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NAVLE ok... > Bovine > Flashcards

Bovine Flashcards

1
Q

Bovine Leukosis Virus
Transmission
Clinical findings
Dx

A

Retrovirus
2nd most common cattle neoplasia after SCC
Transmitted by blood transfer between animals (insect vectors)
4 syndromes: calf, thymic, skin and adult
Calf form: widespread tumor mets
Thymic form: seen in 6 - 8m calves
Skin form: only nonfatal form, seen in young adults - superficial cutaneous tumors that regress after a few weeks
Adult form: 4 - 8y; wide distribution of mets

Dx: need histologic dx; serologic test for adult form, severe lymphocytosis
Control: test and cull

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2
Q

Bovine Respiratory disease (BRD)
Agent
Disease name
CS

A

Manheimia (pasterurella) haemolytica
enzootic pneumonia
CS: bronchopneumonia and fibrinous bronchopneumonia and pleuritis

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3
Q

Bovine corona virus

A

Neonatal calf diarrhea or winter dysentery
Fecal-oral respiratory transmission
Zoonotic - causes diarrhea in humans

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4
Q

Milk fever Cause Risk factors
CS
Stages
Treatment

A

Cause: onset of heavy milk production which depletes serum Ca so rapidly that hormonal control cant keep up
Risk factors: seen in dairy cattle and island breeds (Jerseys & Guernesy), occurs within 1 - 2 days of calving
CS: recumbency, S shaped neck, severe bloat, death
Stage 1: tachycardia and weakness
Stage 2: flaccid paralysis and muscle fasciculations; S-shaped neck
Stage 3: Lateral recumbency, severe bloat, coma
Treatment: add anionic salts to diet 2 - 3 weeks before calving (aka DCAD diet) you want to acidify the blood to increase Ca mobilization

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5
Q

What are the 3 primary controllers of Ca in the cow?

A
  1. Calictonin = decreases iCa
  2. PTH = increase Ca; decrease P
  3. Vit D = increase Ca; increase P
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6
Q

Explain the pathophys of Mg in the cow

So what are effects of low vs high Mg

A

Mg is used to make AChE which is used to inhibit ACh(excitatory)

High Mg –> too much AChE –> flaccid paralysis
Low Mg –> not enough AChE –> muscle fasciculations

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7
Q

What are the 3 disease processes of Phosphorus and how they lead to decreased P?

A
  1. Severe acute hopophosphatemia: increased PTH = increases P in urine in order to retain Ca
  2. Postparturient hemoglobinuria = reduced 2,3DPG in RBCs prevents Na/ATP pump from working, fluid runs into cells and they burst, leading to anemia
  3. Rickets = distorted long bone growth leading to elongated epiphyses
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8
Q

How do you treat severe acute hypophosphatemia (caused by increased PTH) and postparturient hemoglobinuria?

A

Sodium monophosphate

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9
Q

How do you treat/prevent rickets?

A

Maintain a Ca:P of about 2:1

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10
Q

Where is Mg absorbed in adults?

A

Rumen

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11
Q

Where is Mg absorbed in calves?

A

SI

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12
Q

What type of diet can cause hypoMg?

Give 3 examples

A

A diet high in N and K –> they inhibit Mg absorption

3 examples:

  1. Rapidly growing grass pasture especially in the spring or fall
  2. Heavily fertilized pastures (too much N)
  3. Cereal grains
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13
Q

Why is it so important to maintain Mg in the diet?

A

Bc there is no hormonal system to regulate Mg in the body; Mg must be continually ingestested in order to maintain normal Mg.q

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14
Q 
Grass tetany
What is it
How is it caused 
CS
Dx
Treatment
Prevention
A

HypoMg - caused by eating a diet too high in N and K that it inhibits Mg absorption
CS: early: muscle fasciculations and aggressive behavior. Late signs: recumbent, repetitive muscle contractions, convulsions, seizures
Dx: measure Mg in blood or urine (not very reliable), CSF post mortem
Tx: emergency! IV CMPK and oral Mg oxide
Prevention: feed legumes (avoid rapid growing grasses), Mg blocks

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15
Q

Most common cause of hypoK in the cow?

