Internal diseases of swine I Flashcards
Explain congenital muscle tremor and types.
Cases of newborn “shaking piglets” have been reported since the 1920s both in Europe and abroad.
They are unable to properly suckle milk.
- Type A causes microscopic changes in the brain and spinal chord.
- Type B causes no visible changes.
Old theory about congenital muscle tremor in piglets.
A1 type:
A1: Classical swine fever (CSF) infection of sow during 10-50 days of gestation.
Morbidity 40%, high mortality.
Both sexes and all breeds affected.
Non-recurrent in next litters of the same parent pigs.
- Piglets with muscular tremor, ataxia
- Unable to stand, suck
- Does not disappear in piglets of 1 month of age.
Old theory about congenital muscle tremor in piglets.
A2 type:
A2 type believed to be caused by viruses like PCV2, Aujeszky’sdisease, Japanese encephalomyelitis infection of sow at 10-50 days of gestation.
Most litters affected simultaneously.
Morbidity up to 80%, low mortality.
Both genders and all breeds affected.
Non-recurrent in next litters of the same parent pigs.
Symptoms may disappear at 8 weeks old.
Old theory about congenital muscle tremor in piglets.
A3 type:
A3 type: genetic problem, not associated with infections. Mostly affects Male Landrace piglets (carried by sows so X-chromosome related).
Tremor of the head and the anterior part of the body.
Slight tremor of the head and shoulders can occur with adult boars too.
Possibly recurrent in next litters of the same parent pigs!
Low mortality
Old theory about congenital muscle tremor in piglets.
A4 type:
A4 type also genetic, not infection related.
Associated with breed British Saddlebacks
High mortality (up to 25%)
Recurrent in next litters of the same parent pigs because genetic.
Old theory about congenital muscle tremor in piglets.
A5 type:
A5 type associated with Trichlofon or Neguvon (organophosphate insecticide), during days 45 and 79 of gestation. Non-dependent on gender, breed.
Most animals will be affected within a month.
- Rhythmic tremor
- Stumbling
- Difficulty in sucking
Old theory about congenital muscle tremor in piglets.
Type B:
Type B etiology still unknown.
High tactile and nervous sensitivity.
Symptoms may occur with piglets of 3 days of age.
Symptoms may disappear.
Maybe related:
* Inbreeding
* Toxins
* Feeding
But its not for sure.
New theory about congenital muscle tremor in piglets.
Novel atypical porcine pestivirus (APPV) potentially behind A2-type.
Stillbirth and sudden death of young piglets (Bungowannah virus, Australia).
Present in the semen and saliva. Carriers.
Transmission to the piglet at a stage of gestation.
Mobidity up to 80%
Mortality up to 30%
- Splay legs
- Changes in nerve fibres on histology.
- Identification of virus for diagnosis.
New theory about congenital muscle tremor in piglets.
Post mortem lesions: (5)
Excoriations of the legs
Alveolar lung edema
Alveolar lung emphysema
Scattered petechiae in the renal cortex
Characteristic hypomyelination in the CNS
What is rickets and what is its etiology.
Is a piglet disease that interferes with cartilage ossification causing bowed legs.
Deficiency of vitamin D and Ca in feed.
Wrong Ca:P ratio in feed (1.6 : 1 – 1.2 : 1).
Diseases of the digestive system can predispose (gastritis, entheritis, parasitosis etc.).
Why is vitamin D important? (5)
Increases the transport of Ca and phosphates in the intestinal epithelium.
Participates in the formation of bone matrix and mineralization of bone growth zones.
Participates in release of Ca and P from bones (with parathyroid hormone).
Contributes to Ca2+ re-absorption in the kidneys.
Keeps Ca2+ and Phosphorus balance in blood serum.
Clinical signs of rickets in pigs. (8)
Anorexia, eating disorder
Difficulties with getting up and moving around.
Cannibalism
Squealing when standing up
Growth reduction
Callosities (enlargement) at the ends of long bones and ribs (pictured).
Bone deformation
Cramps as in tremors.
