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AVBS3005 > Cattle Health and Diseases > Flashcards

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
Q

What is Dry Cow Therapy

A
  • 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
Q

Summary of mastitis

A
  • 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
Q

Clinical Signs of Lower Respiratory Tract Disease

A

› 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
Q

Pneumonia

A

› 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
Q

What is the diff between morbidity and mortality?

A
  • Morbidity (how well it spreads)
  • Mortality (how well it kills)
30
Q

Pneumonia - Pathogenesis

A

› 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
Q

Pneumonia (Viral vs bacterial)

A

› 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
Q

Innate Host Defences aganist pnemonia

A

› Filtration by the nasal cavity
› Muco-cilliary escalator
› Laryngeal reflex - stops aspiration
› Sneezing
› Cough reflex
› Alveolar macrophages
› IgA secretion from the respiratory epithelium

33
Q

Risk factors for pneumonia

A

› 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
Q

On-Farm Pre-Conditioning (Yard Weaning)

A
  • 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
Q

Stock Handling Prevention

A
  • 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
Q

Pneumonia in Dairy Calves

A

› 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
Q

Risk Factors

A

› 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
Q

Prevention of Pneumonia in Dairy Calves

A

› 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
Q

Lameness in dairy cattle

A
  • 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
Q

Epidemiology of lameness

A

90% lameness in feet (easy fix)
75% all claw lesions involve lateral claw (of hind feet)

41
Q

Why is lameness important?

A

Compromised Welfare
Poor Reproductive performance
Reduced Milk Yield
Increased risk of culling

*expensive disease

42
Q

Signs of lameness

A

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
Q

Foot lesions

A
  • 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
Q

Footrot risk factors, path and clinicla signs

A

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
Q

Digital dermitits

A

Ulcerative lesions
can cause lameness

poor foot hygiene
most cases in hindfeet
moisture/mud

46
Q

Claw lesions

A
  • Sole Injury
  • Sole Bruising
  • Axial wall Crack
  • White Line Disease
47
Q

Sole injury

A

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
Q

Sole bruising

A

extra calw factors
thin soles/ weak
rushed foot placement

red or yello satining
flat thin soles
multiple claws/feet

49
Q

Axel wall crack

A

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
Q

White line disease

A

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
Q

Laminitis

A

infalmed laminaw
common in feedlots with diet cahnges
hardship lines
rotation and sinking of P3

Chronic laminitis –> recommend culling

52
Q

Coriosis pathogenesis

A

mechanical
- restricted movement
- excessive hard surfaces
- reduced lying time

Metabolic
- partruition
- diet (subacute ruminal acidosis)

AVBS3005 (8 decks)

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