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Y2S1 - LAM I > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

How long does Caprine Arthritis Encephalitis virus (CAEv) persist in the host?

A

For life - results in chronic disease course

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2
Q

How is Caprine Arthritis Encephalitis virus (CAEv) transmitted?

A

*Ingestion of colostrum/milk
Doe to kids (licking, breathing)
Close contact between goats
Contaminated fomites

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3
Q

What is the economic significance of Caprine Arthritis Encephalitis virus (CAEv)?

A 
Increased culling rates
Decreased milk production
Increased dx/tx costs
Increased replacement rates
Higher value of CAEv-free breeding stock
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4
Q

How is Caprine Arthritis Encephalitis virus (CAEv) diagnosed?

A

Elitest (cELISA for OPPv/CAEv)

*positive test ONLY indicates infection, not diagnostic for cause of clinical problem

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5
Q

How is Caprine Arthritis Encephalitis virus (CAEv) treated?

A

Only palliative tx

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6
Q

How is Caprine Arthritis Encephalitis virus (CAEv) controlled?

A 
Pasteurized rearing program 
Avoid iatrogenic transmission
Serologic testing 6-12 months
Breed seronegative animals together
Milk CAEv(-) first
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7
Q

What is involved in a “pasteurized rearing program”?

A
  1. Induce parturition with 2-3mL Lutalyse/Prostamate IM
  2. Attend kidding 30-32 hours post-injection, remove kids from dam immediately
  3. Rear kids in isolation on safe colostrum/milk
    - Heat-treated colostrum (131ºF 1 hour)
    - Pasteurized milk (165ºF 15 seconds)
  4. House CAEv-free animals separately from infected animals
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8
Q

What are the four disease presentations of Caprine Arthritis Encephalitis virus (CAEv)?

A

Kid neurologic form
Arthritis
Mastitis
Pneumonia

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9
Q

Which animals get the neurologic form of CAEv?

A

2-6 month-old kids

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10
Q

How does the neurologic form of CAEv present clinically?

A

Progressive paresis > irreversible paralysis (over weeks) > often die of 2º disease

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11
Q

How can the neurologic form of CAEv be diagnosed?

A

CSF - mild to mod increase in cell counts and protein

Histo - multifocal mononuclear inflammatory leukoencephalomyelitis with extensive demyelination

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12
Q

DDx for the neurologic form of CAEv?

A 
Copper deficiency
Vertebral body/spinal cord abscess
Congenital abnormalities of cord/column
Cerebrospinal nematodiasis (P. tenuous)
Listeriosis
Polioencephalomalacia
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13
Q

How is the neurologic form of CAEv treated?

A

No treatment. Humane euthanasia

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14
Q

How does the arthritic form of CAEv present clinically?

A

Initial swelling of anterior aspect of carpus with fluid accumulation in carpal bursa
Progressive arthritis of one or more joints (knees and hocks most common)

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15
Q

How is the arthritic form of CAEv diagnosed?

A

Arthrocentesis - elevated mononuclear cells

Rads - calcification of joint capsule, tendon/sheaths, osteophyte formation

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16
Q

How is the arthritic form of CAEv treated?

A

Palliative options:

  • adequan injections (weekly-monthly)
  • cosequin (PO daily)
  • flunixin meglumine (PRN)
  • meloxicam (PO daily)
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17
Q

How does the mastitic form of CAEv present clinically?

A

Bilaterally hard udder at kidding

Scant milk, but appears normal

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18
Q

How is the mastitic form of CAEv diagnosed?

A

Herd history

Biopsy and histo - lymphoid follicle formation especially around ducts, lobular atrophy, increased fibrous CT

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19
Q

How is the mastitic form of CAEv treated?

A

Steroids may help

Some goats spontaneously increase milk production in 2-3 weeks

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20
Q

How does the pneumonia form of CAEv present clinically?

A

Exercise intolerance, dyspnea, wasting, coughing

Onset following stress

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21
Q

How is the pneumonia form of CAEv diagnosed?

A

Rebreathing bag - squeaking sound
Rads - interstitial pneumonia
Lung biopsy/histo - peribronchiolar accumulation of monos, proliferation of type II pneumocytes, alveoli filled with eosin material

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22
Q

How is the pneumonia form of CAEv treated?

