Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

GI2 > Farm 2 > Flashcards

Farm 2 Flashcards

(100 cards)

Start Studying
1
Q

What are the bacterial causes of salivation in ruminants?

A

Calf diphtheria (necrobacillosis), F. necrophorum, necrotic laryngitis
Actinobacillosis (Wooden tongue)
Actinomycosis (Lumpy jaw)

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

What are the traumatic causes of salivation in ruminants?

A

Choke
Drenching gun/bolus injuries/oral burns
Teeth
Vagal nerve damage

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

Which viral diseases affect the oral cavity of ruminants?

A 
FMD 
Rabies 
BVDV 
BHV-1 (infectious bovine rhinotracheitis) 
MCF (malignant catarrhal fever, ovine herpes virus-2) 
Bovine papular stomatitis (BPSV) 
Orf (parapox virus) 
Bluetongue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the orf vaccine

A

Live attenuated vaccine
Scratch vaccine done behind the elbow
VMD product database (do not vaccinate close to lambing, vaccination will not protect lambs via colostrum)

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

What are the clinical signs of bluetongue in sheep?

A

Eye and nasal discharges which becomes thick and crusty
Drooling as a result of swelling and/or ulcerations in the mouth
Swelling of the neck and/or the face, especially around the eyes and the muzzle
Severe lameness affected sheep are reluctant to rise
Haemorrhages into or under the skin
Inflammation and pain at the coronary band
A “blue tongue” is rarely a clinical sign of infection

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

What are the clinical signs of bluetongue in cattl?

A 
Possibly no signs of illness 
Nasal discharge
Swelling of the neck and head, especially around the eyes and muzzle
Conjunctivitis
Lameness
Saliva drooling out of the mouth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the causative agent of ‘wooden tongue’?

A

Actinobacillus lignieresi, gram -ve, facultive anaerobe, oxidase +ve, urease +ve, commensal of the MM

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

What are the clinical signs of wooden tongue?

A

Painful, sometimes fever
Stomatitis, glossitis, fibrous tissue, cellulitis evolving in pyogranulomatous infection
Swollen tongue, often protrudes, hard to the touch, submandibular swelling, enlarged Lnn
Salivation and reluctant to eat
Can also affect skin, oesophageal groove, rumen wall etc
May lead to vagal nerve injury

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

What is the treatment of wooden tongue?

A

Antibiotics (daily IM >10days)
Sodium iodide (IV, repeate every 10 days) risk it may cause restlessness, tachycardia and staggering
NSAIDs
Prevention: isolate cases and review feeding

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

What is the causative agent of lumpy jaw?

A

Actinomyces bovis, gram +ve rods , anaerobic or fa, NON-spore forming, form fungus like branched networks

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

What are the clinical signs of lumpy jaw?

A 
Swelling 
Abscesses 
Fistulous tracts
Fibrosis 
Mucosal damage 
Painful 
Suppurative granulation of the mandible and maxilla 
Hard immobile lesions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is lumpy jaw treated?

A

Antibiotics: procaine benzylpenicillin (daily IM >10 days)
Sodium iodide
NSAIDs
The bone deformation will remain after treatment.

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

What is the causative agent of calf diphtheria (necrotic stomatitis)?

A

Fusobacterium necrophorum

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

What is the aeitiology of calf diphtheria (necrotic stomatitis)?

A

Trauma to buccal mucosa, erupting teeth, contaminated buckets, rough feed

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

What are the clinical signs of necrotic stomatitis?

A 
Common in calves under 3 mo
Necrotic lesions in the pharynx and larynx 
Swollen cheeks 
Salivation 
Foul smelling breath 
Painful swallowing 
Cough 
Inspiratory dyspnea 
Laryngeal form with stertor more common in older calves 3-18 mo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is calf diphtheria (necrotic stomatitis) treated?

A

Isolation
Antibiotics (procaine benzylpenicillin daily IM >5 days)
NSAIDs
TLC
Tracheostomy
Can affect groups so discuss control with the farmer

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

What are the causes of stomatitis?

