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Farm 3 Flashcards

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1
Q

What is vagal indigestion?

A

An extreme cause of atony involving the rumen, reticulum and abomasum due to interference with vagal innervation of the medial walls by peritoneal adhesions following FB penetrations. The rumen fills with fluid (saliva and drinking water) or in rare occasions gas.

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2
Q

What are the clinical signs of botulism?

A 
Flaccid paralysis 
Recumbency 
Constipation 
Lack of tone in the tail 
Difficult prehension and mastication 
Difficulty ruminating and eructating
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3
Q

What are the clinical signs of tetanus?

A 
Tonic spasm of the reticuloruminal musculature 
Raised tail 
Stiff movement 
Erect ears 
Degree of trismus 
Constipation
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4
Q

When is rectal prolapse most likely to occur?

A

Most often piglets and lambs, occasionally in calves; commonly associated with long-term colitis and/or diarrhoea, e.g. coccidiosis.

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5
Q

List 4 conditions of the abomasum

A

Left displaced abomasum (LDA)
Right displaced abomasum (RDA)
Abomasal torsion/volvulus (AV)
Abomasal ulceration

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6
Q

What is the pathophysiology of an LDA?

A

There is decreased dry matter intake at calving leading to high starch diet, hypocalcaemia, systemic disease, SARA and fat infiltration of the liver. This leads to decreased abomasal activity and a build up of fluid and gas in the abomasum.
Decreased rumen fill and increased space in the abdomen after calving also contribute.

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7
Q

How does a displaced abomasum lead to ulceration?

A

After the abomasum there is continued secretion of acid -> dilation -> increased intraluminal pressure -> mucosal damage -> ulceration

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8
Q

What are the risk factors of abomasal disease?

A

Things that decrease DMI around calving (over fat cows, poor calving management, periparturient disease, poor feed access/palatability)
Lack of long dietary fibre (decreased rumen fill)
Poor control of energy balance around calving
Sudden increased concentrate feeding at calving
Hypocalcaemia
Peak incidence in spring (may be due to lack of long dietary fibre in the grass)

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9
Q

What are the clinical signs of LDA?

A

Decreased yield (classically 5-10 ltrs)
Decreased feed intake (especially concentrate)
Poor rumen turnover
May be signs of underlying primary disease (e.g. metritis, mastitis)
May show mild colic (rare)

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10
Q

How is an LDA diagnosed?

A

Percussion auscultation producing a ‘ping’
Spontaneous abomasal noise on the left ‘tinkling’
Splashing/tinkling/ping on ballotment behind the last rib
ALWAYS look for underlying primary disease
May come and go ‘swinging LDA’

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11
Q

What are the 3 broad treatment categories for treating an LDA?

A

Conservative
Semi surgical
Surgical

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12
Q

How can an LDA be treated conservatively?

A

Roll the cow (cast onto RHS, slowly roll through dorsal recumbency, may do a brief stop/shake in dorsal recumbency)
May use oral propylene glycol, oral fluids/electrolytes, oral probiotics, systemic prokinetics, long fibre diet as well

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13
Q

What is the relapse rate of LDAs treated with conservative management?

A

~75-80%

But may be a good option while you manage underlying conditions

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14
Q

How can an LDA be treated semi-surgical?

A

The roll and toggle method

  • Roll as for conservative treatment (+/- sedation)
  • Insert toggles through a trochar into the abomasum while the cow is in dorsal recumbency
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15
Q

What are the 5 different surgical approaches for treating an LDA?

A 
Paramedian approach 
Bilateral flank approach 
Right flank approach 
Left flank approach 
Laparoscopic
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16
Q

Describe a paramedian approach LDA surgery

A

Sedation and local analgesia
Open the abdomen to visualise the abomasum
Suture the abomasal fundus to the ventral body wall (partial thickness), often include the abomasum the closure of the muscle layer

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17
Q

Describe a bilateral flank approach LDA surgery

A

Requires 2 surgeons and a standing cow
Local anaesthesia (e.g. paravertebral) and skin prep
Paralumbar fossa incision on each side
Left surgeon – identifies and decompresses the abomasum with 16G needle and tubing, checks there are no adhesions, passes under the abdominal contents via the ventral midline to the right surgeon
Right surgeon – bkrings the abomasum to the right side and fixes it into place with omentopexy, pyloropexy

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18
Q

What is an omentopexy?

