Bovine repro Flashcards
Where are GnRH, FSH, LH, oestrogen and progesterone produced from? What do they act on?
GnRH: hypothalamus, acts on pituitary to produce FSH and LH
FSH and LH: anterior pituitary, FSH acts on follicles, LH acts on egg
Oestrogen: follicle
Progesterone: corpus luteum
Stages of follicle growth? What does growth of follicles depend on?
Initiation of follicle growth -> recruitment -> selection and dominance -> ovulation
Primoridal follicles -> primary follicles -> secondary follicles (antrum formation)
Atresia of follicles along the way
Preantral follicle growth for 3 months - GF dependent, gonadotropin influenced
Antral follicle growth for 2 oestrus cycles - gonadotropin dependent, GF influenced
Stages of the bovine oestrus cycle?
Day 0: ovulation - follicle releases oocyte for fertilisation, collapsed follicle develops into CL
Day 6: CL is mature, secretes progesterone
Day 16: luteolysis
Oestrus -> metoestrus -> dioestrus -> protestrus
Follicles continue developing in waves through dioestrusbut hormones prevent ovulation
How big is a dominant follicle?
> 9mm
Hormone levels after calving? When does the first follicle wave emerge postpartum for dairy and beef cows? Does the first dominant follicle ovulate/what does it depend on? How long until first oestrus? Nature of first ovulation?
Low progesterone and oestrogen
Resumption of FSH surges increases within 3-5d, at 7-10d intervals
Emergence of first follicle wave: 5-10d post partum
First post partum follicle wave -> first dominant follicle
Ovulates if sufficient E2 from DF for LH/FSH surge
Capacity for E2 secretion depends on DF size, LH pulse frequency (nutrition, health), IGF-I bioavailability (nutrition)
First oestrus: 2-3 weeks in dairy unless ill/NEB, 3w-3m in beef as increased inhibition
Nature of 1st ovulation: silent
What regulates the LH pulse frequency post partum?
Declining NEB BCS at calving DMI Disease state Suckling and calf presence (beef)
What does success of AI depend on?
Use of proven/fertile sires
Reliable oestrus detection
Best time to inseminate cows?
In oestrus not dioestrus!
12h before ovulation?
Duration of cow signs of heat?
Coming into oestrus: 6-24h (mucus discharge, swelling of vulva, holding milk, bawling, restless, mounts other cows)
Standing oestrus: 6-18h (all above plus stands to be mounted)
Going out of oestrus: 12-24h (same as coming into)
Signs of a cow in oestrus?
Sniffing vulva Chin resting Licking Bunting Mounting head to head Standing to be mounted (only 50% of cows will do)
Methods of oestrus detection of cows?
Visual observation
Paint/chalk/kamar - not all animals show standing heat
Record keeping - start looking 18d after last oestrus
Teaser bull
Chin balls
Milk progesterone
Activity meters - pedometers
What must be done to increase pregnancy rates with AI routine?
Tweezers not fingers Thaw at 37 degrees for 40 seconds Keep warm Chilling once thawed is bad Dry thoroughly
Early embryonic development stages?
Fertilisation -> zygote -> 2-cell -> 4-cell -> 8-cell -> morula -> blastocyst
Which hormone is crucial for embryo growth?
Progesterone
What controls calving?
ACTH from calf pituitary -> cortisol from calf adrenal gland -> increased prostaglandin and reduced progesterone from placentomes
Infusion causes premature labour
Ablation causes prolonged pregnancy
How is submission rate calculated?
No. animals served/No. eligible/3 week cycle
First service submission rate: eligible = all animals after earliest service date who have not yet been served
All services submission rate = all animals after earliest service date who are not yet pregnant
What is ‘pregnancy rate’? What is ‘preg rate’?
Pregnancy rate: % pregnant of those served
Preg rate: number pregnant/number eligible to be served/3 weeks
When does ovulation occur in cows?
24h after heat
Timeline of physiological events to calf between ovulation and calving? When can embryo transfer be done? When does failure of inseminsation occur cumulatively?
24h after heat, day 0: ovulation (2% failure)
Day 2: fertilisation (15% failure)
Day 4: entry into uterus (16-32 cells)
Day 6-7: ET can be carried out
Day 8-13: maternal recognition of pregnancy (45% failure)
Day 21-23: interdigitation and expansion
Day 23: heart begins beating
Day 28: amnion remains spherical
Weeks 5-6: distension of uterus (50% failure)
Weeks 6-7: Sexual differentiation of foetus
Weeks 8-9: genital tubercle migration
Length of normal bovine oestrus cycle? Type of breeder? Type of ovulation? Which ovary ovulates?
18-24 days
Non seasonal
Spontaneous ovulation
Right ovary has 60% of ovulations
What happens during regeneration of the endometrium post-calving?
Septal mass = early evidence of necrosis of septum
Sloughing of necrotic septal mass 5d post partum, fully sloughed by 10-15 days, leaves vascular stubs
Smooth surface of stratum compact by 19d post partum
Normal by 25d+
Why are retained foetal membranes a problem?
Delays involution of uterus
Reduces milk yield
Problems with uterine infections?
Damages the uterus
Suppresses hypothalamic GnRH and pituitary LH secretion
Localised effects on ovarian function
Main uterine infection pathogens?
E.coli Trueperella pyogenes Dichelobacter nodosus Fusobacterium necrophorum (BoHV4)
Risk factors for uterine bacterial infection?
Dystocia
Abortion
Twins
RFM
Reduced DMI in dry period NEB after calving Milk fever/vitamin D Vit E/selenium Vitamin A Iodine
Definition and grades of metritis?
= Inflammation of the uterus caused by bacterial infection, with a reddish-brown (purulent), soul smelling uterine exudate detectable in the vagina, within 21d after parturition
Grade 1: enlarged uterus and purulent uterine discharge but no pyrexia/illness
Grade 2: ‘puerperal metritis’ - overt systemic illness (decreased milk yield, fever >39.5C, reduced appetite)
Grade 3: ‘toxaemic metritis’ - signs of toxaemia (cold extremities, dullness)
Definition, diagnosis and treatment of pyometra in cows? Cause?
= Intrauterine accumulation of pus in the presence of a CL and a closed cervix
Mixed bacterial infection, similar to endometritis
Diagnosis: no signs of heat, enlarged uterus, CL, US for pus
Treatment: PGF
Definition of clinical endometritis?
= Inflammation of the endometrium, with a purulent uterine discharge detectable in vagina 21 days or more post partum (usually caused by bacterial infection)
Uterine discharge scoring?
0 = clear or translucent 1 = flecks of white or off-white pus 2 = <50ml exudate containing <50% white or off-white material 3 = >50ml exudate containing purulent material, usually white or yellow but occasionally bloody
Average calving-conception?
80 days
What factors increase the calving-conception time in order from worst first?
Drop in social status Caesarean Bad calving Lameness Endometritis RFM Dystocia Mastitis Milk fever Low BCS
Sub clinical endometritis? What is it? % affected? Risks?
Inflammation of the endometrium, usually caused by bacterial infection Increased PMN in cytology Not necessarily any bacteria cultured 5-50% of cows in herd affected Risks: NEG/ketosis, metritis
Cystic ovarian disease: Clinical signs? What do follicular cysts look like and do? What do luteal cysts look like? When most common?
Anoestrus -> nymphomania Follicular cysts: - fluid filled - internal diameter >25mm - thin wall <3mm, - ovulates within 10 days - secrete oestradiol for first half of cyst lifespan - other follicles cannot develop during oestrogen phase - prolonged oestradiol inhibits LH surge - turnover of persistent follicles does occur but rarely do they luteinise - repeated waves of anovulatory follicles Luteal cysts: - luteinised follicular cyst - >25mm external diameter - thick wall >3mm (indicates progesterone production) - fluid filled lacuna - duration 10 days Most common <60 DIM
Factors associated with cystic ovarian disease?
High milk production NEB and ketosis - raised NEFAs Twinning and periparturient problems Genetic predisposition Higher parity Excess BCS at drying off
Diagnosis of cystic ovarian disease?
Palpation/ultrasound - degree of uncertainty
Milk progesterone
First stage labour in cows - what is it? how long can it takes? signs?
= dilation of cervix
May take 3-6h
Separates herself
Appetite decreases
May frequently alternate between lying and standing
Thick string of mucus often seen hanging from vulva
Towards end, bouts of abdominal straining occur more frequently, usually every 2-3 mins - pushed uterine contents against cervix, giving more stimulation to dilate
Second stage of labour in cows - What is it? What happens?
= delivery of calf
Begins with appearance of membranes (water bag) at vulva
May last several hours
Water bag ruptures with sudden rush of fluid
Cervix dilates with further pressure from calf
Powerful reflex and voluntary contractions of abdominal muscles and diaphragm (straining) expels the calf
Third stage of labour - What is it? How quick should happen?
Expulsion of placenta
Usually happens within few hours
RFM if not expelled within 12 hours after delivery of calf?
What are ideal calving facilities?
Individual pen 12 x 12ft+ - like to calve alone Easy to clean out between calvings Gate +/- quick release headlock -to easily catch cow for examination/assistance ofcavling Milking facility Well bedded and dry Good access to food and water Good lighting Well ventilated Quiet
When to intervene with a calving? Problem if intervene too early?
If intervene too early when cow in first stage labour, can prevent full dilatation of cervix
Only intervene if:
- no progress after 1h of water bag showing
- showed signs of first stage labour but has not progressed to second stage after 6h (possible twisted uterus)
- appears in extreme discomfort
- significant bleeding from vulva
Most common causes of dystocia?
Malpresentation
Foeto-maternal oversize - large calf, fat dam, young/poorly grown dam, dead emphysematous calf
Congenital abnormality - Schistoma reflexus, spina bifida, hydrocephalus
Hydrops allantois
Schmallenberg virus
Primary inertia - hypocalcaemia
Diagnosis of dystocia?
History - age, parity, breed, previous problems, how long straining, attempts by farmer, water bag broken?
Cow attitude, BCS, behaviour
General examination e.g. if recumbent and not bright/bloated
Obstetrical examination - vulva slackened, vaginal exam, rectal exam
What to pay attention to during vaginal examination for dystocia?
Lesions (tears) or haemorrhage Position of uterus and calf Relaxation and dilatation of vulva, vagina, cervix Signs of life from calf Possibility of extraction Position of umbilical cord
What to do if dystocia confirmed?
Restrain Clean Lubricate Identify 3 Rs: reposition, repulsion, rotation Extract!
Aids to help delivering calf with dystocia?
Position cow downhill or uphill
Best lube = J-lube
Pump warm water and lube into uterus - fill her up, makes space
Sink plunger for repulsion
Epidural anaesthesia
Clenbuterol - relaxes uterus but she won’t help in delivery, increases uterine blood perfusion
Phone colleague if no progress in 20 mins or need help e.g. lots of bleeding, twisted uterus, breech, needs caesarean
Ropes/chains - above fetlock has higher risk of leg fracture, below fetlock has higher risk of slipping off, double loop has minimal chance of leg fracture or slipping off
How to decide if calf in anterior presentation can be delivered per vaginum?
