Clostridial Disease in Lambs (Sudden Death) Flashcards
Name the clostridial diseases which casue sudden death in lambs (5)
Pulpy kidney - Cl. perfringens type D Blackleg - Cl. chauvyoei Black disease - Cl. novyi Braxy - Cl. septicum Cl. sordelli
Describe the pathogenesis of pulpy kidney
High amounts of undigested CHO permits multiplication. Trypsin causes cleavage of protoxin to E toxin. This toxin increases in the brain and casuse tight cell junctions to deteriorate, lose capillary integrity and increase ICP which casues liquefactive necrosis of brain, perivascular oedema and haemorrahge.
Systemic absorption of toxin causes increased intestinal permeability, liver and kidney damage
Death in 12-24hrs
When is pulpy kidney generally seen?
Non-immune lambs 4wks - 8 months old
Often big, strong singles
Losses occur in weaned lambs following dietary improvement e.g. concentrate introduction, move to lush pasture
What are the clinical signs of pulpy kidney?
Sudden death
If alive - severe depression, abdominal pain, bruxism, neurological signs (opisthotonus, seizures)
How is pulpy kidney diagnosed?
Hx of recent move to rich feeding
PCR, ELISA - toxin detection
Gram stain and culture
PM - 10-20ml clear fluid in body cavities, petechial haemorrhage on lungs and epicardium, pulpy kidneys, glycosuria, fluid SI content, focal symmetrical haemorrhage in basal ganglia of brain, focal symmetrical encepholomalacia
Describe the pathogenesis of blackleg
Associated with skin wounds e.g shearing, castrating
Affects skeletal and cardiac muscle
Spores ubiquitous in soil, produce a potent neurotoxin (tetanospasmin) in anaerobic conditions
What are the clinical signs of blackleg?
Sudden death 2-3d Dullness Pyrexia >41 degrees Toxic mm Severe lameness Progressive stiffness and limb rigidity Progress to convulsions Oedema Emphysema
Describe the pathology of black disease
Unique to sheep and affects all ages
Late autumn/winter, peaks Sep - Nov
Associated with liver fluke
Migration of larvae creates an area of hypoxia in which clostridia grow and produce toxin which is absorbed systemically
What are the clinical signs of black disease?
Sudden death Severe depression Anorexia Pyrexia/hypothermia Respiratory distress Muffled heart sounds
Describe the pathogenesis of braxy
Associated with frosted forage (damages abomasal wall?)
Young, non-immune sheep (hogs, store lambs)
Cl. specticum infects abomasla wall and produces alpha toxin which causes local and systemic effects - abomasitis, abomasla and duodenal wall thickening, oedema, haemorrhage, necrosis, excess turbid peritonel fluid, epicardial petechiae
Cell lysis and release of K and haemoglobin
What are the clinical signs of braxy?
Sudden death Sudden onset of illness with weakness Anorexia Inability to keep up with group \+/- pyrexia
How is braxy diagnosed?
Hx of frost
Absence of vaccination
PM - gram stain of mucosal lesions and heart, immunohistochemistry, toxin in tissue or body cavity fluid
Ddx - CCN, ruminal acidosis (but won’t see intestinal necrosis)
Describe the pathogenesis of Cl. sordelli
Primary pathogen of sheep intestine
Abortion and subsequent death in ewes
Invades abomasal mucoas and produces 2 toxins (haemolysin and lethal toxin) which cause abomasal ulcers which rupture and cause enteritis
Vaginal prolapse - compromised cervix allows entry of Cl to uterus = abortion and death
What are the clinical signs of Cl. sordelli?
Sudden death
Lambs 3-10wks old - acute abomasitis
Abomasitis in lambs 6-12 months old (finishing)
How are clostridial diseases treated?
Penicillin @ 2-3x dose and 2x frequency
Tx will kill bacteria but won’t stop toxin circulation, delay between tx and toxin excretion.
