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Ruminant Final > Anemia > Flashcards

Anemia Flashcards

1
Q

What are signs of RBC regeneration in ruminants?

A

Reticulocytes, macrocytic +/- hypochromic, anisocytosis, Howell-jolly bodies, rubricytosis, codocytosis, basophilic stippling

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2
Q

What are causes of hematuria in ruminants?

A

Pyelonephritis, cystitis, urolithiasis, enzootic hematuria, embolic nephritis

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3
Q

What are causes of hemoglobinuria in ruminants?

A

Leptospirosis, bacillary hemoglobinuria, copper toxicity, post-parturient hemoglobinuria, cold water intoxication

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4
Q

What are causes of myoglobinuria in ruminants?

A

Ionophore toxicity, cassia toxicity, capture myopathy

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5
Q

What type of Anaplasma affect cattle and small ruminants?

A

Cattle- Anaplasmosis marginale subsp. centrale
Small ruminants- Anaplasmosis ovis

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6
Q

Where in the US is Anaplasma endemic?

A

Western US

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7
Q

How is Anaplasma transmitted?

A

Tick borne or from biting flies (or iatrogenic)

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8
Q

When is Anaplasma usually spread?

A

Late spring and summer

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9
Q

Describe the pathology of Anaplasma

A

Replicates in red blood cells causing bacteremia, leads to splenic and hepatic macrophage mediated phagocytosis of RBCs, release of APP and inflammatory response

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10
Q

What are the clinical signs of Anaplasma?

A

<1 year old- subclinical
>2 years old- fever, depressed, anorexia/GI stasis, anemia, icteric or pale, aggression, death

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11
Q

How is Anaplasma diagnosed?

A

Identification of organism on blood smear, PCR, CBC, serology for carriers

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12
Q

How is Anaplasma treated?

A

Blood transfusions, tetracyclines, supportive care and minimizing stress

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13
Q

How is Anaplasma prevented/controlled?

A

Tick control, insecticide impregnated ear tags, new vaccine (only in CA)

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14
Q

How is Theileria transmitted?

A

By Asian longhorn tick

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15
Q

What is the causative agent of babesiosis?

A

Babesia bigemina and Babesia bovis

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16
Q

How is babesiosis spread?

A

Tick borne- Rhipicephalus and Ixodes

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17
Q

What are the clinical signs of babesia?

A

Fever, depression, diarrhea-constipation, icterus, anorexia, tachycardia/tachypnea, anemia, death

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18
Q

What are the signs of the cerebral form of babesia?

A

Hyperexcitability, aggressive, convulsions, coma, death

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19
Q

Which kind of babesia is more likely to cause cerebral disease?

A

Babesia bovis

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20
Q

Which animals are more prone to babesia?

A

Cattle >6 months and <5 years old moved to rough pasture

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21
Q

How is babesia diagnosed?

A

Blood smear, serology, or CBC

22
Q

How is babesia treated and controlled?

A

Imidocarb, blood transfusion if needed, control ticks

23
Q

What signs of babesia signal that the disease is advanced and prognosis is poor?

A

Icteric, black urine, weak and low temperature, hemic murmur heard on approach, PCV <10 or HR >140

24
Q

Describe bacillary hemoglobinuria

A

Caused by Clostridium novyi type D/ Clostridium hemolyticum, associated with Fasciola. Has acute onset- pyrexia, jaundice, abdominal pain, port-wine colored urine, usually fatal with short course. Vaccinate for prevention.

25
Q

What is the host specific type of Leptospirosis found in cattle in the US?

A

Leptospira hardjo bovis

26
Q

Describe the symptoms of Leptospira hardjo bovis

A

Chronic interstitial nephritis, infertility, stillbirth, abortion, weak calves, milk drop syndrome, agalactia/mastitis/bloody milk

27
Q

Is Leptospira hardjo bovis shed for a long duration?

A

Yes, may have lifelong shedding

28
Q

Describe the symptoms of non-host adapted Leptospirosis in cattle

A

Severe acute disease- interstitial nephritis, tubular nephrosis, abortion possible

29
Q

Is non-host adapted Leptospirosis shed in urine for the animal’s lifetime?

A

No, only shed for short duration

30
Q

How is Leptospirosis diagnosed?

A

Dark field microscopy, silver stain, PCR, microscopic agglutination test

31
Q

How is Leptospirosis treated and prevented?

A

Treatment- oxytetracycline
Prevention- vaccination, drain/fence off standing water, limit wildlife contact

32
Q

How does copper toxicity lead to icterus?

A

Copper accumulates in liver -> necroses parenchymal cells -> Kupffer cells swell -> blood glutathione reduced -> RBC fragility and hemoglobin oxidation and methemoglobin formation -> IV hemolysis

33
Q

What species is most sensitive to copper toxicity?

A

Sheep

34
Q

What are the clinical signs of copper toxicity in sheep?

A

Abrupt onset depression, anorexia, weakness, hemolytic crisis (anemia, methemoglobinemia, hemoglobinuria, icteric-muddy membranes)

35
Q

What are the clinical signs of copper toxicity in cattle?

A

Dyspnea, head pressing, ataxia, circling

36
Q

How is copper toxicity diagnosed?

A

CBC showing anemia and hemolysis, increased liver and renal enzymes on chem panel, increased copper levels in serum and liver
Post mortem- liver yellow/friable with centrilobular necrosis, hepatic fibrosis, and bile duct hyperplasia, “gunmetal blue” kidneys

37
Q

How is copper toxicity treated?

A

Ammonium molybdate, sodium thiosulfate, D-penicillamine, fluids, diuretics, blood transfusion, oxygen therapy, Vitamin E, molybdenum in the feed for animals less severely effected

38
Q

Which animals get water intoxication most commonly?

A

Calves on milk replacer who are then turned out to pasture

39
Q

What are the clinical signs of water intoxication?

A

Acute hemoglobinuria, hypothermia, salivation, muscle tremors, star gazing, ataxia, convulsions, IV hemolysis

40
Q

How is water intoxication treated?

A

Restrict water temporarily, provide hypertonic saline, corticosteroids, mannitol

41
Q

Describe post-parturient hemoglobinuria

A

Severe acute hypophosphatemia in first 4-6w of lactation, usually in high producing multiparous cows, seen as depression, weakness, anorexia, drop in milk yield, anemia, icterus, and hemoglobinuria

42
Q

Describe the causative agent of anthrax

A

Bacillus anthracis- gram positive rod that forms spores

43
Q

How is anthrax spread?

A

Spores are ingested in soil/plants

44
Q

What are the clinical signs of anthrax poisoning?

A

Blood tinged discharges from orifices, caudal vena cava thrombosis, bleeding ulcers, jejunal hemorrhage syndrome, lack of rigor mortis

45
Q

How is anthrax poisoning diagnosed?

A

Cytology and culture of blood sample or vitreous humor

46
Q

How is anthrax treated/prevented?

A

No treatment- REPORTABLE, ZOONOTIC, DO NOT NECROPSY
Prevent with vaccine, carcass disposal

47
Q

What are the clinical signs of abomasal ulcers?

A

Decreased appetite and milk production, melena, anemia, bruxism, tachycardia, abdominal pain/ileus, rumen stasis, dehydration, recumbency and cold extremities

48
Q

How are abomasal ulcers diagnosed?

A

Difficult- fecal occult blood is specific but not sensitive, mild cases often diagnosis of rule-out
CBC/chem showing anemia, hypoproteinemia, neutrophilia/penia, hemoconcentration, etc.
Abdominocentesis with malodorous, discolored, toxic changes in cells and intracellular bacteria for severe cases

49
Q

How are abomasal ulcers treated?

A

Treat concurrent disease, minimize stress, correct dietary problems, can give PPIs or H2 antagonists or sucralfate, supportive care

50
Q

Which abomasal ulcers have a good vs. bad prognosis?

A

I-III fair prognosis
IV grave prognosis

51
Q

What are the clinical signs of Haemonchus contortus?

A

Anemia, hypoproteinemia, submandibular edema, weakness, collapse

Ruminant Final (12 decks)

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