Head should be easily lifted into pelvis and remain there without flopping back into uterus - C section if not
Forelimbs crossing over = insufficient room for calving per vaginum as cow’s pelvis is putting pressure on humeri and width of shoulders is too large
Should be able to easily bring calf up so fetlocks are a hands breadth out of vulva - means shoulder is within pelvic canal, failure to achieve means too big for extraction per vaginum
Should be able to easily slide hand between foetal cranium and maternal sacrum - c section if not
How to decide if calf in posterior presentation can be delivered per vaginum? What to check?
Assess space by sliding hand over tail head
2 people should be able to exteriorise limbs to point where hocks are past vulva - failure = rules out per vaginum
Check position of umbilical cord - if round hock will break cord as pull calf and may die/drown before out - advise farm of risk, can do c section or calve and take risk
When is an episiotomy done? What must be done prior? How done?
Uncommonly used in cattle - almost totally reserved for heifers
In HF heifers, 5-10% may need
Narrow vestibule and vulva - vulva not fully slackened and dilated but cervix dilated and calf entering pelvic canal
Try manually stretching vulval lips with arms for 20mins before resorting to episiotomy
Perineum area contamination risk high - requires antibiotics
Caudal epidural anaesthesia
Cut at 10-11 O’clock or 1-2 O’clock position
Controlled cut, rather than tear vulva during traction
Make incision when calf’s head passing through vulva
Sutures - interrupted deep dissolvable, interrupted or continuous skin sutures
Complications of episiotomy?
Wound infection and breakdown
Distorted vulva conformation - pneumo-vaginum, uro-vaginum (poor conception rates)
Weak point to muscles which may affect ability to calve naturally in future
If cut at 12 O’clock - rectovaginal fistula
Embryotomy of calf? Drugs needed? When are full and partial embryotomies done?
Must have sufficient space
Caudal epidural anaesthesia
Clenbuterol
Sufficient lubrication
Full embryotomy:
- large dead calf
- abnormal calf (foetal monster)
Partial embryotomy:
- hip locked (euthanasia if still alive, cut off trunk as close to vulva as poss, pass wire to split pelvis, reps one hindquarter and remove other)
- head back, unable to correct and dead calf (remove head using passing method)
- leg back, unable to correct and calf dead (remove leg with passing method, must ensure elbow shoulder and scapula removed or no narrowing will be achieved)
Passing method of placing wire for embryotomy?
Pass wire by hand around area of calf needing removal
Where appropriate attach curved snare director or another form of weight
Thread wire through each side of embryotome, tighten, check wire in correct place by palpation before sawing
Cleat method of placing wire for embryotomy?
Place obstetric chain on limb
Thread wire through embryotome
Place the loop of wire in between the cleats on the leg
Advance embryotome laterally up limb to just past top of scapula/anterior aspect of greater trochanter
Unhook wire from between cleats, pass obstetric chain through loop, to allow wire to be tightened up the medial aspect of the limb to lie in axilla or between hindlimbs
Check position of wire before sawing
How to remove head and trunk for embryotomy?
For head:
- cut as far caudal along neck as poss
- embryotome placed lateral or ventral
- avoid cutting cervix or vaginal wall
For thorax/trunk
- using obstetric hook advance the trunk
- remove as much of trunk as possible by using passing method of wire placement
- pull/cut out any parts of GIT interfering with ability to feel remnants of foetus
- remove rest of trunk if necessary or leave hind quarters
- split pelvis using passing method
- extract one hindlimb at a time
Check for twin
Check for damage to uterus, cervix, vagina
Remove foetal membranes if possible
Anti-inflammatories and antibiotics advised
Complications of embryotomy/foetotomy?
Uterine/cervical/vaginal tears - from sharp bone edges or incorrect rough handling of embryotome
RFM
Metritis
Adhesions
When do most uterine torsions occur? Risk factors? Which way do most twist?
Most occur at onset of parturition Risk factors: - poor rumen fill - space in abdomen - hilly land - process of standing up/laying down Majority are anti-clockwise (when stood behind cow) 90->360 degrees
Signs of uterine torsions at calving? Examination findings?
Appear to start calving but don’t progress
No straining as Ferguson’s reflex not stimulated
May just see slightly raised tail
Dry cow off colour/down/toxic
Vaginal exam - arm ‘corkscrews’, may just feel ‘lip’ in front of cervix, may not be able to feel cervix or calf
Rectal exam - palpation of torsion
Correction methods for uterine torsion?
‘Swing’ calf with coordinated allotment of abdomen to flip calf and uterine horn back into correct position - must be able to reach and firmly grasp calf by hand/rope
Twist legs of calf and uterus may twist too
Roll cow - majority of cows require cow to be rolled from left lateral onto back and into right lateral, if calf can be reached grasp leg firmly or place calving rope and hold firmly while cow rolled, if calf can’t be reached can place plank across abdomen and weighed down to apply pressure to abdomen while rolled
C section - if unable to untwist uterus
Complications of uterine torsions?
If high degree of torsion -> blood supply occluded -> friable tissue -> dead emphysematous calf and toxic cow if not noticed early
Indications for C section?
Foetal oversize/foeto-maternal disproportion
Irreducible uterine torsion
Insufficient cervical dilatation
Foetal malpresentation if unable to reposition
Abnormal calf where embryotomy not feasible
Dead/emphysematous calf where embryotomy not feasible
Constricted vagina and vestibule where massage has not relieved constriction
Elective: double muscled breeds, embryo transfer calves (wait for 1st stage labour)
C section of cow - Anaesthesia? Sedation? Pre-op meds? Position?
Anaesthesia - caudal epidural (block Ferguson’s reflex), paravertebral nerve block
Sedation - avoid unless unsafe without, xylazine will cross placenta and decrease viability, clenbuterol must be used as uterine tone increased but exterioristation of uterus may still be difficult
Pre-op meds:
- Tocolytic (clenbuterol)
- NSAID
- antibiotic
- calcium if appropriate
Position - standing or right lateral (either way, must stay that way)
C section of cow - method?
Left flank approach
Clip and sterile prep flank
Incise from 1 hands breadth below transverse processes, approx length from tip of finger to point of elbow - angled or vertical
Locate uterine horn containing calf and exteriorise
Incise uterus
- normal presentation: incise greater curvature from point of hock to tip of toe
- breech: incise greater curvature from carpus to tip of toe
- avoid cutting placentomes - ligate any bleeding caruncles
Remove calf
- locate umbilical cord and ensure not torsed, prevent early rupture and rupture too close to body wall on extraction
- extend incision if needed carefully
Check for twins
Remove foetal membranes
Suture uterus - 2 layers, inverted, absorbable, round bodied needle, monofilament
Clean off contamination from uterus, rumen and remove blood clots from abdomen
Close muscle and peritoneum in 2 layers, and skin
Apply antibiotics to muscle layers - shown to reduce risk of wound infection
Post op meds - oxytocin, calcium if needed
How to alter C section method if emphysematous calf?
Paramedian incision
Very low flank incision
Sedation/drop - large epidural, xylazine, xylazine and ketamine
C section complications? Signs? Treatment?
Haemorrage: post op check may show cow off colour, tachycardia/murmur, pallor - re-open, locate site of bleeding and ligate
Peritonitis: off colour, pyrexia - re-open, identify any site of leakage, flush abdomen with sterile fluid, if palpable on rectal exam 7d post-op then poor prognosis
Localised adhesions
RFM
Metritis
Wound infections/seroma/breakdown/emphysema
Poor fertility due to: delayed uterine involution, RFM, endometritis, salpingitis, adhesions, abortion
Factor affecting uterine prolapse in cows post partum? Survival? Effect on production?
Hypocalcaemia
2 week survival 80% (better if live calf)
50 day increase in calving-conception
Replacement technique for uterine prolapse of cow?
Standing or sternal with hindlimb extended out behind her
Caudal epidural +/- clenbuterol
Protective cover under uterus
Removed foetal membranes and clean off contamination
Apply lube and gradually feed back in - avoid using finger tips as may rupture uterus, feed in sections starting close to vulva or every from horn yips
Once replaced, ensure horn tips fully everted by using a bottle to extend the reach of your arm, or fill uterus with water
Give oxytocin, NSAIDs, antibiotics, calcium
Buhner’s suture?
What are the main factors affecting cyclicality of cows?
Lameness
Low BCS
High yield
Risk factors for milk fever?
Difficult calving
RFM
Endometritis
Subclinical low Ca
Effect of post partum mastitis, BCS loss and lameness on oestrus and luteal activity etc?
Mastitis:
- first CL and first oestrus are later
- smaller follicles
- reduced fertility
- take longer to ovulate if synchronised
Increased BCS loss:
- increased days to first ovulation after calving
- lower first service pregnancy rate
Lameness:
- first CL and first oestrus are later
- lower intensity of oestrus
- reduced oestrus behaviours
- don’t respond as well to a progesterone synchronisation regime
Effect of milk yield on oestrus signs?
Shorter duration of being mounted (e.g. 6h)
Lower incidence of standing oestrus
Shorter duration of standing
More silent heats
What does oestradiol production by first dominant follicle depend on 1-21d after calving?
IGF-1
Define abortion in cows?
Calving that occurs before 270d gestation
Must be reported (due to Brucella risk)
Measures to monitor for Brucellosis in cows?
All abortions to be reported
Monthly routine bulk milk sampling
APHA decides if individual case to be testing
Stat testing = dam’s blood + vaginal swab + milk
Which infectious agents causing bovine abortion have vaccines?
Lepto
BHV1
BVDv
Brucella
How much does a replacement animal cost following a culled cow?
£1500-2000
Definition of primary abortive agents?
Destroys integrity of foeti-maternal unit
E.g. placentitis due to hypoxia
Allows opportunistic pathogens to invade placenta and foetus
Alters microbiological profile within pregnant uterus
What primary infectious abortive agents are there in cows?
Brucella abortus BVDv Leptospirosis borgpetersensii (commensal in repro tract) Neospora BHV1 Parainfluenza 3 Bacillus licheniformis Fungi
Define secondary (opportunistic) abortive agents of cows?
Usually associated with chorionitis/amnionitis
Placental steroidogenesis abolished (progesterone)
Associated inflammatory cascade and prostaglandins causes:
- luteolysis
- relaxation of cervix
- foetus expelled
What secondary abortive agents of cows are there?
Gram +ve: - T pyogenes - Listeria monocytogenes - Staph aureus - B-haemolytic Strep Gram -ve: - E.coli - Fusobacterium necrophorum - Histophilus somnis - Leptospirosis borgpetersensii - Pseudomona aeruginosa - Salmonella dublin/typhimurium Others: - Mycoplasma bovigenitalium - Yersinia pseudotuberculosis - Ureaplasma divers
What are the 3 possible routes of infection of bovine abortive agents?
