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C2 Flashcards

1
Q

What is the difference between a notifiable and exotic disease?

A

Notifiable is one that the government wants to keep an eye on. Often endemic (eg. anthrax, salmonellosis)
Exotic= diseases outside of Australia

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2
Q

What are the causative agents of the following?

  • Pleuro
  • Bovine TB
  • Bovine brucellosis
  • Enzootic bovine leukosis
  • Haemorrhagic septicaemia
  • Theileriosis
  • Lumpy skin disease
  • Heartwater
A
  • Pleuro: Mycoplasma mycoides ssp mycoides
  • Bovine TB: Mycobacterium bovis
  • Bovine brucellosisL Brucella abortus
  • Enzootic bovine leukosis: EBL virus
  • Haemorrhagic septicaemia: Pasteurella multocida
  • Theileriosis: T. parvum and T. annulata
  • Lumpy skin disease: poxvirus
  • Heartwater: Erlichia ruminantium
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3
Q

What is one of the biggest emergencies in cattle medicine?

A

Lateral recumbency

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4
Q

What are the 4 types of abomasal ulceration? How are they generally dx?

A
  1. Erosions + non-perforating ulcers
  2. Ulcers with profuse intraluminal bleeding
  3. Perforated with local peritonitis
  4. Perforated with diffuse peritonitis

Dx: pallor of mm, malaena, colic

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5
Q

What are the two main syndromes of abomasal ulceration recognised?

A
  1. Peritonitis (localised or diffuse)

2. Internal haemorrhage

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6
Q

What are the average feeding periods in feedlots for beef cattle?

A

100-120d

unless Wagyu or Fresian and then it is >300d

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7
Q

What is the minimum entry weight and age for a feedlot?

A

300-400kg

12-18 months

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8
Q

What are the major markets for grain fed slaughtered beef?

A

Japan, South Korea, US

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9
Q

What are some common respiratory diseases encountered in beef feedlots?

A
  1. Bronchopneumonia
  2. Fibrinous pleuropneumonia
  3. Pericarditis
  4. Lung abscess
  5. Exudative necrotic tracheitis
  6. Tracheal oedema
  7. Atypical interstitial pneumonia
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10
Q

What are the 3 top causes of morbidity and mortality in beef feedlots?

A

Morbidity: BRD, Buller, Musculoskeletal
Mortality: BRD, Other, Musculoskeletal

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11
Q

What are some limitations to the dx of BRD in beef feedlots?

A
  1. subjective scale (visual assessment)
  2. Depression and resp scores are the basis of assessment
  3. Average of 0.2secs per cow examinations
  4. no gold std. Typically a.m. assessment only
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12
Q

How can BRD be prevented and managed in feedlots?

A

Prevention:

  • backgrounding
  • resp vaccine
  • procurement strategy
  • biocontainment strategies
  • induction procedures/ vacc
  • nutritional management
  • remove BVDV PIs

Management:

  • optimal timing of ID and efficacious tx
  • good supportive tx
  • metaphylaxis
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13
Q

What are some sequellae to BRD in feedlots?

A

Mycoplasma bovis and Histophilus somnii infections

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14
Q

What are causes of ruminal hypermotility?

A

Vagus indigestion

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15
Q

What are some DDx for left sided pings?

A 
LDA
Normal rumen gas cap
Pneumoperitoneum
Air in intestines
Physimetra (air in uterus)
Gas in more than one place
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16
Q

What is “succussion”?

A

(Shake abomasum)

Presence of fluid in abomasum making tinkling or splashing sounds

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17
Q

What are some differentials for right sided percussion?

A 
RDA
Right abomasum volvulus
Caecal dilation/ volvulus
Spiral colon/ SI gas
Physometra
Pneumoperitoneum
Air in rectum (post rectal exam)
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18
Q

What are typical clinical signs of an LDA? What are Ddx?

A

Ping on the left side
Fluid splashing on succussion
Ketonuria
Scant faeces on per rectal exam

Ddx?
Other causes of pings
Rumen atony (hypocalcaemia)
Indigestion
Traumatic reticuloperitonitis
Ketosis
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19
Q

What is the typical history of an RDA?

A

A recently called cow that is suddenly off her milk (ie has no milk in udder), looks sick and has abdominal pain

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20
Q

What are some clinical indication of intestinal phytobezoars?

A

Green discharge from nares*
Sudden severe depression in milk yield
Dehydration
Faeces that look like “wasabi mayonnaise”
(may detect fluid splashing sounds in abdomen)

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21
Q

How long does it take for bloat to occur after exposure to relevant pasture?

