Other Causes of Lameness in Cattle Flashcards

1
Q

What is the aetiology of sole haemorrhage/bruising?

A

Traumatic damage to the corium between the pedal bone and the sole results in bleeding which is incorporated into the sole horn as it is produced. This haemorrhage or “bruising” becomes visible as the sole grows out or when the foot is trimmed. NB The sole horn itself cannot bruise once it has been produced (it is avascular).

Sole haemorrhage and discoloration can occur as a result of movement of the pedal bone (as discussed in the lecture) and inadequate cushioning provided by the digital cushion. That is bruising has a similar aetiology to sole ulceration and should probably be considered simply as an earlier and milder manifestation of the same disease.

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2
Q

What are the clinical signs and presentation of sole haemorrhage/bruising?

A

Animals will often present with low-grade lameness or tenderness (short strides where the hind feet do not track up to the forefeet), sometimes on more than one foot. When examined the sole contains areas of bruising. On some occasions the bruising will not become obvious until the sole horn has grown out (or been trimmed back) to become weight bearing which may take a number of weeks

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3
Q

How do we diagnose sole haemorrhage/bruising?

A

Diagnosis is usually apparent as soon as the foot is examined. In cases where areas of sole bruising have not yet reached the weight-bearing surface the only sign may be pain when the area is percussed or “pinched” with hoof testers or by excluding other causes of lameness.

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4
Q

How do we treat sole haemorrhage/bruising?

A

Treatment depends on the degree of lameness and the severity of lesions. Overgrown feet should be therapeutically trimmed to restore correct weight bearing. Recent UoN research has demonstrated that animals benefit from the application of a block to the unaffected claw and a course of NSAIDs even at this early stage of disease. Alternatively, animals often respond well if kept on straw beds for a week or two.

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5
Q

How can we prevent sole haemorrhage/bruising?

A

Ensure optimal underfoot conditions and comfortable housing to maximise lying times. Institute routine foot trimming of all animals.

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6
Q

What is the aetiology of foreign body penetrations?

A

Penetration of the foot in areas other than the white line (usually the sole) with foreign bodies from the environment is not an uncommon finding. Objects commonly found imbedded in the sole are nails, sharp stones, black thorns, pieces of metal & glass and molar teeth which have been cast into the environment. Foreign bodies carry infection through the sole to the corium which then establish infection and abscesses in a similar fashion to WLD.

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7
Q

What are the clinical signs and presentations of foreign body penetrations?

A

Similar to WLD, although lameness is often peracute in onset and severe if the foreign body is still in the sole

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8
Q

How do you diagnose foreign body penetrations

A

Diagnosis is straight forward if the foreign body is still present. If not black tracks in the sole leading to sub-sole abscesses are diagnostic.

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9
Q

How do you treat foreign body penetrations?

A

As for WLD. Ensure that the amount of sole removed is sufficient to prevent reimpaction of the affected area with debris from the environment.

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10
Q

What is the prognosis of foreign body penetrations?

A

Good as for WLD. Occasionally foreign bodies will penetrate into the deep structures of the foot establishing deep digital sepsis. In these cases the prognosis in much worse.

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11
Q

How do we prevent foreign body penetrations??

A

Ensure that the environment is kept free of potential foreign bodies.

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12
Q

What is the aetiology, clinical signs and presentation of heel horn erosion (slurry heel)?

A

The result of standing in wet corrosive slurry (a combination of faeces, urine and occasionally silage effluent) during the winter housing period leads to the soft horn of the heel becomes eroded leading to the formation of pits and fissures in the heel. If severe or left untreated the heel eventually disappears completely.

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13
Q

How do you diagnose and what are the differentials of heel horn erosion (slurry heel)?

A

Presenting clinical signs are diagnostic and cannot be confused with any other condition.

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14
Q

What is the treatment of heel horn erosion (slurry heel)?

A

Regular formalin foot bathing through the winter will harden the feet and limit the effects of heel erosion. Gently trim away loose and fissured horn to remove pocket but spare healthy heel as excessive trimming this will exacerbate the problem. Corrective trimming attempts to increase the angle of the front wall to the ground to reduce the pressure on the sole ulcer site.

