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Hemolymphatic Diseases Flashcards

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1
Q

What are the different causes of anemia?

A
  • Blood loss
  • Intravascular hemolysis
  • Extravascular hemolysis
  • Decreased production
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2
Q

What are the general laboratory findings seen with blood loss?

A
  • anemia + hypoproteinemia
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3
Q

What are the general laboratory findings seen with intravascular hemolysis?

A
  • Pink plasma
  • hemoglobinuria
  • regeneration +/-
  • hyperbilirubinemia
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4
Q

What are the general laboratory findings seen with Extravascular hemolysis?

A
  • Icterus
  • +/- Regeneration
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5
Q

What are the general laboratory findings seen with decreased production of erytherocytes?

A
  • No regeneration
  • Hyperproteinemia
    • ⇡ globulins
    • dehydration
    • possibly hyperfibrinogenemia
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6
Q

What clinical signs are seen with anemia due to blood loss?

A
  • Exercise intolerance
  • tachycardia
  • tachypnea
  • pallor
  • aggression (hypoxia)
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7
Q

What are common causes of blood loss anemia?

A
  • Acute:
    • Trauma
    • Surgical
    • Coagulopathy
    • DIC
    • Sepsis
    • Post-Caval Syndrome
    • Uterus (prolapse)
  • Chronic:
    • Parasites
    • Ulcers
    • Trauma
    • Urinary - Bracken Fern
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8
Q

What are causes of whole blood loss in cattle?

A
  • Trauma (external/internal)
  • Parasites
  • Abomasal Ulcers
  • Coagulopathy
    • Moldy Sweet Clover
    • BVD
  • Post-Caval Syndrome (Terminal)
  • Enzootic Hematuria (chronic Brackenfern)
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9
Q

What causes Abomasal ulcers?

A
  • High producing animals, show animals
  • Diets high in starch, low fiber content
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10
Q

What are the types of abomasal ulcers?

A
  • 4 Classifications based on severity
    • Type I - mucossal
    • Type IV - perforation, hemorrhage
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11
Q

What clinical signs/pathology are seen with abomasal ulcers

A
  • Signs:
    • anorexia, decreased forestomach motility, +Fecal occult blood/melena
    • Pallor, decreased milk production, shock, sepsis
  • Pathology:
    • Fecal occult blood + (usually)
    • ⇣ PCV, normal to ⇣ Protein
    • W/ perforation expect peritonitis:
      • leukocytosis/leukopenia
      • hyperfibrinogenemia
      • fever
      • scleral injection
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12
Q

What is the treatment for abomasal ulcers?

A
  • Dietary and stress managment
  • High quality hay, stall rest
  • Oral alkalinizing agents (i.e. Megnalax)
  • Pepto?
  • Sepsis: blood transfusions, antibiotics
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13
Q

What happens when cattle eat moldy sweet clover?

A
  • Natural coumarins are converted to dicumarol by the mold
    • degree dependent upon moisture content of hay
  • Decreased synthesis of factors II, VII, IX, X by inhibition of Vit K
  • Pathology:
    • prolonged PT, followed by prolonged APTT
    • Normal platelet count
    • Absence of fever and liver failure
  • Signs:
    • Epistaxis
    • melena
    • swollen joints
    • hematomas
    • effusive hemorrhages in body cavity
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14
Q

What is the “Lee-White” clotting time?

A
  • blood should clot in a red top tube w/in 5 minutes
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15
Q

What happens when cattle ingest Bracken Fern?

A
  • Toxic compound - ptaquiloside
    • all parts, live or dried
  • Acute:
    • coagulopathy
    • septicemic crises w/ bone marrow suppression
  • Chronic:
    • Enzootic Hematuria
      • hemorrhagic cystitis w/chronic blood loss anemia
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16
Q

How can Bracken fern toxicity be differentiated from other causes of hemorrhagic cystitis?

A
  • Hemoglobinuria by red cell sedimentation
  • No hemoglobin
  • Thickened bladder
  • Obstruction or pollakiuria
  • Usually multiple cases, mild bacteriuria, pyuria, and anemia
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17
Q

How is Enzootic hematuria diagnosed at necropsy?

A
  • Marrow hypoplasia
  • Urinary bladder pathology
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18
Q

What hemolytic diseases commonly effect food animals?

A
  • Anaplasmosis
  • Mycoplasma Haemollama (camelids)
  • Bacillary Hemoglobinuria
  • Leptospirosis (calves/feedlot)
  • Babesia
  • Water intoxication
  • Neonatal Isoerythrolysis
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19
Q

What is Anaplasmosis?

