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
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
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
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
5
Q
How is Caprine Arthritis Encephalitis virus (CAEv) treated?
A
Only palliative tx
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
7
Q
What is involved in a “pasteurized rearing program”?
A
- Induce parturition with 2-3mL Lutalyse/Prostamate IM
- Attend kidding 30-32 hours post-injection, remove kids from dam immediately
- Rear kids in isolation on safe colostrum/milk
- Heat-treated colostrum (131ºF 1 hour)
- Pasteurized milk (165ºF 15 seconds) - House CAEv-free animals separately from infected animals
8
Q
What are the four disease presentations of Caprine Arthritis Encephalitis virus (CAEv)?
A
Kid neurologic form
Arthritis
Mastitis
Pneumonia
9
Q
Which animals get the neurologic form of CAEv?
A
2-6 month-old kids
10
Q
How does the neurologic form of CAEv present clinically?
A
Progressive paresis > irreversible paralysis (over weeks) > often die of 2º disease
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
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
13
Q
How is the neurologic form of CAEv treated?
A
No treatment. Humane euthanasia
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)
15
Q
How is the arthritic form of CAEv diagnosed?
A
Arthrocentesis - elevated mononuclear cells
Rads - calcification of joint capsule, tendon/sheaths, osteophyte formation
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)
17
Q
How does the mastitic form of CAEv present clinically?
A
Bilaterally hard udder at kidding
Scant milk, but appears normal
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
19
Q
How is the mastitic form of CAEv treated?
A
Steroids may help
Some goats spontaneously increase milk production in 2-3 weeks
20
Q
How does the pneumonia form of CAEv present clinically?
A
Exercise intolerance, dyspnea, wasting, coughing
Onset following stress
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
22
Q
How is the pneumonia form of CAEv treated?
A
Abx therapy may help if secondary bacterial pneumonia
23
Q
What is the etiologic agent of caseous lymphadenitis?
A
Corynebacterium pseudotuberculosis
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
25
How is caseous lymphadenitis transmitted?
Draining external abscesses
Aerosolization of lung abscesses
Skin via microtrauma
26
What is the pathogenesis of caseous lymphadenitis?
Localizes in regional LN > extension along LN chain / systemic travel > hair/wool loss as abscess matures > spontaneous rupture
27
How does external caseous lymphadenitis present?
Abscess formation in LN (parotid common) or SQ - non-painful with gradual hair loss
Pus is odorless, creamy white/yellowish/greenish
28
How does visceral caseous lymphadenitis present?
"thin ewe syndrome"
| Weight loss, neurologic signs, pneumonia-like symptoms
29
How is caseous lymphadenitis diagnosed?
Culture of abscess
Synergistic Hemolysis Inhibition test (SHIT)
-High titers = internal abscessation
-CANNOT distinguish vax from dz
30
How is caseous lymphadenitis controlled?
ID infected animals
Depopulate / separate herd
Vaccinate (sheep 1 year booster, goats 6 month booster)
31
How is caseous lymphadenitis treated in individual animals?
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
32
What classifies "safe use" of a drug?
Includes safety to animal, to persons associated with the animal, and environmental impact
33
What classifies "effective use" of a drug?
Assumes accurate dx can be made
drug properly administered
and course of dz can be followed to assess success of drug
34
What labelling must be on rx products?
Caution: Federal law restricts this drug to use by or on the order of a licensed veterinarian
35
What labelling must be on VFD drugs?
Caution: Federal law restricts medicated feed containing this VFD drug to use by or on the order of a licensed veterinarian
36
What is AMDUCA?
The Animal Medicinal Drug Use Clarification Act of 1994
| Established conditions for legal extra-label use of drugs in animals
37
What are the requirements for extra-label drug use under AMDUCA?
1. On the order of a licensed vet
| 2. Within the context of a vet-client-patient relationship
38
What are the exceptions to extra-label drug use under AMDUCA?
Does not apply to:
1. Drugs in feed
2. Drugs that result in a violative food residue
39
Which antibiotics are prohibited from ALL food animals?