A

Used to fix the abomasum in place in LDA surgery

A continuous suture is put through the omentum and each end of the suture material is sutured to the muscle layer

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19
Q

What is a pyloropexy?

A

Used to fix the abomasum in place in LDA surgery

Put a partial thickness suture through the pylorus and suture to the muscle wall

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20
Q

Describe a right flank approach LDA surgery

A

One surgeon, cow standing
Paralumbar fossa incision on the right hand side
The abomasum is palpated by reaching behind the rumen onto the left side (may be difficult with short arms)
+/- abomasum deflated using a needle and tubing
The abomasum falls or is guided to the ventral midline
Abomasum is located and pulled up to the incision
Fixed into place with omentopexy, pyloropexy

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21
Q

Describe a left flank approach to LDA surgery

A

One surgeon, cow standing
Paralumbar fossa incision on the left had side
The abomasum is identified and a continuous suture line is placed into the fundus. The ends of the suture are left very long ~2m
Abomasum is decompressed if needed
Needle attached to one end of suture material and passed ventrally through abdomen (guarded!) and poked out through ventral body wall to assistant
Repeated with second needle, two ends of material secured on outside as abo repositioned

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22
Q

Describe a laparoscopic approach to LDA surgery

A

Various techniques, some involve rolling and some are done standing

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23
Q

How can LDAs be prevented?

A

Maximise DMI around calving/early lactation e.g. check for stress, correct diet and access
Transition diet: some but not too much concentrate, sufficient long fibre
Fresh calved diet: sufficient long fibre
Early lactation energy balance
Check milk fever control
Check incidences of other diseases (e.g. metritis, milk fever and dystocia) and association with LDA cases

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24
Q

What is the pathophysiology of a right displaced abomasum

A

There is abomasal atony leading to dilation of the abomasum. The abomasum then becomes displaced onto the RHS. Abomasum is susceptible to torsion when dilated.

