Farm 4

Question 1

What are the options for a BVD positive herd?

Answer 1

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

Question 2

How does the UK control BVD?

Answer 2

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

Question 3

How does clostridia usually cause disease?

Answer 3

The potent toxins they produce

Question 4

What is clostridia and where are these organisms found?

Answer 4

Ubiquitous organisms
Gram+, anaerobic bacilli
Produce spores
Soil, rotting vegetation, decomposing matter
Commensal in gut of livestock species

Question 5

What are the risk factors for clostridial disease?

Answer 5

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

Question 6

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

Answer 6

Lamb dysentery – common

Question 7

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

Answer 7

Struck – rare

Question 8

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

Answer 8

Pulpy kidney – most common

Question 9

What are the predisposing factors for C. perfringens infection?

Answer 9

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

Question 10

When is pulpy kidney most likely to occur?

Answer 10

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

Question 11

What are the clinical signs of pulpy kidney?

Answer 11

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)

Question 12

What toxin causes pulpy kidney?

Answer 12

ε toxins

Question 13

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

Answer 13

Lambs <1-2 weeks of age

Question 14

What are the clinical signs of lamb dysentery?

Answer 14

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

Question 15

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

Answer 15

Seen in neonates and adult sheep

Necrotic enteritis, jejunal ulceration, usually found dead

Question 16

How is C. perfringens diagnosed?

Answer 16

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

Question 17

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

Answer 17

Pulpy kidney: cerebral lesions (focal encephalomalacia)

Lamb dysentery: ulcerations intestinal mucosa

Question 18

How are histotoxic clostridia diagnosed?

Answer 18

Gross pathology, confirmed by histopathology with IFAT on tissue

Question 19

What causes braxy?

Answer 19

C. septicum

Question 20

When is braxy seen?

Answer 20

Autumn and winter, when the fields are frosted

Question 21

What are the clinical signs of braxy?

Answer 21

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

Question 22

What causes blacks disease (infectious necrotic hepatitis)?

Answer 22

C. novyi type B

Question 23

What are the clinical signs of blacks disease?

Answer 23

Sporadic death in older sheep but rarely cattle

Question 24

What is the trigger for blacks disease?

Answer 24

Fluke larvae migration

Question 25

How can blacks disease be diagnosed?

Answer 25

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

Question 26

How is clostridial disease treated and prevented?

Answer 26

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

Question 27

What is the prognosis of clostridial disease?

Answer 27

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

Question 28

What are the compliance issues around vaccination of clostridial vaccines?

Answer 28

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

Question 29

What are the histotoxic clostridia?

Answer 29

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)

Question 30

What are the neurotrophic bacteria?

Answer 30

They produce potent neurotoxins C. tetani C. botulinum

Question 31

What are the enterotoxic bacteria?

Answer 31

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

Question 32

How is FMD transmitted?

Answer 32

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

Question 33

Which different species are affected my FMD?

Answer 33

Sheep, goats, pigs and cattle

Question 34

Which species are maintenance hosts of FMD?

Answer 34

Sheep and goats

Question 35

What species is an amplifier host of FMD?

Answer 35

Pigs

Question 36

What species is an indicator host of FMD?

Answer 36

Cattle

Question 37

Which species are carriers of FMD?

Answer 37

Sheep, goats and cattle | Pharyngeal tissue 4-6 months

Question 38

What are the clinical signs of FMD in cattle?

Answer 38

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

Question 39

Does FMD have a high mortality rate?

Answer 39

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

Question 40

What is the morbidity rate of FMD?

Answer 40

100% in a susceptible population

Question 41

Why is control of FMD challenging?

Answer 41

Spreads very quickly | A lot of virus has been shed before you see clinical disease

Question 42

What are the clinical signs of FMD in pigs?

Answer 42

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

Question 43

What are the clinical signs of FMD in sheep?

Answer 43

Mild or absent – fever, oral lesions, lameness | This makes diagnosis and prevention of spread more difficult

Question 44

List some vesicular diseases other than FMD

Answer 44

Vesicular stomatitis Swine vesicular disease Vesicular exanthema of swine

Question 45

What are the differential diagnoses for FMD in pigs?

Answer 45

Foot rot Chemical and thermal burns Vesicular disease

Question 46

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

Answer 46

``` 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) ```

Question 47

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

Answer 47

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

Question 48

How is FMD prevented and controlled?

Answer 48

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

Question 49

Why do we keep the UK FMD free?

Answer 49

Gives more opportunity for trade and higher meat prices

Question 50

What is the aetiology of copper deficiency?

Answer 50

Primary dietary deficiency | Secondary due to antagonism by sulphur, iron and molybdenum

Question 51

What are the clinical signs of copper deficiency?

Answer 51

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

Question 52

How is copper deficiency diagnosed?

Answer 52

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

Question 53

How is copper deficiency treated?

Answer 53

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

Question 54

What is the aetiology of selenium and vitamin E deficiency?

Answer 54

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

Question 55

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

Answer 55

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

Question 56

How is selenium and vitamin E deficiency diagnosed?

Answer 56

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

Question 57

How is selenium and vitamin E deficiency treated?

Answer 57

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

Question 58

What is the aetiology of cobalt deficiency?

Answer 58

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

Question 59

What are the clinical signs of cobalt deficiency?

Answer 59

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

Question 60

How is cobalt deficiency diagnosed?

Answer 60

Improved growth following vitamin B12 injection

Question 61

How is cobalt deficiency treated?

Answer 61

Vitamin B12 injections weekly for several weeks | Intraruminal bolus

Question 62

What is the aetiology of iodine deficiency?

Answer 62

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

Question 63

What are the clinical signs of iodine deficiency?

Answer 63

``` 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. ```

Question 64

How is iodine deficiency diagnosed?

Answer 64

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.

Question 65

How is iodine deficiency treated?

Answer 65

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