Farm 1 Flashcards
What is the mean calf mortality between birth and 3 months?
3-10% - at least half of this due to disrrhoea
What are the important points to consider in the eepidemiology of a calf diarrhoea case?
- infectious/non- infectious
- most agents are ubiquitous/endemic
- mixed infectios are very common
- zoonotic implications
- dairy/ suckler
- housed / outdoor
Zoonotic organisms in calf diarrhoea?
- Crypto
- E.coli
- Salmonella
Need to remember to warn farmers about this.
Common causes of calf diarrhoea?
- E.coli
- Rotavirus
- Coronavirus
- Coccidiosis
- Cryptosporidiosis
What factors influence pathogenic challenge to the calf?
- Source of infection (i.e. diseased animals or clinically normal carriers)
- Pathogen load (related to hygiene, stocking density, isolation of clinical cases, separation of young from adults)
What factors influence the calf’s immunological defence?
- Colostrum status
- Stress and stocking density (Over stocking –> dirty environment and more stress )
- Intercurrent disease (e.g. BVD, respiratory disease)
- Correct feeding
- Trace element status (vitE, selenium and vitamin A have immunological functions)
What are the clinical signs in a scouring calf?
- Colour and consistency of the faeces (may give some indication of causative agent)
“White” & pasty – E. coli or nutritional?
Dark and/or bloody – coccidiosis or salmonellosis - Dehydration (increased thirst skin tent, sunken eyes, cold nose/extremities, weak, collapsed, progressive shock)
- Acidosis -> hyperK (poor suck reflex, depressed, recumbent, comatose, increased respiratory rate, poor response to rehydration)
What are the clinical signs of enterotoxigenic e. coli (ETEC) in calves?
- Watery diarrhoea in young calf (<6d)
- Rapid progression to collapse
- Usually sporadic (single case)
- Some similarities with “watery mouth” in lambs (Entry via GIT, bacteraemia, hygiene/colostrum important, D+ less common in lambs)
What are the clinical signs of salmonellosis?
- Often bloody diarrhoea with pyrexia
- Occurs at all ages
What are the clinical signs of coccidiosis in calves?
- Often less severe D+/systemic signs
- Sometimes darker, stiff faeces +/- blood
- Often tenesmus
- Usually peri-/post-weaning
What are the signs of neonatal diarrhoea in other ruminants?
- Very similar clinical picture and agents to calves
* Important agents in lambs include clostridial endotoxemia and coccidiosis
What are the clinical signs of clostridial endotoxaemia (lamb dysentery)?
Very acute onset, usually <2wks old
Often sudden death
Abdominal pain, bloody scour
Localised haemorrhagic lesions on post mortem
Why may it be important to diagnose the causal agent in calf diarrhoea?
Treatment decisions - If there is a specific treatment for a specific agent e.g. antibiotics for bacterial agents, coccidostats etc.
Prevention strategies - E.g. vaccination
Zoonotic risks
Diagnosing the causal agent can be very expensive and may not yield a useful result.
Which scenario fits best with diarrhoea caused by ETEC?
a) Group of 10d old, moderately dehydrated scouring calves
b) Individual 2d old collapsed calf with watery scour and subnormal temp
c) Group of 5wk old calved with pyrexia and bloody scour
d) Group of 8wk old calves with dark, slightly bloody scour and tenesmus
b) Individual 2d old collapsed calf with watery scour and subnormal temp
Which scenario fits best with salmonellosis?
a) Group of 10d old, moderately dehydrated scouring calves
b) Individual 2d old collapsed calf with watery scour and subnormal temp
c) Group of 5wk old calved with pyrexia and bloody scour
d) Group of 8wk old calves with dark, slightly bloody scour and tenesmus
c) Group of 5wk old calved with pyrexia and bloody scour
How can you diagnose the cause of an outbreak of calf diarrhoea?
Post mortem examination (VLA) - Ideally early in course of disease
Faecal sampling
- Viral antigen (rota/coronavirus/crypto) - snap test
- Parasitology (crypto/cocci) - Can see signs of disease without oocyst present in faeces so negative test doesn’t rule out, may need multiple samples
- Culture (Salmonella spp/E. coli) - Intermittent shedding so negative test doesn’t rule out, may need multiple samples
Describe a basic diagnostic plan for the diagnosis of calf diarrhoea
Diagnosis in calf scour outbreak is more about working out which management factors were “wrong” than deciding which was the causal agent. May be worth considering going further with specific diagnosis if initial management not successful.
- Decide if lab testing justified
- Assess nutritional/management factors
- Assess factors affecting host defences
- Assess factors affecting level of challenge
What is the mainstay of treatment in calf diarrhoea?
Most causes of calf diarrhoea are self-limiting, so supportive therapy is the most important.
Fluid therapy will help to correct dehydration and acid-base balance.
What are the options for fluid therapy in cattle?
Oral - Quick and easy BUT dangerous if the calf is weak and can’t hold its head up
Intravenous - Safe in weak calves, more rapid effect, more time and skill required
What are the different types of oral rehydration solutions?
1st generation (Na/K/(small amount of)Glu) 2nd generation (Na/K/(small amount of)Glu/HCO3 3rd generation (Na/K/¬Glu/HCO3) - Enough glucose to give energy 4th generation (Na/K/ ¬Glu/HCO3/Glutamine) - Glutamine to promote intestinal repair Gels (similar content) - Add to milk
What are the different types of IV fluid therapy?
Commercial (usually need to add bicarb, otherwise is acidogenic. Adding bicarb to hartmanns will precipitate out Ca salts)
DIY (water + salt +/-HCO3)
Should we correct acid base in the sick calf?
Measuring base deficit on farm difficult
Sometimes clinical signs can be suggestive of acidosis (more common in beef calves and when there is a lack of suck reflex)
If acidotic - can prepare a ‘spike’ (35g/400ml) and add to the normal saline drip (13 g NaHCO3/l).
Evidence suggesting that acid base will correct itself once sufficient fluids are provided, so fluid therapy on its own is likely sufficient.
Treatment for calf diarrhoea caused by ETEC?
Systemic antibiotics (bacteraemia/toxaemic) e.g. Cephalosporins, amoxycillin, florfenicol NSAIDs - commonly used, one off does, give fluids at the same time, more resistant to the nephrotoxic effects
Treatment of salmonellosis in calves?
Systemic antibiotics (some debate but on balance usually used) e.g. Potentiated sulphonamides, potentiated amoxycillin Antibiotic resistance relatively common
Treatment of coccidiosis in calves?
Generally environmental management more important Diclazuril and toltrazuril - Licensed for prevention - Commonly used to treat clinical cases as well (nothing licensed for treatment) - Oral drench Decoquinate - Used for prevention - Feed additive (fed in concentrate)
Treatment for cryptosporidiosis?
Halofuginone
- Licensed for prevention
- Oral drench
- Has been used to treat clinical case (usually not necessary)
- May be useful where hygiene/colostrum management has failed to control crypto problem
What supportive treatments should be considered in calf diarrhoea?
Fluid therapy NSAIDs Multivitamins Nursing (isolation, warmth, easy access to food and water) Isolation
How much colostrum should calves get in the first few hours after birth?
2L in the first hour
5L over the next 6 hours
There is little transfer of maternal antibodies possible after 24hrs
Should calved be tube fed?
Only if necessary!
Milk should flow via the reticulo-groove (reflex) from the oesophagus to the abomasum. If the milk reaches the rumen then there is bacterial overgrowth leading to ruminal acidosis and scours from fermentation.
What is a zinc sulphate turbidity test?
Tests calves for passive transfer of maternal antibody
The test is a measurement of immunoglobulins in serum
Blood sample from calf at least 24hrs old
What factors may compromise passive transfer of maternal immunity?
Maternal factors - disease during gestation, premature lactation, maiden dam
Delivery factors - abnormal parturition, placental abnormalities
Neonatal factors - prematurity, dysmaturity, maternal rejection, multiple birth, or any other condition limiting neonatal mobility and strength
What is the causative agent of Johnes?
Mycobacterium avium subsp. paratuberculosis (MAP)
What is Johnes disease?
Incurable disease of cattle and other ruminants characterised by wasting and diarrhoea
What is the disease course of Johnes?
Infection -> carriage -> subclinical -> clinical
80% of natural infections occur within the first month of life, risk of infection much smaller to adults.
What are the clinical signs of an animal SUBCLINICALLY infected with Johnes disease?
Look clinically normal but have lower milk production or lower fertility
What are the clinical signs of an animal CLINICALLY infected with Johnes disease?
Diarrhoea (Intermittent -> chronic)
Decreased milk yield
Weight loss/emaciation
+/- oedema (e.g. “bottle jaw”) – it is a PLE -> hypoprotinaemia
Disease normally develops at 2-6 years of age
What are the sources of infection for Johnes disease?
Faeces from shedding cattle
Faeces from shedding goats/sheep
Colostrum/milk from infected cattle
Environment/fomites - clinical significance is uncertain (Lasts up to 1yr in water or slurry, 4 yrs in soil)
Wildlife reservoirs? - clinical significance is uncertain
What are the 2 basic approaches for the diagnosis of Johnes disease?
Detect MAP in faeces - Better at detecting end stage animals
Detect immune response to MAP (antibody) - Better earlier in the disease course
Advantages of detecting MAP in faeces
Demonstrates shedding/danger of transmission
Excellent specificity
Sensitive methods that allow for MAP detection in faeces are available
Can use pooled samples
Disadvantages of detecting MAP in faeces
Faecal shedding often doesn’t occur until late in disease and can be unpredictable and intermittent
Will detect very few animals early in the course of infection – more likely to detect later in the disease as shedding increases
Some techniques are not very sensitive at detecting MAP in faeces
Some tests have long turnaround times e.g. culture
What are the techniques for detecting MAP in faeces?
ZN staining of faecal smear
Faecal culture
PCR
What are the problems with ZN staining a faecal smear for MAP detection?
Very low sensitivity
Dependant on skill of operator
What is the sensitivity and specificity of faecal culture for MAP detection?
Sensitivity 30-50%
Specificity >99.9%
What are the advantages and disadvantages of using faecal culture for MAP detection?
Advantages – no false positives so positive results are diagnostic
Disadvantages – takes a long time, poor sensitivity (esp.in young subclinical animals), expensive
What is the sensitivity and specificity of using PCR for detecting MAP in a faecal sample?
Sensitivity 30-50%
Specificity >99.9%
What are the advantages and disadvantages of using PCR for detecting MAP in a faecal sample?
Advantages – no false positives, cheaper and quicker cf culture
Disadvantages - poor sensitivity (esp.in young subclinical animals), expensive
What are the advantages and disadvantages of using PCR to detect MAP in bulk milk?
Advantages – no false positives, cheaper and quicker cf culture
Disadvantages – poor sensitivity due to number of animals contributing to the bulk tank and the nature of shedding, gives no information on disease prevalence, may be due to contamination with faeces rather than direct shedding into milk
What is involved in immunodiagnosis of johnes disease?
Antibody evaluation in blood and milk
What are the advantages of using immunodiagnosis for diagnosing Johne’s?
More sensitive early in the disease course
Cheap, easy and quick
Specificity ~99%
What are the disadvantages of using immunodiagnosis for diagnosing Johne’s?
Blood sampling is more costly and requires handling cows
Bulk milk ELISA is very insensitive (20-30%)
Not very good at detecting asymptomatic carrier animals
Why does the sensitivity of Johnes tests vary?
The tests become more sensitive as the disease progresses. There is recrudescence of the disease when the cow is under stress and the immune system is low. Ab count will go up which will be picked up more easily by the test.
What is the definition of Johne’s group J0?
Green
Low risk – no evidence of infection
Repeat ELISA negative – min. 2 tests
What is the definition of Johne’s group J1?
Green
Low risk – no evidence of infection
ELISA negative – 1 test only
What is the definition of Johne’s group J2?
Yellow
Moderate risk – evidence of infection and may be shedding MAP, should be managed as a risk for calving and milk/colostrum
ELISA negative but positive within previous 3 tests
What is the definition of Johne’s group J3?
Yellow
Moderate risk – evidence of infection and may be shedding MAP, should be managed as a risk for calving and milk/colostrum
ELISA negative but positive on previous test
What is the definition of Johne’s group J4?
Yellow
Moderate risk – evidence of infection and may be shedding MAP, should be managed as a risk for calving and milk/colostrum
ELISA positive – first positive test
What is the definition of Johne’s group J5?
Red
High risk – evidence of infection and highly likely to be shedding MAP
Repeat ELISA positive – minimum 2 tests
Two or more positive results in any 4 consecutive tests at any time in individual cow test history
How would you manage Johne’s in an individual animal?
No treatment
Survival time from diagnosis very variable
May get brief remission
Usually cull as soon as possible
What are the 2 main objective for managing Johnes in the herd?
Prevent transmission
Maintain herd biosecurity
How do you prevent transmission of Johnes within a herd?
This is the main focus for positive herds
Focus on replacement heifer calves
Several potential sources of infection (faeces»colostrum>milk>other) – separate young stock (up to 1yr old) from potential sources of infection
How can you reduce the risk of johnes transmission?
Individual calving that is cleaned between – exposure to faeces is a risk so need to reduce contact as much as possible (individual calving and removing calf from mother)
Better hygiene
Cleaning environment
Cleaning PPE
Vets treating calves before adults
Don’t pool colostrum / pasteurise (can still find MAP in pasteurised milk)
Do not feed calved from infected cows
Useful to know the Johnes status of each animal so you can better focus calving management
Why are test and cull schemes used for Johnes eradication?
May speed up rate of eradication in herd but won’t eradicate disease by itself because you will miss the animals early in the disease process
Can we vaccinate against Johnes disease?
There is a vaccine that can be imported from Spain
Why may farmers choose not to vaccinate against Johnes?
It prevents clinical disease but not infection
You need to keep doing it for several generations
It may interfere with TB test results and give false positives
Do other species get Johnes disease?
Common in goats and sheep
Disease is very similar to cattle
Why may Johnes be more difficult to manage in sheep and goats?
It is more difficult to control what happens around birth in these species.
What are the differential diagnoses of the acute abdomen in cattle?
Acute/chronic & local/diffuse peritonitis
Right torsion abomasum
Caecal torsion
Bloat: primary/secondary
Photosensitive dermatitis? - painful so can present like a peritonitis
What diagnostic methods can be used in the acute abdomen?
History taking Clinical exam Exploratory laparotomy Ultrasonography Peritoneal tap? Biochemistry/Haematology?
What would you expect to find in a clinical examination of an acute abdomen?
Reduced feed intake, drop in milk
Pyrexia (24-36h)
Hypovolaemia, toxaemia, shock (acute)
Reduced rumen activity/intensity, GI stasis, scant feces, abdominal distension
Rectal exam - Fibrinous adhesions abdomen, distended SI on rectal examination
Signs of abdominal pain - Reluctance to move, arched back, grunt, treading hind legs, kicking abdomen, recumbency, pain tests (withers pinch and bar test - traumatic reticular peritonitis) HR/RR
What are the causes of diffuse peritonitis?
Urethral obstruction Acute acidosis/rumenitis Toxic mastitis Postpartum metritis Perforated abomasal ulcer
What are the causes of local peritonitis?
LDA/RDA
Caecal torsion
TRP traumatic reticular peritonitis
Uterine torsion/rupture, dystocia, caesarean, vaginal tear
Intestinal obstruction, volvulus, strangulation, intussusception, perforation (iatrogenic)
Splenic/Hepatic/Umbilical abscess
Post surgical complications
What factors predispose a caecal torsion?
Early lactation dairy cow
Hypocalcaemia
How does a caecal torsion occur?
There is caecal atony which may lead to dilation (common). If the free end kinks over it will cause a torsion (rare – cow will die in 24hrs).
What is intestinal strangulation and how commonly do they occur?
A prolapse of the SI through a mesenteric tear or a persistent urachus.
They are rare.
What is a volvulus and how commonly do they occur?
Rare. Torsion of the root of the mesentery.
How common are intussusceptions in cattle?
Rare
How common and intestinal obstructions in cattle?
Rare
How would you diagnose strangulations, volvulus, intussusceptions, and intestinal obstructions in cattle?
Exlap with a right flank approach.
What is bloat?
Vets use the word bloat to describe ruminal dilation and farmers use the word bloat to describe abdominal distention. The rumen is the most common cause for abdominal distention.
What are the 2 distinct aetiologies for ruminal bloat in adult cattle?
Frothy (primary) bloat: often a herd problem Free gas (secondary) bloat: failure to eructate, often in individual animals
How can you differentiate a frothy bloat from a free gas bloat?
In a frothy bloat you can pass a stomach tube but the stomach doesn’t decompress.
What is the cause of frothy bloat?
High protein grass (e.g. alfalfa and clover) increases the viscosity of ruminal fluid. This forms froth that prevents eructation.
How can you treat frothy bloat?
Anti-foaming agents (e.g. mineral oil and poloxalene – should be given to all animals on this pasture)
Decompress with rumenotomy
Diet management – take off pasture, late morning grazing, strip grazing, feed hay before grass
What are the causes of free gas bloat?
Obstruction (‘choke’) Hypercalcaemia Prolonged lateral recumbency Vagal nerve damage Tetanus Actinobacillus Outside pressure (carcinoma, papilloma, EBL, bTB)
Where are the most common sites for obstruction that causes free gas bloat?
Oropharynx, thoracic inlet, heart base
How can you teat a free gas bloat?
Relieve rumen tympany if severe (trocar)
Administer spasmolytic e.g. buscopan
Attempt removal of any obstruction with using fingers or stomach tube/ leave to macerate if trocar present
How does hypocalcaemia cause free gas bloat?
Hypocalcaemia -> lateral recumbency -> failure to eructate
Why does vagal nerve damage cause free gas bloat?
Vagal nerve damage causes dysfunction in the rumen
What causes vagal nerve damage?
Hardware disease – can cause adhesions near the vagal nerve
Actinobacillus – can get into the rumen/reticulum which may affect the vagal nerve
What are the possible causes of abomasal bloat in calves?
Dietary changes (feeding routine)
Poor milk clot formation
Clostridia toxins may be involved
What are the clinical signs of abomasal bloat in calves?
Acute abdominal distension and pain
Rapid dehydration
Usually young calves (pre-weening)
How can abomasal bloat in calves be managed?
Not releved by a stomach tube
Deflate using a large bore needle
Manage the metabolic consequences
Take a thorough history to find the underlying cause
When do calves most commonly get ruminal bloat?
Usually in slightly older calves often just after weening
What are the causes of ruminal bloat in calves?
Poorly understood, related to poor rumen development
What are the clinical signs of ruminal bloat in calves?
More chronic
Often recurrent
May follow concentrate feeding
How do we manage cases of ruminal bloat in calves?
Can create a fistula or use a long term trocar
What is the function of saliva in ruminants?
Act as a buffer in the rumen (maintain normal pH) to allow survival of the ruminal flora.
How will oral cavity disease present in ruminants?
Anorexia/inappetance, relative/complete
Ptyalism/drooling (lesion, obstruction, failure to ingest/chew/swallow)
Swelling head/lips/mandible
Protrusion of the tongue
Oedema submandibular space
Partly chewed lumps of food present (‘quids’)
Bloat (‘ping or ‘dull thud’)
Penetrating wounds outside or inside oral cavity
What equipment is required for examination of the oral cavity in a ruminant?
Good light source
Mouth gag/towel
Halter/bulldog
Sedation - may want to avoid this as you will reduce gut motility
What are the viral causes of salivation in ruminants?
BVD MCF (Ovine herpesvirus-2) IBR (BHV-1.1, 1.2 respiratory) Bovine papular stomatitis / orf (parapox virus) Rabies, FMD, BTV
