Diseases and reproduction of swine Flashcards

1
Q

Peri-Natal losses in piglets

A

Farrow - 3days
50% of losses in this time

Hypothermia

  • no brown fat
  • 30-35 degree optimal temp (environmental)
  • farrow house (18-20 degrees) –> uterus (30-35 degrees)
  • glucose is used to maintain BT as shivering uses glucose this causes positive feedback

Hypoglycaemia

  • result of low glycogen stores in liver
  • inability to suckle, usage of stores from shivering in cold
  • apply milk or intraperitoneal glucose solution (4-6 hrs)

Splay leg

  • multifactoral (nutritional, environmental, genetic, infectious)
  • seen as dog sitting and inability to rise
  • lack of suckling –> hypoglycaemia
  • tie legs (5-8cm) and massage

Congenital tremor - myoclonia congenita

  • genetic, circovirus-2, poisoning/toxins
  • 2 Types
  • -A - brain/SC lesion
  • -B - No brain/SC lesion
  • usually improves with age, however if severe can inhibit suckling
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2
Q

Peri-Natal losses in piglets

A

Farrow - 3days
50% of losses in this time

Hypothermia

  • no brown fat
  • 30-35 degree optimal temp (environmental)
  • farrow house (18-20 degrees) –> uterus (30-35 degrees)
  • glucose is used to maintain BT as shivering uses glucose this causes positive feedback

Hypoglycaemia

  • result of low glycogen stores in liver
  • inability to suckle, usage of stores from shivering in cold
  • apply milk or intraperitoneal glucose solution (4-6 hrs)

Splay leg

  • multifactoral (nutritional, environmental, genetic, infectious)
  • seen as dog sitting and inability to rise
  • lack of suckling –> hypoglycaemia
  • tie legs (5-8cm) and massage

Congenital tremor - myoclonia congenita

  • genetic, circovirus-2, poisoning/toxins
  • 2 Types
  • -A - brain/SC lesion
  • -B - No brain/SC lesion
  • usually improves with age, however if severe can inhibit suckling
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3
Q

Post-natal losses in piglets

A

Anaemia

  • low Fe in sow milk and low stores in piglet
  • Cs anaemia
  • fe supplement

Thrombocytopaenic purpura (maternal isoeryhtrolysis)

  • 7-10 days after colostrum intake –> clotting issues and purpura –> cyanosis and hburia
  • give colostrum from surrogate
Greasy pig - exudative skin 
-staph hyicus 
-skin commensal --> fighting or tail docking 
- toxins --> liver + kidneys 
Cs: greasy dark exudative skin 

Purulent dermatitis

  • Staph/strep pyogenes
  • small vesicles with pus

Hypotrichosis cystica suis

  • large vesicles on the back and ears with coiled hairs inside
  • usually self limiting –> severely affect sebaceous Glands removed

Pityriasis roseca

  • high incidence in landrace breeds
  • usually harmless skin rash
Nutritional 
-hypo Vit A: muscle development and hydrocephalus
-hypo Vit E: Mulberry heart disease 
Hypoglycaemia
Anaemia
Mycotoxins 

Infectious gastroenteritis

  • e.coli, corona/rota, eimeria, strongyloides + ascaris
  • Cs of GE

Infectious arthritis

  • mycoplasma hyosynoviae
  • Cs of arthritis
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4
Q

Nutritional, physical and chemical skin diseases

A

NUTRITIONAL
Fat deficiency
-scaly dermatitis

Sodium deficiency
-illthrift

Fe + Co deficiency

  • anaemia (co - transport of Fe)
  • pale skin + cyanosis

Zn deficiency

  • cant absorb P from phytic acid in plants
  • P binds Zn in gut to absorb
  • parakeratosis

Vit E + Sel
-dermatitis

Vitamins

  • B1: exudative dermatitis
  • B2: resembles greasy pig
  • B3: parakeratosis
  • B5: dermatitis
  • A: sebborrhic dermatitis
PHYSICAL
photosensitivity 
-Photodynamic agents --> UV sensitivity 
-plants or fungi (phytomyces)
-long drug use (oxytetracyclines or sulphonamides)

Sunburn

  • behind ears
  • offer cover/mud

Trauma –> (Auth)heamatoma
-higher incidence in mixed age, sex, breed

Pressure sores

  • joint and teats highest incidence
  • apppropriate bedding

Frost bite
-esp. teats

CHEMICAL
Contact dermatitis
-toxins, sprays, bedding, oil/fuel
-Oil (Naphtalenes) –> hypertrophy and keratinisation

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5
Q

Viral skin diseases

A

FMD (aphtovirus)

  • vesicles –> teats, coronary band, mouth
  • Rapid DDX required
  • OIE + emergency vaccine
  • Survailance and destruction zones

SVD (enterovirus)

  • Only coronary bands not found on teats or in mouth
  • sudden lameness
Vesicular exanthema (circovirus)
-Similar to FMD + SVD but deeper infiltration + granulation

Vesicular stomatitis (vesiculovirus)

  • spread by biting insects (heamatopinus suis)
  • Found in mouth and on coronary bands
  • far less infective than FMD (fewer pigs in herd affected)

Suispox

  • poxvirus
  • spread by biting insects (heamatopinus suis)
  • vesicles with straw coloured contents on ventrum (where lice bite)

Papillomatosis
-Sexually transmitted + rare

Parvoviral dermatitis
-Vesicular disease –> snout + CB

Porcine dermatitis and nephropathy syndrome

  • PCV-2 or Pasturella multocida
  • looks like CSF with purpural lesions on the body and ears

CSF + ASF
-purpura on ears and back

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6
Q

Bacterial skin diseases

A

Necrotic ear disease

  • erysipelas + salmonella (unconfirmed)
  • necrotic pinnae
  • infection through wounds (biting)

Ulcerative spiroceatosis

  • borellia suis
  • ulcerative and purulent dermatitis

Malignant oedema
-clostridium septicum
-anaerobic (deep wounds) –> inoculation –> toxins –> oedema –> ischemia –> necrosis –>gangrene
-necrosis and skin sloughing –> black muscles
T: metronidazole + mycins

Greasy pig disease 
-staphylococcus hyicus 
-Toxins--> Kidneys + liver
-greasy + flakey skin especially piglets and weanlings 
T: mycins, oxytetracycline 
Diamond skin disease 
-erysipelathrix rhusiopathiae 
-2 froms - arthritic + cardiac 
CS: diamond black skin lesions 
T: penicillin + Vancomycin (aerobic gram +)
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7
Q

Mycotic, parasitic and neoplastic skin disorders

A
MYCOTIC 
Dermatophytosis (ringworm)
-microsporum nanum
-trychophytoon verucosum
Most spread by rodents 
Cs: small red alopetic lesions (resembles ptyriasis rosesca)
Dx: scrape T: fluconazole, limesulfer 
PARASITIC 
Lice (pediculosis)
-heamatopinus suis 
-sucking lice 
-blood loss and high burdens 
-spread mycoplasma + suispox 
-Dx: tape/scrape T:ivermectin
Mites
-Sarcoptes scabei 
-burrowing mite 
-Cs: 
--acute - pruritis and head shaking 
--chronic: Waxy ears and thickened skin
Dx: deep scrape 
T: ivermectin 

Demodex - unimportant

Flies 
Biting flies 
-stomoxys (stable), similidae (black)
-irritations and dermatitis 
-spread mycoplasma + pox

Myasis

  • calliphora (blow)
  • cochlimya (screw)
  • flies lay engs in deep mounds –> larvae eat flesh
  • can see larvae in wounds

Ticks
Unimportant in pigs

NEOPLASIA
melanoma
Hgh incidence in large white + saddleback
highly malignant proliferation of melanocytes
T:excision

GENETIC
epitheliogenesis imperfecta 
-often seen on legs and flank 
-if severe = death 
-T: time (skin may grow), grafts 

Pityriasis rosesca

  • landrace
  • Purpural lesions all over the body
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8
Q

Viral respiratory diseases

A

2 Categories
1 - lots of pigs infected but usually self-limiting (PRRS, PCV-2)
2 - high morbidity and high economic importance (Atrophic rhinitis)

PRRS (PRRS virus)
-sow - reproductive symptoms (abortion, mastitis, anoestrus)
-piglets and growers - respiratory
-destroys MO’s –> IS
-Cs: signs of pneumonia
-Chronicity = wasting + pneumonia
co-infections –> complications of pneumonia –> death

Swine flu (orthomyxovirus)

  • H1N2 H1N2 H3N2
  • 100% morbidity 1% mortality
  • HIT

Aujesky’s (SHV-1)
respiratory signs in adults (replicates in URT)
develops to CNS issues in young

inclusion body rhinitis (cytalomegalovirus)

  • rhinitis + brown occular discharge
  • 3 wks of age highly susceptible
  • IB in nasal biopsy

Reovirus
-Enteric, respiratory, reproductive

Porcine Respiratory and neurological syndrome (Henipavirus)

  • fruit bats transmit
  • barking dogs
  • encephalitis

RRDS (PorcRespDisSyn)

  • multi factorial
  • -Infectious, environmental, genetic, husbandary
  • inf: atrophic rhinitis, PRRS, flu
    husbandry: density of herd, vaccination and hygiene
    environment: ventilation, cleanliness
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9
Q

