LA Hepatobiliary Disease- Differential Diagnoses

Question 1

list common causes of hepatobiliary disease in horses

Answer 1

acute:
1. theiler’s disease/equien parvovirus or hepacivirus
2. hepatic lipidosis
3. toxic hepatopathy

chronic:
1. chloelithiasis/cholengiohepatitis
2. pyrrolizidine alkaloid toxicity (crotolaria)

both: secondary hepatic injury and/or cholestasis

Question 2

describe Theiler’s disease

Answer 2

1. also called acute hepatic necrosis or serum-associated hepatitis
2. due to equine parvovirus (EqPV-H) and equine hepacivirus (EqHV)
3. transmission:
   -equine biologic products: tetanus antitoxin most common offender!

-blood transfer or blood vector transmission?

-direct transmission

4. pathologic effects are limited to the liver
   -centrilobular hepatocellular necrosis

Question 3

describe clinical findings, diagnosis, and prognosis of theiler’s disease

Answer 3

clinical findings:
1. acute to subacute, rapidly progressive
-hepatic encephalopathy common
2. few may recover but become chronic carriers and/or develop chronic liver disease

diagnosis:
-viral PCR on blood (preferred)
-liver tissue sample

prognosis:
-poor to grace with severe encephalopathy, hemorrhage, or hemolysis; good to guarded if survive >1 week

-no preventative: judicious use of equine biologics, test blood donors

Question 4

describe hepatic lipidosis pathogenesis

Answer 4

1. obese animals:
   -metabolic horses, ponies, minis, donkeys
2. increased metabolic demand:
   -pregnancy, lactation, concurrent illness
3. fat is mobilized for energy

Question 5

describe clinical findings, diagnosis, and prognosis of hepatic lipidosis

Answer 5

clinical findings
1. mentation changes, ataxia
2. mild colic, diarrhea
3. fever
4. sudden death can occur with hepatic rupture
5. other signs of primary disease

diagnosis:
1. hyperlipidemia: triglycerides >500mg/dL
2. concurrent lab evidence of liver disease
3. fat ID on US (suspect) or liver biopsy (definitive)

prognosis:
1. guarded even with treatment
2. prevent obesity!

Question 6

describe acute toxic hepatopathy

Answer 6

1. relatively uncommon in horses
2. due to chemicals, drugs, mycotoxins, and plants
3. centrilobular hepatic necrosis
   -rule out theiler’s
4. acute onset, possible more than one animal affected
5. dx by exposure and rule out

Question 7

describe secondary liver disease

Answer 7

1. fairly common
2. due to:
   -hypoxia: heart failure, anemia

-inflammation: enteritis, colitis, peritonitis

-occlusion: right dorsal displacement

3. liver is not the primary problem, but
   -SDH and GGT may temporarily increase (rarely bile acids), then resolve when primary disease resolves

Question 8

describe bacterial hepatitis

Answer 8

1. primary bacterial cholangiohepatitis rare in adults
2. secondary bacterial cholangioheptatitis is possible
3. bacterial septicemia may lead to hematogenous, multifocal hepatitis in neonates

Question 9

describe Tyzzer’s disease

Answer 9

1. rare, acute bacterial hepatitis due to clostridium piliformis that causes microabscesses in the liver
2. transmission: oral ingestion

clinical findings:
1. only reported in foals (tYzzers for Young animals)
2. non-specific signs
3. frequently causes sudden death

diagnosis:
1. confounded by peracute onset and sudden death
2. silver stain or PCR post mortem usually

prognosis: guarded to grave

Question 10

describe cholelithiasis

Answer 10

1. calculi in biliary tree
   -common overall
   -occasionally results in disease and/or insufficiency
   -common to have concurrent ascending bacterial hepatitis
2. clinical findings:
   -usually in horses >3 years old
   -colic, fever, icterus
   -intermittent and recurrent
3. diagnosis:
   -clinical signs
   -increased GGT and bile acids
   -US: dilate bile ducts, shadowing choleliths
   -endoscopy
   -exploratory
   -liver biopsy: concentric fibrosis around bile ducts
   -culture
4. prognosis: variable based on number and location of choleliths, severity of signs, extent of fibrosis

Question 11

describe pyrrolizidine alkaloid toxicity

Answer 11

1. sometimes called chronic megalocytic hepatopathy
2. caused by ingestion of PA containing plants (can be growing on land where you are growing hay and get incorporated into bales!!)
   -PAs are metabolized to toxic pyrrole derivatives which inhibit hepatocyte division
3. results in big hepatocytes (megalocytes)
4. fibrosis replaces dead cells that cannot be replaced
5. requires chronic exposure (1-4 months)

Question 12

describe clinical findings, diagnosis, and prognosis of pyrrolizidine alkaloid toxicity