A
  • Anaplasma marginale - cattle, wild ruminants
  • Most prevalent tick-transmitted disease of cattle
  • Intracellular parasite of RBCs
    • Cattle become lifelong carriers and serve as reservoirs
  • Transmission:
    • Boophilus annulatus, D. andersoni, Tabanids, Chrysops
    • Iatrogenic (dehorners, tattoos, etc)
  • severity:
    • Calves <1yr - subclinical
    • Acute but rarely fatal in animals <2yrs
    • Often fatal in animals >2yrs
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20
Q

What happens with persistently infected cattle with anaplasmosis

A
  • Low-level (~0.1%) of parasitized erythrocytes
  • Permanent cycles of rickettsemia occurring at 3-5wk intervals
    • New antigenic variant of A. marginale arises
      • structural changes of surface antigens msp2 and msp3
      • Immune response to each new variant
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21
Q

How often is anaplasmosis transmitted in utero? (vertical transmission)

A
  • 16 - 20% of calves born to PI cows are infected in utero
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22
Q

What are the clinical signs and pathology of Anaplasmosis?

A
  • Signs:
    • weakness, lethargy
    • exercise intolerance
    • dyspnea/tachycardia
    • aggression due to hypoxia
    • GI forestomach hypomotility - constipation
    • Icterus (often profound)
    • Extravascular hemolysis!
  • Pathology:
    • Enlarged orange liver
    • marked icterus/pallor of tissues
    • splenomegaly
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23
Q

How is anaplasmosis diagnosed?

A
  • direct blood smear - visualize intracellular parasite
  • cELISA
  • PCR
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24
Q

How is Anaplasmosis treated?

A
  • Parenteral Oxytetracycline
    • Baytril 100-CA1 conditional approval
    • 100 mg/ml:
      • 22mg/kg IM/IV SID x5d
      • 11mg/kg IM/IV SID x10d
    • 200 mg/ml:
      • 20 mg/kg SID for 4 treatments at 3 day interval
  • Blood transfusions in acute cases
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25
Q

How is anaplasmosis controlled (medically)?

A
  • Oxytetracycline 200mg/ml
    • 20mg/kg SC q 21-28 days
  • Chlortetracycline in feed
    • control of active infection
      • NOT clinical disease, and NOT prevention
      • NO ELDU
    • <700lbs: 2.0mg/lb/day
    • >700lbs: 0.5mg/lb/day
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26
Q

What is Mycoplasma haemollama

A
  • Camelid RBC “Epi”-cellular parasite
    • Attaches to membrane via small fibrils
    • a clear zone separates parasites from the membrane
    • easily dislodged w/ blood smear
  • Clinical signs and treatment similar to anaplasmosis in cattle
  • Definitive diagnosis and screening with PCR
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27
Q

What are health impacts of Mycoplasma haemollamae

A
  • Variable severity
    • mild to severe anemia
    • Depression, lethargy
    • weight loss
    • Death - especially in crias
    • fever
    • tachycardia/tachypnea
  • May be an incidental finding in clinically “normal” animals
  • “cyclical” in peripheral blood
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28
Q

How is Mycoplasma haemolamae diagnosed?

A
  • Poor sensitivity and specificity w/ direct visualization
    • Low numbers of parasites to visualize when animal is also anemic
    • organisms easily fall off and may look like stain precipitate
  • PCR assay- Oregon State
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29
Q

How is Mycoplasma Haemolamae treated?

A
  • Oxytetracycline (1st choice), Florfenicol (2nd)
    • Camelids may become chronic carriers
    • Normal, healthy camelids may clear infection w/out treatment
  • Blood transfusion
  • Fluid therapy
  • Rule out other diseases
    • aplastic anemia
    • myelofibrosis
    • Myelodysplastic syndromes
    • Anemia of chronic disease
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30
Q

What is Mycoplasma Weyoni

A
  • Eperythrozoonosis
  • Blood borne protozoal disease
  • Animals <3yrs
  • Signs (short <1 wk)
    • Edema of ventrum, limbs, udder, scrotum
    • Fever (103-106)
    • hyperpnea
    • rales
    • anorexia
    • depression
  • Pathology
    • Mild anemia
      • normocytic to microcytic
    • leukocytosis
    • Organisms present on periphery of RBC, stain poorly
      • pleomorphic - tennis rackets to signet ring
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31
Q

What is Babesiosis?