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15
Q

What is the prognosis of heel horn erosion (slurry heel)?

A

Good if treated before the disease has completely destroyed the heel. If this has been allowed to happen the foot rotates backwards. This causes the front wall of the hoof to meet the ground at a shallower angle leading to overgrowth of the hoof at the toe. At the same time the pressure exerted by the caudal palmer edge of the pedal bone increased which can lead to pinching of the corium the development of sole haemorrhage and eventually sole ulcers.

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16
Q

How can we prevent heel horn erosion (slurry heel)?

A

Improving underfoot conditions during the winter period will decrease the severity of the condition although a certain amount of heel erosion is almost inevitable in housed cattle. Routine bathing in formalin footbaths will often limit the severity of disease.

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17
Q

What is the aetiology of vertical fissures (sand cracks)?

A

The periople is responsible for producing a thin waxy layer that prevents the horn of the wall from drying out. If it or the underlying wall producing corium becomes damaged vertical cracks can appear in the wall of the hoof that appear to extend as the wall grows. Common causes of damage are digital dermatitis lesions on the front wall of the foot and trauma. Alternately the condition can occur in very hot dry sandy conditions during the summer months.

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18
Q

What are the clinical signs and presentation of vertical fissures (sand cracks)?

A

Often asymptomatic, however if the underlying laminae are involved or the crack becomes infected severe lameness can ensue.

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19
Q

How can you diagnose, and what are the differentials for vertical fissures (sand cracks)?

A

Presenting clinical signs are diagnostic and cannot be confused with any other condition.

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20
Q

How can you treat vertical fissures (sand cracks)?

A

The crack should be opened up and any underlying abscess exposed and allowed to drain. However on occasions if the crack is opened and there is movement between the two wall sections granulation tissue can develop and protrude through. In these cases the granulation tissue should be resected and a block applied to the sound claw to limit sheering forces.

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21
Q

What is the prognosis for vertical fissures (sand cracks)?

A

Generally good although some can be quite difficult to treat and require multiple trims before the wall returns to normal. If the periople has been permanently damaged leading to continued production of defective wall the long term prognosis is poor.

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22
Q

What is the aetiology of horizontal fissurres (hardship lines)?

A

Complete, circumferential horizontal fissures will occur if the production of wall horn is interrupted as it is being produced at the coronary band. Any severe toxic condition e.g. mastitis, metritis, or acute acidosis can results in a temporary but complete absence of horn production. When horn production restarts there will be a complete circumferential fissure often round all 8 claws

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23
Q

What are the clinical signs and presentation of horizontal fissurres (hardship lines)?

A

Often asymptomatic unless the fissure and the underlying laminae either become infected or the pinching forces result in the production of a granuloma. Many show clinical signs when the fissure has grown down the wall to the point that “thimbles” of wall and sole are formed on all claws. At this point movement of the thimble relative to the rest of the wall results in lameness, infection and granulomas.

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24
Q

How can you diagnose horizontal fissurres (hardship lines), what are the differentials?

A

Presenting clinical signs are diagnostic and cannot be confused with any other condition.

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25
Q

How can you treat horizontal fissurres (hardship lines)?

A

If infection has become established the crack should be opened up and any underlying abscess exposed and allowed to drain. Any granulation tissue should be resected. It is often difficult to block the other claw as very often all claws are affected.

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26
Q

What is the prognosis for horizontal fissurres (hardship lines)?

A

Prognosis varies depending on the severity of the disease. Sometimes thimbles grow out and are eventually shed asymptomatically, on other occasions if all claws are seriously affected it may be necessary to cull the affected animal.

On many occasions the disruption in horn production is not complete, instead a thinning of the wall occurs. As these thinner areas grow down the wall they become apparent as a series of ridges or “hardship lines”. As the wall grows at approximately 5mm per month is it possible to calculate how long ago the insult causing the thinning occurred.

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27
Q

What is the aetiology for a fracture of the distal phalanx?

