Cardiovascular Disease of Cattle, Pt. 2 Flashcards
In what cattle is bovine leukemia virus infection most common? How does it typically develop?
dairy (80%) > beef (30-50%)
- asymptomatic carrier stage = 60%
- persistent lymphocytosis = 30%
- enzootic bovine LSA = <5%
Can carrier status of BLV resolve?
NO —> unless it presents in young cattle with colostrum protection (within 6 months)
- calves will likely test positive due to antibody transfer from colostrum, recommend to being testing after 6 months
What are the 2 ways BLV is transmitted? What is required?
- vertical - secretions from positive cattle
- horizontal - in utero (higher risk in calves born to cows with persistent lymphocytosis)
positive lymphocyte transfer by horseflies, blood transfusions, needles, palpation sleeves, or surgical instruments used for dehorning and tattooing
In what cattle is enzootic bovine lymphosarcoma development from BLV infection most common? What are the 3 most common signs?
those > 3 y/o
- enlarged superficial or internal lymph nodes (popped eye due to large retrobulbar LN
- lameness, unusual gait, paraysis (in spinal cord!)
- progressive debility
(other signs dependent on spread of neoplasia to other organs)
What are the top 5 places of metastasis of bovine LSA?
- heart - increased jugular pulse, tachycardia, murmur, arrhythmia
- abomasum (pylorus) - abdominal distension
- LNs
- uterus
- spinal cord - paresis, paralysis of hind limbs
Bovine LSA, mediastinal LN:
vagus nerve involvment = GI signs
Bovine LSA:
exophthalmos due to enlarged retrobulbar LN
How do cattle with persistent lymphocytosis from BLV present?
typically no signs of LSA, but will have abnormally high lymphocyte counts
What are the 3 sporadic types of lymphoma/LSA in cattle?
NOT ASSOCIATED WITH BLV, more common in younger stock
- juvenile (< 6 m/o)
- thymic (6-30 m/o)
- cutaneous (1-3 y/o)
What age of cattle is most commonly associated with thymic LSA? What is it? What are the most common signs?
6-30 m/o
massive lymphocytic infiltration of the thymus
- dyspnea, tachypnea
- distention of jugular veins, muffled heart sounds
- cough
- SQ emphysema in brisket, dewlap, forelimbs, and ventral abdominal walls
What age of cattle is most commonly affected by juvenile LSA? What are the most common clinical signs?
RARE - under 6 m/o
- generalized enlargement of LN
- infiltration of BM and internal organs
- anorexia, dyspnea, difficult ambulation (based on site of enlarged LNs)
What is the most sensitive test available for diagnosing BLV? What is commonly done first? What are other hints?
PCR/RIA
clinical diagnosis based on enlarged LN based on palpation or necropsy
- lymphocytosis (unreliable)
- AGID (most common)
What does a BLV positive test on a 6 y/o cow mean?
a. cow will die of lymphosarcoma
b. cow is persistently infected with BLV
c. cow has clinical lymphosarcoma
d. cow was recently infected, but should clear the virus in 1-2 months
B
What does a BLV positive test on a 6 m/o heifer mean?
a. cow will die of lymphosarcoma
b. cow is persistently infected with BLV
c. cow may or may not have BLV
d. cow was recently infected, but should clear the virus in 1-2 months
C
- at this age, colostrum maternal antibody protection is a possibility, recommend testing again once she is a little older
When is it normal to see udder edema?
periparturient dairy cows —> increased blood flow to mammary glands around the time of calving
more abnormal in beef cattle, suggestive of LSA blocking venous return from mammary glands to the heart
Is treatment available for BLV?
NO —> none are economic or curative, recommend euthanasia at proper time, since LSA is fatal eventually
What are the 3 methods used to control/prevent BLV?
- test and eliminate - prevalence should be low enough to economically make sense, requires constant surveillance, government compensation
- test and segregate - don’t replace stock, keep positives together and away from negatives while slowly culling positives to decrease new infections, constant surveillance and more facilities needed
- test and manage - most cost effective but least effective in preventing new cases, requires strict adherence to control measures
How is BLV prevented? Is there a proper vaccine?
