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Diseases of Dairy Cattle

(based on Dr. Swists notes)

PATB 4110 - Diseases of Food Animals and Horses

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Diseases of specific concern in dairy cattle

2

The Big Three: mastitis; lameness; fertility

And three important infections:
Salmonellosis
Johnes
Tuberculosis
Retained placenta
Brisket

[personal interest]

Milk fever ( calcium)

Grass tetany ( magnesium)
Ketosis

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General Concepts
3

Nutritional & management problems vs. infectious disease

(contagious vs. non-contagious)

Clinical vs. subclinical disease
Cost of diseases
Veterinary & drug expenses
Loss of production (unrealized income)
Early culling/death
One animal vs. the herd
Prevalence

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Disease can often occur in a predictable sequence or cascade

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Overconditioning
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Optimal BCS for a cow at calving is 3.5-3.75/5

Overconditioning increases susceptibility to

all metabolic disorders

Alters hormonal balance

Greater decreases in feed intake prepartum
Faster rate of body weight loss

Rapid fat mobilization to meet energy needs

Decreased milk yields

Longer period of negative energy balance

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Body condition score in dairy cattle

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Displaced abomasum
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Displaced abomasum
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Repositioned abomasum from right ventral side of

abdominal cavity

Twisting from repositioning slows or stops flow of digesta

Gas buildup leads to bloat appearance

Pinging detected with stethoscope by thumping the cow near last

rib and listening on left flank

85-90% left-sided
75% occur within 1st 14 days post calving
Rare in heifers

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Normal Abomasum Position

Displaced Abomasum

D
A

B
C

Abomasum = A

C = Omasum

Rumen = B

D = Liver
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Symptoms of DA
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Dramatically decreased feed intake

Drastic drop in milk production
Pain (b
(back arched))

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Causes and Risk Factors

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Etiology is multifactorial, although abomasal

hypomotility & gas production major contributors to

displacement or volvulus
Abomasal hypomotility:

Hypocalcemia
Mastitis/metritis-endotoxemia & decreased rumen fill

Hypomotiliy also associated with:

Ingestion high-concentrate, low-roughage diets ( VFA)
Diets also result in gas production
Changes in position of organs and fetus prior to birth
Genetic predisposition; deep-bodied cows
Ketosis
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Displaced Abomasum
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Non-surgical
Removal of gas from abomasum
Rolling cow over, taking on rough trailer ride
Tethering of right hind leg

87% recovery rate

Surgical
Move abomasum into place and attach it surgically to
body wall

Open incision or blind tack

92% recovery rate

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Displaced Abomasum
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Prevention

Ensure rapid increase in rumen volume following calving

Feed a total mixed ration
Avoid rapid dietary changes
Maintain adequate roughage in diet
Cows should be in proper body condition at parturition
Prevent hypocalcemia & other metabolic disease

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Bovine Tuberculosis
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Bovine Tuberculosis (TB)

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Historic Disease:

Bovine TB caused more losses among US farm animals in early

1900s than all other infectious diseases combined
Meat inspection: looking for TB esp.
1917, USDA/APHIS began national eradication program; 2010 TB
nearly eliminated
Highly contagious to all warm-blooded animals & humans
Reportable disease in WY & US
Wildlife can spread TB to commercial cattle (and cattle to wildlife)
Mycobacteria
M. bovis, M. avium & M. tuberculosis

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Transmission & clinical signs

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Transmission:

Aerosol>ingestion(milk)>intrauterine/sexual
Clinical signs: Depends on organ/location

Usuallyy chronic disease but can have acute episodes

p
General: emaciation, lethargy, weakness, anorexia, fever
Granulomatous inflammation/disease

i.e., Lung, liver, lymph nodes

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Emaciated Cow

Lung & liver

granulomas

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Lung & lymph node granulomas

Acid fast stain of Mycobacterium

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Diagnosis TB
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Most important diagnostic test:

Intradermal tuberculin test

Diagnosis on clinical signs alone difficult even w/advanced

cases
Other :
Radiographs, microscopic exam sputum/fluids
Meat inspection
Necropsy

Definitive diagnosis:

Isolation & ID of bacteria ~4-8wks

PCR ~2-4 days
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TB Tuberculin skin test

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Animal exposed to tuberculin

Mycobacterial antigen- M. bovis or M. tuberculosis

Checked for reaction after 72 hrs

Delayed type hypersensitivity

If host
h t a reactor,
t antigen
ti
stimulates
ti l t llocall iinflammation
fl
ti c/o
/ skin
ki
swelling
Test sites vary in sensitivity & between countries ~neck, anal or
caudal fold of tail

Disadvantage: Poor specificity-cross reacts with other

Mycobacteria spp. & Nocardia spp.

