Small Ruminant - Haemolymphatic Dz Flashcards
In what breed of sheep is combined vitamin-K dependent factor (II, VII, IX, X) deficiency reported? What is the mode of inheritance of this disease?
- Rambouillet sheep.
- Autosomal recessive.
What is the clinical manifestation of combined vitamin-K dependant clotting factor deficiency in sheep?
- Excessive s/c haemorrhage and umbilical bleeding in lambs.
- Prolonged APTT and PT (intrinsic and extrinsic pathway involved).
What aetiologic agent is responsible for Anaplasmosis in sheep and goats?
- Anaplasma ovis.
- Gram negative rickettsial bacteria.
- Rarely causes clinical dz, but if it does CSx similar to Bovine Anaplasmosis.
List a cause of Heinz body anaemia in sheep that is unique to the causes reported in horses.
Low molybdenum formulate diet –> chronic Cu toxicity.
Copper is an essential trace mineral for ruminants, however it has a narrow therapeutic window. List ruminants in order from most to least susceptibility to copper toxicity.
- Lambs > adult sheep and goats > cattle > horses.
- Dietary requirements for growing sheep: 4-6 ppm.
- Toxicity occurs at 10-20 ppm.
Describe normal copper metabolism in ruminants.
- Ingested Cu is absorbed through enterocytes by carrier proteins and transported to blood bound to Alb and AAs.
- 20% of total plasma copper is ionised copper; 70-90% of this is internalised by hepatocytes –> bile –> packaged in lysosomes in protein complexes or used for formation of ceruloplasmin.
- Hepatic storage buffers Cu intake initially but eventually become saturated.
Describe the pathophysiology of copper toxicity in ruminants.
- Hepatocytes saturated w copper die spontaneously or in response to envrio stress/diet change –> release large amount of Cu into circulation.
- Cu is an oxidant –>
- Lipid peroxidation and oxidative denaturation of proteins within RBCs –> Heinz body formation and methaemaglobinaemia –> intra-/extra-vascular haemolysis.
- Vitamin E is denatured –> enhances cellular susceptibility to further oxidants.
- Sources of excess copper: minerals designed for other species (e.g. cattle mineral given to sheep), inapprop form grain mixtures, chicken litter, Cu-containing fungacides, palm kernel oil, Cu pipes, overdose of C salts.
- Low Mb (soil high in sulfates, Cu:Mb > 6:1) –> Cu tox as Mb binds Cu in rumen making it insoluble and non-absorbable.
List clinical signs of copper toxicity in ruminants.
- Asymptomatic for weeks until onset of hepatic necrosis.
- CSx are of co-existing anaemia, myopathy, neuro, hepatic and renal dz.
- Inappetence, lethargy, weakness, recumbency, pallor, cool extremities, grey MMs.
- Marked tachycardia, low BP, tachypnoea, hypothermia.
- Dark red urine; dark or yellowish faeces.
- +/- petechiation of conjunctival mucosa.
- +/- abortion; ewes tend to have dystocia if survive.
- Death.
Describe findings on necropsy of animals that have died from copper toxicity.
- Tissues are pale and icteric w petechial and ecchymotic haemorrhages on serosal surfaces.
- Liver often pale and yellow.
- Kidneys black w metallic sheen due to Hg.
- Urinary bladder filled w serosanguinous urine.
- Histo: tubular nephrosis, necrosis of splenic follicles and hepaticytes; biliary duct proliferation and cholangitis; spongy degeneration of pons and brainstem.
List diagnostic test findings in ruminants with copper toxicity.
- Plasma copper conc 2.4-20ug/mL diagnostic.
- Normal plasma conc may occur with toxic liver levels.
- Hepatic Cu conc 16mmol/kg DM are threshold for haemolytic crisis; renal conc 15 ppm dry weight.
- Changes occur 24h prior to haemolytic crisis –> inc cytosolic hepatic enzymes and sharp rise plasma Cu.
- Acute crisis: haemoglobinaemia, Heinz body formation, methaemoglobinaemia, anaemia, inc bilirubin, AST, GGT, ALP, CK, creatinine, BUN, plasma ceruloplasmin; urine dark brown to black w protein, blood, Hg casts.
Outline treatment of copper toxicity in ruminants.
- Acute haemolytic crisis: InO2, Vit E, packed RBCs, D-penicillamine (inc urinary Cu excretion), anhydrous sodium sulphate (bind rumen C) and ammonium molybdate (binds rumen Cu, enhances biliary excretion of Cu).
- IV ammonium tetrathiomolybdate + xylazine –> reduced cytosolic and lysosomal hepatic Cu, inc Cu excretion in bile, transient inc blood Cu.
Describe the aetiology and clinical signs of copper deficiency in ruminants.
- Copper deficiency due to inadequate copper in soil or milk, excess molybdenum or dietary zinc/sulphur imbalances.
- Cu is co-factor in wide variety of enzymatic reactions, therefore –> mulitple CSx in young, growing animals incl red growth rate, rough and depigmented hair, diarrhoea, osteoporosis w spontaenous fractures and anaemia.
- Enzootic ataxia/swayback in lambs: demyelinating dz assoc w Cu deficiency.
Describe the pathophysiology of copper deficiency-associated anaemia in ruminants.
- Cu plays an important role in transport of iron from the GIT to the BM and incorp of Fe into heme molecule.
- Anaemia is moderate, slowly progressive, microcytic, hypochromic.
- BM aspirate differentiates from true iron deficiency as revealed sideroblasts (intracellular iron acumm).
- Dx by measuring serum Cu as ceruloplasmin, erythrocyte superoxide, dismutase or Cu content of hair, liver or kidney.
Describe Corynebacterium pseudotuberculosis.
- Gram positive, intracellular, non-motile, pleomorphic, rod-shaped, facultative anaerobic bacteria.
- Two biotypes: small ruminant strains are nitrate negative, strains from horses are nitrate positive, strains from cattle are both.
Describe epidemiology of Corynebacterium pseudotuberculosis infection in large animals.
- Infection occurs worldwide.
- Natural cross-species trans doesn’t appear to occur.
- Different genotypes cause infection in diff US states.
- Soil-bourne org, survives months to years.
- Year-round infection in small ruminants; spread via infected exudates (wounds), long incubation.
- Horses: spread by flies, vectors, contam-soil; highest incidence ext abscess Autumn, internal Winterl incubation period 3-4 weeks.
- Cattle: spread by flied or fomites; spring and summer.
- Bacteria enters via wounds/abrasions –> s/c of submucosal lymphatics –> phagocytosed by macro –> survive intracellulary and can survive lymphatic necrosis and thrombosis.
