Cattle Health and Diseases Flashcards

1
Q

High prevelance of salmonella linked to:

A

large herd size
use of flush alleys

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2
Q

How does salmonella impact cattle

A

 Disease and production losses in cattle
 Public concern
 zoonotic pathogen (beef and dairy products)
 emergence of antimicrobial resistant strains

*causes diarrheoa in calves

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3
Q

characteristics of salmonella

A

 Facultative anaerobe
 Facultative intracellular pathogen
 Survives pH range 4.5 - 9
 Multiplies at temperatures of 8 to 45oC
 Requires water activity of >0.95 to
multiply
 Survives in dust and feces for years

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4
Q

clinical signs of salmonella in calves

A

 Anorexia
 Fever
 Diarrhea
 Death (Initially 7-10 days and then 5 - 7 days)

*smaller the dose, less sick you get
*antibodies concentrated in colostrum, so calf has to drink enough colostrum to get enough antibodies.

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5
Q

Sources of Pathogen Exposure

A

 Purchased Livestock
 Feed
 Water
 Environment
 Equipment (Rendering trucks)
 People (Veterinarians)
 Wildlife

 Introduced by contaminated feed.
 Feed contaminated by irrigation water.
 Irrigation water contaminated by human effluent.
 Herd exposure preceded outbreak by 7 months.
 Salmonellosis in cows precipitated by
 Gossypol toxicosis
 Unbalanced transition ration
 Hot weather
 Numerous salmonella serotypes isolated
 Mortality associated with Salmonella
typhimurium
 Contributing factors
 Failure of passive transfer
 Colostrum pooling
 Calf milk handling practices

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6
Q

Calf Immunity

A

 Born immunologically naïve
 Colostrum provides antibodies, energy,
vitamins and laxatives
 Colostral quality
 Antibody content
 Microbial contamination

*if greezy storage containers, that is where the hygiene problem is

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7
Q

Options to Mitigate Risk of
Contaminated Milk

A

 Avoid feeding “Waste” or “Hospital Milk”
 Pasteurize
 Refrigerate milk during storage
 Feed milk replacer

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8
Q

Variables Influencing Calf Immunity

A

 Cow Health (Gestation and colostrum production)
 Nutrition (Energy/protein, metabolic)
 Heat Stress (Blood flow to placenta)
 Intra uterine infections (BVD)
 Passive Transfer
 150 grams of IgG required
 The effectiveness of colostral transfer is
determined by cow and calf management.
 Environment
 Temperature (Heat and Cold increase energy
expenditure)
 Wind
 Moisture
 Nutrition calves should be fed whole milk at ~ 12 to 15% of
their body weight per day
 Vaccination

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9
Q

Passive Transfer

A

– Minimum 150 gm’s IgG per calf
– 50 gm IgG per L of colostrum recommended. (Holstein Brix 22%+, Jersey
18+%)
– Colostral quality influenced by
– Timing of harvest relative to calving
– Parity (Cows generally better than heifers)
– Volume (High volume often lower IgG content than low)
– Pooling increases risk of transmitting contagious pathogens
– First feed 10 % body weight within 3 hrs
– Second feed 5% around 12 hours of age
– Calves left with cows  65% failure
– Efficiency of absorption is reduced by ~ 50% by 6-9 hrs of age.
– Assessment of Passive Transfer Calf Sera 48 hr (Brix > 8.3 %)

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10
Q

pathogens found in milk

A

 BLV
 Johnes
 BVD
 Salmonella
 Mycoplasma
 Staphylococcus aureus

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11
Q

Summary of HPE

A
  • Environmental conditions may impact both the
    pathogen and the host
  • Environmental conditions influence the survival and
    potentially the proliferation of pathogens in the
    environment. This leads to fluctuations in the
    challenge dose to the host.
  • Environmental conditions may adversely impact host
    immunity. For example hot conditions may lead to
    dehydration and increased susceptibility to infection
  • The outcome of host pathogen interactions reflect
    the balance between the hosts immunity and the
    pathogen dose and virulence
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12
Q

What is mastitis

A

– Inflammation of the
mammary gland most
commonly secondary to
bacterial infection.