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Control
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#1:Test & slaughter

Only

way to assure eradication

of reactors detected by tuberculin test
In affected herd, test every 3 mo.
UM&R
Slaughter

#2: Test & segregate

#3: Chemotherapy

Elephants, nonhuman primates, humans

Routine hygiene
Clean & disinfect contaminated food, water troughs, etc.
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Control
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Nationwide slaughter plant surveillance activities

If positive found, trace back to herd of origin
Test
T t & slaughter
l
ht h
herd
d if necessary
Depopulation voluntary, so may quarantine

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Wyoming Livestock Board: Animal Import Rules

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Import permit required on all bovines entering WY

Certificate of Veterinary Health Inspection required
Bovine originating from a state not accredited TB free must

meett USDA/APHIS requirements

i
t ffor TB
Cattle must be tested prior to movement
Based on status of state/zone and class of cattle
(breeding, sexually intact vs. spayed heifers and steers for
feeding)

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Mastitis
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What is it?
Inflammation of the mammary gland

Healthy Udder & Mammary gland tissue

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Healthy mammary gland tissue

Mastitis
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Causes of Mastitis
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Infectious mastitis
Invasion of bacteria into gland
Clinical or sub-clinical

Many more subclinical cases than clinical

Non
Non-infectious
infectious mastitis
Due to injury, chilling, bruising, improper milking

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Mastitis Quick Facts

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All dairy herds have cows w/subclinical mastitis

Varies from 15-75%
Of cows affected, 5-40% are infected in more than one quarter
On average, 2 infections per lactation

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Mastitis
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Above totals are from 1996. USDA/APHIS Dairy report: From 19962007 % of cows w/clinical mastitis increased 13.4 to 16.5%. The
total economic loss is closer to $250/cow.
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Mastitis
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Clinical mastitis
Visible inflammation in udder (swelling, heat, pain, redness)

Systemic-fever, anorexia & shock

Abnormal milk (e.g., color, fibrin clots)

Subclinical mastitis
Infection and inflammation without clinical mastitis or
systemic involvement (asymptomatic)

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For each clinical mastitis case (Orange), 15-40

subclinical cases (Green)
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Mastitis pathogens
33

Co
Contagious
tag ous
Environmental

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Contagious mastitis
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Pathogens colonize mammary gland

Spread by milking machines, milkers & cow to cow
Staphylococcus aureus
Streptococcus agalactiae
l i
Corynebacterium bovis
Other Streptococcus spp. & Staphylococcus spp.
Mycoplasma spp. can spread from cow to cow through
aerosol transmission

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Contagious mastitis
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Staphylococcus aureus
Worst of the contagious agents
Penetrates deep into glandular epithelium
Not very responsive to antibiotics resistance common
Immune response of cow not as successful in eliminating
infections as with other pathogens
Once established in herd, difficult/impossible to eradicate
Dry treat or cull
Survives in multiple locations in cow
Transmitted esp. by hands

Streptococcus agalactiae
Obligate infection of mammary gland
Readily eradicated with antibiotics
Multiply in milk and on mammary epithelial surfaces
Will not survive in the environment

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Mycoplasma
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Primarily respiratory pathogen

Can infect many tissues

Spreads through multiple routes

Contagious and environmental

High shedding rate

Severe purulent mastitis in multiple quarters
No treatment - identify and cull

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Environmental mastitis
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Pathogens do not normally infect mammary gland

Infection when cows environment, milking machine

or teats/udder are contaminated access through

teat canal

Streptococcus uberis & other non-agalactiae Streptococcus

spp.
Escherichia coli and Klebsiella sp. (coliforms)
Arcanobacterium pyogenes

Important to maintain good sanitary conditions

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Environmental mastitis
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Infect cows between milkings

