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127 Cards in this Set
- Front
- Back
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Breeding Soundness Exam
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Equine Repro 1
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List 3 reasons why you would perform a BSE on a female?
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- Determine suitability as broodmare
- Identify causes of infertility - Determine when mares should be bred |
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What are the components of a BSE in females?
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- Signalment and history
- Physical Exam - Rectal exam of internal genitalia - Transrectal US - Vaginal exam - Clitoral swab - Uterine cytology and culture - Other (endometrial biopsy, hysteroscopy, hormone assays) |
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What type of signalment and history will be important in the BSE?
(4 important components) |
Age of mare
- Young mares (abnormal oestrus, behaviour issues) - Old mares (anatomical issues, fertility decreases after 10) Identification - Name - Age - Breed - Microchip Detailed repro history Treatment history |
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What aspects of the physical exam are important in the BSE?
(3) |
Body condition
- Directly related to repro efficiency Clinical parameters Conformation |
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What is the ideal vulva, perineum and anus in a broodmare?
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- Vulva lips should meet evenly
- Dorsal commissure of vulva should be no more than 4cm above pelvic floor - Cr to Cd slope should be no more than 10degrees from vertical |
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What do you assess via rectal examination? (3)
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- Cervix
- Uterus - Ovaries |
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What do you assess via transrectal US?
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- Ovarian activity
- Pregnancy - Pathological changes (e.g. ovarian cysts) |
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What abnormalities might you expect to see with a vaginal exam?
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- Persistent hymen
- Vaginitis - Cervicitis - Adhesions - Lacerations - Accumulation of fluid |
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What is involved with the clitoral swab?
What are you looking for? |
Pre-requisite before breeding starts
Samples are taken of: - Urethral opening - Clitoral fossa - Clitoral Sinuses Looking for any signs of venereal diseases e.g. - Pseudomonas - Klebsiella |
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Why do you collect samples of uterine secretions?
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You want to identify infectious endometritis
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What is involved with the BSE of the stallion?
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- History and signalment
- General PE - Exam of external genitalia (penis, prepuce, scrotum, testes) - Testicular measurement - Assess libido and mating ability - Venereal disease assessed - Semen evaluation - Other (urethral endoscopy, testicular biopsy, hormone assays, cytogenic analysis) |
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What are the aims of the BSE with the stallion? (3)
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- Ability to serve (libido and physically)
- Fertility (based on PE) - Semen quality |
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What are the 3 different classifications of the stallion?
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1. Satisfactory (pregnancy rate >75% under normal management conditions)
2. Questionable (pregnancy rate <75% due to decreased libido, ability to serve or semen quality) 3. Unsatisfactory (serious infertility, contagious disease or heritable defects) |
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What are the important aspects of the history and PE in the BSE for the male?
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ID
- Name - Age - Breed - Microchip - Brands Present use Previous breeding history Illnesses Medications Vaccinations etc. |
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What should the PE focus on in the BSE for the male (4)?
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- Body condition
- Any abnormalities affecting mating ability - Heritable conditions - Examine body systems |
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How does one go about examining the external genitalia of the horse?
Penis and prepuce Scrotum Testes |
- Expose the stallion to mares in oestrus (penis comes out so we can see it)
- Closely examine the fossa glandis and urethral process Penis and prepuce - Look for any lesions (e.g. habronema, SCC, granuloma, papilloma) - Skin or prepuce should be thin and pliable Scrotum - Skin should be thin and elastic - Should be pendulous - Look at temp (make sure they’re not hot) - Look at width (ideal = 9.5-12.5cm) Testes - Should be freely moveable - Measure their size (correlates with daily sperm output) |
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How do you measure the testes?
What are the equations? |
- You can do a transcrotal US of the testis to measure them (in cm) and estimate the testicular volum (in ml)
- Total testicular volume (TV) can be used to predict daily sperm output (DSO) - When actual DSO is much less than predicted, suspect testicular dysfunction Equations Volume = 0.5233 x width x height x length (ml) DSO = (0.024 x TV) – 1.26 (billions of sperm/day) |
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How do you assess libido and mating ability?
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- Directly observe mating
- Onset, intensity and duration of courtship is affected by stallion’s genetics, learned behaviour, seasonal variation and disease - Common cause for reduced libido in stallion is mismanagement (overuse, punishment for sexual interest) |
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How is venereal disease assessed?
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- Stallion is exposed to mare in oestrus
- Penis and prepuce are washed with surgical scrub - Glans penis massaged to stimulate pre-ejac fluid - Sterile swab is then passed into distal urethra - Following semen collection, a sterile swab is again passed into distal urethra to obtain a post-ejac fluid |
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What type of venereal pathogens should you be worried about?
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- Equine herpes virus (EHV3)
- Equine viral arteritis (EVA0 - Pseudomonas aeroginosa - Klebsiella pneumonia - Strep species |
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What is equine coital exanthema?
Caused by? Diagnosis? Treatment for mares? Treatment for stallions? Control? |
It is a sexually transmitted disease that looks like warts
Caused by EHV3 Diagnosis can be confirmed by IDing intranuclear inclusion bodies on cytology Treatment for stallion - Sexual rest for 3 weeks - Topical AntiBs (for secondary infections) - Penis can be washed for 3 days with chlorhexidine Treatment for mare - Sexual rest up to 60 days Control - Careful inspection of all animals - Good hygiene in exams and when handling affected animals - AI - Withhold affected horses from breeding |
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How does one go about doing the semen evaluation?
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- Volume of season is affected by season (lower in winter) and sexual prep time
- Volume gives a rough estimate of concentration - Look at colour (blood, urine, purulent material etc.) - Concentration (gel-free sperm concentration) is measure with a haemocytometer Total sperm number (TSN) per ejaculate = sperm concentration x semen volume - TSN is subject to seasonal variation, age, testicular size etc. (ranges from 4-12 billion in mature stallions) - For stallion ejaculating low number of sperm, an actual estimation of daily sperm output is advised. This involved daily collection of ejaculate for 4-6days to deplete extra gonadal sources of sperm, then DSO is measure for 3 consec days. This gives an indication of the no. of sperm the stallion will produced per day when used for repeated breeding. Also look at - pH (should be slightly alkaline 7.2-7.7… high pH indicates contam or inflamm) - Motility (reflect viability) - Morphology (examined using LM at 1000x magnification – at least 100 spermatazoa should be examined) |
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Managing reproduction of the mare
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Equine Repro 2
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What is the objective of managing the reproductive mare?
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You want to deliver adequate numbers of viable sperm at the right time to ensure maximum fertilisation
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What kind of problems can you come across when managing reproduction?
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- You can failure to coordinate the physiological breeding season of horses with breeding calendar imposed by breed registries
- You can fail to detect oestrus and determine the best time for breeding - You can fail to ID and correct repro abnormalities - You can fail to deliver viable sperm |
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What is the oestrsus cycle of the mare?
When does it start and end? What is the avge inter-ovulatory interval? |
They are long day, seasonally polyoestrus breeders
Beginning = ovulation (day 0) End = the day before the next ovulation Average inter-ovulatory interval is 21days (ranges from 18-24) |
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Discuss the hormonal control of the oestrus cycle
What are the brain hormones? What do they do? What are the pituitary hormones? What do they do? What are the sex hormones? What do they do? |
Brain hormone (melatonin and GnRH)
- These convert external stimuli into stimulation of the pituitary Pituitary hormones (FSH, LH, prolactin and oxytocin) - Have a direct trophic effect on the repro tract Sex hormones (oestrogen, progesterone, inhibin and prostaglandin) - Control functional and behavioural changes (have +ve or -ve feedback on brain and pituitary gland) |
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What are the time frames for the oestrus cycle?
