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Large Animal Medicine > Midterm 2 > Flashcards

Midterm 2 Flashcards

1
Q

If an animal has a high relative erythrocytosis, what may be occurring?

A
  1. Hemoconcentration

2. Splenic contraction in horses

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2
Q

If an animal has a high absolute erythroctysosis, what may be occurring?

A
  1. Physiological response to chronic hypoxia

2. Neoplastic production

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3
Q

What are the clinical sign of anemia?

A
  1. Pale mucous membranes
  2. Lethargy/obtunded
  3. Anorexia
  4. Exercise intolerance
  5. Tachycardia
  6. Tachypnea
  7. Systolic murmur
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4
Q

What are the necropsy findings of an anemic large animal?

A
  1. Pale tissues
  2. Thin blood
  3. Scenic contraction/splenomegaly
  4. Centrilobular hepatic necrosis
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5
Q

What are the causes of anemia?

A
  1. Loss of RBCs from hemorrhage
  2. Destruction of RBCs due to intra or extravascular hemolysis
  3. Decreased production of RBC’s
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6
Q

What will you see with RBC morphology when looking at regenerative anemia in ruminants?

A
  1. Anisocytosis
  2. Polychromasia
  3. Macrocytosis
  4. Basophilic stippling
  5. Reticulocytes
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7
Q

What would auto-agglutination suggested on RBC morphology?

A

Immune Mediated Anemia

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8
Q

What do Howell-jolly bodies on a blood smear suggest?

A

RBC regeneration except in a horse

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9
Q

What do Heinz bodies suggest on a RBC smear?

A

Oxidative damage (red maple or onion ingestion )

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10
Q

What common hemoparasites can be evident on a blood smear in large animals?

A
  1. Babesia bovis
  2. Babesia caballi (Equine)
  3. Anaplasma marginale
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11
Q

What are some unique features of the equine erythron (RBC)?

A
  1. Unstable PCV due to scenic contraction
  2. No peripheral signs of regeneration aka no macrocytosis, polychormasia, or reticulocytes
  3. Rouleaux formation
  4. Icteric plasma
  5. Howell-holy bodies as a normal morphological characteristic
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12
Q

How can non-regenerative anemia be characterized?

A

Evaluation of the iron status through:

  1. Serum iron concentration
  2. Serum ferritin
  3. Total iron binding capacity (TIBC)
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13
Q

What would a normal ferritin level in a horse suggest?

A

Bone marrow dysfunction

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14
Q

A horse has a low total iron binding capacity (TIBC) level with a low serum iron concentration..what does this suggest?

A

Anemia of chronic disease

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15
Q

What would iron deficiency anemia looks like on a iron panel?

A

Low serum iron concentration and high total iron binding capacity (TIBC) OR
A low serum iron concentration, normal TIBC, and low ferritin levels

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16
Q

If a horse presents with a normal TIBC, a low FE, and a low ferritin level, what does this suggest?

A

Iron deficiency

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17
Q

A horse presents with low Fe values, normal ferritin, and normal TIBC, what does this suggest?

A

Anemia of chronic disease

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18
Q

A ruminant presents with anemia, there are immature RBC’s present and the TP is low…what does this suggest?

A

Acute blood loss anemia

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19
Q

What parameters would be abnormal in a ruminant with hemolytic anemia?

A

There would be immature red blood cells present indicating regeneration and the TP levels would be normal.

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20
Q

What type of anemia will a ruminant likely have if there are no immature red blood cells present and the TP is low?

A

Acute blood loss anemia that needs to be reevaluated in 72 hours.

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21
Q

A cow presents with anemia. There are no immature RBC’s present,the TP is normal, and there is no evidence of hemolysis ..what is going on?

A

A non-regenerative anemia

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22
Q

What are the steps in the diagnosis when an animal is anemic?

A
  1. CBC
  2. Urinalysis
  3. Feces for occult blood
  4. U/S or PE of body cavities
  5. Coomb/s test/flow cytometry
  6. Coggin’s test if a horse
  7. Bone marrow aspirate or biopsy
  8. Coagulation assays
  9. Evaluation of bleeding time
  10. AT-III levels
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23
Q

If a large animal has non-regenerative anemia of chronic disease, what will be on the CBC?

A

Neutrophilic leukocytosis due to stress or inflammation

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24
Q

What tests can be used to evaluate hemorrhage in an animal with anemia?

A
  1. Urinalysis with a dipstick, microscope to look for RBCs and to distinguish between hemoglobin and myoglobin
  2. Feces for occult blood
  3. Body cavities with U/S
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25
Q

What tests can be used to evaluate hemolysis in a large animal with anemia?

A
  1. Coombs test with flow cytometry

2. Coggins test (horse)

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26
Q

If a horse has a positive coggins test, what does this mean?

A

Equine Infectious Anemia

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27
Q

If a large animal has a positive coomb’s test, what does this mean?

A

Immune mediated anemia

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28
Q

What is needed to demonstrate a regenerative anemia response when the M:E ratio is normal (1:1 to 2:1)?

A

Bone marrow aspirate or biopsy

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29
Q

What is the M:E ratio when a large animal has a regenerative anemia?

A

< 0.5:1

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30
Q

What tests are part of a coagulation assay in large animals?

A
  1. PT
  2. APTT
  3. ACT
  4. Fibrin/fibrinogen degradation products
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31
Q

What are the steps in treating anemia?

A
  1. Control hemorrhage
  2. Treat underlying cause
  3. Support tissue oxygen volume with IV fluid therapy
  4. Reasses and determine is blood transfusion needed
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32
Q

What is the main indication in an anemic large animal for a blood transfusion?

A
  1. 10 L blood lost ( more than 25%)

2. PCV < 15% and Lactate > 4mmol/L

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33
Q

What is the universal blood donor for horses?

A

Aa & Qa negative

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34
Q

Which diseases should a donor horse/ruminants blood be free of?

A
  1. EIA
  2. EVA
  3. BLV
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35
Q

How long will transfused RBC’s stay in a recipient for?

A

2-4 days

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36
Q

You need to do a blood transfusion in a horse, but there is no universal donor and the patient has received a previous transfusion..what do you do?

A

Do a major and a minor cross match

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37
Q

What is the difference between a major and minor blood cross match?

A

Major: Donor’s RBC’s with recipients serum

Minor: Recipients RBC’s with donor serum

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38
Q

What is the safe blood donor volume from an adult large animals?

A

1.6% donor BW

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39
Q

How do you determine the blood volume needed in a patient?

A

Patient BW x 0.08 x (desired PCV-receipent PCV/Donor PCV)

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40
Q

What is the target PCV for a large animal needing a blood transfusion?

A

15-20%

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41
Q

What premedication should be administered prior to a blood transfusion?

A
  1. Antihistamine

2. NSAIDS

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42
Q

What is the rate at which you should give a blood transfusion in large animals and what steps are involved ?

A
  1. Start slow at 0.1ml/kg/hr
  2. Monitor TPR, attitude and watch for hives
  3. Increase rate gradually every 5-10 min if no Rxn
  4. Limit to 20ml/kg/hr
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43
Q

When and why does a tranfusion reaction usually occur?

A

Due to donor-recipient blood group incompatibilities and can occur during the first transfusion

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44
Q

What are the clinical signs of a blood transfusion reaction?

A
  1. Tachypnea
  2. Tachycardia
  3. Urticaria
  4. Pyrexia
  5. Pulmonary edema
  6. Colic
  7. Shock/collapse
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45
Q

What are the steps when dealing with a blood transfusion reaction?

A
  1. Slow/stop transfusion and give crystalloid fluids instead
  2. NSAIDS or antihistamines
  3. Dexamethason/prednisone
  4. Epinephrine if there is anaphylaxis
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46
Q

What are some blood substitutes that can be used in a blood transfusion?

A
  1. Oxyglobin
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47
Q

What is TRALI and when does it occur?

A

Transfusion-associated lung injury occuring 1-2 days after a blood transfusion

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48
Q

What are blood transfusion reactions that can occur “late”?

A
  1. TRALI
  2. Hemolysis
  3. SIRS
  4. Serum hepatitis (Theiler’s diease )
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49
Q

What disease in horses is commonly associated with the administration of tetanus antitoxin given 4-6 weeks before clinical signs occur?

A

Theiler’s disease ( serum hepatitis)

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50
Q

A horse is suffering from anemia…other than a blood transfusion, what can you treat with?

A
  1. Iron supplements
  2. Vitamin B12
  3. Copper glycinate
  4. Anabolic steroids
  5. Oral therapy with RED CELL
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51
Q

What are some important causes of acute hemorrhage?

