Musculoskeletal diseases Flashcards
Musculoskeletal diseases in piglets
Congenital defects: Splay leg
Abrasions, trauma and foot lesions
Arthritis: Streptococcus suis I, Staph. spp., T pyogenes.
Musculoskeletal diseases in weaners and growers
Arthritis: G. parasuis, E. rhusiopathiae. Strep. suis, Mycoplasma hyorhinis.
Musculoskeletal diseases in finishers
Arthritis: Mycoplasma hyosynoviae
Bursitis and shoulder abrasions
Trauma: fractures and muscle injury
Porcine Stress Syndrome
Musculoskeletal diseases in adults
Degenerative Diseases: Osteochondrosis, epiphysiolysis.
Foot lesions: Erosive lesions and hoof rot, laminitis, overgrowth.
Miscellaneous and nutritional: white muscle disease, Kyphosis / ricketts, biotin deficiency
Less significant: osteomalacia, osteodystrophia fibrosa, rickets, proliferative osteitis.
Incidence of splay leg in piglets
An important abnormality that may severely compromise the survival of neonatal piglets.
Quite common. Seen especially in Landrace, Large White and Welsh breeds; also hybrids.
Aetiology of spley leg in piglets
A polygenic hereditary abnormality but also caused or exacerbated by a choline deficiency or fusarium (mycotoxin) toxicity.
Pathology of splay leg in piglets
Myofibrillar hypoplasia and associated with reduced diameter of motor neurons.
Epidemiology of splay leg in piglets
Affects up to 4% UK neonatal piglets.
Morbidity in litter can be 25% and mortality of affected piglets 50%.
Death usually caused by crushing injuries, as piglets can’t take evasive action, and also through hypoglycaemia or hypothermia.
Both sexes affected but males more so than females.
Affected animals often have a low birth weight.
Clinical signs of splay leg in piglets
Affected piglets recognised within a few hours of birth.
Can’t stand on their hind legs, which are splayed out laterally.
The forelegs may be normal or also splayed.
Piglets can suck milk if they can get to the teats.
Treatment of splay leg in piglets
Piglets are helped by loosely tying their hind legs together with a figure of eight tape just above the hocks- as soon as possible after birth.
Will help up to 50% piglets walk quite normally.
Help needed for a few days only by which time piglets walking normally.
Low impact/less common congential disorders in piglets
Crooked/kinky tail
Polydactyly
Legless piglets
Arthrogryphosis
Kyphosis and scoliosis
Pietrain creeper syndrome
Dwarfism
Congenital porphyria
Abrasions, trauma, and foot lesions in young piglets
Foot lesions very common- 100% show sole bruising by 24 days, with large numbers showing sole erosions, carpal abrasions, and healed wounds.
Can allow entry of pathogens- local or systemic infection
Treatment of Abrasions, trauma, and foot lesions in young piglets
Temporary improvements to environment (bedding).
Antibiotics to control infection (penicillin, amoxicillin)
Prevention of Abrasions, trauma, and foot lesions in young piglets
Improved hygiene and floor maintenance.
Existing housing: use of floor mats, renew concrete or cover with rubberised pain, provision of bedding.
Refurbish housing with updated plastic flooring.
Incidence of Infectious arthritis (joint ill) in young piglets
Common.
Piglets affected in the first 10 days of life.
Aetiology of Infectious arthritis (joint ill) in young piglets
T. pyogenes, Streptococcus spp including Strep suis type 1, Staphylococcus spp.,
In many clinical cases the actual cause is unknown and is not determined.
Ascending tenosynovitis.
Epidemiology of Infectious arthritis (joint ill) in young piglets
Infection gains access through tonsil or other vulnerable access points (umbilicus, tail-dock lesion) soon after birth.
Infection spreads haematologically through the body.
Infection can also gain access through dirty syringes and needles, poor teeth clipping technique, and through abrasions, trauma and foot lesions.
Clinical signs of Infectious arthritis (joint ill) in young piglets
Reluctant to take weight on all four legs.
Hot to the touch and are pyrexic.
One or more joints distended, warm and painful.
Hock, carpus and stifle most commonly affected.
CNS signs rarely occur but occasionally signs of meningitis in which case Strep suis Type 1 may be the specific cause.
Diagnosis of Infectious arthritis (joint ill) in young piglets
Age, clinical signs.
