent: Dictyocaulis hadweni, Dictyocaulus filaria, Dictyocaulus vivparus.
Dictyocaulis spp have been isolate from bison in Kansas (49), Montana (42), Oklahoma (43), and Alberta(19). Mature lungworm live in the bronchi of the lungs of infected animals. They produce eggs that hatch into larva, which are swallowed and passed out in the feces. The larva can survive overwinter on pasture. Dry, warm and sunny weather will destroy larva. Lungworm larvae that are consumed by bison on pasture pass through the wall of the bison's intestinal tract and then enter the venous drainage of the intestine. Once in the circulatory system the larvae pass through the heart and lodge in the lung.
 
Clinical signs:
The clinical signs associated with lungworm in bison include increased respiratory rate, cough, slight nasal discharge, increased heart rate, mild fever (19).These clinical signs are difficult to recognize in bison on pasture. Often the first indication of clinical lungworm infection is dead bison (19). The disease is most commonly seen in late summer (19).
 
Postmortem findings:
Postmortem findings include pulmonary edema, emphysema and large quantities of bloody froth in the trachea and bronchi containing adult lungworm (19).
 
Diagnosis:
Fecal samples can be examined for the presence of lungworm larva. Routine flotation techniques will not detect lungworm larva. A Baerman sedimentation procedure must be performed on fecal samples. The ideal time for testing is the spring (April, May, June), to determine if any lungworm have been maintained in the herd over winter. In areas where lungworm has been a problem in previous years, bison should be tested in late July and August to determine if they are becoming infected while on pasture.
 
Treatment:
Ivermectin, oxfendazole, fenbendazole, albendazole, febantel, and levamisole have been used to treat lungworm infection in cattle (9).None of these products have been approved for use in bison.
Treatment should be instituted in late spring, just before the herd goes out to pasture. Reducing the worm load in bison at this time will result in a reduction in the number of eggs that are deposited on the pasture over the course of the summer. Pregnant cows, and cows with calves at foot will be difficult to handle during the spring of the year. If lungworm is suspected, oral fenbendazole can be provided in the feed, or in the salt.
If outbreaks occur in the summer, yearlings and two-year-olds can be rounded up and treated with ivermectin. Cows with calves at foot can be treated, on pasture, with fenbendazole in the salt. Routine treatment of bison in the late fall or early winter with ivermectin may not prevent the occurrence of clinical cases of lungworm. During the winter lungworm in the bronchi of cattle may enter a hyperbiotic state. When lungworm larva are in this state they stop growing, and may be resistant to agents that would otherwise kill them.
 
Control:
Programs to control lungworm in bison should include well timed administrations of anthelmintics as well as pasture management programs that are aimed at reducing the number of larva consumed by bison while on they are on pasture.
Since lungworm larva cannot withstand dry, sunny and warm conditions, contaminated pastures should not be grazed early in the spring. In areas where lungworm is endemic, pastures that have been grazed during the late summer should not be grazed until mid summer of the following year. Often even a few weeks of warm, dry weather will be enough to destroy most of the existing lungworm larva on the pasture. A simple two-pasture rotation system can be setup, in which one pasture is used for spring to early summer grazing and another is used for summer and fall grazing.
In endemic areas, bison should be treated with anthelmintics just prior to being turned out to pasture. If anthelmintics were to be used during the summer, it would be advantageous to administer them just before bison are moved from one pasture to another.
Fecal sampling should be part of any lungworm control program. Surveys of the herd should be done in early spring (March, April, May) to determine if bison in the herd are shedding lungworm larva. If they are, the herd can be treated at that time to reduce the number of larva shed onto the pasture. Fecal sampling should also be done during mid to late summer to predict whether clinical cases are impending. If so, treatment can be instituted.
 
