Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI2 > Farm 4 > Flashcards

Farm 4 Flashcards

1
Q

What are the options for a BVD positive herd?

A

‘do nothing’ – some natural immunity will occur
Eradication – cull PIs
Vaccination – protect before first breeding
Eradication and vaccination – most rapid and complete option

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does the UK control BVD?

A

Voluntary national control schemes in England and Wales
Compulsory scheme in Scotland
Mandatory screening, restrictions on untested or “non-negative” herds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does clostridia usually cause disease?

A

The potent toxins they produce

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is clostridia and where are these organisms found?

A 
Ubiquitous organisms
Gram+, anaerobic bacilli
Produce spores
Soil, rotting vegetation, decomposing matter
Commensal in gut of livestock species
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the risk factors for clostridial disease?

A

Management: diet change, handling
Parasites: e.g. fluke
Injury: abrasion of the skin or mucosa allows the spore to enter an anaerobic environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the common name for C. perfringens type B and how common is it?

A

Lamb dysentery – common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the common name for C. perfringens type C and how common is it?

A

Struck – rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the common name for C. perfringens type D and how common is it?

A

Pulpy kidney – most common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the predisposing factors for C. perfringens infection?

A

Low proteolytic activity in neonatal intestine (trypsin inhibitors in colostrum)
Incomplete establishment of normal flora in neonates
Dietary influences
Abrupt diet change, gorging energy rich diet (e.g. moving from milk to forage)
Intestinal hypomotility, consequence of overeating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When is pulpy kidney most likely to occur?

A

In lambs at growing (4-10 weeks) and finishing (>6 months)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the clinical signs of pulpy kidney?

A

Often affects the best lambs as they are the first to be fed and get the most food
Lambs are found dead or with neurological signs
Rapid kidney autolysis (although this is a normal PM change)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What toxin causes pulpy kidney?

A

ε toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When is lamb dysentery (type B) most likely to occur?

A

Lambs <1-2 weeks of age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the clinical signs of lamb dysentery?

A

Haemorrhagic enteritis with ulceration in small intestine, usually found dead, abdominal pain, collapse, blood-stained scour, CNS signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the clinical signs of struck (type c)?

A

Seen in neonates and adult sheep

Necrotic enteritis, jejunal ulceration, usually found dead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is C. perfringens diagnosed?

A

Isolation of C. perfringens means nothing - it is a normal commensal of the GI tract that will overgrow after animal has died
Culture on its own not useful
Isolation of toxins (not diagnostic) also need relevant clinical signs and history
Get relevant suspect history and PM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What PM changes will you see in pulpy kidney and lamb dysentery?

A

Pulpy kidney: cerebral lesions (focal encephalomalacia)

Lamb dysentery: ulcerations intestinal mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How are histotoxic clostridia diagnosed?

A

Gross pathology, confirmed by histopathology with IFAT on tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What causes braxy?

A

C. septicum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

When is braxy seen?

A

Autumn and winter, when the fields are frosted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the clinical signs of braxy?

A

Sudden onset, pyrexia, colic, abomasitis, coma and death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What causes blacks disease (infectious necrotic hepatitis)?

A

C. novyi type B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the clinical signs of blacks disease?

A

Sporadic death in older sheep but rarely cattle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the trigger for blacks disease?

A

Fluke larvae migration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How can blacks disease be diagnosed?

A

Hepatic necrosis; characteristic lesions at PM (sharply delineated yellow necrotic areas of liver) / evidence of migratory fluke
IFAT on impression smears

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How is clostridial disease treated and prevented?

A

Early treatment with antibiotics (5 days penicillin) and NSAIDS
Vaccination (toxins are used to produce most of the vaccines- very effective) – often vaccinated prior to birth to pass clostridial immunity to the young
Good management – dietary management, low stress, removal of affected pasture, reduce risk of injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the prognosis of clostridial disease?

A

Depends on how early treatment starts, generally poor as there is too much toxic damage and often the animals are already dead

28
Q

What are the compliance issues around vaccination of clostridial vaccines?

A

Improper storage e.g. wrong temperature
Improper administration – incorrect route, not given at all, timing, no booster, wrong product, other products given concurrently
Unfit, poorly conditioned animals with a poor immune response

29
Q

What are the histotoxic clostridia?

A

They produce exotoxins that cause localised tissue necrosis and systemic toxaemia
C. chauvoei ((true) black leg)
C. septicum ((false) blackleg, malignant oedema)
C. novyi ((false) black leg)
C. novyi type B (Black disease)
C. sordellii (gas gangrene)
C. haemolyticum (bacillary haemoglobinuria)

30
Q

What are the neurotrophic bacteria?

A

They produce potent neurotoxins
C. tetani
C. botulinum

31
Q

What are the enterotoxic bacteria?

A

Bacteria commonly found in the gut in low numbers
C. perfringens (type A) – haemorrhagic enteritis
C. perfringens (type D) – Pulpy kidney

32
Q

How is FMD transmitted?

A 
Direct contact 
-Ingestion of animal products 
-Mating/AI
-Direct contact with infected wildlife 
-Wind borne 
Indirect 
-Fomites
33
Q

Which different species are affected my FMD?

A

Sheep, goats, pigs and cattle

34
Q

Which species are maintenance hosts of FMD?

A

Sheep and goats

35
Q

What species is an amplifier host of FMD?

A

Pigs

36
Q

What species is an indicator host of FMD?

A

Cattle

37
Q

Which species are carriers of FMD?