A

20 mins

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22
Q

What are some tx options for bloat? What are some preventative options?

A 
Tx:
-Mineral oils or detergents
-Stomach tube
-Rumenotomy (stab) following by oil drench 
Px:
-diet
-oils
-detergents
-monensin
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23
Q

How does monensin work with regard to bloat?

A

=ionophore AB. changes ratio of volatile fatty acids produced in the rumen
->improved feed efficiency and reduced methane gas pdn

Comes as powder or capsule that releases it for 100 days

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24
Q

What are some causes of secondary (free gas) bloat?

A

Acute:

  • oesophageal obstruction
  • recumbency
  • hypocalcaemia

Chronic:

  • Simple indigestion
  • Vagus indigestion
  • Tetanus
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25
Q

How might you treat simple indigestion?

A

Epsom salts several times daily (encourages rumen emptying)
Alkalising agents (if xs grain)
VInegar (if xs protein)

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26
Q

Vagus indigestion leads to hypomotility of the rumen with weak and ineffective contractions. T or F?

A

F. It causes HYPERMOTILITY of ruen (3-6 contractions per min) but weak and ineffective contractions

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27
Q

How might you treat secondary bloat due to vagus indigestion?

A

address primary cause (ABs such as oxytet, TMS or neomycin-pen or anti-inflamms. such as ketoprofen or flunixin)

Also stimulate contractions with feed/ appetite stim. +/- rumenotomy

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28
Q

What are some Ddx for right abdominal distension in a cow?

A
  • Abomasal impaction or volvulus
  • RDA or caecal torsion
  • Phytobezoars
  • Hydrops amnion or allantois
  • Ascites
  • Uroperitoneum
  • Udder oedema (flag)
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29
Q

A ruminal pH below 5 is suggestive of what?

A

carbohydrate engorgement

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30
Q

What is the grunt test?

A

Sharp pressure applied over xiphoid whilst listening for a grunt. Indicative of peritonitis

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31
Q

What nutritional factors are implicated in the development of LDA?

A 
Transition period management (period prior to calving)
BCS
Lead feeding
Hypocalcaemia
Post partum disorders
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32
Q

What are typical clinical signs of an RDA?

A 
Suddenly off her milk
Abdominal pain
Ping high up on right side
\+/- meleana
HR > 120-130
May palpate abomasum per rectum
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33
Q

Grey, yellow faeces, that are very pasty and malodourous are pathognomonic for what condition in cows?

A

Intestinal phytobezoars

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34
Q

What approach do you take for treatment of intestinal phytobezoars in cattle?

A

Right paralumbar approach

Then close using a double layer inturning suture

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35
Q

A banana-shaped lesion palpated per rectally indicates what condition? what CSs are seen with this condition?

A

Intussusception
Colic, completely off milk, anorexia, fast and weak pulse, dehydration, reduced faeces with blood and mucus. also, abdo distension

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36
Q

What are important aspects of cattle history that may lead to acute rumen acidosis? What is the best way to dx this?

A
  • Sudden intro of CHO
  • Sudden increase in intake of CHO
  • Sudden decrease in fibre

Rumen tap to check pH (pH<5)

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37
Q

What bacteria is primarily responsible for pdn of lactate in the rumen?

A

Strep bovis

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38
Q

What is SARA?

A

Sub acute rumen acidosis= herd problem rather than individual. pH 5-5.5. Dominance of gram -ve bacteria
-> mild diarrhoea, foamy faeces, undigested grain in faeces, reduced milk fat (<3%)

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39
Q

How can you prevent rumen acidosis?

A
  1. Change the feed slowly (Start at 4kg/ day, change by less than 20% every few days)
  2. Buffers in feed (NaHCO3/ MgO)
  3. Eskalin in feed (takes 2 weeks to work. Kills 2. bovis selectively)
  4. Tylosin in feed (prevent secondary hepatic abscessation)
  5. Get the diet right
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40
Q

What are the mechanisms by which parasites cause disease? (give examples)

A
  1. Reside in gut lumen absorbing nutrients (eg. cestodes)
  2. Penetrating and destroying mucosal cells (eg. ostertagia)
  3. Feeding on mucosa (Trichostrongylus)
  4. Sucking blood (haemonchus)
  5. Physical obstruction (tapeworms, large roundworms sometimes)
  6. May end up in other organs or mat cause hypersensitivity
41
Q

Plasma pepsinogen in cattle can be used as what type of measure?

A

Measure of ostertagia damage to the abomasum

42
Q

What species of cooperia do we see in cattle in Australia?

A

C. punctata and C pectinata

43
Q

What is the intermediate host for moniezia bendeni and M. expansa (tapeworms)?

A

pasture mites

44
Q

What are the potential outcomes for a cow infected with pestivirus?

A
  • > BVD
    1. if naive and not preg= mild or no clinical disease. develop immunity
    2. If infected early in preg (<100d) can lose preg or can have immunotolerant and PI calves
    3. If preg and infected 100-150d -> PI calf or calf with high Ab levels. May have neurological signs
    4. If preg >150 days, no effect. Calf has immune system and seroconverts
45
Q

How can you diagnose JD (Mycobacterium pesudotuberculosis)?

A

Faeces- demonstration of acid-fast organisms, culture of bacteria, PCR
Serology- ELISA, Agar gel diffusion, CFT

46
Q

What are the four main mechanisms of diarrhoea?

A

Primary osmotic effect
Maldigestion/ malabsorption
Hypersecretion
Increased permeablity

47
Q

What congenital defects might be seen in a calf that has been infected with bovine pestivirus between day 100 and 150 of gestation?

A 
CNS:
-cerebellar hypoplasia
-hydranencephaly
-spinal hypomyelinogenesis
Ocular:
-micropthalmia
-cataracts
-optic neuritis
48
Q

What are some ddx for Yersiniosis?

A

Coccidiosis
Salmonellosis
Ostertagiasis
Paramphistomiasis

49
Q

What is a common cause of macrocytic, normochromic non-regen anaemia in cattle?

A

B12 deficiency

50
Q

What is the signalment for brackern fern poisoning?

A

Youngstock grazing brackern. Pale calves with pneumonia and petechial haemorrhages. Fern suppresses bone marrow-> thrombocytopaenia, anaemia, leukopaenia

51
Q

What are some potential consequences of brassica ingestion? How about clinical signs of brassica poisoning?

A 
Haemolytic anaemia
Photosensitization Carb overload
Choke/ bloat
GIT upset
Polioencephalomalacia

CSs: Letahrgy, weakness, depression, anorexia, red urine, pale mm, dyspnoea, tachycardia

52
Q

How might you treat an abomasal ulcer?

A

Tx is usually futile. Can give Abs (neomycin/ penicillin) and blood transfusion

53
Q

What is imidocarb?

A

Treatment for babesiosis. Also gives 4 week protection. Kills protozoa
Has 14d milk WHP

54
Q

What are some indications for blood transfusions in cattle?

A

Acute blood loss
Intravascular haemolysis
HR>100, rapid RR, pallor, PCV<10-13%

55
Q

What are the tick vectors for babesiosis, theileria and anaplasma marginale?

A

Rhipicephalus microplus
Rhipicephalus microplus and R. sanguineus
Haemaphysalis longicornis

56
Q

How might you treat benign theileriosis?

A

Oxytet +/- imidocarb
blood transfusion
decrease stress and movement

57
Q

One litre of blood will raise a PCV by how much in a 550kg cow?

A

0.75% (therefore 4-6L needed to raise PCV from 8% to 12%)

58
Q

What are the three Qs of colostrum?

A

Quickly- first 6-8 hours
Quality- SG >1.060 or Brix reading of >22%
Quantity- aim for 4L

59
Q

At what age does the umbilicus normally fall off?

A

10-14 days

60
Q

What are some physiological consequences of diarrhoea in calves?

A
  1. Dehydration-> decreased BP, CO and perfusion
  2. Acidosis (na loss, bicarb into lumen, increased lactic acid pdn and VFA pdn)
  3. Electrolyte imbalances
  4. Hypoglycaemia
  5. Overgrowth of bacteria in SI
61
Q

When should you give antibiotics to a scouring calf?

A
  1. diarrhoea plus systemic signs
  2. blood/ mucus in faeces
  3. FPT
  4. Bacterial disease
  5. Diarrhoea syndrome
62
Q

What are some examples of bacteriocidal antibiotics? How about bacteriostatic?

A

Cidal:

  • 3rd gen cephalosporins (ceftiofur)
  • aminoglycosides
  • BS penicillin
  • potentiated sulphonamides (TMPS)
  • fluoroquinolones

Static:

  • sulphonamide
  • tetracyclines
63
Q

What is the organism responsible for Bacillary haemoglobinuria in cows?What does it cause?