 
 
Sarcocystis
 
Causative agent: Sarcocystis spp
The life cycle of sarcocystis begins with a carnivore, such as a dog or coyote, consuming muscle from infected intermediate hosts such as bison, moose, elk, sheep, goats, cattle, mule deer, white tailed deer, bighorn sheep, mountain goats, and pronghorn antelope. The parasite develops in the stomach and intestinal tract of the carnivore and produces sporocysts that are passed out in the feces. The sporocysts are resistant to most environmental conditions. The intermediate hosts (bison) become infected when they consume contaminated food or water that contains the sporocysts. In the intermediate host (bison), the sporocysts develop into sarcocysts, which localize in the muscles.
Sarcocystis sporocytes have been found in the muscle of bison in Alberta and Montana (58,59,60,61,62). Bison have been experimentally infected with sarcocystis, by oral inoculation of sporocytes that originated from infected cattle (63). In most cases, intermediate hosts that are infected with sarcocystis do not develop clinical disease.
 
Clinical signs:
There have been no clinical signs associated with natural sarcocystis infections of bison. Bison calves experimentally infected with large doses of sarcocystis sporocytes became anemic, anorexic, lethargic and had elevated body temperatures (63). It is highly unlikely that bison would be exposed to natural infections as high as those used in this experiment. In Alberta, sarcocystis was found in the muscle of 94% of bison of healthy bison (58). In Montana, sarcocystis was found in the muscle of 13% of healthy bison (61).
 
Diagnosis:
Diagnosis in the live animal is very difficult. Muscle biopsies can detect the presence of sarcocystis sporocytes in infected bison, but since sarcocystis sporocytes can be found in the muscle of normal bison, their presence does not mean they are the cause of disease.
 
Treatment:
In cattle, amprolium or salinomycin may reduce clinical signs. There have been no treatment protocols reported for bison. Presently, the risk of bison developing clinical signs associated with sarcocystis is minimal.
 
Control:
There have been no reasons to develop programs to control sarcocystis in bison.
 
 
 
Stomach and Intestinal Worms
 
Causative agents:
The following stomach and intestinal parasites have been identified in bison (42, 43, 47, 48, 50, 51,52,53):
Cooperia spp.
Haemonchus contortus
Monezia benedeni
Nematodirella alcidis
Nematodirus spp
Oesophagostumum radiatum
Ostertagia spp
Seratia
Trichostrongylus spp
Trichuris ovis, and other unidentified Trichurus spp.
This array of intestinal parasites causes a wide variety of disease syndromes in cattle, ranging from very mild or nonexistent, to very severe and life threatening. In cattle, many of these parasites are also associated with unthriftiness, reduced rates of growth or reduced productivity. Parasitic disease in cattle is often associated with overcrowded or wet conditions especially during the summer, when parasite survival on the ground is highest.
Neither reduced growth rate, loss of productivity, lack of vitality, unthriftiness, nor any other disease syndrome, has been associated with the infection of bison by any of these parasites, other than Ostertagii.
In bison, ostertagia has been the only species reported to cause clinical disease and mortalities. Ostertagii larva can penetrate the glands of the abomasum and there they can enter into a dormant, hypobiotic, state. While they are in this state they cause no damage to the abomasum. If large numbers of larvae emerge from this state at the same time they cause serious damage to the abomasum, resulting in clinical disease and death. This form of ostertagiosis called Type II ostertagiosis has been reported in 3 bison herds in New York State (53).
In ranched bison in Northern Alberta that were tested by fecal analysis, Cooperia was the predominant fecal parasite identified, accounting for 96% of all parasites found in calves and 92% of all parasites found in cows (51).
 
Clinical signs:
The clinical signs associated with Type II ostertagiosis in bison include: anorexia, weight loss, weakness, dull hair coat, severe diarrhea, anemia, hypoproteinemia, lymphocytopenia, neutorphilia and death (53).
 
Postmortem findings:
Pathological findings associated with Type II ostertagiosis in bison include: emaciation, and irregular thickening of the abomasal mucosa, giving it a morocco-leather appearance (53).
 
