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Midterm

POPM 4230 Midterm: Midterm 2 Summary Notes
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17 Pages
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Department
Population Medicine
Course Code
POPM 4230
Professor
Terri O' Sullivan

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HerdPatternFollowingVirus
Introduction
Acute Disease in
Susceptible Animals
Abortions and
Early
Embryonic
Death
PI Animals
Weak or
deformed
calves
Principles of Infectious Disease Control in the context of Dairy Cattle Health
Disease: Complex interactions, result of a combination of risk factors
Biology of the individual and Biology of interactions of the individuals (herd effect) and agent and environment
Health and Disease in Balance
Control of disease is based on management of risk factors that may change over time
Eliminate at Herd, Regional, or National Level
Prevent entry into a (erd or Country that doesnt have disease
Control to keep it a manageable level in a Herd or Country ~ our only plan of action in some cases
BIOSECURITY a Definition
= the protection of people, animals and ecological systems against disease and other biological threats
Australian biosecurity CRC - biosecurity is achieved through systems that aim to protect public health, animal and plant industries, and the
environment, from the entry, establishment and spread of unwanted pests and diseases
Stop movement of things that can cause disease infectious disease control ~ need to understand disease to control disease
SCENARIO
- expanding vxd dairy herd, bought in springing heifers last month
- several milking cows develop severe diarrhea w. fevers and drop in milk production 2 die, 3 recover
- 2 wks later, 2 of these and 4 other cows and heifers abort, 2 other heifers give birth to weak calves that have difficulty walking
~a lot of diseases target an age group but this is targeting them all
BVD in ONTARIO 1991-1995
- 200 + dairy farms w. outbreaks of acute BVD
- many herds were vaccinated for BVD, BUT many animals were NOT immunized for BVD
- our failure to use vx correctly over many years was detected by the BVD virus
~ all herds were supposedly vxd but found holes in vx programs
BOVINE VIRAL DIARRHEA VIRUS
2 Genotypes of the BVD Virus: Type I and Type II
- Type )) was isolated in acute clinical cases from Canada and NE USA in the Mid s
- Both types are capable of causing severe disease (~ even though genetically different)
- Some, BUT Incomplete Immunological Cross-Protection between Genotypes
- Therefore, most vaccines contain both Type I and Type II strains
BVDV
For BVDV the BIOTYPE is defined by the growth characteristics of the virus in cell culture
- Cytopathic (CV) strains kill cells in culture
- Non-Cytopathic (NCV) strains do NOT kill cells in culture (associated w. PI animals)
- Biotype does NOT relate to Acute Virulence
PERSISTENT BVD INFECTION
Infection of Fetus w. Non-Cytopathic BVDV < 125 days of gestation can result in production of a PI Calf
- virus NOT recognized as Non-Self
- virus shedding is continuous for most of animals life AND most do NOT survive adulthood (good news)
- - BUT if they do survive adulthood they are a continuous source of infection for the herd (bad)
EPIDEMIOLOGY of BVDV
- worldwide distribution in cattle
- some European countries are actively engaged in eradication programs
- PI animals are the main reservoir of BVDV in the bovine population
- estimate 0.5-2% in population
- mostly < years old many P)s develop mucosal disease and die by then
BVD TRANSMISSION
- spreads by direct contact w. shedder
- mainly through viral shedding in saliva, mucus, semen, (manure) - OR, in Utero ( PI)
- Shedding:
- PI (large numbers and constant)
- Acute, virulent Type II (shorter duration)
- Other Acutely ill animals
BVDV INFECTION
- upper respiratory tract and lymphoid tissues are the sites of virus replication
- destruction of lymphoid tissue immune suppression
- Viremia starts 3 days to 8-10 days after infection by duration may be as short 2-3 days for some cattle
- 70-90% of infections are subclinical