A
  1. Coagulopathies
  2. Thrombocytopenia
  3. DIC
  4. Guttural pouch mycosis in horses
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52
Q

What are some important causes of chronic hemorrhage?

A
  1. Coagulopathies
  2. Thrombocytopenia from EIA and BVD
  3. GI loss
  4. Internal parasites
  5. Aromas always ulcers in ruminants
  6. Caudal vena cava syndrome in ruminants
  7. Jejunal hemorrhage syndromes in ruminants
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53
Q

How would you diagnose guttural pouch mycosis?

A

Endoscopy

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54
Q

How is guttural pouch Mycosis treated?

A

Surgically, as there is not time for medical treatment since it can take 6 months

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55
Q

What is the main clinical sign of vena caval thrombosis and in what species?

A

Bilateral epitaxis in cattle

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56
Q

What is the pathogenesis behind vena cava thrombosis ?

A

Ruminal Acidosis- lliver abscess-thrombus in the caudal vena cava -metastatic pneumonia- erosion of pulmonary veins

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57
Q

How is vena canal thrombosis diagnosed and treated?

A

Endoscopy and U/S

It is fatal

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58
Q

A high producing dairy cow presents with hyperglycemia, hypermagnesemia hyponatremia, hypochloremia, hypokalemia along with anorexia, tachycardia, and hypothermia. She is bleeding from her rectum. What may be going on?

A

Jejunal hemorrhage syndrome

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59
Q

What causes jejunal hemorrhage syndrome?

A

Poor diet and management

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60
Q

What will jejunal hemorrhage syndrome look like on ultrasound?

A

Distended loops of intestine

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61
Q

How is jejunal hemorrhage syndrome treated?

A

Surgery , but prognosis is guarded

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62
Q

What are the most common causes of hemoperitoneum in large animals?

A
  1. Spleen trauma in mares
  2. Reproductive tract injury with uterine artery rupture
  3. Neoplasia
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63
Q

What clinical signs are seen in a horse with hemoperitoneum?

A
  1. Anemia

2. Colic

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64
Q

How is hemoperitoneum diagnosed?

A
  1. Swirling echogenic fluid on U/S

2. Abdominocentisis

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65
Q

How is hemoperitoneum treated?

A
  1. Fluid therapy
  2. Blood transfusion
  3. Antifibrinolytics and procoagulant agents
  4. Restricted physical activity
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66
Q

What is a signal that a horse will have a poorer prognosis with hemoperitoneum?

A

Prepartum hemorrhage

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67
Q

What is the prognosis for a large animal with hemoperitoneum?

A

Fair with 54 to 74% survival rate

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68
Q

What large animal species is more susceptible to nematode infection?

A

Goats

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69
Q

What type of abomasal ulcer is most often associated with anemia in cattle?

A

A grade 2 ( bleeding,non-perforation)

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70
Q

What are the causes of a anemia causing ulcer in cattle?

A
  1. Lymphosarcoma
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71
Q

How are abomasal ulcer diagnosed?

A

Fecal occult blood tests

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72
Q

What it’s the treatment for abomasal ulcers?

A

Treat the underlying disease that is leading to ileus, feeed more fiber and less grain, and don’t used oral gastroprotectants as they don’t work

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73
Q

What causes hemophilia A?

A

It is a sex linked recessive traits affecting males that involves a factor VIII deficiency

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74
Q

What diagnostic signs will you see with hemophilia A?

A

Prolonged PTT dues to the intrinsic pathway being compromised from a factor VIII deficiency

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75
Q

What diseases are associated with vasculitis in horses?

A
  1. Equine Purpura hemorrhagica (EPH)
  2. Equine Viral arthritis (EVA)
  3. Equine Infectious Anemia (EIA)
  4. Equine Anaplasmosis
  5. Idiopathic
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76
Q

What disease are associated with vasculitis in ruminants?

A
  1. Malignant catarrhal fever (cattle)

2. Bluetongue (sheep)

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77
Q

What is the definitive diagnosis for vasculitits?

A

Full thickness punch biopsies at least 6 mm of the skin analyzed with histopathology

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78
Q

What is the cause of purpura hemorrhagica?

A

Type III hypersensitivity response to bacterial/viral antigens

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79
Q

What are the clinical signs of purpura hemorrhagica?

A
  1. Limb edema
  2. Purpura
  3. Myositis
  4. Colic
  5. Reluctance to move
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80
Q

What bacteria/viruses can cause purpura hemorrhagic in horses?

A
  1. Streptococcus spp.
  2. Corynebacterium
  3. Influenza virus
  4. Strangles vaccination
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81
Q

How is purpura hemorrhagica treated?

A
  1. Treat underlying cause
  2. Corticosteroids for 2-4 weeks
  3. Treat edema
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82
Q

What is the cause of Equine anaplasmosis?

A

Anaplasma phagocytophilum

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83
Q

Where does anaplasma replicate?

A

Granulocytes- neutrophils

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84
Q

What are the clinical signs of equine anaplasmosis?

A
  1. Vasculitis with fever and limb edema

2. Secondary IMHA

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85
Q

How is Equine anaplasmosis treated?

A
  1. Oxytetracycline
  2. NSAIDS
  3. IV fluid therapy
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86
Q

T/F: Equine anaplasmosis patients have the ability to spontaneously recover in 2-3 weeks

A

True

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87
Q

How is anaplasmosis diagnosed?

A
  1. Morulae in neutrophils after 3 days of fever
  2. PCR positive for three weeks
  3. Seroconversion after 12 days
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88
Q

What is the vector for equine anaplasmosis?

A

Ixodes Pacificus

I. Scapularis

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89
Q

What are the 3 mechanisms of thrombocytopenia?

A
  1. Abnormal sequestration
  2. Shortened platelet survival
  3. Decreased/absent platelet production
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90
Q

What are the clinical consequenes of thrombocytopenia?

A

1Petechial hemorrhage and bruising

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91
Q

What are the causes of Immune-mediated thrombocytopenia?

A

Primary causes are idiopathic. Secondary:

  1. Penicillin or ceftiofur administration
  2. Lymphosarcoma
  3. EIA or BVD infections
  4. Alloimmune in foals
  5. Autoimmune
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92
Q

A patient has thrombocytopenia and the platelet level is < 40,000/ul, what does this indicate?

A

Hemorrhage in response to trauma

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93
Q

A patient has thrombocytopenia and the platelet level <10,000/ul , what does this indicate?

A

Spontaneous bleeding

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94
Q

How is immune mediated thrombocytopenia diagnosed?

A
  1. CBC- Platelet counts <100,000/u, mild anemia, and hypoproteinemia
  2. Coagulation panel: prolonged bleeding time with normal PT, PTT and fibrinogen
  3. Bone marrow biopsy: megakaryocytic and erythropoietin hyperplasia
  4. Flow cytometry: Ig on platelet surface
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95
Q

What is the gold standard diagnosis for immune mediated thrombocytopenia?

A

Flow cytometry with Ig on platelet surfaces

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96
Q

What is the treatment for immune mediated thrombocytopenia?

A
  1. Stop triggering medications and treat underlying disease
  2. Immunosuppresion with corticosteroids ( dexmethasone/prednisone)
  3. Blood transfusion
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97
Q

How long would you treat a horse with immune mediate thrombocytopenia with corticosteroids

A

10-21 days with a platelet count normal for at least 5 days

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98
Q

What would you see on a bone marrow biopsy with immune mediated hemolytic anemia?

A

Megakaryocytic and erythyroid hyperplasia…aka a regerative response

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99
Q

What infectious agents are likely to cause immune mediated thrombocytopenia in large animals?

A
  1. Type II BVD in cattle
  2. Equine infectious anemia in horses
  3. Anaplasma phagocytophila in horses
  4. Enzootic lymphosarcoma in cattle
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100
Q

What are the clinical signs of DIC?

A
  1. Generalized thrombosis and/or hemorrhage

2. Multiple ischemia organ failure (MODS)

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101
Q

How is DIC diagnosed?

A
  1. Thrombocytopenia
  2. Prolonged PT, PTT, reduced fibrinogen and elevated D-Dimers
  3. Clinical signs

Need 3 or more lab changes and C/ S to diagnose

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102
Q

What is the cornerstone of treatment for DIC?

A

manage/treat the underlying disease

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103
Q

Besides treating the underlying cause of DIC, what other treatments can be used?

A
  1. IV fluid therapy
  2. NSAIDS like flunixin meglumine
  3. Heparin for At-III
  4. Whole blood/plasma transfusions
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104
Q

What toxin is a common cause of DIC in large animals?