```
Chloramphenicol
Clenbuterol
DES
Dipyrone
Gentian violet
Glycopeptides (eg. vancomycin)
Nitrofurans (including topicals)
Nitroimidazoles (including metronidazole)
Phenylbutazone (in adult dairy cattle)
```
40
How do the FDA define lactating (adult) dairy cattle?
Any dairy breed female >20 months regardless of milking
41
Which drugs are prohibited from extra-label use?
```
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)
```
42
Which antibiotic class is strongly discouraged in cattle? Why?
Aminoglycosides
| -insufficient data for withdrawal
43
What is the MUMS Animal Health Act?
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
44
How is ovine progressive pneumonia virus (OPPv) transmitted?
Aerosols/saliva
| Common needles
45
Which cell type does ovine progressive pneumonia virus (OPPv) infect?
Lymphocytes
46
How does ovine progressive pneumonia virus (OPPv) present clinically?
Poor milk production
-udders are firm, indentable, bilaterally symmetric
Emaciation
Secondary pneumonia
47
How is ovine progressive pneumonia virus (OPPv) diagnosed?
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
48
What are some differentials for emaciation in sheep?
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
49
What is the control strategy for ovine progressive pneumonia virus (OPPv)?
Elitest ELISA for testing
Avoid housing young lambs with older OPPv+ sheep
TMEM154 testing available in Lincoln, NE
50
Are sheep or goats more susceptible to foot rot/scald?
Sheep
51
What infectious agents cause footrot/scald?
Dichelobacter nodosus
| Synergistic effect of Fusobacterium necrophorum
52
T/F: Health certificates can be signed if footrot/scald is present as long as it's being treated?
FALSE, it's still an infectious disease
53
How is footrot treated?
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)
54
How is foot scald treated?
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
55
When should sheep be culled for footrot/scald?
If lame more than twice a year or not responding to treatment
56
How can footrot/scald be controlled?
```
Regular footbaths (10% zinc sulfate)
*No vaccination available in US
```
57
What generalities are true for all clostridial diseases?
Highly fatal, sudden onset
Often affect thriftiest animals
Therapy ineffective once ill
Vaccination is cost-effective and works well
58
How is C. tetani treated and prevented?
```
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
59
What clinical signs are associated with botulism?
Lack of muscle tone, progressive weakness > recumbence
60
What is the main risk factor for botulism?
Spreading poultry litter on land that produces pasture, hay, baleage, or silage in same year
61
Is botulism zoonotic?
No
62
What is the causative agent of braxy? What does it look like clinically?
C. septicum
| Gangrenous abomasitis in young lambs and calves
63
What are the causative agents of clostridal myonecrosis? What are the various disease names?
C. chauvoei, septicum, sordellii, or mixed infections
| Blackleg, Malignant edema, Gas gangrene
64
What are the clinical signs of clostridial myonecrosis?
Lameness, fever, depression
Crepitus and swelling (bubble wrap muscles)
Rapid deterioration with up to 100% mortality
65
DDx for sudden death in ruminants?
```
Clostridium
Bloat
Lightning strike
Grass tetany
Atypical interstitial pneumonia
```
66
How can clostridial myonecrosis be diagnosed?
PCR sample of affected muscle
67
How can clostridial myonecrosis be treated? What's the prognosis?
IV K penicillin
| Poor
68
What is the causative agent of bacillary hemoglobinuria? What is its common name? What species does it infect?
C. haemolyticum / novyi type D
"Red water"
Cattle
69
What is the pathogenesis of bacillary hemoglobinuria?
Fluke liver infection > liver damage creating anaerobic environment > beta, eta, and theta clostridial toxins > localized hepatic necrosis and IV hemolysis
70
What clinical signs are associated with bacillary hemoglobinuria?
Red urine, bleeding from other orifices
| Sudden death
71
What necropsy findings are consistent with bacillary hemoglobinuria?
Ischemic hepatic infarct with zone of hyperemia next to viable liver tissue
Widespread serosal and mucosal hemorrhages
Red-tinged fluid in abdomen and thorax
72
What is the causative agent of black disease? What species does it infect?
C. novyi type B
| Sheep
73
What clinical signs are consistent with black disease? What is a major risk factor?
Infectious necrotic hepatitis
Similar to bacillary hemoglobinuria but NO red urine or bleeding from orifices
Liver fluke (F. magna) major risk factor
74
What is the causative agent of enterotoxemia?
| What are two common names for the dz?
Clostridium perfringes type D
| Pulpy kidney dz, overeating dz
75
Who does enterotoxemia typically affect? What is the main risk factor?
Feedlot lambs
| High CHO in diet (even lush pastures)
76
What clinical signs are consistent with enterotoxemia?
| How long does disease last?
Ataxia, trembling, opisthotonus, rapid progression to convulsions, coma
Peracute dz, lasts <2 hours
77
What is the main differential for enterotoxemia?
Polioencephalomalacia
78
What necropsy lesions are consistent with enterotoxemia in SHEEP?
```
Pulmonary edema
Congested intestines
Hydropericardium with soft fibrinous clot (jello)
Hyperglycemia and glucosuria
Pulpy soft kidney if fresh carcass
Focal symmetric encephalomalacia
```
79
What necropsy lesions are consistent with enterotoxemia in GOATS?
Fibrinohemorrhagic enterocolitis
Pulmonary edema
Renal tubular necrosis
Edema of mesenteric LNs
80
What vaccination schedule should be followed to prevent enterotoxemia?
Sheep q12 months, goats q6 months
| Incoming feedlot animals: vax 2x 1 month apart and work up on feed slowly
81
What is the causative agent of necrohemorrhagic enteritis?
C. perfringes type C or A
82
Who does necrohemorrhagic enteritis typically infect? What is the pathogenesis?
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
What clinical signs are consistent with necrohemorrhagic enteritis?
Depression, anorexia, rapid progression to death
84
What necropsy findings are consistent with necrohemorrhagic enteritis?
Necrosis of duodenal and/or jejunal mucosa, hemorrhagic mesenteric LNs
85
How is necrohemorrhagic enteritis diagnosed?
PCR
86
How is necrohemorrhagic enteritis treated and prevented?
Antitoxin
Broad-spectrum abx (PO metronidazole)
Milk withdrawal 24 hours
Pre-partum vaccination with type A
87
When do anthrax outbreaks typically occur?
July-September following flooding
88
How is anthrax transmitted?
Soil, vegetation, water
Insufficiently cooked infected meat, dead carcasses
Blow fly bites
89
What are anthrax's virulence factors?
```
Protective antigen (PA)
Lethal factor (LF)
Oedema factor (OF)
2 phase life cycle (spore and virulent)
```
90
What clinical signs are consistent with anthrax?
Peracute septicemia characterized by failure of blood to clot
Apathy or excited bellowing
Abortion with massive uterine hemorrhage
91
DDx for sudden exudative hemorrhage?
```
Lightning strike
Dehydration
Acute plant/chemical poisoning
Salmonellosis enteritis
Leptospirosis
Babesiosis
Clostridial infections
Purpura
```
92
How can anthrax be diagnosed in the field?
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
How can anthrax be diagnosed in the lab?
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
How is anthrax treated? What is the prognosis?
Parenteral tetracyclines or penicillin
| Prognosis good unless advanced
95
How is anthrax prevented?
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
What are PCV normals for horses, cows, and camelids?
Horse: 32-48
Cows: 24-46
Camelids: 26-42
97
What clinical signs are expected in anemia?
```
Exercise intolerance
Tachycardia / tachypnea
Pale mms
Weakness
Low systolic murmur (d/t watery blood)
Depression
```
98
How does clinical pathology differ in cases of acute vs chronic blood loss?
Acute: reduced TPP, but maybe normal PCV
Chronic: reduced TPP and PCV (mild clinical signs)
99
What are the various clinical manifestations of bracken fern toxicosis?
