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Midterm

POPM4230 Midterm: POPM 4230; Midterm II Review Notes

20 Pages
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Fall 2015

Department
Population Medicine
Course Code
POPM 4230
Professor
Cathy Bauman
Study Guide
Midterm

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POPM 4230 Animal Health
Midterm II
Lecture 09: Reproductive Health & Udder Health
Freemartin: heifer is born co-twin to a male, 90% are freemartins (chimera XX/XY)
-Female sex characteristics androgenized, abnormal external and/or internal genitalia
-95% are sterile
-No affect on male twin
Lactation / gestation periods are influenced by
breed
-Let them dry up to build up the udder,
nutritional status allow rest time
-If not given dry period, colostrum will not
have as many Ab, protein, etc.
Parturition: time from when they start to show signs
that they are going to calf to time there is a calf on ground
-Time to complete = heifer 2-4h, cow 20min-2h
-Ligaments are first relaxing during first birth with a heifer (takes longer)
-Stage I: relaxation of the pelvic ligaments (tail head “up”)
oMaking room for calf to come through birth canal
oRelaxation & dilation of the cervix
oFetus changes position
oPlacental membranes push against cervix by rhythmic contractions of the uterus
oCan take 2-3 days for this stage to complete to Stage II
-Stage II: allantois ruptures, amniotic sac ruptures, fetus is expelled from uterus by abdominal
contractions, uterine contractions & fetal movement
-Stage III: expulsion of fetal membranes (< 12h is normal), uterine involution (< 28d)
Calving: presentation, position, posture (hooves & head first)
Dystocia: difficult birth
-Failure of the cervix to dilate common in sheep, cattle if fetus is malpositioned or uterus torsed
-Obstruction of vagina too much pelvic fat in heifers
-Failure of vulva or vagina to dilate (more common in heifers)
-Uterine torsion = uterus twists around long axis
-Uterine inertia = milk fever or exhaustion (need minerals, i.e. Ca, P, etc., for muscle tension to push)
-Maternal-fetal disproportion = fetus is too large for pelvis
oWant to breed heifer to bull that has good calving offspring (i.e. small shoulders)
-Abnormal presentation, position, posture; twins
-Malformed fetus (shistosomus reflexus where the belly wall does not close)
Use chains to pull legs out because of slipperiness after membranes have ruptured
-Do not want to use full force, some situations need C sections
-If pasterns are > 15 cm past vulva, then shoulders are clearing birth canal
-If presentation is okay, can leave (cows = 30min-1 h, heifers = 1-2h)
-Maximum force = 2 people’s arms
-Keep clean, use lots of lube, follow natural downward arc in delivery, rotate calf during delivery
Consequences of dystocia
-Death of fetus
-Vaginal tears, uterine tear
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-Obturator nerve paralysis (calving too tight, damages pelvic nerves of cow)
-Sciatic nerve paralysis (down too long), muscle damage due to being down
Long-term issues to dystocia
-Prolapsed uterus (after difficult calving or with milk fever, rupture uterine arteries)
-Fracture of ribs or long bones of calf
-Stillbirth
Retained placenta (RP): failure to expel fetal membranes by 24h post-calving
-Risk factors: dystocia, twins, abortion, milk fever, Caesarian section, induced delivery
-Immune function is greatly reduced in cows with RP
-RP is a major risk factor for subsequent metritis (serious systemic illness) and/or endometritis (chronic
localized inflammation with reduced fertility)
-Impact of RP depends on ability of cow’s immune system to deal with it
Normal postpartum involution
-Process of restoration of reproductive tract to ability to
support subsequent pregnancy
-Shrinkage & repair of uterus & cervix
-Lochia = sloughing of endometrium
-Clearance of bacterial contamination within 3wks
-Ideally: gross – 21d, histologic – 40d
-Restoration occurs in parallel with return to cyclicity
(resumption of estrous cycles)
-“Voluntary waiting period” (VWP) = ~50 days in milk (DIM)
Postpartum anestrus: several recent studies indicate that 20-25% of dairy cows may not cyclic by 60 DIM
-May be pronounced in 1st lactation