A

Decreased feed intake

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16
Q

Clin path associated with hypoK?

A

K <2.5 mEq/L

Increased muscle enzymes (CK & AST)

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17
Q

How do you treat hypoK?

A

K supplementation Iv and oral
IV max rate = 0.5 mEqkg/hr

KCl is most common oral salt

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18
Q

Why are ketotic cows at risk for hypoK?

A

Bc you treat ketosis with dextrose
These drugs divert K into the cell
Alkalosis causes a decrease in K

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19
Q

In a negative energy balance what 3 things mobilized to make glucose?

A
  1. Glycerol (fat mobilization
  2. Aminio acids (msucle catabolism)
  3. Glycogen (from liver)
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20
Q

What are the 3 types of ketone boies commonly seen?

A
  1. Acteone
  2. Acetoacetate
  3. Beta-hydroxybutyrate
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21
Q

Difference between primary and secondary ketosis

A

In secondary ketosis, the diet is fine (unlike primary ketosis), the ketosis occurs secondarily form a separate disease-induced inappetance.

This is far more common

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22
Q

What puts a cow at risk for ketosis

A
  1. A cow 6 weeks from parturition
  2. A high performance (milk production) cow
  3. Overcrowding
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23
Q

How is ketosis most commonly diagnosed?

A

Urine dipstick - it measures acetoacetate - not betahydroxybutyrate

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24
Q

What are the most commont treatments (3) for ketosis?

A
  1. Dextrose - short-term solution (rapidly increases blood glucose)
  2. Ethylene glycol
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25
Q

How many teeth do cows have?

What is their dental formula?

A

32
2(I 0/3; C 0/1; P 3/3; M3/3)

Some include this “canine” as a 4th incisor

Read this as incisors: 0 on both maxillas, 3 on both mandibles. Premolars: have 3 on both maxillas, and 3 on both mandibles. Etc.

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26
Q

How do you age a cow thru teeth?

A

Easiest way to think about it is the first permanent incisor erupts at 1.5 years, the 2nd at 2.5, the 3rd at 3.5 and the 4th at 4.5 years old.

You can’t really use teeth to age after they reach 4.5 years old.

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27
Q

Which teeth are most commonly affected for tooth root abscesses?

A

Mandibular molars

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28
Q

What are the clinical signs and treatment of a tooth root abscess?

A

Hypersalivation

Tx: penicillin (anaerobes)

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29
Q

Name the agent of wooden tongue and describe the clinical signs, clin path changes, and treatment

A

Actinobacillus ligniersi (normal inhabitant; gram (-)
CS: hypersalivation, weight loss, granulomatous inflammation of oropharynx though tongue is most common
Clin path: increased fibrinogen and neuts
Tx: Na iodide and/or tetracycline

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30
Q

In general, when you see pus in the cow, what organism is responsible for it?

A

Trueperella pyogenes - gram (+) and anaerobe

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31
Q

Lumpy Jaw

What organism causes it? Describe common presentation, clin path changes and treatment

A

Actinomyces bovis a gram (+)
CS: penetrates soft tissue AND bone (unlike actionbacillus), hypersalivation, difficulty eating, mandible most commonly affected
Clin path: increased fibrinogen and neutrophils
Treatment: Na iodide and penicillin

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32
Q 
Malignant catarrhal fever 
causative Agent
3 common clinical signs 
Transmission
Dx
Tx
A

Ovine herpesvirus 2
CS: ocular signs!! Corneal edema and epiphora; HIGH fever, vasculitis of viscera (tarry diarrhea, hematuria, oral erosions, etc)
Transmission: sheep are the carrier they are the major risk factor
Dx: PCR, ELISA
Tx: unsuccessful