A

Abx therapy may help if secondary bacterial pneumonia

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23
Q

What is the etiologic agent of caseous lymphadenitis?

A

Corynebacterium pseudotuberculosis

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24
Q

Where is C. pseudotuberculosis found? Is it persistent in the environment? For how long does it infect animals?

A

Ubiquitous worldwide
Months in environment, but killed by regular disinfection
Lifelong infection

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25
Q

How is caseous lymphadenitis transmitted?

A

Draining external abscesses
Aerosolization of lung abscesses
Skin via microtrauma

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26
Q

What is the pathogenesis of caseous lymphadenitis?

A

Localizes in regional LN > extension along LN chain / systemic travel > hair/wool loss as abscess matures > spontaneous rupture

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27
Q

How does external caseous lymphadenitis present?

A

Abscess formation in LN (parotid common) or SQ - non-painful with gradual hair loss
Pus is odorless, creamy white/yellowish/greenish

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28
Q

How does visceral caseous lymphadenitis present?

A

“thin ewe syndrome”

Weight loss, neurologic signs, pneumonia-like symptoms

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29
Q

How is caseous lymphadenitis diagnosed?

A

Culture of abscess
Synergistic Hemolysis Inhibition test (SHIT)
-High titers = internal abscessation
-CANNOT distinguish vax from dz

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30
Q

How is caseous lymphadenitis controlled?

A

ID infected animals
Depopulate / separate herd
Vaccinate (sheep 1 year booster, goats 6 month booster)

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31
Q

How is caseous lymphadenitis treated in individual animals?

A

Option to cull or isolate
Surgical removal (expensive, facial paralysis possible)
Lance and flush abscesses (dilute iodine/chlorhex)
*Refractory to parenteral abx
*Do not use formalin - meat residues

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32
Q

What classifies “safe use” of a drug?

A

Includes safety to animal, to persons associated with the animal, and environmental impact

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33
Q

What classifies “effective use” of a drug?

A

Assumes accurate dx can be made
drug properly administered
and course of dz can be followed to assess success of drug

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34
Q

What labelling must be on rx products?

A

Caution: Federal law restricts this drug to use by or on the order of a licensed veterinarian

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35
Q

What labelling must be on VFD drugs?

A

Caution: Federal law restricts medicated feed containing this VFD drug to use by or on the order of a licensed veterinarian

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36
Q

What is AMDUCA?

A

The Animal Medicinal Drug Use Clarification Act of 1994

Established conditions for legal extra-label use of drugs in animals

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37
Q

What are the requirements for extra-label drug use under AMDUCA?

A
  1. On the order of a licensed vet

2. Within the context of a vet-client-patient relationship

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38
Q

What are the exceptions to extra-label drug use under AMDUCA?

A

Does not apply to:

  1. Drugs in feed
  2. Drugs that result in a violative food residue
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39
Q

Which antibiotics are prohibited from ALL food animals?

A 
Chloramphenicol
Clenbuterol
DES
Dipyrone
Gentian violet
Glycopeptides (eg. vancomycin)
Nitrofurans (including topicals)
Nitroimidazoles (including metronidazole)
Phenylbutazone (in adult dairy cattle)
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40
Q

How do the FDA define lactating (adult) dairy cattle?

A

Any dairy breed female >20 months regardless of milking

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41
Q

Which drugs are prohibited from extra-label use?

A 
Sulfonamides (adult dairy cattle)
Fluoroquinolones
Medicated feeds
Ceftiofur (modified prohibition)
-can be used for specific dz tx if dose regimen is followed for labelled species (even if dz is extra-label)
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42
Q

Which antibiotic class is strongly discouraged in cattle? Why?

A

Aminoglycosides

-insufficient data for withdrawal

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43
Q

What is the MUMS Animal Health Act?

A

Minor Use Minor Species
Provides ways to use FDA authorized drugs for:
1. Conditions in minor species where tx are unavailable
2. Uncommon animal disease conditions in major species

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44
Q

How is ovine progressive pneumonia virus (OPPv) transmitted?

A

Aerosols/saliva

Common needles

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45
Q

Which cell type does ovine progressive pneumonia virus (OPPv) infect?

