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Ruminant Medicine Spring 2016 > L11: Ruminant Hemolymphatic Diseases (Maunsell) > Flashcards

L11: Ruminant Hemolymphatic Diseases (Maunsell) Flashcards

1
Q

Anemia etiology

A

A decrease in RBC mass as measured by reduced RBC numbers, PCV, and hemoglobin levels

  • reduced ability of blood to supply oxygen to the tissues
  • results from blood loss, hemolysis, and/or decreased production
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2
Q

Normal PCV fro ruminants

A

27-48%

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3
Q

PE of the hemic system

A
  • mm (color, CRT, hemorrhages)
  • color and consistency of urine and feces
  • eval the heart
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4
Q

CS of anemia

A
  • tachycardia
  • tachypnea, dyspnea
  • mm pallor icterus
  • heart murmur
  • weakness
  • exercise tolerance
  • collapse, death
  • signs specific to cause of anemia (ie. Melena)
  • acute vs. chronic manifestation of signs
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5
Q

Chronic anemia: usually won’t see CS until PCV is?

A
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6
Q

Acute anemia: usually won’t see CS until PCV is?

A
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7
Q

Approach to anemic ruminants (10 steps)

A

1) complete hx and PE
2) check urine for hemaglobinuria since most hemolytic anemias in ruminants will cause this (except anaplasmosis)
3) PCV/TP, look at plasma color
4) fecal float
5) CBC: regenerative or non-regenerative?
6) Chem +/- blood gas
7) fecal occult blood
8) thoracic/abd U/S and/or rads, ab tap
9) bone marrow aspirate sometimes indicated
10) copper/toxin testing

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8
Q

If during anemia work-up the plasma is discolored, what should you do?

A

Work-up for destruction

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9
Q

If during anemia work-up the plasma is not discolored and protein is low, what should you do?

A

Work-up for external loss

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10
Q

If during anemia work-up the plasma is not discolored and protein is normal, what should you do?

A

Work-up for chronic disease, iron/copper/cobalt deficiency, bone marrow toxins

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11
Q

Approach to anemic camelids

A
  • bone marrow evaluation remains the best way to evaluate red blood cell regeneration
  • camelids produce retics as a regenerative response, but rarely >1.5%. Therefore retics, anisocytosis, polychromasia, and nucleated RBCs are not predictable in magnitude
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12
Q

Site of bone marrow aspirate in ruminants

A

3rd or 4th sternal vertebrae

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13
Q

Site of bone marrow aspirate in camelids

A

3-4cm dorsal to the callous on ventral sternum

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14
Q

Indications for ruminant blood transfusions

A
  • based on CS***
  • low but STABLE PCV of 12-20% does NOT necessitate
  • PCV 25% above normal
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15
Q

How long do cross-matched cells survive after transfusion?

A

2-4 days

25% RBCs survive 4 days
2nd transfusion may only last a few hours
must treat primary cause!

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16
Q

When NOT to transfuse

A
  • maniacal behavior
  • poor temperament (stress from handling can –> death)
  • animal over the crisis and stable
  • anaphylaxis
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17
Q

How to determine how much blood to transfuse for a ruminant >50kg

A
  • 10ml/kg or calculate
  • usually don’t give >6L total

Def = [(desired PCV - recipient PCV)/donor PCV] x recipient BW x Bl volume (ml/kg)

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18
Q

How to determine how much blood to transfuse for a ruminant

A

Calculate deficit using BV = 100 ml/kg neonates, 70-80 for adults. Replace 20-50%

Def = [(desired PCV - recipient PCV)/donor PCV] x recipient BW x Bl volume (ml/kg)

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19
Q

How much blood can a (nonpregnant) donor donate?

A

20% of its blood volume (10-15 ml/kg) at 2-4 week intervals

4-6L for adult cattle
0.5-1 L for adult sheep goats
1-2 L for adult camelids

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20
Q

Causes of anemia

A
  • blood loss
  • hemolytic anemias (infectious and non-infectious)
  • inadequate production
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21
Q

Cattle with what antigen more commonly get transfusion reactions?

A

J positive

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22
Q

Cattle donors should test negative for what diseases to be blood donors?