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25
What are the clinical signs of an RDA ?
Similar to LDA (decreased yield, decreased feed intake, poor rumen turn over, signs of underlying primary disease) but more sever May show mild colic if torsion has occurred
26
How is an RDA diagnosed ?
Auscultation during percussion and ballottment | Similar sounds to LDA, but in a different location as the gas cap is more dorsal
27
What are the broad treatment categories for RDA?
Conservative | Surgical
28
How are RDAs conservatively managed?
This is first line treatment if no signs of torsion Gastric motility modifiers (metoclopramide (unlicenced), Buscopan (little evidence and can’t be used in lactating cows), erythromycin?) NSAIDs (meloxicam) IV Ca Dietary management – more long fibre
29
Why would you choose to treat an RDA surgically?
If there is significant colic, increased HR or conservative treatment fails
30
How do you surgically treat RDA?
Standing right flank approach The abomasum is decompressed (best done by exteriorising and emptying, although tube can be used) Check for signs of ulceration Pyloropexy usually performed to prevent torsion
31
How does the prognosis of an RDA compare to the prognosis of an LDA?
RDA has poorer prognosis
32
When do cattle usually get abomasal torsion?
As a sequela of RDA – the RDA may not present until torsion occurs
33
What are the clinical signs of a abomasal torsion?
Similar to the signs of an RDA but usually more sever colic signs, increase HR (>80-100bpm), little faecal material in rectum, signs of circulatory compromise (low temp, pale mm, dehydration, poor pulse quality)
34
How is abomasal torsion treated?
``` Standing right flank laparotomy Empty abomasum as much as possible Identify and correct torsion (often several axes of torsion so may be very difficult) Perform pyloropexy and close Supportive treatment – fluids and NSAIDs ```
35
What is the prognosis for an abomasal torsion?
Guarded/ poor prognosis
36
What are the predisposing factors for abomasal ulceration?
LDA/RDA Stress Concurrent disease Ingestion of soil/sand
37
What are the clinical signs of abomasal ulceration?
Mild colic, inappetence, pain on ballotment of the right ventral abdomen, melaena/ faecal occult blood, signs of peritonitis Signs are often mild and self cure, even if the abomasum is penetrated the omentum may just seal it off. However may also cause sever signs (colic and poor production) and may be fatal.
38
How is abomasal ulceration managed?
Euthanasia (often advocated once melaena is established) Surgery Analgesia – care with NSAIDs as may be ulcerogenic Antacids? Antibiotics
39
What is the main threat to GI health in ruminants?
A fall in the rumen pH ‘ruminal acidosis’ | If VFAs are produced faster than the cow can absorb the ruminal pH will drop
40
What is the aetiology of ruminal acidosis?
Carbohydrates produce acetic, butyric and propionic acid which is buffered by saliva. High carb diets that need little chewing produce a lot of acid and very little saliva so decrease the rumen pH.
41
What is the aetiology of acute ruminal acidosis?
A large amount of food over a short period of time (e.g. grain overload) causes and acute drop in the rumen pH. This causes bacterial death which will lead to a reduced rate of digestion and decreased dry matter intake. Rumen contractions will cease, there will be no eructation so a gas bloat will occur. This can cause death if sever. A more acidic rumen will also favour lactic acid producing bacteria. Lactic acid is a big osmotic draw which can lead to dehydration and profuse scour.
42
What are the clinical signs of acute ruminal acidosis?
``` 12-36 hours after mass concentrate intake (e.g. animals break into feed store) Anorexia Bloat Ataxia Weakness Blindness Diarrhoea Increased resp. rate Decreased temperature ```
43
How can acute ruminal acidosis be treated?
If animal is recumbent: rumenotomy, empty, flush, +/- repopulate, IV fluids, Ca, glucose B vitamins If animal is standing: oral antacids (e.g. Mg(OH)2), IV fluids, B vitamins
44
What are the possible sequelae of acute ruminal acidosis?
Chronic ruminitis | Liver abscessation
45
What is subacute ruminal acidosis (SARA)?
A chronic but mild suppression of rumen pH | A herd level problem
46
What causes SARA?
Chronic exposure to a high starch low fibre diet (more VFAs and less chewing)
47
How can SARA be prevented?
Need effective long fibre in the diet i.e. a long chop length that requires chewing Can also be related to the feeding system
48
What different feeding systems are used in cattle and what is their effect on rumen pH?
Component feeding (in parlour) – concentrate feed is split between 2 feeds, with every concentrate feed there is a large drop in pH Component feeding with mid-day feed – adding a mid-day feed means meals can be smaller and there will be a smaller drop in rumen pH Component feeding out of parlour – reduces meal size again Total mixed ration – provides the most stable rumen pH, all components of diet are fed ad lib. Partial mixed ration – TMR ad lib and concentrates in the parlour, more dramatic drop in pH after milking but not as bad as component feeding
49
What are the risk factors for SARA?