A

Lymphocytes

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46
Q

How does ovine progressive pneumonia virus (OPPv) present clinically?

A

Poor milk production
-udders are firm, indentable, bilaterally symmetric
Emaciation
Secondary pneumonia

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47
Q

How is ovine progressive pneumonia virus (OPPv) diagnosed?

A

Serology (AGID / cELISA)
-*indicates lifelong infection only
Udder biopsy - chronic lymphocytic indurative mastitis

Necropsy:
Lungs are grossly enlarged/discolored (orange to grey/blue), rib impressions may be seen

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48
Q

What are some differentials for emaciation in sheep?

A
  1. Ovine progressive pneumonia virus (OPPv)
  2. Parasitism (Haemonchus, Teladorsagia, Trichostrongylus, Fascioloides magna)
  3. CLA (internal form)
  4. Johne’s dz
  5. Chronic bacterial pneumonia
    Others: malnutrition, teeth problems, scrapie, neoplasia
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49
Q

What is the control strategy for ovine progressive pneumonia virus (OPPv)?

A

Elitest ELISA for testing
Avoid housing young lambs with older OPPv+ sheep
TMEM154 testing available in Lincoln, NE

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50
Q

Are sheep or goats more susceptible to foot rot/scald?

A

Sheep

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51
Q

What infectious agents cause footrot/scald?

A

Dichelobacter nodosus

Synergistic effect of Fusobacterium necrophorum

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52
Q

T/F: Health certificates can be signed if footrot/scald is present as long as it’s being treated?

A

FALSE, it’s still an infectious disease

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53
Q

How is footrot treated?

A
  1. Isolate lame sheep
  2. Minimal or no foot trim
  3. 1 long-acting injection of tetracycline / gamitromycin
  4. Spray lesion with tetracycline spray
    (FARAD meat withdrawal 90 days)
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54
Q

How is foot scald treated?

A

Individual ewes: treat as for footrot
Individual lambs: spray with oxytetracycline, re-treat if still lame after 5 days
Flock outbreaks: footbath, 10% zinc sulfate

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55
Q

When should sheep be culled for footrot/scald?

A

If lame more than twice a year or not responding to treatment

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56
Q

How can footrot/scald be controlled?

A 
Regular footbaths (10% zinc sulfate)
*No vaccination available in US
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57
Q

What generalities are true for all clostridial diseases?

A

Highly fatal, sudden onset
Often affect thriftiest animals
Therapy ineffective once ill
Vaccination is cost-effective and works well

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58
Q

How is C. tetani treated and prevented?

A 
Dark, quiet location
Tube feed
Acepromazine to sedate and minimize seizures
Debride wound and give penicillin
Give antitoxin if early in dz course

Long-acting penicillin at tail docking
Remove tail/testicles in 3-5 days post-banding
Vaccinate ewes prior to lambing

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59
Q

What clinical signs are associated with botulism?

A

Lack of muscle tone, progressive weakness > recumbence

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60
Q

What is the main risk factor for botulism?

A

Spreading poultry litter on land that produces pasture, hay, baleage, or silage in same year

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61
Q

Is botulism zoonotic?

A

No

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62
Q

What is the causative agent of braxy? What does it look like clinically?

A

C. septicum

Gangrenous abomasitis in young lambs and calves

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63
Q

What are the causative agents of clostridal myonecrosis? What are the various disease names?

A

C. chauvoei, septicum, sordellii, or mixed infections

Blackleg, Malignant edema, Gas gangrene

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64
Q

What are the clinical signs of clostridial myonecrosis?

A

Lameness, fever, depression
Crepitus and swelling (bubble wrap muscles)
Rapid deterioration with up to 100% mortality

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65
Q

DDx for sudden death in ruminants?

A 
Clostridium
Bloat
Lightning strike
Grass tetany
Atypical interstitial pneumonia
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66
Q

How can clostridial myonecrosis be diagnosed?

A

PCR sample of affected muscle

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67
Q

How can clostridial myonecrosis be treated? What’s the prognosis?

A

IV K penicillin

Poor

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68
Q

What is the causative agent of bacillary hemoglobinuria? What is its common name? What species does it infect?

