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Ag Animal II > Hematopoietic disorders - Infectious causes of Anemia > Flashcards

Hematopoietic disorders - Infectious causes of Anemia Flashcards

1
Q

Definition of anemia

A
  • absolute reduction in circulating red cell mass
  • Inadequate oxygen transport
  • Interference with organ function
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2
Q

History of anemia

A
  • Trauma
  • Dietary history
  • Parasite (Haemonchus)
  • Hemorrhage or other illness
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3
Q

Clinical presentation of anemia

A
  • Weakness
  • Depression
  • Lethargy
  • Dementia or disorientation
  • Exercise intolerance
  • Pale mucous membranes
  • Tachycardia
  • Tachypnea
  • Debilitation associated with chronicity
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4
Q

Where to check mucous membranes?

A
  • Conjunctiva

- Vulva

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5
Q

PE findings of canemia

A
  • Pallor
  • Icterus if RBC destruction (won’t happen as much with liver disease)
  • Fever
  • Systolic murmur
  • Signs of blood loss (epistaxis, melena, hematuria, hematochezia)
  • Edema from protein loss
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6
Q

Diagnosis of anemia

A
  • Decreased PCV or HCT
  • Decreased Hemoglobin
  • Decreased RBC count
  • Indices (MCV, MCHC) work well in ruminants
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7
Q

What does MCV represent?

A
  • Average RBC volume (Mean Cell Volume)
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8
Q

Increase in MCV

A
  • Regenerative anemia
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9
Q

Decrease in MCV

A
  • Fe and Cu deficiency

- Or healthy calves

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10
Q

MCHC meaning

A
  • Cellular hemoglobin concentration per average RBC

- Mean cell hemoglobin concentration

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11
Q

Meaning of a decreased MCHC

A
  • Fe deficiency anemia
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12
Q

Increased MCHC

A
  • Usually always false
  • Hemolyzed, icteric, or lipemic samples
  • Heinz bodies
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13
Q

What are the two main categories of anemias?

A
  • Regenerative

- Non-regenerative

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14
Q

How long for regenerative bone marrow response to occur?

A
  • 5-7 days
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15
Q

What are the two categories of regenerative anemias?

A
  • Hemorrhage (blood loss)

- RBC destruction

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16
Q

Non-regenerative anemia

A
  • Bone marrow doesn’t respond

- Inadequate erythropoiesis

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17
Q

What characterize regeneration in ruminants and camelids?

A
  • Reticulocytes and nucleated RBCs
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18
Q

How long for camelids to regenerate?

A
  • Can tkake months
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19
Q

Causes of acute blood loss

A
  • Epistaxis
  • Surgical procedures
  • Ruptured liver, spleen or lung
  • Large vessel bleed
  • Clotting defect
  • Gastric ulcer
  • Hemoperitoneum
  • Hemothorax
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20
Q

Signs of acute blood loss

A
  • Obvious source of loss (although might not see in deep chested ruminants, GI loss, or animals with omentum that can wall it off)
  • Hypovolemic shock (tachycardia, tachypnea, cold extremities, pale mm, muscle weakness, and death eventually
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21
Q

Diagnosis of acute blood loss a

A
  • Change in PCV/TP

- Hemoperitoneum and hemothorax (ultrasound, abdominocentesis, thoracocentesis)

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22
Q

Treatment for acute blood loss

A
  • Stop hemorrhage
  • Treat hypovolemic shock (shock rate with isotonic crystalloids +/- small volume hypertonic saline +/- whole blood transfusion)
  • Whole blood transfusion really only feasible in small ruminants and calves
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23
Q

At what % of total blood volume do you see signs of hemorrhagic shock?

A
  • 30%
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24
Q

What is total blood volume?

A
  • 8% total BW in kgs
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25
Q

When do you start seeing signs of overt blood loss/anemia?

A
  • 8% of blood volume
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26
Q

In a 500 kg Holstein:

  1. What is total blood volume?
  2. How much blood loss for signs of anemia?
  3. how much blood loss for signs of hemorrhagic shock?
A
  1. 40 L
  2. 3.2 L for signs of anemia
  3. 12 L for signs of hemorrhagic shock
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27
Q

Blood typing for whole blood transfusion

A
  • High variability among blood groups and types amongst ruminant species
  • single transfusion is generally safe
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28
Q

Monitoring during whole blood transfusion

A
  • Temperature
  • Urticaria
  • Vomiting
  • Dyspnea
  • Increased HR
  • Have banamine or diphenhydramine ready to give if signs of reaction
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29
Q

Chronic blood loss - when will you see clinical signs?