A

Fracture of the distal phalanx is an uncommon occurrence but causes rapid onset acute lameness without any other obvious clinical signs. Typical claws affected are the medial claw of front feet following trauma during “bulling” (slipping off cows whilst mounting) or hind feet after slipping of the steps of abreast parlours. Herd “outbreaks” have been associated with fluoride poisoning.

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28
Q

What are the clinical signs and presentation for a fracture of the distal phalanx?

A

Acute onset severe lameness with no other obvious clinical signs. If the medial claw of front feet is affected animals often stand “cross legged” so as to take the weight on the unaffected lateral claw

29
Q

How can you diagnose fracture of the distal phalanx?

A

Radiographical examination is required for a definitive diagnosis

30
Q

How can you treat a fracture of the distal phalanx?

A

The distal phalanx is splinted well by the hoof capsule. The only treatment usually necessary is the application of a block to the unaffected claw

31
Q

What is the prognosis for a fracture of the distal phalanx?

A

Good providing no complicating factors exist e.g. fluoride poisoning.

32
Q

What is the aetiology for interdigitial skin hyperplasia (interdgitial corns/growths/fibromas/granulomas)?

A

Interdigital hyperplasia is thought to be caused by chronic irritation of the interdigital area. Irritation can be caused by chronic infection or impaction of dirt / small stones. Foul in the foot may predispose to the condition later in life. A hereditary component has been postulated but remains unproven.

33
Q

What are the clinical signs and presentation for skin hyperplasia (interdgitial corns/growths/fibromas/granulomas)?

A

Skin hyperplasia is often asymptomatic being noted during routine foot trimming or inspection. Cases cause lameness if the overgrowth of skin becomes infected e.g. Foul or Digital dermatitis or becomes so large that it becomes pinched between the claws during locomotion.

34
Q

How can you diagnose skin hyperplasia (interdgitial corns/growths/fibromas/granulomas)?

A

Straight forward once the foot is examined, however as many cases are asymptomatic care must be taken not to assume that the skin hyperplasia is the cause of lameness without examining the remainder of the foot.

35
Q

How can you treat skin hyperplasia (interdgitial corns/growths/fibromas/granulomas)?

A

If the hyperplastic area is infected treating the infection will often resolve the lameness. In cases where the pinching is mild “dishing” out the horn from the interdigital area will often alleviate the clinical signs. In severe cases or in cases where corrective trimming does not succeed it may be necessary to surgically remove the hyperplastic skin under local or intravenous regional anaesthesia.

36
Q

What is the prognosis for skin hyperplasia (interdgitial corns/growths/fibromas/granulomas)? How can we prevent?

A

Prognosis - Good

Prevention- Ensure underfoot conditions are optimal during the winter housing period.

37
Q

Suprascapular paralysis:

A) Aetiology?

B) Clinical signs and presentation?

A

A) C6 & C7 outflow provide motor innervation of suprasinatus and infrasinatus muscles of the scapular. Usually damaged by trauma to prescapular or scapular area.

B) Limb can be advanced but abducts when weight bearing. Stride may be shortened. Atrophy of suprasinatus and infrasinatus muscles can be partial or almost complete.

38
Q

Radial paralysis:

A) Aetiology?

B) Clinical signs and presentation?

A

C7, C8 and T1 outflow provide motor innervation of carpus and digit extensors and sensation to lateral side of limb. Excessive traction on limb (e.g. during calving), trauma to the scapulohumeral area and recumbancy can damage the nerve.

Clinical signs and presentation – Damage to the nerve proximally leads to the limb being held in flexion with the elbow dropped. The cranial wall of the hoof “scuffs” the floor during locomotion. If the nerve is damaged distally innervation to the elbow is often normal but the carpus and fetlock are held in flexion.

39
Q

Brachial Plexus Paralysis:

A) Aetiology?

B) Clinical signs and presentation?

A

A) C5 to T2 outflow make up the principal nerves innervating the forelimb (radial, median and ulner). Excessive traction on limb (e.g. during calving), traumatic abduction and prolonged lateral recumbency can all damage the brachial plexus.

B) Total loss of muscle control of the forelimb. The limb is held flaccid and entirely non weight bearing. The hoof will drag on the floor.

