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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
Q

Another name for bacillary hemoglobinuria

A

Redwater

26
Q

What is bacillary hemoglobinuria?

A

Acute
Fatal
Clostridial disease
Causes Liver infarct, toxemia, intravascular hemolysis

27
Q

What causes bacillary hemoglobinuria?

What is the major toxin and what does it do?

When do most outbreaks occur?

A

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
Q

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 ________.

A

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
Q

Life cycle of flukes

A

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
Q

Main clinical sign of bacillary hemoglobinuria

A

Sudden death

31
Q

Antemortem clinical signs of bacillary hemoglobinuria

A

Less common - die fast

Depression, anorexia, fever, tachypnea
Rectal bleeding
Severe hemoglobinuria - port wine colored
Pale and icteric mucous membranes

32
Q

Bacillary hemoglobinuria - clin path and DX

A

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
Q

DFDX Bacillary hemoglobinuria

A

Anthrax
Leptospirosis

34
Q

TX bacillary hemoglobinuria & prognosis

A

High dose ABX: Penicillin or tetracycline
Supportive care: multiple blood transfusions

Grave prognosis

35
Q

Prevention of bacillary hemoglobinuria

A

Liver fluke control

Vaccination - commercial bacterin/toxoids; highly effective but short immunity; time with liver fluke season

Destroy carcasses

36
Q

Four non-infectious causes of hemolytic disease

A

Heinz body anemia
Copper toxicity
Water intoxication
Post-parturient hemoglobinemia

37
Q

What causes Heinz body anemias?

Which species is more susceptible?

What are the toxins involved?

A

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
Q

Heinz body anemia - pathophysiology

A

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
Q

________ is rare with Heinz body anemia

A

Hemoglobinuria

40
Q

Clinical signs of Heinz body anemia

A

Variable

Weakness, lethargy, anorexia, exercise intolerance
Death losses
Pale mucous membranes +/- icterus
Elevated HR/Resp rate with normal temp
Decreased production

41
Q

Heinz body anemia clin path and DX

A

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
Q

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:

A

Ruminants
Lambs and llamas
Sheep 20-110 mg/kg
Cattle 220-880 mg/kg
6:1
Mixing errors, injections

43
Q

Pathophysiology of copper toxicity

A

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
Q

Clinical signs of acute copper toxicity

A

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
Q

Clinical signs of chronic copper toxicity

A

Onset of clinical signs can take weeks
Acute onset depression, anorexia, thirst
HEMOGLOBINURIA
Anemia, icterus
Death in 24-48 hours

46
Q

Copper toxicity clin path

A

Heinz bodies
Methemoglobin
Decreased PCV
Increased liver enzymes, creatinine, BUN
UA: dark brown/black with increased Hgb and protein

47
Q

Copper toxicity DX

A

Increased serum copper levels ( 0.6-1.5 ppm)
Increased liver and kidney copper levels (lab dependent)

48
Q

Site of liver biopsy in sheep and cattle (think of a photo)

A
49
Q

Treatment of copper toxicity:

Prognosis:

A

Supportive care - transfusion, O2 support
Methemoglobinemia - methylene blue?
Chelators
- D-penicillamine ($100/tx)
- sodium thiosulfate
- ammonium molybdate

Prognosis very poor

50
Q

Copper toxicity prevention

A

Restrict copper supplementation, especially in sheep

Dress contaminated pastures with molybdenum phosphate

Increase zinc

Y3 SPRING (40 decks)

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