-Risk factors relate largely to cow’s health during this transition period – nutrition (negative energy
balance – NEB), body condition score (BCS) & underlying metabolic disease (e.g. ketosis & displaced
abomasum)
-Sometimes difficult to identify affected individuals
Postpartum uterine disease
-Metritis: acute, bacterial uterine infection (< 10
DIM)
oSystemic signs: T > 39.5, off feed, toxemia
oCow is systemically ill (fever, off feed)
oMay or may not also have RP
oUterine discharge is watery, red-brown,
foul smelling (E. coli & anaerobic bacteria)
oNormal discharge is thick, often red (lochia)
oLargely a problem of postpartum immune function
oTreatment: systemic antibiotics
oEconomic loss due to antibiotic treatment, culling & death, milk loss, reproduction (highest costs
are antibiotic & reproduction)
-Endometritis: infection/inflammation of uterus
oNo systemic signs (> 21 DIM), clinical signs is purulent vaginal discharge (15-20%), cytological
(subclinical) endometritis (15-20%)
oLocalized inflammation of the uterus
oCharacterized by delayed involution – disease only exists if the process is impaired or
prolonged
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oDevelopment depends on the immune response of the cow
oTreatment is intrauterine (IU) antibiotic 4-6 weeks post-partum
oEconomic impact of endometritis is reproductive inefficiency (additional days open, conceive
later, could fail to become pregnant, may have to cull (1.2-1.7× risk), increased early pregnancy
losses possible) & milk discard due to antibiotics
-Physiology vs. pathology almost all cows have bacterial contamination of the uterus after calving
oSame immune system mediators appear to be involved in healthy & affected cows (TLR4, IL-1,
IL-6, IL-8, IL-10, TNF )α
oDifference lies in magnitude, regulation, duration & effectiveness of the response
-Cystic ovarian condition: ovarian follicle that fails to ovulate or regress & grows to abnormal size (>
2.5cm diameter) – cyst
oTraditionally thought that cysts were persistent & stopped the estrus cycle, but may impair
reproduction in the short-term
oOver-diagnosed & generally overrated as a problem
oTreatment: induce luteinizing hormone (LH) surge (Ovsynch) ± supplemental progesterone
For a profitable reproductive management, need estrus detection, intensity, accuracy, systematic breeding
management program while monitoring / treating dystocia, RP, abortion & uterine disease
Abortion: premature expulsion from the uterus of the embryo or non-viable fetus
-Etiology: impairment of the function of the placenta, damage to fetus (non-infectious or infectious – non-
contagious or contagious)
-Non-infectious abortion: early embryonic loss (15-25% of pregnancies diagnosed at 28d gestation are
lost by 60d), twins, heat stress, fetal genetic anomalies, iatrogenic (accidental prostaglandin hormone
administered)
-Infectious non-contagious abortion: disease agent may be introduced by circulation or up repro tract
oSporadic abortion (expected incidence 3-5%) - infectious, does not represent danger to herd
Fungal (through bloodstream) or opportunistic bacteria (other maternal disease,
inflammatory response may cause abortion, e.g. E. coli mastitis)
-Infectious contagious abortion: agents are contagious & have predilection for causing abortion (i.e.
infectious bovine rhinotracheitis, bovine virus diarrhea, leptospirosis, neospora)
oReproductive manifestations of a BVD
Conception decreases or EED before 42d
Create a persistently infected calf (PI)
Abortion of congenital anomalies at 125-170d
No fetal harm, born seropositive between 170d-280d
oNeospora caninum is a coccidian parasite that infects cattle, dogs
Totally subclinical in infected adults & infection is lifelong
Manifestation is abortion (4-7 months); if fetus is not aborted, calf likely to be infected
Cattle that aborts is likely to do so again
No effective treatment, eventual culling of cows that have aborted due to Neospora
Seropositive cows that have not aborted are not bred as herd replacement source
Life cycle of N. caninum
Dog is definitive host, tissue cysts are ingested by dog, unsporulated oocysts are
passed in feces
Oocysts in food, water, soil; ingested by intermediate hosts (cattle, sheep, etc.)