Bacterial + parasitic respiratory diseases

A
Enzootic pneumonia (mycoplasma hyopneumoniae)
- usually harmless infection unless co-infection occurs 

Atrophic rhinitis

  • co infection of mycoplasma + one other agent
  • destruction of turbinates through toxin disruption of osteoblasts in nose
  • 2 forms
  • -non-progressive: bordatella or ammonia
  • -progressive: pasturella toxins (commensal)

necrotic rhinitis
-fuscobacterium necrophorum
-damage to roof of mouth, commensal of mouth invades nose –> purulent rhinitis
Cs: swelling of nose, purulent discharge
DDx: atrophic (shrunken nose), necrotic (swollen nose)

Pasturella multocida
-commensal of nose that can contribute to enzootic pneumonia, PRDS, atrophic rhinitis

Gässers diseases - heamatophilus parasuis)

  • Attacks epithelium (is commensal) of lungs, joints and reproductive tract
  • if sow infected mAb –> piglet unaffected
  • if infected after clearance of mAb’s (3-6months) = severe disease

Tuberculosis

  • Mycobacterium bovis, avium, paraTb
  • Bovis - caseous lesions
  • avium - granulomatous reaction
  • Generalisation
  • -early = milliary form
  • -late = tubercule form
  • Dx: acid fast (ZN stain)

Actinobacillosis

  • A. pleuopneumonia
  • commensals that produce toxins that damage the lungs
  • PM:characteristic darkened and ulcerative lungs

staphylococcus suis

  • High mortality in piglets
  • usually a commensal
  • can cause speticaemia and polyvalent organ failure (including pneumonia)
PARASITIC 
-metastrogylus elongatus 
-earthworm is IH 
-lung worm --> cough --> swallow --> GIT --> eggs
Dx: floatation 
T: Albendazole
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10
Q

Non-infectious, Infectious and neoplastic diseases of the heart

A
NON-INFECTIOUS 
Mulberry heart disease 
-Vit E + Selenium deficiency 
-myocardial degeneration 
-Cs: pale, dyspnea, lameness
seen in piglets 
PM: Nutmeg liver
CONGENITAL 
PDA
Valve insufficiencies 
ToF
Atrial + ventral septal defects 
PAA
INFECTIOUS 
Oedema disease 
-E.Coli 
-10 day piglets
-toxin --> vascular contraction --> hypertension --> bleeding + oedema (GIT + CNS)
Cs: oedema + bloody D

Actinobacillus Suis
-Suis –> endocarditis + polyarthritis

Viral encephalitis (Cardiovirus)

  • Myocardial degeneration
  • PM: yellow foci on heart
  • encephalitis + repro failure

Erysipelas

  • E. rhusio
  • Acute: Diamond skin disease
  • chronic = endocarditis + arthritis

CSF (pestivirus)

  • transmitted contact, vertically or sexually
  • Offspring born after transplacental –> carrier and shed continuously
  • Lethal hemorrhagic disorder seen as cyanotic ears, erythema, purpura, bloody D+, abortion
ASF (asfavirus)
-as CSF + ticks and insects
-DDx:
--CSF :cheese (necrotic) tonsils 
--ASF: Marbled LN's + splenomegaly 
T: Cull + OIE + servaile and destroy  

BVDV + Boarder disease
-pestivirus similar to CSF

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11
Q

Diseases of Blood and Lymph

A
BACTERIAL 
ulcerative lymphangitis 
-streptococcus porcini 
-contact with abscess infect
-replicate in tonsils --> LN's
Cs: lymphangitis 
T: clindamycin, vancomycin, penicillin 

Erythropozoonosis
- mycoplasma suis
-originally thought to be ricketsia now known to be mycoplasma
-spread but biting insect (H.suis, flies)
-causing heamolytic anaemia
-Dx: ZN stain (acid fast - seen inside rbcs)
T: macrolides, oxytetracycline, floroquins

Anthrax - bacillus anthracis

  • spores ingested from the soil
  • anthratoxins cause clotting issues –>DIC, internal bleeding, anaemia, jaundice

Salmonella

  • S. cholera-suis, dublin
  • septicaemic form of salmonella
  • clotting issues (DIC), petichae, splenomegally (no lesions)
  • DDx from CSF w/ no lesions on spleen

PARASITIC

  • Babesia trautmanni (L), perroncitoi (S)
  • transmitted by rhiphicephalus tick
  • piroplasmids work by infecting rbcs, multiplying and causing heamolysis –> anaemia, Hburia and jaundice
  • Dx: Giemsa Blood smear
  • T: imidocarb
NEOPLASIA 
Lymphoma 
-uncontrolled division of lymphoid tissue such as that found in LN's 
-Cs: Enlarged LN's 
Dx: biopsy 

Leukosis/leukaemia
-uncontrolled division of leukopeitetic tissue such as bone marrow
-increase in abnormal WBC’s
-

NUTRITIONAL
Fe, Cu, Co deficiency
-Cu + Co play role in transport and absorption of Fe
-lack of any can result in Fe deficiency anaemia
-10-14 days post partum (colostrum is low in Fe, piglets have stores)
-Dx: <8g Hb/100ml of blood = anaemia
-Physiological = 9-15g Hb/100ml
-T: IM Fe dextran

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12
Q

Non-infectious diseases of mouth, oesophagus and GIT

A
MOUTH 
Stomatitis 
-peridontal disease 
-poor tooth clipping --> trauma 
-glossitis, gingivitis 

Cleft lip / Cleft palate
-dysphagia

OESOPHAGUS
obstruction
-anatomical: dysgenesis
-mechanical: stricture, diverticulum (T/F), rupture, neoplasia (intra,extramural)
-functional: MG, Megaoesophagus
-Cs: regurgitation (not V+), dysphagia, gagging

STOMACH
Gastric ulceration
-sows + growers
-dietary due to low protein and fibre + high fat
-finely ground feed
-stress and environmental temperature fluxuations
-if chronic: anaemia, melana, hematemesis
-may result in scarring and stricture of hiatus oesophagii

GIT 
ileus 
-anatomical: atresia anii, dysgenesis 
-mechanical: stricture, hernia (incarceration/strangulation), intussusception, obstruction (constipation, torsion)
-functional: loss of peristalsis 

Torsion

  • occurs in sows + growers
  • usually due to increased abdominal space post partum
  • depending on degrees determines severity (>180 is dire)
  • Cs: V+, obstipation/constipation, dehydration

herniation

  • Direct: touching skin = adhesions
  • indirect: covered by peritoneum or tunica vaginalis = no adhesions
  • Umbilical: most common, usually congenital or can be due to high abdominal pressure (cough, D+, farrowing)
  • Inguinal: mostly male due to failure of inguinal ring closure after descension of testes

Constipation

  • dry feed or dehydration
  • dried bolus of digesta stuck in the GIT
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13
Q

Viral diseases of GIT

A
CORONAVIRUS 
Viral gastroenteritis/transmissible gastroenteritis 
-Mostly sows 
-villous atrophy --> malabsorptive D+
-PM: villi atrophy 

Enzootic viral D+
-similar to VGE/TGE however less common as herds build immunity quickly and it is passed to offspring

V+ and wasting disease
Rare. clinical only in <4days old
V+ and D+ —> develop in CNS issues (encephalitis)

ADENOVIRUS 1-4

  • 1+4 are most common
  • Inclusion body enteritis
  • IB’s found in PP’s
  • D+, illthrift

PCV-2
Post-weaning multi-systemic wasting syndrome
-common in piglets as passed to them via mother (feeding + bedding)
-Cs: wasting, D+, ulcers

ROTAVIRUS

  • Usually of low clinical signifcance unless co-inf with E.Coli
  • Yellow pasty D+

CSF/ASF
-button ulcers on GIT (CSF), Heamorrhagic D+ (ASF)

BVDV + Boarder disease

SEMDI

Teschen disease

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14
Q

Bacterial diseases of GIT

A
SPIROCHAETS 
Intestinal spirochaetosis (Brachyspira pirosicoli)
-destruction of mucosa --> malabsorptive D+
Swine dysentery (Brachyspira hyodysenteriae)
-destruction of LI mucosa --> malabsorptive D+
Hypertrophic enteropathy (Lawsonia intercellularis) 
-invades LI and causes hypertrophy of mucosa resulting in lowered absorption --> watery D+

SALMONELLOSIS
s. cholerasuis, typhimurium, typhisuis
-Typhimurium - enteritis
-cholerasuis - enteritis + septicaemia
-typhisuis - necrotising enteritis
-seen as profuse watery/bloody D+ as well as necrotising proctitis
Multiple Dx samples - intermittent shedding

E.COLI

  • enterotoxaemic form (0175) - released toxins causing –> water into GIT –> yellow/green D+
  • heamorrhagic form (OEDEMA DISEASE) - hypertension in GIT arterys –> odema –> necrosis –> melana
  • VACCINATE

OTHERS
Clostridium perfringes C
-young at highest risk
-bloody D+

Campylobacter coli, jejuni

  • commensal that takes hold in immunosuppressed piglets
  • profuse watery D+

Yersinia pseuoTB, enterocolitica
-PTB: diffuse ulceration of GIT
-EC: Profuse D+
DDx: cross reacts with brucella