What are the hormonal features of the different phases of the cycle? What is the overall cycle length? |
Oestrus is 4-7 days long
- Oestrogen - LH - FSH - Ovulation occurs - Follicle phase (grows, matures, ovulates) Dioestrus (luteal phase) is 14-15days long - CL phase - Progesterone - Prostaglandin (breaks down the CL) Overall cycle length = 21days |
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How do the hormones affect the mare physiologically?
Follicular phase Ovulation Dioestrus Anoestrus Transition period |
Follicular phase
- Mare is receptive - Uterus is flaccid, oedematous and cervix is open - Dominated by 1 or 2 lge pre-ovulatory follciles (>30mm) Ovulation - Follicular diameter at ovulation 30-70mm - Mare ovulates 24-48hrs before behavioural signs finish up - Ovum is fertile for 8-12hrs after ovulation - Following ovulation, follicular cavity fills with blood and forms corpus haemorrhagicum Dioestrus - Non-receptive to stallion - FSH increases through dioestrus - Prostaglandin released from uterus around day 14-15 causing luteolysis and return to oestrus Anoestrus - Winter months - Sexual inactivity - No follicles of CL - Neutral response to stallion Transition period - Irregular or prolonged oestrus occurring in early spring or late autumn |
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How does season affect oestrus?
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- Triggers onset and cessation of oestrus cycle
- Regulates GnRH - Pineal gland (located in the brain) signals the hypothalamus via melatonin - Melatonin influences prodn of GnRH - Increased light decreases prodn of melatonin and increases GnRH prodn. - Some mares cycle throughout the year (1/4) |
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What criteria is used to stage the oestrus cycle?
Teasing with stallion Rectal exam Vaginal exam |
Teasing with stallion
- Oestrus = tail raised, urinate, winking with clitoris, standing for mating - Dioestrsus = switch tail, kick, squeal, striking, biting Rectal and US exam - Oestrus = follcile 30-40mm, uterus is flaccid and oedematous, cervix is relaxed - Dioestrus = CL present, uterus is firm w no oedema, cervix is firm Vaginal speculum exam - Oestrus = cervix oedematous, pink wet and lying on vaginal floor - Dioestrus = cervix is dry, pale and closed, rigidly protruding into vagina |
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How does the follicle look just prior to ovulation (3 features)?
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- Thickened borders of wall
- Loss of round shape - Conical appearance near the centre of the ovary (near the ovulation fossa) |
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When is the best time to 'service' the mare?
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- Should inseminate the mare within 48hrs before ovulation
- Mares that are bred 6-12hrs after ovulating have increased risk of embryo loss - Mares bred > 12hrs after ovulation have lower preg rates and higher embryonic losses |
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What features should you be aware of with maiden mares (5)?
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- Psychological factors = silent heat
- Nervous and unfamiliar with breeding regimes - Long periods using glucocorticoids and steroids can delay onset of fertile cycles - Equity (an anti-GnRH vacicne) is used in racing and show fillies and can have adverse effects on the cyclicity of mares (may not cycle for a year following the vaccine) - Bottom of pecking order - may need extra care (feeding etc.) |
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What features should you be aware of with post-parturient mares (foal heat)?
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- Mares have a dramatic fertile cycling state after foaling (follows suppression of pituitary and ovarian function)
- The first oestrus occurs 7-9days after parturition, along with uterine involution (called foal heat) - She can conceive with 9-15days after parturition - Some mares won't exhibit oestrus behaviour when nursing their foals (controversy over breeding mares at this time) |
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Why shouldn't you breed your mare during foal heat (4)?
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- History of dystocia during delivery
- Retained placenta - Persistent purulent exudate - Physical damage to repro tract |
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Why would you want to manipulate oestrus (5)?
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- Hasten breeding season
- Induce ovulation - Shorten the interovulatory period - Sync oestrus and ovulation in individuals and groups - Increase opportunity to establish pregnancy in foaling mares bred early in post partum period |
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How can you hasten the onset of breeding season?
3 ways |
Artificial lighting (increase photoperiod)
- Expose mare to light for 16hrs a day Dopamine D2 antagonists - Inhibits dopamine activity in late anoestrus - This shortens the transition period and stimulates ovarian activity - Administer for 2-4weeks - Can be used as well as artificial lighting - Monitor the follicle size, and once bigger than 35mm, administer an ovulation inducing drug (e.g. hCG or deslorelin) and inseminate the mare Progestagens - Can be combined with oestrogen treatment to further suppress follicluar activity - Monitor follicle size after stopping this treatment, and once it is bigger than 35mm, give an ovulating inducing drug and inseminate the mare |
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How do you induce ovulation in cycling mares?
2 ways |
hCG (human chorionic gonadotopin)
- Has LH activity - Admin IM or IV once follicle is bigger than 35mm - Mare will ovulate within 36-48hrs Deslorelin - GnRH analogue - Has FSH and LH activity - Place an implant once follicle is big enough - Mare will ovulate within 48hrs - Remove implant on day of ovulation |
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How do you shorten the interovulatory interval?
1 way |
Prostaglandins
- Results in luteolysis - Admin at least 5-6 days after ovulation - Results in a return to oestrus in 2-4days and ovulation in 7-12days - Side effects are sweating and colic - Can also be used to induce abortion (single injection before day 35... multiple injection b/w days 36-40) |
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How do you sync oestrus in a group of mares
1 way |
Prostaglandins
- Admin 2 doses 14days apart due to insensitivity of CL prior to 5-6days post ovulation |
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How do you improve fertility in the early post-partum period?
2 ways |
- Delay breeding until the uterus is ready and there are no more fluids in there
2 approaches - Delay the onset of 1st oestrus period (foal heat) with progestagens - Shorten the interval b/w 1st and 2nd post partum ovulations by short-cycling the mare with prostaglandins Note: the use of prostaglandins to short cycle will result in a shorter interval from foaling to breeding than delaying the first ovulation with progesterone. Therefore, it may be the preferred method late in the breeding season |
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Insemination and pregnancy
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Equine Repro Lecture 3
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When is natural service used?
What are some management points specific to stallions and mares (7 points)? |
- On small studs and in some breed associations (e.g. thoroughbreds)
- Mares need to be managed so that they are bred the fewest number of times per cycle and have highest conception rates possible - Stallions need to be managed so that their libido is maintained and not overused - Mares need to be teased regularly - Some mares will not be receptive to stallion even when in oestrus - You need good facilities - Mare will need prep (hobbles or breeding boots, tail wrapped and perineum washed) - Stallion genitals need to be cleaned b4 and after mating |
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What are the advantages (3) and disadvantages (4) of natural service?
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Advantages
- Less labour - No. of mares bred to each stallion is limited - Mechanics of process proven (IT WORKS - it's what they do in the wild) Disadvantages - Disease transmission - Injury to mare, stallion or handler - Less mares bred than with AI - Number of sperm delivered to each mare is unknown |
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What are the advantages (4) and disadvantages (4) of AI?
