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Ag Animal II > Proliferative Disorders of the Lymphoid and Myeloid System > Flashcards

Proliferative Disorders of the Lymphoid and Myeloid System Flashcards

1
Q

What characterizes bovine lymphoma?

A
  • Frequency of occurrence
  • Age at onset
  • Organ involvement
  • Etiologic agent
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2
Q

4 forms of sporadic lymphoma

A
  • Calfehood (juvenile)
  • Thymic (Adolescent)
  • Cutaneous
  • Multicentric (Atypical)
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3
Q

Etiology of sporadic lymphoma in calfhood

A
  • Unknown cause, rare
  • NOT ASSOCIATED with BLV
  • Age of onset is 3-6 months
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4
Q

Prognosis of sporadic lymphoma in calfhood

A
  • Grave
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5
Q

History of sporadic lymphoma in calfhood

A
  • Slight depression, weight loss, weakness, lymphadenopathy

- Less common signs are fever, ruminal tympany, enlarged liver, ataxia, and diarrhea

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6
Q

PE of sporadic lymphoma in calfhood

A
  • generalized bilateral enlargement of lymph nodes
  • Pale mucous membranes
  • Tachycardia
  • Hyperpnea
  • Cough
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7
Q

Etiology of thymic sporadic lymphoma

A
  • very rare
  • Calves 6-24 months old (newborns up to 4 years)
  • Not associated with BLV
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8
Q

Prognosis of thymic sporadic lymphoma

A
  • 2-9 week course of disease

- Fatal, and most patients die from bloat (vagal indigestion or bloat from impingement on the esophagus)

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9
Q

Clin path of thymic sporadic lymphoma

A
  • Generally unremarkable
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10
Q

Etiology of cutaneous sporadic lymphoma

A
  • Not associated with BLV

- 1-3 years of age (tends to be younger)

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11
Q

Dfdx for cutaneous sporadic lymphoma

A
  • Squamous cell carcinoma
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12
Q

History of cutaneous sporadic lymphoma

A
  • Cutaneous swellings around anus, vulva, shoulders, and flank
  • 1-3 month periods
  • SIgns may regress and reoccur
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13
Q

Clinical signs and presentation of cutaneous sporadic lymphoma

A
  • Raised or ulcerated lesions
  • Associated with other organ involvement (e.g. cardiac insufficiency, brisket edema, jugular pulse)
  • Enlarged lymph nodes
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14
Q

Atypical sporadic lymphoma - how common?

A
  • SUPER rare

- may be associated with BLV

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15
Q

Bovine leukosis virus other name

A
  • Enzootic bovine leukosis
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16
Q

Etiology of bovine leukosis virus

A
  • Causes adult lymphoma

- Most common neoplastic disease of cattle

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17
Q

What type of virus is bovine leukosis virus

A
  • Oncogenic retrovirus
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18
Q

Epidemiology of bovine leukosis virus

A
  • Herd size positively correlated with rate of disease

- Infection more common than disease

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19
Q

How old are most cattle that show clinical signs of bovine leukosis virus associated disease?

A
  • > 2 years
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20
Q

Economic losses of bovine leukosis virus

A
  • Heavy!
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21
Q

Transmission of bovine leukosis virus

A
  • Horizontal
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22
Q

Clinical signs of BLV

A
  • History: loss of condition, drop in milk production
  • Diarrhea, ataxia, paresis, ketosis
  • Infertility
  • Enlarged lymph nodes
  • Exophthalmos
  • Partial to complete anorexia
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23
Q

PE of BLV

A
  • Reflects organ system failure from tumor involvement
  • Cardiac dysrhythmia, tachycardia, tachypnea, hyperpnea
  • Often peripheral lymph node and internal iliac lymph node enlargement
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24
Q

Common tumor sites of BLV

A
  • Heart, Uterus, Lymph nodes, Abomasum

- Also rumen/reticulum, kidney, spinal cord, retrobulbar space

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25
Q

Clinical signs if GI involvement with BLV

A
  • Scant pasty feces or melena
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26
Q

CBC of BLV

A
  • Unremarkable
  • May be microcytic hypochromic anemia if GI hemorrhage
  • +/- Elevated fibrinogen
  • Only 30% of infected cows develop lymphocytosis
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27
Q

Cytology of BLV vs biopsy in terms of sensitivity

A
  • FNA of PLN has low sensitivity (41$)

- Biopsy of PLN has high sensitivity (100)%

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28
Q

Diagnosis of BLV

A
  • Serology for ELISA of blood or milk
  • PCR for BLV nucleic acid (don’t do by itself)
  • ELISA + PCR has increased sensitivity
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29
Q

What is ELISA for BLV looking for?

A
  • Antibodies to 51-kD envelope glycoprotein (gp51)
  • Presence of antibodies does not equal disease or mean that they will get sick
  • If they have signs of lymphoma, they are guaranteed to have a high titer if positive
  • If they’re not showing signs, no guarantees that they’ll test positive even if infected
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30
Q

Treatment of BLV

A
  • No curative treatment
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31
Q

Control BLV

A
  • reduce blood transmission (donors, needles, etc.)
  • Reduce physical contact among infected and non-infected (more practical in smaller herds)
  • Colostrum from BLV positive dam may be protective**
  • Fly control may help
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32
Q

What is BLADs?

A
  • Bovine leukocyte adhesion deficiency
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33
Q

Inheritance pattern of BLADs?

A
  • Autosomal recessive

- Heterozygous carriers are clinically normal

34
Q

% of Holstein calves impacted by BLADs?

A
  • 6% in the US
35
Q

Signs of BLADs

A
  • Chronic bacterial infections

- Can’t fend off invaders like normal

36
Q

Pathophysiology of BLADs

A
  • Leukocytes lack surface glycoproteins called Beta-integrins
  • Without surface proteins, adhesion and migration to chemotactic factors is inhibited
  • Basically leukocytes continue to roll and can’t extravasate
37
Q

Clinical signs of BLADs

A
  • Infectious processes
  • Calf diarrhea
  • Pneumonia
  • Hyperplastic lymph nodes
38
Q

Clin path of BLADs

A
  • Mature neutrophilia (>40,000/L) without significant left shift, lymphocytosis, and monocytosis
  • Hypoalbuminemia, hypoglobulinemia
  • Low serum creatinine, BUN, glucose
39
Q

How to test for BLADs?

A
  • Holstein Association of America
40
Q

Anthrax - where is it?

A
  • Endemic
  • Worldwide
  • Texas and Plains region in the US
41
Q

Etiology of anthrax

A
  • Bacillus anthracis
  • vegetative cells in tissue
  • Will form spores when conditions limited
42
Q

What determines sporulation of anthrax?

A
  • Oxygen!
  • SPores thrive in high pH with high levels of calcium and magnesium
  • Often outbreaks are seen following earth-disturbing activities
43
Q

Spread of anthrax

A
  • blood sucking insects (Tabanid flies)
  • Scavenging animals
  • Carcasses of infected wildlife can be a source too
44
Q

Three routes of anthrax transmission KNOW THESE

A
  • Ingestion
  • Cutaneous
  • Inhalation
45
Q

Which route of anthrax transmission is most common in cattle?

A
  • Ingestion
46
Q

Pathogenesis?

A
  1. bacteria produce dormant spores that can live in environment for awhile
  2. When spores get into the body of an animal or person, they can be activated and turn into active growing cells
  3. When active, the bacteria can multiply, spread out in the body, produce toxins, and cause severe illness and death
47
Q

What are the four main virulence factors in anthrax?

A
  • Capsule
  • Protective antigen
  • Lethal factor
  • Edema factor
48
Q

Capsule purpose

A
  • Survives in macrophages, which cannot kill it
49
Q

Protective antigen role

A
  • Makes pores to enter cells
50
Q

Lethal factor and edema factor roles

A
  • Cell lysis, inflammation, prevent clotting

- This is what prevents signs of rigor

51
Q

Clinical signs of anthrax

A
  • Depends on route of infection
  • Fever, depression, respiratory distress, congestion of mucous membranes (due to lethal factor) and convulsions
  • May see bloody diarrhea, hematuria, and localized tissue swelling
52
Q

Diagnosis of anthrax

A
  • DO NOT open carcasses of suspect animals
  • THis is reportable and zoonotic
  • Microscopic smears of blood or tissues and bacterial cultures
  • YOU MUST ALWAYS notify the lab if you suspect anthrax
53
Q

Which tissues to submit to a lab fo ranthrax?