How do you diagnose rickets in pigs?
How do you tx it?
Based on clinical signs and feed analysis.
Tx is more prevention by adjusting mangement and feeding a more balanced feed.
Etiology of osteomalacia.
Aggravated decalcification of bones due to Ca, P or vit. D deficiency in fodder. Unfavorable feeding and management.
Affects adult pigs whereas rickets affects piglets. More frequently seen in pregnant and nursing pigs.
Sometimes associated with diseases of endocrine glands.
Clinical signs of osteomalacia. (8)
Eating disorder
Frequent bone fractures
Joint sprains
Abnormal bending of bones
Standing up with curved spine
Arthritis
Cramps/muscle tremors
Abortions
What does diagnosis of osteomalacia involve? (4)
Clinical signs
Feed analysis
Radiography
Pathological finding
Tx of osteomalacia. (3)
Fix feeding and management.
Supplement calcium chloride, phosphates.
Deformed bones will not return to normal.
Severe cases should be euthanized.
Etiology of osteochondrosis (leg weakness, OCD).
A developmental bone disorder causing cartilage defects at articular surfaces (epiphysis).
- Rapid growth contributes.
- Large muscle mass contributes.
- High stocking densities increase the incidence.
- High levels of vitamin A (in excess of 20,000 iu/kg) particularly in the younger growing pigs.
Severity depends largely on the environment. Such as slippery floors because trauma contributes to damage.
Full confinement of pregnant gilts when they are still growing can be a major contributing factor.
The modern hybrid gilt often produces large litters and large amounts of milk which depletes her body calcium and phosphorous.
Pathophysiology of osteochondrosis in pigs.
Standing pressure, growth stresses, lack of adequate movement (when crated) and poor conformation reduce the oxygen supply in the epiphyses and articular cartilages resulting in abnormal growth and consistency of the cartilage.
Damage to the cartilage tends to be progressive and irreversible, the damaged cartilage is replaced by fibrous tissue.
Cartilage damage produces shortening and bending of the bones near the joints and at the extremities of the long bones.
Weak epiphyseal plates then fracture and cartilage covering the joint surfaces splits and forms fissures.
Sows that are susceptible to leg weakness are straight legged with little angulation of the bones between the joints and the back tends to be arched. This alignment increases stress on the growth plates.
Clinical signs of acute osteochondrosis. (4)
- Separation or fracture of the bones at the epiphyseal plate (epiphyseolysis) associated with sudden movement.
- Sudden fractures in the knee and elbow joints.
- Crepitus or rubbing of the broken bones together.
- Fractures of the vertebrae in the spine during lactation and immediately post weaning.
Clinical signs of chronic osteochondrosis. (4+front+hind)
The onset is gradual.
- Abnormal leg conformation (can be a cause and a sign of).
- Gait with or without stiffness and pain.
- Joints will not be swollen unless there are fractures.
Front legs:
* Legs are straight and pig walking with a long step on its toes.
* The knees may be bent inwards or flexed which causes the pig to walk with short steps.
* The pasterns may be dropped. This is common in old sows due to shortened bones and slack tendons.
* The feet may be rotated or twisted.
Hind legs:
* These are straight with a swinging action from the hips as the pig moves. Bit of a waddle.
* The legs are tucked beneath the body.
* The hocks turn inwards and are close together.
* Likewise in old sows, the pasterns may be dropped.
Abnormal gaits arise from pain.
Osteochondrosis lesions.
NB Severe clinical signs can be with joints appear normal and vice versa.
Otherwise, cartilage damage and arthritis, particularly in the hip, knee and elbows.
How is osteochondrosis diagnosed? (2)
Clinical signs
Post-mortem examinations may be misleading.
Ddx:
Mycoplasma hyosynoviae
Erysipelas
No specific treatment.
Etiology of Porcine Stress Syndrome. (4)
- Congenital
- Autosomal recessive gene
- Muscle problems (increased sensitivity)
- Stress triggers anaerobic glycolysis, loss of muscle metabolism control.