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15
Q

Parasitic + Neoplastic diseases of GIT

A
PARASITIC 
Giardia duodenalis 
-F-O 
-trophozoites attach to SI mucosa and damage 
-Malabsoptive D+
-Faust float 
-Metro 

Eimeria pomoni

  • 2cyst 4 zoites
  • Villous atrophy caused by endogenous mesogony
  • F-O
  • Dx: float
  • T:baycox (toltrazuril)

Isospora suis

  • 2 cysts 4 zoites
  • F-O
  • Seen as GIT form but can also cause CNS signs in young
  • float
  • T:
Cyrptosporidium parvum 
-Water, food, opportunistic, zoonosis 
-auto-infection can occur (20%/80% - thin/thick shells)
-Atrophy in LI --> watery D+
Dx: ZN acid fast stain
T: nitazoxamide 

Balantidium coli

  • LI
  • Grey D+
  • T: sulphonamides

Strogyloides ransomii
-skin, transmammary, ingestion
-burrows into SI mucosa damaging it –> D+
Dx: float T:benzi

Hyostrongyulus rubidus

  • burrows into STOMACH
  • ingestion, transplacental and mammary
  • hypobiosis until pregnant or lactating
  • forms nodules –> malabsorption
Ascaris suum
-Ingest --> hepatopulmonary migration 
-Worms + beetles acts as PH
-PM: Milk spots on liver 
Cs: respiratory 

Trichuris suis

  • whipworm –> ingest egg
  • burrow into mucosa of LI
  • Bloody D+

Oesophagostomum dentatum
-burrowing forms nodules

Macracanthorhynchus hirudinaceus

  • acanthocephala
  • cockroach IH
  • Hemorrhagic D+ due to mucosa burrowing
  • can cause peritonitis

NEOPLASTIC
Papilomabirus
-can cause papules in mouth or around anus

Hypertrophic lawsoniosis

  • lawsoni intercellularis
  • replaces muscosa with adenomatous tissue
  • crypt hyperplasia and villous atrophy
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16
Q

Diseases of the Liver, Spleen & pancreas

A

Anthrax - Bacillus anthracis

  • spores ingested
  • releases toxin that attacks muscles or heart and skeletal muscles, blood vessels and liver
  • resulting in hemorrhage and oedema of liver
  • Chronic form (acute is Ru)
  • Cs: haemorrhagic disathesis
  • Dx: no rigor mortis, blackberry jam spleen, no clotting
  • T: tetracyclines

Ecchinococcosis

  • E. granulosus or multilocularis
  • Granulosus - hydatid cyst
  • multilocularis - buds
  • affinity for liver + lungs
  • cyst formation destroys parenchyma
  • Dx: floatation
  • T: Albenadzole

Cysticercosis

  • cysticercus cellulose
  • forms cysts in liver and spleen

Ascaris suum

  • Hepatopulm migration
  • milk spots on liver
  • heavy infection can block the bile duct

Fatty liver

  • high fat diet
  • lipid deposits in the liver as fat is too high in diet
  • T: dietary changes + Vit A

Hepatosis dietica

  • Vit E + Selenium deficiency
  • excess Vit A
  • free radical formation –> necrosis of parenchyma
  • Cs: Jaundice, ascites, cardiomegaly
  • Dx: AST, ALT, GGT, Glu Dehydro
  • T: supplement

Yersinia pseudoTb
-Diffuse abscessation on liver + spleen

NEOPLASIA
cholangiosarcoma
hemangiosarcoma

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17
Q

Diseases of urinary system

A

PCPC - Porcine cystitis-pyelonephritis complex (PCPC)

  • actinobacillus suis, e.coli
  • ascending uti
  • pig has wide ureter and alkaline urine (good conditions for bacterial growth)
  • red-brown urine
  • Cs: heamaturia, stranguria, casts, urine pH (7-8),
  • Dx: culture of bacteria in urine, USG

Porcine dermatitis and nephropathy syndrome (PDNS)

  • PCV + PRRS indicated
  • Ag-Ab complexes deposited causing damage
  • seen as strang/oliguria, haematuria, petichiae or cyanosis of ears

Glomerulonephritis

  • Drugs, infection (CSF, PDNS)
  • Ag-Ab
  • damage to glomerulus –> decreased GFR
  • Cs: oedema, polyuria, oliguria
  • Dx: hypoproteinaemia, proteinuria, creatinine, BUN
  • T: Fluid therpy

Interstitial nephritis

  • Usually leptospirosis
  • lepto Ag’s accumulate on kidneys
  • white spotted kidney

Embolic nephritis

  • Septic (bacterial) emboli (actinobacillus, erysipelas)
  • Microabscesses
  • blocks blood flow to kidneys –> ischemia
  • necrosis occurs due to lack of blood

ischemic tubular necrosis

  • usually associated with prolonged hypotension/shock
  • types of shock: hypovolemic, septic/endotoxic, cardiogenic

nephrotoxic tubular necrosis

  • Nephrotoxic substances act on the tubule of the kidney
  • Mycotoxins - aflatoxin (aspergillus)
  • Drugs - sulphonamides
  • heavy metals - lead, arsenic
  • Toxins/chemicals

Hydronephrosis

  • dilation of renal pelvis due to obstruction of urine outflow
  • dilation compresses parenchyma –> atrophy

Urolithiasis

  • stones formed in the ureters/urethra
  • Ca:P balance
  • acidity of urine
  • stranguria/oliguria, haematuria
  • results in hydronephrosis if complete obstruction

Stephanurus dentatus

  • kidney worm
  • SI –> LN –> peritoneal cavity –> liver –> kidney
  • encysts in the kidney and sheds –> spreading in urine
  • Cs: stranguria, haematuria
  • Dx: urinalysis
  • T: benzimidazoles

NEOPLASIA
Nephroma/nephrosarcoma

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18
Q

Disorders of Ca and P metabolism

A

CALCIUM

  • Increased by: PTH (release from bone and kidney retention) + Vit D3 (increases absorption from GIT)
  • decreased by Calcitonin (increased bone absorption and down regulates Ca retention)

PHOSPORUS

  • In relationship with Ca especially in bone
    1. 6:1 - Ca:P

Rickets

  • Seen in juvaniles due to low Ca or Vit D
  • leads to bowing of bones and depletion in the quantity of bone present
  • may lead to fail of growth plate fusion

Osteomalacia (downer sow)

  • decrease is quality of bone even though there is a regular amount. Lack of mineral portion.
  • Seen in adult with chronic low Ca, P or Vit D3
  • increased demand - lactation/gestation
  • increased elimination from bone - HyperPTH
  • decreased absorption - hypovitaminosis D
  • Cs: generalise pain, lameness
  • Dx: serum Ca + P

Osteoporosis

  • Decrease in the quantity of bone causing larger holes in trebeculae
  • Cs: Non-painful, lameness
  • Dx: Serum Ca + P maybe normal
Osteofibrosa dystrophia 
-Severe calcium deficiency 
- Ca:P 1:2
-Mineralised bone is replaced with fibrous tissue due to chronic low levels of calcium 
-

Perpurial tetany/eclampsia

  • Increased excitability of neurons to sodium = tetany
  • caused by low Ca or Mg (Mg is calming)
  • often occurs in sows 7 days before or after farrowing due to large demand for calcium in gestation and lactation respectively.
  • Dx: dyspnea, recumbency, hyper-reflexive limbs

Nutritional tetany

  • Deficiency in dietary Ca, Vit D3, P, Mg or too much Fe
  • As above but due to decreased absorption maybe due to kidney issues, lack of vit d, enteritis, or pure lack of intake in diet.

Post-partum Hburia

Enzootic calcinosis

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19
Q

Trace element disorders

A

Fe

  • Def: diet, absorption, transport (Cu transports Fe)
  • -Hb synthesis impairment
  • Ex: Iatrogenic supplement
  • -Oxidative damage to cells –> Trembling/bruxism

Cu

  • Def: Diet, Molybdenium toxicity (binds Cu)
  • -Neurotransmitter synthesis –> enzootic ataxia
  • Ex: over ingestion
  • -Accumulates in liver –> oxidative damage –> haemolysis
  • -Signs of liver damage and haemolytic anaemia

Co

  • Def: dietary
  • -use to form Vit B12 –> folate metabolism –> RBC maturation –> macrocytic anaemia
  • -Use to binds FA’s –> Fatty liver
  • Ex: Energy production
  • -anorexia, alopecia

I

  • Def: Legume diet (goitrogen)
  • -essential for thyroid hormone –> cant control metabolism –> goitre
  • -Reproductive failure + peri-natal mortality of piglets
  • Ex: rare
  • -suppresses thyroid gland –> impaired growth + reproductive failure

Mo

  • Def: Sulfur and copper toxicity (binds Mo)
  • -Damages liver –> jaundice
  • Ex: low sulfur or copper diet (cant bind Mo)
  • -illthrift

Mg

  • Def: excess Ca + P (inhibits absorption of Mg)
  • -Reproductive failure and ricketts

-Ex: Disrupts Fe absorption –> anaemia

Zn

  • Def: Concentrate feeds often lack Zn
  • -Paraketosis, alopecia + swollen joints
  • Ex:Ingestion
  • -zn forms salts in liver and kidney –> haemolysis