Joint fluid is increased in volume and may be turbid and hypercellular.
Recently euthanized piglets should be submitted to APHA for collection and culture of joint fluid.
Differential diagnoses of Infectious arthritis (joint ill) in young piglets
When possible the cause should be ascertained to determine whether a specific infection such as Strep suis Type 1 is present.
Treatment of Infectious arthritis (joint ill) in young piglets
The whole litter, affected and unaffected, should be treated.
A full 3 - 5 day course of antibiotics should be given.
Penicillin / streptomycin or ampicillin.
Single shot long acting preparations such as tulathormycin (Draxxin) and ampicillin may be appropriate.
Clavulanic acid with amoxyicillin is also effective.
Small doses of steroids or NSAIDs speed recovery in severely affected animals.
Incidence of Chronic septic arthritis in weaners and growers
Common and likely to increase.
There are both economic and welfare issues to be addressed
Aetiology of Chronic septic arthritis in weaners and growers
A range of organisms especially T. pyogenes although this may not have been the primary organism.
Glaesserella parasuis, E. rhusiopathiae, Streptococci, Staphylococci, Actinobacillus suis and possibly the mycoplasmas may have contributed to the primary pathology.
Epidemiology of Chronic septic arthritis in weaners and growers
Many cases were victims of an outbreak of arthritis as younger piglets - especially joint ill at a few days of age
Clinical signs of Chronic septic arthritis in weaners and growers
Lameness and deformity.
One or more joints are affected and there is often severe loss of muscle mass caused by atrophy of disuse.
The affected joints are swollen and sometimes abscessated.
They may have opened with thick pus exuding.
In many cases the joint movement range is greatly reduced and there may be total ankylosis.
Affected animals are often in very poor condition and are unable to compete for food and water.
Diagnosis of Chronic septic arthritis in weaners and growers
History, clinical signs and orthopaedic evaluation.
Most affected commercial pigs are not economic to treat, further diagnosis is not justified.
For pet pigs an X - ray is essential if treatment is contemplated and economic to check that irreversible pathology is not already present.
Treatment of Chronic septic arthritis in weaners and growers
This is seldom economical, or justifiable on welfare grounds, and euthanasia may be the best option.
However chronic joint infection of high value / pet pigs can be treated with some success.
Antibiotic therapy, NSAIDs, joint drainage and lavage may be appropriate in some situations where there is suitable nursing care available.
Control of Chronic septic arthritis in weaners and growers
Environmental and managemental improvements, alongside effective individual pig care.
Early detection and treatment of properly diagnosed disease, with completion of courses of treatment, are effective in dealing with most joint infections in pigs.
Glasser’s disease
World wide occurrence.
Caused by Glaesserella parasuis.
This organism can cause polyarthritis.
Affects pigs from weaning - 4 months of age (sometimes older).
Occasionally, pre-weaned pigs affected.
Serotypes 4,5 believed most prevalent but some studies indicate serotype 10 is more relevant in UK.
Clinical signs of Glasser’s disease
Sudden onset of lameness and fever; may also see CNS signs and respiratory signs.
Joints swollen and affected pigs walk with short strides.
May also see polyserositis with pleurisy, peritonitis, pericarditis on necropsy of found-dead pigs.
Diagnosis of Glasser’s disease
Isolation of organism from joints or other non-respiratory locations (non-virulent strains of GPS reside in the URT and can descend to lungs as by-stander organisms).
Use chocolate agar or Staph streak (NAD dependent).
Serotyping of the isolate is useful for determining if commercial vaccines are suitable for use.
Treatment of Glasser’s disease
Parenteral penicillin / streptomycin, oxytetracycline or trimethoprim sulpha for 3 days.
Metaphylaxis for in contacts can be done using oxytetracycline or amoxycillin in drinking water.
Alternatively, inject all pigs with tulathromycin (Draxxin) a prolonged action product, if there are doubts over water/fed intake.
Prevention of Glasser’s disease
Vaccination (Intervet and Zoetis) but these vaccines are directed only against serotypes 4 and 5.
Protection against other serotypes can be achieved through autogenous vaccination.
Streptococcus suis type 1
A common infection of pigs in the10 - 14 day age group.
Carried by sow and enters piglets body via tonsillar crypts leading to septicaemia with involvement of joints and other organs.