A

C. haemolyticum / novyi type D
“Red water”
Cattle

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69
Q

What is the pathogenesis of bacillary hemoglobinuria?

A

Fluke liver infection > liver damage creating anaerobic environment > beta, eta, and theta clostridial toxins > localized hepatic necrosis and IV hemolysis

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70
Q

What clinical signs are associated with bacillary hemoglobinuria?

A

Red urine, bleeding from other orifices

Sudden death

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71
Q

What necropsy findings are consistent with bacillary hemoglobinuria?

A

Ischemic hepatic infarct with zone of hyperemia next to viable liver tissue
Widespread serosal and mucosal hemorrhages
Red-tinged fluid in abdomen and thorax

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72
Q

What is the causative agent of black disease? What species does it infect?

A

C. novyi type B

Sheep

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73
Q

What clinical signs are consistent with black disease? What is a major risk factor?

A

Infectious necrotic hepatitis
Similar to bacillary hemoglobinuria but NO red urine or bleeding from orifices
Liver fluke (F. magna) major risk factor

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74
Q

What is the causative agent of enterotoxemia?

What are two common names for the dz?

A

Clostridium perfringes type D

Pulpy kidney dz, overeating dz

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75
Q

Who does enterotoxemia typically affect? What is the main risk factor?

A

Feedlot lambs

High CHO in diet (even lush pastures)

76
Q

What clinical signs are consistent with enterotoxemia?

How long does disease last?

A

Ataxia, trembling, opisthotonus, rapid progression to convulsions, coma
Peracute dz, lasts <2 hours

77
Q

What is the main differential for enterotoxemia?

A

Polioencephalomalacia

78
Q

What necropsy lesions are consistent with enterotoxemia in SHEEP?

A 
Pulmonary edema
Congested intestines
Hydropericardium with soft fibrinous clot (jello)
Hyperglycemia and glucosuria
Pulpy soft kidney if fresh carcass
Focal symmetric encephalomalacia
79
Q

What necropsy lesions are consistent with enterotoxemia in GOATS?

A

Fibrinohemorrhagic enterocolitis
Pulmonary edema
Renal tubular necrosis
Edema of mesenteric LNs

80
Q

What vaccination schedule should be followed to prevent enterotoxemia?

A

Sheep q12 months, goats q6 months

Incoming feedlot animals: vax 2x 1 month apart and work up on feed slowly

81
Q

What is the causative agent of necrohemorrhagic enteritis?

A

C. perfringes type C or A

82
Q

Who does necrohemorrhagic enteritis typically infect? What is the pathogenesis?

A

Beef calves/lambs <1-2 weeks only
Neonate ingests organism from environment > protease-deficient neonatal GIT allows for rapid multiplication > hemorrhagic diarrhea d/t beta toxin > necrosis of intestinal/abomasal epithelial cells

83
Q

What clinical signs are consistent with necrohemorrhagic enteritis?

A

Depression, anorexia, rapid progression to death

84
Q

What necropsy findings are consistent with necrohemorrhagic enteritis?

A

Necrosis of duodenal and/or jejunal mucosa, hemorrhagic mesenteric LNs

85
Q

How is necrohemorrhagic enteritis diagnosed?

A

PCR

86
Q

How is necrohemorrhagic enteritis treated and prevented?

A

Antitoxin
Broad-spectrum abx (PO metronidazole)
Milk withdrawal 24 hours

Pre-partum vaccination with type A

87
Q

When do anthrax outbreaks typically occur?

A

July-September following flooding

88
Q

How is anthrax transmitted?

A

Soil, vegetation, water
Insufficiently cooked infected meat, dead carcasses
Blow fly bites

89
Q

What are anthrax’s virulence factors?

A 
Protective antigen (PA)
Lethal factor (LF)
Oedema factor (OF)
2 phase life cycle (spore and virulent)
90
Q

What clinical signs are consistent with anthrax?

A

Peracute septicemia characterized by failure of blood to clot
Apathy or excited bellowing
Abortion with massive uterine hemorrhage

91
Q

DDx for sudden exudative hemorrhage?

A 
Lightning strike
Dehydration 
Acute plant/chemical poisoning
Salmonellosis enteritis
Leptospirosis
Babesiosis
Clostridial infections
Purpura
92
Q

How can anthrax be diagnosed in the field?

A
  1. Lack of rigor mortis, rapid putrefaction, bloody fluid at nares and other body orifices
  2. Obtain blood smear from jugular or knick ear
  3. Aspirate peripheral LN for culture
  4. Examine spleen (right side)
93
Q

How can anthrax be diagnosed in the lab?

A
  1. Direct smear with Wrights/Giemsa
  2. Characteristic capsule (M’Fadyean reaction) when stained with polychrome methylene blue
  3. Immunochromatographic field assay to detect PA
94
Q

How is anthrax treated? What is the prognosis?

A

Parenteral tetracyclines or penicillin

Prognosis good unless advanced

95
Q

How is anthrax prevented?

A
  1. Vaccination of healthy animals on anthrax farms (Thraxol-2)
  2. Quarantine affected farms for >2-4 weeks past last case
  3. Unopened animals should be burned/buried >6 feet deep and covered with quick lyme
  4. Spray contaminated area with cleaner
96
Q

What are PCV normals for horses, cows, and camelids?

A

Horse: 32-48
Cows: 24-46
Camelids: 26-42

97
Q

What clinical signs are expected in anemia?

A 
Exercise intolerance
Tachycardia / tachypnea
Pale mms
Weakness
Low systolic murmur (d/t watery blood)
Depression
98
Q

How does clinical pathology differ in cases of acute vs chronic blood loss?

A

Acute: reduced TPP, but maybe normal PCV
Chronic: reduced TPP and PCV (mild clinical signs)

99
Q

What are the various clinical manifestations of bracken fern toxicosis?

A

Swine and horses: neurological signs
Short-term exposure in ruminants (2-8 weeks): bone marrow suppression
Chronic exposure (months to years) in ruminants: enzootic hematuria

100
Q

What is the pathogenesis of anemia caused by bracken fern toxicosis?

A

Aplastic anemia and subsequent pancytopenia:

  1. Thrombocytopenia > widespread hemorrhage
  2. Leukopenia/neutropenia > SBIs
  3. Nonregenerative anemia
101
Q

What clinical signs are associated with bracken fern toxicosis?

A

Sudden onset
Fever, melena, epistaxis, hyphema, petechial/ecchymotic hemorrhages
Death in 1-3 days

102
Q

How is bracken fern toxicosis treated? What is the prognosis?

A

Supportive care: IV fluids, abx, tranfusions
Avoid stress/trauma
Grave prognosis

103
Q

What is the etiology of purpura hemorrhagica?

A

Immune-mediated vasculitis of horses

Type III hypersensitivity reaction to streptococcal antigens (often secondary to strangles)

104
Q

What clinical signs are consistent with purpura hemorrhagica?

A

Widespread edema, petechial hemorrhages, laminitis, DIC, mild anemia

105
Q

How is purpura hemorrhagica treated?

A

Corticosteroids and penicillin (if S. equi)

106
Q

What is the pathogenesis of DIC?

A
  1. Severe underlying disease (eg. endotoxemia, intestinal accidents, enteritis, sepsis, trauma, renal failure)
  2. Widespread fibrin deposition in microcirculation
  3. Ischemic damage to multiple tissues/organs
  4. Hemorrhage and/or thrombosis (more common in horses)
107
Q

How is DIC diagnosed?

A

3 of 5 criteria needed:

  1. decreased AT-III
  2. FDPs >40 µg/mL
  3. PT > 10.5 sec
  4. aPTT > 60 sec
  5. PLT <100,000/µL
108
Q

How is DIC treated?

A

Treat underlying condition!

IV fluids, NSAIDs, heparin (provided adequate AT-III levels), blood/plasma as needed

109
Q

Which species mostly affected by moldy sweet clover poisoning?

A

Ruminants

110
Q

What is the pathogenesis of moldy sweet clover poisoning?

A

Dicoumarol competitively inhibits vitamin K > deficiency of II, VII, IX, X > impaired coagulation and hemorrhage

111
Q

What does labwork look like in a moldy sweet clover poisoning case?

A

CBC - anemia (maybe)
Increased PT, PTT, and ACT
Normal PLT counts

112
Q

How is moldy sweet clover poisoning treated?