A

Traumatic injuries e.g. drenching gun
Foreign bodies e.g. sticks and root vegetables
Caustic substances on farm

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

How is stomatitis treated?

A

Remove decaying food material
Broad spec antibiotics (amoxicillin 5 days
NSAIDs
Discuss management practices

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

What is the life cycle of fasciola hepatica?

A

Eggs pass out in faeces
Eggs hatch, miracidians penetrate snail (Galba truncatulata)
Cercariae encyst on submerged/wet vegetation (metacercariae develop)
Ruminants ingest metacercariae
Metacercariae excyst in the duodenum, penetrate wall, enter peritoneum and invade Glissons capsule
Migration to the liver
Flukes reach sexual maturity (in ruminant bile duct)
Minimum period for life cycle completion is 17-19 weeks

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

What is the pathology of fasciola hepatica?

A

Parenchymal destruction during migration leading to inflammation and fibrosis
Rarely will damage large blood vessels leading to haemorrhage
Fluke in the bile duct can feed on animals blood leading to anaemia and cholestasis
Anaerobic environment can lead to Blacks disease (infectious necrotic hepatitis)

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

What are the acute clinical signs of fascoiola hepatica in sheep?

A 
Late autumn / early winter
Large numbers of migrating fluke in liver
Anaemia – Pale mucus membranes / weak
Hypoalbuminaemia
Rapidly fatal, animals often found dead
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the clinical signs of sub-acute fascioloa hepatica in sheep?

A 
Late autumn / early winter
Rapid condition loss
Anaemia
Oedema (Submandibular “Bottle Jaw” or brisket oedema )
Colic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the clinical signs of chronic fascioloa hepatica in sheep?

A 
Winter / Early spring
Adult fluke sucking blood in bile ducts
Poor condition
Anaemia
Hypoalbuminaemia
Submandibular oedema
Chronic scour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How do goats present with fasciola hepatica?