Tissue cysts in intermediate hosts, tissue cysts ingested by dog
Sporulated oocysts can also contaminate food & water, eaten by cow &
tachzoites are transmitted through placenta, infecting the fetus
Neospora abortion patterns
Endemic Epidemic
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Description
POPM 4230 Animal Health Midterm II Lecture 09: Reproductive Health & Udder Health Freemartin: heifer is born co-twin to a male, 90% are freemartins (chimera XX/XY) - Female sex characteristics androgenized, abnormal external and/or internal genitalia - 95% are sterile - No affect on male twin Lactation / gestation periods are influenced by breed - Let them dry up to build up the udder, nutritional status → allow rest time - If not given dry period, colostrum will not have as many Ab, protein, etc. Parturition: time from when they start to show signs that they are going to calf to time there is a calf on ground - Time to complete = heifer 2-4h, cow 20min-2h - Ligaments are first relaxing during first birth with a heifer (takes longer) - Stage I: relaxation of the pelvic ligaments (tail head “up”) o Making room for calf to come through birth canal o Relaxation & dilation of the cervix o Fetus changes position o Placental membranes push against cervix by rhythmic contractions of the uterus o Can take 2-3 days for this stage to complete to Stage II - Stage II: allantois ruptures, amniotic sac ruptures, fetus is expelled from uterus by abdominal contractions, uterine contractions & fetal movement - Stage III: expulsion of fetal membranes (< 12h is normal), uterine involution (< 28d) Calving: presentation, position, posture (hooves & head first) Dystocia: difficult birth - Failure of the cervix to dilate → common in sheep, cattle if fetus is malpositioned or uterus torsed - Obstruction of vagina → too much pelvic fat in heifers - Failure of vulva or vagina to dilate (more common in heifers) - Uterine torsion = uterus twists around long axis - Uterine inertia = milk fever or exhaustion (need minerals, i.e. Ca, P, etc., for muscle tension to push) - Maternal-fetal disproportion = fetus is too large for pelvis o Want to breed heifer to bull that has good calving offspring (i.e. small shoulders) - Abnormal presentation, position, posture; twins - Malformed fetus (shistosomus reflexus where the belly wall does not close) Use chains to pull legs out because of slipperiness after membranes have ruptured - Do not want to use full force, some situations need C sections - If pasterns are > 15 cm past vulva, then shoulders are clearing birth canal - If presentation is okay, can leave (cows = 30min-1 h, heifers = 1-2h) - Maximum force = 2 people’s arms - Keep clean, use lots of lube, follow natural downward arc in delivery, rotate calf during delivery Consequences of dystocia - Death of fetus - Vaginal tears, uterine tear - Obturator nerve paralysis (calving too tight, damages pelvic nerves of cow) - Sciatic nerve paralysis (down too long), muscle damage due to being down Long-term issues to dystocia - Prolapsed uterus (after difficult calving or with milk fever, rupture uterine arteries) - Fracture of ribs or long bones of calf - Stillbirth Retained placenta (RP): failure to expel fetal membranes by 24h post-calving - Risk factors: dystocia, twins, abortion, milk fever, Caesarian section, induced delivery - Immune function is greatly reduced in cows with RP - RP is a major risk factor for subsequent metritis (serious systemic illness) and/or endometritis (chronic localized inflammation with reduced fertility) - Impact of RP depends on ability of cow’s immune system to deal with it Normal postpartum involution - Process of restoration of reproductive tract to ability to support subsequent pregnancy - Shrinkage & repair of uterus & cervix - Lochia = sloughing of endometrium - Clearance of bacterial contamination within 3wks - Ideally: gross – 21d, histologic – 40d - Restoration occurs in parallel with return to cyclicity (resumption of estrous cycles) - “Voluntary waiting period” (VWP) = ~50 days in milk (DIM) Postpartum anestrus: several recent studies indicate that 20-25% of dairy cows may not cyclic by 60 DIM - May be pronounced in 1 lactation - Risk factors relate largely to cow’s health during this transition period – nutrition (negative energy balance – NEB), body condition score (BCS) & underlying metabolic disease (e.g. ketosis & displaced abomasum) - Sometimes difficult to identify affected individuals Postpartum uterine disease - Metritis: acute, bacterial uterine infection (< 10 DIM) o Systemic signs: T > 39.5, off feed, toxemia o Cow is systemically ill (fever, off feed) o May or may not also have RP o Uterine discharge is watery, red-brown, foul smelling (E. coli & anaerobic bacteria) o Normal discharge is thick, often red (lochia) o Largely a problem of postpartum immune function o Treatment: systemic antibiotics o Economic loss due to antibiotic treatment, culling & death, milk loss, reproduction (highest costs are antibiotic & reproduction) - Endometritis: infection/inflammation of uterus o No systemic signs (> 21 DIM), clinical signs is purulent vaginal discharge (15-20%), cytological (subclinical) endometritis (15-20%) o Localized inflammation of the uterus o Characterized by delayed involution – disease only exists if the process is impaired or prolonged o Development depends on the immune response of the cow o Treatment is intrauterine (IU) antibiotic 4-6 weeks post-partum o Economic impact of endometritis is reproductive inefficiency (additional days open, conceive later, could fail to become pregnant, may have to cull (1.2-1.7× risk), increased early pregnancy losses possible) & milk discard due to antibiotics - Physiology vs. pathology → almost all cows have bacterial contamination of the uterus after calving o Same immune system mediators appear to be involved in healthy & affected cows (TLR4, IL-1, IL-6, IL-8, IL-10, TNFα) o Difference lies in magnitude, regulation, duration & effectiveness of the response - Cystic ovarian condition: ovarian follicle that fails to ovulate or regress & grows to abnormal size (> 2.5cm diameter) – cyst o Traditionally thought that cysts were persistent & stopped the estrus cycle, but may impair reproduction in the short-term o Over-diagnosed & generally overrated as a problem o Treatment: induce luteinizing hormone (LH) surge (Ovsynch) ± supplemental progesterone For a profitable reproductive management, need estrus detection, intensity, accuracy, systematic breeding management program while monitoring / treating dystocia, RP, abortion & uterine disease Abortion: premature expulsion from the uterus of the embryo or non-viable fetus - Etiology: impairment of the function of the placenta, damage to fetus (non-infectious or infectious – non- contagious or contagious) - Non-infectious abortion: early embryonic loss (15-25% of pregnancies diagnosed at 28d gestation are lost by 60d), twins, heat stress, fetal genetic anomalies, iatrogenic (accidental prostaglandin hormone administered) - Infectious non-contagious abortion: disease agent may be introduced by circulation or up repro tract o Sporadic abortion (expected incidence 3-5%) - infectious, does not represent danger to herd  Fungal (through bloodstream) or opportunistic bacteria (other maternal disease, inflammatory response may cause abortion, e.g. E. coli mastitis) - Infectious contagious abortion: agents are contagious & have predilection for causing abortion (i.e. infectious bovine rhinotracheitis, bovine virus diarrhea, leptospirosis, neospora) o Reproductive manifestations of a BVD  Conception decreases or EED before 42d  Create a persistently infected calf (PI)  Abortion of congenital anomalies at 125-170d  No fetal harm, born seropositive between 170d-280d o Neospora caninum is a coccidian parasite that infects cattle, dogs  Totally subclinical in infected adults & infection is lifelong  Manifestation is abortion (4-7 months); if fetus is not aborted, calf likely to be infected  Cattle that aborts is likely to do so again  No effective treatment, eventual culling of cows that have aborted due to Neospora  Seropositive cows that have not aborted are not bred as herd replacement source  Life cycle of N. caninum  Dog is definitive host, tissue cysts are ingested by dog, unsporulated oocysts are passed in feces  Oocysts in food, water, soil; ingested by intermediate hosts (cattle, sheep, etc.)  Tissue cysts in intermediate hosts, tissue cysts ingested by dog  Sporulated oocysts can also contaminate food & water, eaten by cow & tachzoites are transmitted through placenta, infecting the fetus Neospora abortion patterns Endemic Epidemic Occurrence Common Less common Transmission Vertical Horizontal Abortion rates > 5% / Up to 30% / year year Abortion risk 3-7× risk Up to 40× risk Stage Cows 4-5 months Much more 3-7 months Variable Heifers Problems in cattle reproduction - At calving = dystocia / still birth o Caused by fetal-maternal malproportion, fetal posture and/or incorrect assisted delivery - Before open = failure to cycle o Due to nutritional/endocrine lack of LH surge or BCS in true anestrus, or cystic ovarian condition o Failure to detect heat / inseminate can also occurs during open - After being open = failure to conceive o Inhospitable uterus (i.e. endometritis, ▯ urea-N, heat stress, Trichomonas, Campylobacter) o Can also fail to detect heat / inseminate during this time - During pregnant = early embryonic death, abortion o Early embryonic death can be due to nutritional endocrine lack of P4, failed recognition of pregnancy, genetic / developmental anomalies, heat stress, mastitis, BVD o Abortion can be caused by Neospora, BVD, IBR, mycotic, leptospirosis, salmonellosis, iatrogenic reasons, listeriosis, ureaplasma, toxic Udder anatomy – 4 quarters or mammary glands that each has an associated teat, suspensory ligament holds up the udder keeping it healthy anatomically (up & away from the environment) - Teat purpose is for calf to access milk - Teat duct (streak canal) purpose is acting as a barrier for infection Udder health in heifer - Supernumerary teats: extra teats, a birth anomaly in 50% of heifers o Most do not open into a gland (no streak canal/duct), removed before 2 months of age - Nutrition – do not overfeed - Clean environment – can pick up mastitis pathogens Mastitis: inflammation of mammary gland, frequently associated with bacterial infections - Typically 1 cow in 5 has ≥1 case of clinical mastitis per lactation - Often the most economically important disease on a dairy farm ($120-300 per case, ~$5,000-$12,000 per 100 cows per year) & the #1 reason for use of antibiotics in dairy cows - Reduces milk production (cannot sell milk from cows with clinical mastitis, costs to treat; cows with subclinical mastitis produce less milk), reduces profits o Consumers want nutritious, safe milk from healthy cows o Food safety & welfare issue - Mammary gland is susceptible because mastitis-causing organisms are common on cow’s skin & in environment, milk is difficult place for immune cells & Abs to function (viscous, pH, fat content) & blood- milk barrier in the gland limits the help the immune system can provide - Clinical mastitis: visibly abnormal milk, severity is not well correlated with the etiologic agent o Mild = flakes, clots or watery milk, normal quarter o Moderate = abnormal milk with swollen/hard quarter o Severe = abnormal milk, quarter & systemically ill cow o Typically 3-10 days of production lost (non-saleable milk) per clinical case o Costs include: milk discarded (waste milk), cow treatment costs (vet visit, medication), labour (hand-milking, treating), risk of drug residues (penalties), risk of infection to other cows o With optimal management, the goal is < 2% clinical case rate per month o Majority of clinical cases occur in the first month after calving o Major clinical mastitis pathogens were S. aureus, E. coli, etc. - Subclinical mastitis: inflammation without visibly abnormal milk, detection by somatic cell count (SCC) [somatic cells are the immune cells, neutrophils, in milk] o Routinely measured weekly (in bulk milk, all herds) and/or monthly on individual cows in herds on DHI (dairy herd improvement) → SCC is associated with the probability of bacterial infection o California mastitis test is a simple cow-side test that qualitatively assesses SCC (not exact)  Detergent in solution reacts with DNA in neutrophils to form gel  Cheap, fast & provides information at the quarter level - Diagnosis is visual or SCC – based on bacteriologic culture (takes at least 12-24h, up to 3-4d) o Identifying causative agent important for treatment decisions, prognosis, preventative measures - Transmission o Contagious – cow-to-cow, reservoir, infected cow’s udder is transmitted often during milking  Streptococcus agalactiae  Staphylococcus aureus o Environment to cow (reservoir = bedding, stalls, manure)  Environmenal streptococci = S. uberis, S. dysgalactiae  Coliforms = E. coli, Klebsiella - Contagious – Staph. aureus o Tends to establish chronic infections  Intermittent high SCC, periodic clinical flare-ups, progresses to chronically high SCC & scarring of udder  > 90% of herds have ≥1 infected cow o Very poor response to antibiotics ∴ antimicrobial resistance can be a problem  Often micro-abscesses in glands  Can survive inside macrophages  Better to treat cows when dry (higher cure rate than IMM therapy while lactating) o Prevention is critical  Milk hygiene (washing udders, individual towels), segregation or elimination of infected quarters, milking infected cows last in the milking line, selective culling - Environmental strep’s generally cause clinical mastitis o Group of various species of varying virulence, chronicity & response to therapy o Duration of infection can last days to weeks o Generally respond well to IMM antibiotics (may benefit from extra-label, extended duration therapy, but may cause antimicrobial resistance) - Environmental coliforms o E. coli lives in manure, generally causes clinical mastitis & a short duration of infection (1-3d)  Can be severe (endotoxemia), not response to antibiotics o Klebsiella is similar to E. coli, tends to establish chornic infection  High SCC with or without chronic clinical mastitis o Bacteria invade udder & grow rapidly, infection is short but nasty o Endotoxin (gram – bacterial cell wall component) absorbed into blood, hijacks cow’s immune system, causing excessive inflammatory response o Cow can go from normal to severe mastitis in 12-24h o Outcomes: recovery, loss of quarter, loss of lactation, abortion, death - Control of environment mastitis o Reduce teat end contamination (clean stalls, sand bedding, good ventilation, clean floors / yards, milking hygiene i.e. pre-dip) o Vaccination against coliforms o Nutrition to support immune function - Majority of clinical cases occurs in first month after calving Dry period – within ~2 weeks after dry-off, keratin plug forms in streak canal to seal teat - ~25% of teats fail to close, most new infections occur in these quarters - Once involuted, gland is very resistant to new infection, but existing infections or new IMI acquired in early dry period frequently become clinical in early lactation - Dry cow therapy o Antibiotic = long-acting formations (~2 weeks), eliminate existing infections, prevent new IMI during involution o Teat sealant = inert physical barrier in the teat end to prevent new IMI throughout the dry period Lecture 10: Dairy Transition Management Lactation cycle = ~365 days - Heifers calving at ~2 years - 305 day lactation cycle - Inseminate or provide bull – 12-13 month calving interval - 9 month gestation - Cease milking ~2 months before calving, calve out & join the milking herd Transition: change from being a dry cow in late pregnancy to milking, 3 weeks before & 3 weeks after calving Dry-off: cessation of milking, can be abrupt or gradual - Far-off dry: early dry period, refers to time to calving (8-4 weeks pre-calving) - Close-up dry: late dry period (4 weeks to calving) Grouping - Single dry cow group = move one into maternity pen at a time - Two group dry cow groups = move far-off together, to close-up, to maternity pen all together Challenges of transition groups - Dietary adjustments → may have 3 different diets from early dry period (far-off) to late dry period (close-up), rumen & gut adaptations to new diets - Group changes → social disruption, takes 2-3 days to stabilize social structure with each addition - Immune function o Acute & chronic stresses (pen additions, fighting for resources) o Decrease in immunity of pregnancy o Inflammation due to calving (pain, swelling) o ▯ bacterial challenge of calving & lactation (teat canal open to environment during lactation) - Physiological adaptations o Each diet change requires rumen & gut adaptation (takes ~10-14 days) o Impending calving: adaptation of mammary gland for milk production takes ~3wks, relaxation of cartilage - Calving o Inflammation (pain, swelling) o Exhaustion & change in time budget (no longer laying down for long periods of time, less time spent sleeping, getting restless) o Potential for injury o Dystocia – increased risk for other problems (need assistance calving) o Retained placenta - Energy partitioning o Growing fetus & lactation  Ca &+  energy demand) o Within last week before calving, drop 30% of DMI, consistent drop in feed intake  Gradual decrease two weeks prior to calving, steep decline a week before calving  Ramp up again eventually after calving  Reasons for intake drop are not completely understood  Decrease in rumen space from growing fetus (little evidence)  Acute stress of impending calving  Roles of insulin & leptin (changes focus of putting on fat into breaking down fat)  Increase in non-esterified fatty acid (NEFA) (decreases appetite)  Competition for space at feed bunk or stall space, lack of feed access  Group changes & social disturbances  Dietary changes  Heat stress o Negative energy balance (NEB): milk energy required exceeds food energy obtained, start of lactation has a large energy requirement 30-50% of cows will have infectious or metabolic disease around the time of calving - Transition diseases include milk fever, retained placenta, metritis, clinical & subclinical ketosis, displaced abomasum, (early) clinical mastitis, endometritis - Milk fever has an incidence rate of 5-15% (increases in older cows) - Clinical ketosis has an incidence rate of 2-3% - Subclinical ketosis has an incidence rate of 15-40% - Displaced abomasum (DA) sees an incidence rate of 2- 5% Disease / Disorder Days (Calving to Diagnosis) Milk fever At calving Retained placenta < 1 day Metritis 3 – 7 days Ketosis 7 – 12 days st Left DA 8 – 12 days (90% in 1 6 wks) Subacute ruminal 1 – 20 days acidosis (2 groups) 45 – 150 days Disease occurs in first 4 weeks - Can happen together as well - Transition diseases are interconnected o Having ketosis increases risk of having left-DA o Having milk fever increases risk of having left-DA o Having milk fever increases risk of having ketosis Cost of poor transition - Unrealized milk production (lower production), reduced reproductive performance - Treatment costs, discarded milk - Culling & death Direct costs (DA, ketosis, milk fever) = $175 - $450 per case Milk fever – hypocalcemia, or parturient paresis - No agent → is not an infectious disease - Large outflow of body Ca into colostrum after calving 2+ 2+ - 10L of colostrum includes ~232+of Ca from a single milking (9× amount of Ca available in plasma) - Cow needs to replace the Ca through increased bone resorption & absorption from the diet - Risk factors o Disease likelihood increases with increasing lactations (3+) o Jerseys are more prone to milk fever - All cows will experience some degree of Ca drain - There are clinical & subclinical diseases - If Ca drains are too large, can disrupt muscle function (Ca is an important signaling molecule) o Causes weakness o Could result in a down cow - Calcium regulation & milk fever o Bones are quick & large source of 2+ Ca , so body increases bone 2+ resorption to increase blood Ca levels to make colostrum o More acidic blood pH will improve resorption o Low Mg inhibits bone resorption o Thyroid gland also produces more parathyroid hormone to upregulate the activation of vitamin D which leads to increased passive & active transport of calcium absorption from the diet (this is too slow, but will help) - Clinical milk fever o Stage I (< 1h)  Unsteady  Cool extremities (skin, ears)  Can be hyper-excitable o Stage II (1-12h)  Unable to rise, lying in sternal  Depressed, head on flank o Stage III  Lying in lateral (flat out on their side)  Susceptible to bloat  Death if untreated  Lateral lying position can cut off blood flow to legs, muscle dies off without nutrients & oxygen & necrotic tissue produces toxins  Also affects heart muscle signaling - Consequences of subclinical milk fever o Increased odds of DA, increased odds of culling o Loss in milk yield in early lactation (production-limiting) o Decreased immune function (predisposed to bacterial infection) o Altered fatty acid metabolism - Prevalence of subclinical milk fever in SW Ontario = 32% of tested cows (429 sampled), almost a third had no clinical signs - Treatment of milk fever o Clinical milk fever requires immediate attention o IV calcium infusion at Stage II & III  Short duration of effect < 4h  May require Mg supplementation (no longer inhibits bone resorption) 2+ o Ca supplements at Stage I & subclinical  Calcium gel, bolus, drench  Subcutaneous calcium injection - Treatment outcomes o Not fully recovered = production loss, risk of other diseases o Possibility of relapse o Down Cow Syndrome = lack of blood flow to limbs (ischemic necrosis), appears healthy but cannot rise (be aware of other diseases that cause Down Cow Syndrome) - Prevention of milk fever o Body has sufficient Ca mostly within bone ∴ must be able to mobilize Ca fast enough o Dietary absorption can help but cannot compensate fast enough o Old theory was to prime the system by reducing dietary Ca pre-partum, but you cannot restrict levels low enough for this to work (not practically manageable) o Create a mildly acidic blood environment to aid in resorption, optimizes osteoclast function  Negative DCAD diet – dietary cation anion difference diet + + -  (Na + K ) – (Cl + S)  Lowering DCAD creates mild metabolic acidosis  Adjust diet by reducing forages with K, feed anionic salts & use Ca binders  Anionic salts are unpalatable, need to be careful that intakes do not drop o If cow does not eat, it will exacerbate the NEB NEB occurs in every cow around calving - Space between energy we need & energy we can get from the diet - Primary fuel source is carbohydrates (glucose) o Dietary carbs (starch & fiber) are fermented to volatile fatty acids = acetate (70%), butyrate (10%), propionate (20%) o VFAs can be stored as lipids & converted to milk fats o Glucose is produced through gluconeogenesis using propionate & AAs o When glucose is not available, fats are mobilized as non-esterified fatty acids (NEFA) o Drop in DMI prior to calving, see more fats being mobilized & peaks in NEFA at calving - Dietary carbs are broken down into VFAs, moves through the bloodstream to the liver where propionate & AA are made into glucose to feed to the fetus / growing calf or the udder where the glucose is changed to lactate - Insufficient glucose being produced, body mobilizes NEFAs where they are processed in the liver o NEFAs & ketones will be used by the muscle, used for milk & the fetus after processing - In the liver, NEFA can be processed in 3 ways o Can be completely oxidized for energy, producing acetyl-CoA o It can be re-esterified into triglycerides & stored or exported to mammary gland o It can be partially oxidized into ketones (β- hydroxybutyrate, acetoacetate, acetone) Adaptive response to NEB - Spare glucose → use fat as fuel o Issues are that pre-partum, the fetus needs glucose & post-partum, lactation needs glucose ∴ these two instances that preferentially are stealing glucose - Increase gluconeogenesis & burn NEFA o Only can use propionate in gluconeogenesis o To use FAs for energy, glucose is required in the intermediate stages - NEFA leads to an increase in ketones & possibly fatty liver - Usually, processing of NEFA is in balance – most are being fully oxidized & some ketone bodies are being produced - A maladaptive response to NEB would see a lack of balance o The more NEFA the liver gets, the more that will be partially oxidized into ketones o Can partially oxidize some, but most are partially oxidized or stored o Lots of ketone bodies are being produced & causing fatty liver - Elevated NEFA pre-partum (above a threshold), it is associated with an increased risk of disease o Increased risk of DA, RP, ketosis o Decreased neutrophil function (early immune response is decreased) - Successful transition depends on the degree of NEB & a successful adaptation to NEB - Hard to monitor as there is no on-farm test (must send blood sample, costing time & money) Ketosis = occurs due to excessive NEFA breakdown (partial oxidation) - No agent - Elevation in circulating levels of ketones (acetone, acetoacetate, β-hydroxybutyrate) - β-hydroxybutyrate (BHB) is the main circulating ketone & most stable for detection - Unlike NEFA, can produce both subclinical & clinical disease - Most cows will have some ketones in circulation around calving, those that do not adapt well to NEB will have higher concentrations - Clinical ketosis occurs at different concentrations of BHB o Clinical signs: drop in feed intake, drop in milk production, dry manure, loss of body condition, nervous signs (less common, but will see wonky, look blind, throwing head around) - Subclinical ketosis (or hyperketonemia = high blood levels of ketones) o Ketones in circulation above threshold without clinical signs o Primary ketosis = due to maladaptation to NEB o Secondary ketosis = drop in feed due to other disease o Cannot really tell the difference - Prevalence of subclinical ketosis in Michigan & Ontario = 40-43% ketotic o Ranges depend on farm (management factors, genetic factors) - Risk factors for ketosis o Increasing number of lactations (more common in older cows) o History of being ketotic previously o Over-conditioned cows (possibly mobilize mo
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