A

Cl. haemolyticum (sometime Cl. novyi Type D)

Toxaemia, dark red/ brown urine and rapid death

64
Q

Dysuria in a cow (frequent urination/ straining) is usually due to involvement of the ________. Potential causes include: a-d

A

lower urinary tract

a. cystitis (e.coli)
b. pyelonephritis
c. obstructive urolithiasis
d. vaginitis

65
Q

What causes pyelonephritis in cows? what are the CSs?

A

Corynebacterium renale.

-> haematuria, pyura, painful micturition

66
Q

What are some risk factors for urolithiasis? How may it be treated?

A

Increased concentrate feeding, high silicate pastures, low water intake

  • urethrostomy or salvage slaughter
  • ammonium chloride/ sulphate
67
Q

How might you treat vaginitis?

A

IM penicillin. Minor episodes may resolve without intervention though

68
Q

What may cause post-parturient haemoglobinuria? Which animals are more at risk? How might you tx?

A 
Prolonged phosphorus deficiency
High producing older cows
Tx:
-Give P IV or SC (60g Na acid phosphate in 300ml water)
-Give P orally (DCP powder)
-blood transfusion (5L IV)
69
Q

What is the difference between Acute and Chronic copper poisoning in cattle?

A

Acute-> GIT signs, fluid accumulation and eventual IV haemolysis. Caused by accidental exposure to Cu salts

Chronic: only haemolytic and icteric signs. Cu-rich soils or areas exposed to industrial contamination

70
Q

What is a Gartner’s cyst? What is a freemartin?

A

Remnant of mesonephric duct

Heifer with a make co-twin-> XX/Xy chimera

71
Q

What is the treatment for lepto pomona in calves? what is a ddx?

A

Streptomycin

Cold water toxicosis

72
Q

Maintenance for a 500kg dairy cow= ___
Milk= ___MJ/L
Average diet= ____MJ/ Kg
Req in KgDM=______

A

60MJ
5MJ/L
10MJ/kg
half the litres + 6

73
Q

What are some consequences of copper deficiency in cattle?

A
  1. Coat colour change
  2. Diarrhoea
  3. Reproductive failure
  4. Gait abnormalities
  5. Falling disease
  6. Anaemia
  7. Humerus fractures
  8. Illthrift
74
Q

What are some rules of thumb regarding the intake of neutral detergent fibre?

(What is NDF?)

A
  1. Optimum intake is achieved when NDF = 28-34% of total diet DM
  2. Max NDF from forage should equal 1% of cows body weight
  3. Max intake in total ration should equal 1.2% of cows body weight

(Hemicellulose, cellulose and lignin)

75
Q

What is falling disease?

A

Aortic rupture due to weak collagen as a result of Cu deficiency

76
Q

What treatment options are there for copper deficiency in cattle?

A 
Oral:
-topdress pasture with fertiliser
-trace element pellets added to ration
-trace element licks
-add to water
-copper bullets
Parenteral:
-2ml injection (Cu-edetate takes 7d to translocate to liver, Cu-glycinate takes 21d) 
DO NOT inject Cu within 5 weeks of or during joining
77
Q

What causes white muscle disease (aka nutritional muscular dystrophy)? How does the disease present?

A

Se def

Acute NMD-> sudden death in first 3d of life. Involves myocardium and diaphragm. Animals found in sudden lateral recumbency, look limp, have normal neuro reflexes

Subacute NMD-> presents at 1-4 months of age. Precipitated by stress. Get paresis of skeletal muscles and recumbency

“Beef looks like chicken”

78
Q

What are some syndromes of Se deficiency?

A
  1. Illthrift
  2. Heinz body anaemia
  3. NMD
  4. Suboptimal milk yield
  5. Sub optimal fertility
  6. RFMs
  7. Subclinical mastitis
  8. Premature/ stillborn calves
  9. Almost anything!!!
79
Q

What trace element deficiency leads to skin and hoof problems?

A

Zn

80
Q

What may the following postures indicate?

  1. Frog-legged
  2. Splay-legged
  3. Sternal recumbency
  4. Lateral recumbency
A
  1. Frog-legged:
    Femoral n injury; preg tox
  2. Splay-legged:
    pelvic fracture, hip dislocation, muscle rupture or obturator (or sciatic nerve) paralysis
  3. Sternal recumbency:
    MS, mild toxaemia, mild milk fever
  4. Lateral recumbency: Severe milk fever, severe systemic/ toxic disease
81
Q

What is the function of the following nerves?

