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Y3 SPRING > AG MED - Hematopoeitic Disorders 2 > Flashcards

AG MED - Hematopoeitic Disorders 2 Flashcards

1
Q

5 infectious causes of RBC destruction

A

Anaplasmosis
Babesiosis
Haemobartonellosis (Eperythrozoonosis)
Leptospirosis
Bacillary hemoglobinuria

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2
Q

Which infectious cause of RBC destruction is eradicated in ruminants in the US?

A

Babesiosis

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3
Q

Babesiosis is caused by an _________ of RBCs.

Name 2

Transmission of babesiosis is by ______.

A

Obligate intracellular parasite

Babesia bovis
Babesia bigemina

one-host tick: Rhipicephalus spp (formerly Boophilus)

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4
Q

Clinical signs of babesiosis

A

2-3 week incubation
Pyrexia (104 - 107.6 F)
Depression, icterus, anorexia, tachycardia, tachypnea
Anemia: intravascular destruction of RBCs by escaping merozoites
Hemoglobinemia
***Hemoglobinuria
Abortion
Death
Cerebral babesiosis

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5
Q

Babesiosis - Clin path

A

Anemia with regeneration

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6
Q

Babesiosis - DX

A

ID Babesia on Giemsa-stained blood smear (acute infections)

Serology IFA/ELISA (Ab present 7 days post infection)

PCR

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7
Q

Babesiosis - TX

A

Imidocarb
Diminazene
Phenamidine
Amicarbalide

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8
Q

What are two indications of poor prognosis for Babesiosis?

A

PCV < 10% and neuro signs

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9
Q

Babesiosis - Prevention

A

Removal of tick vector
(Experimental) immunization - live organisms into calves

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10
Q

Haemobartonellosis
Etiology for cattle, sheep, camelids and swine

A

Hemotropic mycoplasmas

Cattle - Mycoplasma wenyonii
Sheep - Mycoplasma ovis
Camelids - Mycoplasma haemolamae
Swine - Mycoplasma suis

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11
Q

Haemobartonellosis - Epidemiology

Location:
Age and condition:
Transmission:

A

Worldwide but generally a minor disease
Young, stressed animals; carrier animals
Transmission via blood - insects, needles, castration
Intrauterine transmission = lifelong infection

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12
Q

Haemobartonellosis - Clinical Signs

Incubation period:
Cattle CS:

A

Incubation period = 1-3 weeks

Cattle
- RARE clinical disease
- fever, stiff gait
- decreased milk production; udder edema
- diarrhea
- lymphadenopathy - prefemorals
- scrotal swelling
- swollen legs / stocked up

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13
Q

Haemobartonellosis - Clinical signs in sheep

A

RARE sudden death with hemoglobinuria and icterus

Less severe disease with fever, depression, anemia and weight loss

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14
Q

Haemobartonellosis - Camelids

Clinical Signs
Mode of Transmission
DX

A

Variable clinical signs
Anemia, depression, fever, weight loss
Hypoglycemia common in camelids
Mode of transmission - infected blood: biting insects, needles, etc.
In utero transmission - 2006 case report
PCR available for dx

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15
Q

Haemobartonellosis - DX and Clin path

A

Epicellular parasite on RBC
Anemia

CF, ELISA, PCR

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16
Q

Haemobartonellosis TX

A

Oxytetracycline
LA 200
up to 50 days
May not eliminate carrier state

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17
Q

Is leptospirosis zoonotic?

A

YES

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18
Q

Syndromes of leptospirosis

A

Abortion
Hemolytic anemia
Septicemia
Mastitis
Combination of above

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19
Q

Leptospirosis is caused by:

Which serovars have hemolysins and yield hemolytic diseases?

What are the other four serovars?

A

Leptospira interrogans

Pomona and icterohemorrhagia

Grippotyphosa
Hardjo
Swajizik
Bratislava

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20
Q

Leptospirosis

Incubation:
Age / animals affected:

What are the clinical signs for the hemolytic form of leptospirosis?

When does death occur?

What is the recovery timeline?

A

Incubation 3-7 days
Young calves, lambs, kids, crias (adults)

Fever
Anorexia, depression
Petechia
*** Hemoglobinuria
Anemia
Icterus
Tachycardia, dyspnea