A

BLV
BVDV

(CAE for goats)

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23
Q

Steps of blood transfusion

A

Collect from donor using aseptic technique:

2) clip and prep donor
3) place catheter
4) collect into sterile commercial kit bags or into bottles containing ACD
5) administer to patients through an in line filter to remove small clots, fibrin strands, and debris
6) initially administer slowly (0.1 mg/kg) for the first 10-15 minutes then up to 20 ml/kg/hr

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24
Q

Signs of transfusion rxn

A
  • anaphylaxis or CV overload
  • urticaria, shivering, sweating early
  • tachycardia
  • tachypnea
  • fever
  • colic
  • pulmonary edema
  • hemaglobinuria
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25
Q

Tx for severe transfusion reaction

A

-epinephrine

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26
Q

Tx for mild transfusion rxn

A
  • slow transfusion
  • flunixin meglumine
  • corticosteroids
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27
Q

Causes of inadequate production or bone marrow suppression leading to anemia

A
  • nutritional (Fe, Cu, Co deficiencies)
  • chronic dz
  • renal dz
  • BM toxins (bracken fern, citrus)
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28
Q

Causes of hemolysis

A
  • infectious
  • Heinz body hemolytic anemia (due to toxicity)
  • post-parturient hemaglobinuria
  • water intoxication
  • other (congenital porphyria, IMHA)
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29
Q

Causes of acute blood loss

A
  • injuries during birth
  • trauma
  • castration, dehorning
  • secondary to other disease (abomasal ulcer, caudal vena cava syndrome)
  • bleeding from umbilicus at birth
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30
Q

Common causes of CHRONIC blood loss

A
  • internal parasites
  • external blood-sucking parasites
  • abomasal ulcers
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31
Q

Causes of anemia due to hemostatic dysfx

A
  • moldy sweet clover (dicoumarol) toxicity

- DIC (rare)

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32
Q

Etiology of moldy sweet clover (dicoumarol) toxicity

A
  • most common in north-central states
  • natural coumarols in the plant are converted to dicoumarol by molds during poor storage conditions
  • causes increased PT, aPTT, normal platelet count
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33
Q

CS of dicoumarol toxicity

A
  • lameness
  • epistaxis
  • melena
  • SC hematomas
  • bleeding from injection sites
  • hematuria
  • bloody milk
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34
Q

Tx of dicoumarol toxicity

A
  • remove access to moldy feed
  • Vit. K1
  • transfuse if anemia is life-threatening
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35
Q

Clinical progression of anemia

A

Acute: present with hypovolemic shock
After 12-24h: decreased PCV/TP, increased retics (esp. w/ acute loss), no icterus or hemaglobinuria

After 4d: polychromasia, basophilic stippling, Howell-Jowell bodies
Chronic: iron stores eventually depleted –> poor regenerative response

36
Q

CS of hemolytic anemia

A
  • varies w/ underlying disease and severity
  • fever common
  • hemaglobinuria and hemaglobinemia if large amount of IV hemolysis
  • icterus
37
Q

Clin path of ruminant hemolytic anemias

A
  • regenerative response usually observed
  • may have intra or epi-cellular organisms, or Heinz bodies
  • increased UNCONJUGATED bilirubin (if conjugated, more likely due to liver disease)
38
Q

Infectious causes of hemolytic anemia

A
  • anaplasma marginale* (most important in US cattle)
  • Eperythrozoonosis (most important in camelids)
  • Babesia (eradicated)
  • Bacterial infections (Leptospira interrogans, Clostridium haemolyticum)
39
Q

Bovine Anaplasmosis**

A
  • rickettsial parasite of cattle
  • causes anemia via reticuloendothelial phagocytosis of RBCs
  • acute infection causes 5-70% of RBCs to be parasitized!
  • suspect if have severe anemia + icterus + no hemaglobinuria**
40
Q

How long does it take to see a regenerative response after an acute hemolytic event in cattle?

A

4d

41
Q

Hemotrophic mycoplasmas by species

A

M. Wenyonii –> cattle
M. Ovis –> sheep and goats
M. Haemolamae –> camelids

42
Q

Etiology of hemotrophic mycoplasmas by species

A

Cattle and goats: most infections latent
Sheep: uncommon cause of anemia in young lambs
Camelids: important cause of hemolytic anemia in crias

*pathogenesis poorly understood; causes IV and EV hemolysis

43
Q

Transmission, Dx, and Tx of hemotrophic mycoplasmas

A

Trans: blood-sucking vectors, iatrogenic, and vertical
Dx: blood smears (low sensitivity), PCR
Tx: oxytetracycline, supportive care, transfuse PRN

44
Q

Etiology of Bovine babesiosis

A
  • Cause: Babesia bovis, B. Bigemina, and B. Divergens parasites
  • most important arthropod-borne dz of cattle worldwide**
  • also affects deer, bison, buffalo
45
Q