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33
Q 
Bluetongue
Causative agent
Transmission
Reservoir
Clinical signs
Treatment and control
A

Orbivirus!
Transmission: culicoides
Cattle are the reservoir; see clinical disease most often in SHEEP
CS: see signs around fly season (summer and fall), edema of face and muzzle, nasal discharge, oral erosions, ABORTION
Tx: abx and NSAIDs

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34
Q 
BVD (bovine viral diarrhea)
Virus type
Biotype (behavior of virus)
Who are the natural hosts?
How is it transmitted?
A

Pestivirus
Biotype: non-cytopathic form is most common; the cytopathic form is uncommon and is considered a mutation of hte non-cytopathic form
Natural hosts: cattle
Transmission:
persistently infected cattle: when a pregnant dam becomes acutely infected with the non-cytopathic type BVD and fetus is < 125 days in gestation

Can also get from DIRECT CONTACT - body fluids, flies, fomites, etc.

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35
Q

What are common clinical signs of BVD

A

Subclinical - will just cause immunosuppression

Clinical - oral erosions, oculonasal discharge, diarrhea, inappetence, etc. usually < 3 years old

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36
Q

What are uncommon clinical signs of BVD?

A

Persistently infected: unthrifty and small
Mucosal disease: when NCP mutates to CP it causes mucosal disease - will see erosions around mouth and anus. They will die of this.

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37
Q

How is BVD diagnosed?

Treated?

A

Dx: Ab detection (indicates exposure or vaccination); Ag detection - immunohistochemistry on skin or antigen capture ELISA

Tx: supportive care

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38
Q

What is the GI route for cattle?

A

Esophagus –> reticulum –> rumen –> omasum –> abomasum –> SI –> cecum –> LI

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39
Q

Describe the process of fermentation in the rumen

A
  1. Sugars are used to produce pyruvate
  2. Pyruvate is reduced to the VFAs: acetate, proprionate and butyrate.
  3. Acetate and butyrate –> Acetyl Co-A
  4. Proprionate –> directly makes glucose in liver
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40
Q

How is the eosphageal groove formed and what is its function?

How is it controlled?

A

Formed from muscular folds of the reticulum and allows for liquid (ie milk) to bypass the rumen and proceed directly to the abomasum for digestion.

Controlled by suckling and milk proteins

41
Q

What should you remember about the omasum?

A

Its the one with the leaves; dont really know what its for

42
Q

Abomasum - what side is it on? What type of digestion does it do?

A

Its on the R side - cranial and ventral

Glandular digestion

43
Q

When evaluating rumen fluid, what does
Black-green fluid indicate?
Milk gray-brown?

A

Black - green = rumen stasis

Gray-brown = lactic acidosis

44
Q

Rumen acidosis
How does it occur?
What does it lead to?
What is the pathophys?

A 
Occurs from excessive carb consumption
Leads to acidosis and hypoMg
Initially gram (-) bacteria like strep bovis proliferate and drop the ph to 5 which causes gram (-) bacteria to die and Lactate producing bacteria (gram +) to proliferate and make acidosis worse dropping ph to 5 or lower killing all microflora.
45
Q

What are the 3 major sequlae from rumen acidosis?

A
  1. Osmotic draw - fluid is drawn from vascular space into rumen, can cause CV collapse and rumen distention.
  2. Systemic acidosis - D-lactate produced by bacteria in rumen can leak into vasculature (this is unable to be metabolized by animals bc they produce L-lactate)
  3. Acid damage to rumen - causes bacterial translocation and can lead to endotoxic or septic shock
46
Q

With regards to septic shock induced by ruminal acidosis, what organism is likely to be the inciting cause?

A

Fusobacterium necrophorum gram (-)

47
Q

What syndrome is likely to arise from acid damage to the rumen from ruminal acidosis?

A

Caudal vena cava syndrome
Septic emboli dislodge from liver and lodge in pulmonary vessels and can lead to life-threatening epistaxis in cattle

It is the most impt cause of epistaxis in cattle!!!