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
What is the pathogenesis of anemia caused by bracken fern toxicosis?
Aplastic anemia and subsequent pancytopenia:
1. Thrombocytopenia > widespread hemorrhage
2. Leukopenia/neutropenia > SBIs
3. Nonregenerative anemia
101
What clinical signs are associated with bracken fern toxicosis?
Sudden onset
Fever, melena, epistaxis, hyphema, petechial/ecchymotic hemorrhages
Death in 1-3 days
102
How is bracken fern toxicosis treated? What is the prognosis?
Supportive care: IV fluids, abx, tranfusions
Avoid stress/trauma
Grave prognosis
103
What is the etiology of purpura hemorrhagica?
Immune-mediated vasculitis of horses
| Type III hypersensitivity reaction to streptococcal antigens (often secondary to strangles)
104
What clinical signs are consistent with purpura hemorrhagica?
Widespread edema, petechial hemorrhages, laminitis, DIC, mild anemia
105
How is purpura hemorrhagica treated?
Corticosteroids and penicillin (if S. equi)
106
What is the pathogenesis of DIC?
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
How is DIC diagnosed?
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
How is DIC treated?
Treat underlying condition!
| IV fluids, NSAIDs, heparin (provided adequate AT-III levels), blood/plasma as needed
109
Which species mostly affected by moldy sweet clover poisoning?
Ruminants
110
What is the pathogenesis of moldy sweet clover poisoning?
Dicoumarol competitively inhibits vitamin K > deficiency of II, VII, IX, X > impaired coagulation and hemorrhage
111
What does labwork look like in a moldy sweet clover poisoning case?
CBC - anemia (maybe)
Increased PT, PTT, and ACT
Normal PLT counts
112
How is moldy sweet clover poisoning treated?
Stop feeding clover or dilute component
Vitamin K1 (NOT K3)
Transfusion (only need 1L to restore clotting factors)
113
What is hemophilia? Which large animals does it affect?
Inherited factor VIII deficiency
| Horses (thoroughbreds, standardbreds, arabians, quarter horses)
114
How does hemophilia appear clinically? What does lab work show?
```
Characterized by hemarthrosis and hematoma formation d/t coagulation defects
aPTT prolonged (intrinsic pathway)
```
115
How is hemophilia treated?
No treatment.
116
What is the pathogenesis of ITP (immune-mediated thrombocytopenia)?
Antibody-mediated destruction of platelets
| Idiopathic or secondary to drugs/dz/neoplasia
117
What does labwork look like in ITP?
PLT <40,000 (clinical signs)
Anemia and hypoproteinemia
PT, aPTT, fibrinogen all NORMAL
Prolonged bleeding times
118
How is ITP treated? What's the prognosis?
Dexamethasone
Transfusion for severe anemia
Good prognosis (dependent on cause)
119
Which infectious agents are most likely to cause thrombocytopenia in large animals?
BVDV
EIAV (mild)
Anaplasma phagocytophila
120
What might cause oxidant-induced hemolytic anemias (Heinz body anemias) in large animals?
```
Phenothiazine (horses)
Wild onions (cattle and horses)
Red maple leaf (horses
```
121
Do Heinz body anemias cause primarily intra or extravascular hemolysis?
Intravascular
122
What clinical signs are associated with Heinz body anemias?
Acute and profound signs of anemia
Hemoglobinuria / methemoglobinuria (maple leaf)
Hypoxia-induced neuro signs
123
How are Heinz body anemias diagnosed?
New methylene blue stain on blood slides
124
How are Heinz body anemias treated?
Remove source of oxidizing agent
Supportive care
Methylene blue reduces methemoglobin in cattle, but not horses
125
Which species is most susceptible to copper toxicity?
Sheep
126
How do acute and chronic copper toxicity differ?
Acute:
Colic, diarrhea, renal/hepatic failure, hemoglobinuria, icterus (maybe)
Chronic:
Hemolytic crisis (icterus, hemoglobinuria, etc.)