Streptococcus dysgalactiae and Streptococcus

uberis

Escherichia coli

Symptoms confined to mammary gland

Easily out-competed (opportunistic)

Easily eradicated (antibiotics, immune system)
Toxins released when killed

Systemic

effects (fever, depression, death)

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Pathways for Infection

40

Most common route of entry is streak canal

Smaller diameter streak canals more resistant to mastitis
If keratin plug compromised, animals more susceptible to
mastitis

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In udder...
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Bacteria proliferate, destroy secretory cells

Some release toxins when killed
Destroy more secretory cells
Absorbed
Ab b d iinto bl
bloodstream
d

systemic effects (fever, low appetite)

Milk ducts blocked by clotted milk

Blood vessels dilate, slowing blood flow
Interferes with treatment access

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Acute mastitis:
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Udder hot, hard, tender

Increased temperature, refusal to eat, dull eyes,

rough coat
Increased blood proteins and leukocytes in

mammary tissue and milk

Blood vessels greatly dilated
Milk ducts compressed

Treatments more likely to be unsuccessful under these conditions

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Chronic Mastitis
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If treatment unsuccessful
Scar tissue
Ducts permanently blocked
Loss
L
off function
f
ti iin glands
l d may b
be permanentt

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Mastitis signs and symptoms

45

High somatic cell count (SCC) indicates mastitis

Composed of neutrophils from the blood and epithelial
secretory cells
Neutrophils in milk = response to infection
Epithelial cells in milk
Each doubling of SCC >50,000 cells.ml = loss of 0.5 kg/milk/day

In chronic mastitis, only symptom is milk thick or

lumpy

Terms you will hear:

Summer mastitis = A. pyogenes = loss of quarter
Gangranous mastitis = various causes; life-threatening
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Milk quality changes

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Altered composition
Decreased fat, protein, lactose
Increased chlorides
Lower total solids

As low as 1/3 normal milk

Poor flavor (salty)

Clumping of somatic cells
Clumpy, stringy milk
Only 2-3% of all cases show clinical symptoms

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Risk factors
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Majority of new infections occur during:

First 3 weeks of dry period

Milk left in udder
First month after parturition
Immune system compromised

Frequency of milking affects risk of infection

Pathogen load decreased by evacuating milk more frequently

Position of the gland

More exposed to environment, greater the risk

Chilling on cold ground
Improper ventilation and dampness
Injury

Heritability (conformation of udder/teat)

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Prevention and control

48

Clean and dry environment

Clean and dry teats at milking
Good hygiene, esp. for environmental causes
Teat dips (pre- and post-milking)
Well maintained equipment
Segregate clinical cases
Early identification
Prompt treatment
Milking machine maintenance
Dry cow treatment
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Uncomfortable free stalls increase the incidence of mastitis by increasing

exposure to environmental pathogens

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Latex Gloves
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Backflush systems reduce spread of contagious pathogens, such as S. aureus, by

sanitizing milkers between groups of cows
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Teat dips only effective if adequate coverage of all teats

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Barrier teat dips useful to prevent mastitis in dry & transition cows

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Barrier dips block bacterial access to the animal and can be used to protect cut
areas where the skin barrier compromised.

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Treatment
55

Antibiotics
During lactation
Dry period
Frequent milking
Reduce
R d
ability
bili to proliferate
lif
Oxytocin
Reduce volume of media
Reduce pathogen population
Fluid therapy for endotoxemia

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Treatment
56

Treatments used on dry cows most effective

method of treating Staphylococcus aureus

infections

Long-lasting antibiotic preparations

Should not be used if cows will not have full dry period

All intramammary infusions should be conducted

aseptically

Clean teat ends with alcohol

Insert infusion tube only as far as necessary

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Cannulas on commercial mastitis treatments should only be inserted one-quarter

inch into the teat end to minimize keratin removal

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Treatment
58

Many reasons to avoid antibiotic contamination of

milk supply

Illegal - contamination results in financial penalties

Development of antibiotic resistance

Keep treated milk separate

Use separate equipment

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