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13
Q

HPE of mastitis

A

Host
* Immune function
Pathogen
* Contagious
* Environmental

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14
Q

What are the mammry gland defenses

A

The Teat
- streat canal, keratin excreting, like sticky fly
paper for bacteria
Phagocytes
- # increase with mastitis (#WBC)
frequent milking
Antibodies
Lactoferrin

barrier into mammary gland. Barrier to
bacteria (streat canal)
Milking cows properly decreases risk, frequent
milking
floods and poweroutages, common that cows get mastatis as cows not milked properly

Teat sphincter (closed initially when goes to get milked. Relaxed cow means sphincter relaxes down and allows milk out
Takes 20 minutes after milking for the sphincter to go back up. Feed cows after milking so stand up eating and don’t lye down while it is closing.

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15
Q

What are teat lesions and what do they do?

A

Compromise the integrity of the teat sphincter
* Lead to bacterial colonization of the teat skin.
* Causes
* Trauma
* Milking Equipment – Excessive or insufficient teat end vacuum, poorly fitting liners.
* Teat Dips – Chemical injury or excessive drying.
* Adverse Climatic Conditions – frostbite, photosensitization.
* Skin pathogens

hyper keratosis (rough skin at end of teats, sphynicter doesn’t close properly)

too much vaccum causes congestion in the teat

Not enough vacuum, takes longer to milk cow

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16
Q

When are high risk periods for intramammary infections

A
  • After dry off (Cessation of milking) - drip milk out , teat sphincter open

– Prior to and immediately following calving - mammary glands engorged, can start dripping milk, if lying down and dripping milk out, bacteria can get in
Can get odema

Harder to milk cows after partution, can’t get milk out as cups don’t stay on udder properly during milking so still have some milk in udder, sphyincter stays open, lies down in paddock and get pathogens

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17
Q

Milking Procedure

A

collect milk sample to see if cow has mastitis before putting machine on to stop spreading into tank
Looking for clumps and change in colour (occansional)

  • Pre dip (to reduce risk of environmental mastitis).
  • Fore strip each quarter (To identify mastitic quarters).
  • Wipe teats dry with a single service towel.
    – (Contact time 20 – 30 seconds, pre dip removed to avoid contamination of the milk)
  • Attach milking machine.
  • Shut off vacuum and remove milking cluster when milk stops flowing
  • Post dip (prevents contagious mastitis)
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18
Q

Preparation Prior to Milking

A
  • Cows should be handled quietly so they are relaxed and let down milk normally.
    Poor milk let down can prolong milking leading to teat end lesions.
  • Minimise bacterial contamination on teats prior to and following milking (clean
    lanes and entry and exit alleys)
  • Milking machines should be applied to clean dry teats. (Pre milking wash and dry
    may be necessary under adverse environmental conditions)
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19
Q

Clinical Manifestations of Mastitis

A
  • Abnormal
    – Secretion (Mild)
  • Abnormal Gland (Moderate)
    – Swelling
    – Redness
    – Pain
    – Temperature (Warm/Cold)
  • Abnormal Cow (Severe)
    – Fever
    – Depressed Mentation
    – Altered Gait
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20
Q

Contagious Mastitis Pathogens

A
  • Streptococcus agalactiae
  • Staphylococcus aureus
  • Mycoplasma spp.
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21
Q

Transmission of Contagious Mastitis Pathogens

A
  • Transmission generally occurs at milking time.
    – Milking equipment
    – Milker’s hands
    – Contaminated milk
    – Teat washing materials
    – Treatment procedures
    – fluctuations in vacuum causing teat
    impacts
  • Poor teat health
22
Q

Contagious Mastitis Control Strategies

A
  • Post
    -milking teat disinfection (dip)
  • Prepare teats properly prior to milking * Use adequately sized, properly
    functioning milking equipment and
    appropriate milking technique
  • Backflush or disinfect contaminated
    equipment
  • Segregate infected cows * Consider culling chronically infected
    cows
  • Lactating cow treatment * Dry cow therapy * Maintain a closed herd * Avoid feeding heifer herd replacements
    mastitis milk.
23
Q

Environmental Mastitis Pathogens

A
  • Streptococcus uberis, Streptococcus
    bovis and other environmental
    streptococci
  • Coagulase negative Staphylococcus
    spp.
  • Coliforms
  • Truperella pyogenes
  • Yeast
  • Corynebacterium bovis
  • Prototheca spp.
24
Q

