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Diseases of Dairy Cattle (based on Dr. Swist’s notes)

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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  Johne’s  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 4

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Overconditioning 5

 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 6

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Displaced abomasum 7

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Displaced abomasum 8

 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

D A

B

B C

C

A

Abomasum = A

C = Omasum

Rumen = B

D = Liver 9

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Symptoms of DA 10

 Dramatically decreased feed intake  Drastic drop in milk production  Pain (b (back arched))

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Causes and Risk Factors 11

 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 9/8/2010

Displaced Abomasum 12

 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 13

 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 14

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Bovine Tuberculosis (TB) 15

 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 16

 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 18

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Diagnosis TB 19

 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 9/8/2010

TB Tuberculin skin test 20

 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 21

 #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. 9/8/2010

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Control 22

 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 23

 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 25

 What is it?  Inflammation of the mammary gland

Healthy Udder & Mammary gland tissue

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Healthy mammary gland tissue

Mastitis 26

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Causes of Mastitis 27

 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 28

 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 29

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. 9/8/2010

Mastitis 30

 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) 31

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Mastitis pathogens 33

 Co Contagious tag ous  Environmental

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Contagious mastitis 34

 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 36



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 37

 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 38

 Pathogens do not normally infect mammary gland  Infection when cow’s 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 39

 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... 41

 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: 42

 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 44

 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 9/8/2010

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Milk quality changes 46

 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 47

 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) 9/8/2010

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 9/8/2010

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Uncomfortable free stalls increase the incidence of mastitis by increasing exposure to environmental pathogens

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Latex Gloves 50

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Backflush systems reduce spread of contagious pathogens, such as S. aureus, by sanitizing milkers between groups of cows 9/8/2010

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Teat dips only effective if adequate coverage of all teats 9/8/2010

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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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