40
Q

Obturator paralysis:

A) Aetiology?

B) Clinical signs and presentation?

A

A) L4, L5 and L6 outflow make up the obturator nerve, which innervates the adductor muscles of the hind limb. Usually damaged during dystocia due to foetal oversize when the nerve is crushed as it runs through the pelvic canal.

B) Can be unilateral or bilateral and causes an inability to adduct the limb leading to abduction. If severe animals may slip causing severe abduction and trauma to the leg, hip and pelvis.

41
Q

Femoral Paralysis:

A) Aetiology?

B) Clinical signs and presentation?

A

Femoral paralysis:

A) The femoral nerve is composed of outflow from L4, L5 & L6 and innervates the iliopsoas and quadriceps muscles. Usually damaged in calves during dystocia caused by “hiplock” when the calf’s limb is hyperextended during traction.

B) The limb is virtually non-weight bearing because the stifle cannot be extended, instead it “hangs” in a flexed position with the digits resting on the floor.

42
Q

Sciatic paralysis:

A) Aetiology?

B) Clinical signs and presentation?

A

A) The sciatic nerve is composed of outflow from L6, S1 & S2. It is responsible for all motor innervation distal to the stifle joint and all skin sensation except for the medial aspect of the thigh. Also commonly injured during dystocia caused by foetal oversize (it may be part of “calving paralysis”) and occasionally during prolonged periods of lateral recumbency and iatrogenically during intramuscular injections into the hind limb.

B)The limb is non-weight bearing. The stifle and hock are held in extension and the distal joints of the foot are flexed. The foot is “knuckled” over. The limb is dragged along by extension of the hip only.

43
Q

Tibial paralysis:

A) Aetiology?

B) Clinical signs and presentation?

A

A) A branch off the sciatic nerve responsible for motor innervation of the extensors of the hock and flexors of the digit. Damage is rare and usually caused by extensive trauma to the gastrocnemius area.

B) Damage to the tibial nerve causes hock flexion and extension of the digits causing weight bearing to be shifted onto the heels. The animal can walk but with a “jerky” motion.

44
Q

Peroneal paralysis:

A) Aetiology?

B) Clinical signs and presentation?

A

A) A branch off the sciatic nerve responsible for motor innervation of the flexors of the hock and extensors of the digit. It is damaged during period of prolonged recumbency and sudden falls that damage the lateral aspect of the stifle joint.

B) Damage causes the fetlock to become flexed “knuckled” and the hock extended. Animal can weight bear and walk but tends to “knuckle over” and stumble

45
Q

How do we diagnose nerve paralysis and what are the differerntials?

A

Presenting signs and history are often highly suggestive. Differential diagnoses depend on the presenting signs and the nerve affected but include fractures, dislocations, subluxations and damage / rupture to tendons and ligaments.

46
Q

What is the treatement for nerve paralysis?

A

Treatment of all nerve injuries relies on keeping the animal comfortable (i.e. deep soft bedding) and on “non slip” surfaces to avoid making the situation worse after falls that may cause other injuries. Anti-inflammatory drugs to reduce swelling around damaged nerves may help in the early stages. In some cases supportive dressings are appropriate to “hold” the limb in the correct position.

47
Q

What is the prognosis for nerve paralysis?

A

The prognosis will depend on the nature and extent of the nerve damage. Cases which involve “bruising” or swelling of the nerve will usually respond well to conservative therapy, however the prognosis in cases which involve complete rupture of the nerve will be very poor.

48
Q

Limb fractures:

A) Aetiology?

B) Clinical signs and presentation?

A

A) Limb fractures are not an uncommon occurrence in cattle and the usually the result of severe trauma e.g. falling off bullying cows, trapping legs between bars e.g. in crushes, road and farm traffic accidents, jumping gates and falling down grids and potholes. The nature of the injury often means that limb fractures are comminuted, open and grossly contaminated by the time they are first seen.

B) The limb is usually none weight bearing. Significant swelling caused by soft tissue injury may be apparent. Very often especially if the fracture is open evidence of severe trauma is obvious.

