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Ruminants > Liver disease > Flashcards

Liver disease Flashcards

1
Q

How much liver mass must be lost before clinical signs become apparent?

A

75%

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2
Q

What are clinical signs indicative of liver disease?

A

Weight loss, ascites and edema, diarrhea, hepatic encephalopathy, photosensitization, hemorrhage, abdominal pain

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3
Q

Is weight loss a common sign of chronic or acute liver disease?

A

Chronic

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4
Q

When might you see icterus in ruminants?

A

In cases with severe liver failure or complete bile duct obstruction (rare)

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5
Q

How does liver failure cause ascites and edema?

A

Severe cirrhosis can cause portal hypertension which causes ascites. Hypoalbuminemia secondary to liver failure causes edema.

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6
Q

How does liver disease cause diarrhea?

A

Hypoalbuminemia causes intestinal edema, portal hypertension and bile deficit cause malabsorption

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7
Q

What are clinical signs of hepatic encephalopathy?

A

Dullness/depression, tenesmus, head pressing, blindness, mania, ataxia, vocalization

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8
Q

How does liver disease cause photosensitization?

A

Phylloerythrin is unable to be removed by the liver so it accumulates and causes a reaction with sun in lightly pigmented skin which releases energy and causes dermatitis.

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9
Q

How does liver disease cause hemorrhage?

A

Terminal stage liver failure causes inadequate production of clotting factors

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10
Q

Why does liver disease cause abdominal pain?

A

Due to enlargement of liver and stretching of capsule or inflammation of capsule

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11
Q

What diagnostic results are consistent with liver disease?

A

Hypoglycemia, hypoalbuminemia, elevated SDH, elevated AST (less specific), elevated GGT, elevated OCT

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12
Q

What does an elevated SDH indicate?

A

Hepatocellular damage (current/ongoing)

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13
Q

What does elevated AST indicate?

A

Hepatocellular or muscle damage, could be current or previous

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14
Q

What does elevated GGT indicate?

A

Damaged to the biliary tract, could be current or previous

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15
Q

What is the most sensitive and specific indicator of hepatocellular damage in ruminants?

A

Ornithine carbamoyl transferase (OCT)

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16
Q

How is bilirubin usually affected in ruminants with liver disease?

A

Unconjugated bilirubin is usually elevated
Conjugated bilirubin may also be elevated if there is severe bile duct obstruction

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17
Q

Where can you visualize the liver of a ruminant on ultrasound?

A

On the right side between the 10th and 12th intercostal spaces

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18
Q

Describe liver biopsy in ruminants

A

Can be performed blindly or with ultrasound guidance on the midpoint of the 11th intercostal space on the right side. Can confirm or rule out diffuse disease such as hepatic lipidosis. Cannot rule out focal disease like abscesses or flukes. Should not be performed if an abscess is suspected. Can also be used to assess mineral status.

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19
Q

What predisposes cows to liver abscesses?

A

High grain diets, being dairy or feedlot cattle

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20
Q

What are the primary agents in liver abscesses?

A

Fusobacterium necrophorum, Arcanobacterium pyogenes, Streptococcus, Staphylococcus, Bacteroides

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21
Q

What are sources of bacteria that cause liver abscesses?

A

Grain overload, infection of the umbilical vein, septicemia, foreign body penetration from the reticulum

22
Q

Describe the pathophysiology of F. necrophorum in liver abscesses

A

F. necrophorum is a normal GI inhabitant. In cases of grain overload and rumen lactic acidosis, rumenitis can occur and F. necrophorum can invade damaged rumen wall and access the portal circulation. The organisms lodge in the liver and produce leukotoxin which forms abscesses. These abscesses are encapsulated by connective tissue but continue to grow and can cause obstruction or erosion into the caudal vena cava causing thrombus, portal hypertension, and ascites. The thrombus can shed emboli and cause metastatic pneumonia, aneurysms, hemorrhage, and death.

23
Q

What clinical signs are associated with liver abscesses?

A

Reduced rate of gain, feed efficiency, and milk production; livers condemned at slaughter, intermittent fever, cranial abdominal pain, and weight loss may be seen

24
Q

How is a liver abscess diagnosed?

A

CBC showing chronic inflammation, chemistry panel showing elevated globulins and normal to slightly elevated liver enzymes with normal liver function tests. Ultrasound can be used for diagnosis, but can miss the abscess.

25
Q

How are liver abscesses treated?

A

Not usually diagnosed antemortem unless sequela are present- if sequela present, prognosis is poor. Can manage with penicillin, oxytetracycline, or a macrolide. Surgical drainage can be performed in valuable cattle.

26
Q

How can liver abscesses be prevented?