A

Chronic form is most common although sub-acute is seen. Very rare to see sudden death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are the clinical signs of acute fascioloa hepatica in cattle?
Rare in cattle Fibrous nature of liver Acquired immunity does develop and provides protection (NB whilst antibody can be detected in sheep it appears to be non-protective)
26
What are the clinical signs of chronic fascioloa hepatica in cattle?
Similar presentation to sheep | Brisket and ventral oedema also seen
27
What are the clinical signs of subclinical fascioloa hepatica in cattle?
Increasingly recognised Poor performance (reduced growth rate / reduced yield / loss of condition / predisposes to other disease) Increased risk of Salmonella dublin?
28
How is faciola hepatica diagnosed?
Post mortem (fluke in parenchyma and bile duct) Elevation of liver enzymes AST / GLDH (acute and chronic disease) / gGT (chronic disease bile duct damage) Faecal egg count (adults must be present so only of use in chronic cases) Eosinophilia – indicates parasitic infection (useful in subclinical cases) Blood / bulk milk antibody ELISA (only indicates exposure)
29
What are the blood biochemistry changes in a faciola hepatica infection?
``` Aspartate aminotransferase (AST) - Not liver specific, also produced from cardiac and skeletal muscle Gamma glutamyltransferase (γGT) - Good indicator of bile duct damage Glutamate dyhydrogenase (GLDH) - Liver specific, elevated in acute disease Sorbitol dehydrogenase (SDH) - Liver specific, elevated in acute disease Bilirubin - Conjugated increased with bile duct obstruction, unconjugated increased in haemolytic anaemia ```
30
What drugs can be used to treat liver fluke?
``` Triclabendazole Nitroxynil Closantel Clorsulon Oxyclozanide Albendazole ```
31
Which drug can be used to treat immature fluke in sheep and cattle?
Triclabendazole
32
Which drug can be used to treat adult and late immature fluke in cattle?
Nitroxynil
33
Which drugs can be used to treat adult and late immature fluke in sheep?
Nitroxinil and closantel
34
Which drugs only treat adult fluke in cattle?
Clorsulon, oxyclozanide and albendazole
35
Which drugs only treat adult fluke in sheep?
Oxyclozanide and albendazole
36
How should acute fluke be treated?
Needs activity against early immature fluke (i.e. triclabendazole)
37
How is fluke treatment delivered?
Drench or subcutaneous injection
38
Which fluke products are licenced during lactation?
Oxyclozanide and albendazole
39
How can fluke infection be prevented?
Limit snail habitat Prevent access to snail habitats (fence of marshy areas) Application of molluscicides to pasture Introduction of a predator e.g. geese Prophylactic treatment (e.g. routine regular treatment of stock, treat when evidence of disease, treatment based on fluke forecast)
40
What other liver trematodes are there?
Fasciola gigantica Fasciola magna Dicrocoelium dendriticum
41
What is the aetiology of liver abscesses in large animals?
Bacteraemia from navel ill or another nidus of infection (e.g. ruminitis, FB) Usually T. pyogenes or Fusobacterium necrophorum
42
What happens if a liver abscess is found at slaughter?
Liver is discarded and the rest of the animal is eaten as normal
43
What are the clinical signs of liver abscessation?
``` Vague clinical signs, often subclinical Poor performance (poor yield, poor BCS, reduced growth rate) ```
44
How can liver abscessation be prevented?
Limit subclinical ruminal acidosis | Add small quantities of roughage to the diet
45
What complications may result from bacteraemia in large animals? (e.g. from a septic focus in the liver)
Peritonitis, endocarditis, caudal vena cava thrombosis syndrome
46
What happens in caudal vena cava thrombosis syndrome?
Extension of infection into the caudal vena cava Septic foci seed out in lungs establishing local abscesses Erosion into major vessels can cause per-acute fatal haemorrhage Animals usually found dead in a huge pool of blood
47
What is the cause or ruminitis?
Chronic low rumen pH -> inflammation of the rumen mucosa | Common in barley beef animals fed 100% cereal diets +/- small quantities of forage
48
What happens to the rumen mucosa in ruminitis?
Enlargement and hardening of the papillae Excessive keratinization of the mucosa including food material and bacteria Eventually rumen wall abscessation can occur which may extend into the liver
49
What is the pathogenesis of Ragwort?
Contains pyrrolizidine alkaloids which are toxic to hepatocytes The degree of liver damage depends on dose Toxicity can be acute or chronic It is often subclinical due to a large functional liver reserve
50
What are the clinical signs of ragwort poisoning?
Dull, depressed, weight loss, poor doing, jaundice, subcutaneous oedema (due to hypoalbuminemia), colic, scour, photosensitization Hepatic encephalopathy can occur - staggering, circling and blindness
51