- prevent spread of blood and tissues between cattle (needles, palpation sleeves, insects, work BLV negative cattle first)
- maintain a closed herd, with any incoming cattle testing negative before integration
- test stock > 6 months every 6 months
NO
What can/should be done with BLV-positive cow’s colostrum?
a. feed it to pigs
b. risk is low, so it can be fed to all calves
c. feed it to bull calves
d. drink it yourself
A, C, D
- pigs not susceptible
- bulls not worth as much and will likely be sent to slaughter before exhibiting any signs
- no risk to humans, high in protein!
How can BLV spread be prevented?
- feed only colostrum and milk from BLV-negative cows
- pasteurize milk/replacer
- use AI or negative bulls when breeding
What is the most common cause of anemia in cattle? Second most common cause?
chronic infection or inflammation
traumatic hemorrhage —> abomasal ulcers, blood parasites
What are common differentials for a unilateral swelling of the mammary region of the abdomen in cattle?
- abscess
- hematoma from udder vein trauma; not recommended to open, pressure can provide hemostasis
- seroma
- hernia
In what cattle is cold water toxicity most commonly seen? What is the most common sign recognized by owners? What causes it?
calves or show cattle given access to unlimited cold water
hemoglobinuria —> massive water intake causes hypotonicity, which leads to intravascular hemolysis of RBCs
What is indicative of anaplasmosis on a blood smear? What species most commonly affects cows and causes clinical signs?
round or oval basophilic staining bodies located marginally on RBCs
Anaplasma marginale
- centralis does not commonly cause clinical cases
Where is anaplasmosis endemic?
southeast and west central US
How is anaplasmosis transmitted? What are the only 2 reservoir hosts?
- blood-sucking insects and arthropods - ticks
- winged insects with contaminated mouthparts - able to affect cows in a 1 mile radius, must feed on two hosts within 5 mins (horse flies, stable flies, mosquitoes, deer flies)
- blood transfer - dehorning, castrating, vaccination, nose tongs, rectal palpation, surgery
cattle and black-tailed deer
What is the most common age of cattle affected by anaplasmosis? What seasons cause an increase in development?
> 2 years has the highest mortality, while those younger than 2 tend to have subclinical disease (quicker at removing RBCs) —> especially if they’re new to a herd
- late spring to early summer = tick associated
- late summer to early fall = insect associated
Anaplasmosis, age of susceptibility:
What are the most common clinical signs associated with anaplasmosis?
- pale MM due to anemia (usually only seen with 40-50% RBC loss)
- thin and watery blood sample
- icterus
- bronze bullet feces
- abortion, infertile bulls
NO hemoglobinuria
What are some differentials associated with anaplasmosis? How does it differ?
- babesiosis
- cold water intoxication
- leptospirosis
no hemoglobinuria with anaplasmosis —> A. marginale alters the shape of RBCs, which does not destroy them within the vessel, rather they are sent to the spleen and broken down by extravascular hemolysis
What provides a definitive diagnosis of anaplasmosis? What can be done if this is difficult to find?
demonstration of A. marginale bodies in RBCs with a blood smear stained with Wright Giemsa
in later stages, bodies are harder to find on the smear, so a fluorescent antibody test is useful
What is the drug of choice for treating anaplasmosis? What else is commonly done?
Tetracycline
blood transfusion (1-3 gallons if hemoglobin is especially low)
How can the developmental and convalescent stages of anaplasmosis be differentiated? Does this change treatment plans?
- DEVELOPMENTAL = clinical signs, anemia
- CONVALESCENT = recovery indicated by appearance of reticulocytes (better prognosis)
no - treat at any stage, less likely to need a transfusion at the convalescent stage
What herd treatment is recommended in cases of anaplasmosis? How often is this recommeded?
stop an outbreak by treating all members with LA 200/300 (tetracycline)
repeat with 28 day intervals all throughout vector season or provide continuous access to oral chlortetracycline in feed
Why is a 28 day interval recommended for treating herds with tetracycline for anaplasmosis?
minimal incubation period of A. marginale is 21 days and the average developmental stage is 7 days
- offers a way to decrease costs of drugs
What is the pathogenesis of anaplasmosis like?
- DAY 1 = invades mature RBCs
- DAY 2-21 = infects 1% of RBCs (incubation)
- DAY 21+ = infected RBCs double each day for 4-10 days —> developmental stage with decreased RBC survival, autoantibodies, and destruction in the spleen = ANEMIA
What are the 4 stages of anaplasmosis?