A
  • Eradicated from US
  • B. bigemina, B. bovis
    • tick vector - Boophilus annulatus
  • Signs:
    • Fever
    • icterus
    • anemia
    • tachypnea
    • tachycardia
    • hemoglobinuria/hemoglobinemia due to intravascular hemolysis
    • abortions
    • death
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32
Q

What causes Bacillary Hemoglobinuria?

A
  • Focal hepatic infection with C. hemolyticum
    • releases toxins (phospholipase C beta toxin)
    • produces hepatic necrosis and degradation of lipid membranes ⇢ intravascular hemolysis
  • Bacterial spores reside in liver until anaerobic conditions present allowing de-sporulation and toxin production
  • Hepatic damage often caused by liver fluke, primary inciting cause
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33
Q

When does Blood loss result in death vs anemia?

A
  • Acute los of >⅓ of circulating blood volume (~8% bw) ⇢ death from shock
  • Gradual loss (>24hr) of up to ½ (50%) of blood volume may be tolerated (anemia)
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34
Q

What is hemolytic anemia? signs?

A
  • RBCs either become fragile and burst (toxicity) or are targeted by the immune system (infectious)
  • Signs:
    • Icterus (usually circulatory in cattle, rather than liver disorder)
    • hemoglobinemia/hemoglobinuria
    • fever
    • tachycardia
    • tachypnea
    • depression
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35
Q

How can extravascular destruction of RBCs be differentiated from intravascular destruction?

A
  • Icterus without hemoglobinuria is associated with extravascular destruction
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36
Q

What are common causes of hemolytic anemias in cattle?

A
  • Bacterial
    • Bacillary Hemoglobinuria
    • Leptospirosis
  • Protozoal
    • Anaplasma
    • Eperythrozooan
    • Babesia
  • Toxic
    • rape and kale
    • onion
    • copper
    • pharmaceuticals
  • Other:
    • Postparturient hemoglobinuria
    • Water intoxication
    • Neonatal isoerythrolysis
    • Autoimmune
37
Q

What is Suppression/depression Anemia?

A
  • Decreased erythropoiesis either due to impairment or lack of hemopoietic stimulation
    • Due to some failing physiologic factor due to lack of cofactors (ie vitamin/mineral deficiencies) organ disease of a stimulator organ or anatomic disruption of marrow progenitor cells
38
Q

What causes depression anemia in cattle

A
  • Chronic infection
  • Chronic renal disease (pyelonephritis, amyloidosis)
  • Parasites
  • Acute Bracken fern (myelodysplasia)
  • Malignancy
39
Q

What is Post-Caval Syndrome

A
  • Usually result of liver abscesses in close proximity to the posterior vena cava or large pulmonary vessels eroding through the vasculature wall
  • Presents as epistaxis and hemoptysis
  • Cattle may die suddenly or present with signs of blood loss anemia
    • anemia + hypoproteinemia
40
Q

What is the treatment for Acute blood loss anemia?

A
  • Stop hemorrhage
  • Fluids
  • Whole blood transfusion
41
Q

How/why are blood transfusions done in cattle?

A
  • do not expect to completely replace RBCs
    • More interested in the cofactors (proteins, clotting factors, etc)
  • Cells will only last a few days - provides support not resolution
  • Procedure:
    • Collect blood:
      • up to ~10-15% of donors blood volume (BV = BW * 8%)
        • start at about 10-12 ml/kg
    • Transfuse:
      • Try to replace 20-40% of calculated blood loss in recipient
        • Ex: 450kg cow - 36L blood volume
          • PCV decreased from 30% to 15% ⇢ lost about 18L of blood ⇢ Replace 40% (7Liters!)
      • Rate starts at 0.5ml/kg/hr (2-3 drops/sec) for the first 5 -10 minutes then increase to 10ml/kg/hr
42
Q

Does blood need to be cross-matched in cattle for transfusions?

A
  • No!
  • transfusion reactions rare in cattle
43
Q

What are abomasal ulcers?

A
  • Common in cattle fed high carb, low fiber diets
    • high producing dairy cattle, show cattle, etc
  • High incidence in first month after calving
  • Contaminant diseases increase incidence
    • mastitis, metritis, ketosis, etc
  • Ulcers:
    • May be mild mucosal erosion, deep layer ulceration, or complete perforation
    • Can progress rapidly to perforation, acute peritonitis and death before clinical signs can be seen or diagnostics can be performed
44
Q

What are the clinical signs of abomasal ulcers?