49
Q

Limb fracture:

A) diagnosis and differentials?

B) Treatment?

A

A) In many cases diagnosis is obvious especially if the fracture is open or the causal trauma is witnessed e.g. jumping gates, trapped in crush. In other cases fractures must be differentiated from other causes of none weight bearing lameness such as dislocations. Manipulation of the affected limb will often reveal atypical movement and crepitus unless the fracture is high up the limb when muscular contraction will often stabilise the fracture making diagnosis more difficult. Radiographical examination will obviously provide a definitive diagnosis but is only of use in fractures of the lower limb and is rarely cost effective.

B) Treatment will depend on the age, weight, nature of fracture and value of the animal affected. In all but the most expensive adult cattle emergency slaughter will almost certainly be the most appropriate option.

Fixation of distal limb fractures is possible especially in young animals with uncomplicated breaks. Reduction of the fracture can be difficult especially if there is a delay before presentation for treatment. Both internal and external fixations are possible, although external fixation using splints and casts are usual because of the costs associated with internal fixation. Heavier animals and fractures higher up the limb are much more difficult to treat and effectively immobilise

50
Q

Limb fracture:

A) Prognosis?

A

Prognosis will depend on the site and nature of the fracture and the age and weight of the animal. Uncomplicated distal limb fractures in young animals will usually respond well to casting. The prognosis in older animals with open fractures higher up the limb is usually hopeless.

51
Q

What are growth plate injuries?

A

Injuries to the growth plates of calves are not uncommon following forced traction at calving. Usually the distal metacarpus and metatarsus joints are affected usually by separation or displacement. They usually respond well to casting but can be more complicated if both limbs are affected because animals have difficulty rising.

52
Q

Pelvic fractures:

A) Aetiology?

B) Clinical signs and presentation?

A

A) Pelvic fractures are not common. The usual site affected is the tuber coxae which is broken following lateral falls onto hard surfaces or “pushing / racing” through narrow entrances and doorways. Occasionally the pelvic symphysis can become separated during calving when excessive traction is used on young animals. Other fractures of the pelvis are very uncommon.

B) Clinical signs vary depending on the site of the fracture. Some pelvic fractures make weight bearing impossible. Fractures to the tuber coxae are usually obvious because the bone fragment usually becomes displaced ventrally.

53
Q

Pelvic fractures:

A) Diagnosis and differential diagnosis?

B) Treatment?

C) Prognosis?

A

A) Pelvic asymmetry is apparent in many cases. Crepitus will often be noticed during walking or palpation for many fractures. Rectal and vaginal examination can be helpful to assess the fracture and associated soft tissue injury.

Differential diagnoses include dislocations, and pelvic haematomas and abscesses.

B) Fractures to the tuber coxae respond well to box rest although the piece of bone may form a sequestrum. Often an open draining tract develops from the sequestrum which requires surgical removal for treatment. In many cases of pelvic fracture slaughter may be necessary. An initial period of closely confined box rest will often indicate whether this alone will be adequate for treatment. If there is no response slaughter should be considered.

C) Prognosis depends on the nature of the fracture. It is good in uncomplicated fractures of the tuber coxae. The prognosis for fracture which destabilise the pelvis are poor.

54
Q

Osteochondrosis:

A) Aetiology?

B) Clinical signs and presentation?

C) Diagnosis?

D) Treatment?

E) Prevention?

A

A) A condition of very fast growing animals, therefore almost exclusively confined to beef animals especially those on a cereal beef system (very rapid weight gain). Cartilage flaps form when nutritional supply can not keep pace with the rate of cartilage growth.

B) Mild progressive lameness usually in fast growing bull beef animals. Coxofemoral, femoropatellar, femorotibial and tibiotarsal joint of the hind limb and scapulohumeral, humororadial, radiocarpal and metacarpophalangeal joint of fore limb have all been reported as affected.

C) Diagnosis may be difficult because of the mild and fluctuating nature of the lameness. Joint pain and crepitus may be apparent. Radiography is diagnostic but not usually financially viable.