- INCUBATION - invasion of cells without signs, ends with first rise in rectal temp
- DEVELOPMENTAL - clinical signs appear, anemia develops and ends when reticulocytes appear (regenerative)
- CONVALESCENCE - return to normal blod values
- CARRIER - disappearance of detectable anaplasmosis bodies, can last a lifetime
How can carrier status of anaplasmosis be detected?
- complement fixation test
- card agglutination card (in the field, least accurate)
- cELISA (very sensitive)
Is there a recommended vaccine available for anaplasmosis? How can it be prevented?
NO - Plazvax is no longer available, may not have been successful
- oral antibiotics (Chlortetracycline) in feed or salt-mineral mixes to begin before vector seasons
- control biting insects and ticks
How are herds with anaplasmosis handled?
- separate into positive (carriers, convalescent, developmental) and negative groups
- treat all and repeat at 28 day intervals
antibody titers may persist for 130 days
What are the 2 causative agents of bovine babesiosis (Texas Cattle Fever)? Where is infection most common? What are the most common signs?
B. bigemina and B. bovis
along Mexican border, Puerto Rico
anemia, hemoglobinuria, jaundice
What causes anthrax? How do cattle become infected?
Bacillus anthracis - spore-forming, aerobic
infection by spore ingestion, inhalation, or cutaneous penetration
What are 2 incidences that can facilitate infection with anthrax?
- grazing of abrasive forages = penetration of spores into oral mucosa
- heavy rainfall or flooding preceded by drought/dusty conditions expose spores from lower layers of the soil
What is indicative of death caused by anthrax? What states have highest incidence?
sudden death resulting in a nonautolyzed carcass with bloody discharges and marked splenic swelling
plains states in the summer months (not common east of the Mississippi River)
How should a carcass suspected to be infected with anthrax be handled?
- DON’T OPEN —> vegetative organisms rapidly destroyed in 1-2 hours
- soil contamination commonly occurs due to bloody exudates, predation, and oxygen exposure —> proper burial at least 2 m and cover with quicklime or burn (spore HIGHLY resistant to chemical and physical agents in the environment!)
What is indicative of a chronic form of anthrax?
localizes edematous swelling of the shoulders, ventral neck, and thorax
What treatment is recommended for anthrax (if caught in enough time)? Is there a vaccine?
procaine penicillin G
yes, but not commonly used
What are the 4 hallmark signs of anthrax? What offers a definitive diagnosis?
- black, tarry exudates from body orifices
- failure of blood to clot
- incomplete rigor mortis
- splenomegaly*
organisms seen on blood smear or intact eyeballs/spleen —> medusa hair appearance
What is postparturient hemoglobinuria associated with in cattle? How is it treated?
hypophosphatemia
treat with blood transfusions and fleet enemas containing phosphate
What are 4 causes of depression anemia?
- nutritional - iron, copper, cobalt, vitamin B12, folic acid deficiency
- inflammatory disease - chronic infection/inflammation, neoplasia
- organ dysfunction - chronic renal or GI disease, chronic parasitism
- BM damage or dysplasia - aplastic anemia, bracken fern/soybean meal poisoning, myelophthisic disorders
What is iron deficiency anemia associated with? In calves? How is it treated?
chronic blood loss —> internal/external parasitism, GI lesions, hemostatic defects
veal calves on an all-milk diet with no exposure to soil
iron administration
In what areas is copper deficiency most common? Why?
bottom lands
excess molybdenum —> tailings of coal or uranium mines
What causes Heinz body hemolytic anemia? What are 5 examples?
oxidizing agents
- onions, rape, kale, wilted maple leaves
- phenothiazine
- methylene blue
- acetylphenylhydrazine
- rye grass or selenium deficient pastures
How do Heinz bodies develop on RBCs?
oxidative denaturation of hemoglobin results in aggregation of protein globins, appearing as inclusions withing RBCs
What determines the extent of signs seen with Heinz body hemolytic anemia? What is commonly seen?
specific toxin, amount ingested, time of course, complicating second factors
- weakness, depression, anorexia
- exorcise intolerance
- pale MM
- icterus
- elevated HR and RR
- discolored urine
How is Heinz body hemolytic anemia diagnosed? Treated?
- observation of profound anemia, Heinz body inclusions, hemoglobinemia/uria
- elevated bilirubin
remove source of toxicity and give blood transfusions