Abrasive environmental conditions and insufficient colostral derived immunity are factors.
Chronic joint infection can carry over to post-weaning phase.
Clinical signs of Streptococcus suis type 1
May see occasional sudden death and /or several members of litter lame with swollen joints, fever, and reluctant to move.
May see CNS signs and occasionally endocarditis.
Diagnosis of Streptococcus suis type 1
Isolation of organism.
Joint fluid is sero-sanguinous.
Treatment of Streptococcus suis type 1
Immediate treatment with parenteral penicillin, ampicillin or trimethoprim sulpha for 3 - 5 days.
Tulathromycin (Draxxin) or other prolonged action antibiotic injectable options.
NSAIDs (ketoprofen) may help cases.
Incidence of Swine Erysipelas
Quite common.
Chronic arthritis caused by erysipelas is probably less common than that caused by other organisms such as T. pyogenes.
In many cases the cause of arthritis is not determined but the clinical signs of erysipelas are quite specific.
Mostly affects pigs >12 - 16 weeks (possibly after decline of colostral antibody).
Aetiology of swine erysipelas
Potential zoonosis
Erysipelothrix rhusiopathiae
Epidemiology of Swine Erysipelas
Chronic erysipelas may follow the acute form of the disease but often there is no history of this.
The changes in the joint are of a non-suppurative proliferative arthritis.
Damage to the articular cartilages can result in their loss and the joints become dry and ankylosed.
Clinical signs of peracute Swine Erysipelas
Sudden death
Congestion and discolouration of the skin
Clinical signs of acute Swine Erysipelas
Diamond shaped skin lesions: classic rhomboid urtical lesions (septicaemia)
Pyrexia, leading to fertility problems (abortion in sow/poor semen quality boar)
Clinical signs of chronic Swine Erysipelas
Lameness, paralysis
Cyanosis, skin necrosis
DIagnosis of Swine Erysipelas
Clinical signs and progression of the untreated disease.
At post-mortem the joint capsule is thickened and the synovial membrane is proliferative with areas of granulation tissue.
In advanced cases there is loss of articular cartilages.
A definitive diagnosis is based on culture of the organism from the joints.
Differential diagnoses of Swine Erysipelas
Other causes of lameness eliminated by careful clinical evaluation and culture of joint contents and synovial membranes.
Specific diseases include Glasser’s disease (G. parasuis), Streptococcus suis Type 2, Mycoplasma infections, leg weakness and diseases of the foot.
Treatment of Swine Erysipelas
Can be unrewarding.
In cases where there are chronic pathological changes in the joints euthanasia may be advisable as the chance of recovery and normal growth are poor.
In early cases parenteral injections of penicillin for at least five days are advised.
NSAIDs including ketoprofen or oral aspirin may be used.
Prevention of Swine Erysipelas
Vaccination of sows
Higher challenge may require vaccination of growing pigs
Streptococcus suis types 2 and 14
A zoonotic organism.
A common and important disease in the UK usually affecting weaned or finishing pigs - usually affects older animals than Strep. suis Type 1.
Infection often follows stresses such as mixing and moving.
Zoonotic infections reported for serotypes 1,2,14.
Clinical signs of Streptococcus suid types 2 and 14
Occasional sudden death and then several pigs in group show signs. Piglets - 2-6 weeks (peak at 6 weeks).
Pyrexia 40-41 degrees, lameness, swollen joints.
May see acute polyarthritis. May also see meningitis and CNS signs.
Diagnosis of Streptococcus suid types 2 and 14
History and clinical signs.
Isolation of organism from pathological sites with serotyping – can be done on a smear by FAT.
Culture from tonsils may be confused by co-existent non-virulent strains.
Some labs have developed PCR tests to discriminate virulent strains but these are not 100% specific.
Treatment of Streptococcus suid types 2 and 14
Aggressive course of antibiotics such as penicillin, ampicillin or trimethoprim sulpha for 3 - 5 days.
Long acting preparations of tulathromycin (Draxxin) or other antibiotics can be useful by single injection.
NSAIDs may help painful cases but a welfare endpoint must be agreed on a case by case basis, particularly if meningitis also present.
Control of Streptococcus suid types 2 and 14
strategic medication of the group with in-feed or in water antibiotic (amoxicillin, potentiated sulphonamide)
Incidence of Mycoplasma hyorhinitis
Exact incidence unknown but quite common.