D)Conservative treatment can include confinement and housing on soft bedding. Surgical treatment is not financially viable.

E) If “outbreaks” occur the growth rate of the group should be reduced.

55
Q

Hip dysplasia:

A) Artiology?

B) Clinical signs and presentation?

C) Diagnosis?

D) Treatment?

A

A) Uncommon occurrence in fast growing beef bulls (usually Hereford and Aberdeen Angus) between 4 and 12 months of age. May be inherited? Erosion of the cartilage of the acetabulum and femoral head eventually leading to subluxation and joint degeneration.

B) Slow onset lameness which eventually leads to reluctance to weight bear and move. Animals will loose condition. In the early stages lateral swinging of the affected limbs may be seen.

C) Clinical signs are suggestive. Crepitus may be detected in affected limbs. Radiography may be of value in small animals

D) None, therefore slaughter

56
Q

Hip Dislocation:

A) Artiology?

B) Clinical signs and presentation?

C) Diagnosis?

D) Treatment?

A

A) Usually seen in adult cows after traumatic abduction (“partial splits”) of the hind legs soon after calving when relaxation of ligaments is maximal. In most cases (~80%) the femoral head is displaced craniodorsally.

B) Clinical signs and presentation: Acute onset hindlimb lameness, usually non weight bearing. After craniodorsal dislocation the leg tends to be rotated outwards. The pelvis and hips will often appear asymmetrical if viewed from behind.

C) Manipulation of the leg will often reveal the dislocation because of restriction in hip movement and detection of crepitus. Vaginal and rectal examination can be helpful in the detection of movement and crepitus if the leg is manipulated at the same time. Radiographical examination can be used to confirm a diagnosis in valuable and small animals.

D) Dislocations can be replaced by manipulation or surgically. The surgical approach in through the gluteal muscles cranial to the greater trocanter. The femoral head is visualised and reintroduced to the acetabulum with the help of an assistant manipulating the leg.

The hip can often be manipulated back into position (especially if attempted soon after dislocation) with the animal heavily sedated (Xylazine). The hip is forcible replaced by a combination of rotation to loosen the soft tissue contraction, leverage and pressure on the femoral head.

However the dislocation is replaced the animals should be kept comfortable and housed on a non slip surface to allow soft tissue healing.

57
Q

What is the prognosis for a hip dislocation?

A

Good providing cases are uncomplicated (i.e. no fractures) and replacement is attempted early. The prognosis in cases which have been dislocated for a while is much poorer.

58
Q

Patellar luxation:

A) Aetiology?

B) Clinical signs and presentation?

C) Diagnosis?

D) Treatment?

A

A) 3 types. Dorsal luxation occurs occasionally and sporadically in mature cattle. Medial and lateral luxations appear to be congenital and are rare.

B) If the patella is fixed in dorsal luxation the leg is held out stiff and straight behind. Animals walk with a jerky action in which the leg suddenly snaps forward. Affected steps may be intermittent. In some cases the leg becomes fixed in extension for long periods. Animals suffering from medial and lateral luxation are unable to bear weight on the affected leg because the stifle collapses if weight is borne. Both legs may be affected.

C) Presenting signs are suggestive for all 3 conditions. The abnormally placed patella can be visualised and palpated out of position.

D) Doral patella luxation is corrected by sectioning the medial patella ligament under local anaesthesia with the animal standing. Medial and lateral patella luxation can be treated with a joint overlap procedure. In lateral luxation the medial joint capsule is overlapped and visa versa.

59
Q

Degenerative Joint Disease:

A) Aetiology?

B) Clinical signs and presentation?

C) Diagnosis?

D) Treatment?

A

A) Chronic non infectious degeneration of joints. Associated with age and excess weight.

B) Rarely presents clinically, although a common post mortem finding. Mild to moderate slow onset chronic lameness. Animals are unwilling to flex and extend affected joints giving a stilted gait. Affected joints may be painful, demonstrate crepitus when manipulated and show mild swelling.

C) Diagnosis is difficult due to the non specific nature of the signs. Exclude other diagnoses. Care should be taken not to use “arthritis” as a coverall for more serious conditions and as excuse to allow obvious welfare cases to exist on farms.