Femoral n (L4-L6)
Sciatic n (L6-S2)
Obturator n (L5-L6)
A

Femoral: Innervates quads and draws HL fwd

Sciatic: Peroneal portion innervates dorsal and lateral aspects of foot; tibial innervates caudal and medial

Obturator: innervates medial thigh muscles to adduct HL

82
Q

What is the treatment for hypoCa?

A

Calcium borogluconate

83
Q

What is transit tetany? What are some predisposing factors?

A

=Non parturient hypocalcaemia (cows on lush grass)

recent oestrus, low levels of Ca in diet, low Mg, high Zn, not eating….

84
Q

What is pregnancy toxaemia? How is it treated?

A

=type of hepatic lipidosis seenin late preg beef cows that are fed inadequate diet during last two months of preg

Ketol (propylene glycol= glucose)

85
Q

What is protein energy malnutrition?

A

Insufficient provision/ quality of feed-> thin late preg cows that can’t get up

86
Q

What are the aims of an integrated approach to transition nutrition?

A
  1. Reduce ruminal disruption (milking cows are vulnerable to lactic acidosis and SARA)
  2. Minimise macromineral deficiencies (Ca, Mg, P)
  3. Minimise lipid mobilisation disorders (ketosis, fatty liver anf pregnancy toxaemia)
  4. Avoid immune suppression (a/w lack of energy or protein intake)
87
Q

What are components of an integrated transition diet that need to be considered?

A

Energy and protein; macrominerals and DCAD; microminerals; rumen modifiers (eg. monensin); buffers and other possible additives

88
Q

What is the normal urine pH of Holstein cows and Jerseys?

A 
HF= 6.2-6.8
Jerseys= 5.8-6.3
89
Q

Briefly, what are the three stages of milk fever?

A

Stage 1: excitable, hypersensitivity/ tremors, progressive ataxia and rumen stasis
Stage 2 (1-12hrs): sternal recumbency/ depressed, ruminal stasis and bloat, uterine inertia, dull/depressed, often won’t try to get up
Stage 3: Lateral recumbency, flaccid paresis, tachycardia, bloat, hypothermia/ regurgitation

90
Q

What are some ddx for milk fever?

A
  1. Acute toxic mastitis (IV calcium will kill these cows)
  2. Calving paralysis
  3. Grain overload (rumen pH)
  4. Other infections
  5. Grass tetany (mentation)
  6. Fat cow syndrome (look for ketones)
91
Q

What are some risk factors for grass tetany?

A
  • fresh, lush, rapidly growing pastures heavily fertilised with N & K and low in Mg
  • cereal crop with high K
  • rapid growth after cold wet weather
  • very fat or very thin cows
  • decreased intake
92
Q

For a recumbent cow, what are some important questions to ask?

A
  1. How long has she been down for? (assess secondary damage)
  2. When did she calve?
  3. How old is she? (2 yo unlikely to have milk fever or grass tetany)
  4. Are others affected?
  5. What treatment have you given?
93
Q

What are some indicators for a poor prognosis for a down cow?

A
  1. recumbency > few hrs
  2. can’t maintain sternal recumbency after calcium
  3. abduction of HLs
  4. Attempts to rise using FLs only
  5. no attempts to rise
  6. HLs out backwards or extended forwards
  7. Very high CK
  8. Inability or reluctance to correctly nurse the cow
94
Q

What are some ddx for a group of cows found suddenly dead?

A
  • Electrocution
  • Anaphylaxis
  • Nutritional Poisoning
  • Potent poisons
  • Nutritional deficiency
  • Septicaemia or Toxaemia
95
Q

What is the difference between spastic an flaccid paralysis?

A

Spastic: loss of voluntary movement; increased tone of muscles; increased spinal reflexes

Flaccid: loss of voluntary movement, decr. muscle tone, absence of spinal reflexes, muscle wasting

96
Q

What causes hypovitaminosis A? What are some CSs?

A

Lack of carotene in diet. Occurs in animals with a lack of green feed (younger>older)

Staggery, convulsions, night blindness (tx with parenteral vit A)

97
Q

What are some clinical signs of tetanus in cattle?

A

Spasticity, “saw-horse” stance, stiff gait, passive flexion not possible, 3rd eyelid prolapse, locked jaw and bloat

98
Q

What is the difference bw a tremor, tic, myoclonus and tetany?

A 
Tremor= continuous repetitive twitching of skeletal muscle (usually palpable and visible)
Tics= spasmodic twitching movement made involuntarily by muscles normally under voluntary control
Myoclonus= repetitive rhythmic contractions of skeletal muscles (occurs in sleep)
Tetany= continuous tonic spasm of a muscle

DVM3 (13 decks)

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