A
  • make sure you CALL the state vet if you suspect

- Submit unclotted blood, intact eye, and regional lymph node

54
Q

Appearance of anthrax on a slide

A
  • Boxcar look
55
Q

Treatment of anthrax

A
  • Grave prognosis
  • Often unrewarding
  • Penicillin and tetraycline for minimum of 5 days
56
Q

One main feature on necropsy of animals with anthrax

A
  • Rigor doesn’t seem to set in
57
Q

Control and prevention of anthrax

A
  • REPORTABLE!
  • DO not open the carcass
  • Quarantine if outbreak and psosibly vaccinate
  • Pasture management
58
Q

How to manage an outbreak of anthrax?

A
  • Quarantine
  • Vaccinate normal animals prophylactically
  • Insect control
59
Q

Vaccination of anthrax

A
  • Prophylactic vaccination in some endemic areas
60
Q

Public health and anthrax

A
  • Zoonotic disease
  • Humans develop 3 forms
  • Cutaneous, inhalational, GI
  • Rare in US - cutaneous most common
  • Vets are an at risk group
61
Q

What causes caseous lymphadenitis

A

Corynebacterium pseudotuberculosis

  • 2µm, gm positive, intracellular, nonmotile, pleomorphic, rod-shaped facultative anaerobe
62
Q

When to assume caseous lymphadenitis?

A
  • In any small ruminant with a bump until proven otherwise
63
Q

Which species gets nitrate positive CL vs nitrate negative CL?

A
  • Nitrate positive in horses
  • Nitrate negative in Small ruminants (thick capsules)
  • Both in cattle
64
Q

CL epidemiology - where does it come from?

A
  • Soil borne organism

- Can last for several months ot years in the soil

65
Q

Seasonality of CL

A
  • Not seasonal
66
Q

Transmission of CL

A
  • Direct contact, insects, and fomites
67
Q

Incubation period of CL

A
  • Long
68
Q

prevalence of CL

A
  • up to 5-10%
69
Q

Pathophys of CL

A
  • Organism gains access via wound or abrasion and spreads to SQ or submucosal lymphatics to macrophages
  • Organism survives intracellularly due to high lipid content
  • Replicates in phagolysosomes
70
Q

Virulence factors of CL

A
  • Exotoxins
  • Phospholipase D and Sphingomyelinase
  • Corynomycolic acid + PLD
71
Q

Role of PLD and sphingomyelinase in CL

A
  • Hydrolyze and degrade cell wall
  • Increase vascular permeability
  • Help it extravasate
  • PLD helps form the capsule too
72
Q

Corynomycolic acid and phosphlipase D role

A
  • Induce inflammation, edema, pain
73
Q

What happens when an abscess ruptures with CL?

A
  • Organisms released into the environment
74
Q

Signs of CL in sheep and goats

A
  • Poor performance
  • External abscesses
  • Internal abscesses
  • Parotid LN often but al others too
75
Q

Dfdx for CL

A
  • Trauma, seroma, hematoma, FB, injection reaction, tumor
76
Q

Clin path of CL

A
  • Anemia of chronic disease
  • Leukocytosis with neutrophilia
  • Elevated fibrinogen (internal abscesses more likely)
77
Q

Diagnosis of CL

A
  • ELISA
  • Synergistic hemolysin inhibition test (SHI)
  • Definitive diagnosis is isolation of organisms
78
Q

SHI or synergistic hemolysin inhibition test

A
  • Measures IgG response to exotoxin in patient’s serum
  • More helpful in a high prevalence herd
  • SErial testing on a herd level basis is most helpful
79
Q

Treatment of CL

A
  • Drainage would be contamination of environment
  • Complete excision of abscess preferred
  • Antibiotics are usually unrewarding
  • Large operations may cull, but that’s pretty expensive
80
Q

Prevention of CL

A
  • isolation of infected animal, fly control, good sanitation, and careful disposal of bedding
  • Immunization

Ag Animal II (13 decks)

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