48
Q

What are the clinical signs of rumen acidosis?
Clin path?
the tx?

A

CS: POLIOENCEPHALOMALACIA (decreased thiamine - thiaminase producing bacteria proliferate with acidosis) signs of this are blindness, recumbency and death. Other signs include: diarrhea and scleral injection

Clin path: dehydation acidosis (decreased HCO3 and increased anion gap)

Tx: Mg hydroxide, IV bicarb, broad spec abx (ceftiofur). Severe cases can have rumenotomy and recommend 30 days abx to prevent liver abscesses

49
Q

How do you prevent rumen acidosis?

A

Increase fiber in diet

50
Q

What is the difference between ruminal acidosis and sub-acute rumen acidosis (SARA)?

How is SARA diagnosed?

A

Similar but SARA is related to the fermentation of carbs in smaller amounts over longer period of time. Not immediately life-threatening like ruminal acidosis but can lead to serious consequences.

Rumen pH of >12 animals - consider SARA high risk if >25% have rumen pH <5.5.

51
Q

Free gas bloat

What is an indication of free gas bloat?
Tx

A

No eructation (not enough DM)
Indication of underlying disease
Causes: hypoCa, cant ercutate, inflammation

Will deflate when orogastric tube is placed
Pass tube, give Ca if hypoCa suspected

52
Q

Frothy bloat

What is an indication of frothy bloat?
Tx

A

Too much concentrated food (grains, lush hay like alfalafa)
These feeds increase the surface tension of the fiber mat

Will NOT deflate with orogastric tube

Reduce surface tension with poloxalene or laundry detergent to destabilize the mat and allow gas to be eructated

53
Q

Reticulorumen milk accumulation
How does it occur?
CS?
Tx

A

Occurs when esophageal groove fails to close
CS: milk ferments and putrities - gray chalking color poop that stinks, recurrent bloat, acidosis

Tx: wean sooner (discontinue milk @ 6 weeks)

54
Q 
Traumatic reticulo-peritonitis causes disease where?
CS
Signs of pericarditis/pleuritis:
Dx
Tx
A

Causes disease: peritoneum, pleural space and pericardium
CS: fever, kyphosis (hunched back), tachycardia, bruxism (grinding teeth)
Signs of pericarditis/pleuritis: muffled heart sounds, pericardial friction rub, R-sided heart failure (edema, jugular distension, jugular pulses)
Dx: leukocytosis, increased fibrinogen, increased globulins, anemia
Tx: florifenicol, magnet!

55
Q

Vagal indestion: Type 1
Functional causes
Mechanical causes
Treatment

A

Failure of eructation
Functional causes: vagal neuritis from pneumonia or reticulitis
Mechanical: esophageal obstruction, tetanus, hypoCa

Tx: treat underlying cause, reversible

56
Q 
Vagal Indigestion type 2
Functional cause
Mechanical cause
CS
Tx
A

Omasal Transport Failure

Cause: functional: damage to enteric nervous system; mechanical cause - mass, FB

57
Q

Vagal indigestion type 3
Functional vs mechanical cause
CS
How to differentiate between type 2 and type 3

A

Functional: damage to enteric nervous system
Mechanical: pyloric lymphosarcoma
Abomasal Transport Failure
CS: identical to type 2 - L-shaped rumen, scant greasy feces with long hay fibers and hypermotile rumen

Differentiate by testing Cl in serum
Type 2 = normal Cl
Type 3 = LOW Cl serum

58
Q

Vagal Indigestion type 4

A

Vagal Indigestion of Late Pregnancy

Gravid uterus maysimply block pyloric outflow; resolves after parturition

59
Q

Describe an LDA and when it is most likely to occur

A

when the abomasum becomes trapped between the rumen and the left abdominal wall.

usually occurs about 6 weeks post-partum

60
Q

describe an RDA and its implications

A

when the abomasum is displaced between the liver and the right abdominal wall.

it is an EMERGENCY bc it always involves some degree of torsion of the pylorus.