Resident flora of reproduction tract during pregnancy - at time of service in cattle e.g. Ureaplasma diversum
Transplacental (contaminate amnion) - Bacillus licheniformis in cattle, Chlamydophila abortus in ewes
Haematogenous - viruses e.g. BVDv, BHV-1
What foetal lesions are associated with transpacental infection of abortive agents in cows?
Ureaplasma diversum -> conjunctivitis, bronchopneumonia, peri-bronchiolar cuffing
T progenies -> bronchopneumonia
What foetal lesions are associated with haematogenous infection of BHV-1 in cows?
Peri-bronchiolar mononuclear inflammatory cell infiltration and vasculitis
Centrolobular necrosis of liver
Foetal lesions associated with iodine deficiency?
Thyroid hyperplasia (foetal weight in kg/2to3 = expected weight of thyroid in g)
Foetal lesions associated with selenium/vitamin E deficiency?
Cell membrane protein associated with removal of oxidation products
Myocardial degeneration
Mixed inflammatory cell infiltration with some mineralisation - chorionitis
What foetal lesions are associated with haematogenous infection of BVDv in cows?
Pale liver without autolysis
Fatal focal myocarditis with mononuclear inflammatory cell infiltration
Radio-opaque lines
Cerebellar hypoplasia
Formula to relate foetal tibial length to gestational age?
If tibial length <58mm, days = 68 + (1.7xL)
If tibial length 58-163mm, days = 114 + (0.91xL)
If tibial length >160mm, days = 105 + L
Approximate timing of bovine abortions?
BVD, Salmonella, T progenies, M tuberculosis - any time
Trichomonas - 2-4 months
Neospora - 4-6 months
Campylobacter - 4-8 months
Mycotic, lepto, listeria, IBR, IPV - 4-9 months
Bacillus/Chlamydia - 5-9 months
Brucella - 6-8 months
Foetal immunity - when does T cell recognition of self occur? When are antibodies produced?
T cell recognition of self: 90-120 days The more complex the antigenic stimulus, the later in gestation Abs are produced - BDVv after day 140 - Salmonella dublin after day 165 - Fungi after day 200
IBR - Agent? Signs? Diagnosis? Prevention?
BHV-1 Unusual to have resp and retro symptoms Latent carriers - trigeminal ganglion Recrudescence - stress Serology - ELISA Swabs - IF Vaccines - protection in face of outbreak (into-nasal, marker vaccine)
Neospora caninum - What is it? Phylum? Definitive host? When does it cause abortion? Transmission? Outcome?
Intracellular parasite
Definitive host - canidae
Phylum = Apicomplexa
Dogs: bradyzoite ingestion -> oocysts in faeces, transplacental transmission -> puppies may have disease (neonatal paresis), Ab response
Most commonly diagnosed cause of abortion
Usually 4-6 month gestation
May cause early embryonic death - manifests clinically as infertility (rare)
Congenitally infected heifers most at risk of abortion in first gestation
Cows infected by oocysts ingestion (exogenous) -> abortion or PI calf born
Recrudesence of infection in cow -> transplacental (endogenous) -> abortion of PI calf born
10%: Abortion
80%: Birth of clinically normal PI calf
10%: Birth of clinically normal uninfected calf but may be weak
95% of calves born to infected dams are themselves infected
Endemic abortion pattern:
- annual abortion rate >3%
- endogenous transpacental transmission
- very efficient, common route
Epidemic abortion pattern:
- abortion storm >10% of at risk cows abort over a 12 week period
- associated with exogenous transplacental transmission
Diagnosis of Neospora in cows?
Maternal serology (ELISA) fluctuates though reproductive cycle
- nothing at 12-18mo (little use screening young stock)
- use increasing levels as evidence of recrudescence
- test in second half of pregnancy
- eliminate other causes
Test calf at birth - indicates dam infected if calf +ve
PM of dead foetus - brain histopath, non suppurative encaphalitis
Control of Neopsora?
Keep dogs away from cattle feed and water and don’t allow to eat placentas
Identify positive cows - serology of whole herd
Cull seropositive animals and offspring - often not practical as high prevalence so expensive
Breed to beef and do not keep or sell as replacement heifers
Use sexed semen to get more heifers from uninfected animals
Embryo transfer to negative recipients
PI cows are immune to further challenge but may recrudesce
Causes 35% of abortions in UK
BVD - Type of virus? Incubation period? When are Abs present? Genotypes? Biotypes? What happens if infection during pregnancy?
Pestivirus
Incubation period 5-7d
Abs present 14-21d after initial infection
Genotype I - mildly/moderately pathogenic, most common type in N Europe
Genotype II - virulent type, problem in N America, severe diarrhoea and moderately mortality rates (30%)
2 biotypes within each genotype:
- non cytopathic: rarely causes clinical disease (unless genotype II) but crosses foeti-maternal barrier
- cytopathic: associated with mucosal disease in PI animals
Infection during pregnancy of non cytopathic:
- First trimester (0-95d): foetal resorption or abortion
- 95-120d: immunotolerance (PI)
- 120-285d: seropositive foetus +/- congenital lesions, abortion may occur due to placentitis
Consequences of BVD?
Lowered pregnancy rates - reproduction tract epithelia and follicles affected
Abortion - compromised foeti-maternal barrier allows secondary bacterial infection (placentitis and foetal pathology)
PI calves
Congenital abnormalities - cerebellar hypoplasia, microphthalmia, cataracts
Mucosal disease - PI animals then infected with cytopathic biotype
Problems with BVD PI calves?
Don’t recognise virus as foreign as infection occurs before immune system development
Ab negative, Ag positive (serum for Ab, heparin for Ag)
Susceptible to MD if encounter secondary infection with cytopathic virus (don’t mount an immune response) - usually via mutation of resident strain
Often poor-doers as BVD is immunosuppressive - but can make to adulthood and produce PI calves
Clinical signs of BVD mucosal disease?
Ulceration of mucosal (particularly tongue, soft palate, gingiva and oesophagus)
Ill thrift
Diarrhoea
+/- Concurrent respiratory disease (immune suppression)
Diagnosis of BVD?
Seroconvert over 3 weeks
Bulk milk Abs (quarterly) - vaccination will render useless
Detect PI in blood from 1mo (<30do MDA interferes)
Ear notch tissue test when tagged
Check test (5 bloods per group_
Bulk tank PCR detection limit one in 300
Probably 50% dairy herds are but tank BVD Ab+ve (70% in UK cattle)
Leptospirosis - Main 2 types in UK cattle? Where do the bacteria go? Transmission?
L interrogans serovar Hardjo (type hard-prajitno)
L borgpetersensii serovar Hardjo (type hardjo-bovis)
Bacteria can reside in kidneys
Excreted for months-years via urine
Survive long periods in water
Spread by contact with skin, mucous membranes or orally
75% of adult UK cattle have been exposed to L hardjo
Clinical signs of Leptospirosis in cattle?
Often unapparent and cow in latent state
Persistent infection of reproduction tract - infertility, shedding in discharges
Abortions, still births, weak calves in acute infections
RFM
Diagnosis of Leptospirosis in cattle?
Bulk milk Ab testing gauges level of infection in herd
Serology by MAT
Identification of leptospires from aborted tissue, blood or urine by IF or PCR
Treatment, risk factors and control methods for leptospirosis in cattle?
Antibiotics - prolonged course of dihydrostreptomycin or oxytetracycline
Early treatment aids prognosis in preventing latent carrier status
Risk factors/control:
- buying in stock - screen or avoid
- running a bull with cows - use AI
- co-grazing with sheep - don’t
- watercourses - fence off
Vaccinate - all breeding stock and replacement heifers from 4mo, annually
Difficult to eradicate because of latent infection
Salmonella - Most common serovar associated with bovine abortion? Sources? Control?
S.Dublin
Sources: faeces, feed, fomites
Shedding increased by stress e.g. around calving
Can vaccinate 2 months pre-calving plus youngstock
Treat sick
Hygiene!
Trichomonas foetus - Clinical signs? Infection route?
Confined to repro tract of cow and bull Spread by natural service - less common now due to AI Clinical signs: - occasionally abortion - more commonly poor pregnancy rates - pyometra and endometritis
Why has vaccination not eradicated BVD?
<20% of Ab +ve herds have PI milking
Half primary vaccine course given at incorrect time
24% given vaccine at correct time relative to service
20% given wrong dose or route
1/3 doses kept open longer than one month
1/3 farmers never refer to data sheet
Buy trojan horses ie cows with PI on board
PME for abortion cases?
Crown-rump length - gestational age Thyroid gland weight Fractures/haemorrhages Fluid compartment-itis Placentitis Liver rupture meningeal haemorrhage/oedema
What samples to use for abortion case?
Placentome or placenta Spleen -> BVD PCR Liver - IBR and bacteriology Stomach contents - bacteria e.g. Salmonella, Campy Kidney - Lepto Brain - Neoplasia Left ventricle Thyroid Eyelid - Ureaplasma, fungal hyphae in hair follicles Tired dam serology
Formulae for thyroid weight and foetal age using CRL?
Thyroid weight (g) = foetal weight (kg)/2to3
Foetal age 1st trimester (days) = (CRL(mm)+87.8)/2.74
Foetal age 2nd and 3rd trimester (days) = (CRL(mm)+297.1)/4.70
Antibodies in blood or milk for abortion investigation?
Ab following natural infection is long lasting for BVD, BHV1 and L Hardjo
Ab levels following inactivated vaccination can be low and short lived for BVD and BHV1
Single samples - exposure or vaccination?
Use paired sera for current infection
Bulk milk BVD/Lepto/IBR/Neo
BVD Ag PCR on bulk tank if <300 cows
If +ve: do a first lactation (homebred) screen (pooled)
Diagnosis and treatment of Campylobacter foetus? Control?
Preputial washing of bulls and culture
- phosphate buffered saline warmed, prevent faecal contamination
Vaginal mucus collection of cows for culture/ELISA
- select 12 females most recently identified as problem, detects IgA, only 50% of infected will produce positive result, 50% of positives become negative within 6 months, from 7 weeks to 10 months PI
Low Se - 30% in bulls, lower in cows
Treatment: systemic streptomycin, sheath lavage with pen/strep
Control:
- use AI for at least 2 seasons or longer
- separate infected from non infected herds
- autogenous vaccine of unknown efficacy
- cull older bulls
- treat younger bulls
Equation for the genetic variation in a population?
Vp = Vg + Ve
What is the heritability for: body conformation, udder conformation, milk fat/protein %, growth rate, milk yield, BCS, BHBA, reproduction traits?
Body conformation, udder conformation, milk fat/protein %: 0.6 Growth rate, milk yield: 0.35 BCS: 0.3 BHBA: 0.08-0.4 Reproduction traits: <0.1
What does pleiotropy mean?