D) None, symptomatic treatment such as anti-inflammatories may ameliorate clinical signs in the short term. Animals should be culled when lameness starts to cause welfare problems.

60
Q

What is the aetiology of white muscle disease?

A

Selenium along with vitamin E are powerful antioxidants (glutathione peroxidases, GSHPx) that protect cells against peroxidases that damage cell membranes. It is also thought to improve immune function. Vit E and Se probably “spare” each other.

Selenium deficiency has a primary aetiology in both cattle and sheep. Animals fed on diets low in Se risk clinical signs. Usually associated with grazing pastures growing in areas where the soil contains low Se levels (soils on granite or volcanic rocks). It does not proved possible to induce disease such as muscular dystrophy through depletion of Se and Vit E levels alone. It is though that high level of poly unstaturated fatty acids (PUFA) in the diet e.g. spring grass, are also necessary as PUFA leads to the production of lipid peroxides.

61
Q

What are the clinical signs for white muscle disease? Cattle and sheep?

A

Cattle –

  1. Muscular dystrophy (White muscle disease) in growing animals
    1. Peracute – Sudden death, or animals found dead
    2. Acute – Lateral recumbancy, dull, respiratory disease, tachycardia. Death within 24 hours.
    3. Subacute – Stand and walk stiffly, reluctance to move, weakness and reluctance to stand. The animal eats normally and the heart and respiratory rate may be normal or slightly elevated.
    4. Chronic – Ill thrift and poor weight gains. Lower survival rates.
  2. Retained cleansing, metritis and cystic ovarian disease in adults
  3. Depressed immune function – Has been shown to decrease phagocyte function in vitro. Possibly decreased resistance to disease e.g. mastitis, although yet to be definitively proven.
  4. Heinz body anaemia in growing calves

Sheep

  1. Muscular dystrophy (Stiff lamb disease) in lambs
    1. Lambs still born or born weak / die within a few days (often from cardiac arrest)
    2. Acute - 0–4 months, stand and walk stiffly, reluctance to move, weakness and reluctance to stand. Often confused with joint ill.
    3. Chronic - Ill thift and poor weight gains. Lower survival rates.
  2. High embroyonic mortality and infertility in ewes
  3. Heinz body anaemia in growing lambs
62
Q

How do you diagnose white muscle disease?

A

1.Clinical signs

  1. PME – White plaques in heart muscle, white striations in skeletal muscle.
  2. Whole blood Se – Difficult and expensive to measure but reflects Se status at the time of sampling
  3. Erythrocyte GSHPx – Easier to measure than Se, however erythrocytes are turned over slowly so this is a historical measure of Se status. It may take upto 4 months for GSHPx levels to reflect Se intake.
  4. Creatine Kinase – Serum / plasma CK levels will be elevated because of release from damaged muscles.
  5. Response to treatment / supplementation
63
Q

How do we treat and prevent white muscle disease?

A

1.Parenteral injection – s/c or i/m injection (nb s/c less damaging to carcase) or Se preparations usually in combination with Vit E e.g. Vitenium or Vitesel (Cattle & sheep). May require redosing every week or every two weeks. Depo injection in oily bases are available e.g. Deposel Injection (Cattle & sheep).

  1. Addition to feedstuffs – Levels of Se and Vit E in feed can be increased
  2. Selenium boluses – Cosecure (Cattle & sheep, Co, Cu & Se), Zincosel (Cattle & sheep, Co, Zn, Se), Ionox (Cattle, Co, I, Se), All-Trace (Cattle only, multivitamin & mineral)
  3. Addition of selenium to drinking water – Ensure medicated water is the only available supply e.g. Aquatrace Selenium (Cattle only, Se only), Aquatrace Ex-Sel (Cattle and Sheep, multivitamin & mineral), Aquatrace Trio Cattle (Easi-calver) (Cattle only, Cu, I and Se)
  4. Free access minerals, blocks and licks – Individual animal intake can be very variable.
  5. Drenches - Labour intensive, requires repeat doses e.g. Aquatrace Ex-Sel (Cattle & sheep, multivitamin & mineral preparation used as a drench)
  6. Application of Se salts to soils
64
Q

Flexoral Limb Deformities:

A) Aetiology?

