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