Death in 2-3 days
Slow recovery

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21
Q

Leptospirosis clin path

A

Moderate leukocytosis
Elevated fibrinogen
Hemoglobinemia
Hemoglobinuria

22
Q

Leptospirosis DX

A

Based on demonstration of organism in urine, milk, or fetal tissues

MAT, PCR, FAT

23
Q

Treatment of leptospirosis

A

Oxytetracycline
Streptomycin
Procaine Pen-G
Supportive care

24
Q

Prevention of leptospirosis

A

Vaccination
Removal of carriers - dogs, cats, vermin

25
Another name for bacillary hemoglobinuria
Redwater
26
What is bacillary hemoglobinuria?
Acute Fatal Clostridial disease Causes Liver infarct, toxemia, intravascular hemolysis
27
What causes bacillary hemoglobinuria? What is the major toxin and what does it do? When do most outbreaks occur?
Clostridium novyi type D Beta toxin causes hepatic necrosis, hemolysis, and damage to capillary endothelium Most outbreaks in summer/early fall - usually follow flooding
28
Bacillary Hemoglobinuria - Pathophysiology ______ ingested by animal cross intestinal mucosa and are transported to the _____ via ________. Persist in ________ cells. Localized ______ areas promote germination - ____________. Release of toxins increase anaerobic environment causing further ____ and ______. Absorption of toxins causes ________.
Spores ingested by animal cross intestinal mucosa and are transported to the liver via macrophages. Persist in Kupffer cells. Localized anaerobic areas promote germination - liver fluke tracts. Release of toxins increase anaerobic environment causing further bacterial growth and hepatic necrosis. Absorption of toxins causes intravascular hemolysis, icterus, hemoglobinuria, death.
29
Life cycle of flukes
Metacercariae (viable on grass for several months) ingested Flukes migrate through liver and mature Eggs shed 10-12 post infection Miracidium hatch after 2-4 weeks Mud snail Cercaria shed from snail after 6 weeks
30
Main clinical sign of bacillary hemoglobinuria
Sudden death
31
Antemortem clinical signs of bacillary hemoglobinuria
Less common - die fast Depression, anorexia, fever, tachypnea Rectal bleeding Severe hemoglobinuria - port wine colored Pale and icteric mucous membranes
32
Bacillary hemoglobinuria - clin path and DX
Rare to get chem panel and DX antemortem Anemia High AST, GGT, bilirubin Hemoglobinuria DX: fluorescent antibody test on impression smears of liver infarct Area, hx, clinical signs, necropsy
33
DFDX Bacillary hemoglobinuria
Anthrax Leptospirosis
34
TX bacillary hemoglobinuria & prognosis
High dose ABX: Penicillin or tetracycline Supportive care: multiple blood transfusions Grave prognosis
35
Prevention of bacillary hemoglobinuria
Liver fluke control Vaccination - commercial bacterin/toxoids; highly effective but short immunity; time with liver fluke season Destroy carcasses
36
Four non-infectious causes of hemolytic disease
Heinz body anemia Copper toxicity Water intoxication Post-parturient hemoglobinemia
37
What causes Heinz body anemias? Which species is more susceptible? What are the toxins involved?
Brassica plants - rape, kale, turnips - cattle more susceptible Goitergenic effect, atypical interstitial pneumonia, choke Toxin = S-methyl cysteine sulfoxide —> converted to dimethyl sulfide in the rumen Onion toxicity - allium family - all ruminants susceptible Toxin = n-propyl disulfide and s-methyl cysteine sulfoxide Prediction of toxicity is difficult - sheep up to 50% - cattle see signs at 5%
38
Heinz body anemia - pathophysiology
Heinz body formation by precipitation of oxidatively denatured Hgb RBCs are less deformable and removed from circulation by RES in spleen and phagocytized and broken down
39
________ is rare with Heinz body anemia
Hemoglobinuria
40
Clinical signs of Heinz body anemia
Variable Weakness, lethargy, anorexia, exercise intolerance Death losses Pale mucous membranes +/- icterus Elevated HR/Resp rate with normal temp Decreased production
41
Heinz body anemia clin path and DX
Early stages: may see high % of RBC with Heinz body inclusions Erythrogenic response in 3-4 days TP WNL +/- hemoglobinemia and hemoglobinuria +/- signs of renal failure (UA changes) Negative Coombs test
42
Copper toxicity is common in _______. Most susceptible: Toxic doses for sheep and cattle: Diets with copper/molybdenum ratios over ___ more likely to result in copper toxicity. Sources:
Ruminants Lambs and llamas Sheep 20-110 mg/kg Cattle 220-880 mg/kg 6:1 Mixing errors, injections
43
Pathophysiology of copper toxicity
Ionized copper internalized by hepatocytes Hepatocytes become saturated Liver necrosis Large amounts of cuprous copper released into blood Free inorganic copper is an oxidant and causes oxidative stress Production of Heinz bodies and methemoglobinemia RBCs lyse intravascularly or sequestered by spleen
44
Clinical signs of acute copper toxicity
Ingested Abdominal pain, severe diarrhea Vomiting, green feces Severe shock, dehydration Death in 24 hours Injected Anorexia, depression, dehydration Ascites, pleural transudate HEMOGLOBINURIA Dyspnea Head pressing, ataxia, aimless wandering
45
Clinical signs of chronic copper toxicity
Onset of clinical signs can take weeks Acute onset depression, anorexia, thirst HEMOGLOBINURIA Anemia, icterus Death in 24-48 hours
46
Copper toxicity clin path
Heinz bodies Methemoglobin Decreased PCV Increased liver enzymes, creatinine, BUN UA: dark brown/black with increased Hgb and protein
47
Copper toxicity DX
Increased serum copper levels ( 0.6-1.5 ppm) Increased liver and kidney copper levels (lab dependent)
48
Site of liver biopsy in sheep and cattle (think of a photo)
49
Treatment of copper toxicity: Prognosis:
Supportive care - transfusion, O2 support Methemoglobinemia - methylene blue? Chelators - D-penicillamine ($100/tx) - sodium thiosulfate - ammonium molybdate Prognosis very poor
50
Copper toxicity prevention
Restrict copper supplementation, especially in sheep Dress contaminated pastures with molybdenum phosphate Increase zinc

Y3 SPRING (40 decks)

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