B) Clinical signs?

C) Diagnosis?

D) Treatment?

E) Prognosis?

A

A) A relatively common congenital abnormality. More common in some breeds e.g. Belgian Blues. May be associated with abnormal limb position in a cramped uterus.

B) Calves are born with varying degrees of rigid flexion usually in the fore limbs. Less commonly there is extensor rigidity in the hocks. The condition is usually bilateral and can range from mild (just off straight) to severe.

C) Diagnosis is straight forward.

D) Mild cases are usually self limiting and correct them selves as calves start to walk. Physiotherapy and walking on hard surfaces may help. In more serious cases it may be necessary to splint (padded guttering works well) the legs in extension leaving the hooves exposed to encourage normal walking. In the most severe cases surgery can be helpful. Ligaments and tendons causing the most restriction in movement can be identified and resected hopefully encouraging more normal weight bearing.

E) Good in mild cases, treatment of severe cases can be difficult and disheartening as animals will often thrive but leg position will not improve.

65
Q

Spastic Paresis:

A) Aetiology?

B) Clinical signs?

C) Diagnosis?

D) Treatment?

E) Prevention?

A

A) Unknown. Most common in the German and Dutch Friesians and the Aberdeen Augus.

B) Chronic and progressive contraction of the gastrocnemius muscles. Young animals between 6 weeks and 6 months of age. Hock is nearly straight. Animals walk with a stiff and stilted gait. Limbs may jerk intermittently at rest.

C) Pathognomonic.

D) Surgical resection of the gastrocnemius and superficial flexor tendons or neurectomy of the tibial nerve.

E) Hereditary predisposition. Affected animals should not be used for breeding.

66
Q

Hock Cellulitis, Bursitis and Trauma:

A) Aetiology?

B) Clinical signs?

C) Diagnosis?

D) Treatment?

E) Prevention?

A

A) Hock abrasion, enlargement and damage are the result of trauma suffered during the winter housing period. Animals rub hock on cubicle beds, cubicle frames and other objects in the environment.

B) In the initial stages there is hairloss over the bone protuberances of the hock. As the condition develops the hock swells because of soft tissue damage and swelling and the development of tarsal bursitis. In severe cases the skin overlying the hock can become ulcerated, which can lead to the development of a secondary infectious bursitis and even infectious arthritis. In the early stages animals are usually not lame. However if swelling is severe or lesions become infected a mild to moderate lameness may develop.

C) Straightforward. Swollen and damaged hock in winter housed animals.

D) Not usually necessary unless secondary infection exists. A course of antibiotics will usually relieve the lameness. Lesions SHOULD NOT be incised and drained. Most lesions almost completely resolve during the summer months when animals are out of winter housing.

E) Identify and correct the underlying cause. A certain amount of hock damage is inevitable in winter housed cattle especially those in cubicles. However if the prevalence is high the predominant causative factor should be identified by watching cattle rising from cubicles and corrected e.g. cubicle flooring, abrasive edge to cubicle step.

67
Q

What is carpel bursitis?

A

Carpel bursitis is similar to hock bursitis is aetiology and presentation. It is more common in winter housed cattle and resolves in the summer months. Animals present with large swollen carpi. If swelling is severe, lesions can be aseptically drained.

68
Q

Rupture of the Gastrocnemius Muscle:

A) Aetiology?

B) Clinical signs?

C) Diagnosis?

D) Treatment?

E) Prognosis?

A

A) Unclear, often associated with periods of prolonged recumbency, excessive weight and possible mineral imbalance.

B) The Gastrocnemius muscles ruptures usually at the musculotendon junction and usually bilaterally. Weight bearing is almost impossible because the hock drops almost to the floor.

C) Signs are pathognomonic

D) Animals should be closely confined with the limbs splinted in extension for a number of weeks to allow healing and fibrosis of the muscles to occur.

E) Guarded, animals are unlikely to recover fully, re-rupture may occur.