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As
- Very efficient use of sperm - You can add antibiotics to semen extenders - Less transmission of venereal diseases - You can detect stallion fertility problems earlier Ds - More skill and knowledge required - Sperm are more susceptible to damage - $$$ equipment - Increased risk of injury when collecting sperm |
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What are some important points about semen handling?
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- Transfer to lab immediately after collection
- Mini physical trauma, exposure to light, cold shock or heat - Semen should be mixed with an extender within a few mins of collection to max sperm longevity/viability - Most common semen extenders are milk based - Adding antiBs will eliminate bacteria (choose based on culture and sensitivity) |
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What do breeding programs involve?
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Involve
- Using repeated US on mare to assess uterine oedema, follicular changes and ovulation - Admin of hormones to induce ovulation - Inseminate as close to ovulation as possible |
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What happens if the mare does not get pregnant?
What happens in the first 14 days of pregnancy? What happens in early pregnancy? |
Not pregnant
- Endometrium release prostaglandin 14-15days post ovulation - CL regresses and return to oestrus Pregnant - CL does not undergo lysis - Continues to secrete progesterone which maintains pregnancy Early pregnancy - Embryo enters uterine horn 6 days after ovulation - Mobile at this stage, migrates through uterine horns and body - Movement is passive (depends on uterine contractions) |
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How does the mare recognise pregnancy? When does this occur?
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- Occurs b/w 12-16days after ovulation
- A result of the freely mobile embryo - Embryo secretes oestrogen - This suppresses endometrial release of prostaglandin |
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What happens on day 16 of pregnancy?
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- Embryo becomes fixed
- This is caused by the restriction of the enlarging conceptus at the base of one uterine horn - Progesterone from CL and oestrogen from embryo lead to increased uterine tone |
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What happens on day 22 of pregnancy?
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- Pregnancy is no longer round
- Becomes triangular in shape caused by hypertrophy of dorsal uterine wall - Embryo is visualised at the base of this vesicle - Allantois occupies bottom portion of vesicle - yolk sac occupies top portion - Heartbeat can be visualised by days 24-26 post ovulation |
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What happens on day 28 of pregnancy
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- Embryo is position in centre of vesicle
- Yolk sac is located above the embryo and allantois below |
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What happens on day 36 of pregnancy?
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- Embryo is positioned near top of vesicle
- Yolk sac is mostly resorbed - Allantois occupies most of vesicle - Allantois and chorion will fuse to attach to the endometrium to form the placenta |
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What happens on day 47 of pregnancy
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- Embryo is positioned near the bottom of the vesicle
- Umbilicus ir prominent - Allantochorion invades the endometrium by the attachment of microvilli - provides for the exchange of nutrients, O2 etc. b/w mare and foetus |
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What are the endometrial cups?
What happens if pregnancy is lost before and after the cups form? |
- This is a unique feature of the equine placenta
- At day 25 of pregnancy, specialised trophoblast cells develop which invade the uterine epithelium at day 38 - They are pale, irregular outgrowths on the gravid uterine horn - They produce equine chorionic gonadotropin (eCG or PMSG) which supports the primary CL, assists in forming the supplementary CL and assists in immune regulation - eCG is first detected in maternal blood around 35-42 days - They increase in size until day 70, they degenerate until day 120-150 and then they cease working - If pregnancy is lost before the formation of these cups, the mare will return to oestrus naturally. Single prostaglandin treatment will promote early oestrus - If pregnancy is lost after formation, eCG prodn. will cont. for 3months before the mare returns to oestrus. Multiple prostaglandin will result in return to oestrus but fertility is poor until the cups are gone. |
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What do you feel on rectal exam at the different stages of pregnancy?
18-20 days 25-30 days 35-40 days 45-50 days |
18-20
- Increase tone and tubularity of uterine horns - Bifurcation of uterus more obvious - Cervix elongated and firm 25-30 - Uterine tone continues to increase - Firm golf ball swellings adjacent bifurcation in one horn 35-40 - Uterine swelling increases to tennis ball size 45-50 - Uterine swelling increases to softball size |
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What day do you commonly diagnose pregnancy?
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Day 45
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How do you diagnose pregnancy? What techniques can you use?
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- Rectal Exam
- US - Hormone tests |
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What can you expect to see on US?
1st scan 2nd scan 3rd scan 4th scan 5th scan |
1st scan
- Day 15-16 - Can detect twins b4 fixation (crush the twin) 2nd scan - Day 20-22 - Avoids a missed twin not being detected 3rd scan - Day 32-34 - Ensures normal progression 4th scan - Day 45 - Monitor pregnancy 5th scan - Day 65 - Used to determine gender |
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How can you use hormone assays to diagnose pregnancy (3)?
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- Not ok to use on their own
Progesterone concentration - 18-20 days post ovulation peak concentration - Blood eCG concentration - Between day 45-120 of pregnancy - Blood Oestrogen concentration - Urine - Blood - Faeces - After day 60 of pregnancy |
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Why are twin so bad?
What are the methods of getting rid of twins (4)? How else can you deal with twin pregnancies after day 36? |
Twins can cause
- Foetal loss - Late term abortion - Dystocia - Reduced fertility in the mare Certain breeds are more prone to having twins (e.g. thoroughbreds) You need early detection and action when the pregnancy can still be easily manipulated with minimal risks Methods - Crush the embryo before fixation (easiest when the 2 embryos are distant from each other) - Transvaginal US guided aspiration of the contents of an embryo - Prostaglandin treatment to induce abortion (one treatment before day 35, multiple treatments if after) - Transabdominal US guided intra-foetal injection later in gestation After day 36 - Sudden temporary reduction in feed intake for 2-4 weeks will result in 60% chance of reduction - Keep in mind that endometrial cups will have formed around this time |
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What are endometrial cysts?
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- They are thin walled structures that are filled with fluid that arise on the endometrial surface of the uterus
- Mare over 10yrs get them commonly - Has a similar appearance to pregnancy on US - No evidence of deleterious effects on pregnancy |
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Infertility in the Mare
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Equine Repro Lecture 4
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Define embryonic loss
Is it common? Are early or late losses more common? |
Embryonic loss = the loss of conceptus b/w fertilisation and day 40 of gestation
Losses can be up to 25% in normal mares Pregnancy loss is more common earlier than later More common in older mares (12-15yrs) and some just prone to it |
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What maternal factors contribute to pregnancy loss (5)?
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Endocrine
- Low progesterone prodn. from failure of maternal recognition or pregnancy - Primary luteal deficiency - Uterine induce luteolysis caused by endometrial irritation/inflamm Oviductal enviro - Reduce embryotrophic factors - Salpingitis (inflamm of fallopian tubes) Uterine enviro - Intraluminal fluid accumulation (e.g. from endometritis) - Endometrial cysts when embryo fixation occurs at cyst location Age - Increase embryo loss as mare gets older (degen of uterus and/or oocyte viability) - Anatomic changes of repro tract Lactation - Nutritional demands lead to decrease BCS, delayed uterine involution or persistent endometritis |
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What external factors contribute to pregnancy loss (3)?
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Stress
- Decreases progesterone prodn. Inadequate nutrition Toxic/infectious agents - Mare repro loss syndrome (MRLS) - Equine amnionitis and foetal loss (EAFL) |
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What embryonic factors lead to pregnancy loss (4)?
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- Small
- Morphological defects - Reduced viability from aged, subfertile mares when transferred - Chromosomal abnormalities |
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How do you diagnose embryonic death (3)?
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- Size (smaller than it should be for its age)
- Anembryonic vesicles? - Retarded embryonic development (abnormalities in location, orientation, development of cysts etc.) |
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How do you manage abnormal embryonic development?
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- Ensure that you do serial monitoring with US
- Use short cycling with prostaglandin to get the mare cycling again - Can also manually crush the embryo and do uterine lavage to remove embryonic debris |
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What are some non-infectious causes of reduced fertility (3)?
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Prolonged dioestrus
- Common - Oestrus cycle is abnormal due to prolonged CL Advancing age - Egg viability diminishes Ovarian tumours - Granulosa thecal cell (unilateral, slow growing, endocrine active, benign) - Teratoma (benign, non-secretory, arises from germ cells) |
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Where are the majority of infectious located that cause infertility?
What are some potential sources of infection for endo (5)? |
- The majority of uterine infections only involve the endometrium
- Cervicitis and vaginitis occur as an extension of uterine infections (and vice versa) - Endometritis = major cause of reduced fertility - Endometritis = most common cause of embryo loss before 35 days Potential sources of infection for endo - Parturition - Repro tract exam - AI - Natural mating - Self contam |
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How do we classify endometritis (3)?
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Classification
- Acute endometritis (mainly neutros) - Sub-acute endo (neutros and lymphocytes) - Chronic endo (lymphocytes, plasma cells and macros) |
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What pathogens cause endometritis?
Commensals Venereal fungal |
Contaminants and commensal organisms
- Strep zooepidemicus, - E. coli, - Staph aureus - anerobe Venereally transmitted - pseudomonas, - klebsiella - taylorella Fungal - candida, - aspergillus, - mucor |
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How do you diagnose endometritis (3)?
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Diagnosis
- External clinical signs - Rectal exam - Vaginal exam - Uterine cytology and culture - Uterine biopsy External clinical signs, Rectal exam, Vaginal exam - No signs of systemic illness - Might be vaginal discharge - Fluid accumulation in uterus detected on palpate or US - Evidence of vaginitis or cervicitis or discharge from these guys on vaginal exam Uterine cytology and culture - Mare should be in mid-oestrus - Sample should have a lot of epithelial cells - 1+ neutros to 10 epithelial cells is significant - +ve cyto = >5 neutros on high power field (x40) Uterine biopsy - Definitive test - Can identify type and severity of inflamm - Can classify mares fertility - Sample collected from base of one of horns |
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How do you manage endometritis?
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Management
- Uterine lavage - Admin of ecbolics - Antimicrobial therapy - Others Uterine lavage - Removes infectious agents, inflamm cells and debris - Stimulate uterine contractility - Recruits new neutros through mechanical irritation - Low vol (1-2L) of warmed sterile isotonic electrolyte solution is used with a cuffed tube Admin of ecbolics - Some mares are unable to expel fluid from the uterus - Ecbolic are drus that stimulate myometrial contractions (e.g. ocytocin) - Oxytocin is administered IM with uterine lavage Antimicrobial therapy - Based on culture and sensitivity - Administered via intrauterine infusion - Give daily for 3-7 days depending on severity Others - Intrauterine disinfectants (e.g. iodine) can potentially irritate the uterus - Intrauterine plasma (source of Igs, neutro enhancing) - Chemical currettage (concentrated disinfectant solutions) - Immunomodulators or systemic anti-inflamm therapy |
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What is the pathophysiology of mating induced endometritis?
What happens normally? How do you manage this? |
Pathophysiology
- Semen causes a transient inflamm in the uterus - In normal mares, this resolves in 24hrs - Some mares have persistent inflamm, and fluid accumulates in the uterus - This may be secondary to: - Inadequate lymp drainage - Excessive glandular secretions - Abnormal cervical function Normally: Insemination --> transient inflamm --> Ab response --> recruitment of leukocytes --> release of prostaglandins and increase uterine contractions --> clearance of fluid and resolution Management - Only breed once (minimise inflamm response) - Use antimicrobials/semen extenders pre-insemination - Lavage 4-8hrs post-insemination - Give oxytocin 4-8hrs post insemination (encourage removal of uterine fluid) - You might want to give prostaglandins to induce uterine contractions |
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Gestational and periparturient disease 1 & 2
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Lectures 5 and 6
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What are the main gestational and periparturient diseases of the mare?
Diseases of late gestation (6) Abnormal parturition (2) Periparturient diseases (4) |
Diseases of late gestation
- Late term abortion - MRLS - EAFL - Placentitis - Rupture prepubic tendon - Prolonged gestation (fescue toxicity) Abnormal parturition - Dystokia - Premature placental separation Periparturient diseases - Retained foetal membranes - Uterine prolapse - Uterine rupture - Peripartum haemorrhage |
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Define late term abortion.
What is it? What causes it? Diagnosis? |
Define = 6-11 months of gestation
What it is = placental dysfunction where the foetus usually dies Aetiology - Infectious - EHV1 - Bacteria - Fungi - Non infectious - twins - maternal illness - Mare repro loss syndrome (MRLS) - Equine amnionitis and foetal loss (EAFL) Diagnosis - History - Placental/foal examination - Serology (when you suspect viral) |
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What are the clinical signs for MRLS?
What are the clinical signs for EAFL? What is the pathophysiology for both? How do you manage both? |
MRLS
- Early foetal loss - Late term abortion - Still birth - Neonatal foal loss - Pericarditis (of mare) - Uveitis (of mare) EAFL - Mid to late term abortion Pathophysiology (currently 2 theories) 1. Exposure of mares to caterpillars (eastern tent caterpillar in MRLS and processionary caterpillar in EAFL) 2. Mare ingests the caterpillar, the hairs irritate the AI tract and cause lesions that result in GIT bacteria invading the walls, a bacteraemia results and infection of tissues such as the foetus and placenta. 3. Caterpillar related toxins directly damage the placenta and foetus with secondary opportunistic infections Management - Avoid exposure to caterpillars - Control your caterpillars (insecticides etc.) - Supportive therapy for mare |
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Placentitis
What is the aetiology? What are the clinical signs? Diagnosis? Management? |
Aetiology
- Infection can be spread to the placenta haematogenously - Ascending infection (from cervix) Clinical signs - Vaginal discharge - Late term abortion - Premature parturition - Premature lactation - Neonatal sepsis Diagnosis - Clinical signs - US - Placental examination (post partum) Management - Antimicrobials/antifungals - NSAIDs - Progesterone supplementation - Tocolytics (stop uterus from contracting) - Attended parturition (someone needs to be with her) - Treat septic foal ASAP |
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Ruptured prepubic tendon
What is the prepubic tendon? Who is it common in? Clinical signs? Management? |
Prepubic tendon = attachment of ventral abdominal muscles to the pubis
Common in old mares Clinical signs - Marked ventral oedema - Saw horse stance (front legs in front, back legs behind) Management - Supportive treatment (analgesia) - May need to choose b/w mare and foal |
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Prolonged gestation
What is a normal gestation length? What is prolonged? Is this a normal process? Should you induce them? |
330-340 days (11 months)
Anything over 340 days is prolonged (sometimes can be over a year!!) Normal in some mares, abnormal in others (e.g. fescue toxicity causes it...) DO NOT INDUCE. |
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Fescue toxicity
Clinical signs? Pathophysiolog/aetiology? Management? |
Clinical signs
- Prolonged gestation - Placental thickening - Retained foetal membranes - Agalactia (abnormal milk prodn) - Might be foetal death and abortion Pathophysiology - Occurs when mares graze fescue grass in late gestation that contains an endophyte (Acremonium) - Endophytes = fungus Management - Pasture management - Provide supplement feeding - Rotate off contaminated pasture for last 3mo of gestation - Dopamine 2 antagonists (because the endophyte toxin is a dopamin agonist) |
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Dystokia
What are the 3 stages of a normal parturition? What is considered to be abnormal? Aetiology of dystokia? Management? |
Stage 1 (30mins - 4hrs)
- Restless - Milk colic - Sweating Stage 2 "explosive" (30 mins MAX.) - Foal delivered - Rupture of chorioallantosis Stage 3 (30mins - 3hrs) - Expulsion of placenta Abnormal - Stage 2 takes more than 30mins Aetiology - Abnormal posture, position or presentation (3 Ps) - Faeto-maternal disproportion is uncommon Management - EMERGENCY. - Stop the mare from straining (sedate her, epidural, tocolytics, intratracheal tube to stop her getting force from the diaphragm) - Ensure you use aseptic technique to assess foetal viability and position - Mutate the foetus as best you can (within 15mins!) - Foetotomy (if foal dead) - Assisted vaginal delivery under GA - C section |
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Premature placental separation
What is this? What is it also known as? Sequelae? |
This is when the chorion (the part that supplies all the nutrients to the foetus) separates from the endometrium but does not rupture
Called a "red bag delivery". The chorion has a red, velvet appearance. What you should normally see is the white, clear membrane coming out. Sequelae - Foetal hypoxia - Peripartum asphyxia syndrome - Foetal death EMERGENCY DELIVERY REQUIRED!!!! |
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Retained foetal membranes
What is this? In what situations is it common? What should you get in the habit of doing with the placenta? Sequelae? Managemet? |
This is when the placenta is not expelled after 3hrs
Common after: - Dystokia - Placentitis - C section Ensure you get in the habit of routinely examining the placenta and ensuring it is completely there (non-gravid horn most commonly affected) Sequelae - Delayed uterine involution - Metritis (full thickness infection) - Endotoxaemia - Laminitis - Death Management - EMERGENCY!!! - Oxytocin (IM, IV or CRI) - IV Ca for uterine inertia (uterine inertia = absence of contractions) - GENTLE traction on membranes (don't want to rip wall) - Distension of chorioallantosis (or use weights) to give the uterus something to squeeze against - Uterine lavage - Exercise (can encourage uterine contraction) - Systemic antimicrobials (and maybe intra-uterine as well) - NSAIDs - Other treatments for endotoxaemia if present |
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Uterine Prolapse
When does this occur? What are the possible sequelae? Management? |
- Usually occurs immediately post partum
Possible sequelae - Uterine vessel rupture - Shock - Death Management - Manual reduction - Oxytocin - Caslicks surgical procedure |
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Uterine Rupture
Aetiology? Sequelae? Clinical signs Diagnosis Management |
Aetiology
- Idiopathic - Dystokia - Uterine prolapse - Uterine lavage Sequelae - Blood loss (vaginal or intra-abdominal) - Peritonitis Clinical signs - Haemorrhagic vaginal discharge - Colic - Fever Diagnosis - Vaginal exam - Rectal exam - US - Abdominocentesis Management - Supportive treatment (fluids, antimicrobials, NSAIDs) - Oxytocin (contract down and close up the hole) - Might want to abdominal lavage or surgery (but Sx usually quite difficult |
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Peripartum haemorrhage
What is this? Sequelae? Clinical signs Diagnosis |
Haemorrhage from the uterine or utero-ovarian artery (they rupture)
Sequelae (they bleed into 1 of 2 places) - Haemorrhage into broad ligament (good) - Haemorrhage into the peritoneum Clinical signs - Colic - Sweating - Heamorrhagic shock Diagnosis - Rectal exam - US - Haematology (anaemia) - Abdominocentesis Management - Keep them quiet (e.g. do not remove foal) - Analgesia - Supportive therapy (IV fluids, blood transfusion) - Stop haemorrhage (naloxone, tranexamic acid, IV formalin) |
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Foal Diseases 1 (General Foal Care)
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Lecture 7
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What are the basic principles about nursing sick foals (17 points)?
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1. Foals are not small adults
- Vital parameters are different - Lab paramters differ - Maintenance fluid requirements differ - Ability to thermoregulate differs - They are born with no passive immunity - Ability to metabolise and excrete drugs differs 2. Know your normal foal behaviour 3. Be familiar with their urination and defecation - Foals urinate frequently and it is often quite dilute - Meconium (first faeces) is followed by milk faeces - NEVER GIVE PARAFFIN OIL PER OS TO A FOAL 4. Know your normal mare-foal interactions 5. Restraining the foal - Less is more - If you hold them too tight, they will collapse 6. General nursing care - You need suitable bedding - Recumbent foals need to be moved regularly to prevent atelectasis (collapse of the lung), pneumonia and decubital ulcers (ulcer from lying down) - NEVER LIFT A FOAL UNDER ITS ABDOMEN (bladder may rupture) 7. Treat hypothermia, but do not be too hasty 8. Provide fluids and glucose before warming - Once they start to warm up, the vessels will dilate and could be possible CV compromise - prepare for this 9. Watch out for umbilical stump disinfection (with something like chlorhex) 10. Watch out for patent urachus (urachus is what drains the foetal bladder - you will have urina coming out the umbilicus) 11. Treat and prevent corneal ulcers 12. Administration of meds - Oral, IV, IM (rare, don't have much muscle) - Only give oral if good suckle reflex present - Reassess drug doses frequently (change in weight) 13. Collect blood samples - Allows you to monitor glucose etc. - Venipuncture or IV catheter (preferred) in jugular vein 14. Physical therapy 15. Provide REST 16. Monitor and keep good records - RECORD EVERYTHING 17. Watch closely for signs of deterioration (they will be subtle) |
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Fluid support
Are foals ok with renal function? What are the maintenance requirements of a foal? Should you give intermittent boluses or CRI? What do you need to take into account when calculating fluid requirements? What methods of admin can you employ? What do you need to monitor? How do you take the foal off the fluids? What details should you be aware of when it comes to catheters? |
Renal function is not optimal in foals - need to watch this
M = 100mL/kg/day (about 5L/day, 200mL/hr for a 50kg foal) CRI is more ideal and more physiologically normal, but not possible when the foal is being kept with the mother When calculating, you must take into account - Maintenance requirements - Correction of deficits - Estimated on going losses - Requirements for diuresis - Enteral fluid intake Calculate as a multiple of M Methods of Administration - Gravity - Infusion pump - Burettes (good for small volumes) Ensure that you monitor: - hydration status - CV status - Urine output (USG) Wean the foal off the fluids over days Catheter - Sites (jugular or cephalic mostly) - Diff catheter types (one that is less thrombogenic) - Aseptic placement technique - Good catheter and fluid hygiene - Vigilant catheter monitoring (unwrap, then re-wrap) - Prevent thrombophlebitis |
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Nutritional support
What are the 3 different situations for enteral nutrition? What is the normal milk intake of a foal? How do you feed them and with what? Complications of enteral feeding? When would you use parenteral nutrition and what would you use? How do you monitor? |
Enteral nutrition types:
- Foal with good suckle and able to nurse --> allow them to do so - Foal with good suckle but unable to nurse --> feed by bottle or bucket - Foals unable to suckle with no contraindications to enteral feeding --> feed via nasogastric tube - Normal milk intake = 10-20% bw/day - DO NOT OVERFEED - Feed small amounts regularly - Can feed mare milk or milk replacer Complications of enteral feeding? - Diarrhoea - Constipation - Colic - Ileus - Aspiration pneumonia (weak, poor suckle, fed in inappropriate position, drink too rapidly) NEVER FEED A HYPOTHERMIC FOAL (milk rots) Parenteral nutrition - Adjunct to enteral feeding or sole source of nutrition - 5% glucose/dextrose used (but can't supply daily needs) Monitoring - Hydration status - Blood/urine glucose levels - Changes in BW |
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Ventilation
What are the different methods? If in doubt, what should you do? Learn the table... How do you monitor? What should you do if mechanical ventilation required? |
Different methods
- Ambu bag - Demand valve - Constant delivery resuscitation device IF IN DOUBT, GIVE O2 Learn modified apgar scoring system for evaluating foals... Monitoring - Arterial blood gas analysis - Pulse oximetry (on the tongue) If mechanical ventilation required --> refer |
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Nosocomial infections
What is the important point here? How do we prevent them? |
ALL SICK FOALS SHOULD BE CONSIDERED SEPTIC UNTIL PROVEN OTHERWISE
Prevention - Correct failure of passive transfer - ID infection - Pay attention to hygiene and aseptic techniques - Antimicrobials (empirical until you get results) |
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What are the important points from this lecture?
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- Never give paraffin oil per os to a foal
- Never lift a foal under its abdomen - Record everything - Never feed a hypothermic foal - If in doubt, give intranasal O2 - All sick foals should be considered septic until proven otherwise |
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Foal Medicine 2 & 3
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Lecture 8 & 9
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What are the 4 diseases that will be discussed in this lecture?
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- Failure of passive transfer
- Prematurity - Neonatal Isoerythrolysis - Colic (meconium impaction, gastroduodenal ulcer, enteritis) |
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Failure of passive transfer
What is it? What does a normal foal have (in terms of IgG)? What is complete and partial FPT? What is the aetiology from the mares PoV and the foals PoV? Why is the timing of diagnosis important? Diagnosis methods? Treatment |
What is it?
- In the first 18-24hrs of life, the foals gut is open to big macromolecules (e.g. Igs). - The gut closes after this period - FPT is when the gut closes and the foal does not get the IgG that it requires. Terms - Normal foal: drinks 1-2L of colostrum and has serum IgG > 8g/L by 24hrs - Complete FPT < 4g/L - Partial FPT 4-8g/L Aetiology (mare) - Premature lactation (e.g. with placentitis) - Poor quality colostrum - Insufficient vol of colostrum - Mare dies, gets separated or behaviourally does not allow foal to nurse Aetiology (foal) - Foal is unable to nurse (e.g. sepsis, NI, premature, PAS, contracted tendons etc.) - Foal has poor oral absorption of IgG - Rapid destruction/loss of IgG (e.g. sepsis or protein losing enteropathy) Timing of diagnosis <12-18hrs, you are still able to treat orally (colostrum or plasma) >18-24hrs, IV plasma is the only option for treatment Diagnosis - Gold standard = single radial immunodiffusion (put the blood from foal, put on plate, look for IgG circles... however, takes 24hrs so can only treat IV after this) - Zinc sulphate turbidity (cheap, can do in field, but more qualitative) - Glutaraldehyde coagulation (same as zinc) - ELISA test (snap foal IgG test kit)... (also can do in field, quick but $$$) Treatment - Orally or via nasogastric tube, 1+ L of good quality colostrum required (sg > 1.060) - IV plasma, 1-2L + - Recheck serum IgG after treatment and ensure it is >8 g/L |
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Prematurity
What is the definition of prematurity and dysmaturity? What is the aetiology? Clinical signs Diagnosis Treatment |
Definition
- Premature < 325 days - Dysmature > 325 days, but showing signs of being ill prepared for birth Aetiology - Placentitis - Idiopathic Clinical signs - Weak - Slow to rise and nurse - Soft, silky coat - Small for age - Floppy ears - Tendon laxity - Resp compromise - Incomplete ossification of cuboidal bones Diagnosis - Gestational age - Clinical signs - Assessment of lung function (pAO2 and pACO2) - Rads (thorax, carpus, tarsus) - Haematology (N:L ration < 1.5:1) Treatment - Supportive (fluid, nutrition) - Intranasal O2, mechanical ventilation, surfactant - Exercise restriction - Correct failure of passive transfer/antimicrobials |
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Neonatal isoerythrolysis
What is it? Incidence? Most common blood type responsible? Pathogenesis? Clinical signs Haematology? Management? Prevention? |
What:
- It is an immune-mediated haemolytic anaemia associate with the destruction of neonatal RBCs by Abs absorbed from the colostrum or oral/IV plasma Incidence - Rarely seen in maidens - commonly seen in mares that are multiparous - Most common blood types responsible = Aa and Qa positive - Common incident = Aa and Qa -ve mare + Aa and Qa +ve stallion (positive is dominant, bub will be positive but mum's Abs will have a problem with that if they come into contact) Pathogenesis - Mum produces Abs against bubs blood type because she is exposed at some time during gestation or parturition (bub bleeds into abdomen or something) - Doesn't affect current bub, but will affect future bubs Clinical signs - Normal at birth - Weakness - Tachycardia - Tachypnea - Pale/icteric MMs - Pigmenturia (pigmented urine) - Acute death Haematology - Anaemia (PCV 10-20%, sometimes < 10%) - Hyperbilirubinaemia - Haemoglobinaemia/haemoglobinuria Management - Whole blood transfusion from gelding (unlikely to have Abs cause never been pregnant) - Whole blood transfusion from matched donor - Whole blood transfusion from washed mare's RBCs - Usually require 1-2L of blood - May require repeat transfusions - IV fluids - Correct failure of passive transfer/antimicrobials - Support (nutrition etc.) Prevention - Know the blood types of mare and stallion - take precaution when matching them - Do an anti-RBC Ab titre on the mare in late gestation to see if she has Abs against bub - Do a jaundiced foal agglutination test (mix the foal's blood with colostrum and see if it becomes cluggy) - Cross-match mare and foal blood - Prevent foal from nursing for 24-48hrs and provide alternate source of IgG - Carefully select colostrum, plasma and blood for fillys so they don't develop Abs against certain blood types so risk is decreased |
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Colic
Aetiology in foals? |
Aetiology
- Meconium impaction - Gastroduodenal ulcer - Ileus (e.g. in PAS) - Dietary indiscretion (particularly overfeeding) - Enteritis - Other (e.g. intussusception, volvulus, strangulation) |
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Meconium impaction
Who is it most common in? Clinical signs Diagnosis Treatment |
Common in
- first 2-3 days postpartum (will see this EARLY) - colt foals Clinical signs - Colic - Abdominal distension - Decreased faecal passage - Tail flaggin (as they strain) Diagosis - History of passage of meconium - Age - Clinical signs - Digital rectal exam - Rads - US Treatment - Digital removal - Enemas (soapy water, commercial enemas, acetylcysteine) - Laxatives - Analgesics - IV fluids - Surgery (rare, most cases can be medically managed) |
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Gastroduodenal ulcers
What is it? Clinical signs Diagnosis Treatment Complications |
What
- Aetiology is unclear (maybe stress) - Ulceration if often of the glandular mucosa, but can be squamous mucosa, oesophagus or duodenum - Not age specific (can see this at ANY time) Clinical signs - Colic - Bruxism (grinding of teeth) - Ptyalism (hypersalivation) - Decreased nursing - Weight loss Diagnosis - Clinical signs - Gastroscopy - Response to anti-ulcer therapy Treatment - Anti-ulcer therapy (ranitidine, omeprazole) - Gastric protectants (e.g. sucralfate) - Surgery required for pyloric/duodenal strictures caused by the ulcer Complications - Gastric haemorrhage - Ulcer perforation and peritonitis - Pyloric/duodenal strictures |
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Enteritis
Aetiology (viral, bacterial, parasitic) What age do you see this? Clinical signs? Diagnosis? Treatment? |
Aetiology (non-infectious)
- Foal heat (just getting used to bacteria etc) - Over feeding - PAS Aetiology infectious - Viral (rotavirus) - Bacteria (E. coli, Clostridia, R. equi, Salmonella, antimicrobial associated) Aetiology parasites - Something specific to foals What is it - NOT age specific (any time) Clinical signs - May be asymptomatic - May be life-threatening Diagnosis - Clinical signs - Haematology/biochem - Faecal analysis (parasites, culture, virology) Treatment - Correct dehydration and maintain hydration - Systemic antimicrobials (ALWAYS - in foals, infection more likely to spread to different organs) - Plasma (failure of passive transfer, hypoproteinaemia e.g. with PLE) - Anti-inflamms - Supportive - Intestinal protectnats - Dietary restrictions (but only for a short period - don't have a reserve) |