Bovine babesiosis vectors

A 
Rhipicephalus ticks
(Mechanical transmission can also occur)
46
Q

CS of bovine babesiosis (by age)

A

Calves: usually subclinical (become asymptomatic carriers/reservoir)
1-2 yrs: moderate dz
>2 yrs: often fatal

47
Q

Etiology of babesiosis outbreaks

A

Endemic areas: outbreaks occur when stress/naive cattle are introduced, or exposure of young animals to ticks is interrupted

Marginal or previously tick-free areas: major epizootics with high morbidity and mortality in cattle

48
Q

Lifecycle of bovine babesiosis

A
  • transovarial transmission in the tick
  • infects bovine RBCs
  • merozoites emerge causing IV RBC destruction
  • incubation period = 2-3 weeks
49
Q

Cerebral babesiosis –>

A 
Ataxia
Hyperexcitability
Convulsions
Opisthotonus
Coma 
Death
50
Q

Control of babesiosis

A
  • Bos indicus more resistant
  • tick control and eradication
  • live vaccines
51
Q

Tx of babesiosis

A
  • supportive care only

- treat anemia

52
Q

Bacillary hemaglobinuria agent

A

Clostridium haemolyticum

-common soil contaminant in poorly drained regions of the US where liver flukes occur

53
Q

Etiology of Bacillary Hemaglobinuria

A

Liver fluke damage and spores ingested –> vegetative stage, proliferation –> exotoxins causing IV hemolysis, necrosis of liver

54
Q

CS of bacillary hemaglobinuria

A
  • often found dead

- fever, hemaglobinuria

55
Q

Dx/Tx/Prevention of bacillary hemaglobinuria

A

Dx: coagulative necrosis in liver, impression smears reveal large G+ rods, FA diagnostic

Tx: penicillin or oxytet, fluids/transfusion, supportive care. Often found dead

Prevent: vaccine effective but short-lived. Must re-vax q6 mos.

56
Q

Lepto in cattle etiology and transmission

A
  • causes acute hemolytic syndrome in calves and lambs
  • L. Interrogans usually
  • uncommon in North America
  • not host adapted; shedding is short-lived if animal survives
  • transmitted via contact w/ env, urine-contaminated feed or water
57
Q

Acute hemolytic syndrome in lepto

A
  • pathogenesis poorly understood
  • anemia partially immune-mediated
  • only occurs in young animals
  • interstitial nephritis occurs
58
Q

CS of lepto

A

-fever
-depression
-icterus
+/- signs of anemia
-petechia
-hemoglobinuria

59
Q

Dx of lepto

A
  • serology (Microagglutination test)

- Ag detection

60
Q

Tx and control of lepto

A

Tx: oxytet, cephalosporins; supportive care, transfusions if anemia life-threatening
Prevent: routine vaccines annually or q6mo.

61
Q

Heinz body hemolytic anemia: etiology

A

Toxic agent –> oxidative denaturation of Hb –> aggregation of globin protein, appearing as Heinz body inclusions

  • anemia occurs due to IV rupture of cells and EV removal
  • renal damage 2ary to severe hemaglobinemia and acute renal failure are common
62
Q

Brassica and onion toxicities

A
  • ingestion of large amounts of Brassica family plants or small amounts of onions –> non-specific signs of anemia, icterus, hemaglobinuria, +/- fever (Heinz body hemolytic anemia)
  • tx = stop exposure, provide supportive care, fluids +/- transfusion
63
Q

2 toxicities that –> Heinz body hemolytic anemia

A
  • Brassica/onion

- Copper

64
Q

Cause of copper toxicity

A
  • chronic Cu >20 ppm or relative excess if Molybdenum is deficient (Cu:Mb >6:1)
  • inappropriate sulfur lvls in the diet
  • culprits: horse or pig feed, poultry waste used as feed or fertilizer for crops
65
Q

Susceptibility to Cu toxicity: Sheep vs goats vs cattle

A

Sheep > goats > cattle

66
Q

Distribution of plasma Cu in the body. Where does excess Cu go?

A

80% protein-bound
20% ionized and internalized by hepatocytes and stored to be used for ceruloplasmin synthesis

-high dietary Cu is buffered by hepatic storage until critical threshold is breached, causing hepatic necrosis, release of large amt. of Cu into the blood, and massive oxidative damage to RBCs and IV hemolysis –> Heinz body formation, methemoglobinemia

67
Q

CS of copper toxicity

A
  • hemaglobinuria, methemaglobinuria
  • icterus
  • abortion
  • metallic kidneys
  • pale yellow liver
68
Q

Dx of copper toxicity

A
  • Excessive liver Cu

- plasma Cu will be elevated in acute toxicity or crisis, but may be normal in chronic Cu

69
Q

Tx/prevent of copper toxicity

A
  • supportive care
  • ammonium tetrathiomolybdate IV
  • oral Cu-binders

Prevent: species appropriate feed, watch Cu:Mo balance

70
Q

Post-parturient hemoglobinuria etiology

A
  • syndrome of dairy cattle worldwide
  • occurs in high producing multiparous cows, usually in first month post-calving
  • assoc. w/ hypophosphatemia
  • not fully understood
  • occurs sporadically
71
Q

CS of post-parturient hemoglobinuria

A
  • severe anemia
  • icterus
  • hemoglobinuria
  • marked hypophosphatemia
  • anemia regenerative after 4 days
72
Q

Tx/prevent of PP hemoglobinuria

A

Tx: supportive care, transfusion PRN, supplement phosphorus IV and oral

Prevent: correct diet

73
Q

Water intoxication etiology

A
  • massive water intake can cause hypotonicity of body fluids and IV hemolysis due to osmotic lysis
  • dairy calves most susceptible (esp. Before 5 months old)
74
Q

CS/clin path of water intoxication

A
  • depression, resp. Distress, convulsions, coma
  • severe hemoglobinuria
  • anemia, hypoproteinemia, hyponatremia, hypochloremia, hyposmolality
75
Q

Tx of water intoxication

A
  • temporarily restrict water intake

- correct sodium imbalance slowly w/ hypertonic saline

76
Q

Causes of anemia due to decreased RBC PRODUCTION

A
  • mineral deficiency (Fe, Cu, Co)

* characterized by NO icterus, hemolysis, and non-regenerative)

77
Q

Fe deficiency anemia

A
  • usually due to chronic blood loss, not low dietary iron
  • causes a microcytic hypochromic anemia
  • tx: must tx primary problem (ie. Parasites); can give oral Fe supplements
  • injectable Fe products in ruminants can cause liver necrosis, anaphylaxis
78
Q

Copper deficiency etiology

A
  • can be primary or secondary to high dietary Mo, sulfates, Zn, or Fe
  • young growing animals most susceptible
  • Cu required for transport of Fe and incorporation into heme molecules
79
Q

CS of Primary Cu deficiency

A

Primary:

  • poor growth
  • depigmented hair coat
  • diarrhea
  • spontaneous fxs
  • epiphysitis
  • “Sway back” (demyelinization) in lambs
  • anemia (moderate, progressive, microcytic hypochromic)
80
Q

CS of 2ary Cu deficiency

A
  • profuse watery diarrhea
  • weight loss
  • unthriftiness
81
Q

Cu and cobalt deficiency results in:

A

Salt Sickness

-most common in S. FL cattle

82
Q

Dx/Tx of Cu deficiency

A

Dx: liver biopsy
Tx: dietary supplementation of Cu and correction of Cu:Mo imbalances when possible

83
Q

Anemia due to decreased RBC production

A
  • anemia secondary to CHRONIC disease ie. Chronic inflammation from parasites, abscess, Johne’s dz, cancer
  • chronic elevations in pro-inflammatory cytokines and acute phase proteins stimulate sequestering of iron in liver and BM
  • results in mild chronic normocytic normochromic anemia
  • tx: treat the primary dz process
84
Q

Bracken Fern Toxicosis

A
  • cattle most susceptible
  • causes bone marrow depression, pancytopenia
  • CS: fever, melena, epistaxis, hematuria, petechia, bleeding
  • Tx: supportive care, transfusion, remove from source
  • Poor prognosis
85
Q

Causes of anemia due to LOSS in camelids

A
  • intestinal parasites
  • trauma
  • hemorrhage
  • GI ulcers
  • coagulopathy
86
Q

Causes of anemia due to LYSIS in camelids

A
  • red maple toxicity
  • immune mediated
  • M. Haemolamae
  • copper toxicity
  • hypophosphatemia
87
Q

Causes of anemia due to DECREASED PRODUCTION in camelids

A
  • chronic inflammation/infection
  • renal dz
  • neoplasia
  • Fe deficiency

Ruminant Medicine Spring 2016 (18 decks)

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