A

Moldy sweet clover

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105
Q

What is the toxic principle of moldy sweet clover?

A

Dicoumarol from improperly cured hay or silage

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106
Q

How does moldy sweet clover cause DIC?

A

The toxin is a vitamin K antagonist with interferes with production of factors II, VII, IX, and X

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107
Q

How is moldy sweet clover poisoning treated?

A
  1. Stop feeding clover
  2. Administer vitamin K1
  3. Whole blood/plasma transfusion as required
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108
Q

What diseases in large animals are caused by RBC loss?

A
  1. GP mycosis
  2. Vena Caval Thrombosis
  3. Jejunal Hemorrhage syndrome
  4. Hemoperitoneum
  5. Intestinal parasites
  6. Abomasal ulcers
  7. Hemophilia A
  8. Purpura hemorrhagica
  9. Equine anaplasmosis
  10. EIA
  11. IMTP
  12. Moldy sweet clover poisoning
  13. Warfarin toxicosis
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109
Q

Which diseases in large animals are associated with intravascular hemolysis?

A
  1. Equine Piroplasmosis
  2. Bovine Babesiosis
  3. Bacillary hemoglobinuria
  4. Leptospirosis
  5. Heinz body anemia’s
  6. Copper toxicity of ruminants
  7. Water intoxicating of calves
  8. Post-parturient hemoglobinura
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110
Q

What disease in large animals are associated with extravascular hemolysis?

A
  1. Immune-Mediated hemolytic anemia
  2. Equine infectious Anemia
  3. Anaplasmosis in ruminants
  4. Mycoplasma haemolame in camelids
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111
Q

What anemia in large animals are associated with decreased RBC production?

A
  1. Depression anemia

2. Anemia of chronic disease

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112
Q

What are the causes of depression anemia in large animals?

A
  1. Vitamin/mineral deficiency
  2. Inflammatory chronic disease
  3. Renal or hepatic failure
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113
Q

What vitamin/mineral deficiencies can cause depression anemia in large animals?

A
  1. Iron
  2. Copper
  3. Cobalt (B12)
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114
Q

Hemoglobinemia and hemoglobinuria are associated with ________ hemolysis, while hyperbilirubinema is associated with ________ hemolysis.

A

Intravascular

Extravascular

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115
Q

What causes equine piroplasmosis and how is it transmitted?

A
  1. Babesia caballi
  2. Theileria equi

Both spread by tick vectors

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116
Q

What is the equine piroplasmosis infectious agent that is reportable?

A

Theileria equi

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117
Q

What are the clinical signs of equine piroplasmosis?

A
  1. Fever
  2. Obtunded
  3. Anorexia
  4. Incoordination
  5. Nasal/ocular discharge
  6. Hemoglobinemia/Uria
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118
Q

On blood smears, what is seen with babesia caballi versus theileria equi?

A

Large piroplasms with B. caballi and small piroplasms with T. Equi…the piroplasms are in RBC’s

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119
Q

How is Equine piroplasmosis treated?

A

Imidocarb

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120
Q

Which infectious agent that causes equine piroplasmosis is harder to clear and has more severe Clinical signs?

A

T. Equi

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121
Q

Wher does bovine babesiosis occur?

A

Not in the USA

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122
Q

What is the other name for bacillary hemoglobinura and what clinical signs are seen?

A

Red Water

  1. Sudden death
  2. Port wine urine form hemoglobinuria (intravascular hemolysis)
  3. Fever
  4. Bloody nasal/rectal distract 5. Palor/icterus
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123
Q

What causes bacillary hemoglobinuria?

A

Clostridium hemolyticum B toxin

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124
Q

What parasite is bacillary hemobloginuria associted with?

A

Faciola hepatica

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125
Q

How is bacillary hemoglobinuria treated?

A
  1. Penicillin or oxytetracycline IV or IM

2. Blood transfusion

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126
Q

How is bacillary hemoglobinuria diagnosed?

A
  1. Post Mortem with necrotic hepatic infarction with clostridium overgrowth
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127
Q

What are the clinical signs of leptospirosis infection in large animals?

A
  1. Hemorrhage in the kidney, eyes, reproductive tract and lungs
  2. Abortion
  3. Uveitis
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128
Q

What two lepto serovars are associated with acute hemolytic syndrome?

A
  1. L. Pomona

2. L. Icterohaemorrhagicae

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129
Q

What are the causes of Heinz body anemia?

A
  1. Phenothiaine tranquilizers
  2. Toxic plants
  3. Selenium deficiency
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130
Q

What type of hemolysis does Heinz body anemia cause?

A

Intra and extravascular

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131
Q

What clinical signs are seen with Heinz body anemia?

A
  1. Methemoglobinemia

2. Hemoglobinemia

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132
Q

What toxic plants can cause Heinz body anemia?

A
  1. Red maple (equids)
  2. Brassica spp.
  3. Wild onion
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133
Q

What is the toxic principle of brassica and wild onion toxicity?

A

S-methylcysteine sulfoxide metabolize to dimethyl disulfide which causes RBC oxidation

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134
Q

How is Heinz body anemia treated?

A
  1. Remove toxic source
  2. Activated charcoal
  3. Methylene blue in ruminants
  4. Vitamins C
  5. IV fluid therapy
  6. Blood transfusion
  7. Don’t give NSAIDS if kidney disease an can cause colic
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135
Q

Why would you want to be careful giving an NSAID in an animal with Heinz body anemia?

A

It can cause colic and kidney issues

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136
Q

What can cause primary copper toxicity in ruminants?

A

Excessive ingestion/injection of copper

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137
Q

What can cause secondary copper toxicity in ruminants?

A
  1. Molybdenum deficiency

2. Hepatotoxic plants

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138
Q

Which large animal species is most susceptible to copper toxicity?

A

Sheep

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139
Q

How is copper toxicity diagnosed?

A

High serum and liver copper levels

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140
Q

If a sheep is in the acute hemolytic phase of copper toxicity, how it is diagnosed?

A

Non-regenerative anemia with high serum/liver copper levels

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141
Q

If a sheep is in the pre-hemolytic phase of chronic copper toxicosis, how it it diagnosed?

A

Elevate liver enzymes and high copper in liver biopsy

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142
Q

How is copper toxicity treated?

A
  1. Measure copper levels in liver
  2. Identify/ remove sources of copper
  3. Supplement with zinc and iron and decrease molybdenum
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143
Q

A calf presents with serum hypo-osmolarity, mild anemia, and hemoglobinemia/nuria..what is likely going on?

A

Water intoxication

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144
Q

How does water intoxicating lead to clinical signs in calves?

A

Rapid ingestion of water causes osmotic lysis of RBC’s

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145
Q

A dairy cow presents with hypophosphatemia and hemoglobinemia/uria 1 month after calving..what is going on?

A

Post-parturient hemoglobinuria

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146
Q

What may post-parturient hemoglobinuria be associated with?

A

Copper and selenium deficiency

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147
Q

What can cause secondary immune mediated hemolytic anemia?

A
  1. Penicillin

2. Lymphosarcoma

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148
Q

What are the clinical signs of immune mediated hemolytic anemia?

A
  1. Fever

2. Tachycardia with pallor-anemia

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149
Q

How is immune mediated hemolytic anemia diagnosed?

A
  1. Saline agglutination test
  2. Direct Coomb’s test
  3. Flow cytometry
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150
Q

How is immune mediated hemolytic anemia treated?

A
  1. Treat underlying cause
  2. Dexamethasone
  3. Blood transfusion if needed
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151
Q

This disease is lifelong in horses, causes extravascular hemolysis, is transmitted via blood and is caused by a lentivirus…what is it?

A

Equine infectious anemia

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152
Q

How does a persistent infection of equine infectious anemia occur?

A

The virus persists in monocytes

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153
Q

T/F: Equine infectious anemia is reportable.

A

True

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154
Q

What are the c/s of equine infectious anemia?

A
  1. Vasculitis
  2. Glomerulonephritis
  3. Hepatitis
  4. Thrombocytopenia
  5. Anemia in subacute to chronic cases
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155
Q

What is the difference between acute and chronic equine infectious anemia?

A

Acute occurs within 7-30 days while chronic is > 30 days. Acute has no anemia.

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156
Q

How is EIA diagnosed?

A

Coggins test with AGID and ELISA

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157
Q

When can EIA be diagnosed via a coggins test?

A

10 days post-infection (seroconversion)

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158
Q

What is the treatment for EIA?

A

None, must be euthanized or permanently quarantined

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159
Q

How do ruminants become infected with anaplasmosis?

A

The blood of carrier animals taken up by tick or flies

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160
Q

How does anaplasmosis in ruminants cause clinical signs?