A

Slowly increase grain content and do not exceed 55%, add buffers to food, add Tylosin to food, vaccines are available for F. necrophorum but are not as effective as antibiotics

27
Q

What is the most common cause of liver disease in ruminants?

A

Fasciola hepatica

28
Q

Where is Fasciola hepatica found?

A

In the Gulf states and pacific northwest

29
Q

What is the intermediate host of F. hepatica?

A

A snail

30
Q

Describe the pathophysiology of F. hepatica

A

Fluke eggs are passed in the feces of cattle, become miracidia in water, infect snails, develop into metacercaria, and migrate up to vegetation where cattle ingest them. In the small intestine, they migrate through the intestinal wall to the liver where they mature (6-8w) then enter the bile duct and are shed in the feces.

31
Q

What clinical signs are associated with F. hepatica?

A

Production losses, liver condemnation at slaughter. Can result in rough hair coat, weight loss, anemia, depression, hypoproteinemia with edema, and anorexia

32
Q

Which species are more likely to show clinical signs of F. hepatica infection?

A

Sheep and goats

33
Q

What is seen at necropsy of animals with F. hepatica?

A

Areas of liver necrosis with a thickened bile duct and dark bile

34
Q

How is F. hepatica diagnosed?

A

Fecal sedimentation (>5eggs/g), ELISA available but not frequently used, chemistry panel shows hypoproteinemia and elevated GGT

35
Q

How is F. hepatica treated?

A

Flukecidal treatment for 2-3 months after the end of transmission season. Cloruson is most commonly used.

36
Q

What species gets infectious necrotic hepatitis most commonly (black disease)?

A

Sheep

37
Q

What is the causative agent of infectious necrotic hepatitis (black disease)?

A

Clostridium novyi type B

38
Q

Describe the pathophysiology of infectious necrotic hepatitis (black disease)

A

C. novyi is ubiquitous and is ingested by cattle. Spores cross the intestinal barrier and spread throughout the body in macrophages, particularly to Kupffer cells in the liver. Anaerobic conditions lead to spore germination and proliferation. Necrotic/anaerobic areas of the liver (usually from fluke migration) become infected. Alpha and beta toxins are produced and cause systemic endothelial damage and further hepatic necrosis.

39
Q

What clinical signs are associated with infectious necrotic hepatitis (black disease)?

A

Mostly signs of fluke migration; once infected the disease is rapidly fatal so animals are usually found dead. If found before dying, they may be depressed, febrile, and tachypneic

40
Q

How is infectious necrotic hepatitis (black disease) diagnosed?

A

Necropsy with coagulative necrosis of the liver with gram + rods. Subcutaneous tissues may appear hemorrhage and black and putrefy quickly. C. novyi can be cultured and the toxin culture proves diagnosis.

41
Q

How is infectious necrotic hepatitis (black disease) treated?

A

Usually not treated as it is fatal. Can treat with penicillin IV.

42
Q

How is infectious necrotic hepatitis (black disease) prevented?

A

Control fluke population, vaccinate against clostridium (q6-12m, perform before onset of fluke season)

43
Q

What is the causative agent of bacillary hemoglobinuria (red water)?

A

Clostridium hemolyticum (C. novyi type D)

44
Q

Which species does bacillary hemoglobinuria (red water) occur in?

A

Cattle, rarely sheep

45
Q

Describe the pathophysiology of bacillary hemoglobinuria (red water)

A

Spores of C. hemolyticum lodge in Kupffer cells and germinate in anaerobic conditions (usually fluke migration). C. hemolyticum produces high concentrations of toxins which cause hepatic necrosis and intravascular hemolysis.

46
Q

What clinical signs are associated with bacillary hemoglobinuria (red water)?

A

Usually found dead- prior to death depressed, tachypneic, febrile, have dark colored urine and possibly bloody nasal discharge and diarrhea +/- icterus

47
Q

What are common necropsy findings in bacillary hemoglobinuria (red water)?

A

Subcutaneous petechia and ecchymoses, increased hemorrhagic pleural and peritoneal fluid, dark red urine, autolysis, necrotic zones of the liver with pale centers and zones of hyperemia between necrotic and normal tissue. Liver impression smears show gram positive rods.

48
Q

How is bacillary hemoglobinuria (red water) diagnosed?

A

Gram positive rods with C. hemolyticum and toxin culture, or fluorescent antibody test

49
Q

How is bacillary hemoglobinuria (red water) treated?

A

Rarely attempt to treat- treatment would be IV penicillin and whole blood transfusion

50
Q

How can bacillary hemoglobinuria be prevented?

A

Bury or burn affected animals. Control fluke population and vaccinate for clostridial species.

Ruminants (10 decks)

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