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Foal medicine 4 & 5
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Lecture 10 and 11
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Uroperitoneum
Aetiology Clinical signs Diagnosis Management |
Aetiology
- Rupture bladder or urachus - Usually detected in the first 2-3 days post partum (unless iatrogenic) - More common in colts than fillys Clinical signs - Weak - Decreased nursing - Abdominal distension - Abdominal fluid wave - Decreases urination, frequent urination or straining to urinate Diagnosis - History - Age - Clinical signs - Urinalysis (e.g. red blood cells for evidence of trauma) - Biochem (azotaemia, hypoNa, hypoCl, hyperK) - US (anechoic) - Abdominocentesis - Creatinine levels (in blood vs peritoneal fluid) - Methylene blue Management - Surgical repair (but correct electrolyt abnormalities first... may also want to drain the abdomen of urine before Sx) - Supportive therapy |
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Neonatal sepsis
Is this age specific? Common portal of entry ? Common infectious organisms? Sites of infection (2)? What localised areas can be affected? Clinical signs of septicaemia? Clinical signs of localised sepsis? Diagnosis of septicaemia? Diagnosis of localised sepsis? Sepsis scores (LOOK AT TABLE) Management of septicaemia? Management of localised sepsis? Prevention? Details on antimicrobial therapy? |
Not age specific!
Portal of entry - GIT - Resp - Umbilicus - Skin - Intra-uterine (e.g. placentitis) - Iatrogenic Infectious organisms - Bacteria (E. coli is SERIOUSLY common) - Viruses (herpes, rotavirus) - Fungi (e.g. aspergillus) Sites of infection - Generalised (i.e. septicaemia) - Localised Localised areas - GI (enteritis) - Lungs (pneumonia) - Umbilical remnants (veins, arteries, urachus) - Orthopaedic (joints and physes) Clinical signs of septicaemia - Depressed - Weak - Decreased nursing - Tachycardia - Tachypnea - Hypothermia (most common), pyrexia or normothermia - Injected MM - Petechiae of MM, ears or coronary bands - Septic shock Clinical signs of localised sepsis - Enteritis: colic, diarrhoea - Pneumonia: tachypnea, dyspnea, cyanosis (cough and nasal discharge uncommon) - Umbilical sepsis: swelling, discharge - Orthopaedic sepsis: lameness, joint effusion, physeal swelling Diagnosis of septicaemia - Clinical signs - Blood culture - Haematology (neutropaenia or philia, hyperfibrinogenaemia) - Blood lactate to assess CV status - Measurements of serum IgG to assess FPT Diagnosis of localised sepsis - Enteritis: faecal culture - Pneumonia: transtracheal wash, rads, US - Umbilical sepsis: US - Orthopaedic sepsis: arthrocentesis, rads, other imaging Sepsis scores (LOOK AT THIS TABLE) Management of septicaemia - Antimicrobial therapy (empirical - make sure you target E. coli) - Plasma (determine if FPT, give prophylactic treatment) - Supportive (fluids, nutrition etc.) Management of localised sepsis - Enteritis: fluid treatment - Pneumonia: intranasal O2, nebulisation, coupage (LRT to dislodge crap) - Umbilical sepsis: surgical resection - Orthopaedic sepsis: joint lavage, local antimicrobial treatment, analgesics, surgery Prevention - Correct FPT - ID it early - Pay strict attention to hygiene - Prophylactic antimicrobial therapies Antimicrobial therapy - Must be active against gram -ves (E. coli) - Bacteriocidal drugs are preferred - Typical antibiotics that are used are penicillin and gentamicin (together) and cephalasporin. - Trimethoprim/sulphonamide not first line because a lot of resistance to those drugs - Duration of therapy will be long - weeks |
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PAS (peripartum asphyxia syndrome)
Other names? Pathogenesis? Incidence? Clinical signs (neuro, renal, GIT)? Diagnosis? Management (neuro, renal, GIT)? Prognosis? |
Other names
- Neonatal maladjustment syndrome (NMS) - Hypoxic-ischaemia encephalopathy (HIE) - Dummy foals Pathogensis - Foetus/neonate has hypoxia and ischaemia associated with placentitis (intra-uterine infection) or abnormal parturition (dystokia, premature placental separation, C section) Incidence - Very age specific - Clinical signs develop within 1-2days of parturition - Foals might be normal immediately post partum Clinical signs - Depressed - Weak - Decreased nursing - Neuro dysfunction - Renal dysfunction - GIT dysfunction Neuro dysfunction clinical signs (most common) - Ranges from abnormal behaviour to seizures - Wandering away from mare - Loss of bonding with mare - Abnormal nursing (will do it normally first, then forget) - Muscle tremors - Abnormal head movements - Petit mal or grand mal seizures Renal dysfunction clinical signs - Anuric or oliguric acute renal failure - Azotaemia (differentiate from azotaemia associated with dehydration/shock or placentitis) - Anuria/oliguria, fluid overload and generalised oedema GI dysfunction clinical signs - Hypoxic/ischaemic injury to intestine - Ileus - Gastric reflux - Colic - Diarrhoea (non infectious or clostridial) Diagnosis - History - Age - Clinical signs - Rule out other CNS diseases (e.g. meningitis which is rare and trauma, causes of renal failure and GI dysfunction - May have concurrent sepsis Management - Supportive - Many mildly affected foals will recover w/in 2-5 days with only supportive therapy Neuro management (more severe) - Anti-oedema therapy (e.g. mannitol, diuretics etc) - Anticonvulsants (e.g. diazepam, phenobarbitone, pentobarbitone etc) Renal management - Fluid diuresis - Dopamine CRI (to increase kidney perfusion) - Furosemide (CRI or boluses) - DMSO or mannitol GIT management - Limit enteral feeding - Reflux gastric contents - Prokinetics (e.g. lignocaine0 - Treatment for clostridiosis if present (e.g. penicillin) Prognosis - Good for those with mild signs - Not so good for those with severe neuro signs, or renal/GIT signs... |
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Flexural limb deformities
Laxity - Which joint is usually involved - What age foals is it common in - How do you treat it? Contracture - Why is this a problem? - How do you treat it conservatively? - How do you treat it surgically? |
Laxity
- Usually the fetlock involved - Common in premature foals - Many correct in a few days - If persistent, place heel extensions Contracture - Can prevent nursing leading to FPT, dehydration and weakness (they can't get up) - Conservative management = encourage weight bearing and ambulation, bandages/splints, toe extensions, analgesia, oxytetracycline (causes limb laxity) - Surgical management = DDFT desmotomy of accessory ligament, SDFT desmotomy of the accessory ligament |
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Angular limb deformities
What different deformities occur? |
Different types
- Valgus (lateral deviation) - Varus (medial deviation) Diagnosis - PE - Rads Note: you need to do something before the growth plate closes Growth plate closure times - Distal radius = 6mo - Distal MC/T 3 = 4-6weeks - Distal tibia = 6-8mo Conservative management - Confinement - Corrective hoof trimming - Valgus, lower lateral wall of hoof - Varus, lower medial wall of hoof - Corrective shoeing - Valgus, apply medial hoof extension - Varus, apply lateral hoof extension Surgical management - Growth acceleration (periosteal strip) - Valgus (strip lateral) - Varus (strip medial) - Growth retardation (using screws and wire or staples across physis, or a screw through the physis) - Valgus, place implants medially - Varus, place implants laterally - Implants must be removed to avoid over correction!! (i.e. going to need 2 surgeries) |
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Biosecurity
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Lecture 12
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What is the definition of biosecurity?
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Describes those procedures use to both prevent the intro of an infectious disease into an animal popn and control the spread of those infectious agents already present in the pon
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What are the 3 major components of biosecurity?
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1. General infection control practices and protocols whose goal is to prevent the spread of contagious infectious agents from animal to animal and from animal to human within a facility
2. Surveillance of the facility and/or animals within for particular infectious agents, with the aim of IDing enviro contamination and potentially averting outbreaks of disease 3. ID, investigation and management of disease outbreaks |
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What are the current equine infectious agents that are of biosecurity concern in Aus?
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- Enteric salmonellosis
- Enteric clostridiosis - Rotavirus infected foals - Crypto in foals - Equine herpes (resp, neuro and abortogenic) - Step equi var equi (strangles) - Hendra - Lyssa virus - Dermatophytosis - All equine exotic diseases - Agents that may infect immunocompromised animals or humans (e.g. rhodococcus equi) - MRSA |
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What factors are important in developing appropriate biosecurity strategies?
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- Type of organism and clinical signs of infection
- Appropriate diagnostic methods and treatment - Epidemiology of infections in your area - Assessment of virulence and level of contagion, patient morbidity/mortality rates - Modes of transmission - Ability to infect other species (including humans) - Ability to survive in enviro - Susceptibility to disinfectants - Existence of and methods of diagnosing carriers |
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What are some general infection control practices?
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- Attention to personal hygiene and other non-phamacologic methods of preventing disease spread are vital for infection disease control practices to be successful
- These methods should be employed during routine day to day activities with ALL patients (not just sick ones) - Patients may spread of acquire a contagious disease w/out being suspected of such by the vet E.g. - Patients in the incubation period - Patients with atypical clinical signs - Patients with sub-clinical infections or carriers - Patients that are at risk of developing an infection from their own flora or enviro |
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What are the 3 basic approaches that must be applied to control the spread of disease?
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1. Methods to decrease (or prevent) direct spread
2. Methods to decrease (or prevent) fomite spread 3. Methods to decrease enviro pathogen load |
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Discuss methods to decrease direct spread.
5 |
1. Physical separation
- House animals to be protected as far away as possible from those with a contagious disease - Do not admit a horse with a contagious disease to hospital unless they REALLY need the services. 2. Choose a site within a facility to isolate animals - Must be able to prevent direct contact with others - Must be able to prevent exposure of other horses to bodily fluids - Must be able to prevent exposure via common water sources (or run off) - Minimise human and vehicle traffic around them 3. All vet hospitals should have a designated area that can be used for isolation - Preferably an inside horse box than outside in the yard due to difficult disinfecting later on - Distance of necessary separation depends on pathogen 4. In some scenarios, decreasing pathogen spread by physical contact may involve quarantine of whole facility with restricted movements in and out of property 5. Golden rule = IF IN DOUBT, ISOLATE |
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Discuss methods to decrease fomite pathogen spread
4 |
1. Fomites represent one of the easiest methods to spread a disease
2. Most important thing to do is wash your hands 3. Clean clothes and footwear 4. Barrier nursing - Physical separation of patient - Provision of suitably sized transitional exclusion zone b/w dirty and clean areas - PPE - Use of disinfectant foot baths at entrance and exit - Provision of 1 hand washing facility in exclusion zone and another close to the exclusion zone to allow hand washing events after leaving the isolated area - Dedicated equipment to use in the dirty area - Protocols for movement of equipment in and out - Protocols for movement of patient in and out - Procedures for decreasing enviro load of infectious agent |
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Discuss methods to decrease enviro pathogen load
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1. Clean isolated areas during treatment of patient
- remove waste - Remove soiled bedding - Use barrier nurse procedures - Soiled bedding can be incinerated or composted 2. Thorough cleaning and disinfecting of areas contaminated by isolated patient - Clean all surfaces with soap or detergent to remove organic matter - Kill microorganisms with disinfectant Factors to consider when selecting disinfectant - Spectrum of activity - Activity with organic matter - Temp dependent? - Diluted with water, still as good? - Efficacy decrease with time once prepared? - Residual activity after drying? - Cost? - Easy to apply? - Toxic to people or animals or enviro? - Corrosive to surfaces or equipment? NEVER MIX DISINFECTANTS |
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What is the aim of surveillance?
What does it include? |
Aim
- To ID enviro contamination and potentially avert outbreaks of disease Includes - Enviro cultures and/or PCR facilities housing patients w contagious diseases after depopulating, cleaning and disinfection - important for organisms that are known to be either difficult to kill or able to survive in the enviro for long periods of time - Routine enviro testing for the presence of specific infectious agents - Routine testing of asymptomatic horses to ID carriers or shedders Often this is only implemented after an outbreak of a nosocomial infection |
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What specific things should you be aware of when it comes to an ambulatory vet?
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- Can spread b/w horse facilites
- Can lead by example with horse owners - Greatest risks are those that are difficult to kill with disinfectant or last for long periods (e.g. strangles, salmonella and rotavirus) - All biosecurity principles apply to the ambulatory vet Ambulatory vets should have the following with them at all times - PPE - Waterless hand washing product - Material to clean and disinfect reusable equipment of duplicates of such equipment - Biohazard bags for transporting dirty equipment - Disinfectant and hand pump to spray vehicle |
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What are some specific biosecurity policies for equine vet practice?
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- Must have a written biosecurity policy that outlines what steps to be taken when contagious disease is admitted to the hospital
Policy should be - Accessible to staff at all times - Tailored for individual space and most likely contagious organisms to come in - Revised periodically to reflect changes in prevalence of disease - Actually used |