- no overt disease, seroconversion ie. successful immune response
~ produces whole spectrum of symptoms from really bad to not much going on
RISK FACTORS FOR BVD DISEASE
- herd has a hx of inadequate immunization
- NO MLV used or failure to give primary series of killed vx
- animals are purchased
- screening tests for BVD NOT performed
- new purchases are NOT isolated
MucosalDisease
NCV
CV
NCV & CV
PI Animal
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CLINICAL PRESENTATIONS OF BVD
Mucosal Disease only in P)s
Peracute BVD high fever, off feed, diarrhea, death w. in 48 hours
- hemorrhagic syndrome-fever, diarrhea, severe platelet depression, death
Acute BVD fever, diarrhea, pneumonia, abortion
Immune Suppression and secondary pneumonia (or other disease)
BVD associated Reproduction Problems abortions, congenital anomalies
~ whole spectrum of disease, doesnt help us figure it out
MUCOSAL DISEASE
- PI animals only, usually < 2yrs old
- Morbidity low (few animals) BUT case fatality ~ 100%
- fever
- oral erosions (~ on soft palate)
- diarrhea sometimes w. blood
- die in 5-7 days
~ a new strain not exposed to before usually ends up killing them (different than in utero strain)
BVD CONGENITAL DISEASE
- Cerebellar Hypoplasia
- Blind or Cataracts small unthrifty
- Lack of hair (~pattern baldness, patches of missing hair)
~ exposure likely happened months prior
BVDV and REPRODUCTION
- best available vx ~ 80-90% effective at fetal protection
- reproductive problems can persist despite an aggressive immunization program (difficult to rigorously quantify)
- a PI Dam will always have PI Calf
ECONOMIC COSTS of BVDV
- very small percentage of all BVDV infections are clinical
- acute disease of highly pathogenic strain may kill 25-40% of infected animals and cause severe milk depression and weight loss
- abortions
- smoldering reproductive problems
BVD TREATMENT
- no specific tx
- supportive care and antibiotics for secondary infections in acute BVD
- PI calves generally die of mucosal disease OR should be euthanized (source of virus to herd)
BVD CRITICAL CONTROL POINTS
Prevent/eliminate PIs and Prevent Acute Disease
- adequate, correctly implemented vx program
- MLV for Fetal protection
- Introductions: NO nose to nose or manger/waterer contact for 3 wks
- Test for BVD-Pi in Quarantine (~before intro to herd)
- Vaccinate purchases in Quarantine
- Isolation of animals w. diarrhea and respiratory disease
SALMONELLOSIS
- numerous serotypes
- infection shedding disease
- Sporadic and Epidemic associated w. parturient disease and stress
- prevention of introduction unlikely (- rodent/wildlife control)
- following outbreak infection becomes Endemic
- cows = wks mths (- yrs) VS - farm = years
- many strains of various virulence (host adapted VS non-host adapted)
- infects any species w. an intestinal tract
- organism is prevalent
- disease is opportunistic
- ZOONOTIC
Clinical Signs of Salmonellosis
Most Salmonella Species:
- diarrhea bloody, fibrin casts (in severe strains) and commonly in fresh cows
- fever, off-feed
- drop in milk
- abortions ~ if serious enough
- calf septicemia, diarrhea, death in calves (~rarely kills cows but will kill calves)
different …Salmonella Dublin **
- emerging disease ~ different then Salmonellas were used to due to resp signs, sudden outbreak of resp disease in calves
- Causes Respiratory signs
- diagnosed in dairy herds in northern USA and in Quebec .. and on veal farms
- sporadic cases on ONT dairy farms
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SALMONELLOSIS TRANSMISSION
- Fecal >> Oral/nasal/urine (septicemic)
- infected does not mean clinical and clinical does not mean septicemic
- Clinicals shed up to 109 /g manure
- rumen VFAs protective
- infectious dose in healthy adults = 109
- infectious dose in off-feed cows = 102 -103 ~ infectious dose drops dramatically in animals w. depressed feed in take, after calving
- opportunist of calves and peripartum cows
Salmonellosis Critical Control Points
- INTRA-herd biosecurity restrict movement of manure/fomites
- separate hospital and calving pens
- rational Abx use
- emphasize separation of calves and cows in outbreak
- NO vaccine!