A
  • Signs:
    • partial to complete anorexia
    • Decreased GI motility (rumen, SI)
    • Positive fecal occult blood test
      • visual melena possible
    • Pale mucous membranes
    • Decreased milk production
    • perforating ulcers may present as signs of severe colic, septic or hypovolemic shock
45
Q

What clinical pathology test can be done with abomasal ulcers

A
  • Fecal occult blood test
    • good specificity, sensitivity erratic
  • Anemia, TP low normal to decreased
  • Test for BLV
  • CBC/Chemistry may provide prognostic support
46
Q

What is the treatment for abomasal ulcers?

A
  • Decrease grain intake, increase fiber
    • increased hay will help alkalinize abomasal environment
  • Magnesium hydroxide orally
    • cathartic and alkalinizing
    • 2-3 doses
      • systemic sever alkalosis may occur with excessive doses
  • Bismuth Sulfate (Peptobismol), Kaolin-pectalin (kaopectate)
  • Antibiotics
  • Blood transfusion is severe bleeding
    • most useful for providing clotting factors and proteins
47
Q

Which sweet clover causes coagulopathies?

A

Melilotus spp

48
Q

What are the clinical signs of Moldy Sweet Clover toxicosis?

A
  • Same as coagulopathy
  • Anemia
  • epistaxis
  • melena
  • swollen joints (hemorrhagic)
  • hematomas
  • petechia
  • hemorrhagic effusions of body cavities
  • Not a hemolytic disease - mild icterus may develop due to breakdown of RBCs from large volumes of blood in tissues from ongoing hemorrhage
49
Q

How is moldy sweet clover toxicosis diagnosed?

A
  • History of exposure and compatible clinical signs
  • Anemia w/normal platelet count
  • No indications of liver disease/failure
  • Prolonged clotting time
    • blood should clot in a red top tube w/in 5 minuts
50
Q

What is the treatment for Moldy Sweet clover toxicosis

A
  • Gentle handling
  • Remove source
  • Vit K1 injection:
    • 1-3mg/kg IM or SQ BID/TID for 2-3 days
51
Q

What happens when cattle eat Bracken fern (Pteridium aqualinum)

A
  • Enzootic hematuria or acute bracken fern toxicosis
  • Both can result in hemolymphatic crises
  • ptaquiloside compound is toxic and in all parts of the plant
52
Q

How are Enzootic Hematuria and Acute Bracken fern Toxicosis (caused by the same plant) different?

A
  • Enzootic Hematuria = chronic
    • consuming 1-3% of BW for months to years
    • Hemorrhagic cystitis and urinary bladder neoplasia
  • Acute Toxicosis
    • primary hemolymphatic crisis due to bone marrow suppression
    • Consuming equivalent BW over 3wks to 3 month time period
    • Fever, depression, weakness, uncontrolled hemorrhage
53
Q

How is Enzootic Hematuria/Acute Bracken Fern Toxicosis diagnosed?

A
  • CBC:
    • anemia (mild to severe)
    • severe pan-leukopenia (acute toxicosis)
  • Necropsy - Bone marrow hypoplasia
54
Q

What are the clinical signs of Bacillary Hemoglobinuria?

A
  • Acute onset w/ rapid progression
  • Depression
  • Anorexia
  • Fever (104-106)
  • Head and neck extension, arched back
    • visceral/liver pain
  • Hemoglobinemia/hemoglobinuria (~24hrs after start)
  • Icterus
55
Q

How is bacillary Hemoglobinuria diagnosed?

A
  • High case fatality rate - Dx usually post-mortem
  • Hepatic Infarct and necrosis
    • conically shaped w/ hyperemic zone
  • Dark red urine in bladder
56
Q

What is the treatment for Bacillary hemoglobinuria

A
  • Supportive - Prognosis is GRAVE
  • Procaine Penn G (40K units BID)
  • Fluids
  • Transfusions
57
Q

What is Leptospirosis

A
  • L. pomona and L. icterohemorrhagica most common
  • Causes wide clinical syndromes:
    • septicemia, interstitial nephritis, abortion, mastitis, ophthalmia, hemolytic anemia
  • Zoonotic
58
Q

What are the clinical signs of Leptospirosis

A
  • Hemolytic syndrome almost exclusively in calves <1mo
  • Depressed
  • Icerus
  • Pallor
  • Fever (105-107)
  • Tachycardia
  • Dyspnea
  • Anemia - most likely immune-mediated
  • Petechial mucosal hemorrhage
  • Hemoglobinuria
59
Q

How is Leptospirosis diagnosed?