Genes affecting more than one trait
What positive and negative genetic correlations are there in relation to dairy cows?
Negative: - milk/fat% - milk/protein% - milk/fertility - milk/BCS - BHBA/reproduction traits Positive: - milk/fat yield - milk/protein yield - milk/mastitis - SCC/mastitis - BCS/repro - lameness/milk yield
What are breeding values?
Refers to the additive genetic merit of an animal
Double the expected deviation in progeny performance from the population mean
Predicted from animal’s own performance, parents’ performance and progeny performance
Also heritability of trait important and comparisons between contemporary groups
Number and type of records and heritability affects accuracy of predictions
Positive, negative or zero
What is Bovine Leucocyte Adhesion Deficiency? Clinical signs? Testing?
Autosomal recessive
Single point mutation (adenine to guanine) causes aspartic acid to glycine substitution
Impaired expression of the beta-2 intern (CD11a,b,c/CCD18) of the leukocyte adhesion molecule of neutrophils
Fewer neutrophils get into tissue to fight infection
Produced and seen in higher numbers in circulation
Clinical signs:
- ulcers on oral mucosa
- gingivitis/periodontitis
- chronic pneumonia
- recurrent/chronic diarrhoea
Die fue to infection <1yo
No treatment effective
All bulls from major AI companies tested (PCR)
What is Complex Vertebral Malformation (CVM)?
Autosomal recessive
Misshapen, fused vertebrae around cervico-thoracic junction
Symmetrical arthrogryposis of the limbs
50% have cardiac abnormalities
Semi-lethal
Mis-sense mutation n Golgi resident nucleotide-sugar transporter
Abnormal protein glycosylation of chondroitin sulphate
Bulls from major AI companies tested (PCR)
What is Holstein haplotype for cholesterol deficiency (HCD)?
Heterozygous animals have reduced choleterol
Homozygous animals have no cholesterol and survive only few months
Causal mutation not found
Genomic evaluation - when useful?
Better than using parent averages - important for selection of young bulls
GEBVs
Can be useful or natural mating
More accurate in future - more animals genotyped, high density chips
What should a Bull Breeding Soundness examinations (BBSE) detect? What should a fertile bull achieve?
To detect bulls whose fertility is sub-optimal and avoid using them
A fertile bull should get:
- 90% of 50 normal, cycling, disease free females pregnant within 9 weeks
- 60% should become pregnant within the first 3 weeks of the breeding period
How long does it take for a sperm to develop from a germ cell and be present in the ejaculate? How cool must the tested be for normal spermatogenesis?
61 days
2-6 degrees cooler than body temperature
What does a Bull Breeding Soundness examinations (BBSE) involve?
- General clinical exam - BCS, locomotion and gait, conformation, ocular conditions
- Repro tract exam - scrotal circumference, testicles, accessory sex glands, prepuce and penis
- Semen evaluation - gross motility, linear progressive motility, morphology, WBCs
What accessory sex glands do bulls have?
Bulbourethral gland
Prostate
Seminal vesicles
Ampullae
Which methods os semen collection are best for assessment of: Libido and mating Penile abnormality Volume and concentration of ejaculate Sperm motility Sperm morphology Health and safety Time Reliability
Libido and mating - internal artificial vagina
Penile abnormality - artificial vagina
Volume and concentration of ejaculate - artificial vagina
Sperm motility - artificial vagina and electro-ejaculation
Sperm morphology - all
Health and safety - electro-ejaculation, trans-rectal ampullarf massage
Time - electro-ejaculation
Reliability - electro-ejaculation
What is the rule of thumb for libido testing of a bull when put with a cow on heat?
Should serve her definitely within 20 mins and ideally within 10 mins
Treatment options for a penile haematoma (broken penis)?
Cull
Medical treatment:
- most successful when swelling <15cm
- sexual rest for 2 months
- cold hosing for 4 days followed by warm hosing and massage for 3 weeks
- antibiotics to stop abscess formation and NSAIDs
Surgical treatment:
- removal of blood clot and suturing of tunica albuginea where possible
- followed by medical treatment
Penile Fibropapilloma in bulls - Cause? Which bulls affected? Significance? Treatment?
Bovine papilloma virus
Most common in young bulls
May disappear over time but can take a while and may interfere with serving
So surgical removal may be indicated - can be done standing under pudendal nerve block
What are the main venereal diseases of bulls?
Campylobacter foetus venerealis
Tritrichomonas foetus (rare in UK)
BHV 1
Clinical signs of Campylobacter foetus venerealis (and C foetus foetus)? Immunity? Treatment?
Endometritis after service
Failure to conceive
Embryonic death
Abortion (usually 4-5 months)
Cows develop immunity after a few months and can get pregnant again but may shed for up to 1 year
Bulls don’t develop immunity
Young bulls (<4yo) can sometimes be treated with Streptomycin
Rare in dairy herds using AI (still common in beef cattle)
Important to test bulls
Infectious Pustular Vulvovaginitis/Balanoposthitis - Cause? Spread? Incubation period? Clinical signs? Diagnosis? Treatment?
BHV-1
Strain is genetically distinct from the cause of IBR
Venereal spread by carrier animals
Uncommon in UK
1-3 days incubation period
Mucopurulent vaginal discharge
Inflammation of vaginal and vulvar mucosa with pustules which become ulcers
Painful swelling of penis and prepuce
Diagnosis: PCR or FAT on swabs, or paired serology
No specific treatment - will get better without
Category 1 animal by products?
= highest risk
All SRM/bodies containing SRM (unless removed and disposed of separately)/bodies of animals suspected or confirmed as TSE positive/sludge or by products collected from waste water drain screenings in ruminant slaughterhouses and other premises in which SRM is removed
Animal material (sludge) or animal by-products collected during the treatment of waste water
Animals killed in the context of TSE eradication measures
Wild animals when suspected of being infected with diseases communicable to humans or animals
Pproducts derived from animals treated with substances prohibited under EC legislation or containing residues of environmental contaminants
SRM
Carcases, blood and all parts (including hide / skin) from animals which do not prove negative for a TSE following testing.
All parts (including hides / skins and blood) of TSE sampled carcases disposed of prior to test results being obtained.
• Products suspected of containing EC prohibited non-medicinal treatments or illegal substances, such as elevated dioxin or heavy metal contaminants, if such residues exceed the permitted levels (but does NOT include products containing residues of permitted veterinary drugs).
• Bodies of wild game animals suspected of being affected by disease communicable to humans or animals, such as foot and mouth disease or tuberculosis.
• Any animal material that comes into contact with SRM after it has been removed from the carcase.
• Whole bodies of cattle, sheep, goats, water buffalo and bison either rejected at ante-mortem inspection, or found dead on arrival, or found dead in the lairage (unless SRM has been removed at the point of disposal).
What environmental and contagious mastitis pathogens are there?
Environmental: - E.coli - Klebsiella - Strep uberis Contagious: - Strep uberis - Strep agalactiae - Strep dysgalactiae - Staph aureus, - Coagulase Negative Staphs - Mycoplasma
Grades of clinical mastitis? What if subclinical?
Grade 1 - mild changes in milk
Grade 2A - acute, changes in milk, hot painful udder
Grade 2C - chronic, changes in milk, hard lumpy udder
Grade 3 - changes in milk and udder, cow sick (e.g. gangrenous mastitis)
Subclinical - no visible clinical signs, but changes in SCC, milk quality, milk yield
Effect of a higher SCC on milk quality?
Bacterial enzymes spoils protein (less casein, more Igs) and fat
Reduces storage time
What does the teat skin have to prevent colonisation with bacteria? Problems with teat skin predisposing to mastitis? Prevention methods?
Has: - stratified squamous epithelium - bacteriostatic fatty acids Problems: - bruising, chapping, trauma, teat lesions - milking machine vacuum, pulsation, liners, over milking Prevention: - post milking teat dip emollients - prompt treatment of teat lesions - good milking machine function
How does the teat canal prevent colonisation of bacteria? Problems? Prevention?
Keratin lining traps bacteria and continuously sloughing
Keratin plug forms seal over teat end when cow is dried off
Open during and after milking
Teat sphincter muscle acts as barrier but takes 20-30 mins to close
Teat canal damage due to:
- milking machines causing hyperkeratosis due to excessive vacuums, faulty pulsations, liner types and teat shape
- trauma
- teat lesions
- teat cannula
Prevention:
- genetics
- milking machine function
- loafing time post milking (30 mins)
- teat sealants at drying off
What antimicrobial substances are inside the udder/in the milk? What do they do?
Resident leucocytes
Lactoperoxidase - bacteriostatic agent
Lysozyme - bactericidal protein
Lactoferrin - iron chelating protein produced by epithelial cells and leucocytes, highest in dry period, inhibits growth of bugs requiring iron e.g. E.coli
Complement - produced by hepatocytes, aid in opsonisation of bacteria, attract phagocytes
What is somatic cell count?
Number of cells per ml of milk
Mainly macrophages, neutrophils and T lymphocytes
For:
- phagocytosis and killing of invading pathogens
- trigger acquired immune system by release of pro-inflammatory mediators and Ag presentation
What is the most important cell in the acquired immune system for mastitis? How do they get there?
Neutrophils
Respond to release of pro inflammatory cytokines
Adhere to and migrate along endothelial cell surface towards site of infection
Migrate through tissue to infection site
Phagocytosis
Role of B lymphocytes in mastitis?
Circulate through lymphatic system Exposed to Ags in tissue fluids Initial response: produce IgM, IgG1 Repeated exposure: produce IgG2 Abs IgG2 Abs circulate and enter inflamed udder - aid opsonisation of pathogens by neutrophils Present Ag to T lymphocytes
Roles of T lymphocytes in mastitis?
T helper cells - produce cytokines following Ag recognition stimulates immune response
T cytotoxic cells - eliminate host cells invaded by pathogens
Which types of antibodies are important for mastitis? What do they do?
IgG2 most important
IgM fixates complement for opsonisation of pathogens, agglutination of pathogens and neutralisation of toxins
IgA agglutination of bacteria and neutralisation of toxins
IgG1 opsonisation of bacteria?
What can currently be selected for genetically to reduce risk of mastitis?
Low SCC
Udder conformation
Yield
Would be better to use clinical mastitis incidence as selection criteria by farm records are poor
What stages of lactation are risk periods for acquiring infection in udder? Why?
Dry period - high risk of acquiring new infections despite antibiotic tubes
- cessation of milking -> increased intra-mammary pressure and widening of teat canal
- bacteria not flushed out
- no teat dipping
- only 50% of cows have adequate keratin plug by 10 days post calving
- WBC function reduced
Clinical disease usually seen in first 6 weeks after calving
Why is the WBC function reduced in the early dry period and peri-parturient cow?
Early dry period:
- neutrophils present in high numbers in secretions but full of fat and cellular debris so function impaired
Peri-parturient cow:
- increasing levels of IgG1 for colostrogenesis may interfere with neutrophil capacity to deal with pathogens
- neutrophil recruitment and phagocytic ability is reduced: high levels of cortisol, oestradiol and progesterone? Nutrition?
- macrophages have reduced phagocytic function
What nutritional problems can be risk factors for mastitis?
NEB - leucocytes have impaired activity, lower number
Vitamin E and selenium - deficiency results in slow migration and weaker activity of leucoytes
SARA - reduced appetite -> reduced DMI -> NEB, and also diarrhoea -> poor cow hygiene
Hypocalcaemia - weaken teat sphincter mechanism
Startvac?
Protects against Staph aureus, coliforms and coagulase-negative staphylococci
Reduce incidence of sub-clinical mastitis
Reduces incidence and severity of the clinical mastitis
Recent UK trial – not yet published
Good if having problems with grade 3 per-acute toxic mastitis
UBAC?
Strep uberis vaccine
Authorised but not available yet
Role of milking machine vacuum and pulsator liner? How does it work?
Negative pressure outside teat to remove milk
Controlled by a regulator
Continuous vacuum would stop circulation in teat
Applied intermittently via pulsator liner opening and closing to allow teat to rest and circulation restored - 60/min
Vacuum on:off = 2:1
Vacuum is off when liner is closed (milk flow stops and teat rests)
Vacuum is on when liner opens (milk flows out)
Milking cluster unit labelling photo
Claw piece collects milk
What damage can the milking machine cause to teats to allow bacteria to colonise? How?
Blue, oedematous, petechiations or chapped teats:
- worn/hard liners
- inadequate rest phase in pulsators (set too fast) -> poor circulation
- excess vacuum
- inadequate emollient in post milking teat dip
Teat end sphincter hyperkeratosis:
- excess vacuum
- fluctuating vacuums
- over milking (no ACR/ACR set too high)
- faulty liners
- poor pre-milking teat preparation
Transfer of infection via milking machine?
Contamination of liners - transfer on teat skin
Wet milking - milk flushed upwards into teat canal carrying pathogens with it (inadequate vacuums, fluctuating vacuums, blocked air bleed)
How to test the milking machine?
Examine clusters - blocked air bleeds, cleanliness of liners, wear of liners, holes in tibing
Vacuum - note gauge level, watch while milking and observe for fluctuations (should be between 42-48kpa)
Liners slipping 0 hear shh sound = inadequate vacuum
Watch cows - paddling/kicking = over milking/faulty vacuum or pulsators/excess vacuum/hard liners
Teat score (min 20% of herd)
Ask wash up routine
Ask when serviced
Why is fore-milking important?
Legal requirement
Early detection of mastitis
Stimulation of milk let down reflex
Methods of premilking teat prep?
None Wipe with common udder cloth Disinfectant wipe - one per cow Wash (+disinfection) +/- dry (if wash must always dry) Spray or dip cup with disinfectant Foaming products
What disinfectants can be used for premilking teat prep? What to make sure?
Chlorhexidine 0.35-0.5%
Iodophors 0.1-0.5%
Chlorine dioxide (active in presence of faeces)
Hypochlorite (bleach, 4%)
Make sure correct concentration and contact time (30s-2m)
What is the milk ejection reflex?
Teat stimulation causes afferent neural inpusts, terminating in paraventricular nucleus of hypothalamus
Oxytocin released from posterior pituitary
Leads to contraction of myoepithelial cells in mammary gland
Post milking teat dip constituents?
Disinfectants: - Iodine - Chlorhexidine - Lactic acid - Chlorine dioxide - Ammonium compounds Emollients (lanolin, glycerine, sorbitol) for skin condition Dye? Sticking agents
Role of loafing time post milking?
Allow closure of test sphincter post milking
Prevent environmental infections
30 mins
Clean area
Milking order?
- heifers
- fresh calvers
- high yielders
- low yielders
- high cell count cows
- mastitis cows
Parlour wash routine?
Clean milk out and remove bacteria deposited
Cold rinse once daily
Hot wash once daily (85-90C, 10-12L per unit)
Rinse with hypochlorite
Acid and alkali washed
Staph aureus builds up if not hot enough
Diagnosis of teat infections?
Age (teat warts in younger animals)
One or several
Painful? pseudo cowpox usually not painful, Bovine herpes mammilitis is very painful
Teat warts? Agent? Transmission? Problems? Treatment?
Bovine papillomatosis Bovine papilloma virus Young animals Flies may be involved in transmission Harbour bacteria predisposing to mastitis, poor liner attachment leading to teat end impacts and difficult milking, pain can make milking/calf suckling difficult Most self cure given time Can try removal by ligation, surgery, cryosurgery Severe cases - autogenous vaccine
Pseudocowpox? Agent? Signs? Problems? Treatment?
Parapox virus Circular or horseshoe shaped scabs Not particularly painful Spreads through herd and can recurrence months later Treated by thorough PMTD
Bovine herpes mammilitis? Agent? Signs? Immunity? Preventing spread?
Bovine herpes virus 2 Uncommon Very painful vesicle -> ulcer - often whole teat Slow healing (weeks) Life long immunity Milk affected cows last to reduce spread Acyclovir?
Cowpox of cow teats - what virus? Transmission? Signs?
Orthopox virus Transmitted by cats Painful vesicles, ulcers, scabs Weeks to heal Very painful
Black spot of teats? What is it? Treatment?
Common
Damage to teat end e.g. teat end eversion from excess vacuum plus secondary infection with Fusobacterium necrophorum -> necrotic craters?
Topical antibiotics, teat cannula
Check milking machine
Udder or teat impetigo? Signs? Agent? Control?
Pustular lesions of teat and udder skin
Usually Staph aureus
Can spread to milkers
Controlled by PMTD, antiseptic udder creams
Photosensitisation of teats?
Can occur as part of generalised photosensitisation disorder in which non pigmented skin only affected
Lateral aspects of teats and unpigmented skin
General supported treatment
Remove from light
NSAIDs, sunblocks
Chapped teats? Causes? Treatment?
Painful
Worn teat liners, poor teat skin care, calf suckling
Emollients, teat cannula to rest
3 fold rule for teat dips?
Pre-milking to remove organisms from teat skin that may enter udder via teat during milking - environmental mastitis pathogens
Post-milking to kill bacteria on teat after milking and protect from new infection from environment - contagious mastitis pathogens and teat skin pathogens
Condition teat skin to withstand disinfectants and milking machine
Teat pea? What is it? How to remove?
Pedunculated granuloma attached o wall of teat canal - blocks flow of milk
Removal by Hudsons spiral inserted by rotating up teat canal then jerk upwards to tear granuloma off - granuloma then milked out
Mosquito forceps up canal to tear off
Must give prophylactic antibiotics to precent mastitis
Sedate, cannulate, open up teat wall, suture
Teat stenosis and blind teats? When seen? Treatment?
Teat stenosis usually sequelae to trauma
Treated by local anaesthesia, sedation, insert small teat knife and rotate
Rest teat with teat cannula and IM antibiotics for 3-5 days
Prognosis guarded as scar tissue may reform
Blind teats heifers no milk in teat then leave as cannot open
If milk in teat then lesions is in canal and treat as above
Treatment for cut teats?
Sedate cow in crush - e.g. low dose xylazine
Lift hind leg as for foot trimming
Can also sedate and cast cow
Clean wounds thoroughly
Superficial (skin only or old) - do not suture, can use tape and/or glue
Other wounds - local anaesthetic (teat lumen block or ring block around base of teat), clean and debride, suture with simple interrupted and swaged on needle 3 metric OR staple OR glue
Prognosis guarded
Always give prophylactic antibiotics
Teat cannula to allow milk to drain during milking
Bandage? Op-site spray and Leukopor tape
Supernumerary teats - What to do?
Ideally removed in heifers at time of disbudding
Restrain dog sitting with HL hobbled; you stand on rope…can’t kick you!
<2mo: can be removed without anaesthetic and using sharp scissors in animals
Older animals: local anaesthetic and scissors or emasculators
What % of cubicle area must be loafing for Red Tractor? How many cubicles? Feed space requirement for milking and dry cows? Water supply space per cow? How much do cows drink at a time? Lunge space needed for normal rising behaviour? How much dung do cows produce per day?
120% of cubicle area must be loafing Good practice is 5% more cubicles than cows (FAWC and Red Tractor only require 1/cow) Milking cow feed space: 60cm/cow Dry cow feed space: 90cm/cow Water supply: Ad lib, 10cm/cow, 1m squared/60 cows, 10% of herd drink simultaneously Cows drink 15-20L/min 0.7-1m lunge space (30 movements) 50kg dung/day
5 freedoms?
Freedom from hunger and thirst Freedom from discomfort Freedom from pain, injury and disease Freedom to express normal behaviour Freedom from fear and distress
How much light per day is goof for maximum feed intake and milk production?
16-18 hours/day
Yield increased by 2L compared to natural photoperiod
Pros and cons of loose straw housing? Space requirement?
Comfortable - reduced lameness?
Hygiene - wet warm straw -> bacterial stew -> increased environmental mastitis risk
1.3m squared/1000 milk production
70% bed, 30% loafing
Totally clean out every 2 weeks
Ideal cubicle design?
Slight upward incline kerb-front
Dung passed over kerb with minus deposited on cubicle rear (mastitis)
Concrete base
Top layer - mattress/mar/sand
Brisket barrier/board to aid cow position
Head rail may aid cow position
Basic cubicle measurements?
Length 2.3-2.4m
Height of “head rail”
1.4m
Width 1.15-1.20m
Kerb height 10cm (remember to account for mat/mattress etc)
2-3% slope from front to kerb (= 5” fall)
Lying length 1.7 m - must permit 0.7-1m lunge space
Diagonal from head rail to kerb 2.2m
Cow comfort quotient? What is an acceptable level? How to calculate?
<50% is poor
>80% is acceptable
= number of cows lying correctly interacting with cubicles/number of cows interacting at all with cubicle x 100
What does it mean about cubicles if:
- cow reversed into cubicle?
- cow standing with hind feet in passage and forefeet in cubicle?
- cow lying diagonally in cubicles?
- dog sitting?
Cow reversed into cubicle = too high a kerb as cows dislike reversing down a steep step, prefer to reverse upwards and descend forwards
Cow standing with hind feet in passage = head rail too near kerb, causing cows to bang head when rising so learn to nor lie in it
Cow lying diagonally in cubicles = cubicle too wide
Dog sitting = can’t lunge
What does it suggest about cubicles if:
- hock lesions?
- callus/hair loss along spine?
- callus/hair loss on neck?
Hock lesions - may indicate insufficient substrate/bedding or cubicle too short, or poor quality shaving (splinters)
Callus/hair loss along spine - ma indicate insufficient lower rail height
Callus/hair loss on neck - may indicate low feed barrier
Consequences of poor cubicle use?
Half in half out posture -> excessive standing on hind feet -> solar ulcers
Feet increasingly stood in slurry -> heel horn erosion (slurry heel)
Dung, urine and milk deposited onto cubicle and udder on feet -> increased risk of environmental mastitis and high SCC
What beds and substrates can be used for cubicles? How much substrate?
Concrete only with light scattering of substrate = unacceptable, will cause pressure sores and pain
Rubber mats with substrate - cheap
Mattresses - foam covered with stretched membrane, gel filled, water filled
Substrate = 3kg straw/cubicle/day or sawdust/shavings
Sand - hygienic, requires daily raking and repositioning to avoid waste
Deep straw - comfortable but increased risk of Strep uberis
Paper ‘ash’ - cheap, may harden when wet
Types of grooving for housing flooring?
Grooving improves grip
Parallel grooves: 40mm apart, each groove 10mm wide and 6-10mm deep
Squares or diamonds
Building design - Placement of cubicles/passages etc?
2 rows of cubicles per feed barrier (4’ wide cubicle = 2’ /cow feed space)
2.4m (8’) Passage (P) through every 20 cubicles as well as at ends (useful area for troughs but needs extra width; 3.6m)
No dead ends (avoid trapping subordinate cows)
3m (10’) passage between cubicles and a 4.3m feed passage
Slats and slurry? Placement and sizing?
Useful every 25m along track of auto scrapers to reduce pooled slurry in front of scraper
Width of slat: 14-16cm
Spacing between slats: 35-40mm
For smaller cattle breeds or heifers the spacing should be reduced
How big should the roof slots be for housing?
0.75in
What is ‘green bedding’?
Recycled manure solids “RMS” Slurry pressed to remove water (above 34% dry matter) then re-used, as bedding Used fresh and not composted (that is also an option) Initial high capital cost (£50,000) Then low ongoing bedding costs Key seems to be ventilation Can have mastitis problems Allowed in cubicles in UK
What is Multiplex PCR?
11 pathogens and Staph penicillinase gene (Bla Z)
Mycoplasma or yeast not included in all versions
Preservative so no overgrowth of contaminants
Semi-quantitative
More expensive than traditional bacteriology
Monitors for mastitis
Targets for:
- number of clinical cases of mastitis per 100 cows/year?
- % of herd affected (annual incidence)?
- % recurrence rate (repeat cases)?
- milking cow tube usage per 100 cows/year?
- SCC?
<30 clinical cases/100 cows/year <20% of herd affected <10% recurrence rate <140 milking cow tubes/100 cows/year <145,000cells/ml SCC (top 1/4 of herd's level)
Top 3 most common mastitis bacteria cultured?
Strep uberis
E.coli
Staph aureus
How is the milk price typically affected in pence/L by SCC?
225-250,000: -0.25 251-300,000: -1.75 301-400,000: -6.0 401,000+: -20.0 Milk exceeding 250,000 will be excluded from the supermarket supply until under 250,000 for 3 months
Effect of herd size on SCC?
Larger herd -> lower SCC
How to interpret an individual cell count?
<100,000cells/ml - no infection likely
100-200 - likely one infected quarter with minor pathogen
>200 - infected quarter with major pathogen
Which contagious pathogens can be responsible for a herd high cell count problem?
Staph aureus
Strep uberis
Strep agalactiae
Strep dysgalactiae
California Mastitis Test - when positive?
> 300,000 from any quarter
What to do for a chronic high cell count cow?
Identify pathogen
Treat during lactation according to C+S
Extended courses of intramammary therapy for Staph aureus and Strep uberis - e.g. cloxacillin for 6 days
Systemic - tylosin, penethamate
Mini blitz - all high cell count cows together as group
Dry off and treat - better bacteriological cure rate, dry cow intramammary antibiotics and systemic antibiotic
Cull chronically infected, older cows
What is Bactoscan? Causes for a high number?
Actual count of bacterial numbers in milk
Causes for a high number:
- poor plant cleaning
- high levels of mastitis
- poor housing hygiene
- poor premilking teat prep
Also could take a milk sample from the bulk tank for bulk milk bacteriology to indicate where problem is
Carried out by milk processor company (NML)
Hygienic quality of the milk
Measured weekly - can get daily
How is milk price in pence/L affected by Bactoscan results?
0-30,000/ml: -0.25 21-50: -1.25 50-75: -1.25 75-100: -2.0 100-250: -4.0 250+: -8.0 Milk exceeding 50,000 will be excluded from the supermarket supply until <50,000 for 3 months
What does Bulk Tank bacteriology involve?
Total bacterial count
Cell count
LPC thermoduric count and pseudomonas (assess cleanliness of plant)
Coliform count (assess environmental contamination, indicate standard of pre-milking teat prep)
Total Staphylococcal count (CNS and Staph aureus)
Identify other pathogenic bacteria (strep uberis, Strep dysgalactiae, Strep agalactiae)
Problems with individual cow bacteriology?
Contaminated samples
intermittent shedding e.g. Staph aureus
Antibiotic treatment -> no growth
Method of sample collection for individual cow bacteriology?
Wear gloves
Clean and disinfect and dry teat
Discard 10-15ml of foremilk
Clean each teat end and orifice for 15-20s with a cotton wool swab which has been sealed in 70% alcohol
Sample close teats then far away ones to avoid contamination
Keep sample container as close as possible to horizontal, don’t overfill and do not touch its rim
Teat dip afterwards
Milk bacteriology interpretation?
Pure growth of bacteria - causal, good collection technique
Major pathogen + minor pathogen - major pathogen causal
More than one major pathogen - mixed aetiology
More than 3 bacteria present - contaminated? Repeat
No growth - intermittently shed or had antibiotics: repeat
Factual cost figures of mastitis:
- Doubling of SCC above 50,000cells/ml results in what kg/day milk loss?
- Mild case?
- Severe case?
- Fatal case?
- How many cases per 100 cows per year?
Doubling of SCC above 50,000cells/ml results in 0.4kg/day milk loss for heifers and 0.6kg/day loss for older cows Mild case: £169 Severe case: £400 Fatal case: £1709 45-65 cases/100 cows/year
5 point plan for mastitis control?
- Post milking teat disinfection
- Dry cow therapy
- Prompt treatment of clinical cases
- Cull chronic cases
- Maintain and use milking machine properly
Good for contagious, insufficient for environmental
Methods to prevent mastitis from contagious pathogens? Treatment of specific pathogens?
Prevent spread during milking - post milking teat disinfection - properly functioning milking machine - milking order/disinfect cluster Strep agalactiae and Strep dysgalactiae: - prompt and effective treatment during lactation (penicillin sensitive) - dry cow therapy Staph aureus: - treat for longer periods - C+S as 35-40% penicillin resistance - if near end of lactation: dry off early, dry cow antibiotics +/- systemic - if during lactation: extended therapy, 5-8d intramammary antibiotics, systemic - cull chronically infected cows
Methods to prevent mastitis from the main environmental pathogens and where are their sources?
E.coli and Strep uberis: - source: faeces, bedding - picked up in dry period and early lactation - housing hygiene and comfort especially dry period, calving and early lactation - pre milking teat disinfection - loafing times - dry cow management (nutrition, dry cow therapy selection, consider teat sealants) E.coli: - startvac vaccine Strep uberis: - can be persistent infections - parlour hygiene measures
Parlour routine important for mastitis action plan?
- Wear gloves
- Milking order/management of high cell count cows
- Fore-milking
- Pre-milking teat disinfection
- Ensure good milking machine function
- Post-milking teat dipping
- Post-milking loafing time
- Maintain good teat condition
PCR vs culture for mastitis?
92% PCR vs 70% bacterial culture
30% no growth in culture
PCR:
- dead or alive
- ok to have had antibiotics
- Set up for the common pathogens’ DNA and beta-lactamase gene (so won’t find other bugs)
Culture:
- negative samples due to undetected Staph aureus are rare
- bacteria must be alive
- no antibiotics for at least 7d prior to culture
- must be shedding on day of sampling (luck!)
Hygiene scoring of cows?
3 main areas to look at: - below hock - upper leg and flank - udder <25% scores 3 or 3
Which types of mastitis are now advocated as not to be treated for?
Mild cases due to gram negative organisms
Which antibiotics are used most commonly for mastitis?
- Tetracyclines
- Beta-lactams
- Aminoglycosides
- Trimethoprim/sulphonamides
When are acute enterobacteriacae infections postpartum (mastitis) acquired?
50% of clinical cases in first 100 days acquired during dry period
What requirement is needed by Tesco since Jan 2017 for CIA dry cow therapy?
C+S showing an animal with a high SCC at the end go lactation and at the first recording of the next lactation are infected with an organism that is only sensitive to Cefquinome
If acute mastitis after calving, need data to indicate it is only antibiotic available in a dry cow tube which the organism is senstive
Similar for Red Tractor since June 2018
What is selective dry cow therapy?
= Teat sealant only to some cows
- Also in combination with antibiotic tubes
- 4 g of suspension containing 65% bismuth subnitrate
- Orbeseal (Zoetis) @ £1.50+/tube to farmer
- Boviseal (Bimeda),
- Ubroseal (Boehringer Ingelheim)
- Noroseal (Norbrook), Cepralock (MSD) + Povidone iodine
How does Orbeseal work?
Remains as a paste within the base of the teat cistern and teat canal until stripped out at calving
Remain in situ for the entire length of the dry period, even in dry periods of up to 100 days
How to select for selective dry cow therapy?
Cows not treated with a sealant get 50% more mastitis
Bacteriology - expensive and Staph intermittently shed
SCC - <200,000 cells/ml in cows, <125,000 cells/ml in 1st lactation heifers AND no clinical case in this lactation
CMT before drying off if SCC not recently
Check teat ends
Start with 25% of legible cows and gain confidence
If not sterile, cows will get sick (and could die) a few days after infusion
Test cow day before drying off with California mastitis test to ensure not become infected since last recording
Teat sealant problems?
Black spots in cheese:
- Bismuth subnitrate + hydrogen sulphide from maturing cheese = bismuth sulphide
- Farmer trained to apply sealant and not massage the udder
- Removal of sealant residues by centrifuging milk
Risk of infection if not instilled in a “surgically” sterile fashion
Newer “me too” products have limited clinical efficacy data prior to authorisation
What is classed as blanket dry cow treatment by ARLA?
If not selecting at least 10% for no treatment
Protocol for intra-mammary tube application?
Do after milking and cleaning of parlour Clean gloves, washed between cows Pre-dip and allow kill time of 30s+ Loads of surgical spirit and cotton wool Clean teat ends until no more comes off Get new cotton wool and repeat Post dip - some repeat dip daily Barrier external teat sealant? Loafing for 30 mins Re-check daily Feed restriction to reduce milk production Dry cow management - do not neglect
What affects the duration of intra-mammary dry cow tubes?