JOHNEs DISEASE
Mycobacterium avium, subsp. paratuberculosis (MAP)
- thick walled bacteria very resistant to environmental destruction
- can infect cattle, deer, bison, sheep and goats
- very slow growing (~ hard to work w., have to wait ~16 wks for it to grow on special media)
- mainly in ileum (distal S.I)
~ time until clinical disease also takes a long time, takes years
TRANSMISSION of JD
= mostly fecal-oral
- organism shed in manure
- contaminate feed, pasture, water, calving pen oral ingestion of bacteria
- in advanced stages of disease organisms may pass from dam to fetus in utero OR in colostrum
- generally thought to infect calves <6 months old, highest risk is newborns BUT evidence that older calves can be infected
~ utter contaminated, calf ingests manure and grows to develop JD but wont see it until  yrs down the road
EPIDEMIOLOGY of JD
- animals exposed as adults may become infected but we dont know infective dose
- many animals will never develop Clinical disease
- Clinical disease onset from 18 months to 6+ year of age
- age of onset of disease may depend on level of exposure as a calf
- bacteria may survive years on pasture
PATHOLOGY of JD
- intestines become thickened w. bacteria and inflammatory cells
- Malabsorptive diarrhea (~ due to thickening of the gut)
~ have diarrhea but do not loose appetite not typical of other diseases
CLINICAL SIGNS of JD
- episodes of profuse diarrhea, weight loss but good appetite, no blood or fever
- often in fresh cows
- diarrhea eventually becomes chronic
- cows usually culled before death
- subclinical infection appears to reduce milk production (~ not huge, but do produce less)
TX and CONTROL of JD
- NO effective tx
- goal is to remove infected animals (selective slaughter) and prevent new infections
- diagnostic tests are very imperfect
- blood or milk EL)SA for Serum Abs to MAP
- Se= 15-45%, Sp= 99.2% for subclinical
- Milk ELISA is useful to estimate herd prevalence
- Fecal culture of individuals or pooled samples
- expensive and takes up to 3 mths
- better sensitivity but still ~40 to 60%
- Direct PCR on feces
~ test produce a lot of False negs (poor sensitivity) for JD
~ dont have tests that allow us to eradicate this disease
BIOSECURITY FOR JD
- dont allow claves to eat manure
- basic control measures will help prevent salmonellosis, calf scours
- risk assessment and management plan
~ use what we know and how we can min disease, evaluate management at different steps, try to get calves away from 1st manure meal
**Johnes Education and Management Assistance Program
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Description
find more resources at oneclass.com Principles of Infectious Disease Control in the context of Dairy Cattle Health Disease: Complex interactions, result of a combination of risk factors Biology of the individual and Biology of interactions of the individuals (herd effect) and agent and environment Health and Disease in Balance Control of disease is based on management of risk factors that may change over time  Eliminate at Herd, Regional, or National Level  Prevent entry into a (erd or Country that doesn▯t have disease  Control to keep it a manageable level in a Herd or Country ~ our only plan of action in some cases BIOSECURITY – a Definition = ▯the protection of people, animals and ecological systems against disease and other biological threats▯ Australian biosecurity CRC - biosecurity is achieved through systems that aim to protect public health, animal and plant industries, and the environment, from the entry, establishment and spread of unwanted pests and diseases  Stop movement of things that can cause disease – infectious disease control ~ need to understand disease to control disease SCENARIO - expanding vx▯d dairy herd, bought in springing heifers last month - several milking cows develop severe diarrhea w. fevers and drop in milk production – 2 die, 3 recover - 2 wks later, 2 of these and 4 other cows and heifers abort, 2 other heifers give birth to weak calves that have difficulty walking ~a lot of diseases target an age group but this is targeting them all BVD in ONTARIO 1991-1995 - 200 + dairy farms w. outbreaks of acute BVD - many herds were ▯vaccinated▯ for BVD, BUT many animals were NOT ▯immunized▯ for BVD - our failure to use vx correctly over many years was ▯detected▯ by the BVD virus ~ all herds were supposedly vx▯d but found holes in vx programs BOVINE VIRAL DIARRHEA VIRUS 2 Genotypes of the BVD Virus: Type I and Type II - Type )) was isolated in acute clinical cases from Canada and NE USA in the Mid ▯▯▯▯▯s - Both types are capable of causing severe disease (~ even though genetically different) - Some, BUT Incomplete Immunological Cross-Protection between Genotypes - Therefore, most vaccines contain both Type I and Type II strains BVDV For BVDV the BIOTYPE is defined by the growth characteristics of the virus in cell culture - Cytopathic (CV) strains kill cells in culture - Non-Cytopathic (NCV) strains do NOT kill cells in culture (associated w. PI animals) - Biotype does NOT relate to Acute Virulence PI PERSISTENT BVD INFECTION NCV Animal Infection of Fetus w. Non-Cytopathic BVDV < 125 days of gestation can result in production of a PI Calf Mucosal - virus NOT recognized as Non-Self - virus shedding is continuous for most of animals life AND most do NOT survive adulthood (good news) CV Disease - - BUT if they do survive adulthood they are a continuous source of infection for the herd (bad) NCV EPIDEMIOLOGY of BVDV - worldwide distribution in cattle CV - some European countries are actively engaged in eradication programs - PI animals are the main reservoir of BVDV in the bovine population - estimate 0.5-2% in population - mostly > Oral/nasal/urine (septicemic) - infected doe9 not mean clinical and clinical does not mean septicemic - Clinicals shed up to 10 /g manure - rumen VFA▯s protective - infectious dose in healthy adults = 10 - infectious dose in off-feed cows = 10 -10 ~ infectious dose drops dramatically in animals w. depressed feed in take, after calving - opportunist of calves and peripartum cows Salmonellosis Critical Control Points - INTRA-herd biosecurity – restrict movement of manure/fomites - separate hospital and calving pens - rational Abx use - emphasize separation of calves and cows in outbreak - NO vaccine! JOHNE▯s DISEASE Mycobacterium avium, subsp. paratuberculosis (MAP) - thick walled bacteria very resistant to environmental destruction - can infect cattle, deer, bison, sheep and goats - very slow growing (~ hard to work w., have to wait ~16 wks for it to grow on special media) - mainly in ileum (distal S.I) ~ time until clinical disease also takes a long time, takes years TRANSMISSION of JD = mostly fecal-oral - organism shed in manure - contaminate feed, pasture, water, calving pen – oral ingestion of bacteria - in advanced stages of disease organisms may pass from dam to fetus in utero OR in colostrum - generally thought to infect calves <6 months old, highest risk is newborns BUT evidence that older calves can be infected ~ utter contaminated, calf ingests manure and grows to develop JD but won▯t see it until ▯ yrs down the road EPIDEMIOLOGY of JD - animals exposed as adults may become infected but we don▯t know infective dose - many animals will never develop Clinical disease - Clinical disease onset from 18 months to 6+ year of age - age of onset of disease may depend on level of exposure as a calf - bacteria may survive years on pasture PATHOLOGY of JD - intestines become thickened w. bacteria and inflammatory cells - Malabsorptive diarrhea (~ due to thickening of the gut) ~ have diarrhea but do not loose appetite – not typical of other diseases CLINICAL SIGNS of JD - episodes of profuse diarrhea, weight loss but good appetite, no blood or fever - often in fresh cows - diarrhea eventually becomes chronic - cows usually culled before death - subclinical infection appears to reduce milk production (~ not huge, but do produce less) TX and CONTROL of JD - NO effective tx - goal is to remove infected animals (selective slaughter) and prevent new infections - diagnostic tests are very imperfect - blood or milk – EL)SA for Serum Ab▯s to MAP - Se= 15-45%, Sp= 99.2% for subclinical - Milk ELISA is useful to estimate herd prevalence - Fecal culture of individuals or pooled samples - expensive and takes up to 3 mths - better sensitivity but still ~40 to 60% - Direct PCR on feces ~ test produce a lot of False negs (poor sensitivity) for JD ~ don▯t have tests that allow us to eradicate this disease BIOSECURITY FOR JD - don▯t allow claves to eat manure - basic control measures will help prevent salmonellosis, calf scours - risk assessment and management plan ~ use what we know and how we can min disease, evaluate management at different steps, try to get calves away from 1 manure meal **Johne▯s Education and Management Assistance Program find more resources at oneclass.com find more resources at oneclass.com **PROACTION = developed by dairy farmers of Canada = QA program for dairy farmers = provides documentation that assessment occurred JD AND HUMAN HEALTH - JD and Crohn▯s disease in ppl are clinically and pathologically similar - is it a ZOONOS)S? Jury▯s still out on this - MAP detected w. increased freq in tissues from Crohn▯s patients than - - healthy ppl or patients w. other )BD▯s - Not all Crohn▯s patients have MAP - probable role of genetic and other host factors - MAP might be factor in only a subset of patients if any - MAP in Crohn▯s patients may not be viable - - not clear if the organism is cause or effect (opportunistic) of lesions in ppl - MAP has been detected in raw milk, meat, water, sewage, wildlife - MAP may survive pasteurization – controversial JD CRTICAL CONTROL POINTS - prevent manure movement from adults to calves - identification and accelerated removal of infected (shedding) individuals - clean maternity pens - immediate calf removal (do not allow to nurse, catch it before it hits the ground) - non-pooled colostrum; not from infected cows - do NOT feed cow feed refusals to heifers - avoid manure spreading in same year as forage harvest JD is Complicated: - very slow to develop to Clinical disease, very hard to diagnose, esp in young animals, farmers believe it is difficult to control! Points from video on JD - drop in milk production, diarrhea, weight loss but still good appetite – could be JD - less than 5 % of infected cows show sickness, 1 sick cow means more infected but not showing - subclinical (secrete spread) stage lasts for years – just bc no clinical signs doesn▯t mean they aren▯t infected - don▯t pool colostrum - need clest MAP free colostrum for calves or use milk replacer - calves mostly infected by that 1 manure meal (or contaminated colostrum/milk) - portable calf pens – mom can be near but calf can▯t nurse from possibly infected utter - handle feed and manure separately (different buckets for skid steer) – cow manure can contaminate - calves and heifers should not come into contact w. manure, test for JD regularly BIOSECURITY Programs for infectious disease control that prevent or reduce the intro or movement of disease on an operation 1. Introduction of pathogens onto farm 2. Movement of pathogens w. farm 3. Transfer of pathogens to humans PRINCIPLES - in dairy herds we tend NOT to take an ALL PERILS approach - decide what you▯re trying to control/prevent - keep diseases you don▯t have OUT and minimize spread of diseases you have (endemic) - emphasize the need for INTRA-herd biosecurity - basic practices will reduce risk of numerous diseases (JD control will help w. calf scours) - assemble groups quickly and maintain BIOSECURITY BASICS – ▯A▯ List ▯for everyone!▯ - correctly implemented vx program - milking time hygiene - restricted manure movementand handling - isolation of sick animals - separate sick and maternity pens - prompt calf removal from cow environment - no colostrum pooling - remote deadstock, cull cow, and veal collection - disease monitoring program BIOSECURITY BASICS – ▯B▯ List - selective sourcing of purchases (buyer beware) - maximize knowledge of sources and animals being purchased (small numbers) - pre-introduction testing - milk replacer instead of milk/waste milk - Metaphylactic treatments find more resources at oneclass.com find more resources at oneclass.com UDDER HEALTH AND MANAGEMENT MASTITIS 101 ▯most costly disease for dairy industry▯– different opinions Mastitis – 1 word – many diseases - 130 + different organisms - bacteria, protozoa, algae  almost always a mix 2 mostly independent forms = Clinical and Subclinical = Contagious and Environmental MASTITIS = inflammation of the mammary gland - practically, associated w. bacterial infection (not always) - typically, 1 cow in 5 has >= 1 case of clinical mastitis per lactation - often most economically important disease on a dairy farm - ~$120-$300 per case - ~$5000-$12000 per 100 cows per year - #1 reason for use of Abx in dairy cows = mastitis The Battleground … - many mastitis causing organisms are common on the cow and in her environment - bacteria have potential to enter mammary gland during & after every milking - blood-milk barrier limits immune system components available to respond to challenge - milk is a difficult place for immune cells and antibodies to function ~ great growth place for bacteria and not a lot of antibody activity - evidence that some cows are genetically programed for a ▯better▯ immune response CLINICAL MASTITIS = visibly abnormal milk MILD = flakes, clots, or watery milk; normal quarter MODERATE = abnormal milk + swollen or hard quarter SEVERE = abnormal milk, quarter and systemically ill cow - severity is NOT well correlated w. the Etiologic agent - typically 3-10 days of production lost (non-saleable) per clinical case - costs include: - milk discard, tx, labor, risk of drug residues, possible risk of infection to other cows - typically, a substantial majority of cases occur in the 1 month after calving ~ risk not uniform across lactation, opens most after calving st ~ 1 mth after calving = highest immune suppression and stress - with optimal management, the goal is <2% clinical case rate per month SUB-CLINICAL MASTITIS - inflammation w. out visibly abnormal milk - detected by somatic cell count (SCC) - Somatic cells = immune cells (neutrophils) in milk - routinely measured - weekly in bulk milk – all herds - monthly on individual cows in herds SOMATIC CELL COUNT – SCC - associated w. probability of bacterial infection - Linear Score (LS) is the log (SCC) - linear relationship w. milk loss - reduced skewing of group avg SCC - SCC 200,000 cells/ml = LS 4 = typically cut-point for assumed infection - regulatory limit in bulk tank milk = SCC <400,000 cells/ml - fines and eventual shut-off if above this Milk loss due to subclinical Mastitis - milk that is never produced due to mammary inflammation, NOT due to discard ~ as linear score goes up milk production decreases CALIFORNIA MASTITIS TEST - simple cowside qualitative SCC - detergent in solution reacts w. DNA in neutrophils to form gel - cheap, fast, and provides information at the quarter level The Challenge of making Mastitis Decisions What can we measure for? Visible SCC, LDH, EC, NAGase - cow has done what supposed to = don▯t give abx - month later see she was challenged but did not respond – on going issue ~ wish we could have identified at start, hard to tell at 1 don▯t want to give abx bc told to limit them find more resources at oneclass.com find more resources at oneclass.com Variability in ▯daily▯ bulk tank SCC QUALITY THRESHOLD = 200,000 bulk tank SSC PENALTY THRESHOLD = 400,000 bulk tank SSC CONTROL OF MASTITIS GENERAL - milking hygiene and technique – clean dry teats, good milk let down, rapid milk out - clean environment - cow comfort - dry cow therapy Vs. PATHOGEN SPECIFIC - abx tx protocols for clinical cases - vaccination - selective culling ~ may need abx at end of lactation to clear infection/keep protected during dry Implement Tools Proven to Prevent Mastitis (20052015) - slip gloves on and change w. each cow (36% in 2005, 61% in 2015) - teat sealant (25%  73%) - use clean towels btw cows (88%  88%) - dipping teats (95%  97%) ~ injectable abx? (??  30%) NMC 10-Step Mastitis Control Program 1. establish udder health goals for the herd 2. maintain a clean and comfortable environment (cows and people) 3. always use proper milking procedures 4. properly use and maintain milking equipment 5. keep good records 6. manage clinical mastitis appropriately during lactation 7. use effective dry cow management – all quarters of all cows? 8. use biosecurity protocols (buyer beware!) and cull chronically infected cows ▯. monitor herd▯s udder health status regularly 10. periodically review the mastitis control program Monitoring of Cow SCC- DHI – Monthly – MUST HAVE! DIAGNOSIS of Mastitis - etiologic diagnosis may be important for tx decisions, prognosis, and specific preventative measures - definitive diagnosis based on bacteriologic culture – takes at least 12-24 hrs, up to 3-4 days ~ knowing what bacteria is causing disease most commonly gives us sense of where to look in environment, cows etc Incidence of New Infections during Lactation AND the Dry period **high infection seen when we stop milking cows – when drying them off ▯drying off▯ DRY COW THERAPY ANTIBIOTIC - long-acting formation (~2wks) - objectives = eliminate existing infections, prevent new IMI during involution TEAT SEALANT - inert physical barrier in the teat end - objective = prevent new IMI throughout the dry period DRY PERIOD - w. in ~2 wks after dry-off a Keratin plug forms in the Streak canal to seal the teat - ~25% of teats fail to close – most new infections occur in these quarters - once involuted, the gland is very resistant to new infection - BUT existing infections, or new IMI acquired in the early dry period frequently become clinical in early lactation CONTAGIOUS MASTITIS RESERVO)R = cow▯s udder, transmitted cow to cow Major Agents = Streptococcus agalactiae(gram +), Staphylococcus aureus(gram +), Mycoplasma bovis ~ 2 categories of bugs Streptococcus agalactiae (Step ag) - extremely contagious - associated w. - a high prevalence of subclinical mastitis (ie. many cows w. high SCC) - poor milking hygiene, lack of post-teat dipping - lack of dry cow therapy - very susceptible to IMM Abx – 90-95% cure rate w. labeled use of penicillin - uncommon, but occasional Epidemics find more resources at oneclass.com find more resources at oneclass.com Staphylococcus aureus - tends to establish Chronic infections - intermittent high SCC, periodic clinical flare ups, progresses to chronically high SCC and scarring of udder - very poor response to abx - direct resistance - micro-abscesses - survival inside macrophages - Lactating IMM therapy 10-40% cure rate - Dry cow therapy 40-60% cure rate ~difficult to treat, need to treat more aggressively - >90% of herds have >=1 infected cow – variable importance as a herd problem - prevention is critical – milking hygiene, dry cow therapy, segregation or elimination of infected quarters or cows ENVIRONMENTAL MASTITIS RESERVOIR = bedding, stalls, manure; transmitted Environment to cow Major Agents = Coliforms and Environmental Streptococci COLIFORMS = E. coli and Klebsiella(both gram neg) ENVIRONMENTAL STREP = Strep. uberis and Strep. dysgalactiae (both gram positive) COLIFORMS E. coli - lives in manure - generally causes clinical mastitis - generally short duration of infection (1-3days) - can be very severe (endotoxemia)  not responsive to Abx (~ vaccination for some colifroms?)  Klebsiella is similar to E. coli BUT tends to establish Chronic infection - - High SCC +- Chronic Clinical Mastitis COLIFORM MASTITIS - bacteria invade udder and grow rapidly - infection is short BUT nasty - Endotoxin (gram (-) bacterial cell wall component) absorbed into blood – hijacks cow▯s immune system ▯excessive inflammatory response) - cow can go from normal to severe mastitis in 12-24 hrs Outcomes = recovery, loss of quarter, loss of lactation, abortion, death ENV)RONMENTAL STREP▯s - a group of various spps of varying Virulence, Chronicity, and Response to therapy - Generally cause Clinical mastitis - duration of infection – days to weeks - generally repond to IMM Abx – 40-65% cure rate - may benefit from extra-label extended duration therapy CONTROL OF ENVIRONMENTAL MASTITIS - Reduce teat end contamination - clean stalls, sand bedding, good ventilation, clean floors/yards, milking hygiene – pre-dip - Vaccination against Coliforms - Nutrition to support immune function ~ dairy is a more targeted approach, VS swine uses keep everything out CALF DISEASES – Current Health Status of Pre-Weaned Calves PERINATAL MORTALITY = a calf carried to term, or at least longer than 260 days and born dead or dying w. in 24-48 hours of birth - 9.6% of calves are stillborn in Canada and 8% of calves are stillborn in US - significantly higher in primiparious heifers VS multiparous cows - approx. 90% of calves, which die in the perinatal period, were alive at the beginning of calving = = much of this loss is preventable! • Mortality risk throughout a dairy cow▯s life.. - Unweaned heifers have the highest mortality rate PRE-WEANED DAIRY CALF MORTALITY and MORBIDITY - 7.5% pre-weaning mortality risk in heifers born alive - – majority due of death due to Diarrhea - 23% of calves treated for diarrhea -21.9% of calves treated for pneumonia • How many calves do we have left? Assume an 8% Perinatal mortality rate - - 7.5% Pre-weaning mortality rate - - and calve 100 cows per year which results in 50 heifer calves CASE #1 - 160 calvings last year Perinatal▯Mortality▯ Pre-Weaning▯Mortality▯ - 10 calves died at birth or w.in 1 48 hrs - 75 heifer calves born alive & died prior to weaning at 60 days - how is farm doing? incidence of perinatal mortality? pre-weaning mortality? find more resources at oneclass.com • find more resources at oneclass.com FACTORS CONTRIBUTING TO PERINATAL and PRE-WEANING MORTALITY DYSTOCIA (main cause = Feto-Pelvic Disproportion, fetus to mother hip ratio) • = difficult or abnormal calving due to a prolonged unassisted parturition process, or due to a prolonged or severe assisted calf delivery *Holstein cows have the highest rate of dystocia (beef is lower) – Factors causing Dystocia - feto-pelvic disproportion – predominant cause - calf presentation - insufficient dilation of cervix - uterine torsion Impacts of Dystocia - internal injuries such as bleeding and fractures - impaired breathing and inadequate supply of oxygen to oxygen dependent organs -impaired ability to thermoregulate  All create a newborn calf w. poor vitality Short term consequences - high perinatal mortality - lower passive immunity transfer ▯2016▯ - higher pre-weaned mortality - higher indicators of physiological stress Long term consequences - impact on milk production - 703 kg reduction in 305-d milk yield in vet assisted calves comparedw. non-assisted calves PREVENTING DYSTOCIA - breeding/genetics - nutrition – prevent OVER conditioning (~over conditioning means a smaller pelvic diameter) - observation of cows/heifers close to calving - appropriate timing of any necessary calving intervention PREVENTING LONG TERM Impacts of Dystocia - Respiratory and thermal support - non-steriodal anti-inflammatory drugs - manual feeding of colostrum (~ifnot feeding need to tube them asap) PASSIVE TRANSFER OF IMMUNITY - placenta of cow separates maternal blood supply  prevents in utero transmission of immunoglobulin▯s ▯)g▯ - calf relies entirely on absorption of maternal Ig from colostrum after birth ** - passive transfer is the absorption of maternal Ig across the SI during the 1 24hrs after birth Why is Passive Transfer Important? - helps protect calf against common calf hood diseases until its own immature immune system becomes functional - immunoglobulin▯s ▯)g▯ specifically bind pathogens to aid in their clearance from the body – particularly important vs. bacteria ~ protects calf for 2 wks before calf antibodies form ComposiAon▯ of▯ Colostrum▯ -▯FYI▯ COLOSTRUM Milking▯Number▯ = first milk after calving – nutrient and Ig dense 1▯ 2▯ 3▯ Milk▯ - produced during the 5 wks prior to calving Specific▯Gravity▯ 1.0561.040▯ 1.035▯ 1.032▯ - ▯Liquid Gold▯ for calves Solids▯ 23.9▯ 17.9▯ 14.1▯ 12.9▯ Protein▯%▯ 14▯ 8.4▯ 5.1▯ 3.1▯ COMPOSITION OF COLOSTRUM Casein▯%▯ 4.8▯ 4.3▯ 3.8▯ 2.5▯ - calories from colostrum 1600 VS. milk 600 calories per liter - energy from colostrum may be just as important as Igs IgG,▯mg/ml▯48▯ 25▯ 15▯ 0.6▯ Fat▯%▯ 6.7▯ 5.4▯ 2.9▯ 3.7▯ - calf has very little energy reserve at birth Lactose▯%▯ 2.7▯ 3.9▯ 4.4▯ 5.0▯ - sufficient for only 1 day survival w. out nourishment - transition colostrum on day 2 or 3following calving remains nutrient dense Vitamin▯A▯ug/l▯ 2950▯ 1900▯ 1130▯ 340▯ Calories/L▯1600▯ 600▯ - common error on dairy farms is to provide 1 day of colostrum and then switch to milk XXX - calf loses advantage of transition colostrum nutrients Components of Successful Colostrum Management Program Quality, Quantity, Quickness, Cleanliness Colostrum – QUALITY - high quality colostrum has an IgG concentration >50 g/L - variable quality (IgG content) - beef cattle > mature dairy > dairy heifers - affected by vaccination, nutritionof dam; heat stress; leaking; cleanliness of harvest - generally inverse relationship of volume and quality, BUT not consistent - 8kg rule: <8kg of colostrum at 1 milking = more likely high quality colostrum - can test - specific gravity of colostrum (colostrometer or refractometer) - Ig or total protein in calf serum (1-7 days old) Colostrum – QUANTITY - key is to deliver and have absorbed an adequate mass of Ig to (help to) protect against disease - target = 1000 mg/dl IgG in serum - estimated by > 5 (5.5?) mg/ml serum total protein - need to deliver >= 100 g IgG (100g = adequate amount of colostrum) - 150 -200 may be necessary or better - based on typical Holstein colostral [IgG] st - calf MUST ingest ~10-12% of BW at 1 feeding = 4L for Holsteins, 3L for Jerseys find more resources at oneclass.com find more resources at oneclass.com Colostrum – QUICKNESS Calf Intestinal Ig absorptive capacity decreases in first 24 hrs ~ want to feed colostrum as soon as possible after birth, not able to absorb w. longer period Quickness – Delayed Colostrum Harvest Concentration of Ig in colostrum is highest immediately after calving - begins to decrease over time when milking delayed - ideally milk cow w. in 2 hours of calving w. maximum delay of 6 hours What if can’t milk cow right away? - Refrigerate - Frozen  thaw slowly using warm water bath, store in small quantities for ease of thawing (1-2 Ls max) - Colostrum replacers - need to absorb 100g IgG but absorption is less w. colostrum replacers (only 35-40%) - provide minimum of 200g IgG from replacer - 2 packages - calves fed w. in 2 hrs of birth 200g IgG w. replacer irrespective of feeding method = no FPT - 100g of replacer by nipple bottle = No FPT - 100 g of replacer by tube = >50% FPT Colostrum feeding strategies - METHODS OF DELIVERY ESOPHAGEAL TUBE FEEDER – no esophageal groove closure = flows directly into rumen – delay in absorption (~increased failure to pass Ig) NIPPLE BOTTLE SUCKLE DAM – not recommended as no control over timing or amount, and increase in pathogen risk Colostrum – CLEANLINESS - bacteria in colostrum interferes w. passive absorption of colostrum - binds free Ig in intestinal lumen and blocks uptake/transport of Ig across intestinal cells Where does contamination occur? - w. strict udder prep, 100% of samples come out of cow acceptable (<100, 000 CFU/ml) - most contamination of colostrum happens in the collection bucket - also think about storage - refrigerate or freeze colostrum w. in 1 hour of collection - refrigerate for 1 day is OK – Add Potassium Sorbate will increase shelf-life to 6-7days - frozen for up to 1 year OK ~ bacteria will grow exponentially if not stored in cold What is Clean? Same as for all milking equipment 1. Take hoses, lids, nipples etc apart 2. Rinse w. warm (105-110F) water 3. Soak in hot (>120 F (50C); use 140-180 F) water w. detergent 4. Scrub all surfaces, including using bottle brushes 5. Rinse w. hot water w. acid (~1 ounce of pipeline acid in 5 gallons) 6. Drain and air dry How are we doing w. colostrum management? Failure of passive transfer – FPT cutoff (5.2g/dL) Bacterial Contamination of Colostrum - cut point is total bacterial count <100,000 colony forming units per ml SHORT TERM CONSEQUENCES Calf Diarrhea - colostrum deprivation resulted in a 74-fold greater risk of mortality during 1 21 days of life in heifer calves - estimated that 31% of all dairy heifer mortality during 1 21 days could be prevented by improved colostrum management
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