Hemolymphatic Diseases Flashcards
1
Q
What are the different causes of anemia?
A
- Blood loss
- Intravascular hemolysis
- Extravascular hemolysis
- Decreased production
2
Q
What are the general laboratory findings seen with blood loss?
A
- anemia + hypoproteinemia
3
Q
What are the general laboratory findings seen with intravascular hemolysis?
A
- Pink plasma
- hemoglobinuria
- regeneration +/-
- hyperbilirubinemia
4
Q
What are the general laboratory findings seen with Extravascular hemolysis?
A
- Icterus
- +/- Regeneration
5
Q
What are the general laboratory findings seen with decreased production of erytherocytes?
A
- No regeneration
- Hyperproteinemia
- ⇡ globulins
- dehydration
- possibly hyperfibrinogenemia
6
Q
What clinical signs are seen with anemia due to blood loss?
A
- Exercise intolerance
- tachycardia
- tachypnea
- pallor
- aggression (hypoxia)
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
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)
9
Q
What causes Abomasal ulcers?
A
- High producing animals, show animals
- Diets high in starch, low fiber content
10
Q
What are the types of abomasal ulcers?
A
- 4 Classifications based on severity
- Type I - mucossal
- Type IV - perforation, hemorrhage
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
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
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
14
Q
What is the “Lee-White” clotting time?
A
- blood should clot in a red top tube w/in 5 minutes
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
- Enzootic Hematuria
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
17
Q
How is Enzootic hematuria diagnosed at necropsy?
A
- Marrow hypoplasia
- Urinary bladder pathology
18
Q
What hemolytic diseases commonly effect food animals?
A
- Anaplasmosis
- Mycoplasma Haemollama (camelids)
- Bacillary Hemoglobinuria
- Leptospirosis (calves/feedlot)
- Babesia
- Water intoxication
- Neonatal Isoerythrolysis
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
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
- New antigenic variant of A. marginale arises
21
Q
How often is anaplasmosis transmitted in utero? (vertical transmission)
A
- 16 - 20% of calves born to PI cows are infected in utero
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
23
Q
How is anaplasmosis diagnosed?
A
- direct blood smear - visualize intracellular parasite
- cELISA
- PCR
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
25
How is anaplasmosis controlled (medically)?
* 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
26
What is *Mycoplasma haemollama*
* 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
27
What are health impacts of *Mycoplasma haemollamae*
* 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
28
How is *Mycoplasma haemolamae* diagnosed?
* 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
29
How is *Mycoplasma Haemolamae* treated?
* 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
30
What is *Mycoplasma Weyoni*
* 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
31
What is Babesiosis?
* 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
32
What causes Bacillary Hemoglobinuria?
* 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
33
When does Blood loss result in death vs anemia?
* 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)
34
What is hemolytic anemia? signs?
* 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
35
How can extravascular destruction of RBCs be differentiated from intravascular destruction?
* Icterus _without_ hemoglobinuria is associated with extravascular destruction
36
What are common causes of hemolytic anemias in cattle?
* Bacterial
* Bacillary Hemoglobinuria
* Leptospirosis
* Protozoal
* Anaplasma
* Eperythrozooan
* Babesia
* Toxic
* rape and kale
* onion
* copper
* pharmaceuticals
* Other:
* Postparturient hemoglobinuria
* Water intoxication
* Neonatal isoerythrolysis
* Autoimmune
37
What is Suppression/depression Anemia?
* 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
What causes depression anemia in cattle
* Chronic infection
* Chronic renal disease (pyelonephritis, amyloidosis)
* Parasites
* Acute Bracken fern (myelodysplasia)
* Malignancy
39
What is Post-Caval Syndrome
* 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
What is the treatment for Acute blood loss anemia?
* Stop hemorrhage
* Fluids
* Whole blood transfusion
41
How/why are blood transfusions done in cattle?
* 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
Does blood need to be cross-matched in cattle for transfusions?
* No!
* transfusion reactions rare in cattle
43
What are abomasal ulcers?
* 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
What are the clinical signs of abomasal ulcers?
* 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
What clinical pathology test can be done with abomasal ulcers
* Fecal occult blood test
* good specificity, sensitivity erratic
* Anemia, TP low normal to decreased
* Test for BLV
* CBC/Chemistry may provide prognostic support
46
What is the treatment for abomasal ulcers?
* 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
Which sweet clover causes coagulopathies?
*Melilotus spp*
48
What are the clinical signs of Moldy Sweet Clover toxicosis?
* 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
How is moldy sweet clover toxicosis diagnosed?
* 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
What is the treatment for Moldy Sweet clover toxicosis
* Gentle handling
* Remove source
* Vit K1 injection:
* 1-3mg/kg IM or SQ BID/TID for 2-3 days
51
What happens when cattle eat Bracken fern (*Pteridium aqualinum)*
* 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
How are Enzootic Hematuria and Acute Bracken fern Toxicosis (caused by the same plant) different?