A

Auto-antibody production leading to extravascular hemolysis

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161
Q

What are the different phases of anaplasmosis in ruminants ?

A
  1. Acute
  2. Convalescent
  3. Chronic carrier
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162
Q

How is anaplasmosis in ruminants diagnosed (acute versus chronic phase) ?

A
  1. Inclusion bodies in RBC’s on fresh blood smear (acute phase)
  2. PCR
  3. cELISA (chronic)
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163
Q

What are the clinical signs of an acute phase of anaplasmosis in ruminants?

A
  1. Fever
  2. Late term abortion
  3. Severe anemia with no hemoglobinuria
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164
Q

What are the clinical signs of an chronic phase of anaplasmosis in ruminants?

A
  1. Weight loss

2. Icterus

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165
Q

What age of ruminants will have more severe clinical signs when infected with anaplasmosis?

A

Older

166
Q

Why does seroconversion not equal organism clearance with anaplasmosis?

A

The organism will no longer be visible in RBC’s but will still be in the animals body lifelong

167
Q

How is anaplasmosis in ruminants treated?

A
  1. Supportive
  2. Blood transfusion
  3. Oxytetracycline
168
Q

A llama from Colorado presents with a moderate, poorly regenerative anemia, fever, and lethargy. There is evidence of extravascular hemolysis. What is the likely cause?

A

Mycoplasma haemolamae

169
Q

How is mycoplasma haemolamae treated?

A

Oxytetracycline, but full cure unlikely

170
Q

How is mycoplasma haemolamae diagnosed?

A
  1. PCR

2. Fresh blood smear

171
Q

How many RBC’s must be affected before clinical signs will be seen in acute anaplasmosis in ruminants?

A

> 1%

172
Q

What is the most common form of anemia in large animals?

A

Depression Anemia

173
Q

A ruminant presents with decreased serum iron and TIBC with normal bone marrow iron stores and ferritin levels. How would you treat?

A

You would NOT supplement with iron as this is anemia of chronic inflammation and this would cause there to be too much iron in the body due to the sequestration in the bone marrow.

174
Q

What chronic disease syndromes can lead to depression anemia in large animals?

A
  1. Liver abscess
  2. GI abscess in small ruminants
  3. Chronic pneumonia
  4. Chronic BVDV
  5. Johns disease
  6. Neoplasia
175
Q

What are tests you can use to measure B cell function in humoral immunity?

A
  1. In vitro lymphocyte blastogenesis test

2. Response to a killed virus vaccine

176
Q

How can immunoglobulin concentration be determined?

A
  1. Total globulins by ELISA, ZNSO4, and RID or routine chem

2. Globulin fractions by protein electrophoresis

177
Q

How can B cell concentrations in blood/lymphonodes be determined?

A
  1. CBC w/ differential
  2. Flow cytometry
  3. HIstopathology
178
Q

How can T cell function be tested in cell-mediated immunity?

A
  1. In vitro lymphocyte blastogenesis test

2. Intradermal injection of phytohemagglutinin (PHA)

179
Q

What are some clinical conditions in large animals that may indicate immunodeficiency?

A
  1. 2 or more episodes of pneumonia in 1 year
  2. Opportunistic organism infections
  3. Multiple sites of infection
  4. Recurrent pyodermatitis
  5. Meningitis or osteomyelitis
  6. 2 or more months on antibiotics with no effect
  7. Failure to gain weight/grow normally
  8. Recurrent infections with history or primary immune deficiency in blood line
180
Q

What occurs if there is failure of passive transfer?

A

Inadequate humoral immunity

181
Q

Why is passive transfer of IgG in colostrum and IgA in milk important?

A

The immune system is competetent but naive at birth and needs time for antigen processing and colonial expansion

182
Q

How is failure of passive transfer treated?

A

Give colostrum within 3-4 hours of birth but no more than 24 hours. GIve plasma if it has been longer than 24 hours since birth.

183
Q

What breed of horse is susceptible to sever combined immunodeficiency disease (SCID)?

A

Arabians

184
Q

What occurs during severe combined immunodeficiency disease (SCID) that causes C/S?

A

Failure to produce function B and T lymphocytes due a autosomal recessive primary immunodeficiency

185
Q

How does SCID progress in foals?

A

Normal for 2-3 months an then start to suffer from bronchopneumonia, enteritis, septic arthritis and/or omphalophlebitis. They die within 5 months.

186
Q

How is SCID diagnosed?

A
  1. Persistent lymphopenia <1000/ul on CBC
  2. Low globulin concentrations ( IgM and IgG)
  3. PHA intradermal test
  4. Lymphoid/thymic hypoplasia at post-mortem
187
Q

How is SCID treated/prevented?

A

No treatment, but prevented with genotypoing

188
Q

An 8 month old foal presents with a history of chronic/recurrent infections and on serology, the persistence IgM levels are < 25 mg/DL…what disease is this?

A

Selective IgM deficiency

189
Q

What type of immunity is deficient in selective IgM deficiency in horses?

A

Humoral due to a primary immunodeficiency

190
Q

What age horses can be affected by selective IgM deficiency

A

All ages as there is juvenile (5 month to 2 years) onset and adult onset ( 2 to 5 years)

191
Q

What is a common clinical presentation in a 3 year old horse with selective IgM deficiency?

A
  1. Recurrent infections

2. Lymphosarcoma

192
Q

How is selective IgM deficiency in horses treated?

A
  1. Antibiotics and other supportive treatment
  2. Plasma transfusions for IgM transfer

Prognosis is poor to grave

193
Q

How would you distinguish common variable immunodeficiency (CVID) and Slective IgM deficiency in horses?

A

The main difference is in CVID, the IgM will be , 25mg/dL AND the IgG will be depleted eventually reaching <200mg/dL

194
Q

A horse presents to you with variable lymphopenia, B cell depletion in bone marrow/lymphoid tissue, and has a lack of response to vaccination with tetanus toxoid due to low IgM and IgG levels and has recurrent fungal infections…what disease is this?

A

Common variable immunodeficiency of Horses (CVID)

195
Q

How is CVID treated?

A

Supportive care and antibiotics short term, but long term prognosis is grave

196
Q

Name the disease: A primary immunodeficiency of the innate immune system due to an autosomal recessive gene inherited in Holstein cattle.

A

Bovine leukocyte adhesion deficiency (BLAD)

197
Q

Which cell is not able to migrate out of the vasculature in response to cytokines in a cow with bovine leukocyte adhesion deficiency?

A

Neutrophils

198
Q

Wht are the 4 forms of bovine lymphoma?

A
  1. Juvenile (calf)
  2. Thymic (adolescent)
  3. Cutaneous
  4. Enzootic
199
Q

At what age are cattle when they suffer from juvenile LSA?

A

< 1 year, usually between 3-6 months

200
Q

Which two forms of bovine lymphoma have similiar clinical presentations?

A
  1. Juvenile (calf) LSA

2. Enzootic

201
Q

What are common clinical signs of juvenile and enzootic bovine lymphoma?

A
  1. Symmetrical generalized lymphadenopathy
  2. Poor growth/ Weight loss
  3. Moderate anemia from bone marrow infiltration
202
Q

What is the age of onset for thymic LSA?

A

6-24 months

203
Q

What are the clinical signs of thymic LSA?

A
  1. Dysphasia from esophageal compression
  2. Dyspnea/cough from tracheal compression
  3. CV insufficiency from blood vessels contraction
204
Q

What causes clinical signs in Thymic bovine LSA?

A

Space occupying mass at the base of neck and cranial thorax ( thymus tumor)

205
Q

What age cattle are infected with cutaneous bovine lymphoma?

A

1-3 years

206
Q

Describe the type of tumor seen on cattle with cutaneous LSA..

A

2-3 cm w/ necrotic center that are raised, circular and ulcerated affecting the skin and very painful, tend to wax and wane and can spread to other organ systems

207
Q

What virus is associated with Enzootic bovine lymphoma?

A

Bovine leukosis virus (BLV)

208
Q

What is the age of onset for enzootic Bovine LSA?

A

> 2 years, most orient > 4 years

209
Q

Why is enzootic bovine LSA not a huge problem for producers?

A

The majority of cattle infected are asymptomatic and there is no difference in economic performance

210
Q

How is enzootic bovine LSA commonly transmitted?

A
  1. Horizontal: Iatrogenic from reused needles/instruments

2. Vertical: Ingestions of infected milk/colostrum

211
Q

What type of immune response does a BLV infection stimulate and why can it lead to enzootic bovine LSA?

A

Humoral response with antibodies that do not clear the infection

212
Q

What percentage of cattle will develop persistent lympocytosis with a BLV infection? Enzootic LSA?

A

30%

1-5%

213
Q

What 7 common organs can enzootic LSA infect in cattle?

A
  1. Peripheral lymph nodes
  2. Retrobulbar lymph nodes
  3. Heart
  4. Uterus
  5. Abomasum
  6. Spleen/kidney
  7. Lumbar spinal cord
214
Q

How is enzootic LSA diagnosed?

A

Demonstration of neoplasticism cells on cytology/histopathology of a biopsy/FNA/fluid sample

215
Q

T/F: A diagnosis of BLV = a diagnosis of LSA.

A

False

216
Q

What does a positive results on a AGID test for enzootic LSA tell you?

A

Confirms an infection of BLV, but not LSA

217
Q

How is enzootic LSA treated?

A
  1. L-asparaginase

2. Dexamethasone

218
Q

How can enzootic LSA be prevented?

A

Since there are no BLV vaccines available, you must ID seropositive cattle and cull them. Minimizing iatrogenic transmission is helpful.

219
Q

What are the types of equine lymphoma?

A
  1. Alimentary
  2. Thymic/mediastinal
  3. Multi centric
  4. Cutaneous
220
Q

What is the most common primary tumor of horses?

A

Lymphoma, specifically the sarcomatous forms

221
Q

What is the etiology of equine lymphoma?

A

Unknown, but it is sporadic

222
Q

What is the average age a horse can develop lymphosarcoma?

A

5-10 years , except alimentary form less than 5 years (16 year average)

223
Q

What parts of the horses body are commonly infiltrated with alimentary lymphosarcoma?

A
  1. Small intestine

2. Intestinal and hepatic lymph nodes

224
Q

What are the clinical signs of alimentary lymphosarcoma in horses?

A
  1. Emancipated w/ good appetite
  2. Recurrent colic
  3. No peripheral lymphadenopathy
225
Q

How is alimentary lymphosarcom in horses diagnosed?

A
  1. Hypoalbuminemia on chem panel

2. Low glucose absorption test from intestinal malabsorption

226
Q

What are the clinical signs of thymic/mediastinal lymphosarcoma in horses?

A
  1. Respiratory signs like labored breathing
  2. Ventral edema
  3. Pleural effusion
  4. Lymphadenopathy
227
Q

How is thymic/mediastinal lymphosarcoma diagnosed?

A
  1. U/S

2. Cytology of pleural fluid

228
Q

What are the clinical signs of multi centric equine lymphosarcoma?

A
  1. Emaciation
  2. Severe depression
  3. Lymphadenopathy
  4. Anemia/leukemia
  5. Organ dysfunction
229
Q

What are the clinical signs of cutaneous lymphosarcoma?

A
  1. Multiple SQ nodules that appear suddenly, then regress

2. Local LN involvement

230
Q

How is equine lymphoma treated?

A
  1. Corticosteroids for immune suppression
  2. Chemotherapy
  3. Supportive
231
Q

What is the most common cause of acute hepatitis and failure in horses?

A

Idiopathic acute hepatitis (IAH)

232
Q

What can cause idiopathic acute hepatitis in 20% of cases?

A
  1. Equine serum products

2. Tetanus antitoxin

233
Q

When will idiopathic acute hepatitis in horses typically manifest as disease?

A

4-10 weeks after administration of a biologic

234
Q

What age and type of horse typically develop IAH?

A
  1. > 2 years

2. Lactating mares 1-3 months post foaling

235
Q

What are the clinical signs of equine IAH?

A

Acute progressive hepatic failure over 2-7 days with:

  1. Jaundice
  2. Photosensitization
  3. Yawning with hepatic encephalopathy
  4. Intravascular hemolysis
  5. DIC
236
Q

What viruses are associted with IAH?

A
  1. Theiler’s disease flavivirus

2. Equine parvovirus

237
Q

What is typically found on blood chemistry with IAH?

A
  1. Elevated bilirubin
  2. Elevated SDH, AST, GGT, and ALP
  3. Low BUN and glucose
238
Q

What will liver function tests looks like in a horse with IAH?

A
  1. High bile acids

2. High ammonia

239
Q

What can be used to diagnose IAH in a horse besides blood chemistry?

A
  1. U/S
  2. Biopsy/histo
  3. Post mortem exam
240
Q

What is seen on ultrasound in a horse with IAH?

A

Decreased parenchyma echogenicity and heterogenous

241
Q

What is seen on biopsy/histo of a horse with IAH?

A

Diffuse necrosis and biliary hyperplasia ( are not very helpful)

242
Q

What is see post-mortem in a horse with IAH?

A

Enlarged, pale, diffusely mottled liver OR

Small “dishrag” LIver

243
Q

How would you treat a horse with IAH?

A
  1. IV dextrose and electrolytes
  2. Plasma transfusion
  3. Liver support drugs/ammonia reduction
244
Q

What is the prognosis for IAH?

A

90% mortality, deat in 5 days or recovery in 7-10 that may not be complete..very expensive to treat

245
Q

How an IAH be prevented in horses?

A
  1. Give the toxoid for tetanus instead of antitoxin
  2. Routine tetanus prophylaxis
  3. Screen horses on property for subclinical infection
246
Q

What is the cause of Tyzzer’s disease and what species does this affect?

A

Clostridium piliforme in foals

247
Q

What does Tyzzer’s disease cause?

A

Acute and highly fatal bacterial hepatitis

248
Q

How do horses become infected with Tyzzer’s disease?

A

It is sporadic and not contagious, but it is shed by healthy mares who are resistant

249
Q

What are the clinical signs of tyzzer’s Disease?

A
  1. Sudden death at 7-42 days old
  2. Fever
  3. Icterus
  4. Seizures
250
Q

What is the prognosis of Tyzzer’s disease?

A

Grave because fatal in 48 hours

251
Q

How is tyzzer’s disease treated?

A

High dose penicillin and gentamicin with support

252
Q

How is Tyzzer’s disease diagnosed?

A

Necropsy with mutlifocal hepatic necrosis and intracytoplasmic bacteria. Can also use PCR or fluorescent antibody

253
Q

What is Black’s disease and what species are affected?

A

Infectious Necrotic hepatitis that infects small ruminants

254
Q

What is the cause of Infectious necrotic hepatitis (INH)

A

Clostridium novi type B toxins

255
Q

Why is infectious necrotic hepatitis called Black’s disease?

A

The clostridium toxin ruptures SQ vessels and causes dark skin

256
Q

What parasite is associated with INH? Why?

A

Faciola Hepatica or magna..or a liver biopsy. The liver fluke cause hepatic damage and sets up for a clostridium infection.

257
Q

How do small ruminants become infected with clostridium that causes infectious necrotic hepatitis?

A

Spores are found in the soil, bowel and liver of grazing animals that are consumed and then disseminated in the respiratory system to the liver

258
Q

What are the clinical signs of infectious necrotic hepatitis?

A
  1. Sudden death in late summer/early fall
  2. Fever
  3. Anorexia
  4. Depression
  5. Separation from the herd
259
Q

What is a differential diagnosis for Tyzzer’s disease?

A

Equine Herpes virus

260
Q

What is a differential diagnosis for infectious necrotic hepatitis?

A

Anthrax

261
Q

How Is infectious necrotic hepatitis (INH) diagnosed?

A
  1. Necropsy
  2. Gram stain liver impression smears
  3. Fluorescent antibody on impression smears
  4. Specific exotoxins identification
262
Q

What is the definite diagnosis of infectious necrotic hepatitis and why is it not used often?

A

Specific exotoxin identification, but not practical in the field

263
Q

What is seen on necropsy in small ruminants that died of INH?

A
  1. SQ hemorrhage
  2. Blood tinged body cavity fluids
  3. Swollen/congested liver with focal coagulative necrosis and fluke migration tracts
264
Q

How do you treat INH in small ruminants?

A

Not usually indicated, but

  1. Penicillin
  2. Oxytetracycline
265
Q

How is INH prevented in a flock?

A
  1. Vaccinate
  2. Mass administration of long acting antibiotics if herd member dies from it
  3. Burn/bury/remove carcasses
  4. Reduce fluke infestation
  5. Commercial bacteria/toxoids
266
Q

When vaccinating a herd against INH, what do you use and how should it be timed?

A

A commercial bacteria/toxoid that will have a 5-6 month effect and should be timed with fluke season with 2 injections 5 months apart in mild climates and 1 injection in harsh climates

267
Q

What cause Bacillary hemoglobinuria?

A

Clostridium novyi Type D toxin

268
Q

What are the clinical signs of bacillary hemoglobinura?

A
  1. Sudden death
  2. Fever
  3. icterus
  4. Blood nasal discharge/feces
  5. Hemoglobinuria uncommon
269
Q

What does bacillary hemoglobinuria do to the liver?

A

Causes localized hepatic necrosis

270
Q

How is bacillary hemoglobinuria diagnosed?

A
  1. Post mortem necropsy 2. History of animal from endemic area
  2. Gram stain impression smears
  3. Fluorescent AB on impression smears
  4. Histopathology
271
Q

What is seen on necropsy in a animals that died from red water?

A
  1. Advanced decomposition
  2. Bloody oriifices
  3. Hemorrhage in SQ, serosa
  4. Coagulative necrosis in liver
272
Q

How is red water treated?

A
  1. Supportive

2. Blood transfusion for intravascular hemolytic anemia

273
Q

How is bacillary hemoglobinemia prevented?

A
  1. Remove carcasses
  2. Administer commercial bacteria/toxoid vaccines for 5-6 month protection
  3. Control liver flukes
274
Q

What is the pathophysiology of red water similiar to?

A

Infectious Necrotic Hepatitis

275
Q

In what species are liver abscess most likely to occur in ? Why?

A

Cattle

Erosions of rumen epithelium from high energy diets inducing lactic acidosis

276
Q

What bacteria is associated with liver abscess formation in Cattle?

A

F. Necrophorum

277
Q

How do neonates typically form a liver abscess?

A

Extension of an umbilical infection

278
Q

What concurrent disease and infectious agent puts goats at a higher risk for developing a liver abscess?

A

Caseous lymphadentitis

C. Pseudotuberculosis

279
Q

What are the clinical signs of a liver abscess that span all species?

A
  1. Weight loss

2. Fever

280
Q

What are some differentials for a liver abscess in cattle?

A
  1. Reticuloperitonitis
  2. Parasitism
  3. Malnutrition
  4. Lymphosarcoma
  5. Johne’s
281
Q

What are some differentials for a liver abscess in horses?

Why?

A
  1. Abdominal abscess
  2. Cholelithiasis

They have intermittent colic

282
Q

What are the primary complications that can arise from a liver abscess, especially in cattle?

A
  1. Caudal vena cava thrombosis
  2. Common bile duct compression
  3. Peritonitis
283
Q

How are liver abscesses in cattle diagnosed?

A

High risk feed ration ( high grain/limited forage and no adjustment period)

284
Q

What will be seen on CBC and chem panel with a liver abscess?

A
  1. Neutrophilia
  2. Anemia
  3. Elevated GGT and AST
285
Q

T/F: You should biopsy a liver abscess.

A

False

286
Q

How are liver abscesses treated?

A
  1. Penicillin or ampicillin combined with rifampin
  2. Metronidazole

But diagnosis usually made post-mortem

287
Q

How can liver abscesses be prevented?

A
  1. Adjust grain/feed change over 3-4 weeks
  2. Feed a good fiber source
  3. Administer approved feedlot antibiotics
288
Q

Describe a good fiber source for cattle to prevent liver abscesses?

A

> 19 cm in length with 1kg/head/day with lactating diary cows recieving a 45: 55 roughage to concentrate diet and 2.3kg stem hay/day

289
Q

What are some feedlot approved antibiotics that can be used to prevent liver abscesses in cattle ?

A
  1. Bacitracin
  2. Chlor or oxy tetracycline
  3. Tylosin
  4. Virginiamycin
  5. Leukotoxin based F. Necrophorum vaccine
290
Q

What are the clinical signs of chronic active hepatitis (CAH)?

A
  1. Weight loss
  2. Icterus
  3. Depression
  4. Behavior changes
  5. Mild colic
  6. Intermittent fever
  7. Aseptic vasculitis (rare)
291
Q

What is the liver enzyme profile in a large animals with chronic active hepatitis?

A
  1. Marked increase in ALP and GGT
  2. Mild increase in AST and SDH
  3. Increased serum bile acids and conjugated bilirubin
292
Q

When performing histopath on a liver biopsy in a horse with chronic active hepatitis, what will you see?

A
  1. Mononuclear cell infiltration
  2. Neutrophils is bacterial infection
  3. Biliary hyperplasia
  4. Hepatocellular necrosis
293
Q

What diagnostics should be done to a liver biopsy in an animal with chronic active hepatitis?

A
  1. Culture

2. Histopath

294
Q

How is chronic active hepatitis treated?

A
  1. Antibiotics if there is an infection for 4-6 weeks

2. Corticosteroids if there is lymphocytic plasmacytic infiltration

295
Q

What antibiotics are used to treat chronic active hepatitis in large animals?

A

Antibiotics for enteric bacteria:

  1. Ampicillin
  2. Chloramphenicol
  3. Penicillin + gentimicin
  4. TMS
296
Q

What corticosteriods can be used to treat large animals with chronic active hepatitis?

A
  1. Prednisolone: better for longer treatment and higher doses
  2. Dexamethasone: more potent, so better for short term and low doses
297
Q

What is suppurative cholangiohepatitis?

A

Neutrophil accumulation within hepatic portal tracts and bile ducts

298
Q

What is the sequelae to suppuratic cholangiohepatitis?

A
  1. Cholelithiasis
  2. Loss of hepatic function
  3. Chronic active hepatitis
299
Q

What are the clinical signs of suppurative cholangiohepatitis

A
  1. Fever
  2. Colic
  3. Icterus
  4. Weight loss
300
Q

What liver enzyme is elevated on blood chemistry with cholangiohepatitis?

A

GGT

301
Q

How is cholangiohepatitis diagnosed?

A
  1. Elevated GGT
  2. Elevated conjugated bilirubin
  3. Inflammatory CBC
  4. U/S
  5. Biopsy
302
Q

What is seen on U/S with cholangiohepatitis?

A
  1. Diffuse increase in echogenicity
  2. Hepatomegaly
  3. Mild biliary distension/biliary wall thickening
303
Q

What does a biopsy determine in a patient with cholangiohepatitis? What is seen on a biopsy?

A

Determines the severity of disease and degree of fibrosis

  1. Nuetrophilic infiltrate
  2. Hepatocyte nerosis
304
Q

What bacteria are commonly cultured on a liver biopsy in a patient with cholangiohepatitis?

A
  1. Salmonella
  2. E.coli
  3. Citrobacter
  4. Aeromonas
  5. Acinetobacter
305
Q

How is cholangiohepatitis treated?

A
  1. Antiobiotics for 4-6 weeks

2. Monitor liver enzymes serially

306
Q

What antibiotics should you use to treat cholangiohepatitis?

A

Gram - and anaerobe effective:

  1. TMS
  2. Penicillin+gentimicin
  3. Chloramphenicol
  4. Enrofloxacin
  5. Ceftiofur
307
Q

What is cholelithiasis?

A

Stones in the left/right bile ducts or gallbladder

308
Q

What is choledocholithiasis?

A

Stones in the common bile duct

309
Q

What is hepatolithiasis?

A

Stones in the intrahepatic bile ducts

310
Q

What large animal species tends to become clinical with cholelithiasis?

A

Horses

311
Q

What is the most common cause of biliary obstruction in large animals?

A

Choledocholithiasis

312
Q

What can cause acute biliary obstruction in horses and what will you see on blood chemistry?

A

Colonic displacements

Elevated GGT, bilirubin, serum bile acids and ammonia

313
Q

What is the most likely reason for cholelithiasis?

A

Ascending inflammation or infection

314
Q

What are equine bile stones made out of?

A
  1. Bile salts
  2. Calcium bilirubinate
  3. Cholesterol
315
Q

What is the triad of clinical signs in a horse with cholelithiasis?

A
  1. Intermittent colic
  2. Fever
  3. Icterus
316
Q

What age horse is most predisposed to cholelithiasis?

A

> 5 years

317
Q

What would indicated that a horse with cholelithiasis has multiple stones or that the bile duct is completley occluded?

A
  1. Photosensitization
  2. Encephalopathy
  3. Weight loss
  4. Icterus (bile duct)
  5. Coli (bile duct)
318
Q

How is cholelithiasis diagnosed?

A
  1. Elevated GGT, ALP, and bilirubin
  2. U/S: hepatomegaly, dilation/thickening bile ducts, diffuse echogenicity, choleliths
  3. Triad of clinical signs
319
Q

On U/S, where is it most likely you will see choleliths?

A

Cranioventral right hepatic lobe between the 7-10th ICS

320
Q

How accurate is diagnosis of cholelithiasis with U/S?

A

50-75%

321
Q

What are differential diagnosis of cholelithiasis?