Answer 12

clinical findings:
1. pathophys is chronic but onset of signs of liver failure are often acute
2. weight loss might appear earlier

diagnosis:
1. liver histopath is classic: megalocytes, fibrosis, biliary hyperplasia

prognosis: variable

Question 13

list common causes of hepatic disease in ruminants and camelids

Answer 13

acute:
1. hepatic lipidosis: bovine, camelids
2. pregnancy toxemia: caprine, ovine
3. toxic hepatopathy: bovine primarily but also the others

chronic:
1. hepatic abscesses: bovine primarily
2. flukes: all, but less common in camelids
3. copper toxicity: most commonly ovine

both: secondary hepatic injury and/or cholestasis

Question 14

describe hepatic lipidosis/pregnancy toxemia

Answer 14

1. hep lip in cattle or camelids, preg tox in small ruminants
   -similar pathophys to horses
2. cattle: typically affects high producing dairy cows during early lactation (occasionally near the end of pregnancy)
3. small ruminants: typically affects does/ewes near the end of gestation, esp damns with twins or triplets
4. ruminants more likely to make ketones

Question 15

describe clinical findings, diagnosis, and prognosis of hepatic lipidosis/pregnancy toxemia

Answer 15

clinical findings:
1. often extreme anorexia
2. signs of liver insufficiency
3. signs of ketosis
4. possible neuro signs: small ruminants seem more predisposed

diagnosis:
1. ketosis: urine or blood sample
2. increase NEFA or TG: blood sample
3. liver enzymes and bile acids variable
4. fat ID on liver ultrasound (suspect) or biopsy (definitive)

prognosis:
1. variable; cattle better than small ruminants
2. in small ruminants, if saving the dam is the priority, recommend induction or c section
3. prevent obesity

Question 16

describe acute toxic hepatopathy in ruminants/camelids

Answer 16

1. similar to horses
2. mycotoxins more likely to affect ruminants
   -aflatoxin produced by aspergillus

Question 17

describe black disease in ruminants/camelids

Answer 17

1. also called infectious necrotic hepatitis
2. clostridium novyi type B
   -spore present in liver
   -anoxic insult occurs (fluke migration)
   -proliferation and toxin production
3. clinical findings:
   -sudden death
4. diagnosis:
   -post-mortem reveals hemorrhagic black tissue and rapid autolysis
   -histopath and fluorescent antibody test or PCR
5. prognosis: grave
   -vaccine available, reduces losses by 50%
   -fluke control

Question 18

describe bacillary hemoglobinuria in ruminants/camelids

Answer 18

1. also called redwater
2. clostridium novyi type D
   -almost identical to black disease
   -BUT also produces hemolytic toxins
3. so will see signs of hemolysis:
   -anemia
   -icterus
   -hyperbilirubinemia
   -bilirubinuria

Question 19

describe hepatic abscessation in ruminants and camelids

Answer 19

1. multifactorial pathophys:
   -excessive grain ingestion
   -rumenitis
   -bacterial translocation into portal blood flow
   -hematogenous seeding of the liver: occasionally emboli to vena cava or lungs too
   -most commonly fusobacterium necrophorum, trueperella, salmonella
2. most common in feedlot cattle

Question 20

describe clinical signs, diagnosis and prognosis of hepatic abscessation in ruminants and camelids

Answer 20

several syndromes:
1. subclinical most common

2. clinical disease often presents with chronic wasting and poor doers
3. uncommon but potential clinical disease presents with pulmonary hemorrhage or epistaxis
   -when septic emboli settle and form abscesses that rupture in the lungs

diagnosis: difficult
1. unspecific inflammation, variable liber enzymes on bloodwork
2. US hit or miss

prognosis:
1. poor and treatment expensive
2. include enough forage and avoid rapid intro of concentrates
3. bacterins available to F. necrophorum have variable efficacy
4. feed additives like tylosin as preventatives

Question 21

describe liver flukes in ruminants and camelids

Answer 21

1. 3 species:
   -fasciola hepatica
   -fascioloides magna
   -dicrocoelium dendriticum
2. occur in both cattle and small ruminants, less common in camelids
3. snails = intermediate host
4. flukes physically invade the liver and cause ischemic necrosis

Question 22

describe clinical findings of liver flukes in ruminants and camelids

Answer 22

clinical findings:
1. most often subclinical in cattle, more often clinical in sheep

2. acute disease due to massive migration
   -hemorrhage
   -acute liver failure
3. chronic disease more common:
   -weight loss
   -hepatic fibrosis

diagnosis:
1. positive fecal sediment exam
2, post mortem
3. clinical response to flukicides

prognosis:
1. variable
2. typically treat in the late summer/early fall in the south

Question 23

describe copper toxicity

Answer 23

1. most common in sheep
2. chronic ingestion leads to storage in liver followed by stress induced or spontaneous release which causes oxidative damage, heinz body formation, and intravascular hemolysis
3. clinical findings: signs of intravascular hemolysis
   -icterus and hyperbilirubinemia
   -pale MM, anemia with heinz bodies
   -pigmenturia
4. diagnosis:
   -increased blood or liver copper levels during hemolytic crisis
5. prognosis:
   -guarded to poor
   -only feed sheep-specific concentrates or supplements to sheep!!