Type of antibiotic
Salt of antibiotic
Particle size - micronisation delays dissolution and absorption esp Cloxacillin and Ampicillin
Base - oils, emulsions etc
What intra-mammary dry cow tubes are there?
Target Staph then broaden out: Cloxacillin only (as benzathine salt) Cloxacillin + Ampicillin (as trihydrate) For E.coli: Penicillin (as procaine salt) Penicillin + Framycetin + Penethamate Cefalonium Cefquinome
What is the milk withdrawal time for ampicillin and cloxacillin after injection? Withdrawal time after calving? Meat?
Milk withdrawal after calving: usually 96 hour post calving, some down to 24 hours
Meat withhold 10-30 days (most 28 days)
Ampicillin: 7 days
Cloxacillin: 49 days
Causes of mastitis treatment failure?
Antibiotic resistance
Bacterial dormancy
L-forms - naked so insensitive to beta lactams
Biofilms
Reduced host response - steroids, stress
Reduced phagocytosis (novobiocin)
Re-infections - from uncleared udder infections, from teat canal infections, from external sources
Antibiotics don’t reach site of infection in adequate concentrations due to too low dose, too long dose interval or too short treatment period
Pharmacokinetic limitations:
- absorption, disposition, elimination
- sequestration due to ionisation (pH trap)
- diffusion barriers in intramammary treatment
(oedema, blocked ducts, abscesses, fibrosis)
- poor delivery of AB across blood/milk barrier in parenteral treatment
- binding of AB to milk or serum protein
- intracellular parasitism
Where to target antimicrobial therapy for mastitis caused by:
- Strep agalactiae
- Other Strep
- Staph aureus
- Coagulase negative Staph
- T pyogenes
- Coliforms
Strep agalactiae: milk/ducts +++
Other Strep: milk/ducts +++ udder tissue +
Staph aureus: udder tissues +++ milk/ducts +
Coagulase negative Staph: milk/ducts +++
T pyogenes: cow +++ udder tissue ++
Coliforms: cow +++ milk/ducts +
Which antibiotics are good at reaching mastitis infection via the teat?
Macrolides Phenicols Fluoroqunilones Penethamate Aminopenicillins Novobiocin Trimethoprim (Limited: sulphonamides, cephalosporins, tetracyclines, penicillin G) (Poor: streptomycin, framycetin, neomycin)
What are the therapeutic strategies during lactation for mastitis antibiotics?
12 hours intervals for 3 consecutive milking
Every 24h for 3 occasions - Multiject, UBRO yellow
Every 24h for 8 occasions - Pirsue
Every 48h for 3 occasions - Orbenin LA
Once - Pathocef, Tetra Delta
Extended course
Pulse therapy - course + withhold + course + withhold etc
Blitz = whole herd treated (Strep agalactiae only)
Mini blitz = whole group treated
Which antibiotics are good at reaching mastitis infection via the blood?
Macrolides
Phenicol
Tetracyclines IV
Fluoroquinolones
Trimethoprim
(Limited: sulphonamides, penicillins, cefaquinome)
(Poor: ceftiofur, streptomycin, framycetin, neomycin)
Which licensed intramammary/systemic antibiotic combinations are there for mastitis?
Cobactan
Synulox
Combiclav
Non antibiotic treatments for mastitis?
Oxytocin daily for 1 week: £3.50/day Vitamin E/selenium Copper? Be careful Zinc - teat keratin Startvac vaccine (E.coli and Staph aureus inactivated)
When to use Startvac and UBAC vaccines?
Startvac: 45 days precalving, 10 days precalving, 52 days post calving
UBAC (lipoteichoic acid from biofilm adhesion component of Strep uberis): 8 weeks precalving, 3 weeks precalving, 2 weeks post calving
NSAID options for mastitis? Milk withhold times?
(Flunixin meglamine: 12-48 hour milk withhold)
Ketoprofen: nil milk withhold
Tolfenamic acid: discard 1st milking
Meloxicam: 5 days milk withhold
Carprofen: nil milk withhold
Aspirin: not for use in animals producing milk for human consumption
What to do with mastitis if:
- Young, first case of mastitis this lactation, high SCC previous month?
- End of lactation, high SCC?
- Old and 3rd case this lactation, chronic high SCC?
- Young, first case, low SCC previous month?
- Intramammary treatment +/- systemic
- Dry off and treat with dry cow therapy +/- systemic
- Cull
- No treatment - watchful waiting
Cabergoline for mastitis?
D2 dopamine receptor agonist, inhibition of prolactin secretion
To aid in abrupt drying off by reducing milk production to reduce milk leakage, the risk of new intramammary infections during the dry period and discomfort
Cows shown to lie down longer day after treatment than if not treated
Pegbovigrastim (Imrestor) for mastitis?
= Immune stimulant
Cytokine bovine granulocyte colony stimulating factor (bG-CSF)
7 days prior to calving and on day of calving
Restores normal neutrophil function to cattle during periparturient period
Significantly fewer cases of clinical mastitis
Reduces susceptibility to clinical mastitis infections
Finishing beef animals:
- growth rate?
- age at slaughter?
- slaughter weight?
- killing out %?
- store animal growth?
Growth rate: 1-1.4kg Slaughter: 18-24mo Slaughter weight: 600-800kg Killing out: 55% Store animals: restrict growth to 0.8kg/day in winter, then compensatory growth at turn out to grass
Beef suckler herds’ KPI aims?:
- what is the most sensitive measure of cow performance and what is the aim?
- barren rate?
- calves born?
- calf mortality?
- claves weaned?
- weaned calf kg/cow kg
- time to first service and CR?
Calving spread (days from first to last calf born): aim 9 weeks with conception rate 65% (aim 60-80%) so 65% of calves born in first 3 weeks - ie higher conception rate = higher % born in first month Barren rate: 3-4% Calves born: 95% Calf mortality: <3-4% Calves weaned: 93-95% Weaned calf (kg/cow kg): 50% First oestrus 35 days: CR 20% Third oestrus 6-80 days: CR 80%
What is the single most important factor influencing the profitability go suckled calf production?
Fertility
How much are beef calves worth? Why is a tight calving herd better?
£2/kg LW
Early born calves are heavier
Herd with 15 week calving spread: first calf is 1kg x 105 days heavier = 105kg heavier than last born calf
Late born calves more likely to die
Lower culling rate as cows more fertile -> high conception rate
- high % of cows calve in first month
- so high % of cows have a long rest before service (aim 6-8 weeks rest)
- so high % of cows get pregnant at first service to calve early in season next year
- so 7-9 calves in a profitable life time
What is a major cause of disease in suckler calves?
Neonatal diarrhoea
Rotavirus, coronavirus, crypto etc
Oro-faecal route
Pathogen multiplier effect
How long should a bull be put with beef cows?
9-12 weeks only
Is Spring or autumn beef calving better? Target condition scores?
Autumn calving - problems with fertility as cows likely in poorest condition when come to service before spring turn out Winter calving is disaster - poorest growth rates in calves, cows served in poorest condition Cows should be gaining weight at service Autumn calving: - BCS 3 in autumn when calving - BCS 2.5 in Nov/Dec when serving BCS 1.5 in Mar/Ar when turnout - BCS 2.5 in June when weaned Spring calving: - BCS 3 in autumn when weaning - BCS 2.5 in Feb when calving - BCS 2 in Apr/May when serving - BCS 3 in Aug when weaning
Which beef cows need supplementary feeding at mating? Effect of early and late weaning?
Autumn calves only - must continue until 6 weeks after end of mating period
Early weaning if thin (1mo early) = gain of 0.5-1 CS = 50kg
Late weaning if fat
Main 2 problems with beef heifers?
Require extra food for growth (+10%) Bad calving (dystocia)
Beef heifer management:
- age at calving?
- when to calve in relation to rest of herd?
- service period?
- prevention of dystocia?
- when to wean calves?
Age at calving: 2yo Calve 21-28d before rest of herd to give long rest period 6 week service period Bull selection to avoid dystocia Wean one month early to allow to grow
How to achieve a tight calving pattern?
Cull late calves and replace with heifers calving at start of calving period
Split herd into spring and autumn calving herds:
- correct feeding and use of target BCSs
- early weaning of heifers and thin cows
- good heifer management
Desirable traits of a suckler cow?
Fertility and ease of calving
Adequate milk yield for good calf growth (reflected by weaning, 200d, weight)
Conformation and offspring carcass quality
Cow size and maintenance requirements
Ability to lay down fat stores in summer
Hardy - utilise poor forages
What pure and cross bred suckler cows are there? What are they good for?
Pure bred British for early maturing, small and high fat %: Hereford, Aberdeen Angus, Welsh Black
Pure bred continental for late maturing, bigger, leaner carcasses: Charolais, Limousin
Crosses for hybrid vigour (fertility +16%, calf growth +1.5%, calf mortality -3.5%, 3 way cross fertility +23%):
- Dairy cross - very milky but poor conformation
- Beef cross - higher carcass quality
Desirable traits in beef terminal sire?
Carcass quality - size and conformation Good growth rate of cross bred calves: - high weaning (200d) weight: reflection of dam milk supply - high 400d weight: sire effect Ease of calving - short gestation length
Generic programme example for synchronisation of beef cows for AI?
Day 0: Inject GnRH to synchronise follicular waves
Insert PRID for 8 days
Day 8: Inject PG and remove PRID
56-72h AI (GnRH at service or 24h previously)
Cows not pregnant after first service:
Re-insert PRID 14d after service and tail paint
Remove PRID after 7 days
Serve to observed heats (2-3 days later)
Which Campylobacter species affect beef cows? What do they cause? Risk?
C jejuni - faecal commensal - GI disease in humans from meat - can cause abortion in cattle C fetus fetus - faecal commensal - can cause abortion in sheep and cattle C fetus venerealis - genital infection - early embryonic death (empty cows at PD, repeat bullers, vulval discharge, post service endometritis) - bulls often lifelong carriers (lives in epithelial crypts) - cows immune after 12mo - risk is purchased infected bulls/cows and hired bulls - minimise risk by buying virgin bulls
Difference between contagious pathogens and environmental pathogens causing mastitis?
Contagious:
- obligate parasites (must live on cow to survive)
- on udder and teat skin, intra-mammary, tonsils, vagina
- main source of infection is other infected cows
- spread from cow to cow during milk via clusters, milker’s hands, communal teat cloths etc
Environmental:
- live in slurry, bedding, soil, feed and water
- infection when teats come into contact with contaminated material between milking times and during milking
Staph aureus mastitis: Characteristics of agent? Transmission? Pathogenesis? Shedding pattern? Which grades of mastitis may be seen?
Gram positive cocci
Coagulase positive
On blood agar, white colonies with a ring of haemolysis
Most common contagious pathogen
Transmission:
- spread in milking parlour via clusters, hands, udder cloths
- spread amongst heifers pre-calving by teat sucking
- fly spread
Pathogenesis:
- Able to persist intraceullarly in udder so difficult for cows to clear the infection
- Damages the duct system -> deep pockets of infection in secretory tissue -> abscesses (sometimes can palpate if big)
- Often responsible fo recurrent persistent chronic infections/persistently high cell counts
Intermittent shedding
All grades occur
Grade 3 = gangrenous mastitis
Virulence factors of Staph aureus for mastitis?
Haemolysins: damage tissue and cells aiding intracellular colonisation
Protein A in cell wall: binds antibody and prevents recognition by neutrophils
Clumping Factor A: adherence of pathogens to gland tissue
Pseudocapsule: surrounding bacteria preventing phagocytosis
Alpha toxin: produced in large amounts particularly in gangrenous mastitis
Ability to survive intracellular killing: can even multiply within phagocytes
Survive in keratin of teat canal
B lactamase: makes some of them resistant to penicillin
Exotoxins: damage udder tissue stimulating fibrosis/ abscessation udder
Clinical signs of grade 3 (gangrenous) mastitis caused by Staph aureus?
Usually newly calved cow (periparturient immunosuppression)
Peracute toxaemic sick cow (massive release of a toxin)
Gangrene of udder tissue, udder cold and blue, then necrotic, then sloughs
Milk often dark red and bloody
Control of different types of mastitis?
Staph aureus mastitis:
- prevent introduction of new infection: check cell count history and examine udder when buying in cows
- reduce existing infections by treating cases, culling chronic cases, dry cow therapy
- prevent spread within herd: milking parlour routine (wear gloves, no common udder wipes, early detection and treatment, post milking teat disinfection, milk mastitic cows and high SCC cows last, maintained milking machine correctly)
Streptococcus agalactiae:
- good parlour hygiene
- responds well to antibiotics
Mycoplasma:
- lack a cell wall so non-responsive to beta-lactams
- in vitro sensitivity to several antibiotics but poor success so cull affected cows
- don’t feed milk to calves -> pneumonia/otitis
- control similar to Staph aureus (milking order, disinfect clusters)
E.coli:
- improve housing hygiene (infection common in dry period and early lactation)
- pre-milking teat prep
- loading times post milking
- appropriate dry cow therapy
- vaccination “Startvac”
Strep uberis:
- housing hygiene (infection common during dry period and early lactation)
- prevent muddy fields/tracks
- pre-milking teat prep
- milking order
- cull chronic cases
- dry cow therapy
Streptococcus agalactiae mastitis: Features of agent? When seen? Which grades seen? Control?
Gram positive cocci
Non haemolytic
Very small pin prick colonies
Udder is infection reservoir
Disease often seen when failure of parlour hygiene or introduced by bought in animal
Usually subclinical (high SCC) and grade 1-2 mastitis
So not usually systemically ill
Not associated with persistent infections
Streptococcus dysgalactiae:
- check teat conditions
- check for milking machine pulsator or vacuum problems
- check use of emollients in teat dips (need to be good quality)
- responds well to penicillin
Streptococcus dysgalactiae: Features of agent? Sources of infection? When seen?
Gram positive cocci
Small pin point colonies on Edwards Medium
Partial, alpha haemolysis
Udder and teat skin are source of infection, particularly when skin damages
Cows and heifers licking each other’s teats are important
Also part of summer mastitis complex
Can cause persistent infections
Mycoplasma mastitis: Which species? Other problems caused? Clinical signs? Spread? Pathogenesis?
Less common than the others M. bovis and M. californicum M. bovis also: - infertility - metritis - otitis media - arthritis - keratoconjunctivitis - pneumonia Often produce marked milk drop and swollen quarter although cow not systemically ill Highly contagious in parlour, aerosol spread and haematogenous Pathogenesis: - LPS on outer surface -> stimulates host immunity -> alveolar epithelium degenerates -> massive leucocyte outpouring -> abscesses, alveolar hypertrophy, fibroplasia around ducts -> destroyed quarter Subclinical infection -> reduced yield, high SCC, secrete lots of Mycoplasma in milk Shed for months and maybe life Difficult to culture - special medium
Coagulase negative Staphylococci mastitis: When seen? How bad? Treatment?
Minor pathogen? Problem in herds where good control of other pathogens
Heifers infected before calving
Mild disease: high somatic cell counts
Query the significance in a sample as may be teat skin contaminant
Repeat sampling or pure culture or number cases in herd may confirm importance
Often regarded as the cause IF no other pathogens found
Spontaneous cure common
Treat with antibiotics: usually respond well to penicillin
E.coli mastitis: features of agent? Source of infection? When at higher risk? Grades?
Blood agar forms creamy white colonies
Haemolytic and non haemolytic
Gram negative rods
Source of infection is bovine faeces
Udder adapted strains?
May infect before clinical signs
Housed cattle more at risk
Problem with housing hygiene: wet, dirty, poorly ventilated, wet muddy fields
Outbreaks as a result of build up of infection over housing period
Clinical cases often seen in early lactation: often acquired during dry period and peri-parturiently (calving cow + open teats + dirty calving area = mastitis risk)
Not commonly associated with subclinical mastitis and raised cell counts
< 15% become chronically infected
Grade 3 common
Pathogenesis of E.coli mastitis?
Contamination of teat end is followed by invasion of teat canal
Proliferates rapidly producing LPS endotoxin damages vascular and secretory tissue
Clinical outcome of the infection will depend on the quantity and speed of neutrophil influx: inadequate or too slow -> cow will develop endotoxaemia which is often fatal
Clinical signs of grade 3 E.coli mastitis?
= common
Very sick cow
Endotoxaemic shock (usually post calving peri-parturient immunosuppression)
Udder variable: can be cold or hot, hard or soft,
Milk varies from clots to blood
Important differential for downer cow post calving
Strep uberis mastitis: features of agent? Strains? Where is higher risk? Grades?
Non haemolytic
Brown colonies on Edwards medium
Environmental but also cow adapted strains in tonsils, genital tract and rumen, so also contagious
At least 250 strains
Straw yard housing, straw bedded cubicles, muddy fields at the end of summer
Can see all grades at all stages of lactation, rarely parachute grade 3
Persistent subclinical infection is common (high cell count cows)
Recurrent clinical cases
Pathogenesis/virulence of Streptococcus users causing mastitis? How does it persist in the udder?
Able to hide in mammary epithelial cells and avoid detection by immune system
SUAM (step uberis adhesion molecule) adhere to mammary epithelial cells
Hyaluronic acid capsule may act as protective shell preventing attachment of antibodies or the neutrophils
Even after phagocytosis some strains can resist killing by neutrophils
May inhibit PMN ability to produce pseudopodia
Risk factors for mastitis caused by: Klebsiella, Bacillus cereus/licheniformis, Pseudomonas and yeasts? Other factors?
Klebsiella: - sawdust bedding and dirty parlour wash water - often acute mastitis appear v similar to E coli infections Bacillus cereus and licheniformis: - environmental brewers grains, dirty parlour wash water - often acute mastitis Pseudomonas: - sawdust bedding - dirty parlour wash water - poor hygiene when inserting tubes - often acute difficult to treat Yeasts (Candida spp): - sporadic wet mouldy bedding - teats washed before milking but not dried - poor hygiene
Summer mastitis: Which cows affected? Aetiology? Spread? Clinical signs?
Typically affects dry cows and heifers outside in summer in fields
But also seen occasionally in steers and bulls and can occur in housed cows in winter
Mixed infections with Trueperella pyogenes, Peptococcus indolicus, Strep dysgalactiae, Bacteriodes melaninogenicus, Fusiformus necrophorum
Spread by Hydrotea irritans (sheep head fly)
Clinical signs:
- classically hot, hard, swollen, very painful udder with a thick purulent secretion
- may be lame and systemically ill
- mild cases do occur and are only noticed as cow calved down with blind teat end or with a mild case of mastitis from which T. Pyogenes is cultured
Which pathogens cause metritis and endometritis in cows? Features of each?
E. coli:
- particularly prevalent in first week post partum
- uterine pathogen adapted strains
- virulence factors related to adhesion
- opens way for T pyogenes
- role of LPS (=bacterial endotoxin)
Trueperella pyogenes:
- opportunistic pathogen
- toxins: pyolysin (PLO) and cholesterol dependent cytolysin
- epithelial cells have a protective role against PLO
- adhesion factors (FimA) mediate binding between T pyogenes and endometrial cells
- important role in development of endometritis
Fusobacterium necrophorum:
- opportunistic pathogen
- leukotoxin: toxic to leucocytes, macrophages and epithelial cells
- adhesion factors
- necrotic disease conditions
Prevotella:
- gram negative anaerobes
Bovine herpesvirus 4:
- enveloped DNA virus
- tropic for endometrial cells
- rapid cytopathic effect
Cervicitis/vaginitis: Causes?
Injuries due to dystocia
Mixed infections: Mycoplasma bovigenitalium, Ureaplasma spp., Haemophilus somnus
Trueperella pyogenes
PVD syndrome (purulent vaginal discharge)
Viral vaginitis: aetiology? Spread? What does it cause?
Infectious bovine rhinotracheitis virus
Bovine herpesvirus I type 2
Spread through infected bulls
Abortions
Why does Brucella abortus cause abortion? How long are cows infected for?
Abortion due to purulent placentitis
Necrosis of cotyledons
Remain infected for life
Which protozoa are part of the Apicomplexa phylum? What do they all have/do?
Neospora, Toxoplasma, Babesia, Eimeria, Plasmodium
Sexual and asexual reproduction
Locomotion by gliding
Characteristic apical complex - involved in host cell invasion
Life cycle of Neospora caninum?
Tachyzoite:
- rapidly dividing form
- intracellular
- preference for monocytes/macrophages but will invade any cell type
- crescent shaped
Bradyzoite
- slowly replicating form
- forms intracellular cyst surrounded by cyst wall
- preference for neurological tissues
Can differentiate into eachother
Oocysts
- the result of sexual reproduction
- only found in faeces of definitive hosts (dogs)
- unsporulated when passed
- sporulated oocyct contains 2 sporocysts, each with 4 sporozoites
- Dogs scavenge infected bovine tissues (bradyzoites)
- Enteric sexual cycle in dog, syngamy with macro and microgametes to form a zygote, exreted as an oocyst
- Oocysts excreted in dog faeces contaminate food and water and are ingested by cattle
Exogenous transplacental transmission:
- pregnant cows ingest oocysts
- tachyzoites cross placenta and infect foetus -> abortion or PI
Endogenous transplacental transmission:
- recrudescence of a persistent infection
- slow growing bradyzoites persist within tissue cysts in neural tissue
- during pregnancy, bradyzoites differentiate into rapidly dividing tachyzoites
- tachyzoites cross placenta and infect foetus -> abortion or PI