A
  1. Chronic liver disease (other forms)

2. Causes of mild recurrent colic like verminous arteritis, internal abscesses, enteroliths, and neoplasia

322
Q

How is cholelithiasis treated?

A
  1. Long term antibiotics and anti-inflammatories
323
Q

When is surgery indicated for cholelithiasis? What surgeries?

A

When there is choledocholithiasis..

  1. Choledocholithotripsy
  2. Choledochotomy
324
Q

Which organ in te body is the first to encounter toxins?

A

Liver

325
Q

What types of toxins are more problematic in cattle and sheep?

A

Chemical

326
Q

What drugs can cause liver toxicity in horses?

A
  1. Erythromycin
  2. Rifampin
  3. Diazepam
  4. Sulfonamides
  5. Aspirin
327
Q

What do mycotoxins cause in the liver?

A

Megalocytosis

328
Q

In what large animal species are mycotoxins more problematic and why?

A

Ruminants because they accept moldy feed

329
Q

What toxin causes chronic megalocytic hepatopathy and chronic, delayed hepatic failure?

A

Pyrrolizidine alkaloid containing plants

330
Q

How does pyrrolizidine toxicity occur when it is unpalatable?

A

If forage is sparse and animals are hungry, dried plants can get into hay/silage, seeds can be includes in the ration

331
Q

What is the lethal dose of pyrrolizidine alkaloids?

A

200-250mg/kg BW

332
Q

What species are resistant to pyrrolizidine alkaloids?

A

Goats and sheep

333
Q

What common plants contain pyrrolizidine alkaloids?

A
  1. Ragwort
  2. Salvation jane
  3. Common heliotrope
  4. Lantana
334
Q

How does pyrrolizidine alkaloids cause liver failure?

A

The toxic pyrroles crosslink double-stranded DNA blocking hepatocytes from dividing leading to chronic megalocytic hepatopathy. This change causes hepatocellular death which are replaced with connective tissue distrupting bloow flow and regeneration.

335
Q

What are the clinical signs of pyrrolizidine alkaloid toxicity in horses? Cattle?

A
  1. Weight loss
  2. Icterus
  3. Hepatic encephalopathy
  4. Abortion
  5. Photosensitization
  6. Diarrhea
  7. Diarrhea
  8. Weight loss
  9. Tenesmus
  10. Proapsed rectum
  11. Ascites
336
Q

Pyrrolizidine alkaloid toxicity is chronic and subclinical until an acute presentation of hepatic failure with photosensitization and hepatic encephalopathy occurs..why does this all of a sudden occur?

A

Loss of hepatic mass reaches a critical threshold

337
Q

What is a poor prognostic indicator in horses with pyrrolizidine toxicosis?

A

Bile acids > 50 umol/L

338
Q

What do hepatic enzymes look like with pyrrolizidine toxicosis?

A
  1. Elevated SDH, LDH< and FLDH if hepatocyte destruction occuring, will be normal if damage has been done
  2. Elevated GGT and ALP
339
Q

How can pyrrolizidine toxicosis be differentiated from other liver disease with a liver biopsy?

A

Megalocytosis with biliary hyperplasia and peri-portal fibrosis

340
Q

What will a liver look like that has been damaged by pyrrolizidine alkaloids?

A

Small, firm and discolored

341
Q

How is pyrrolizidine toxicosis treated?

A
  1. Supportive with control of the hepatic encephalopathy

2. Low protein, high energy diet

342
Q

What is the prognosis of pyrrolizidine toxicosis ?

A

If substantial fibrosis present (bridging), death will occur in 5-10 days once signs of liver failure start. If a horse retains appetite, they may recover. Can serial measure liver enzymes and bile acids to prognosticate.

343
Q

How is pyrrolizidine toxicosis prevented?

A
  1. Check dried feed
  2. Adequate feed to pastured animals
  3. Graze sheep on infested pasture
344
Q

How could you treat abnormal behavior in a large animal suffering from hepatic disease?

A
  1. Sedation: Low dose alpha 2’s
  2. Reduce ammonia production/absorption
  3. Analgesia
  4. Treat cerebral edema
  5. Treat acute hypoglycemia
345
Q

Why should you not use diazepam in large animals with hepatic disease?

A

Exacerbates hepatic encephalopathy through action on GAB, duration of action too short, and worsens ataxia

346
Q

What are poor prognostic indicators in large animals with hepatic disease?

A
  1. Hemolysis
  2. Hepatic encephalopathy
  3. Severe metobolic acidosis
  4. Diarrhea
  5. Bridging necrosis/fibrosis on biopsy
  6. High serum bile acids
  7. Long PT
  8. Low albumin
347
Q

Which large animal liver diseases involve supportive therapy as the main treatment and if there is no evidence of severe chronic changes/fibrosis, have a good prognosis?

A
  1. Theilers

2. Cholangiohepatitis

348
Q

What can ben used to reduce blood ammonia in large animals with liver disease?

A 
1. acetic acid 
2 lactulose 
3. Oral neomycin
4. Metronidazole 
5. Mineral oil 
6. MgSO4
349
Q

T/F: You can combine mineral oil and MgSO2 when reducing blood ammonia.

A

FALSE

350
Q

Why is giving continuous IV fluids with 5% dextrose a good idea for liver disease patients?

A
  1. Decrease effort/energy spend on gluconeogenesis
  2. Decrease blood ammonia
  3. Address dehydration/shock
  4. Improve bile flow
351
Q

When should metabolic acidosis be treated and how?

A

If pH is < 7.1 and use alkalinizing IV fluid like lactated ringers. If they doesn’t work, use NAHCO2 (bicarb)

352
Q

Why do animals with liver disease sometimes develop hypokalemia and how does this contribute to increased serum ammonia levels?

A

The anorexia decreases potassium intake. The low potassium increases production and absorption of ammonia from the kidney and enhances intracellular movement of ammonia.

353
Q

What antioxidants can be used for therapy in hepatic disease patients?

A
  1. DMSO: cholelith destruction
  2. Mannitol: cerebral edema
  3. Vitamin E
354
Q

What anti-inflammatory can be given to hepatic disease large animal patients?

A

Banamine

355
Q

What is pergolide?

A

A medication used to treat hyperlipemic ponies with pituitary tumors

356
Q

What vitamins can you consider giving paraenterally on a weekly basis in hepatic disease large animal patients?

why would you give these?

A
  1. B1
  2. Folic acid
  3. A
  4. D
  5. E
  6. K1
    Given is cholestasis limits their uptake
357
Q

What medications may decrease hepatic fibrosis?

A
  1. Colchicine
  2. Cyclosporine
  3. Pentoxyfilline
358
Q

What herbs/alternative medicine can be used to treat hepatic disease?

A
  1. SAME
  2. Milk thistle
  3. Acupuncture
359
Q

What type of diet should large animal hepatic disease patients receive?

A

High carbohydrate and moderate protein rich in branched chain amino acids that is fed frequently in small portions.
Oat and grass hay best or 2 parts beet pulp: 1 part cracked corn in molasses

360
Q

What are some proteins that are rich in branched chain amino acids?

A

Sorghum, milo, beet pulp and bran have leucine, valine and isoleucine

361
Q

What diets should be avoided in large animals with hepatic disease?

A

High protein like alfalfa, legumes, spring grasses because can exacerbate signs of hepatic encephalopathy due to conversion of urea to ammonia.

362
Q

What large animal species are suceptible to hyperlipemia/hyperlipidemia?

A

Ponies,
Donkeys,
Mini horses

363
Q

How is hyperlipidemia/hyperlipemia caused?

A

A sudden drop of carbs in the diets either by starvation, anorexia, stress, weight loss or lactation leading to fat mobilization with hepatic accumulation

364
Q

What is the difference between hyperlipidemia and hyperlipemia?

A

Hyperlipidemia is reversible with triglycerides still less than 500mg/dL and no evidence of hepatic dysfunction whereas, hyperlipemia has triglycerides above 500, there are severe dysfunctional signs along with insulin resistant hyperglycemia and a high mortality.

365
Q

How is hyperlipidemia reversible?

A

If caloric intake is increased, fat will not be mobilized and stored in the liver.

366
Q

Why are azotemic animals more likely to acquire hyperlipidemia?

A

Lipid removal from the blood is inhibited due to the inhibition of lipoprotein lipase

367
Q

A minature horse presents with anorexia, depression, diarrhea, and a white coating of tongue, azotemia and myopathy. Triclyceride levels are over 500 ug/dL..what disease is this?

A

Hyperlipemia

368
Q

Why do large animals die from hyperlipemia?

