Periparturient losses in does and ewes Flashcards

1
Q

what is the periparturient period in sheep and goats?

A
  • 3 weeks before parturition until 3 weeks after = periparturient
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2
Q

Periparturient losses in ewes and does
* Common and important causes at the herd/flock level:

A
  • Pregnancy toxaemia (pre-parturient)
  • Vaginal prolapse (pre-parturient)
  • Gangrenous mastitis (post-parturient)
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3
Q

sheep abortion causes in does and ewes

A
  • Chlamydia abortus
  • Toxoplasma gondii
  • Coxiella burnetti (Q Fever)
  • Campylobacter jejuni (usually sheep, rarely goats)
  • Campylobacter fetus (sheep only)
  • Iodine deficiency abortion
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4
Q

Pregnancy toxaemia
- what do we see?
- etiology
- seen in who, usually?
- individual animal risk factors

A
  • “Twin lamb disease”
  • Presenting complaint: late gestation ewes or does off feed, down
  • Etiology: Insufficient energy in the diet to meet nutritional requirements of late gestation
  • Usually only seen in ewes/does with multiples – but this online is not sufficient to cause disease!
    <><><><>
  • Individual animal risk factors:
  • Thin (BCS < 2.5)
  • Fat (BCS > 4.0)
  • Any other disease causing a drop intake, or making it difficult to get to the feed (e.g. dental disease, CAE arthritis)
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5
Q

Pregnancy toxaemia
* Flock level risk factors:

A
  • Thin ewes/does due to inadequate energy in the diet, or inadequate energy
    density of the diet, and….
  • Competition (eg. not enough feeder space)
  • Poor water quality or quantity (decrease dry matter intake)
  • Held off feed (eg. for worming)
  • Shearing
  • Inclement weather
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6
Q

Pregnancy toxaemia - pathogenesis

A
  • Inadequate energy in diet
  • Transient hypocalcemia > encephalopathy (often irreversible)
  • Mobilization of lipid stores > elevation in ketone bodies, accumulation of lipids in liver cells, impairment of hepatic function
  • High levels of circulating corticosteroids
  • Fetal death and masceration
  • End stage renal and liver failure
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7
Q

Pregnancy toxaemia
– clinical findings
- progression?

A
  • 6 to 3 weeks before expected parturition
    <><>
  • Early signs: not up with the group, not aggressive to get to grain, grinding teeth
    <><>
  • Later signs:
  • Increasing depression, head pressing
  • Mild to sever optisthotonus/stargazing
  • +/-blindness
  • Fine tremors, ataxia, circling
    <><>
  • May see temporary improvement when fetuses die, but then becomes depressed, down, and comatose
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8
Q

Pregnancy toxaemia – lab diagnosis
- individual vs flock

A

Individual animal diagnostics:
* Positive on urine or blood ketones
* Elevated liver enzymes
* Elevated BHBA in serum
(> 0.8 mmol/L is subclinical threshold)
<><><><>
Flock/herd level diagnostics:
* Sample of ‘at risk’ animals for BHBA
* Normal < 0.7 mmol/L
* Moderate underfeeding = 0.8 - 1.6 mmol/L
* Severe underfeeding = 1.6 - 3.0 mmol/L
* Clinical preg tox typically > 3.0 mmol/L

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9
Q

Pregnancy toxaemia – post mortem

A
  • Fatty liver
  • Dead fetuses
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10
Q

Pregnancy toxaemia – treatment
for mild vs more severe cases

A

If still eating, but not eating grain (mild case)
* Can give 50mL 50% dextrose IV once
* Correct predisposing cause
* Isolate, make grain available
* 60mL glycol orally BID for 3-10 days
<><><><>
If not eating, or neurologic signs (moderate to severe)
* 50 to 100mL 50% dextrose IV once, or 5% drip
* IV fluids (supportive)
* Get fetuses out! (20mg dexamethasone + PG), c-section?
* Hypocalcemia? Give 60mL slow, 60mL SQ
* Antibiotics (penicillin)
* Euthanize if comatose or non-responsive

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11
Q

Pregnancy toxaemia – control

A
  • Address risk factors to prevent more cases
  • Nutrition should be appropriate for energy needs
    > Analyze forages, supplement where needed with grain
    > Feed according to body condition score
    > Scan for fetal numbers
  • Manage feeding to allow for needed consumption
  • Prevent diseases that can reduce intakes
  • Ensure producer is able to recognize and treat disease early
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12
Q

Vaginal prolapse
- when we see it?
- etiology?
- epidemiology / prevalence

A
  • Presenting complaint: 2 to 3 weeks pre-lambing, intermittent or constant prolapse of vagina
  • Etiology: complex, related to risk factors
  • Epidemiology: more common in sheep, normal incidence < 1%, but outbreaks can be up to 25%
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13
Q

Vaginal prolapse
* Risk factors (individual animal)

A
  • Previous history of vaginal prolapse
  • Over conditioned
  • Multiple fetuses
  • Genetics
  • Short dock length (damage to anal musculature)
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14
Q

Vaginal prolapse
* Flock level risk factors:

A
  • Poor quality forage
  • Crowding at the feeder
  • Metabolic disease
  • Plant or mycotoxin estrogenic compounds?
    > Red clover, diseased alfalfa, zeralenone from fusarium in corn
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15
Q

Vaginal prolapse
* Clinical findings

A
  • Intermittent initially
  • Severe may include rectal prolapse, partial uterine prolapse and/or bladder
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16
Q

Vaginal prolapse
* Treatment:
- and control

A
  1. Administer epidural
  2. Replace vagina
    * Wash with non-irritating soap
    * Check for bladder, uterus
    * Elevate hind end if necessary
    * Gently replace
  3. Vaginal spoon
    * lamb over top of the spoon
    * Irritating
  4. Suture vulvar lips (umbilical tape)
    * Must watch very closely
    * Risk of dystocia, tearing, infection
    <><><><>
    * Control – related to risk factors
17
Q

Gangrenous Mastitis
- other name?
- presenting complaint, timing
- agents
- epidemiology, who gets it?

A
  • ‘Bluebag’
  • Presenting complaint: 2 to 4 weeks post-partum, occasionally at weaning, down, dead, lame
  • Etiology: Staph. Aureus (most common), Mannheimia haemolytica, occ. Pseudomonas aeruginosa
    <><><><>
  • Epidemiology:
  • Sporadic within a flock, but may have high prevalence within a group
  • Nursing animals: skin infection, orf, aggressive nursers, M. haemolytica present in lambs nasopharynx
  • Dairy animals: contagious infection (similar to dairy cows)
  • Associated with high stocking density
18
Q

Gangrenous Mastitis
* Clinical findings

A
  • Febrile (> 40C)
  • Off feed, depressed
  • May be lame, commonly down
  • Udder cold, discolored blue, bloody/serum-y secretion
  • If they survive, the affected half of the udder will slough off
19
Q

Gangrenous Mastitis
- dx
- PM

A
  • Laboratory diagnosis via milk culture
  • Post mortem findings: toxaemia, gangrene of udder (may extend beyond)
20
Q

Gangrenous Mastitis
* Treatment
* control

A

Treatment
* Usually too late to save the gland/udder
* Supportive treatment aims to save the animal
* Fluids, systemic antibiotics, NSAIDs
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Control
* Nursing animals:
> Control stocking density (>2 sq meters per ewe/doe)
> Control Orf
> Tilmicosin at weaning or 1 month prior to lambing (sheep ONLY)
* Dairy animals:
> As for dairy cows

21
Q
A
22
Q

Abortion
– common causes
- which are zonnotic?

A
  • Chlamydia abortus (both)
  • Coxiella burnetii (Q Fever) (both)
  • Toxoplasma gondii (both)
  • Campylobacter jejuni (sheep, rarely goats)
  • Campylobacter fetus (sheep)
  • Iodine deficiency abortion (both)
  • ALL INFECTIOUS CAUSES ABOVE ARE ZOONOTIC
23
Q

Chlamydia abortus
- what type of abortions
- lesions
- signs
- spread
- progression / pathogenesis?
- control?

A
  • Fresh abortions
  • Severe placentitis
  • Stillbirths, weak kids/lambs, open ewes/does
  • Infected through aborted materials
  • No pathology until pregnant (50 to 100 day incubation)
  • If infected late gestation –> abort next pregnancy
  • If infected as lambs/kids–> abort first pregnancy
    <><>
  • Control
  • Oxytetracycline injection every 14-21 days after 80 days gestation
  • Vaccination, start with replacements
    <><><><>
  • ZOONOTIC
24
Q

Coxiella burnetii (Q Fever)
- type of abortions / issues?
- lesions
- spread
- control

A
  • Fresh abortions, stillbirths, weak lambs/kids
  • Severe placentitis (intercotyledonary)
  • Infected through fetal fluids, milk, feces
  • Aerosol route of transmission most common
    <><><><>
  • Control–> tetracycline as per Chlamydia, but not as effective
  • Control–> vaccine available, needs import permit, takes 4-5 years to lower flock level shedding
  • ZOONOTIC
25
Q

Toxoplasma gondii
- spread?
- signs / issues
- lesions
- control

A
  • Cats infected through eating rodents, birds, aborted material
  • Pass oocysts which contaminate feed
  • Mummies, abortions, stillbirths, weak/small lambs/kids
  • Coteledonary lesions
  • Control–> cat and rodent control (difficult!), protect feed from contamination with feces
  • Control–> feed monensin or decoquinate during last 14 weeks of pregnancy
  • ZOONOTIC
26
Q

Campylobacter
- transmission
- incubation, presentation
- lesions
- treatment
- prevention

A
  • Infected through aborted fetuses, placenta
  • Carrion birds, contamination of feed from birds?
  • Incubation 7 to 60 days, average 14 to 21 days, so can often appear as a ‘storm’
  • Lesions on liver of fetus, areas of necrosis, fibrin
  • Mild placentitis, edematous cotyledons
  • Antimicrobials in the face of an outbreak (not if C. jejuni – oxytetracycline is not effective, there is a resistant clone)
  • Vaccination available for C.fetus
  • ZOONOTIC
27
Q

Iodine deficiency abortion
- type of abortions
- signs? lesions?
- control

A
  • Late term abortions, stillbirths, weak lambs/kids
  • Large thyroids, less hair
  • Control–> paint tincture of iodine on skin of ewes weekly, supplement iodine throughout gestation, ensure salt being fed is available to all animals
28
Q

Take home messages
* Common diseases occurring during the periparturient period (3 weeks pre- to 3 weeks post- lambing/kidding) include:

A

pregnancy toxaemia, vaginal prolapse, gangrenous mastitis, and abortion

29
Q

Take home messages
* Pregnancy toxaemia – late gestation
> pathogenesis
> control
> presentations, treatment, prognosis
> dx?

A
  • Energy deficit potentiated by muptiple fetuses (inc. demand) also taking up
    more space in the abdomen (less capacity for feed in the rumen)
  • Need a well formulated ration appropriate for the animal (BCS, # of fetuses)
  • Mild symptoms = off feed, dull à treat with glycol, can give dextrose IV
  • Severe symptoms = neurologic, down à these have a poor prognosis
  • Test blood with BHB meter (glucometer) using ketone strips - ≥ 0.8 = ketotic
30
Q

Take home messages
* Vaginal prolapse (pre-lambing/kidding)
- who gets it? presentation
- risks
- treatment

A
  • More common in sheep, normally < 1% but can have ”outbreaks”
  • Risk factors = prev. prolapse, overconditioned, multiple fetuses, short dock length (tail), poor quality forage, crowding at feeder
  • To fix, give an epidural, then replace and use a spoon or suture
  • A spoon is preferred as they can lamb over top (v. suture)
31
Q

Take home messages
* Gangrenous mastitis (post-lambing/kidding)
- pathogen
- presentation
- tx
- prognosis

A
  • Typically Staph aureus
  • Acute presentation, may be dead, down, dying (septic) – fever, off feed, cold blue udder
  • Treatment is based on saving the animal: antibiotics, NSAID, fluids
  • If they survive, the affected half of the udder will slough off
32
Q

Take home messages
* Abortion
* Common causes include:
- nature of abortions?

A

Chlamydia, Toxoplasma, Q-fever (Coxiella), and
Campylobacter – all infectious and zoonotic!
* A non-infectious and non-zoonotic common cause is Iodine deficiency (goiters, hairless lambs/kids)
<><><><>
* Chlamydia: fresh abortions, severe placentitis, vaccine available
* Toxoplasma: mummies, cotyledeonary necrosis, infected via oocysts in cat feces
* Q-Fever: similar presentation to Chlamydia, vaccine available
* Campylobacter: mild placentitis, C. jejuni often multi-drug resistant, often a ‘storm’ in a single lambing/kidding period