L4: Ruminant Liver Disease (Reuss) Flashcards
What lab values are measured for liver function?
GGT SDH ALP AST LDH Bilirubin (can indicate cholestasis vs. hepatocellular dz; >0.5 = cholestasis) Bile acids Ammonia
Where is liver located on ultrasound? What does it look like?
Right ICS 6-12, sharp borders
GB right ICS 9-11, thin walled, round, anechoic
Portal vein round, CVC triangular.
Parallel channel sign
Distended bile ducts parallel to portal veins
CS of liver dysfunction
-portal hypertension, lymphatic leakage, hypoalbuminemia –> ascites
- portal hypertension –> diarrhea
- release of septic emboli from liver abscesses –> caudal vena cava syndrome/massive pulmonary hemorrhage
- loss of factors 2,5,7,9,10 –> hemorrhage
- photosensitization
- hepatic encephalopathy
Hepatic encephalopathy
- char. By behavior change, ataxia, circling, stupor, tenesmus, bellowing
- can cause rectal prolapse
- pathophys: caused by increasing ammonia, glutamine, serum auromatic amino acids, GABA tone
Fasciola hepatica
- liver flukes from ingesting metacercariae on grass
- snails IH
- killed by drought, freeze, sustained heat
- SR most susceptible
- can be fatal/acute, subacute, or chronic depending on burden
Subclinical effects of Fasciola hepatica
- reduced gain/efficiency
- liver condemnation
- increased with periods of nutritional stress/nematode burdens
CS of fasciola hepatica
- weight loss, rough coat, ascites, edema, icterus
- hypoproteinemia
- biliary hyperplasia
- proline-depression anemia
Pathology of fasciola hepatica
-tunnels of coagulative necrosis
-fibrosis (esp. Ventral)
+/- bile duct changes (cholangiohepatitis, calcification of bile ducts, discolored bile) if it’s been 6-8 wks since ingestion
Dx of fasciola hepatica
- Fecal sedimentation (only detects eggs from adults)
- ELISA 2 wks post infection
- inc. GGT, eosinophilia, anemia, hypoalbuminemia
- U/S, cholecystocentesis (look for fluke eggs in the bile)
Fascioloides magna
-liver fluke found in great lakes, NW, gulf coast
-cattle = dead end hosts
-SR = aberrant hosts
-deer, elk = DH
-
Pathology of Fasciola magna in CATTLE
Encapsulate in liver –> closed cysts –> carcass condemnation
Path. Of Fascioloides magna in SR
Continual migration –> extensive tissue damage
Liver fluke tx
- Clorsulon for juveniles
- Albendazole for adults and F. Magna
- prevent snail infection by removing adults about 2 mos. after end of transmission season
Fat cow syndrome
Overconditioned periparturient dairy cows within 1-2 wks of calving at risk for hepatic lipidosis
Pathophys. Of hepatic lipidosis
1) Inc. FFA mobilization –> NEFAs
2) Liver extracts NEFAs and can only release once reesterified into triglycerides
3) TG production overwhelms ability to package into VLDLs, and TG is deposited in liver
4) insulin resistance perpetuates
Dx of hepatic lipidosis
- NEFAs >1000 for lactating, >350 for peripartum
- AST >100 (unreliable)
- ketonuria
- U/S
- Liver biopsy (floats?)
Tx of hepatic lipidosis
- positive energy balance
- IV dextrose, insulin
- propylene glycol
- force feeding, transfaunation
- steroids short-term
- Vit. E, selenium, glucagon
Pyrrolidizine alkaloid toxicity due to what plants?