A

Stop feeding clover or dilute component
Vitamin K1 (NOT K3)
Transfusion (only need 1L to restore clotting factors)

113
Q

What is hemophilia? Which large animals does it affect?

A

Inherited factor VIII deficiency

Horses (thoroughbreds, standardbreds, arabians, quarter horses)

114
Q

How does hemophilia appear clinically? What does lab work show?

A 
Characterized by hemarthrosis and hematoma formation d/t coagulation defects
aPTT prolonged (intrinsic pathway)
115
Q

How is hemophilia treated?

A

No treatment.

116
Q

What is the pathogenesis of ITP (immune-mediated thrombocytopenia)?

A

Antibody-mediated destruction of platelets

Idiopathic or secondary to drugs/dz/neoplasia

117
Q

What does labwork look like in ITP?

A

PLT <40,000 (clinical signs)
Anemia and hypoproteinemia
PT, aPTT, fibrinogen all NORMAL
Prolonged bleeding times

118
Q

How is ITP treated? What’s the prognosis?

A

Dexamethasone
Transfusion for severe anemia
Good prognosis (dependent on cause)

119
Q

Which infectious agents are most likely to cause thrombocytopenia in large animals?

A

BVDV
EIAV (mild)
Anaplasma phagocytophila

120
Q

What might cause oxidant-induced hemolytic anemias (Heinz body anemias) in large animals?

A 
Phenothiazine (horses)
Wild onions (cattle and horses)
Red maple leaf (horses
121
Q

Do Heinz body anemias cause primarily intra or extravascular hemolysis?

A

Intravascular

122
Q

What clinical signs are associated with Heinz body anemias?

A

Acute and profound signs of anemia
Hemoglobinuria / methemoglobinuria (maple leaf)
Hypoxia-induced neuro signs

123
Q

How are Heinz body anemias diagnosed?

A

New methylene blue stain on blood slides

124
Q

How are Heinz body anemias treated?

A

Remove source of oxidizing agent
Supportive care
Methylene blue reduces methemoglobin in cattle, but not horses

125
Q

Which species is most susceptible to copper toxicity?

A

Sheep

126
Q

How do acute and chronic copper toxicity differ?

A

Acute:
Colic, diarrhea, renal/hepatic failure, hemoglobinuria, icterus (maybe)
Chronic:
Hemolytic crisis (icterus, hemoglobinuria, etc.)

127
Q

What does labwork look like in copper toxicity? How is a diagnosis made?

A

Anemia
Methemoglobinemia
Elevated liver enzymes in pre-hemolytic phase of chronic poisoning
Renal failure (pigment nephropathy)

Dx acute: acute hemolytic syndrome + copper in blood and liver
Dx chronic: liver biopsy for copper

128
Q

How is copper toxicity treated?

A

Avoid stress and activity
Acute: Supportive (GI protectants, IV fluids)
Chronic: D-penicillamine (expensive)
PO Ammonium/sodium molybdate and sodium thiosulfate (facilitate fecal excretion)
IV sodium tetrathiomolybdate (protects circulating RBC)

129
Q

What is the causative agent of equine piroplasmosis? How is it transmitted?

A

Babesia caballi and equi
Tropical horse tick Dermacentor niteus
*REPORTABLE

130
Q

What clinical signs are associated with equine piroplasmosis?

A

7-21 days after exposure
Incoordination, lacrimation, swelling of eyelids, hemolytic anemia signs (intra/extravascular)
May die acutely or become a carrier

131
Q

How is equine piroplasmosis diagnosed?

A

Parasites may be visible in RBC in early phase (prior to CS)

CI-ELISA test - seropositive within 14 days

132
Q

How is equine piroplasmosis treated?

A

Imidocarb

BUT not authorized to tx here d/t reportable status

133
Q

Which patients are most often affected by water intoxication?

A

Young milk-fed calves suddenly given unrestricted access to cold drinking water > osmotic lysis of RBCs

134
Q

What does serum biochemistry of water intoxication reveal?

A

Hyponatremia, hypochloremia, decreased osmolarity

135
Q

How is water intoxication treated?