A
  • Urine culture, Fluorescent assay, and dark field microscopy of urine possible for confirmation
  • Serology:
    • >1000 agglutinating antibodies is presumptive
    • best to have rising titers from paired samples 2wks apart
  • Post mortem:
    • anemia/pale tissues
    • generalized hemorrhage
    • raised white spots on kidneys
    • hemoglobinuria
60
Q

What is the treatment for Leptospirosis?

A
  • Oxytetracycline (9mg/lb IV/SQ q24hr for 4 doses)
  • Plus oral tetracycline for one month
61
Q

What is Neonatal isoerythrolysis?

A
  • Rare
  • Dam produces antibody to red cell antigen in calf
    • due to blood transfusions, or vaccination against anaplasmosis with older market vaccine
62
Q

What are the signs of Neonatal Isoerythrolysis?

A
  • Marked icterus and anemia in neonate developing shortly after birth
63
Q

What is water intoxication?

A
  • Acute hemolytic (intravascular) anemia following consumption of large amounts of water
    • Osmotic shock to RBCs
  • Evident hemoglobinuria
  • Most recover w/out treatment
64
Q

What are “Heinz body” hemolytic anemias?

A
  • Host of toxins that result in hemolytic anemia and Heinz body formation
    • Phenothiazines, onions, rape, kale, beets, nitrates (sudan), rye grass
  • Heinz body formation is from the oxidative damage to hemoglobin by the toxin forming an aggregate of insoluble hemoglobin in the RBC
  • Organ failure develops
    • centrilobular hepatic degeneration
    • hemoglobinuric nephrosis
65
Q

What are the clinical signs of Heinz body anemias?

A
  • Weakness, depression
  • Tachypnea/tachycardia
  • Pallor
  • developing icterus
  • Brown discoloration of blood, urine, mucous membranes noted in nitrate/nitrite toxicities
66
Q

How are Heinze body anemias diagnosed?

A
  • Signs of multi-organ involvement
  • Elevated direct and indirect bilirubin
  • Anemia - profound w/ high percentage of Heinz bodies
    • often develops over days resulting in signs of regeneration on CBC
      • anisocytosis, polychromasia, basophilic stippling
67
Q

What are the forms of Bovine lymphoma?

A
  • Sporadic (non-BLV associated)
    • Juvenile (multicentric) calf form
    • Adolescent thymic form
    • Cutaneous form
  • Enzootic (BLV associated)
    • Enzootic Bovine Leukosis
68
Q

What is Juvenile Lymphoma?

A
  • Rare
  • calve <6mo
  • more common in dairy
  • Signs:
    • non-painful, smooth enlargement of peripheral lymph nodes
    • followed by internalized lymphadenopathy, organ involvement and death
69
Q

What is the Adolescent thymic form of Bovine Lymphoma?

A
  • cattle 6mo to 2-3yo
  • Thymic lymphoid tissue becomes a neoplastic mass, pressing on structures in the neck and thoracic inlet
  • Signs:
    • bloat
    • jugular distension
    • dyspnea
  • Dx:
    • palpation/ultrasound
    • mass aspiration
70
Q

What is the cutaneous form of Bovine lymphoma?

A
  • Cattle from 18-36mo
  • nodular lymphoid tumors arise in the dermis
    • resemble urticarial-like wheals
    • non-pruritic
  • hair loss over nodules and hyperkeratotic skin
  • may spontaneously regress
    • recurence of the adult form is likely
71
Q

What is Bovine Leukemia Virus?

A
  • Oncogenic Retrovirus
    • ssRNA virus
  • Once infected develop lifelong antibody response
    • primarily to gp51 envelope and p24 capsid proteins
  • Infects primarily B-lymphocytes
    • both T-cells and monocytes/macrophages may be infected
    • harbor integrated provirus
  • Escapes immune response
    • low levels of replication
    • rare expression of viral proteins on cell surface
  • Lacks Chronic Viremia
  • Long latent period
72
Q

What are the 3 possible outcomes of BLV infections

A
  • Majority - Persistent infection
    • no clinical signs
  • ~⅓ - Persistent lymphocytosis (PL)
  • <5% - Lymphosarcoma
73
Q

How is BLV transmitted?