A
  • PCV is <15%
  • Physiologic adaptation masks signs until then
  • Slow progression
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30
Q

Common causes of chronic blood loss (remember)

A
  • Haemonchus
  • Bleeding GI lesions
  • Some renal disease
  • Hemostatic dysfunction
  • Blood sucking external parasites
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31
Q

Clinical signs of chronic blood loss

A
  • Ill thrift
  • Poor body condition and hair
  • Pallor of MM
  • Edema if protein also chronically lost (albumin)
  • Weakness, lethargy
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32
Q

FAMACHA

A
  • Aenmia guide for owners to get certified

- Trying to figure out when to do deworming

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33
Q

What are the two parts of hemostasis?

A
  • Coagulation and fibrinolysis
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34
Q

Inherited coagulation disorders

A
  • Rare

- Examples are hemophilia A and Factor XI deficiency (autosomal recessive)

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35
Q

Hemophilia A is a deficiency of what

A

Factor VIII deficiency

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36
Q

Acquired hemostatic disorder

A
  • Sweet clover toxicosis
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37
Q

Which species of clover can lead to sweet clover toxicosis?

A
  • Melilotus officinalis and M alba
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38
Q

What type of sweet clover leads to sweet clover toxicosis?

A
  • Moldy sweet clover hay or silage containing dicoumarol
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39
Q

Which states have a problem with sweet clover toxicosis?

A
  • Northern Plains States

- Includes Idaho and Montana

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40
Q

Pathogenesis of sweet clover toxicosis

A
  • Coumarins in legumes and alfalfa converted by molds to dicoumarol
  • Same as warfarin toxicosis
  • Interferes with hepatic synthesis of clotting factors, II, VII, IX, and X by inhibiting Vitamin K
  • Need a certain amount of Dicoumarol over several weeks
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41
Q

Which clotting factors are impacted by moldy sweet clover toxicosis?

A
  • II, VII, IX, and X

- By inhibiting vitamin K synthesis

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42
Q

Which pathways (intrinsic, extrinsic, common) are impacted by moldy sweet clover toxicosis?

A
  • Intrinsic (IX)
  • Extrinsic (VII)
  • Common (X)
  • Also impacts prothrombin (factor II)
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43
Q

Signs of sweet clover toxicosis

A
  • Stiffness and lameness (hemorrhage into joints)
  • Early signs include epistaxis and melena from dark, digested blood
  • Death by massive hemorrhage
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44
Q

Dfdx for sweet clover toxicosis

A
  • DIC, Bracken Fern toxicosis, mycotoxicosis
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45
Q

Clin path for sweet clover toxicosis

A
  • Prolonged PT and PTT
  • +/- Hematuria (not platelets, just clotting factors)
  • Normal platelet count to differentiate from DIC and bracken fern
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46
Q

How do you differentiate sweet clover toxicosis from DIC and bracken fern on CBC?

A
  • Normal platelet count
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47
Q

Treatment for sweet clover toxicosis

A
  • Vitamin K (4 weeks of high dose

- Whole blood transfusions for severe loss

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48
Q

Anaplasma that impacts cattle vs sheep

A
  • A. marginale (cattle)

- A. ovis (sheep)

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49
Q

Vector for anaplasma

A
  • Dermacentor species
  • Biing flies
  • Mechanical vectors
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50
Q

Transmission of Anaplasma

A
  • Intrauterine

- Also mechanical vectors

51
Q

Spread of Anaplasma

A
  • In most states
52
Q

Reservoir for Anaplasma

A
  • Asymptomatic cattle

- Stressed carriers can break with disease

53
Q

Time of year for Anaplasma?

A
  • Late spring and summer
54
Q

Incubation of Anaplasma?

Primary exposure?

At what % decrease in RBCs do you see clinical signs?

A
  • Highly variable - acute severe to subclinical
  • 15-30 day incubation
  • Primary exposure at calfhood
  • Clinical signs seen when 35-50% decrease in RBCs
  • Peracute death
55
Q

Acute signs of anaplasma

A
  • Pyrexia (103-106°F)
  • Subsides in 12-24 hours
  • Subnormal at death due to hypovolemia
  • Anorexia, lethargy, drop in milk production
  • Signs of anemia
  • Mucous membranes pallor or icteric
  • +/- dark brown feces, pollakiuria
  • Abortion
  • DO NOT SEE HEMOGLOBINURIA**
56
Q

Do you see hemoglobinuria with Anaplasma?

A
  • NO
  • Extravascular hemolysis in Anaplasma
  • Intravascular hemolysis required for hemoglobinuria
57
Q

Hemoglobinuria

A
  • Plasma reflects a hemolytic state with icterus potential

- Deep red to black urine

58
Q

Where is the discoloration in the urine with hemoglobinuria?

A
  • Throughout urination
59
Q

Hematuria

A
  • blood in urine
  • Red, brown, or pink
  • RBCs seen on microscopic exam
60
Q

Where can you localize hematuria if seen at beginning of urination?