Mostly affects pigs aged
3 - 10 weeks often just before or just after weaning.
Increasing awareness of its role.
Aetiology of of Mycoplasma hyorhinitis
Mycoplasma hyorhinis.
Epidemiology of of Mycoplasma hyorhinitis
May originate from an older pneumonia case.
The organism is found in the nasal tracts of 60% pigs.
Colonisation from dam or from groups mates at weaning.
Organism gains access to susceptible piglets and septicaemia develops.
Settles in the joints causing a polyarthritis, some strains may also cause pneumonia.
Clinical signs of of Mycoplasma hyorhinitis
Affected pigs are dull, lame and anorexic.
Slight fever, and appetite is depressed.
Growth rate is markedly depressed.
Joints are swollen and warm to the touch - the hock, stifle, shoulder and elbow are most frequently affected.
Diagnosis of of Mycoplasma hyorhinitis
Clinical signs.
Joint fluid is sero-sanguinous or serofibrinous - there is an increase in numbers of plasma cells and lymphocytes.
PM reveals joint changes including villous hypertrophy of the synovial membranes.
M. hyorhinis also causes polyserositis (pleurisy, pericarditis, peritonitis) and low grade pneumonia.
Differential diagnoses for Mycoplasma hyorhinitis
Other causes of lameness including H. parasuis, Strep. suis., E. rhusiopathiae.
Diagnosis is by PCR on fresh or frozen material (from non-respiratory location).
Treatment of Mycoplasma hyorhinitis
Oxytetracycline or tiamulin given for five days by injection or in food or water if piglets are eating.
If untreated (mild cases) self cure occurs in 4 weeks.
Incidence of Mycolplasma hyosynoviae
Quite common in UK and in other pig keeping areas.
Aetiology of Mycolplasma hyosynoviae
M. hyosynoviae - infection often follows stress.
Epidemiology of Mycolplasma hyosynoviae
Clinical signs of Mycolplasma hyosynoviae
Variable from slight to severe acute lameness.
Temperature is usually normal.
May see self cure of mild cases and regression of lameness over a few days.
Affected joints are swollen and may be warm to the touch.
At post mortem the joint contains clear yellow-brown fluid +/- fibrin flakes.
The synoviae are inflamed but the articular surfaces are usually unaffected.
Diagnosis of Mycolplasma hyosynoviae
Clinical signs but to confirm must isolate M. hyosynoviae from joint
Fluid (PCR).
Joint fluid yellow - brown and clear.
DDX - osteochondrosis in breeding stock.
Treatment of Mycolplasma hyosynoviae
Parenteral treatment by injection with tiamulin, tylosin or lincomycin for 3 - 5 days.
Prevention of Mycolplasma hyosynoviae
Where an ongoing repeated problem, then consider prophylactic treatment of group for 2-3 days using Lincomycin in water a few days before the expected appearance of clinical signs.
Repeat the medication 10 days later if experience dictates.
Causes of arthritis pre-weaning
Joint ill: Strep. spp
Joint ill: Staph. spp
Joint ill: T. pyogenes
Cause of arthritis 1-3wk olds
Strep suis 1
Cause of arthitis 5-16 wks old
G. parasuis
Cause of arthritis 6-26wks
Strep. suis 2, 14, other
Cause of arthritis in <12 wks
Actinobacillus suis
Cause of arthritis >12wk olds
E. rhusiopathiae
Cause of arthritis in 3-10wk olds
M. hyorhinitis
Cause of arthritis in 10-26wk olds
M. hyosynoviae
Bursitis
Common in finishers (85%)
Occasionally lameness
If skin damaged, secondary infection possible
○ Abscessation
○ Ulceratio
Negative economic impact of bursitis
Affected tissue needs to be trimmed at the abattoir
0.5kg reduction in carcase weight
Aetiology of burstitis
○ Hard floors/lack of bedding
○ High stocking densities on slats
○ Slats wider than 3cm
○ Heavy pigs
Prevention of bursitis
Adequate bedding
Polypropylene slats
Recording as a negative welfare outcome on assurance schemes should help reduce prevalence
Incidence of limb lesions caused by pressure
Very common, typically noted in finisher pigs.