61
Q

describe an Abomasal volvulus and what it can cause

which cow gets it the most often?

A

twisting of the abomasum on the mesenteric axis - it gets trapped between the liver and right abdominal wall.

it is an EMERGENCY - can induce Vagal indigestion type 3 (low serum Cl) and make the cow become systemically ill: dehydration –> shock –> death

lactating dairy cows get it the most often

62
Q

what concurrent diseases can predispose a cow to a DA? (4 big things)

A

anything that causes reduced abomsum motility can predispose to a DA

  1. ketosis
  2. hepatic lipidosis
  3. metritis or mastitis
  4. hypoCa
63
Q

what are the clinical signs of a DA?

A

normal TPR, decreased production, dehydration, decreased rumen sounds, decreased appetite
LDA: bulge at cranial aspect of left paralumbar fossa
ping

64
Q

clinical signs of an abomasal volvulus?

A

SEVERE tachycardia, severe dehdyration, no rumen motility, anorexic, sharp decrease in production, feces will be scant and dark

(big things to differentiate between this and DA is AV has elevated heart heart rate, completely anorexic, and feces will be scant and dark)

65
Q

what are clin path signs of a DA?

A

hypoCl
metabolic ALKALOSIS (H and Cl are sequestered in abomasum and not reabsorbed in SI)
hypoK, hypoCa,
high lactate

66
Q

what is strange about the UA for cows with DA?

A
  1. they will have a paradoxic aciduria despite having a metabolic alkalosis.
    we expect H+ to be retained but there is a greater drive to retain Na due to dehydration and hypotension so aldosterone kicks out the H+ in favor of the Na+.
  2. bc Cl is sequestered in the abomasum and we are resorbing Na+, we have too many cations and not enough anions. so we dump a different cation to equilbrate –> K+. this leads to hypoK
    * hypoCl, hypoK and paradoxic aciduria*
67
Q

other than clinical signs and clin path changes; what is another way to diagnose DA?

A

Liptak test - used to rule out rumen ping. aspirate fluid ventral to gas ping.

fluid pH <4.5 = LDA

68
Q

what are the non-surgical options for a DA?

A

roll - from left side to right side
roll and toggle - LDA only
blind stich - LDA only

69
Q

what is the most common treatment for a DA? describe it and what its disadvantages are

A

right flank omentopexy
deflate abomasum, pull back tot he right side and create pexy between omentum and right body wall.
disadvantage: must have LONG arms and the abomasum is not in the correct anatomic spot.

70
Q

what are two other common surgical procedrues for DAs?

A

right flank pyloropexy - pexy between pylorus and body wall.
left flank abomasopexy - secures abomasum in NORMAL anatomic position. but it requires even longer arms and requires two people and you cant evaluate the rest of the abdomen.

71
Q

what spinal nerves innervate the flank? (useful for DA surgeries)

A

T13, L1 and L2

72
Q

which cow is more likely to get an abomasal ulcer and what kind are they typically?

A

dairy cattle; perforating

73
Q

what are clinical signs of an abomasal bleeding ulcer?

A

decreased appetite, bruxism, melena, profound anemia

common after calving

74
Q

what are clinical signs of localized perforating ulcers?

A

localized: relatively common, abscess forms and walls it off, adhesions to other viscera will occur. signs are usually subclinial and similar to traumatic reticuloperitonitis

75
Q

what are clinical signs of diffuse perforating ulcers?

A

rapid or massive abomasal leakage. can’t be walled off and septic shock ensues quickly followed by death

76
Q

diagnosis of abomasal ulcers?

A

difficult and often presumptive; can US or abdominocentesis for perforating ulcers

77
Q

treatment of abomasal ulcers

A

PPIs

78
Q

what disease is abomasal LSA associated with?

A

BLV (bovine leukemia virus)

79
Q

what are the 4 main predilection sites for LSA?