How is ragwort poisoning diagnosed?
History of exposure Elevation of liver enzymes in serum Histology of liver (biopsy or PM) Post mortem changes (shrunken, fibrosed, slate-grey or mottled liver)
52
How can ragwort poisoning be treated and prevented?
Symptomatic treatment | Prevent in other animals in the group
53
Which species are most susceptible to copper toxicity?
Sheep | Esp certain breeds e.g. North Ronaldsay, Charollais, Texel and Suffolk breeds
54
Why is copper toxicity becoming more common in cattle?
Over supplementation to avoid infertility
55
What is the pathogenesis of copper toxicity?
Excess Cu is stored in the liver Subclinical liver degeneration Sudden mass release of Cu Acute intravascular haemolysis -> prehepatic jaundice Renal Cu excretion capacity overwhelmed -> nephromegaly and haemoglobinurea
56
What are the clinical signs of acute copper poisoning?
Depression, colic, collapse, death
57
What are the clinical signs of chronic copper poisoning?
Jaundice, anaemia, depression and anorexia, rumen stasis, colic, diarrhoea, recumbency and death This is more common in cattle
58
How is copper toxicity diagnosed?
Clinical signs History of exposure to copper or over supplementation Post mortem (widespread jaundice, hepatomegaly, distended bronze-black kidneys) Plasma Cu >50mmol/L (Live animal) Liver Cu >8,000 mmol/Kg (PM or biopsy?) Kidney Cu >650 mmol/Kg (PM)
59
How is copper toxicity treated?
None if haemolytic crisis has occurred Remove from sources of Cu from diet Ammonium tetrathiomolybdate described but not licensed in UK/EU Fluids and supportive therapy
60
How is copper toxicity prevented?
Only feed sheep concentrate designed for sheep (has low Cu) Never graze sheep on pasture fertilised with pig manure Calculate and monitor Cu intake
61
Why may you do a liver biopsy in farm animals?
Liver copper estimations Diagnosis of fatty liver Histology in case of liver disease
62
What are the dangers of liver biopsy?
Haemorrhage | Infection
63
What are the landmarks for taking a liver biopsy in cattle?
Right had side, 11th rib space, ~20cm below transverse process
64
What is the technique for taking a liver biopsy in cattle?
``` Surgically prepare the site Local anaesthetic in all layers 1cm stab incision through the skin Introduce biopsy needle through the intercostal muscle towards the left elbow Biopsy using standard technique ```
65
What are the predominant salmonella species in adult cattle?
S. Dublin, S. typhimurium
66
What are the clinical signs of salmonella in adult cattle?
Diarrhoea, pyrexia, systemically ill, abortions, septicaemia, pneumonia polyarthritis, ear tip necrosis in calves
67
What are the features of a salmonella carrier state?
Mixed infections common (often fasciola hepatica) Source of infection is usually bought in cattle (or contaminated feed/pasture/water) Can be an active or passive carrier Shedding of the organism can be activated by stress
68
How can salmonella be diagnosed in adult cattle?
``` Is difficult as clinical signs and PM are not unique Enteritis – faecal samples Abortion – foetus, placenta Infected herd – slurry sample Screen for liver fluke ```
69
How is salmonella treated in adult cattle?
Antibiotics e.g. amoxicillin and TMPS IM 5 days – prevent systemic disease but may increase length of carrier state and select for resistant strains (e.g. S. typhimurium DT104) Culture and sensitivity is important
70
What route should systemic antibiotics NOT be given to cattle?
Oral antibiotics will interfere with rumen flora in adult cattle but can be given to calves pre-weaning.
71
What prevention and control measures can be used for salmonella in cattle?
Vaccination of non-clinical animals (dead vaccine, can also be used in face of an outbreak) Closed herd Disinfection protocols Prevention of concurrent liver fluke infection Wildlife biosecurity Feed and pasture contamination Clean water source (mains)
72
What is winter dysentery?
A characteristic syndrome of diarrhoea and milk drop seen in groups of animals
73
What are the clinical signs of winter dysentery?
Self limiting profuse dark diarrhoea, reduced milk yield (10-30%), colic
74
What is the aetiology of winter dysentery?
Causal agent thought to be a corona virus with a tropism of GI and resp tracts
75
What is the epidemiology of winter dysentery?
Very infectious, high morbidity, mortality is rare, short incubation period 3-7 days.
76
How is winter dysentery diagnosed?
Clinical signs and history. Can look for virus in the faeces but this virus also found in normal animals Important to differentiate from other causes e.g. salmonellosis
77
How is winter dysentery treated?
Supportive, the disease is self limiting
78
How can winter dysentery be prevented?
Standard biosecurity measures, infection is hard to control once established but will burn itself out in a couple of weeks
79
What is the differential diagnosis for diarrhoea in adult cattle?
