Anemia

Question 1

What are signs of RBC regeneration in ruminants?

Answer 1

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

Question 2

What are causes of hematuria in ruminants?

Answer 2

Pyelonephritis, cystitis, urolithiasis, enzootic hematuria, embolic nephritis

Question 3

What are causes of hemoglobinuria in ruminants?

Answer 3

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

Question 4

What are causes of myoglobinuria in ruminants?

Answer 4

Ionophore toxicity, cassia toxicity, capture myopathy

Question 5

What type of Anaplasma affect cattle and small ruminants?

Answer 5

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

Question 6

Where in the US is Anaplasma endemic?

Answer 6

Western US

Question 7

How is Anaplasma transmitted?

Answer 7

Tick borne or from biting flies (or iatrogenic)

Question 8

When is Anaplasma usually spread?

Answer 8

Late spring and summer

Question 9

Describe the pathology of Anaplasma

Answer 9

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

Question 10

What are the clinical signs of Anaplasma?

Answer 10

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

Question 11

How is Anaplasma diagnosed?

Answer 11

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

Question 12

How is Anaplasma treated?

Answer 12

Blood transfusions, tetracyclines, supportive care and minimizing stress

Question 13

How is Anaplasma prevented/controlled?

Answer 13

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

Question 14

How is Theileria transmitted?

Answer 14

By Asian longhorn tick

Question 15

What is the causative agent of babesiosis?

Answer 15

Babesia bigemina and Babesia bovis

Question 16

How is babesiosis spread?

Answer 16

Tick borne- Rhipicephalus and Ixodes

Question 17

What are the clinical signs of babesia?

Answer 17

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

Question 18

What are the signs of the cerebral form of babesia?

Answer 18

Hyperexcitability, aggressive, convulsions, coma, death

Question 19

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

Answer 19

Babesia bovis

Question 20

Which animals are more prone to babesia?

Answer 20

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

Question 21

How is babesia diagnosed?

Answer 21

Blood smear, serology, or CBC

Question 22

How is babesia treated and controlled?

Answer 22

Imidocarb, blood transfusion if needed, control ticks

Question 23

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

Answer 23

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

Question 24

Describe bacillary hemoglobinuria

Answer 24

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.

Question 25

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

Answer 25

Leptospira hardjo bovis

Question 26

Describe the symptoms of Leptospira hardjo bovis

Answer 26

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

Question 27

Is Leptospira hardjo bovis shed for a long duration?

Answer 27

Yes, may have lifelong shedding

Question 28

Describe the symptoms of non-host adapted Leptospirosis in cattle

Answer 28

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

Question 29

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

Answer 29

No, only shed for short duration

Question 30

How is Leptospirosis diagnosed?

Answer 30

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

Question 31

How is Leptospirosis treated and prevented?

Answer 31

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

Question 32

How does copper toxicity lead to icterus?

Answer 32

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

Question 33

What species is most sensitive to copper toxicity?

Answer 33

Sheep

Question 34

What are the clinical signs of copper toxicity in sheep?

Answer 34

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

Question 35

What are the clinical signs of copper toxicity in cattle?

Answer 35

Dyspnea, head pressing, ataxia, circling

Question 36

How is copper toxicity diagnosed?

Answer 36

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

Question 37

How is copper toxicity treated?

Answer 37

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

Question 38

Which animals get water intoxication most commonly?

Answer 38

Calves on milk replacer who are then turned out to pasture

Question 39

What are the clinical signs of water intoxication?

Answer 39

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

Question 40

How is water intoxication treated?

Answer 40

Restrict water temporarily, provide hypertonic saline, corticosteroids, mannitol

Question 41

Describe post-parturient hemoglobinuria

Answer 41

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

Question 42

Describe the causative agent of anthrax

Answer 42

Bacillus anthracis- gram positive rod that forms spores

Question 43

How is anthrax spread?

Answer 43

Spores are ingested in soil/plants

Question 44

What are the clinical signs of anthrax poisoning?

Answer 44

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

Question 45

How is anthrax poisoning diagnosed?

Answer 45

Cytology and culture of blood sample or vitreous humor

Question 46

How is anthrax treated/prevented?

Answer 46

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

Question 47

What are the clinical signs of abomasal ulcers?

Answer 47

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

Question 48

How are abomasal ulcers diagnosed?

Answer 48

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

Question 49

How are abomasal ulcers treated?

Answer 49

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

Question 50

Which abomasal ulcers have a good vs. bad prognosis?

Answer 50

I-III fair prognosis IV grave prognosis

Question 51

What are the clinical signs of Haemonchus contortus?

Answer 51

Anemia, hypoproteinemia, submandibular edema, weakness, collapse