Large/infrequent concentrate meals Excessive levels of starch/sugar in diet Too little effective long fibre in diet (e.g. overmixing/fine chopping of ration) Sorting of long fibre (e.g. undermixing) if bits of straw are too long (>5cm) they will cherry pick and leave the straw Poor access to forage component of ration Poor transition/dry cow management Poor cow comfort/housing design
50
What are the clinical signs of SARA?
Variable faecal consistency Poor cow cleanliness Tail swishing Decreased yields and bulk milk butterfat levels Decreased feed intakes Poor reproductive performance - little evidence Increased incidence of lameness and environmental mastitis - little evidence
51
How can SARA be monitored?
Rumenocentesis to monitor rumen pH (3/12 cows with a rumen pH of less than 5.5 indicates SARA) pH sensing rumen bolus (5-6 month life span) but expensive so most farmers will only monitor a few cows.
52
How can you assess if the feed is a risk factor for SARA?
Using a penstate sieve. This will separate the larger pieces from the smaller pieces.
53
How can SARA be controlled?
Limit depression of the rumen pH (this can be more difficult in high yielding cattle) Include buffers or yeasts Avoid rapidly released starch e.g. round wheat Add some long fibre Good transition/calving management to maintain DMI Good mixing of mixed rations
54
How can depression of rumen pH be limited?
Forage:concentrate ratio >40:60 Dietary NDF (neutral detergent fibre – a chemical measure of fibre content) content - >35% NDF from forage ?>20-25% Total sugar and starch content - <25% In parlour feeding – Max 4Kg / feed Distribute concentrate feeds – Mid day feed, out of parlour feeders, TMR Ensure feed intakes/access maximised
55
What are the advantages and disadvantages of feeding forage on a ‘self-feed’ system?
Advantages – cheap and easy | Disadvantages – reduced DMI, often wasteful, more spoilage as more food exposed to air
56
What are the advantages and disadvantages of feeding forage on a ‘ring feeder’ system?
Advantages – easy with big bale silage, max feed space per unit area, can be used in addition to other systems to give more SA Disadvantage – awkward for clamp silage/mixed ration
57
What are the advantages and disadvantages of feeding forage on a ‘trough’ system?
Advantages – easier to feed into, can control the feed environment (smooth and raised), cheap, can be covered Disadvantages – needs lots of space
58
What are the advantages and disadvantages of feeding concentrate in parlour feeders?
Advantages – no competition, can vary feed between cows Disadvantages – all daily concentrates in only 2 meals, cow needs to eat concentrate quickly, measurement of feed weight is often inaccurate
59
What are the advantages and disadvantages of feeding concentrate in out-of parlour feeders?
Advantages – can vary feed between cows, concentrate spread over the day so each meal is smaller Disadvantages – often significant competition of access, expensive to install
60
What are the advantages and disadvantages of feeding concentrate in mid-day feed?
Advantages – cheap and easy, spread over the day, versatile and flexible, variety increases DMI Disadvantages – hassle to feed, competition/variation in access
61
What are the different ways of determining how much food each cow should be fed?
Feed to yield Flat rate Stepped
62
What are the advantages and disadvantages of using feed to yield feeding?
Advantages – simple and easy to follow, mirrors lactation curve Disadvantages – very large concentrate meals in early lactation
63
What are the advantages and disadvantages of using flat rate feeding?
Advantages – simple and easy to follow, costing easier | Disadvantages – underfeeding in peak lactation and overfeeding in late lactation
64
What are the advantages and disadvantages of using stepped feeding?
Advantages – simple and easy to follow, combines advantages of feed to yield and flat rate Disadvantages – doesn’t feed to energy requirements as much as feed to yield
65
What are the advantages of having multiple groups of cows on the farm e.g. high and low yielders?
``` Increased precision (Fed to yield) Avoids thin and fat cows (compared to one group) Improved management (cows at similar stage are together) Decreased standing times helps with lameness ```
66
What are the disadvantages of having multiple groups of cows on the farm e.g. high and low yielders?
``` Increased bullying (when animals moved) - more of an issue around calving Increased complexity (multiple groups, diets etc) Increased time ```
67
What are the 3 macro minerals that commonly cause problems in ruminants?
Calcium Phosphorus Magnesium
68
Why does Mg deficiency cause a problem in ruminants?
They have very small reserves so no homeopathic control | Inhibits nerve transmission leading to staggers, recumbency and coma
69
When are ruminants most likely to get hypomagnesaemia?
Winter/spring grass is a poor source of Mg There is poor availability when N/K fertiliser has been recently applied to the grass When DMI is low esp if animal is shivering
70
How can hypomagnesaemia be prevented?
Provide supplementary feed Add MgCl2 to drinking water Use of bolus in the risk period
71
Which trace elements most commonly cause problems in ruminants?
Copper Cobalt Selenium Iodine
72
What are to most common signs of trace element deficiency in ruminants?
Poor growth | Loss of condition/”ill thrift”
73
What kind of virus is the BVD virus?
Pestivirus
74
What are the 2 biotypes (related strains) of the BVD virus?
Non-cytopathogenic (BVDnc) – persists in the cattle population Cytopathic (BVDc) – arise from the non-cytopathic strain through spontaneous mutation
75
What are the types of BVD and how does this relate to the biotypes?
Type 1 – most common presentations Type 2 – rare form in the UK Both types contain non-cytopathogenic and cytopathogenic biotypes
76
What are the clinical signs of acute BVD infection?
Mild systemic disease (diarrhoea, reduced production, often barely noticeable), immunosuppression (causing respiratory and enteric disease), reduced reproductive performance This is not a disease of primary GI Importance – real importance is fertility and immune compromise
77
How long does it take for virus clearance and antibody response in an acute BVD infection?
Virus clearance 10-14 days | Antibody responses slow…plateau at 10 – 12 weeks
78
What are the possible outcomes if a pregnant cow is infected with BVD?
``` PI calf Normal calf Abortion Congenital defects Embryo loss ```
79
What happens if a pregnant cow is infected with BVD in the first third of pregnancy?
The foetus is not immunocompetent leading to - Embryonic death - Foetal death and mummification - Foetus survives but Is born persistently infected
80
What happens if a pregnant cow is infected with BVD in the middle third of pregnancy?
The foetus is largely immunocompetent so will have an immune response leading to: - Foetal death/abortion - Foetus survives but is born with congenital damage e.g. cerebellar hyperplasia, arthrogryposis, microphthalmia, cataracts, hydrocephalus, musculoskeletal malformations, and alopecia
81
What happens if a pregnant cow is infected with BVD in the last third of pregnancy?
The foetus is immunocompetent leading to - Active foetal antibody response - Calf is normal, virus negative
82
What is a PI calf?
Born to a cow infected with BVD during early pregnancy (93%) or a PI dam (7%). These calves will have circulating antigen all of their lives and will shed large quantities of virus.
83
How do cows get mucosal disease?
Occurs when PIs are superinfected with a cytopathic biotype that has mutated from a non-cytopathic biotype. It is fatal.
84
What are the clinical signs of mucosal disease?
Ulceration of the oral and gastrointestinal mucosa, foul smelling diarrhoea, weight loss, death, +/- resp signs, depressed, anorexic, dehydrated
85
What are the clinical signs of BVD type 2?
Sever disease, often fatal, usually in adults, thrombocytopenia, diarrhoea, haemorrhagic disease
86
What are the possible immune states of BVD?
``` Naïve = Ab -ve , virus -ve Immune = Ab +ve, virus -ve PI = Ab -ve, virus +ve (ncp) MD = Ab -ve, virus +ve (ncp+cp) ```
87
How can bulls bring BVD infection into the herd?
Can be a PI (some look clinically normal) Can be acutely infected Virus can ‘hide’ in the testicles (an immunologically privileged site) blood Ab positive, antigen negative yet still spreading virus, virus only found in semen
88
How can BVD be diagnosed?
Viral antigen and antibody tests in both blood and milk | Can use bulk milk – viral Ag will detect 1 PI in 300 cows
89
How can PI calves be identified?
Virus can be identified in blood samples pre-colostrum or from older calves (care with maternal antibodies) Viral Ag from ear tag tissue samples
90
How can a BVD PI cows be differentiated from acutely infected cows?
Viremia following acute infection lasts up to 2 weeks so to demonstrate a PI animal you need 2 positive antigen tests >3 weeks apart
91
What should happen to BVD PI animals?
Should be culled – they are a major reservoir of infection
92
Why should care be taken when buying a pregnant cow?
The cow may not still be infected with BVD but the calf may be a PI – the ‘Trojan horse’ effect
93
What are the advantages and disadvantages for ear tag biopsy testing for BVD?
Advantages – identifies PIs, allows culling, identifies dams that should be tested Disadvantages – expensive as every animal is tested
94
How do you blood sample a heifer cohort for BVD?
Can test from 8 months of age (after maternal Ab gone), usually sample 8-10 from a group, should be Ag and Ab negative
95
What does it mean if a heifer is Ab positive for BVD?
They must have seroconverted due to infection from a PI or contact with an adult (acute infection or PI)
96
How are the different types of BVD managed?
``` Type 1 -Acute – no treatment or symptomatic treatment if seen -Mucosal disease – cull Type 2 -Symptomatic – grave prognosis ```
97
How can you evaluate a herds current BDV status?
Initial screening is usually bulk milk Ab +/- Ag test or young stock cohort test. Calf tag and test results are also useful. PM and abortion results may also give some indication.
98
What are the biggest risk for BVD virus entry to the herd?
Contact with cattle from another unit (e.g. across fences) Contact through markets or shows Shared, hired or new bull BVDV status of bought-in cattle
99
How is BVDV transmitted?
Virus is shed in nasopharyngeal secretions, urine and (less commonly) faeces Virus has poor survival in the environment
100
How can we prevent transmission of BVD within the herd?
Vaccination Removal of PIs Maintain biosecurity to prevent reintroduction of the virus

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