Aetiology of limb lesions caused by pressure
Unsuitable or inadequate bedding to prevent damage to the skin and deeper tissues over the pressure points of the body.
Epidemiology of limb lesions caused by pressure
Metal mesh flooring, rough concrete surfaces, lack of straw and slatted floors are among surfaces likely to predispose to the above.
Wet, dirty conditions, poor ventilation and overcrowding make matters worse.
Clinical signs of limb lesions caused by pressure
Knees and hocks and less commonly the anterior surfaces of the fetlock joints are most frequently affected.
Areas of excoriation of the skin with local skin necrosis.
In some cases abscess formation occurs in adjacent tissue.
Hygromata - subcutaneous bursae filled with synovial-like fluid - develop and these sometimes also become infected.
Lameness not usually present.
In other cases chronic irritation of the skin causes hyperplasia and the development of calluses. Lameness associated with this group of lesions is relatively uncommon.
Treatment of limb lesions caused by pressure
In the absence of infection no treatment is normally given.
Pigs should be moved to better accommodation or better bedding provided.
Abscesses are drained in the normal way and superficial areas of infection may be treated by application of topical oxytetracycline spray.
Never open and drain an uninfected bursa/hygroma.
Prevention of limb lesions caused by pressure
High prevalence requires review of sleeping areas, slat/slot condition, smoothness of cement floors, availability of bedding etc.
Shoulder abrasion
Very low body condition (BCS 1,2)
Poor flooring, poorly designed farrowing crates
Often obvious during/after lactation especially in younger parities - esp P1-P2 (weight loss)
Treatment based on relieving pressure, and topical anti-infectives/NSAID
Prevention focused thorough clinical and environmental assessment, identifying predisposing factors.
Causes of trauma
Fighting
Falling during mating
Osteomalacia (dietary)
Inappropriate environment/handling facilities
Accidental electrocution (uncommon)
§ Thoracic vertebrae
§ Humerus, neck of scapula
§ Pelvis, neck of femur
§ Burn marks
Clinical signs of trauma
Sudden onset of severe and acute lameness
Unable to take weight on the affected limb(s) - Unfit for transport
Lower limb fractures: deformity of limb
Upper limb fractures: swelling and evidence of haematoma (not always obvious)
Diagnosis of trauma
Clinical examination difficult
§ Heavy musculature and swelling
Abnormal bone mobility, crepitus
Dramatic increase in muscle tone around fracture
Radiography is impractical and costly under field conditions
Differential diagnoses of trauma
Severe foot pathology/abscess
Epiphysiolysis
Spinal abscess
Treatment of trauma
Euthanasia most practical in most commercial situations
Incidence of fractures
Quite common especially in units where handling facilities for large numbers of pigs are not good.
Aetiology of fractures
Trauma - accidental, injuries inflicted by other pigs, falling during mating, falling over rubble in poorly maintained paddocks.
Humeral fractures are also seen in cases of electrocution
Clinical signs of fractures
Sudden onset of severe and acute lameness.
Usually unable to take weight on the affected limb.
Muscle tone in the limb is reduced.
The pedal withdrawal reflex is non - responsive.
In lower limb fractures there may be obvious deformity of the limb.
In upper limb fractures there may be swelling and evidence of haematoma formation.
Clinical examination of fractures
Difficult in suspected fracture cases.
Sedation or general anaesthesia may be necessary.
Upper limb fracturesare difficult to evaluate.
Abnormal bone mobility, dissymetry, crepitus palpated or auscultated and the dramatic decrease in muscle tone around the fracture are often diagnostic.
Radiography can be helpful but can be impractical and costly under field conditions.
Upper hind-limb fractures can be relatively well splinted by surrounding muscle such that affected pigs may go unnoticed initially (e.g. when off-loading at abattoir).
Treatment of fractures
Lower limb fractures can be successfully plastered (resin) although management usually requires the pig being kept in a hospital pen on its own and great care is needed to monitor for tightening of the cast as the pig rapidly grows.
Upper limb fractures have a very poor prognosis.
Internal fixation does not work well in pigs because of their poor bone density.
Euthanasia will likely be required.
Muscle injuries
Muscles can be damaged as a result of fighting or in association with bone damage for example in fractures.
Deep bite wounds penetrating the skin may extend deep into muscle.