A
  • Blood
    • iatrogenic
    • biologic (insect vectors - tabanids)
  • Salivary, nasal, pulmonary secretions may possess infected lymphocytes and are capable of experimental transmission if injected into naive animal
  • In-utero
  • Infected semen
    • chilling and processing semen appears to eliminate BLV
74
Q

How are all retroviruses similar?

A
  • All have at least 3 genes
    • gag, pol, env
      • encoding proteins that are processed posttransitionally into polypeptides needed for viral replication and packaging
75
Q

How do retroviruses infect host cells

A
  • bind to target cells through receptors for the env protein
  • envelope undergoes conformational change to allow for fusion to the target cell, then undergoes penetration through cellular endosomes
  • Viral RNA is reverse transcribed to DNA which is transported to the nucleus
  • Viral DNA is integrated into the host DNA
  • cell produces new gag, pol, and env proteins that are packaged and released from the cell through budding.
76
Q

What lymph nodes and organs are most commonly involved in BLV?

A
  • Lymph nodes:
    • Iliac
    • Intrathoracic
    • Mesenteric
    • Superficial
  • Organs
    • Abomasum
    • Heart
    • Spinal Cord
    • Kidneys
    • Liver
    • Uterus
    • Pulmonary
77
Q

What Clinical signs are seen in EBL?

A
  • Usually a result of the mass effect of the tumor growing in a particular region/organ
  • Abomasal ulcers, signs of vagal indigestion
  • Right sided heart failure, affectin the right atrium
    • jugular distension, brisket and submandibular edema, muffled heart sounds, occasionally abdominal distention due to hepatic congestion and ascites
  • Posterior ataxia, paresis and paralysis
78
Q

How is EBL diagnosed?

A
  • CBC
    • marked crenation
    • lymphocytes - pleomorphic, many features of malignancy
      • large nuclei, irregular chromatin patterns, prominent nucleoli, intensely basophilic cytoplasm, frequent mitotic nuclei
    • Lymphoid leukemia
  • Fine Needle Aspirate/Biopsy
    • 30-40% misdiagnosed
  • Serum AGID, ELISA
  • Blood PCR
  • CSF tap
    • tumors are extra-dural, compressive, and non-exfoliative
    • need to aspirate mass on path to CSF
  • Direct EM, culture
79
Q

What are the indirect tests for EBL?

A
  • AGID
    • tests for Ab against envelope protein gp51 or core protein p24
  • ELISA - a bit more sensitive
  • Predictive value of a negative test is excellent
    • False negative - drop in serum antibodies in periparturient cows
    • False positive - calves due to maternal antibody
80
Q

How does PCR test for EBL?

A
  • Detects proviral DNA
  • Possibly increased sensitivity and specificity
81
Q

What is Caseous Lymphadenitis (CL)?

A
  • Bacterial infection
    • Corynebacterium pseudotuberculosis
      • gram + rod
  • Suppurative infection of lymphatic system
  • 2 forms:
    • Internal (sheep)
    • External (goats)
82
Q

How is CL transmitted?

A
  • Environment/infected animals
  • Skin
  • Mucous membranes
  • Inhalation
  • Ingestion
83
Q

What lymph nodes are most commonly affected by CL in goats?

A
  • External ln
    • Cervical
    • Mandibular
    • Prescapular
    • Prefemoral
84
Q

What signs does CL cause in sheep

A
  • Bloat
  • Respiratory issues
  • Chronic Wasting
  • Infertility
  • Lymphadenitis
  • Characteristics of abscess
85
Q

What are the differential diagnoses for CL?

A
  • Injection site abscess
  • Truperella pyogenes
  • Tooth root abscess
  • Thymoma
86
Q

How is CL diagnosed?

A
  • Clinical signs
  • Direct smear
  • Blood agar growth
  • Synergistic hemolysin inhibition test (serum)
    • cross reacts with mycobacteria
    • Looks for presence of exotoxin
      • Titers of 1:512 indicative of internal abscess
      • Titers of >1:4 indicate exposure
87
Q

What is the treatment for CL?

A
  • En-block removal of entire mass
  • Lance and flush abscess capsule vigorously and express all contents
    • swab remaining capsule lining with strong iodine to ‘cauterize’
    • cover with penicillin
88
Q

Is there a vacccine for CL?

A
  • Yes
  • decreases incidence of abscesses
  • does NOT prevent infection
  • Interferes with screening tests

food animal medicine (43 decks)

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