Prevention of Mastitis

A
  • Provide a clean and comfortable environment
  • Maintain milking machine function
  • Maintain good milking procedures
  • Teat dip
  • Maintain teat health
  • Detect and treat clinical mastitis
  • Assess performance through monitoring the rate of new infections
25
What is Dry Cow Therapy
* The use of teat sealants and or intra-mammary antimicrobial therapy immediately after the last milking of the lactation to prevent new infections and treat existing infections * Dry cow therapy has the following advantages over lactation antimicrobial therapy – Higher dose of antibiotic – Retention time of antibiotic longer – Reduced risk of drug residues * It is important to clean and sanitize teats carefully prior to infusing a quarter poor technique may introduce bacteria and cause infections.
26
Summary of mastitis
* Environmental conditions influence the number of organisms in the environment and subsequently the challenge to the teat end. – Wet, warm conditions favour bacterial growth * Environmental conditions impact cow immunity – Wet / dry conditions can compromise teat skin – Poorly functioning milking equipment compromises teat health and may contribute to bacterial challenge to the teat end * The spread of contagious pathogens is also promoted by environmental compromise – Poorly fitting/functioning milking equipment – Damaged teats
27
Clinical Signs of Lower Respiratory Tract Disease
› Depressed mentation › Anorexia › Fever › Reduced rumen fill › Oculo-nasal discharge › Tachypnoea (increased rate of breathing) › Dyspnea (difficulty breathing) tends to occur in the later stages of disease › Coughing tends to be seen in the later stages of disease › Mortality
28
Pneumonia
› The most common disease of beef cattle in feedlots - Economically important - Morbidity (how well it spreads) - Mortality (how well it kills) - Most common indication for antimicrobial therapy in feedlot cattle
29
What is the diff between morbidity and mortality?
- Morbidity (how well it spreads) - Mortality (how well it kills)
30
Pneumonia - Pathogenesis
› Commensal bacteria - Most bacteria (Pasteurella multocida, Mannheimia hemolytica, Histophilus somni) involved in bronchopneumonia of cattle are commensals normally found in the oral cavity and pharynx. - “Stressors” or viral agents that impair the normal host defences of the lower respiratory system and/or cause immunosuppression enable pharyngeal commensals to infect the lungs, resulting in bronchopneumonia. › Contagious bacterial pathogens - Mycoplasma spp. - Salmonella Dublin
31
Pneumonia (Viral vs bacterial)
› Viral - IBR - BVD (Pestivirus) - Bovine respiratory syncytial virus - Parainfluenza (PI3) - Coronavirus › Bacteria - Mannheimia hemolytica - Pasteurella multocida - Histophilus somni - Mycoplasma bovis – contagious - Salmonella enterica serovar Dublin - contagious
32
Innate Host Defences aganist pnemonia
› Filtration by the nasal cavity › Muco-cilliary escalator › Laryngeal reflex - stops aspiration › Sneezing › Cough reflex › Alveolar macrophages › IgA secretion from the respiratory epithelium
33
Risk factors for pneumonia
› Transport - Stress (glucocorticoids, epinephrine) - Co-mingling (viral exposure) - Dust (overload clearance mechanisms) - Dehydration (compromised muco-cillary clearance) ›Poor Air quality - At the level of the animal - Poor ventilation - High humidity › Nutrition - Shipping fever is largely a disease of feedlot cattle. In experiments where cattle are comingled and fed a lower energy ration (hay) the incidence of pneumonia is lower. - Pneumonia is uncommon on grass fed beef operations - Poor nutritional management increases risk
34
On-Farm Pre-Conditioning (Yard Weaning)
* Management Procedures Best Done Prior to Weaning * Dehorning * Castration * Drenching * Vaccination (bacterial and viral) * Weaning * Yard weaning * Introduction to trough feeding and watering * Training * Walking through yards * Controlled release from yards psychology - separate cow from calf and retain calves in yards and feed them from feed buckets, walking amongst them and controlling how leave from yards, those animals much better adapted when leave for feed lot. Teaching them they get food from a tray, what happens in a feedlot
35
Stock Handling Prevention
* Avoid moving stock in extreme conditions: heat, cold, very dusty * Avoid overcrowding in all situations: grazing, stockyards, transportation. * Avoid sudden diet changes. * Minimize the mixing of herd groups. * Provide appropriate shelter from extreme conditions. * Ensure continual access to clean water. * Separating sick animals from non-infected.
36
Pneumonia in Dairy Calves
› Commonly observed in calves during and immediately following weaning. › Dairy calves are typically weaned at an earlier age than beef calves (6 – 10 weeks of age). › Weaning is associated with dietary change and may predispose to acidosis if not managed carefully. › Weaning may also contribute to nutritional stress (inadequate nutrients) if calves are not adapted to solid feed. › Sometimes management procedures such as dehorning and vaccination are carried out at weaning that may contribute to calf stress › Calves are co-mingled at weaning predisposing to pathogen transfer
37
Risk Factors
› Intercurrent disease - Coccidiosis in dairy calves - Pestivirus › Poor air quality - Inadequate ventilation - Ammonia build up in closed facilities › Nutritional stress - Inadequately adapted to solid feed (insufficient nutrient intake) - Acidosis › Calf mixing
38
Prevention of Pneumonia in Dairy Calves
› Good colostrum management › Good Nutritional management - Well fed (adequate nutrients) - Gradual step down in milk fed - Provision of some roughage to reduce risk of acidosis › If housed - Good ventilation - Bedding management reduce dust and ammonia › Staggered management procedures - Preferably dehorn during first week of life › Constant access to fresh water
39
Lameness in dairy cattle
* Lameness is among the three most costly diseases of dairy cattle after mastitis and poor reproductive performance. 2nd most common disease after mastitis as can't stand as well * It is the #1 WELFARE issue in cattle
40
Epidemiology of lameness
90% lameness in feet (easy fix) 75% all claw lesions involve lateral claw (of hind feet)
41
Why is lameness important?
Compromised Welfare Poor Reproductive performance Reduced Milk Yield Increased risk of culling *expensive disease
42
Signs of lameness
more severe will be at back of herd on way to dairy walking speed, rhythm, stride length and foot placement, weight bearing and back alignment and head position Slowing walking speed after milking, rhythm - not fluid, interrrupted and uneven (non lame front move through quicker), stride length and foot placement (track up on even surface, lameness have shortened stride and rear falls short), weight bearing evenly (lame faver lame leg, opposite take more weight, duclaw sink closer to ground), arched back can equal bad alignment or can equal stomach pain, head alignment below normlaly, bobbing head = lameness
43
Foot lesions
* Lesions involving the Intergital skin * Footrot * Bovine digital dermatitis * Lesions involving claw horn * Sole injury * Sole bruising * White line disease * Axial wall crack * Lesions involving deeper structures * Deep digital sepsis * Laminitis / coriosis Digital dermitits - moisture a risk for both, wet conditions, like being in bath, softer skin, stone graze skin allows bacteria in Interdigital hyperplasia
44
Footrot risk factors, path and clinicla signs
Risk factors - poor hygiene - abrasions Path - secondary infection of interdigital skin abbrasions - anerobes Clinical signs - sudden lameness - symmetrical distal limb swelling - split in interdigital skin with foul smelling exudate
45
Digital dermitits
Ulcerative lesions can cause lameness poor foot hygiene most cases in hindfeet moisture/mud
46
Claw lesions
* Sole Injury * Sole Bruising * Axial wall Crack * White Line Disease
47
Sole injury
Weak/ thin/ flat soles hurried foot placement penetration with sharp object abcess formation between corium and sole haemorraging staining of sole lamenes dark tract on sole, painful to squeeze
48
Sole bruising
extra calw factors thin soles/ weak rushed foot placement red or yello satining flat thin soles multiple claws/feet
49
Axel wall crack
rainfall/fine mud lateral hind claws path poorly understood may cause lameness crack along axial groove impacted with dirt and gravel excessive granulation tisue formation in crack
50
White line disease
white line = sole/wall junction first impact of weight bearing is heel/sole junction poor animal handling twisting or slipping in yards lateral claws of hindlimbs mechanical forces create opening at white line becomeing impacted with foreign material undderun sole deep digital sepsis
51
Laminitis
infalmed laminaw common in feedlots with diet cahnges hardship lines rotation and sinking of P3 Chronic laminitis --> recommend culling
52
Coriosis pathogenesis
mechanical - restricted movement - excessive hard surfaces - reduced lying time Metabolic - partruition - diet (subacute ruminal acidosis)