A
  • Urethra, repro tract
61
Q

Where can you localize hematuria if seen at end of urination?

A
  • Bladder
62
Q

Where can you localize hematuria if seen throughout of urination?

A
  • Kidney
  • Ureters
  • Differentiate from hemoglobinuria
63
Q

Clinical signs of Anaplasma in sheep

A
  • Typically subclinical
64
Q

Clinical signs of Anaplasma in goats

A
  • Rare, severe anemia
65
Q

Clinical signs of Anaplasma in camelids

A
  • rare anemia
66
Q

Clin path of Anaplasma

A
  • IDentify organism on a blood smear
  • Wright’s stain, New methylene Blue, Giemsa stain
  • May see RBC regeneration chronically
67
Q

Where will death occur for a rapid vs gradual PCV drop?

A
  • <20% at rapid

- <10% at gradual drop

68
Q

Diagnosis of Anaplasma

A
  • Serology to ID persistently infected (difficult)
  • Competitive ELISA*** (high sensitivity and specificity; approved by USDA and OIE)
  • PCR (seroconversion in acute disease; confirm diagnosis in acute infection)
69
Q

Which test for diagnosing Anaplasma is approved by USDA and OIE?

A
  • competitive ELISA
  • High sensitivity and specificity
  • Looks for antibody
70
Q

Treatment for Anaplasma

A
  • Oxytetracycline in acute disease

- Supportive care if needed with whole blood transfusion

71
Q

Will treatment for Anaplasma eliminate persistent infection?

A
  • No
72
Q

At what PCV will prognosis for Anaplasma be considered poor?

A

<8%

73
Q

Prevention of Anaplasma

A
  • Decrease transmission by getting rid of tick vectors

- In endemic areas with low transmission rates, there is some conditional vaccination

74
Q

For prevention of Anaplasma in a herd free of it an a non-endemic area?

A
  • Quarantine and serological screening
75
Q

Babesiosis - is it reportable?

A
  • YES
76
Q

Babesia in the US

A
  • Eradicated in the US
77
Q

Organism involved in babesiosis?

A
  • Babesia bovis

- Obligate intracellular parasite of RBCs

78
Q

Transmission of Babesiosis?

A
  • One-host tick
  • Rhipicephalus spp
  • Formerly Boophilus
79
Q

Incubation of babesiosis

A
  • 2-3 weeks
80
Q

Clinical signs of babesiosis

A
  • pyrexia (104-107.6°F)
  • Depression, icterus, anorexia
  • Aenamia with intravascular destruction of RBCs
  • Hemoglobiniemia
  • Hemoglobinuria***
  • Abortion
  • Death
  • Cerebral babesiosis (low RBC, grave prognosis)
81
Q

Clin path of babesiosis?

A
  • Anemia with regeneration
82
Q

Diagnosis of babesiosis?

A
  • ID on Giemsa-stained blood smear in acute infections
  • Serology (IFA and ELISA)
  • PCR
83
Q

Poor prognostic indicators for babesia

A
  • <10% PCV and neuro signs
84
Q

Treatment of Babesia

A
  • Imidocarb
  • Diminazene
  • Phenamidine
  • Amicarbalide
85
Q

Prevention of Babesia

A
  • Tick vector eradication
  • Useful in US
  • Immunization
86
Q

Hemobartonellosis cause

A
  • Hemotropic mycoplasmas
87
Q

Which Mycoplasma causes hemobartonellosis in camelids? ***

A
  • Eperythrozoon sp (M. Haemolamae)
88
Q

Which Mycoplasma causes hemobartonellosis in cattle?

A

E. wenyonii

89
Q

Which Mycoplasma causes hemobartonellosis in sheep?

A
  • E. ovis
90
Q

Where is hemobartonellosis?

A
  • world wide but generally minor disease
91
Q

Who gets hemobartonellosis?

A
  • Most often stressed animals
  • Younger more likely than old
  • Immunosuppression (e.g. splenectomy)
  • carrier animals
92
Q

Transmission of hemobartonellosis

A
  • Blood (insects, needles, castration)

- Intrauterine

93
Q

How long do infections with hemobartonellosis last?

A
  • Life long
94
Q

Incubation period for Hemobartonellosis

A

1-3 weeks

95
Q

Clinical signs of hemobartonellosis in cattle

A
  • Rare clinical disease in cattle
  • Fever, stiff gait
  • < Milk production - udder edema
  • Diarrhea
  • Lymphadenopathy - prefemorals
  • Scrotal swelling
  • Swollen legs
96
Q

Clinical signs of hemobartonellosis in sheep

A
  • “yellow lamb disease”
  • Rare sudden death with hemoglobinuria and icterus
  • Less severe disease with fever, depression, anemia, and weight loss
97
Q

Clinical signs of M. haemolamae (hemobartonellosis in camelids)

A
  • Variable clinical signs: anemia, depression, fever, weight loss
  • Hypoglycemia is common in camelids
98
Q

Mode of transmission of M. haemolamae

A
  • Unknown
  • Biting insects
  • In utero transmission
99
Q

Diagnosis of M. haemolamae

A
  • PCR
  • Can also do a gram stain on a blood smear
  • Epicellular parasite on RBC
  • Anemia
  • CF, ELISA, PCR
100
Q

What should a primary differential in a camelid with anemia be?

A
  • M. haemolamae
101
Q

Treatment for hemobartonellosis

A
  • Oxytetracyclines
  • LA (brand) 200mg/mL (LA 200)
  • Up to 50 days
  • May not eliminate carrier state
102
Q

Leptospirosis issues

A
  • Zoonotic
103
Q

Syndromes associated with Lepto

A
  • late term abortion
  • Hemolytic anemia
  • Septicemia
  • mastitis
  • Combo
104
Q

Etiology - which Leptospira serovars are responsible for majority of disease?

A
  • Leptospira interrogans serovars Pomona and icterohemorrhagia
105
Q

Clinical signs of hemolytic form of leptospirosis

A
  • Young calves, lambs, kids, crias (adults??)
  • Incubation 3-7 days
  • Fever
  • Anorexia, depression
  • Petechiation
  • Hemoglobinuria**
  • Anemia
  • Icterus
  • Tachycardia and sypnea
  • Death in 2-3 days

Slow recovery

106
Q

Clin Path for Leptospirosis

A
  • Moderate leukocytosis
  • Hyperfibrinogenemia
  • Hemoglobinemia
  • Hemoglobinuria
107
Q

Definitive diagnosis of leptospirosis

A
  • Based on demonstration of organism in urine, milk or fetal tissues
  • MAT, PCR FAT
108
Q

Treatment for Leptospirosis

A
  • Oxytetracycline
  • Streptomycin
  • Procaine Pen-G
  • Supportive care
109
Q

Prevention of leptospirosis

A
  • Vaccination
  • Removal of carriers
  • Hygiene
110
Q

What to do if you suspect leptospirosis?

A
  • Go into isolation!
111
Q

Bacillary hemoglobinuria

A
  • Acute fatal clostridial disease

- Liver infarct, toxemia, intravascular hemolysis

112
Q

Etiology of bacillary hemoglobinuria

A
  • Clostridium novyi type D (C. hemolyticium)
113
Q

Major toxin in bacillary hemoglobinuria

A
  • Beta toxin
  • Phospholipase C
  • Causes hepatic necrosis, hemolysis, and damage to capillary endothelium
114
Q

Timing of bacillary hemoglobinuria

A
  • Summer and early fall
115
Q

What events do bacillary hemoglobinuria outbreaks usually follow?

A

Flooding

116
Q

Pathophysiology of bacillary hemoglobinuria

A
  • Spores ingested by animal –> cross intestinal mucosa and transported to liver via mcarophages –> persist in Kupffer cells
  • Localized anaerobic areas promote germination (liver flukes)
  • Release of toxins –> increase anaerobic environment –> further bacteria growth and hepatic necrosis
  • Abrotpion of toxins leads to intravascular hemolysis, icterus, hemoglobinuria, and death
117
Q

Clinical signs of bacillary hemoglobinuria

A
  • Sudden death
  • Antemortem signs are uncommon
  • Depression, anorexia, fever, tachypnea
  • Rectal bleeding
  • Severe hemoglobinuria (port wine colored)
  • pale and icteric mucous membranes
118
Q

Necropsy findings of bacillary hemoglobinuria

A
  • Necrosis in the liver grossly

- Can do an impression smear

119
Q

Clin path of bacillary hemoglobinuria

A
  • rare to get BW and diagnostics antemortem
  • Anemia, high AST, and GGT, high bilirubin
  • Hemoglobinuria
  • FAT on impression smears of liver infarct
  • Area, history, clinical signs, and necropsy
120
Q

Dfdx for bacillary hemoglobinuria

A
  • Anthrax, lightning
121
Q

Treatment for bacillary hemoglobinuria

A
  • Grave prognosis
  • High dose penicillin or tetracycline
  • Supportive care could give blood transfusions
122
Q

Prevention of bacillary hemoglobinuria

A
  • Liver fluke control
  • Vaccination with commercial bacterin/toxoids
  • Highly effective but short immunity
  • Time with liver fluke season

Destroy the carcasses

123
Q

Infectious causes of anemia that have intravascular hemolysis

A
  • Bacillary hemoglobinuria
  • Leptospirosis
  • babesiosis Hemobartonellosis

Ag Animal II (13 decks)

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