A

Restrict free water intake and restore normal blood osmolarity

136
Q

Which patients are affected by post-parturient hemoglobinuria?

A

High-producing multiparous dairy cattle

Onset in first month after calving

137
Q

What is the proposed mechanism for post-parturient hemoglobinuria?

A

Phosphate deficiency disrupts cellular energy metabolism and inhibits RBC defense mechanisms > susceptible to lysis

138
Q

What clinical signs are consistent with post-parturient hemoglobinuria?

A

Intravascular hemolysis

Depression, decreased milk production

139
Q

What lab abnormalities are consistent with post-parturient hemoglobinuria?

A

Marked hypophosphatemia

Anemia with dramatic regenerative response

140
Q

How is post-parturient hemoglobinuria treated?

A 
Blood, IV fluids
IV phosphate (sodium acid phosphate) followed with oral phosphorus supplementation
141
Q

Which breeds are most affected by neonatal isoerythrolysis?

A

Standardbreds and thoroughbreds

142
Q

Which blood antigens are associated with neonatal isoerythrolysis?

A

Foals Aa/Qa +

Mares Aa/Qa -

143
Q

What clinical signs are consistent with neonatal isoerythrolysis?

A 
Appear 2-3 days after birth
Weakness/lethargy
Iceterus
Bilirubinuria
Tachycardia with anemic murmur
Neurological signs (NPI)
144
Q

How is neonatal isoerythrolysis diagnosed?

A 
Anemia (usually <18%)
Elevated bilirubin
Coombs +
Crossmatch mare's serum to foals RBC
Jaundiced foal test (JFT):
-colostrum + foal blood
145
Q

How is neonatal isoerythrolysis treated?

A

Supportive care

Can use mare’s washed RBC for transfusion

146
Q

How is neonatal isoerythrolysis different in calves?

A

Does not occur naturally, a sequela to administration of blood-derived vaccines to dam (eg. anaplasma vax)

147
Q

What is the etiology and transmission of equine anaplasmosis?

A

Anaplasma phagocytophila
tick-borne
Infects neutrophils

148
Q

What clinical signs are consistent with equine anaplasmosis?

A

Mostly subclinical
Limb edema, mucosal petechiation, icterus, ataxia
Anemia is rarely severe

149
Q

How is equine anaplasmosis diagnosed?

A

Pancytopenia (mild)
Inclusion bodies in granulocytes
PCR (+5 days after infection and before CS)
IFA serological test (paired)

150
Q

How is equine anaplasmosis treated?

A

Will spontaneously resolve within 2 weeks
Oxytetracycline (improvement in 2 days)
Supportive care: hydration, limb bandages, easily chewed food

151
Q

What is the etiology of ruminant anasplasmosis? Which cells are infected? Where is disease seen geographically?

A

A. marginale (cattle)
A. ovis (sheep/goats)
Infect RBCs
Southern US states

152
Q

How is ruminant anaplasmosis transmitted?

A

Asymptomatic carrier cattle are major reservoir
Ticks and biting flies
Iatrogenic common

153
Q

Which animals are most affected by ruminant anaplasmosis?

A

Calves least susceptible

Adult cattle most susceptible

154
Q

What is the pathogenesis of ruminant anaplasmosis?

A

Incubation 3-6 weeks
Once inclusion bodies visible, # of affected RBC doubles every 24hrs for 7-10 days
Progressive hemolytic anemia (extravascular)
Animals that recover are carriers for life

155
Q

How is ruminant anaplasmosis diagnosed?

A

Dot-like organisms on RBC margin

Serological testing

156
Q

How is ruminant anaplasmosis treated?

A

Oxytetracycline to shorten disease course

Long-acting oxytet (IM q3 days for 4 treatments) to eliminate carrier state

157
Q

How is ruminant anaplasmosis prevented?

A

Vaccination (different from equine)

158
Q

What is the etiology of Mycoplasma hemollama?

A

Rickettsial disease
Arthropod blood-borne transmission
Affects immunocompromised llamas (sometimes cattle/sheep)

159
Q

What clinical signs are associated with M. hemollama?

A

Usually subclinical
Depression, fever, modest hemolytic anemia
Can be severe in sheep

160
Q

How is M. hemollama diagnosed?