* 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
How is Enzootic Hematuria/Acute Bracken Fern Toxicosis diagnosed?
* CBC:
* anemia (mild to severe)
* severe pan-leukopenia (acute toxicosis)
* Necropsy - Bone marrow hypoplasia
54
What are the clinical signs of Bacillary Hemoglobinuria?
* 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
How is bacillary Hemoglobinuria diagnosed?
* High case fatality rate - Dx usually post-mortem
* Hepatic Infarct and necrosis
* conically shaped w/ hyperemic zone
* Dark red urine in bladder
56
What is the treatment for Bacillary hemoglobinuria
* Supportive - Prognosis is GRAVE
* Procaine Penn G (40K units BID)
* Fluids
* Transfusions
57
What is Leptospirosis
* *L. pomona and L. icterohemorrhagica* most common
* Causes wide clinical syndromes:
* septicemia, interstitial nephritis, abortion, mastitis, ophthalmia, **hemolytic anemia**
* Zoonotic
58
What are the clinical signs of Leptospirosis
* 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
How is Leptospirosis diagnosed?
* 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
What is the treatment for Leptospirosis?
* Oxytetracycline (9mg/lb IV/SQ q24hr for 4 doses)
* Plus oral tetracycline for one month
61
What is Neonatal isoerythrolysis?
* Rare
* Dam produces antibody to red cell antigen in calf
* due to blood transfusions, or vaccination against anaplasmosis with older market vaccine
62
What are the signs of Neonatal Isoerythrolysis?
* Marked icterus and anemia in neonate developing shortly after birth
63
What is water intoxication?
* Acute hemolytic (intravascular) anemia following consumption of large amounts of water
* Osmotic shock to RBCs
* Evident hemoglobinuria
* Most recover w/out treatment
64
What are “Heinz body” hemolytic anemias?
* 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
What are the clinical signs of Heinz body anemias?
* Weakness, depression
* Tachypnea/tachycardia
* Pallor
* developing icterus
* Brown discoloration of blood, urine, mucous membranes noted in nitrate/nitrite toxicities
66
How are Heinze body anemias diagnosed?
* 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
What are the forms of Bovine lymphoma?
* Sporadic (non-BLV associated)
* Juvenile (multicentric) calf form
* Adolescent thymic form
* Cutaneous form
* Enzootic (BLV associated)
* Enzootic Bovine Leukosis
68
What is Juvenile Lymphoma?
* 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
What is the Adolescent thymic form of Bovine Lymphoma?
* 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
What is the cutaneous form of Bovine lymphoma?
* 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
What is Bovine Leukemia Virus?
* 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
What are the 3 possible outcomes of BLV infections
* Majority - Persistent infection
* no clinical signs
* ~⅓ - Persistent lymphocytosis (PL)
* \<5% - Lymphosarcoma
73
How is BLV transmitted?
* 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
How are all retroviruses similar?
* All have at least 3 genes
* *gag, pol, env*
* encoding proteins that are processed posttransitionally into polypeptides needed for viral replication and packaging
75
How do retroviruses infect host cells
* 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
What lymph nodes and organs are most commonly involved in BLV?
* Lymph nodes:
* Iliac
* Intrathoracic
* Mesenteric
* Superficial
* Organs
* Abomasum
* Heart
* Spinal Cord
* Kidneys
* Liver
* Uterus
* Pulmonary
77
What Clinical signs are seen in EBL?
* 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
How is EBL diagnosed?
* 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
What are the indirect tests for EBL?
* 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
How does PCR test for EBL?
* Detects proviral DNA
* Possibly increased sensitivity and specificity
81
What is Caseous Lymphadenitis (CL)?
* Bacterial infection
* *Corynebacterium pseudotuberculosis*
* *gram + rod*
* Suppurative infection of lymphatic system
* 2 forms:
* Internal (sheep)
* External (goats)
82
How is CL transmitted?
* Environment/infected animals
* Skin
* Mucous membranes
* Inhalation
* Ingestion
83
What lymph nodes are most commonly affected by CL in goats?
* External ln
* Cervical
* Mandibular
* Prescapular
* Prefemoral
84
What signs does CL cause in sheep
* Bloat
* Respiratory issues
* Chronic Wasting
* Infertility
* Lymphadenitis
* Characteristics of abscess
85
What are the differential diagnoses for CL?
* Injection site abscess
* *Truperella pyogenes*
* Tooth root abscess
* Thymoma
86
How is CL diagnosed?
* 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
What is the treatment for CL?
* 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
Is there a vacccine for CL?
* Yes
* decreases incidence of abscesses
* does NOT prevent infection
* Interferes with screening tests