A
  1. Metabolic dysfunction
  2. Liver rupture—> hemoabdomen
  3. Laminitis
  4. Lipid in liver, kidney, heart and skeletal muscle causing dysfunction
369
Q

How is hyperlipemia diagnosed?

A
  1. > 500mg/dl triglycerides
  2. White/yellow plasma
  3. Elevated bilirubin
  4. High TP on refractometer
  5. U/S: Hepatomegaly/increased echogenicity/loss of architecture
  6. Don’t need a biopsy
370
Q

How is hyperlipemia treated?

A
  1. Correct primary disease to alleviate anorexia
  2. Give palatable feeds in tube with IV dextrose 5%
  3. Insulin
  4. Wean foals
371
Q

A ewe is in the final 2 weeks of gestation and presents with anorexia, weakness and depression, appears to be blind and is star gazing with tremors and ataxia. What diseases could this be?

A
  1. Pregnancy toxemia
  2. Mastitis
  3. Hypocalcemia
  4. Polioencephalomalacia
  5. Enterotoxemia type D
  6. Toxicosis
372
Q

How is pregnancy toxemia diagnosed?

A
  1. Hypokalemia
  2. Hypocalcemia
  3. Ketonuria
  4. Metabolic acidosis
  5. Elevated free fatty acids
  6. Friable and fatty liver on necropsy
373
Q

What large animals can suffer from pregnancy toxemia?

A

Ewes with more than 1 fetus and does with 3 or more fetuses in the 3rd trimester or if they are underconditioned

374
Q

How does pregnancy toxemia occur?

A

The ewe/doe is unable to meet energy demands with rapid fetal growth and inadequate caloric intake

375
Q

How is pregnancy toxemia treated?

A
  1. Caesarian section/induce parturition with dexamethasone or PGF2
  2. Continuous infusion of glucose
  3. B vitamins
  4. Transfaunation
  5. Glucose precursors like propylene glycol
376
Q

How is pregnancy toxemia prevented?

A
  1. Provide excellent quality forage
  2. Fetal sorting at day 45 to make sure ewe/does with more than 1/2 fetuses get the proper nutrition
  3. Serial measurement of plasma BHB to asses nutritional adequacy
377
Q

What is fat cow syndrome?

A

Mobilizaton of fat to liver of post parturient dairy cows stimulated by negative energy balance and hormonal changes of parturition

378
Q

What are the clinical signs of fat cow syndrome?

A

Over-conditioned cow after calving has anorexia, weight loss, and depression of rumen motility and lactation

379
Q

How is fat how syndrome diagnosed?

A
  1. Ketonuria
  2. Normal liver enzymes
  3. Hypoglycemia (maybe)
  4. Liver biopsy isn’t helpful as lipidosis is present in normal post-parturient cows without disease
380
Q

What percentage of liver fat values on a liver biopsy correlates to clinical signs in fat cow syndrome?

A

> 34%

381
Q

How is fat cow syndrome treated?

A

It has a 25% mortality, so you have to treat predisposing disease and address the negative energy balance and lipidosis

382
Q

How is fat cow syndrome prevented?

A
  1. Prevent obesity in late lactation with a 12-13 month calving interval with make changes before the dry period
  2. Adequate protein in the dry period with good quality roughage with added grain 2-4 weeks prior to calving
383
Q

What is the lancet fluke and where do adults reside/shed eggs and what does this cause?

A

Dicrocoelium dendriticum

Bile ducts where is causes inflammation, cirrhosis, and hepatic insufficiency

384
Q

What part of dicrocoelium infects the definitive host (goats, sheeps, and cattle) ?

A

Metacercariae in ants

385
Q

What are the clinical signs of a dicrocoelium parasitism?

A
  1. Weight loss
  2. Depression
  3. Anemia
  4. Hypoproteinemia
  5. Submandibular edema
386
Q

How is dicrocoelium, faciola hepatic, and fascioloides magna diagnosed and treated?

A
  1. Fecal sedimination exam

2 Albendazole

387
Q

What are the set of differential diagnosis for a Dicrocoelium parasitism?

A
  1. Chronic fascioliasis
  2. GI helminthiasis
  3. Johnes
388
Q

What is the difference between fascioloides magna and fasciola hepatica?

A

Fascioloides magna occurs in greater numbers, has a broader geographic distribution, and is a variety of snail hosts.

389
Q

How is the disease caused by fascioloides magna different in cattle versus sheep/goats?

A

Cattle: It is a dead end host where it rapidly gets encapsulated and only causes condemnation of the liver, but not real significant clinical signs.
Sheep/goats: Unlimited migration that can cause severe hepatic insufficiency

390
Q

When does fasciola hepatica occur and where?

A

In late fall/winter in habitats that are wet for >6 months and >50F…it is very climate sensitive

391
Q

What are the three syndromes fasciola hepatica can cause?

A
  1. Subclinical disease and production loss
  2. Anemia, ill thrift, and hepatic dysfunction
  3. Acute illness and sudden death from Clostridium novyi and haemolyticum
392
Q

What are the clinical signs of a cow with subclinical fasciola hepatica disease?

A
  1. Reduced weight gain, feed efficiency, and lactation

2. Anemia, hypoproteinemia, bottle jaw

393
Q

How is depression anemia and biliary hyperplasia caused by fasciola hepatica?

A

The flukes produce proline which causes the anemia and hyperplasia

394
Q

How long do fasciola hepatica flukes survive and when does the body amount an immune response to them?

A

They survive more than 12 months, but an immune response occurs 5-6 months post infection

395
Q

What species is most susceptible to fasciola hepatic disease? Why?

A

Sheep and goats

Fluke entry to bile ducts can be fatal

396
Q

What are the clinical signs of a bile ducts being invaded by liver flukes in sheep and goats?

A
  1. Ascites (acute and chronic)
  2. Hemoabdomen (acute)
  3. Pallor (acute)
  4. Icterus (acute)
  5. Edema (chronic)
  6. Emaciation (chronic)
397
Q

What is seen on a blood chem and CBC in an ruminant with fasciola hepatica infection?

A
  1. Depression anemia
  2. Hypoproteinemia
  3. Mild eosinophilia
  4. Elevated hepatic enzymes
398
Q

How do you distinguish fasciola hepatica from paramphistomum?

A
  1. If albendazole doesn’t kill off the adult liver flukes and some are still seen on sedimination, it is paramphistomum.
  2. Paramphistomum has smaller, grey eggs
  3. Necropsy
399
Q

What medication can kill juvenile >6month fasciola hepatica?

A

High dose clorsulon

400
Q

What disease that kills fasciola hepatica adults can only be used in lactating animals?

A

Albendazole

401
Q

How should treatment for fasciola hepatica be timed?

A

Treat when flukes are older than 12 months after the transmission season ends and remove treatment while they are < 6 months old

402
Q

What are common clinical signs signs that are very suggestive of liver disease in large animals?

A
  1. Icterus
  2. Hepatic encephalopathy
  3. Secondary Photosensitization
403
Q

What leakage enzymes in large animals indicate possible liver damage? Which are most commonly measured?

A
  1. AST ( most common)
  2. SDH (most common)
  3. ALT
  4. GLDH
  5. LDH 5
404
Q

If unconjugated bilirubin is increased in the plasma, what might this indicate?

A
  1. Hemolysis
  2. Decreased uptake into hepatocytes
  3. Disturbed intracellular protein binding/conjugation
405
Q

If conjugated bilirubin is high in blood serum, what might this indicate?

A
  1. Disturbed secretion of conjugated bilirubin in canaliculi
  2. Intra or extra hepatic bile obstruction
406
Q

What can cause hypoglycemia in horses?

A
  1. Liver failure
  2. Strangulating colic w/ sepsis
  3. Sepsis in foals
  4. Paraneoplastic
  5. Iatrogenic (insulin)
407
Q

What are differentials for hepatic encephalopathy?

A
  1. GI associated hyperammonemia (colic/colitis)
  2. Trauma
  3. Rabies
  4. Viral encephalomyelitis
  5. Leukoencephalomalacia
  6. Brain abscess
  7. Equine protozoal myelitis
  8. Botulism
  9. Heavy metal toxicity
408
Q

In which species is hypoalbuminemia uncommon with hepatic disease?

A

Horses

409
Q

What is sorbitol dehydrogenase (SDH) sensitive for?

A

Acute hepatocellular damage

410
Q

Measuring ALP is heplful in _______, but not _________.

A

Horses; ruminants

411
Q

What liver enzyme increases in young racehorses in training for unknown reasons?

A

GGT

412
Q

What can GGT refelct?

A

1.

Large Animal Medicine (9 decks)

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