``` Johnes disease Liver fluke GI parasites Coccidiosis BVD Babesiosis Malignant catarrhal fever Clostridial disease Endotoxaemia ```
80
What are the causes of acute diarrhoea in adult cattle?
``` Clinical ruminal acidosis Poisoning Endotoxaemia Ingestion/dietary Winter dysentery Malignant catarrhal fever Salmonellosis Abomasal ulcer BVD (transient infection) ```
81
What are the causes of chronic diarrhoea in cattle?
``` Johnes disease Micronutrient deficiency/toxicity Liver fluke Amyloidosis GI parasite ```
82
Causes of diarrhoea in a group of cattle
Micronutrient deficiency/toxicity GI parasites BVD (acute/transient infection) Winter dysentery
83
Causes of diarrhoea in an individual cow
``` Abomasal ulcer Endotoxaemia Malignant catarrhal fever Amyloidosis Johne’s disease BVD (mucosal disease in PI animal) ```
84
Causes of diarrhoea in the individual cow or a group
``` Poisoning Ruminal acidosis Ingestion/dietary Liver fluke Salmonellosis ```
85
What questions would you ask in a case of diarrhoea?
``` Individual or herd outbreak? Acute/subacute/chronic? Any animal movements or new animals onto farm? Nutrition: any changes in feed? Mortality/morbidity? Milk drop? Abortions? ```
86
What can the diarrhoea look like in different conditions of the adult cow?
``` Dark and foul smelling (occult blood) Pale and pasty (rumen acidosis) Watery (endotoxaemia) Air bubbles (Johne’s) Mucus, fibrinous casts (Salmonella) Fresh blood ```
87
Give a diagnostic plan for diarrhoea in adult cattle?
``` History Clinical exam Faecal sample? Blood? PM? Response to supportive treatment? Consideration of zoonotic potential ```
88
What is a treatment plan for diarrhoea in adult cattle?
``` Supportive treatment (remove from current feed, transfaunation, introduce good quality hay) Absorbants such as kaolin Fluids NSAIDs Antibiotics? Rumen supplements (no evidence) ```
89
What factors play a role in whether salmonella infection leads to clinical disease?
``` Serotype Concurrent infection Previous exposure Immune competence Colostrum Strain Viral load ```
90
What is traumatic reticuloperitonitis (TRP)?
Aka. Hardware or tyre wire Caused by fragments of metal being eaten by cattle and progressing to the reticulum where they may penetrate the rumenoreticular wall and migrate through the body. Clinical signs vary
91
What are the 4 main presentations of TRP?
Acute peritonitis Chronic local peritonitis Diffuse peritonitis Sudden death
92
How does acute peritonitis present?
``` Anorexia Milk drop (>50% in 24hrs) Pyrexia Subacute abdominal pain, 'tucked-up' appearance Reduced/absent rumination Firmer faeces Moderate abdominal fill and mild ruminal tympany Grunting Difficulty in rising and laying down Peculiar laying position e.g. lateral ```
93
What are the differential diagnoses for an acute peritonitis presentation?
Traumatic reticulitis Pericarditis Pleuritis Any painful abdominal condition
94
How does chronic local peritonitis present?
Disappointing milk yield Loss of body condition Arched back, tense abdomen, smaller rumen, reduced rumen motility Variable temperature (may be subnormal or slightly elevated) Reduced faecal quantity with an increase in undigested particles Mildly tachycardic Vague signs of ill health, poor production and infertility
95
What are the differential diagnoses for a chronic local peritonitis presentation?
Chronic indigestion Ketosis Pneumonia
96
How does diffuse peritonitis present?
``` Typically in recently calved animals Abdominal enlargement despite anorexia Absent or limited rumen movement Toxaemia and shock (skin tent time of the upper eyelid is more than 3 seconds) Dehydration Tachycardia (>120bpm) Scant faeces Pain on deep rectal palpation ```
97
Why does sudden death occur in TRP?
Sudden death in apparently healthy cattle can result from migration of wire directly through the pericardial sac and perforation of either a coronary vessel or the heart itself
98
How is TRP diagnosed?
History (sudden drop in milk over 24hr period) Clinical exam (reduced rumen size, reduced rumen movement, reduced appetite, change in faecal constancy, reluctance to extend back on withers pinch, grunt on bar test, muffled heart sounds, distention of jugular veins, mild pyrexia) Radiography Ultrasonography Exlap Abdominal paracentesis – may show peritonitis Blood tests (leucocytosis, neutrophilia with a left shift, acute phase proteins e.g. fibrinogen or haptoglobin)
99
What are the 2 methods for rumenotomy?
Method 1 – create a temporary rumenostomy by suturing the edges of the rumen incision to the skin, this can be left as a semi-permanent stoma or closed at the end of surgery Method 2 – using a Weingart frame, this is quicker and easier than rumenostomy
100
What are some causes of chronic ruminal hypomobility syndrome?
Vagal indigestion Botulism Tetanus Peritonitis

GI2 (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions