Bovine Disease Flashcards
What is the heart rate parameters in adult bovine?
60-80bpm
What are the respiration rate parameters in adult bovine?
15-30bpm
What is the temperature parameters of adult bovine?
38-39 C
What is the rumen turnover parameters of adult bovine?
1 every 40 seconds or 2 in 3 minutes
What are the heart rate parameters in calves?
60-80 bpm, up to 100 when handled
What are the respiration rate parameters in calves?
15-30bpm
What are the temperature parameters in calves?
38.5-39.5 C
What are the rumen turnover parameters in calves?
Present from 6/8 weeks of age
Name 7 clostridial diseases of cattle.
Blackleg
Malignant oedema
Tetanus
Botulism
Clostridium Perfringens (Welchii) Diarrhoea
Bacilliary haemaglobinuria
Infectious Necrotic Hepatitis (Black Disease)
What are clostridia?
Gram negative obligate anaerobes. Spore forming – survive a long time in the environment. Infection via wound contamination or ingested spores localise in muscle/liver/spleen.
What is the pathogenesis of clostridial diseases?
Tissue damage and low oxygen tension results in spore activation and toxin production
What is the aetiology of clostridial myositosis?
Blackleg and malignant oedema
What is the pathogenesis of clostridial myositosis?
Toxin production leads to muscle necrosis and toxaemia
What is the epidemiology of clostridial myositosis?
Commonly at pasture but also indoors, usually sporadic affecting small numbers of animals, outbreaks of blackleg may occur
What is blackleg?
Most common in animals 6-24 month sold, good body condition, infection usually by ingestion
What is malignant oedema?
Any age, contamination of puncture wounds, post surgier, IM injection, parturition, bruising of muscle carrying latent spores
What are the clinical signs of clostridial myositosis?
Marked depression
Pyrexia
Tachycardia
Stiffness if sub-lumbar muscles involves
Lameness
Limb swelling
Painful
Emphysema
Swelling of the tongue = respiratory distress
Cardiac signs in blackleg
How is clostridial myositosis diagnosed?
- PM findings
- Demonstration of gram positive bacilli on a smear
- Fluorescent antibody testing for toxins
How is clostridial myositosis treated?
- Penicillin
- Drain and irrigate wounds with antiseptic solutions
- NSAIDs
- Fluid therapy
How is clostridial myositosis controlled?
Vaccinate all animals over 4 months of age prior to turn out, various vaccines available
What is the pathogenesis of clostridium tetani?
- Spore contamination of wounds
- Neurotoxin production reaches CNS via peripheral nerves
- Incubation periods is days to 4 weeks
What are the clinical signs of clostridium tetani?
- Progressive stiffness – limbs, jaw, elevated tailhead
- Muscle tremors
- Hyperaesthesia
- Convulsions
- 3rd eyelid prolapse
- Ruminal tympany – bloated, dilated, non-motile rumen
How is clostridium tetani treated?
- Penicillin IV
- Tetanus antitoxin
- NSAIDs
- Wound management
- Muscle relaxants (Xylazine)
- Nursing
- Dark, quiet surroundings, ample bedding – nursing
How is clostridium tetani controlled?
Vaccination and wound management
What is the aetiology of botulism?
Intoxication or ingestion of pre-formed clostridium botulinum toxins in spoiled or contaminated food and water
What is the pathogenesis of botulism?
Neurotoxins cause flaccid motor paralysis, incubation period (few hours to 14 days), zoonotic
What are the clinical signs of subacute botulism?
Lingual paralysis
Dysphagia
Ataxia
Muscle weakness
Laboured breathing
Recumbency
Constipation
Death
Occasional recovery in 3-4 weeks
What are the clinical signs of peracute botulism?
Sudden onset
Rapid paralysis
Death within 12-18 hours
What are the clinical signs of acute botulism?
Progressive muscular paralysis
Recumbency
Death
How is botulism diagnosed?
- Clinical signs
- Demonstration of toxins in serum, liver or feed
- History may reveal access to poultry
How is botulism treated?
- Symptomatic treatment
- Fluid therapy
- Nursing
- Penicillins, tetracyclines, TMPS contraindicated
How is botulism prevented?
Remove carcasses before applying poultry waste to pasture
Name 2 uncommon clostridial diseases in cattle.
Clostridial dysentery
Bacillary haemoglobinuria and black disease
What is mastitis?
A production disease due to breeding for production and not udder functionality. It is endemic and a a welfare issues in that it causes pain
How is mastitis a public health issue?
- Effects shelf life/taste
- Farmers pay based on absence of infection
- Zoonotic pathogens?
- Transfer of resistance to consumer
How is mastitis an economic issue?
- Loss of milk
- Treatment/veterinary
- Labour
- Culling
How does mastitis affect food sustainability?
- Carbon footprint of dairy
- Wastage
Distinguish mastitis and intramammary infection.
Mastitis in inflammation of the udder and intramammary infection is a pathogen infection of the udder with/without clinical signs.
Distinguish clinical and subclinical mastitis.
Clinical – inflammation with changes in the udder/milk/systemically
Subclinical – inflammation without changes in udder/milk
How can mastitis be epidemiologically classified?
Contagious cow to cow spread or environmental to cow spread
When does mastitis occur?
Dry period origin or lactation origin
Summarise the anatomy of the bovine udder.
Teat cistern leads to streak canal with sphincter muscle and rosette of Furstenburg is made of stratified squamous epithelium.
How does the udder have innate immunity?
Teat sphincter
Keratin plug
Macrophages
Neutrophils
How does the udder have acquired immunity against specific pathogens?
Immunoglobulins and lymphocytes
What happens in udder involution?
- Over 20-30 days
- Decreased section volume
- Decrease in milk components
- Increase immunoglobulins and lactoferrin
- Milk synthesis approaches in 0-48 hours
What happens to the udders during steady state?
Quiescent regeneration
What happens to the udders during transition?
10-15 days
Reverse of involution
Increase in size
Colostrogenesis
Hormones and initiation of milk production
How is subclinical mastitis diagnosed?
- Marker of inflammation associated with intra-mammary infection
- Somatic cells = leucocytes
How is subclinical mastitis important to industry?
- Somatic cell count >400K = unsuitable for human consumption
- Payment premiums and limits for quality milk
- For every doubling of SCC over 100K a cow loses 5% of her production
What is the somatic cell count of non-infected and infected udder quarters as a number of cells per ml of milk?
Non infected quarters 5-200K SCC. Infected quarters 200K-5M.
What milking data do farms record?
- Cows contributing the most to the bulk milk somatic cell count
- Cows to milk separately/last/with separate equipment
- New cases of subclinical mastitis
- Chronic cases of subclinical mastitis
- Cows that need treatment
- Cows that need culling
- Cows to sample for bacterial culture to find causal organisms of mastitis
- Disease monitoring
- Pregnancy diagnosis
Which milk recording data do vets use?
- Identify cows for farm to investigate further – do they have clinical mastitis/need treatment, to sample for bacterial culture
- Analysis of trends – over time, % new infections/calving in with a high SCC, chronic high SCC, dry period cure rate
How does infection affect somatic cell count?
- Number of quarters infected
- Type of pathogen
- Severity of infection
How does age affect somatic cell count?
- More likely to be infected
- Have residual damage from previous infections
- Have greater cellular immune response
How does stage of lactation affect somatic cell count?
- Rise in late lactation
- Increased exposure during duration of milking
- Residual damage from previous milkings
- Fresh cow cell counts are unreliable for the first 5-14 days
How does day to day variation affect somatic cell count?
- Lowest at milking
- Highest in strippings before and after
Describe the 4 grades of clinical mastitis.
Grade 1 – changes to the milk only, in colour and consistency
Grade 2 – changes to the udder, heat, swelling, pain
Grade 3 – changes to the cow (sick cow) and/or gangrenous sloughing of the teat
Grade 4 – signs of toxicity – recumbent cow, raised HR, red mmbs
How is clinical mastitis diagnosed?
- Detected and treated by the farmer for milk and udder changes or sick cow with milk/udder changes
- Vet involvement for sick and toxic cows and those with no response to treatment
- Take a sample of the affected ¼
- On farm culture/PCR
- Practice lab - you won’t know the pathogen at the time of treatment
How is clinical mastitis treated?
- Intramammary antibiotic tube – broad spectrum/multi-product so not knowing at the time of treatment is not a huge deal
- Systemic antibiotic for more severe cases
- Pain relief – NSAID
- Detailed in herd health plan
- Record which cow has been treated
What is the usual length of a cow’s dry period?
60 days
What is the cut off somatic cell count for a diagnosis of subclinical mastitis?
200K
What are the major contagious mastitis pathogens?
Staphylococcus aureus
Streptococcus agalactiae
Mycoplasma species
What are the minor contagious mastitis pathogens?
Corynebacterium bovis
Trueperella pyogenes
Coagulase-negative staphylococci
Describe the mastitis caused by staphylococcus aureus.
- Udder and teat skin, other body sites
- Mainly cow-to-cow
- Persistent infections
- Therapy has poor response in lactation and moderate in dry cow therapy
- Subclinical or clinical
- Gram positive
Describe the mastitis caused by streptococcus agalactiae.
- Only in the udders of infected cows
- Cow-to-cow transmission
- Lactational treatment
- Subclinical but is occasionally clinical
- Gram positive
Describe the mastitis caused by mycoplasma.
- Less common but we see it less often because there is a difficulty in culturing and diagnosis so is probably increasingly found in herds
- Cow-to-cow, on udder
- Mostly subclinical
- Calf pneumonia or herd arthritis often seen
- Poor response to treatment so cull
A farm with 160 cows in a 8 a side parlour milks 2x a day, how often should rubber liners be changed?
Approximately every 4 months
How can you reduce new infection rate to control contagious mastitis pathogens?
Milking routine
Parlour function
Vaccination
Treatment
Culling
Nutrition
Genetics
How can new intramammary infections be reduced with treatment?
- Early identification and treatment – increases effectiveness and reduces spread
- Treatment of cases can occur in 2 ways – in lactation and dry cow therapy
How does staphylococcus aureus mastitis respond to therapy during lactation?
- Poor response 10-30% due to true microbial resistance, and microabscesses and intracellular so hard to get antibiotic to penetrate
- May treat to decrease shedding
- Difficult to assess cure
How is streptococcus agalactiae treated during lactation?
- Treat all cows or all infected cows
- Penicillin-containing IMM tubes
How does mycoplasma respond to therapy during lactation?
Ineffective
How do the contagious mastitis pathogens respond to vaccination?
Staph. aureus ineffective as prevention?
Strep. ag. – not really necessary.
No Mycoplasma mastitis vaccine
How can new intramammary infection be reduced?
- Vaccination
- Culling of chronically affected cows as they are a source of infection to others
- Drying off chronic cows
- Nutrition
- Genetics
Why is reducing duration of infection with dry cow therapy effective?
- Decreased residue risk
- Lengthened therapeutic window
- Close to 100% effective for Streptococcus agalactiae
- Staphylococcus aureus 40-60%
- Same cure risks and not effective for Mycoplasma
When should contagious mastitis cows be culled according to pathogen?
- Cull Mycoplasma cows
- Staph. aureus cows – preferential cull list to go at next opportunity
- Strep. ag. – very rarely need to get culled
Describe mastitis caused by corynebacterium bovis.
- Contagious, but not very virulent
- Teat duct (streak canal) infections
- Good surrogate measure of teat dip effectiveness
- Chronic moderate SCC – usually self-limiting or cured by DCT
Describe the mastitis caused by trueperella pyogenes.
- Relatively rare
- Severe clinical mastitis
- Thick purulent foul discharge
- Dry cows or heifers with a history of teat end damage
- Summer mastitis due to spread by biting flies
- Usually results in culling
What are the major pathogens of environmental mastitis?
- E. Coli
- Strep. uberis
- Klebsiella
- Enterobacter species
What are the minor pathogens of environmental mastitis?
- Steptococcus dysgalactiae
- Pseudomonas aeruginosa
- Nocardia species
- Serratia marcescens
- Yeasts
- Algae
Describe the epidemiology of the major pathogens of environmental mastitis.
- Increase with high humidity, warm temperatures
- Bedding factors – often found in sawdust
- 70-90% of intramammary infections will result in clinical signs
- High self-cure rate – antibiotic therapy can be effective
Describe the mastitis produced by the major pathogens of environmental mastitis.
- Gram negative = endotoxin release
- Classically severe mastitis, but often starts mild and progresses
- Bacteria multiply to peak in 12-24 hours
- LPS released from proliferating and phagocytosed organisms
- Excessive inflammation and systemic signs result = toxic mastitis
Describe the mastitis produced by streptococcus uberis.
- Gram positive
- More persistent
- Udder becomes reservoir
straw, out on pasture - Dry period can be major risk
What are the herd signs of environmental mastitis?
- Increase in clinical mastitis - may include toxic mastitis, early dry period or early lactation
- Elevated SCC in bulk tank and individuals
- Positive bulk tank cultures
How can changes to milking routine reduce new infection rates of environmental mastitis?
- Pre milking teat dip/teat cleaning reduces environmental bacteria entering udder during milking process, approved product, contact time
- Keep cows standing to decrease teat end exposure for 30+ minutes, usually done by putting fresh feed and water out
How can husbandry changes reduce new infection rate of environmental mastitis?
- Keep clean and dry
- Allow space and stocking density
- Bedding types – mattress and top layer very deep bed. Sawdust = klebsiella, straw = streptococcus, green bedding, sand inorganic substrate
- Bedding management
- Scraping frequency
- Ventilation
- Feed and water spaces
- Pasture stocking density, rotation, poaching in wet/boggy areas
- Cow cleanliness
How does vaccination affect environmental mastitis?
Common for coliforms in large herds and little impact on the new IMI rate but decreases severity
When is new intramammary infection rate high for environmental mastitis?
- New IMI rate up to 10x higher than during lactation despite antibiotic therapy
- Risks are high during involution and transition/colostrogenesis and low during involuted steady state
- Mastitis in subsequent lactation in the first 30/100 days of dry period
How does dry cow therapy affect environmental mastitis?
DCT used as reduced duration of infection for contagious pathogens but used to reduce new infection rate for environmental pathogens
How is classic dry cow therapy used?
Dry cows off abruptly, treat each quarter immediately following the last milking. Treat all quarters of all cows in blanket dry cow therapy
How are keratin plugs used as dry cow therapy?
Prevents bacteria from entering the teat streak canal
How are teat sealants used as dry cow therapy?
Administer at dry off, highly viscous paste, removed at calving by stripping/suckling
How is blanket dry cow therapy used?
Herds with BTSCC above 250K, all cows get an antibiotic dry cow tube, irresponsible antibiotic use.
How is selective dry cow therapy used?
For low SCC herds, all cows get a teat sealant, consider which cows need antibiotics, not which cows do not need them, high SCC cows or clinical mastitis would requires antibiotics
How is mastitis caused by coliforms treated?
High self-cure rates
Subclinical to peracute so treat accordingly to clinical signs
How is mastitis caused by environmental streptococci treated?
Moderate self-cure rates, high recurrence rate if untreated
How is mild mastitis without clinical signs treated?
Standard IMM antibiotic protocols
Gram negative or no growth = no treatment
Gram positive = IMM protocol
How is mastitis caused by pseudomonas aeruginoa treated?
- Cause acute CM but more often chronic high SCC and intermittent flare-ups
- Treatment ineffective, usually leads to culling
- Examine wash water, infusion technique, home-made treatments, diluted teat dips
How is mastitis caused by serratia, nocardia, yeasts and algae treated?
All are very difficult to cure, usually result in culling
Which stages of the lactation cycle is the most at risk of infection?
Involution, transition and early lactation
Which of the following are major contagious pathogens?
Staphylococcus aureus and mycoplasma
The result from a milk sample sent for culture comes back as ‘no growth’, what is this likely to mean?
Bacteria no longer present
How important is antibiotic intramammary tubes for control of contagious pathogens?
Not important, dry cows therapy is the best opportunity for cure of contagious pathogens.
As well as intramammary antibiotics what else is important in treatment of clinical mastitis?
NSAIDs
Make brief notes on 3 risk factors associated with spread of contagious pathogens.
Not wearing gloves in the parlour
Improper post dip application or use of spray rather than a cup
Lack of parlour servicing
How is mastitis investigated?
- Data collection and analysis – SCC and clinical cases
- Diagnosis of the problem
- Herd surveys – identification of risk factors
How is contagious mastitis characterised?
Long duration
Poor cure rate
Chronic cases/subclinical (high cell counts individual/bulk milk)
No seasonality
How is environmental mastitis characterised?
Seasonal effects
Higher new infection rate
Less chronic cases
What is udder cleft dermatitis?
- Necrotising lesions between 1/4s of udder
- Secondary/haemtogenous spread of bacteria can have serious consequences
What is udder oedema?
Heifers around 1st calving. Can be quite uncomfortable – present as lameness, treat with NSAIDs
What are teat peas?
Minerals/fats from milk form a mass within the teat – often mobile but can cause problems at milking/obstruct milk flow
What must be considered when undergoing teat surgery?
- Teats do not heal very well – surgical repairs can be frustrating
- Anaesthesia – local techniques, sedation
- Restraint/safe handling
What is a pathogen that commonly causes toxic clinical mastitis?
E.coli
What fluids should be given in response to toxic mastitis?
Hypertonic saline followed by isotonic or oral fluids
At what point would you consider a somatic cell count raised?
200K