Diagnosis:
Fecal samples may be examined to identify the presence of parasite eggs and larvae. The identification of parasite eggs or larvae in the feces of bison should not be considered an indication that parasites are the cause of disease. In cattle, the number of eggs found in fecal samples is not related to the total number of parasites in the hosts stomach or intestinal tract (9).
Fecal analysis should only be used to identify the presence of the parasite in the herd, and to estimate the number of bison that are infected.
Fecal samples should be collected in the spring from April to June. If fecal samples are collected in the late fall or winter, they may be unrewarding since parasites may reduce egg or larva production during this time.
 
Treatment:
The treatment of bison with parisiticides should vary with the geographic location, the species of parasites that are infecting the bison, as well as the housing and pasturing practices on each ranch. In New York state where Ostertagii was present and bison were housed in close quarters, the burden of Ostertagii in bison increased to the point where mortalities occurred (53). In Northern Alberta where bison were maintained on large, spacious ranges in both the summer and winter, Cooperia was the predominantly identified parasite, even though Ostertagii was present in small numbers. Clinical disease was not identified evan after 18 months without parasiticide treatment (51).
In cattle, these parasites have been found to be susceptible to a wide variety of parasiticides, including bezimidazoles, probenzimidazoles, levamisole and ivermectins (9). None of these products has been approved for use in bison.
In bison, ivermectin in a 0.5% pour-on formulation has been found to be effective against Ostertagii at a dose of 1ml/10kg of body weight (54).
 
Control:
Control programs will also vary with the geographic location of the bison and the parasite populations that are endemic to bison in that location. Control programs should include routine fecal egg counts, pasture rotation and judicious use of parasiticides.
 
 
 
Ticks and Tick Paralysis
 
Causative agent: Dermacentor andersoni
Ticks are common vectors of disease. They are bloodsuckers and can cause anemia and reduced growth rates. Some ticks are able to produce a neurotoxin that causes paralysis. Tick paralysis has been reported from bison in Montana (57).
 
Clinical signs:
The clinical signs of tick infestation in bison are associated with tick paralysis. Initially, infested bison have an unsteady gate, and jerky movements. The animals lie down and then are unable to get up. Tick paralysis was only seen in bison calves and yearlings (57).
 
Diagnosis:
The ticks are easily observed on the skin of the bison.
 
Treatment:
Remove the ticks from the bison. There are a number of products that may be used for treating infested cattle . Many of them work well, but most do not have residual effect. Products that have been used in cattle include avermectins, organophosphates, and pyrethroids. Sprays and dips are commonly used to treat cattle with ticks.
 
Control:
Ticks are difficult to control. Rotating pastures, and frequent treatment may reduce the level of ticks on the pasture and on bison, but complete eradication is unlikely.
 
 
 
 
 
Warbles (Grubs)
 
Causative agent: Hypoderma bovis, Hypoderma lineatum
During the spring and summer warble flies, the adult stage of hypoderma, lay their eggs on the legs and lower body of cattle, bison, some species of deer and occasionally horses (9). The eggs hatch into larvae which penetrate the skin and migrate to the esophagus (H. lineatum) or the spine (H.bovis), where they continue growing. As spring approaches the larvae migrate to a position just below the skin along the back. They make an air hole in the skin and then emerge and fall to the ground where they pupate. Adult flies emerge from the pupae to complete the cycle (9).
There is some evidence that hypoderma larvae may not be able to penetrate through the skin and dense hair on the back of bison. In Montana and Yellowstone National Park, bison were found to have dead, discolored larvae from previous years infestations underneath the hide along the back (42).
Hypoderma larvae have been found around the esophagus of bison in Montana (42), Yellowstone National Park (42), and Oklahoma (43). The location of the larvae suggests that the species of hypoderma that infected these bison was H. linatum. In Michigan, hypoderma larvae were found along the spinal chord in bison (44), suggesting that the species of hypoderma in this case was H.bovis.
 