A 
HULA!
H - heart (most common site is RA)
U - uterus
L - LNs
A - abomasum
80
Q

what are the CS of abomasal impaction?

A

CS: “PAPPLE” shaped and/or bilateral ventral enlargement, weight loss, scant feces

blood Cl will be normal

81
Q

diagnosis and treatment of abomsal impaction

A

dx: fluid rumen ingesta (decreased particle length)
tx: cathartics - Mg sulfate, mineral oil; prokinetics - metoclopramide, erythromycin (dont really work); abomasotmy - open abomasum and remove contents

82
Q

how do you prevent abomsal impaction?

A

good quality roughage
access to water
good nutrition quality (avoid undigestible fiber and poor quality roughage in winter months)

83
Q

what abdominocentesis results indicate an “acute abdomen” aka colic?

A

a TP > 3 and WBC >5000

84
Q

what are causes of SI obstruction?

A

hemorrhagic bowel syndrome
mesenteric fat necrosis
intussusception
mesenteric volvulus

85
Q

what are causes of LI obstruction?

A

cecal dilation and volvulus

atresia coli/ani

86
Q

what are some infectious causes of SI dsiease (4)

A
  1. Johne’s disease
  2. Salmonellosis
  3. Clostridiosis (C. perfringens)
  4. Winter dysentery
87
Q

describe hemorrhagic bowel syndrome or jejunal hemorrhage syndrome and its risk factors

A

highly fatal disease of dairy cattle characterized by intraluminal GI hemorrhage

risk factors: Brown swiss cow, first 120 days of lactation, feeding silage

88
Q

clinical signs of hemorrhagic bowel syndrome (jejunal hemorrhage syndrome)

A

usually just one cow
per acute onset and rapid debilitation
hypovolemic SHOCK
scant, bloody, tarry feces

89
Q

clin path changes associated iwth hmeorrhagic bowel syndrome or jejunal hemorrhage syndrome

A 
neutrophilia
leukocytosis
metabolic alkalosis
hypoK
azotemia
hyperglycemia
90
Q

how do you treat hemorrhagic bowel syndrome (jejunal hemorrhage syndrome)

px

A

manual clot massage without opening GI tract (preferred)
enterotomy
high doses of penicillin

px = guarded

91
Q

mesenteric fat necrosis

A

angus and jersies
affects older, fat cattle
CS consistent with obstruction due to extraluminal obstruction from fat necrosis

92
Q

intussusception
who does it occur in?
dx

A

occurs in juveniles but all ages susceptible

dx: bulls eye lesion on US

93
Q

mesenteric root volvulus
CS
tx

A

EMERGENCY
tachycardia, apple shape abdominal distension
rapid deterioration
looks like a colicy horse - rolls around

94
Q

johne’s disease
agent
CS
transmission

A

mycobacterium paratuberculosis
CS: older dairy cow usually, weight loss, pipestream diarrhea, fair appetite, hypo-proteinemia!

fecal-oral, transplacental, shed in milk and semen

95
Q

stages of Johne’s disease infection (4)

A
  1. silent infection - incubating in jejunal and ileal mucosa, undetectable
  2. inapparent shedders, no clinical signs but shedding into environment via feces can dx on PCR, culture
  3. clinical disease - weight loss, diarrhea, normal appetite, shedding a lot!!
  4. advanced clinical disease - emaciation, submandibular edema, animals die of cachexia and dehydration
96
Q

dx and tx of johne’s

A

bacterial culture of feces

97
Q

salmonellosis - which are most common in cattle?

gram - or +?

A

typhimurium and dublin

gram (-)!

98
Q

what are the clinical signs of salmonella and how is it transmitted?
what signs are unique to young animals?
clin path?

A

CS: profuse, fetid diarrhea, fever, inappetence
young animals: arthritis!!
clin path: low neuts and low lymphs!
transmitted: fecal-oral

99
Q

dx of salmonella

A

fecal culture

NAVLE ok... (18 decks)

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