Senecio
Crotalaria
Heliotropium
Cattle 30x more sensitive than SR
Pyrrolidizine alkaloid toxicity pathogenesis
Pyrroles (alkylating agents) –> cross link DNA, have anti-mitotic effect, megalocytes can’t divide, fibrosis, veno-occlusive disease, portal hypertension
-Chronic progressive intoxication
CS of PA toxicity
- d
- wt. loss
- tenesmus, rectal prolapse
- ascites
- photosensitization
- hepatic encephalopathy
Dx of PA toxicity
- increased GGT, ALP, bile acids
- liver biopsy (see fibrosis, bile duct proliferation, megalocytosis)
Tx of PA toxicity
- no cure
- low protein high energy diet
Aflatoxins
- produced by fungi
- inhibit protein synthesis
- cause dec. feed efficiency –> hepatic failure –> hemorrhage, death as dose increases
- carcinogenic to people
GGT comes from what tissues
Liver
Mammary tissue
Pancreas
Infectious Necrotic Hepatitis aka
“Black Disease”
- caused by Clostridium novyi type B
- ALPHA toxin
Pathophys of Infectious Necrotic Hepatitis/Black Disease
- requires pre-existing liver disease (ie. Liver flukes to create anaerobic env. For sporulation)
- causes rapid putrefaction, hemorrhage of SC blood vessels, serosanguinous effusion, coagulative necrosis in the liever
CS of Infectious Necrotic Hepatitis/Black Disease
-sudden death during fluke season
-fever, hypothermia, recumbency, death within hrs
(5-50% morbidity)
-affects well nourished adult sheep
Dx of Infectious Necrotic Hepatitis/Black Water
Gram stain
Culture
Fluorescent Ab
Toxin ID
Cause of Bacillary Hemoglobinuria/”Redwater”
Clostridium novyi type D
-BETA toxin
Pathophys of Redwater
- causes hepatic necrosis, hemolysis, hemorrhage, endothelial damage
- requires anaerobic liver damage
- can be carried in decomposing carcasses, carrier animals
- follows flooding
- affects well conditioned animals >1 yr in poorly drained pastures
- 95% mortality!
CS of Bacillary Hemoglobinuria/Redwater
- sudden death
- fever, arched back, separation from herd
- tachycardia/pnea, agalactia, constipation, diarrhea
- hemolysis –> icterus, hemoglobinuria
Dx/necropsy of Bacillary Hemoglobinuria/Redwater
- ischemic hepatic infarct
- rapid putrefaction
- SC and pulmonary edema
- petechia/ecchymosis
Dx: Gram stain, culture, fluorescent Ab, toxin ID
Tx/Prevention of Clostridium novyi
Tx rarely possible
- penicillin, tetracycline
- antitoxin
Prevent: multivalent vaccines, fluke control, remove carcasses
Incidence of hepatic abscesses on feedlots
1-95% (2ary to high grain diets)
Etiology of hepatic abscesses
- polymicrobial anaerobes
- Fusobacterium most common in cattle (normal in rumen)
- Arcanobacterium (normal in rumen wall)
- SR: Corynebacterium pseudotuberculosis most common
- leading cause of liver condemnation*
Pathophys of hepatic abscesses
1) Portal vein: Rumenitis-liver abscess complex:
- high grain diet –> rumenitis –> colonization of rumen wall –> portal circulation
2) Umbilical vein
3) hepatic a. (Requires primary source of bacteremia)
4) bile duct
5) direct extension (ie. Trauma to wall of liver)
CS of hepatic abscesses
- none, or wt. loss/poor production
- CVC thrombosis syndrome: extension of abscess to CVC –> thrombus, septic emboli –> pulmonary embolus, pneumonia, endocarditis, hemoptysis, epistaxis
Dx/Tx of hepatic abscesses
- U/S
- Necropsy
Tx: penicillin, macrolides; full recovery unlikely
Prevention of hepatic abscesses
- prophylactic abx (ie. Tylosin*)
- vaccine
- prevent ruminal acidosis
Which ruminants most prone to Cu toxicosis?
Sheep»_space; goats > cattle
Etiology of Cu Toxicosis
- eating horse/cattle feeds
- drinking foot baths
- fluke damage, PA toxicity predisposes
CS of Cu Toxicosis
- none in accumulation stage
- stress –> large release –> hemolytic crisis
- weakness, d, coli
Dx of Cu Toxicosis
- anemia, hyperbilirubinemia, azotemia
- hemoglobinuria w/ isosthenuria
- Inc. Cu lvls in serum, liver, kidneys
- “Gunmetal kidney” on necropsy w/ centrilobular necrosis, fibrosis, bile duct hyperplasia
Tx of Cu Toxicosis
- fluids
- blood transfusion
- increase urinary Cu excretion with D-penicillamine or ammonium tetrathiomolybdate
- tx flock with ammonium molybdate, Na thiosulfate
- minimize stress