A

Organisms on RBC (blood smear)

PCR

161
Q

How is M. hemollama treated?

A

Tetracycline (IM/IV)

162
Q

Which large animal species are most often affected by IMHA?

A

Horses

163
Q

How is IMHA treated in large animals?

A

Dexamethasone for immune suppression

164
Q

What is the etiology of equine infectious anemia?

A

Viral disease (retrovirus) causing immune-mediated hemolytic anemia
Affects horses, donkeys, mules
Infected animals are persistent carriers
*REPORTABLE

165
Q

How is equine infectious anemia transmitted?

A

Via blood - arthropods, iatrogenic, in utero

166
Q

How does equine infectious anemia present clinically?

A
  1. Acute (7-30 days post-infection)
    Fever, depression, anorexia, mucosal petechiation
    NO anemia
  2. Subacute to chronic (>30 days post-infection)
    anemia, icterus, intermittent fever, weight loss, generalized edema, death
  3. Chronic asymptomatic
    episodic flare-ups of clinical disease which become less common
167
Q

How is equine infectious anemia diagnosed?

A 
Coggins test (may be neg in first 10-14 days, recommend testing at 45 days)
ELISA (faster but not standardized)
168
Q

What features are unique about the equine erythron?

A
  1. Unstable PCV d/t splenic contraction
  2. Rouleaux formation
  3. Icteric plasma normal
  4. Lack of peripheral regeneration
  5. Howell-Jolly bodies normal (not indicative of regen)
169
Q

Why is testing total serum iron and TIBC useful in the equine? What might it tell you?

A

Helpful to determine regeneration
Low Fe + High TIBC = iron deficiency (chronic blood loss)
Low Fe + low/normal TIBC = anemia of chronic dz

170
Q

What is needed to definitively determine RBC regeneration in horses?

A

Bone marrow biopsy (regenerative E:M = 2:1)

171
Q

How much blood can safely be donated in the equine?

A

BW x 0.08 x 0.2 = L safe to take

20% of blood volume, which is 8% of BW

172
Q

What can be used to anticoagulate blood in an emergent field situation?

A

Heparin, 1 unit/mL blood

173
Q

Calculate how much blood to transfuse to a patient

A

BW (kg) x .08 x (PCV desired - PCV current) / PCV donor

174
Q

How is equine viral arteritis transmitted?

A

Aerosol or venereal

Stallions are main carrier

175
Q

What clinical signs are consistent with equine viral arteritis?

A

Most often asymptomatic

Edema, rhinitis/conjunctivitis, urticarial rash, abortion

176
Q

How is equine viral arteritis diagnosed?

A

Leukopenia
Serology - paired titers
Virus isolation
*Reportable in some states!

177
Q

How is equine viral arteritis treated and prevented?

A

Symptomatic tx, sexual rest for stallions
ARVAC modified live vaccine (breeding stallions in Dec/Jan)
Mares bred by + carrier stallions should be isolated >14 days

178
Q

What clinical signs are consistent with Lyme in horses?

A

Hyperesthesia
Arthritis, recurrent lameness
Encephalitis and uveitis

179
Q

What major r/o’s should be considered for Lyme in horses?

A

A. phagocytophilum
Immune-mediated dz
Leptospirosis

180
Q

How is Lyme diagnosed in horses?

A

Lyme multiplex test from Cornell
*Idexx NOT accurate
Synovial biopsy suggested

181
Q

How is Lyme treated in horses?

A

Oxytetracycline (>2 weeks and retest)

182
Q

What is the etiology and geographic region of pigeon fever?

A

Corynebacterium pseudotuberculosis

West coast

183
Q

What clinical signs are associated with pigeon fever?

A

Fever
Cellulitis and ulcerative lymphangitis
Abscesses - thick walled and deep, common on chest

184
Q

How is pigeon fever diagnosed?

A

Clinical and US evidence of deep abscess
Culture
Serum hemagglutination inhibition test (if suspect occult abscesses)

185
Q

How is pigeon fever treated? What is the prognosis?

A

Lance and drain abscesses
Penicillin or TMS
Good prognosis with simple abscesses, guarded if internal abscesses present

Y2S1 - LAM I (1 decks)

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