Clinical signs:
In cattle, the clinical signs of Hypoderma spp. infestation are associated with poor growth and swellings along the back that are present during the spring (9). Clinical signs associated with hypoderma infestation in bison have not been reported.
 
Postmortem findings:
Postmortem findings of hypoderma infestation in bison include larvae migrating adjacent to the esophagus, along the spinal chord, and underneath the skin of the back (42,43,44).
 
Diagnosis:
Palpating the midline of the back of bison during the spring for swellings containing hypoderma larvae may make the diagnosis.
 
Treatment:
Organophosphates and ivermectins kill Hypoderma spp. larvae. The timing of treatment is very important. Treatment should be instituted before the larvae reach critical areas such as the esophagus and the spinal chord. If the larvae are killed when they are in these areas the dead larvae may cause serious harm to the bison. In Michigan, 23 out 70 bison were killed as a result of improper timing of the treatment of bison with an organophosphate (44). The timing will vary from area to area depending on the time that the peak of the hypoderma fly season occurs. In Michigan, mortalities were associated with organophosphate treatments that were applied to bison in December (44). Bison producers should consult with local veterinarians as to the optimal time for the application of parasiticides to their bison.
 
Control:
There have been no programs reported for the control of hypoderma in bison. In endemic areas, yearly applications of parasiticides for the control of hypoderma will be required.
 
 
 
 
 
Diseases Associated with Nutrition
 
 
 
Bloat /Rumenal Tympani
 
Cause:
The cause has not been established in bison. Bloat is abnormal distension of the rumen and reticulum caused by excessive retention of gas in the rumen and reticulum. In order for normal eructation (burping) to occur, gas produced by fermentation in the rumen must coalesce into a bolus of free gas. When bloat occurs, soluble plant leaf proteins in the feed form foam in the rumen which will not coalesce into free gas. In cattle, bloat can occur with cows on pasture, or on dry feed. Pasture bloat is most often associated with leguminous plants (9). Bloat is not very common in bison but it has occurred (19).
 
Clinical signs:
Sudden death is a common finding in bison (19). In live bison there will be a large swelling on the left side of the animal, just behind the ribs. There may be increased respiratory rate, mouth breathing, and recumbency just before death. During the course of the disease, as the rumen enlarges pressure is exerted on the diaphragm making breathing difficult. Bloated bison that become too excited during handling for treatment will die.
 
Postmortem findings:
The rumen will be grossly enlarged and may still contain foam. There may be anterior congestion and posterior blanching of the carcass.
 
Diagnosis:
The diagnosis can usually be made from the clinical signs.
 
Treatment:
In cattle, mild cases of bloat may be treated by gently chasing (walking) the animal. This may be difficult in bison. Releasing the gas trapped in the rumen with a stomach tube may provide immediate relief. If the situation is life threatening the bison's the rumen may be punctured from outside the body wall with a trocar or a sharp knife. Anti-foaming agents or surfactants such as mineral oil or dioctol sodium succinate can be administered orally.
If bison are on pasture when bloat is detected, they should, if possible, be moved off of the pasture and fed long grass hay until the bloating stops. If the bison are being fed dry leguminous hay, the hay should be changed to long grass hay.
 
Control:
It is not always possible to predict whether a pasture has the potential to cause bloat. Furthermore, the characteristics of any pasture can change in a very short period of time. In cattle, bloat is most commonly seen when lush, rapidly growing, pre-flowering leguminous pastures such as alfalfa are grazed. If a pasture was thought to be potentially dangerous, bison should be prevented from grazing it.
Monensin or salinomycin in the salt may reduce the incidence of bloat in cattle being grazed on legume pastures. The efficacy and safety of these products has not been established in bison.
 
 
 
Copper Deficiency
 
Cause:
Insufficient copper in the diet (primary copper deficiency), or dietary constituents that prevent dietary copper from being absorbed from the digestive tract (secondary copper deficiency). Secondary copper deficiency associated with high sulfur levels in the drinking water, has been reported in bison in Saskatchewan (65).
 
Clinical signs:
Clinical signs of copper deficiency in bison include stiff gait, lameness leading to recumbency, emaciation, diarrhea, and loss of coat color (65).
 
Diagnosis:
The clinical signs of emaciation, lameness, and diarrhea combined with loss of hair coat color would be suggestive of copper deficiency. Normal serum and liver copper levels have not been established for bison. In the reported cases of copper deficiency in bison, serum copper levels were 5.8 mol/l and liver copper levels were 0.02 mol/g. Both of these levels would also be considered low for cattle (65).
 
Postmortem findings:
Postmortem findings were mainly associated with degenerative lesions of the joints, which included thinning of articular cartilage, defects in the articular cartilage and rupture of joint ligaments and capsules. There was as rupture of flexor and extensor tendons as well as fracture of the patellas (65).
 
Treatment:
Treatment protocols have not been reported for copper deficiency in bison. In advanced cases with degenerative joint lesions, such as those that have been reported, treatment would probably be unsuccessful. The diet of affected bison should be supplemented with copper. However, safe dietary levels of copper have not been established for bison. In cattle, copper sulfate can be added to the salt-mineral mix to a level of 3 to 5% of the total mineral mixture (19).
 
Control:
Feed, water, and pasture should be sampled to determine if there is adequate copper available in the diet. They should also be tested to see if there are any elements present, such as molybdenum, or sulfates, that may inhibit the absorption of copper from the diet.
In cattle, the minimum dietary requirement is 10mg of copper per kg of dry matter. Since the minimum dietary copper requirements for bison have not been established, it is not known whether these levels would be adequate. In cattle, over supplementation with copper can produce toxicities. Care should be taken when copper supplements are prescribed. A qualified nutritionist should be consulted to examine both feed and water analysis before supplementation of copper, or other trace minerals is recommended
 
 
 
Grain Overload / Rumen Overload
 
Cause:
Excessive consumption of carbohydrate rich feed. The sudden ingestion of large quantities of highly fermentable carbohydrate rich feed, such as ground or rolled barley, wheat or oats, can cause the rumen to produce excessive lactic acid. The lactic acid kills many of the rumen micro flora and enters the circulatory system to cause metabolic acidosis, a toxic condition causing physical symptoms.
Grain overload can occur when any cereal grains fed. Bison are considered somewhat resistant to grain overload, and the incidence is much lower in bison than in cattle. Cereal grains can be fed to bison with a much greater degree of safety than they can be fed to cattle.
 
Clinical signs:
Grain overload has been seen in bison (19). In the early stages bison may be uncomfortable, mildly 'colicky" and anorexic. Diarrhea always accompanies grain overload. As the condition progresses bison will become depressed, start to stagger, and eventually become recumbent.
In cattle it usually takes 24 to 48 hour after grain consumption for this condition to develop. The mortality rate can be high, and in some cases dead bison are the first indication of a problem. Founder and abortion can follow grain overload.
 
Postmortem findings:
The rumen contents will be very thin. If whole, or rolled grain is being fed, there should be a large quantities of grain in the rumen and abomasum.
 
Diagnosis:
The diagnosis can often be made from the history and clinical signs. The history doesn't always include sudden access to grain. Grain overload can occur in calves that are being fed whole oats on a free choice basis (19).
The pH of rumen fluid that is obtained from sick animals via a stomach fluid can be determined. Cattle being fed a roughage diet have a rumen pH between 6 and 7, those on a high grain diet have a rumen pH of 5 to 6. A rumen pH of less 6 in cattle being fed a roughage diet and a rumen pH less than 5 in cattle being fed a grain diet are considered significant (19). These values have not been established for bison.
 
Treatment:
In mild cases, withhold water for 24 hrs. Remove the grain that is causing the problem, and provide long grass hay free choice. Antacids, such as baking soda and magnesium oxide may be administered orally to correct the acidosis.
In severe cases rumenotomy and rumen lavage have been used in cattle. The efficacy of these treatments in bison is unknown. The stress associated with these procedures may be too severe to warrant their use. Severe cases will be unresponsive to treatment, and slaughter should be considered.
 
Control:
Many bison ranchers provide bison calves and yearlings with grain, especially whole oats, in a free choice manner. The assumption is commonly held by many bison ranchers that bison will only eat what they need. Although this method of feeding bison is commonly practiced, there have been instances when bison have died of grain overload under this management (19). If the incidence of grain overload increases in bison being fed free choice grain, feeding programs that limit quantity of grain being fed to bison need to be implemented.
 
 
 
Nutritional Muscular Dystrophy / White Muscle Disease
 
Cause:
Dietary deficiency of vitamin E and/or selenium.
 
Clinical signs:
White muscle disease has been reported in bison, but the clinical signs have not been described (68). In cattle, clinical signs include sudden death, increased heart rate, stiffness, weakness, recumbency, and dyspnea.
 
Postmortem findings:
The pathological changes associated with nutritional muscular dystrophy in bison have not been described. In cattle, the affected muscle groups can be swollen, edematous and have white or gray streaks in them. There may be cardiac hypertrophy and pulmonary emphysema (9).
 
Diagnosis:
In cattle, the diagnosis is made from determination of serum selenium, creatine phophokinase , glutathione peroxidase levels. Normal bison had serum selenium levels of 0.1 ug/ml. Bison from a herd with white muscle disease had serum selenium levels of 0.026 ug/ml (68). Reference serum levels of creatine phosphokinase and glutathione peroxidase have not been established for bison.
 
Treatment:
Treatment protocols for bison with nutritional muscular deficiency have not been described. Cattle are treated with selenium and DL-alpha-tocopherol injections in preparations that contain 3mg selenium per ml and 150 iu DL-alpha-tocopherol per ml. The cattle dose is 2ml per 45 kg (9). The effectiveness of this dosage has not been established for bison.
The response to treatment of severe cases will be poor. When clinical cases occur, all bison in the group should be treated, since the others in the group will probably be deficient as well. Care should be taken when handling selenium and vitamin E deficient bison because excitement or exercise may precipitate clinical cases.
 
Control:
Preventing the occurrence of nutritional muscular dystrophy will require supplementing the diet with vitamin E and selenium. Selenium can be toxic to cattle when overfed. It would be prudent to analyze selenium and vitamin E in feed sources, and to consult a qualified nutritionist, before supplementation is carried out. Some geographical locations are known to be selenium deficient. In these areas continuous supplementation would be required.
Selenium and DL-alpha-tocopherol can be supplemented in the salt or grain rations. Bison however, do not always consume salt or grain on a consistent basis. Bison have developed white muscle disease even when provided with free choice selenium (68). The daily requirement of selenium and DL-alpha-tocopherol for bison has not been established.
 
 
 
 
 
 
Congenital Abnormalities
 
 
 
Arthrogryposis
 
Cause:
Arthrogryposis is a birth defect. It is seen as a result of inbreeding.
 
Clinical signs:
Clinical signs of arthrogryposis in bison include exaggerated slope of the back, increased angulation of the hock, stilted gait, poor muscling of the hind quarters, poor weight gains and reduced growth potential. Bison with arthrogryposis stand with their hocks abnormally close together or with their hocks crossed (66).
In both of the cases reported, the bison were affected from birth. One case resulted from a sibling mating (66).
 
Postmortem findings:
There will be reduced muscle mass of the carcass, especially of the hind quarters. The hock joints will be in extreme angulation, and will be rigidly fixed around the tibiotarsal joint. There may be thinning and erosion of the articular cartilage of the bones in the hock joint, especially the talus (66).
 
Diagnosis:
The clinical signs would be suggestive of the disease. Normal hematology, serum chemistry, and plasma trace minerals would help to rule out other causes of disease, since these values were within normal ranges for cattle, in the cases reported in bison (66). Radiographs of the hind limbs will be normal (66).
Analysis of the pedigree of affected bison may demonstrate that the disease has a familial trend. Since affected bison have reduced growth rates and are poor doers, the diagnosis may best be made by postmortem examination. Tissues submitted to a pathology laboratory for examination should include the bones and joints of the back legs.
 
Treatment:
Treatment of arthrogryposis in bison has not been reported. It is unlikely that advanced cases of arthrogryposis will respond to any treatment.
 
Control:
Control will involve pedigree analysis of affected animals, and elimination of breeding combinations that result in the production of arthrogrypotic calves. If cows or bulls can be identified as individuals that produce arthrogrypotic calves, they should be removed from the herd.
 
 
 
Atresia Ani and Rectovaginal Fistula
 
Cause:
These are thought to be congenital abnormalities. There is one case reported from a bison herd that was maintained for nearly 20 years by inbreeding (67).
 
Clinical signs:
The clinical signs reported include poor growth, rough hair coat, periodic episodes of diarrhea, and chronic bloat (67).
 
Diagnosis:
The affected bison in the report did not have an anus (67).
 
Postmortem findings:
The rectum ended blindly, and there was a small fistula between the rectum and the vaginal vault (67).
 
Treatment:
The only treatment that would have any chance of success would be surgical correction of the condition. In cattle the condition can sometimes be corrected if the blind end of the rectum is very close to where the opening of the anus should be. Surgical correction was not attempted in the case reported.
 
Control:
A sound breeding program that includes the introduction of out crosses to the herd should prevent the occurrence of most hereditary diseases.
 
 
 
 
 
 
Toxicities in Bison
 
 
 
Urea Poisoning
 
Causative agent: Urea fertilizer
Urea poisoning from consumption of urea fertilizer or water containing urea fertilizer killed 15 of 300 bison in Alaska (70).
 
Clinical signs:
Clinical signs were not reported, since all 15 of the bison were found dead. In cattle, clinical signs of urea poisoning include abdominal pain, frothing at the mouth, muscle tremors, incoordination, weakness, bloat and death (9).
 
Postmortem findings:
Pathological changes associated with urea poisoning of bison include bloat, hemorrhage and congestion of the lungs, hemorrhage of the spleen, pulpy consistency of the kidney, and serosangenous fluid in the pleural cavity and pericardial sac (70).
 
Diagnosis:
In cattle, elevated serum ammonia levels can diagnose urea poisoning. Abnormally high levels of urea or ammonia in the rumen would also be diagnostic.
Control:
There is a commonly held belief among bison ranchers that bison have very discriminate eating habits. This may not be the case. To prevent toxicities bison should be denied access to toxic substances.
 
 
 
Ponderosa Pine Needle Abortion
 
Cause:
Feeding pine needles (Pinus ponderosa) to pregnant bison causes abortion. Abortion caused by consumption of pine needles occurs frequently in pregnant cattle on pasture (71). Naturally occurring abortion from the consumption of pine needles has not been observed in bison (71). Pine needle abortion has only been produced in bison by experimentally feeding pine needles to pregnant bison (71).
 
Clinical signs:
Pregnant bison in late stages of pregnancy fed up to 2.25 kg of pine needles did not develop any clinical signs other than abortion. The calves that were not aborted were all born alive and all survived (71).
 
Postmortem:
There were no bison cow or calf mortalities associated with feeding pine needles to bison (71).
 
Diagnosis:
Establishing the diagnosis of pine needle abortion would be difficult. There were no clinical signs observed in bison cows fed pine needles and the bison calves that were aborted were born as normal healthy calves.
 
Treatment:
There is no known treatment for pine needle abortion in cattle or bison.
 
Control:
It is thought that bison, as opposed to cattle, do not consume pine needles when they are on pasture, even if ponderosa pines are present. Control programs to prevent the consumption of pine needles by bison have not been required.
 
 
 
 
 
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