Sel
-Def: Low dietary intake or excess sulfur (Sel replaces in AA’s)
–Muscle degeneration –> calcification of muscle (White muscle disease - especially in the myocardium)
Dx: CK + AST (muscle enzymes)

  • Ex: WMD therapy iatrogenic cause
  • -Selenium replaces Sulfur in AA’s –> impaired cell function
  • -Acute: Neurons –> blindness and ataxia (blind staggers)
  • -Chronic –> (keratinocytes most affected) –> loss of hair and claws
  • -T: Give sulfur

Dx: Serum blood levels
T: supplementation/elimination/chealating agent (EDTA)

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20
Q

Disorders of vitamin metabolism

A

WATER SOLUBLE
B
-1: Cerebro-coritcal dysgenesis
-2: Skin and eye eruptions and lesions and reduced fertility + abortion
-3:Crabohydrate metabolism –> fat used instead –> hepatosis dietica
-5: Locomotory issues + goose stepping
-6: AA metabolsim –> CNS issues + death
-7: Skin and hooves –> petachiae, cracked hooves
-9: Poor reproductive performance + Anaemia (related to B12)
-12: RBC maturation and utilisation of folate in RBC’s (non-regen anaemia)
-Choline: used in lipid transport and ACh –> CNS issues

C (ascorbic acid)

  • Anti-oxidant
  • Hypo: Bone resorption in pigs, weakness fatigue, dyspnoea, bone pain, haemorrhages of the skin, musculature, adipose tissue and organs, lowered fertility.

LIPID SOLUBLE
D
-Hypo: lack of ca –> oseteomalacia, porosis, rickets, tetany (eclampsia)
-Hyer: calcinosis

E

  • Hypo: works with selenium (anti oxidant) –> MHD/WMD
  • Hyper: Rare, muscle wasting

A (Retinol)

  • Hypo: Degeneration of retinal tissue and pigment in eyes. Blindenss or piglets born with no eyes. Bone growth plate differentiation –> delayed closure and soft bones
  • Hyper: premature closure of GP’s –> stunting

K

  • Hypo: lack of clotting –> haemorrhagic diathesis
  • Hyper: Hypercoagulation –> DIC + embolism
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21
Q

Vices of pigs, cannibalism

A

Unwanted behaviour highly linked to environment, stress and diet

Different behaviours displayed

  • Weanlings (<21days) - tail biting and ear biting
  • Growers (3-8 weeks) - tail necrosis and flank biting
  • Finishers (9-16 weeks)
  • Sows + boars (5-6 months) - vulval biting, masterbation

Factors:

  • Environment - little to no bedding, mix of breeds/litters/age/sex, overcrowding and group housing
  • Husbandary - enrichment, tail docking, teeth clipping
  • Tail length - long tails prone to being bitten
  • nutrition - finely ground feed or not enough feed
  • stress - mix of pigs can cause stress as well as moving pigs close to farrow

Aggression
-contact or non-contact

Vulval biting
- This is done close to farrow as vulva becomes hyperaemic and engorged making it a target for stressed or hungry pigs
-Chronic wounds can cause scarring and stenosis of the vaginal opening –> dystocia
P: 2.7m/sow

Cannibalism

  • Highest incidence in primiparous sows –> infantophagia
  • This is exaserbated by moving of the sow to the farrowing house within 24 hours of farrow. The sow will see all new pigs as “enemies”
  • House gilts with sows to reduce this occurance
  • Give stresnil after 2nd piglet born and separate (reintroduce >20 mins)
  • ensure plenty of bedding, enrichment and food
  • Seen prevalent in duroc and landrace

masterbation

  • Boars will masterbate using the preputial diverticulum
  • ejaculate can stagnate here and cause infection/irritation
  • may also reduce will to breed

Crushing

  • Restless sow
  • recumbant piglets
  • insufficient space/layout of farrowing cage

Bar biting
-stereotypy

Belly-nosing
-replaces foraging behaviour

anal massage

  • pigs do this in overcrowded conditions
  • causes receiving pig to defecate
22
Q

Diseases of locomotor system

A

INFECTIOUS ARTHRITIS
mycoplasma hyosynoviae, arthritis, hyorhinus
-Usually immunity as sows pass mAb
-seen in growers 8-10 weeks (HS), seen in finishers (A, HR)
-fill joints with yellow inflammatory fluid
-Cs: lameness, swollen joints, recumbency
T: macrolides

Erysipelas - erysipelathrix rhusiopathiae
-Spread by rodents and birds - difficult to eliminate
- acute - diamon skin
-chronic - myocarditis + arthritis
Cs: swollen joints + lameness

Haemophilus suis - Glässer’s disease

  • Polyarthritis
  • myocarditis

Streptococcal arthritis
-commensal, sudden onset severe arthritis

PARASITES
Sarcocystis canisuis, hommisuis
-bradyzoites in cysts in muscle
IH: pig

Cysticercosis

  • cysticercus cellulose (T. soleium)
  • encysts in skeletal muscle

Trichinella (Pseudo)spiralis

  • transmitted by wild boar (domestic-sylvatic cycle)
  • nurse cells found in muscle either with or without capsule
BONES, JOINTS, TENDONS 
Osteomalacia, porosis, OCD
-Ca, P, Vit D3
-fast growth 
-loss of communication of bone underlying cartilage (lack of blood supply --> necrosis) - OCD

Epiphyseolysis

  • Breakage of bone through the epiphseal plate
  • SH Type IV - through the growth plate
  • Lack of growth –> stunted

Gyroarthosis
-congenital rounding of joint –> Euth

Foot rot

  • crack in hoof (usually back lateral claw)
  • fuscobacterium necrophorum infiltrates
  • abscess + phelgmon –> penetrate joints and ligs
MYOPATHIES 
MHD/WMD
-Sel + Vit E deficiency 
-Act as muscle anti oxidants --> without oxidative damage to the muscle --> zenkers necrosis and Ca deposition. 
-especially the myocardium 

Porcine stress myopathy syndrome:
Malignant hyperthermia
-similar to exertional rhabdomyolysis
-has a genetic component of sensitive Ca+ channels
-excessive muscle contraction result in LA build up which can be painful and result in furhter contraction creating heat and eventually resulting in acidosis and hyperthermia

Back muscle necrosis
-seen in sows due to stress

PSE (5.6)

  • Anaerobic environment –> permeability to water and protein –> LA accumulation
  • Pale soft and exudative meat

DFD (6.4)

  • Chronic stress –> depletion of glycogen before slaughter –> less LA –> less protein and water leeching
  • dry firm and dark meat
23
Q

Diseases of the nervous system

A

NON-INF
Sunstroke
-no sweat = poor thermoregulation
-environmental: high temp, low water and ventilation

Myoclonia congenital
-Multifactoral: genetic, PCV/CSF, organophosphate poisoning
Severity of tremour ranges

INFECTIOUS
Usually piglets that are affected by the neurological forms of these diseases as adults usually have immunity and the diseases manifest in a different organ system

VIRAL
PRDC (Adenovirus)
-part of PRDC can cause cns in young

Aujesky’s (SHV-1)

  • Usually respiratory (barking pigs)
  • can be cns in young

Teschen disease

  • adults have Ab’s
  • occurance in growers and weanlings
  • damages motor neurones

Viral enchphalitis (cardiovirus)

  • 2 forms
  • -repro
  • -cardiac

Japanese enchpalitis virus

  • pig is reservoir
  • mosquito vector
  • reproductive issues

Blue eye disease - Rhubulavirus

  • neuro-occular disease piglets
  • Reproductive - sows and boars

Porcine Respiratory and neurological syndrome (Henipavirus)

  • Bat vector
  • respiratory and cns

Rabies - lyssavirus
-sudden onset –> death

BACTERIAL
Streptococcal encephalitis
-commensal of URT that can invade brain in immunosuppressed

Listeria monocytogenes
-Encephalic form

Clostridium botulinum
-flaccid paralysis

clostridium tetani
-spastic paralysis

PARASITIC

  • Toxoplasma gondii
  • transplacental is possible
  • Pig is IH (cyst in muscle)
  • CNS issues in cats - FH
24
Q

Disease of mammary glands

A

Teat necrosis

  • trauma from the floor or piglet teeth damage teat skin –> allow bacterial infection –> Necrosis
  • Ergot poisoning can cause vasocontrcition and mammary necrosis as well as agalactia

PPDS (also known as MMA)
-Multifactoral
–Bacterial: bacteria in uterus (metritis) –> endotoxin –> haematogenous –> prolactin and thyroxine inhibition + cortisol + PG’s increase –> Hypogalactia
-Mastitis + hypoCa2+ (nutritional) –> hypogalactia
Hypogalactia –> 3days post partum –> emaciation –>absence of milk ejection (agalactia) –> PPDS –> Neonatal issues –> “Runting syndrome”

Mastitis
-Types
–Environmental - E.Coli + klebsiella (colliform mastitis)
–Strept and staph - non-environemtnal and less severe (acute) than colliform
–Necrotising - pasturella
Acute - red swollen, vaginal discharge, pain
Chronic - consolidated and fibrous lumps with no pain or swelling. absent milk ejection

Udder oedema

  • Breed disposition, arousal or overfeeding before farrowing can cause teat oedema
  • pressure prevent milks flow from acini into ducts for milk ejection

Mammary hypoplasia
-hormonal issue caused by congenital issues or mycotoxin poisoning

Frost bite

25
Q

Mycotoxin poisoning

A

Mycotoxins
-issue in humid countries (tropical occurrence)

ASPERGILLUS 
Aflatoxin 
-most acute toxin 
-causes liver damage and lipid deposition 
-eliminates Vit E + Selenium --> WMD/MHD
-abortion + agalactia in pregnant 
-T: supplement Vit E + Selenium 

Ochratoxin

  • Nephrotoxin –> iterstitual and tubular necrosis
  • Liver spots
  • T: supportive kidney fluids

CLAVICEPS
Ergot
-Cause vasoconstriction –> extremity necrosis (including mammaries)
-inhibits prolactin –> agalactia
-can also result in CNS issues if ischemia of brain

FUSARIUM
Fumonsin (porcine pulmonary oedema PPO)
-inhibits lipid synthesis -->pulmonary oedema 
-abortions 
-hepatotoxicosis 

Trichothecenes

  • vomitotoxin –> V+ and D+
  • lack of feed intake –> Emaciation

zearalenone

  • Oestrogenic mycotoxin
  • BM affects –> soft bones
  • Males are feminised
  • Females experience abortions and infertility

Dx: Very difficult other than using non-specific Cs as such chromographic feed analysis may rule out certain toxins that have photodynamic properties

T:

  • adsorbance (charcoal),
  • dilute with healthy feed,
  • use higher quality feed and give lower quality to Ru (more tolerant)
  • Mould inhibitors - citric acid
26
Q

Diagnosis of fertility disorders in gilts and sows (indications, diagnostic methods and approaches)

A

Of each 100 sows serviced –> 89 will farrow
abortion rate is 0.5-1%
-Investigate the Hypothalamo-pituitary-ovarian-uterine axis
-Management including environment, infectious process, time of mating, status of female and male

Ovarian function test

  • Transrectal USG
  • -expensive + time consuming
  • -will give accurate follicular development in live sow without need for cull
  • -examine follicular/luteal cysts
  • Serum P4 values
  • -can determine best time of insemination as well as cycle timing and status with measurement of blood P4
  • -P4 High –> Dioestrus
  • -P4 low –> anoestrus, prooestrus
  • -CL starts to produce P4 after ovulation this is close to prime fertilisation period

Post mortem

  • Ovarian cysts
  • -Multiple large cysts –> luteal –>P4
  • -Multiple small cysts –> follicular –> E2 –> disrupts cycle length
  • -single small cyst –> no Cs usually incidental finding

-Acyclic
If not CL found or inactive ovary –> acyclic

27
Q

Diagnosis of reproduction diseases in boars (indications, diagnostic methods and approaches)

A

Semen quality is mainly affected by environement and season

Diagnostic methods

  • Anamnesis
  • -Environment, Housing, previous services
  • clinical exam
  • -TPR, BCS
  • genital exam
  • -Check testes and epididymis
  • -temperature, mobility, symmetry, size
  • Physical condition musculoskeletal
  • -willingness to mount and HL stability
  • lack of libido
  • -Age, BCS, history with females (aggression or shyness)
  • semen quality
  • -volume, density (200-1000 x10^6), defects (<20% primary, <10% secondary), pH (alkaline), colour
  • # of matings
  • -year 1 10-20
  • -year 2 20-30
  • -tear 3 35-45
  • test reaction to female in oestrus

Indications
-Failure of erection - blood ischemia (obstruction) to coprus cavernosum

-Abnormal erection - phallocampsis, abnormal sigmoid flexure

  • Penile lesions (failure of intromission)
  • Adhesion with peri-penile tissue
  • -balanopostitis
  • -phimosis/paraphimosis
  • -neoplasia
  • Failure of ejaculation
  • -neuronal issue
  • -stress/pain/shyness
  • Failure of fertilisation
  • -semen parameters
  • -testiculaer hypo/aplasia
  • -orchitis/epididymitis
  • -cryptorchidism
28
Q

Disorders of oestrous cycle as a cause of infertility in gilts and sows (aetiology, clinical signs, diagnosis, differentials, treatment, prevention)

A

Oestrus cycle of pig lasts 21 days

  • pro: 1-3 days
  • oestrus: 1-2 days
  • dioestrus: 14 days

Non-seasonal polycyclic (more fertile in winter, some wild boars are seasonal)

Disorders of the oestrus cycle (anoestrus)

  • causes of anoestrus
  • -incorrect detection of oestrus
  • -premature weaning
  • -disease process (infection, cystic ovaries, mycotoxins)

Dx of anoestrus

  • behaviour
  • -standing agaisnt back pressure and vocalisation = oestrus
  • Clinical exam
  • -lowered feed intake and hyperaemic vulva
  • serum P4
  • -low in pro and oestrus
  • -higher just after ovulation (prime insemination)
  • -remains high during dioestrus and pregnancy
  • -if very low for prolonged period –> no CL so no ovulation, maybe acylic or silent oestrus
  • USG of ovaries
  • -luteal cysts –> P4 –> T: PGF2-a
  • -Follicular cysts –> E2 –> T: GnRH/hCG
  • PM

Treatment
-post weaning acyclicity canbe treated with administration of hCG or eCG 12 hours post ween

29
Q

Non-infectious causes of infertility in gilts and sows (aetiology, clinical signs, diagnosis, differentials, treatment, prevention)

A

Anoestrus

  • causes of anoestrus
  • -incorrect detection of oestrus
  • -premature weaning
  • -disease process (infection, cystic ovaries, mycotoxins)

cystic ovaries

  • follicular –> regular cycle –> E2 –> T:hCG/GnRH
  • luteal –> anoestrus –> P4 –> T:PGF2-a
  • Stress can increased incidence of cysts as corticosteroids –> inhibit LH –> inhibits ovulation

Poor management

  • poor timing of insemination (oestrus only lasts 1-2 days)
  • -service on first day of heat and 24 hours later
  • BCS / nutritional status
  • -Farrowing abortion: feed in morning –> abort in evening
  • Age of female

Male failure

  • Inadequate service
  • inexperienced
  • slippery floor
  • issues with intromission or mounting
  • semen quality issues

Physical abnormalities

  • vaginal anatomical abnormalities (ano-vaginal fistula, double vagina, atresia/a/hypoplasia)
  • musculoskeletal issues, male cant mount
  • -hoof, joints, bones, muscle
  • tubular lesions –> hydrosalpinx/ pyosalpinx

Intersex disorders

  • hermaphrodite
  • ovotestes
  • hypersex (XXY, XYY)
  • Freemartinism

Season

  • although non-seasonal some boars are winter cyclers
  • this is seen as pigs are less fertile during summer due to higher heat, very high heat 7-14 days post-service is very dangerous for piglets viability
  • One litter in spring will often result in anoestrus or abortions during summer/autumn

Light
-12-16 hours light is best for completion of pregnancy

Intoxifications

  • Aspergillus
  • -aflatoxin
  • Claviceps
  • -ergot
  • Fusarium
  • -zearalenone –> oestrogenic –> inhibits by constantly producing low amounts –> retained CL –> anoestrus
30
Q

Intoxifications as cause of infertility in gilts and sows (aetiology, clinical signs, diagnosis, differentials, treatment, prevention)

A

MYCOTOXINS
Fusarium
-Zearalenone
–oestrogenic –> low level inhibition of LH –> inhibits ovulation

Claviceps - ergot

  • vasoconstriction
  • metritis, mastitis, peripheral gangrene (including mammaries)

Aspergillus
-Aflatoxin –> usualy liver lipidosis in piglets but can also result in abortion in pregnant sows

NUTRITIONAL
Iodine –> toxicity can inhibit production of thyroid hormones and cause infantile stunting and peri-natal losses

Gossypol –> cottonseed causes oxidative damages and results in inhibited spermatogenesis and cycle abnormalities (delayed return, anoestrus, silent oestrus)
Dx: also see cardio, hepatic and renal damage

T: Eliminate (give to Ru, higher resistance), adsorbents (charcoal), fluids, dilute feed, use mycotoxin eliminators (citric acid)

31
Q

Bacterial and protozoan infections as a cause of infertility

A
3 Groups:
1 - opportunistic pathogens that infect during oestrus and the uterus is more susceptible to infection 
--Streptococcus suis 
--chalmydophia 
--brucella

2 - pathogenic agents that cause severe disease and are highly contagious infecting an entire herd (usually viruses)

  • -SMEDI
  • -PRRS
  • -PPV

3 - infrequent highly pathogenic and lethal infections

BACTERIAL 
Leptospira interrogans 
-water borne 
-lepto-Ag attack foetus and placenta 
-results in abortion, stillbirth or premature parturition 
-Cs: vaginal discharge, 
-Dx: Lepto Ag
-T: tetracycline 

Listera monocytogenes
-abortive form

Brucella suis 
-spread in afterbirth and semen 
-Cs: orchitis, abortion, arthritis 
-T: Atb
P: B.abortus (Ru) vaccine seem to be effective 

Chlamydophila

  • disrupts materno-foetal nutrient and gas exchange
  • Cs: conjunctivitis, abortion, respiratory issues

Eperythrozoon suis

  • blood borne
  • insects + needles
  • abortion, still birth

PROTOZOAN
Toxoplasma gondii
-spread transplacentally
-1st trimester abortion + premature parturition

32
Q

Viral infections as a cause of infertility in gilts and sows

A

SMEDI - enterovirus (like teschen diease)

  • depending on the time of infection either
  • Stillbirth, mummification, embryonic death or infertility
  • Su can develop immmunity
  • if infected in early gestation can bare a live healthy immune piglet

Porcine parvovirus

  • most common and important cause of infant loss in herds
  • Adult tend to be resistant but causes fatal disease in piglets or cause litter illthrift
  • in males can disrupt spermatogenesis

PRRS - arterivirus

  • Blue ear disease
  • causes late stage abortion, agalactia and delayed oestrus
  • <30 days gest –> reabsorption
  • > 40 days gest –> mummification
  • Last trimester –> still birth

Blue eye disease - rhubulavirus

  • neuro-ocular disease
  • Sows: infertility, abortion
  • boars: orchitis, epididymitis

Aujesky’s - SHV-1

  • usually respiratory
  • can cause abortion

Swine influenza - orthomyxovirus

  • usually respiratory
  • can cause abortion

Japanese encephalitis
-boars pass in semen (orchitis) –> can cause encephalomyocarditis if infected 40-60 days of gest

CSF/ASF

  • haemorrhagic disease
  • still birth and reabsorption
  • sows: infertility and oestrus disorders
33
Q

Embryonal mortality and embryonal losses on the pig farm

A

Embryonal loss - <30days = reabsorption

  • EED = before maternal recognistion = normal oestrus
  • LED = post-maternal recognition = delayed return

Foetal loss - 30-115days = mummification

Causes:

  • Nutritional
  • infectious (PRRS, PPV, Lepto, Blue eye, SEMDI)
  • management (dystocia of sow)
  • tetrogens
  • genetic
  • environmental
Peri natal losses 
->50% of losses occur in this period 
-farrow --> day 3 
-Hypothermia
-Hypoglycaemia 
-Splayleg 
-congenital tremor 
-neonatal isoerythrolysis 
--24-36 hour after colostrum intake 
erythrolysis
-pale pig syndrome --> naval bleeding 
--Anoxia in womb as blood pools in the placenta and the piglet is separated prematurely then the blood is not recalled into the piglet resulting in hypovolemia
34
Q

Dystocia in gilts and sows

A

rare in sows due to foetal-maternal size

Management

  • 3 days pre-farrow –> farrowing crate
  • 24 hours PF –> colostrum let down
  • 60 mins PF –> lay down, bloody discharge, meconium

Parturition (physiological)

  • 1/2 born head first, 1/2 born feet first
  • 15 mins between piglets
  • 2-4 hours PP –> expel placenta

Pathological

  • gestation >116 days
  • passing large amount of bloody discharge and meconium with no straining
  • non-productive straining
  • no afterbirth >4 hours

Placental retention

  • > 4 hours Post farrow
  • Retention is seen as vaginal discharge
  • Oxytocin + Atb

Uterine inertia

  • absolute - foetal size
  • relative - stricture, dropped uterus, torsion
  • Malposition
  • malpresentation
  • malposture
  • Nutritional
  • Infectious (lepto, listeria, PPV, PRRS)
  • Physical - obstruction/torsion

Manual delivery

  • 2 fingers under chin or on hamstrings
  • can use hooks in eyes as last resort

C-Section
-when there is foetal size issue or no response to inertia treatment

End of parturition

  • behaviour is poor indicator
  • closure of cervix (95% accurate)
  • retained foetus’ –> calcify and reabsorb

Aftercare - piglets

  • Remove mucous/clear airway
  • TPR
  • Umbilicus (dip in iodine)
  • colostrum
  • tail dock and teeth clip
  • Fe and TriVit
  • castrate <7 days
  • ID tag

Sow

  • Check for PPDS
  • Check birth canal for trauma
  • Check for placenta expulsion
35
Q

Puerperal diseases

A

Occur 12hours - 3 days post partum

MAMMARIES
PPDS
-multifactoral issues with lack of milk let down
-usually MMA is preface, bacterial infection of uterus –> endotoxins –> prolactin and thyroxane are decreased and cortisol and PG’s are increased
-Nutritional + environement also play a role
-Cs: swollen red mammaries with restless piglets
-ATB + Oxytocin

Teat oedema

  • usually in overfed, dehydrated and inactive sows
  • oedema places pressure on the udders blocking ductus and acini preventing milk ejection
  • seen restless piglets
  • pressing a finger into the udder and seeing an imprint means oedema is present

Mammary hypoplasia

  • congenital
  • mycotoxins
  • poor nutrition

Mastitis
-envionmental (colliform) - E.coli/klebsiella
-staph/strep - less severe and usually only on teat
-gangrenous - pasturella
Acute/Chronic

MMA

  • Usually bacterial infection from teat or ascending upper genital tract
  • occues 12hours - 3 days PP
  • illthrift in piglets

UTERINE
metritis (peri, endo, myo)
- highly susceptible during parturition as cervix opens and if exposed to environment
-Cs: vaginal discharge is normal postpartum but if malodorous or febrile –> treat w/ 2x oxytocin a day

endometritis (prequel to metritis)

Pyometra
-infection during cervical opening –> closure –> pus build up

Uterine, vaginal or cervical prolapse
-seen in older fat sows with large piglets or large litters
-increased abdominal pressure from gas producing feeds
-dystocia
-zearalenone poisoning
T: repositon uterus laprascopically, tack suture on vagina, amputation of uterine horns, euthanisia for wellfare

36
Q

Syndrome of lactation insufficiency in sows

A
MMA --> PPDS
Teat oedema 
Agalactia
Teat necrosis 
Mammary hypoplasia 
Metritis 
Mastitis
37
Q

factors in suckling mortality

A
PERI-PARTUM 
Piglet 
-Hypothermia 
-hypoglycaemia
-splayleg 
-congenital tremor 

Sow

  • neonatal isoerythrolysis
  • pale pig syndrome - naval bleeding
POST-PARTUM 
piglet 
-Fe def anaemia
-neonatal iso 
-greasy pig - S.hyicus 
-pustular dermatitis 
-hypotrichosis cystica
-Pityriasis roseca 
-Arthritis (mycoplasma)

Sow
-Cannibalism (infantophagia)

Anything that affects milk let down

  • PPDS + MMA
  • Mastitis
  • teat oedema
  • teat necrosis/hypoplasia
  • Nutritional / stress (agalactia)

INFECTIOUS
Bacterial
-Clostridium speticum
–wound invasion –> gangere and sepsis

  • Clostridium perfringes C
  • -Enteritis –> severe D+

Viral

  • Rota, corona
  • Aujesky’s
  • Blue eye - Rhubulaviris
  • CSF/ASF
  • PPV
  • SEMDI (entero –> teschen)

Parasitic

  • coccidiosis
  • -Eimeria, isospora, cryptosporidium
  • Toxoplasma gondii - transplacental
  • strongyloides/hyostrongylus –> transmammary
CONGENITAL 
atresia anii 
hydrocephalus 
gyroarthrosis 
cleft lip/palate
hernia (inguinal/ubilical)
38
Q

Non-infectious causes of boar infertility

A

Males service a number of sows based on age
-1 year: 10-20
-2 years: 20-30
-3 years: 35-45
<1year: puberty at 8 months –> only mate one per day to avoid overheating

Cryptorchidism
-high heat –> destroyed spermatozoa but male hormones still produced

Testicular hypo/aplasia

  • congenital, environmental, nutritional
  • poor body condition or malnutrition
  • inadequate amount of germ cells

Testicular neoplasia

  • sertoli cell –> hyperoestrogenism
  • leydig cell –> prostatic hyperplasia

Paraphimosis

  • inability to retract penis
  • during mounting or sex can also occur due to trauma or penile entrapment in the diverticulum
  • oedema and necrosis can result
  • T: lubricate and replace –> stay suture

Phimosis

  • Inabiltiy to protrude penis
  • trauma while sheathed
  • congenital short penis
  • sigmoid flexure anomoly
  • T: remove adhesion, try to protrude, removal of prepuce

Balanopostitis

  • Postitis: inflammation of prepuce
  • balanitis: inflammation of glans penis
  • Trauma (fighting, mounting, sex)
  • Can result in para/phimosis
  • NSAID’s, lubricate, cold compress

Phallocampsis

  • persistent phrenulum
  • prevents protrusion of penis from prepuce
  • frenulum should break down around 6months
  • ligate and cut –> sexual rest 2 weeks

Diverticulum

  • urine scalding, ulceration, diverticulitis
  • ensure clean and clear
  • flush
  • NSAID’s + atb

Penile entrapment

  • penis becomes entrapped in the diverticulum due to masterbation
  • entrapment can result in paraphimosis, oedema and necrosis due to exposure

Failure of copulation

  • lack of libido
  • conformation of penis (abnormal erection - phallocampsis)
  • inexperienced
  • environemntal/husbandary
  • age
  • status

Failure of erection

  • restriction of blood to coprus cavernosum
  • failure of sigmoid flexure

Failure of ejaculation

  • obstruction
  • neuro disorder
  • stress
  • pain

Sperm defects

  • Primary
  • Secondary
  • Azoospermia (aspermia - lack of ejaculate)
  • Oligozoospermia (low sperm count in normal ejaculate)
  • Asthenozoospermia - lack of motility
39
Q

Infectious causes of infertility in boars

A

VIRAL
PRRS - arterivirus
-insect vectors and contact
Cs: reduced semen quality, orchitis, epididymitis

PPV

  • contact, venereal, transplacental
  • reduced sperm count

Blue eye disease - rhubulavirus

  • resp, venereal, vertical
  • Cs: reduced semen quality + corneal opacity
  • PM: Testicular hypotrophy

Aujesky’s - SHV1

  • contact, venereal, vertical
  • usually respiratory
  • results in lower semen quality

Japanese encephalitis - Enterovirus

  • insects
  • sumer infertility however may persist and become chronic

BACTERIAL
listeria
-venereal, contact
-abortive form

leptospirosis

  • from water, vertical
  • Male become inapparent carriers of lepto (fast spread)
  • passed to female and offspring

brucella suis

  • contact, venereal
  • reduced sperm quality, orchitis, epididymitis, accessory gland inflammation, swollen joints

chlamydophila

  • venereal transmission
  • weak piglets, stillbirth
40
Q

Bio-techniques for reproduction management in gilts and sows as a prevention of infertility (indications, methods and approaches)

A

ID Puberty

  • 8months (>85kG)
  • Influenced by day length (light hours), presence of male, BW, age, exogenous factors
  • Induce puberty by administering PG600 (progestagen) at 5-6 months
  • dormitory effect
  • transport stress near age of puberty can induce

Synchronise/control oestrus

  • suppress oestrus with progestagens in feed, remove feed and will cycle in 7-10 days
  • oestrus (1-2 days)
  • signs of oestrus include standing to pressure on back and vocalisation

Return to oestrus PP

  • delayed oestrus can be caused by;
  • -premature weaning (<14 days)
  • -BW (Lactation makes it hard to maintain weight)
  • -Summer (heat)
  • -ensure return with PG600 injection post wean

Timing parturition

  • at 115 days –> PGF2-a –> luteolysis –> parturition
  • If sow is due in 3 days (>112 days) apply PGF2-a and will farrow in 30 mins

Timing insemination
-optimal time is 40 hours from ovulation. Difficult to pin point, so usually done at first sign on standing heat and then again 12-24 hours later

Managing the gilt pool

  • After each farrow. 15-25% of all females are culled to maintain herd strength.
  • Congenital disorders, issues during parturition, small litter sizes and age are all indications for being culled

Eliminating heat stress

  • Pigs originally would birth one litter during winter
  • Susceptible to stillbirth, infection, delayed return to oestrus and infertility during times of high heat
  • Gilts: more male expsoure, water and space
  • Lactating: wet feed, aircon
  • Sows: PG600 is given post-wean to ensure return to oestrus in 3-10 days
41
Q

Analysis of reproduction management in gilts and sows as a prevention of infertility (analysis of reproduction indices and factors affecting sows’ reproduction performance, interpretation of reproduction indices)

A

Reproduction indicies;

  • 2 litters per year
  • S/L/Y: 2.5 (excellent), 2.08 (unacceptable)
  • NPD’s: 3-10 days optimally, to minimise NPD’s;

Oestrus detection

  • P4 Serum, USG, behaviour (standing against back pressure + vocalisation)
  • inseminate at first sign and 12-14 hours later

Technique

  • Detect, inseminate
  • Boar: year 1 - 10-20, 2: 20-30, 3:35-45

Primiparous?
-first litter will always be smaller and there will be a delayed return to oestrus

Weaning age

  • 17 days is literature
  • new study shows better result from 21-28 day wean
  • extra 0.25Kg/day after 17 days

Season

  • Summer (lower likelihood of puberty and successful insemination)
  • Light period - 12-14 hours helps pregnancy
  • Temp: 18-24 ideal
  • air quality - high levels of ammonia associated with disease and lower production

Nutritional BCS

  • BCS and BW has a big impact on puberty and conception rate as well as litter size
  • Flushing (increased feed intake) is done for 2 weeks prior to insemination and prior to farrowing to encourage large litter and good nutritional status for parturition and lactation
  • during pregnancy physiological body temperature raises –> making large feeding sessions inefficient better to change for 3x per day of smaller quantities
  • ensure feed is fresh
  • use of liquid feed, can add water or fats to increase intake + energy
  • Decrease during lactation: 2Kg/day

Water
-10-20 L/day for pregnant, 30-40L/Day for lactating

Stress

  • highly susceptible first 30 days (before implantation at 28 days), and final 30 days
  • stress causes high heat –> fatal for piglets
  • post breed uterus undergoes physiological inflammation

Moving/mixing females
-although used to induce puberty this should be avoided soon to farrow as sow will see new pigs as enemies in an unfamiliar setting –> infantophagia

Male dormitory effect
->10mins/day

42
Q

Anaesthesia and analgesia in swine (indications, methods and approaches, complications)

A

Prior to surgery

  • Fasting 24 hours
  • if abdominal surgery, liquid food and laxative (3 days prior)
  • check for status, no d+, cough or poor BCS

Stages of anaesthesia

  • Stage I: Sedation and disassociation
  • -Planes: 1–>3
  • Stage II: excitment and loss of conciousness
  • Stage III: surgery
  • -Planes: 1–>5
  • Stage IV: overdose, respiratory paralysis

Induction

  • Drugs: ADK (superior) or AAK (inferior)
  • Azeperone (1mg/kg), diazepam(0.2 mg/kg)(midezolam),ketamine (2mg/kg) (tiletamine)
  • Acepromazine, atropine, ketamine (muscle contractions)

Maintainence

  • Propofol (respiratory depression), pentobarbitol
  • Inhalation: iso, sevo, halo (can cause malignant hyperthermia)

Monitoring

  • Resp: 12-15 breaths/min
  • Temp: 39 dgerees
  • Reflexes: corneal, pupillary
  • CRT

Analgesia

  • Buprenorphine
  • butorphanol
  • ketamine
  • detomidine
  • lidocaine (local)
  • Ketaprofen (NSAID’s)
  • carprofen (NSAID’s)
  • meloxicam (NSAID’s)

Epidural

  • Used for surgery caudal to inguinal canal
  • lumbo-sacral space, needle is advanced 10cm caudal, aspiration to ensure no CSF (sub-arachnoid space) and lidocaine is applied (apply half if CSF is present)
  • Wait 10mins –> lasts one hour

Fluids
-10/ml/hr

Recovery

  • pigs are prone to laryngospasm.
  • if dyspnea occurs post-removal of ET tube then place in dorsal recumbency and re-intubate
  • Observe until sternal recumbency
  • do not return to pen mates immediately –> cannibalism

Euthanasia
-Pentobarbitol 150ml/kg

43
Q

Analysis of reproduction management in boars as a prevention of infertility (boars‘ insemination ability, sperm production, fertility)

A

Usage

  • puberty: 6-7 months (2-4x service at this time)
  • introduce female from first sign of puberty
  • first mating should be with a willing, shy gilt
  • Ages: 1 (10-20), 2(20-30), 3(35-45) / week

Environment

  • familiar (prevent distraction)
  • appropriate flooring
  • temperature kept cool to prevent >39 degrees

Nutritional
-high protein and fit

Boar selection

  • # of piglets in litter
  • diseases (infectious or hereditary)
  • lack of libido/behaviour
  • lack of adaptilbity

Mating techniques

  • Pen mating - 1:4
  • hand mating - 1:15-25
  • AI - 1: 150-1250 (semen lasts <72 hours)

Exam

  • Anamnesis + general
  • gonadal exam
  • -physical + infectious
  • -observe copulation/mounting
  • Behavioural/libido exam
  • Semen analysis
44
Q

Castration of piglets and boars

A

Indications

  • Behavioural
  • Boar taint - adrestenone + skatole
  • Cryptorchidism

Ages and legislation

  • > 7 days –> requires GA + analgesia
  • optimum time to castrate piglets is 5 days pre-wean
  • approx day 12 (if weaned at day 17)

Methods

  • Piglets can be open or closed
  • Adult must be closed due to high change of herniation
  • Restrain –> incise –> twist –> crush –> antiseptic powder

Slaughter

  • Adults must be castrated 3 months prior to slaughter to ensure no boar taint
  • GA –> dorsal rec –> incise –> twist –> emasculate –> ligate –> close (abdominal muscles, peritoneum, sub Q, skin)

Cryptorchidism

  • Inguinal, abdominal, ectopic
  • Uni or bi lateral (removed descended one first in uni)
  • 3 months prior to slaughter
  • Incise midline lumbar –> caudal teat
  • can be located in inguinal canal, found in the abdomen with kidneys or GI, ectopic can be found anywhere even in femoral canal

Vasectomy

  • Indicated for teaser boars for inducing oestrus
  • Removal of spermatic cords (bilaterally)
  • Incise from scrotal base to caudal teat and blunt disect out the spermatic cord

Complications

  • hernia –> highly likely in adults with open castrate (inguinal usually)
  • infection –> high risk if >7 weeks old
45
Q

Invasive treatment of boars‘ genitals

A

Preputial prolapse (phimosis)
-Entraps the penis inside the preuce and prevents erection/copulation
-mucosa exposed to the air is at higher risk for trauma, frostbite, infection
Procedure: move prolapse cranial, clamp muscosa and cut. sexual rest for 2 weeks

Penile prolapse (paraphimosis)

  • Entrapment of penis can result in –> strangulation + necrosis
  • usually due to trauma, neurological issue, sigmoid flexure failure or balanitis
  • Procedure: Lubricate + clean –> push back inside –> sexual rest.
  • if reoccured then repeat and add purse string sutures to the urethral opening (remove after 10 days)

Prolapsed rectum

  • Complete: all layers, Incomplete: mucosa only
  • Occurs in older overweight pigs due to increased abdominal pressure (bloat, D+, cough) or mycotoxin poisoning (smooth muscle relax)
  • risk of cannibalism + necrosis
  • Procedure: Lubricate –> replace –> purse-string suture
  • Rectal stricture is very likely

Phallocampsis (persistent frenulum)

  • Usually breaks down during puberty (6-7 months)
  • persistence can interrupt ability to intromit
  • Cut + ligate –> sexual rest 2 weeks

Preputial diverticulum resection

  • penile entrapment
  • diverticulum becomes filled with semen or urine, rsulting in urine scalding, abscesses and pus formation.
  • The entrapped penis cannot escape and disrupts copulation
  • procedure: catheterise the diverticulum to localise it, then find the connection between the preputial orifice and the diverticulum, clamp at base and remove flap

Penile trauma

  • common in boars
  • usually due to mounting or fighting
  • mild trauma –> sexual rest
  • severe trauma (breakage into tunica vaginalis) often has a poor prognosis

Orchitis

  • Seen as inflammation of testicles either due to infection or torsion
  • Acute: swollen, hot, red, painful
  • chronic: fibrous with adhesion and shrunken
  • Unilateral –> infertility, -Bilateral –> Sterility
46
Q

OVH in gilts

A

Indications

  • Jambon iberico: iberian ham made from gilts raised less than 1 years and where oestrus is CI’ed due to inhibition of growth.
  • Behaviour alteration and pyometra risk in PET PIGS
  • Reproductive: neoplasia or avoiding pregnancy

Procedure:

  • GA
  • Lateral approach
  • Ventrolateral incision care to avoid GIT
  • find left ovary –> run loop suture to bifurcation
  • localise right ovary
  • Loop, ligate ovaries and uterus –> cut
  • (In gilts you can twist the ovaries and ligate the uterus)
  • closure of all 3 layers

Older sows: Para-medial approach (uterus drops in older sows)
gilts: para-lumbar approach

Complications

  • incontinence
  • herniation (improper closure of peritoneum)
  • peritonitis (poor hygiene)
  • Intra-abdominal bleeding (slipped knot)
47
Q

Hernitomy

A

Types

  • Inguinal, umbilical
  • direct or indirect

INGUINAL

  • usually after birth, <7 days due to failure of closure of the navel, pulling from the umbilical cord or affixing a navel clip
  • Fairly common and uneventful –> only issue is at slaughter it increases the risk of perforating the GIT

Procedure:

  • non surgical: elastrator ring 7days (necrotises) 21 days hernia sac drops off and skin is closed
  • surgical (herniorphapy): open skin, ligate the base of the hernial sac, cut, close

INGUINAL
-in males is known as a scrotal hernia and forms due to the incomplete closure of the inguinal canal after the testes descend (5x more likely on left side)
-in females it is extremely rare and associated with intersex disorders
Procedure
-non-surgical: scrotal taping (<7 days old)
-surgical: open inguinal ring –> DO NOT penetrate the tunica vaginalis as this holds the intestines –> remove hernial sacand affix spermatic cord and tunica vaginalis to the inguinal canal –> castrate

48
Q

C-section in gilts and sows

A

Indications

  • complicated dystocia - no responce to medical treatment, obstruction or torsion
  • research purposes - obtain pathogen free piglets

Factors:

  • Time spent in parturition so far (<2.5 hours)
  • time spent intervening already
  • birth canal trauma/obstruction

Preparation

  • stabilise: often the sow will be exhausted, stresse and potentially close to shock by the time a C-Sec is indicated
  • catheterise: IV fluids into ear vien
  • peri-op ATB: peritonitis

Procedure:
Radical: shoot sow/gilt, survival: use GA

Lateral recumbancy
-incise: paramedial - old sows, ligate mammary vessels and take care for contamination from the floor (High risk)

  • incise: ventrolateral - usual approach (lower risk)
  • incise: paralumbar - in young/gilts (low risk)
Express uterine horn 
Removal of piglets: incise parallel to oviduct as close to the bifurcation as possible (OVH in radical)
Intrauterine atb + oxytocin 
close uterus (2 layers cushing/utrect)
Close skin (3 layers) 
post-op atb and rest for 2 weeks
49
Q

Hoof correct and amputation

A

Hooves become damaged when:

  • trauma –> crack in hoof
  • chronic wet environment –> softens hoof
  • nutritional –> zinc and biotin deficiency

Lameness grading system of swine

  • 0: physiological
  • 1: signs of lamness on one hoof
  • 2: definate lameness on one or more hooves
    3: inability to rise or stand

Claw lesions:
Toe trimming
dew claw trimming - over growth can result in lameness or breakage of the dew claw
heel overgrowth - should be flat and have coronary band parallel to floor
heel-sole crack - superfical or deep
white line disease - crack that separates coronary band
hoof cracks (vertical and horizontal) - superficial or deep

Procedures:

  • done to reduce lameness and risk of trauma
  • this encourages mobility and increases feeding +growth

-Toe trimming - ensure toes are similat length and not overgrown
-heel-sole balance - lateral often outgrowns medial
Wall straightening - should be flat and have coronary band parallel to floor
-dew claw trimming - 2cm is ideal, longer can result in trauma or breaking the toe

Digital amputation

  • usually due to spetic arthritis
  • prevents the haematogenous spread of purulent bacteria to other parts of the body. If fetlock becomes infected then toe amputation will not be curative

Procedure

  • GA
  • localise lesion and tourniquet
  • incise at 45 degrees
  • exarticulation: use foetotomy wire and cut between joints
  • remove all cartilage to remove risk of infection
  • close with opening –> drainage
  • atb and bandage
50
Q

Embryotransfer in gilts and sows

A

Fewer uses in swine as they have multiple large litters a year

Used for

  • education
  • minimise inherited disease + increase vigor
  • decrease generational time
  • decrease transport costs
  • to obtain pathogen free herds

Selection of a donor

  • Physically healthy and mature (fit)
  • able to cycle and meet oestrus requirements
  • disease/pathogen free
  • genetically viable

preparation of donor
-Oestrus detection - use of serum P4 or USG to accurately determine when oestrus will occur, PG600 can be given to a prepubertal gilt to induce puberty and thus oestrus
OR
-Without detection - behavioural signs used to estimate
-Starve for 24 hours pre collection

Collection of embryo

  • Must be done laparoscopically with GA (VL approach)
  • Oviduct: collect <4 cells from oviduct
  • uterine horn: collect >4cells from uterine horn
  • Ascending collection: water from uterus into oviduct
  • Descending collection: water from oviduct to uterus

Examination of the embryo

  • grading for abnormalities
  • -0: no abnormalities
  • -1: 10%
  • -2: 20-30%
  • -3:>50%
  • -Infertile: degenerated ova

Storage of embryo

  • Short term: <12 hours in phosphate buffer
  • long term: PBS, foetal calf serum, atb, pure water
  • Long term: microclimate (38.5, 100% humidity, 90% N2)
  • Semi-permanent: deep frozen foetal calf serum

Selection of recipient:

  • Strong HL development
  • Age
  • physically healthy
  • BW

Preparation of recipient:

  • Induce oestrus - 1 day lag from donor is ideal for implantation
  • Starve for 24hrs pre-implantation

Transfer

  • GA
  • laparoscopic approach, incise uterine horn/oviduct
  • place embryo (speed > accuracy)
  • same side as CL
  • embryos cooled to -30 –> placed into liquid N –> thawed for 5 seconds in air (30 degrees) –> placed
51
Q

Pre-natal losses

A

Types:
gametopathy: <12 days –> resorption
embryopathy: 13-25 days
-Early ED –> normal cycle
-Late ED –> after pregnancy detection, delayed return to oestrus
Fetopathy: >35 days –> mummification/abortion

Causes
Endogenous - lethal gene defects
Exogenous
-Physical: torsion/dystocia,trauma
-chemical: teratogens: OP’s, drugs (sulfonamindes), mycotoxins (aflatoxin), heavy metals
-Non-inf: poor timing of conception, stress
-Inf: Brucella, toxoplasma, PRRS, SEMDI, CSF, lepto, listeria, jap encp virus, aujesky’s

Foetal death

  • Adsorption: <30 days (Parvo, PRRS)
  • mummification: after cone calacification >30 days (SEMDI)
  • Abortion: death before viability
  • -Non-Inf: Zearlenone/aflatoxin, stress, overeating/starvation/ OP’s
  • -Inf:(Brucella, toxoplasma, aujesky’s, lepto, listeria, chlamydia, erysipelas)
  • Still birth: Death after viability (complicated dystocia)