127
What does labwork look like in copper toxicity? How is a diagnosis made?
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
How is copper toxicity treated?
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
What is the causative agent of equine piroplasmosis? How is it transmitted?
Babesia caballi and equi
Tropical horse tick Dermacentor niteus
*REPORTABLE
130
What clinical signs are associated with equine piroplasmosis?
7-21 days after exposure
Incoordination, lacrimation, swelling of eyelids, hemolytic anemia signs (intra/extravascular)
May die acutely or become a carrier
131
How is equine piroplasmosis diagnosed?
Parasites may be visible in RBC in early phase (prior to CS)
| CI-ELISA test - seropositive within 14 days
132
How is equine piroplasmosis treated?
Imidocarb
| BUT not authorized to tx here d/t reportable status
133
Which patients are most often affected by water intoxication?
Young milk-fed calves suddenly given unrestricted access to cold drinking water > osmotic lysis of RBCs
134
What does serum biochemistry of water intoxication reveal?
Hyponatremia, hypochloremia, decreased osmolarity
135
How is water intoxication treated?
Restrict free water intake and restore normal blood osmolarity
136
Which patients are affected by post-parturient hemoglobinuria?
High-producing multiparous dairy cattle
| Onset in first month after calving
137
What is the proposed mechanism for post-parturient hemoglobinuria?
Phosphate deficiency disrupts cellular energy metabolism and inhibits RBC defense mechanisms > susceptible to lysis
138
What clinical signs are consistent with post-parturient hemoglobinuria?
Intravascular hemolysis
| Depression, decreased milk production
139
What lab abnormalities are consistent with post-parturient hemoglobinuria?
Marked hypophosphatemia
| Anemia with dramatic regenerative response
140
How is post-parturient hemoglobinuria treated?
```
Blood, IV fluids
IV phosphate (sodium acid phosphate) followed with oral phosphorus supplementation
```
141
Which breeds are most affected by neonatal isoerythrolysis?
Standardbreds and thoroughbreds
142
Which blood antigens are associated with neonatal isoerythrolysis?
Foals Aa/Qa +
| Mares Aa/Qa -
143
What clinical signs are consistent with neonatal isoerythrolysis?
```
Appear 2-3 days after birth
Weakness/lethargy
Iceterus
Bilirubinuria
Tachycardia with anemic murmur
Neurological signs (NPI)
```
144
How is neonatal isoerythrolysis diagnosed?
```
Anemia (usually <18%)
Elevated bilirubin
Coombs +
Crossmatch mare's serum to foals RBC
Jaundiced foal test (JFT):
-colostrum + foal blood
```
145
How is neonatal isoerythrolysis treated?
Supportive care
| Can use mare's washed RBC for transfusion
146
How is neonatal isoerythrolysis different in calves?
Does not occur naturally, a sequela to administration of blood-derived vaccines to dam (eg. anaplasma vax)
147
What is the etiology and transmission of equine anaplasmosis?
Anaplasma phagocytophila
tick-borne
Infects neutrophils
148
What clinical signs are consistent with equine anaplasmosis?
Mostly subclinical
Limb edema, mucosal petechiation, icterus, ataxia
Anemia is rarely severe
149
How is equine anaplasmosis diagnosed?
Pancytopenia (mild)
Inclusion bodies in granulocytes
PCR (+5 days after infection and before CS)
IFA serological test (paired)
150
How is equine anaplasmosis treated?
Will spontaneously resolve within 2 weeks
Oxytetracycline (improvement in 2 days)
Supportive care: hydration, limb bandages, easily chewed food
151
What is the etiology of ruminant anasplasmosis? Which cells are infected? Where is disease seen geographically?
A. marginale (cattle)
A. ovis (sheep/goats)
Infect RBCs
Southern US states
152
How is ruminant anaplasmosis transmitted?
Asymptomatic carrier cattle are major reservoir
Ticks and biting flies
Iatrogenic common
153
Which animals are most affected by ruminant anaplasmosis?
Calves least susceptible
| Adult cattle most susceptible
154
What is the pathogenesis of ruminant anaplasmosis?
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
How is ruminant anaplasmosis diagnosed?
Dot-like organisms on RBC margin
| Serological testing
156
How is ruminant anaplasmosis treated?
Oxytetracycline to shorten disease course
| Long-acting oxytet (IM q3 days for 4 treatments) to eliminate carrier state
157
How is ruminant anaplasmosis prevented?
Vaccination (different from equine)
158
What is the etiology of Mycoplasma hemollama?
Rickettsial disease
Arthropod blood-borne transmission
Affects immunocompromised llamas (sometimes cattle/sheep)
159
What clinical signs are associated with M. hemollama?
Usually subclinical
Depression, fever, modest hemolytic anemia
Can be severe in sheep
160
How is M. hemollama diagnosed?
Organisms on RBC (blood smear)
| PCR
161
How is M. hemollama treated?
Tetracycline (IM/IV)
162
Which large animal species are most often affected by IMHA?
Horses
163
How is IMHA treated in large animals?
Dexamethasone for immune suppression
164
What is the etiology of equine infectious anemia?
Viral disease (retrovirus) causing immune-mediated hemolytic anemia
Affects horses, donkeys, mules
Infected animals are persistent carriers
*REPORTABLE
165
How is equine infectious anemia transmitted?
Via blood - arthropods, iatrogenic, in utero
166
How does equine infectious anemia present clinically?
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
How is equine infectious anemia diagnosed?
```
Coggins test (may be neg in first 10-14 days, recommend testing at 45 days)
ELISA (faster but not standardized)
```
168
What features are unique about the equine erythron?
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
Why is testing total serum iron and TIBC useful in the equine? What might it tell you?
Helpful to determine regeneration
Low Fe + High TIBC = iron deficiency (chronic blood loss)
Low Fe + low/normal TIBC = anemia of chronic dz
170
What is needed to definitively determine RBC regeneration in horses?
Bone marrow biopsy (regenerative E:M = 2:1)
171
How much blood can safely be donated in the equine?
BW x 0.08 x 0.2 = L safe to take
| 20% of blood volume, which is 8% of BW
172
What can be used to anticoagulate blood in an emergent field situation?
Heparin, 1 unit/mL blood
173
Calculate how much blood to transfuse to a patient
BW (kg) x .08 x (PCV desired - PCV current) / PCV donor
174
How is equine viral arteritis transmitted?
Aerosol or venereal
| Stallions are main carrier
175
What clinical signs are consistent with equine viral arteritis?
Most often asymptomatic
| Edema, rhinitis/conjunctivitis, urticarial rash, abortion
176
How is equine viral arteritis diagnosed?
Leukopenia
Serology - paired titers
Virus isolation
*Reportable in some states!
177
How is equine viral arteritis treated and prevented?
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
What clinical signs are consistent with Lyme in horses?
Hyperesthesia
Arthritis, recurrent lameness
Encephalitis and uveitis
179
What major r/o's should be considered for Lyme in horses?
A. phagocytophilum
Immune-mediated dz
Leptospirosis
180
How is Lyme diagnosed in horses?
Lyme multiplex test from Cornell
*Idexx NOT accurate
Synovial biopsy suggested
181
How is Lyme treated in horses?
Oxytetracycline (>2 weeks and retest)
182
What is the etiology and geographic region of pigeon fever?
Corynebacterium pseudotuberculosis
| West coast
183
What clinical signs are associated with pigeon fever?
Fever
Cellulitis and ulcerative lymphangitis
Abscesses - thick walled and deep, common on chest
184
How is pigeon fever diagnosed?
Clinical and US evidence of deep abscess
Culture
Serum hemagglutination inhibition test (if suspect occult abscesses)
185
How is pigeon fever treated? What is the prognosis?
Lance and drain abscesses
Penicillin or TMS
Good prognosis with simple abscesses, guarded if internal abscesses present