A

Sheep, goats and cattle

Pharyngeal tissue 4-6 months

38
Q

What are the clinical signs of FMD in cattle?

A

Fever, vesicles (mouth, hoof, teat), abortion

39
Q

Does FMD have a high mortality rate?

A

No, generally adults recover in 2 weeks but can cause death in young stock
<1%
Animals are generally destroyed to prevent spread

40
Q

What is the morbidity rate of FMD?

A

100% in a susceptible population

41
Q

Why is control of FMD challenging?

A

Spreads very quickly

A lot of virus has been shed before you see clinical disease

42
Q

What are the clinical signs of FMD in pigs?

A

Hoof lesions (more severe than cattle), snout vesicles, oral vesicles

43
Q

What are the clinical signs of FMD in sheep?

A

Mild or absent – fever, oral lesions, lameness

This makes diagnosis and prevention of spread more difficult

44
Q

List some vesicular diseases other than FMD

A

Vesicular stomatitis
Swine vesicular disease
Vesicular exanthema of swine

45
Q

What are the differential diagnoses for FMD in pigs?

A

Foot rot
Chemical and thermal burns
Vesicular disease

46
Q

What are the differential diagnoses for FMD in cattle and sheep?

A 
Rinderpest
IBR
BVD
MCF
Bluetongue
Pox virus – pseudocowpox etc 
Plant toxins
Papilloma virus (non-vesicle look alike)
Ulcerative diseases (non-vesicle look alike)
Photosensitisation (non-vesicle look alike)
47
Q

FMD is very rarely zoonotic (only if very immune suppressed). What are the clinical signs in humans?

A

Mild headache, malaise, fever, tingling, burning sensation of fingers, palms, feet, prior to vesicle formation, oral blisters

48
Q

How is FMD prevented and controlled?

A

Animal treatment?
Eradication programs
Vaccinate to kill – vaccinate to slow spread and then kill
Vaccinate to live – only in endemic areas, protects against clinical signs but not infection, affects trade

49
Q

Why do we keep the UK FMD free?

A

Gives more opportunity for trade and higher meat prices

50
Q

What is the aetiology of copper deficiency?

A

Primary dietary deficiency

Secondary due to antagonism by sulphur, iron and molybdenum

51
Q

What are the clinical signs of copper deficiency?

A

Poor growth, de-pigmentation (grey brown discolouration) esp around ears and eyes ‘spectacle’, thin grey sparse hair coat, lameness, diarrhoea, anaemia, reduced fertility
Causes swayback in lambs

52
Q

How is copper deficiency diagnosed?

A

Plasma copper concentrations (7-10 animals should be sampled)
Response to supplementation
Liver biopsy samples can be used to measure copper reserves

53
Q

How is copper deficiency treated?

A

Copper supplemented parenterally or orally (in feed or slow release bolus)

54
Q

What is the aetiology of selenium and vitamin E deficiency?

A

Dietary deficiency
Selenium and Vit E protect cells against damage - skeletal, cardiac and respiratory muscles are most susceptible to damage.

55
Q

What are the clinical signs of selenium and vitamin E deficiency?

A

Congenital form – still birth, weak calf unable to suck
Delayed form – seen in calved 1-4 months old, sings precipitated by sudden unaccustomed exercise, appearance varies depending in muscle affected
Skeletal – stiffness, recumbency, calf otherwise BAR
Respiratory – resp distress
Cardiac – sudden death

56
Q

How is selenium and vitamin E deficiency diagnosed?

A

Measure enzyme concentrations that indicate muscle damage
Post mortem
Biochemical test - whole blood glutathione peroxidase (GSHPx) a selenium containing enzyme

57
Q

How is selenium and vitamin E deficiency treated?

A

Sodium selenate or selenite given by injection
Usually combined with Vit E

Prevention – SC injection of barium selenite, oral supplementation, rumen bolus
Supplementation to the dam in late pregnancy will ensure good supply in colostrum for newborn calf

58
Q

What is the aetiology of cobalt deficiency?

A

Dietary deficiency from grass grown in cobalt deficient soil
Cobalt is required for the manufacture of vitamin B12
More common in sheep

59
Q

What are the clinical signs of cobalt deficiency?

A

Poor appetite, reduced growth, anaemia, skin becomes thin with poor hair quality

60
Q

How is cobalt deficiency diagnosed?

A

Improved growth following vitamin B12 injection

61
Q

How is cobalt deficiency treated?

A

Vitamin B12 injections weekly for several weeks

Intraruminal bolus

62
Q

What is the aetiology of iodine deficiency?

A

Primary deficiency low iodine in the soil
Secondary deficiency from ingestion of the goitrogen thiocyanate found in brassicas and legumes
Or secondary deficiency from selenium deficiency

63
Q

What are the clinical signs of iodine deficiency?

A 
Thyroid enlargement (goitre), poor growth rates, poor milk production and retained placenta.  
Calves born of iodine deficient dams may be stillborn with goitres and areas of alopecia and SC oedema. Weak calves are unwilling to suck leading to high mortality.
64
Q

How is iodine deficiency diagnosed?

A

Clinical exam
Histopathology of the thyroid
Plasma inorganic iodine (PII)measures current daily iodine intake (short term)
T4 levels reflect the thyroid and iodine status of the animal.

65
Q

How is iodine deficiency treated?

A

Oral dosing with potassium iodide (short acting and laborious)
Intraruminal bolus
Free-access minerals, medication of water supply and pasture fertiliser
Added to ration

GI2 (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions