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.

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.

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.

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.

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.

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.

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.

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.

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.

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.