Such wounds require careful evaluation and cleaning, with a severity end-limit, taking into account availability of hospitalisation pens and nursing care.
Some may require surgical repair and 3-5 day courses of antimicrobials.
Incidence of porcine stress syndrome
Has occurred in many breeds.
95% of Pietrains carried the gene.
Breeding companies have progressively excluded the gene from modern breeding stock hybrid strains but it may still be seen in unimproved traditional and pedigree breeds and especially the Pietrain.
Aetiology of porcine stress syndrome
An inherited defect caused by a single nucleotide substitution.
Inherited as an autosomal recessive gene with incomplete penetrance.
Known as the Porcine Stress Syndrome (PSS) gene and also Halothane Sensitivity Gene.
The ryr gene codes for the ryanodine receptor (a calcium gated calcium release channel on the sarcoplasmic reticulum) leading to an alteration in sensitivity resulting in instability.
The muscle becomes hypersensitive to various stresses.
In response to stress there is a rapid onset of anaerobic glycolysis and loss of control of skeletal muscle metabolism.
Affected pigs also show dysregulated metabolism of noradrenaline.
Epidemiololgy of porcine stress syndrome
The genetic background to the condition means that it can be transmitted from one generation to the next with continued serious welfare and economic consequences.
Performance of affected animals may be reduced.
Four main syndromes of Porcine stress syndrome
Porcine stress syndrome
Malignant hyperthermia
Pale soft exudative pork (PSE)
Back muscle necrosis
Porcine stress syndrome
Pigs show an abnormally severe response to stress - including travel, mixing, weighing etc.
Hot ambient temperatures exacerbate the problem.
Initially pigs may show muscle tremors quickly followed by dyspnoea with open mouthed breathing.
Body temperature rises rapidly to very high levels and the pig is very distressed.
The skin is blotched with purple patches.
The pig collapses, muscular spasm is seen and death occurs.
Malignant hyperthermia
Occurs in response to exposure to some anaesthetics (halothane anaesthesia and also to treatment with Succinylcholine (a muscle blocker)).
Within a very short time signs of abnormality are seen - muscle rigidity develops, temperature rises and large amounts of lactic acid are produced.
Heart rate increases and cardiac dysrhythmia is seen.
Death follows.
Pale soft exudative pork (PSE)
Rigor sets in very rapidly after slaughter.
Lactic acid is produced and the pH of muscle falls (<6) meat loses its colour and normal consistency.
The carcase loses its rigor and fluid content drips out due to reduced water retaining capacity of the muscle protein.
Stress just prior to slaughter exacerbates the effects of PSE.
Back muscle necrosis
Necrosis of parts of the longissimus dorsi muscle occur.
There is pain and swelling over the affected area which gradually resolves over a period of two weeks.
Damaged muscle never regenerates and carcase value decreases.
Some deaths occur.
Diagnosis of porcine stress syndrome
Based on the history and clinical signs.
A number of diagnostic tests
can be used:
a) Halothane sensitivity test, and Creatine Kinase (CK) assay were originally used to help in genetic improvement of breeding lines;
b) PCR test for PSS gene is now used as the selection marker and to screen pigs.
c) Post mortem - shows areas of pale muscle, low pH and poor carcass setting qualities.
Treatment of porcine stress syndrome
In most cases the rapidity and severity of the symptoms seen in the various clinical syndromes precludes any effective treatment and most cases end fatally.
Separate from group, adequate ventilation, cooling with water.
Still most cases fatal.
Incidence of porcine osteochondrosis
A very common and important condition in growing and older pigs.
Also referred to as Leg weakness, Arthrosis and Epiphysiolysis.
Actually a form of dyschondroplasia as it appears to be a cartilage developmental problem starting quite early in life.
Aetiology of porcine osteochondrosis
Not entirely clear- likely some genetic predisposition but environmental and nutritional factors also important.
The pathological defect is believed to be a malfunction of cartilage production and its ossification.
Defects of conformation may develop from the disease but also contribute to it.
Epidemiology of porcine osteochondrosis
The problem occurs in up to 80 % of pigs in some surveys with all breeds and both sexes being involved.
Occurs in pigs <18 months.
Not all pigs with orthopaedic pathology show signs of lameness.
The condition is associated with joint abnormalities especially in the long bones, their growth plates, their epiphyses and in the vertebral joints.
Pathology of porcine osteochondrosis
Growing cartilage in the growth plates, some areas are disrupted.
Pathological changes cause abnormalities in various parts of the bone and joints
Physeal cartilage defects: bending and deformity
Articular and epiphyseal cartilage defects: sterile joint abnormalities
Lesions mainly seen on the weight bearing condyles
Clinical signs of porcine osteochondrosis
Animals appear uncomfortable when made to walk or stand.
May walk on knees with carpi flexed and the animal may seem unwilling to extend the carpi whilst the fetlock joints may be over extended.
The toes of the hind legs may be turned in.
May adopt a wide hind leg stance.
May be ataxic and have a swaying gait resulting in swaying movements of the hindquarters.
Diagnosis of porcine osteochondrosis
Definitive diagnosis is by necropsy or abattoir examinations with submission of joints for histopathology.
Osteochondrosis can be detected radiographically showing irregularity of the articular cartilages and sometimes the presence of joint mice.
Synovial fluid increases in the early stages of the disease but later is reduced in quantity.
Cellular content of the synovial fluid is normal and is not increased as it is in cases of septic arthritis.
Differential diagnoses of porcine osteochondrosis
Must be sure that no other causes of lameness are present - requiring a comprehensive clinical examination in every case.
Must check that there are no foot lesions, no infectious diseases of the joints and no injuries including fracture.
Erysipelas.
Mycoplasma hyosynoviae, epiphysiolysis (fracture of the femur/pelvis).
Treatment of porcine osteochondrosis
Is not effective as it is impossible to reverse the abnormalities present.
In valuable breeding animals NSAIDs including ketoprofen or oral aspirin may provide temporary help.
Note long term phenylbutazone may predispose gastric ulcers and is not licensed in pigs.
Control of porcine osteochondrosis
Careful breeding from unaffected animals with monitoring of the performance of groups of siblings may be helpful.
Good nutritional management to ensure strong bone deposition in the face of a rapid increase in body weight.
Epiphysiolysis
Separation of femoral head, ischeal tuberosity, greater or lesser trochanter along lines of the growth plate
Bony proliferative changes
Incidence of Epiphysiolysis
This condition is not uncommon and is most frequently seen in young boars and less commonly in gilts at the beginning of their breeding life.
It is considered to be a specific form of osteochondrosis / dyschondroplasia.
Aetiology of Epiphysiolysis
An existing defect in the epiphysis, possibly the result of dyschondroplasia, may result in a weak link between the femur and femoral head epiphysis.
Trauma sustained in attempts to serve or through fighting may cause the separation to occur.
Clinical signs of Epiphysiolysis
Lameness involving one hind leg.
The severity of the lameness may increase over the course of a few days.
The leg may just touch the ground or may be carried when possible.
Muscle wasting in the ipsilateral gluteal region occurs quite quickly. It may be possible to detect crepitus around the hip joint by touch or via the stethoscope.
Diagnosis of Epiphysiolysis
History and clinical signs are indicative. Confirmation on necropsy.
Differential diagnoses of Epiphysiolysis
Other causes of lameness including the foot but especially femoral shaft fracture - such animals are usually totally non-weight bearing and crepitus may be detected along the femoral shaft - although the muscle mass of the upper limb makes this difficult.
Treatment of Epiphysiolysis
Animals must be euthanised on welfare grounds
Foot lesions in adult pigs
Very common
Over grown claws
Broken claws
Footrot/bush foot/bumblefoot
Overgrown claws
One or both claws of both fore and hind legs may be affected.
Unsuitable diet, lack of exercise and lack of exposure to firm surfaces can all predispose to the problem.
Affected claws may crack and possibly become infected.
They can be trimmed using cattle hoof shears in a feeding pen or farrowing crate.
Sedation may be necessary if offering of food does not prove sufficient to take the pig’s mind off its feet.
Broken claws
may require tidying up or treatment if infected.
If many cracks
Biotin deficiency could be present
Footrot/bush foot/bumble foot
Very common
Reluctant to walk
May actually be pedal sepsis
Toes may be enlarged, warm and very painful to touch
Fusobacter necrophorum, T. pyogenes, and the spiochete spp.
Treat with aggressive antibiotic and NSAID therapy, occasionally surgical drainage
Incidence of White muscle disease
Uncommon
Aetiology of white muscle disease
Vitamin E/Selenium deficiency
Epidemiology of white muscle disease
As in other species the onset of this problem can be sudden.
Vit E deficiency can arise if the diet is rich in unsaturated fats.
Barley treated with priopionic acid can also be low in Vit E.
Vit E is an essential dietary antioxidant and is involved in membrane protection.
Clinical signs of white muscle disease
Sudden onset of pain and swelling in one or more muscle groups.
Pigs in the group may have shown other signs of Vit E deficiency including sudden death.
If muscles in the limbs are affected the animal is reluctant to move.
Affected animals resent getting to their feet, moving and turning.
One or both sides may be involved and painful firm swellings are palpable in the lumbar region.
Diagnosis of white muscle disease
History, feeding (Low Vit E / Selenium levels in diet), clinical signs, heart lesions, histology: myofibrillar degeneration, vit E in liver low inl. CPK, AST.
Treatment of white muscle disease
Injection of Vitamin E / Selenium.
Correct any dietary deficiencies.
NSAIDs may be needed in the acute phase to reduce discomfort.
Incidence of Biotin deficiency in pigs
Modern diets should contain adequate biotin (> 220 g / tonne) but problems can arise with home mixed food.
Levels can be marginal in some cereals.
Aetiology of biotin deficiency
Biotin is essential for the maintenance and integrity of the hooves.
Deficiency can lead to lameness and the development of cracks in the walls and soles of the hooves.
Prolonged biotin deficiency is required to produce symptoms
Clinical signs of biotin deficiency
Several sows in a herd may show signs of lameness and reluctance to take weight on their feet.
Mating can be difficult.
Litter size may also fall in biotin deficient herds.
The feet are sensitive to the touch and affected animals show resentment if their toes are squeezed.
Cracks are seen in the walls (originating near the coronary band) and also in the soles.
The pads of the soles are softer than normal.
Also causes alopecia and dry scaly skin which may progress to dermatitis with brown crusts/petechial haemorrhages.
Diagnosis of biotin deficiency
Clinical signs and low blood biotin levels (<700 ng/L).
Pathology: areas of necrosis in stratum corneum of epithelium of: skin, claws, oral and oesophageal mucosa.
Treatment of biotin deficiency
Supplement biotin levels in diet.
It may take some months for the full benefit of this to be seen.
Pigs with plasma level of 6070ng/litre -> supplementation
400-1250 mg/t of d biotin in all sow rations as Rovimix H (Roche) 40 g premix/t
Levels up to 3000 mg/t may be necessary to reverse hoof lesions
Preventative 500 mg/t
Incidence of kyphosis and rickets
May arise through inadequate levels of Calcium, Phosphorus or Vitamin D especially in home mixed diets, or where there is reliance on plant derived phosphates in the diet.
Phytase is added to diets to release this phosphate but this phytase may be inactivated by pelleting.
Also, high levels of Zinc included for gut stability may reduce uptake of Ca and P
Aetiology of kyphosis
genetic marker candidates have been identified as predisposing but have not been validated by epidemiological studies.
Aetiology of rickets
Classic rickets is linked to deficiency of Ca, P or Vit D in the diet, but some improved genetic lines appear to have increased demand (i.e. driven by an insufficiency rather than a deficiency).
Some cereal based rations have very high Phosphorus levels but are low in Vit D and Calcium.
Epidemiology of kyphosis and rickets
Both forms affect rapidly growing young animals.
Clinical signs of rickets
Lameness, reluctance to move.
Epiphyseal regions of long bones are enlarged and there may be bending of the diaphysis.
Enlargement of the costo - chondral junctions may be seen or palpated (rickety rosary).
Tooth development is delayed or inhibited.
Clinical signs of kyphosis
Usually a sagittal plane deviation (hump back) involving thoracic or lumbar vertebrae; scoliosis (crooked back) sometimes seen.
Sometimes, may also see changes to costochondral junctions but rarely see changes in long bones.
Diagnosis of rickets and kyphosis
Low levels of Ca, P or Vit D in the diet and in analysis of bone.
Radiography shows very poor ossification of the bones.
Treatment of rickets
Correct diet and parenteral injections of Vitamin D.
Treatment of kyphosis
responds well with enhanced phosphate availability – balanced with Ca.
