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4/11/2008

Dr. Shannon Swist Diseases of Food Animals and Horses

Dairy vs. Beef Cattle

Mastitis Bovine Leukosis Johne's Disease Hemorrhagic bowel syndrome Vagal indigestion Laminitis Q: What are Metabolic Disorders the 3 most L i iti important causes of economic Winter Dysentery Fatty liver syndrome industry? losses in the dairy Dilated cardiomyopathy Ketosis of Canadian HolsteinAbomasal Friesians displacement Bovine leukocyte Milk fever adhesion deficiency Ruminal acidosis

Diseases of Dairy Cattle

Contagious Mastitis

Pathogens colonize mammary gland Spread by milking machines, milkers & cow to cow

Streptococcus agalactiae St t l ti Streptococcus dysgalactiae Staphylococcus aureus Mycoplasma bovis

Environmental Mastitis

Pathogens do not normally infect mammary gland Cause infection when the cow's environment, milking machine o teats a d udde a e g ac e or and udder are contaminated ­gain access through teat canal

Streptococcus uberis & other non-agalactiae Streptococcus spp. Escherichia coli Klebsiella Arcanobacterium pyogenes

Important to maintain sanitary conditions

Mastitis Signs and Symptoms

Acute mastitis

Udder is hot, very hard, and tender Increase in temperature, refusal to eat, dull eyes, Q: What is the most common route rough coat of pathogen infection? Increase in 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

Mastitis Signs and Symptoms

Chronic mastitis

If no treatment or if treatment is unsuccessful Scar tissue forms Ducts become permanently blocked Loss of function in these glands may be permanent

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Factors Affecting Risk of Mastitis

Majority of new infections occur during:

First three 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

Factors Affecting Risk of Mastitis

Position of the gland

More exposed to environment, greater the risk

Chilling on cold ground Improper ventilation and dampness Injury

Prevention

Clean and dry environment Clean and dry teats at milking Teat dips (pre- and post-milking) (pre post milking) Properly maintained equipment Early identification Prompt treatment

Heritability (conformation of cow)

Latex Gloves

Uncomfortable free stalls can increase the incidence of mastitis by increasing exposure to environmental pathogens (Courtesy of Monsanto)

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Backflush systems reduce the spread of contagious pathogens, such as S. aureus, by sanitizing milkers between groups of cows (Courtesy of John Smith)

Teat dips are only effective if adequate coverage of all teats is accomplished (Courtesy of Mark Kirkpatrick)

Barrier teat dips are useful for preventing mastitis in dry and transition cows (Courtesy of Mark Kirkpatrick)

Barrier dips simply block bacterial access to the animal and can be used to protect cut areas where the skin barrier has been compromised (Courtesy of Mark Kirkpatrick)

Treatments

Antibiotics

during lactation dry p y period

Treatment

Treatments used on dry cows are most effective method of treating staphylococcus aureus infections

Long-lasting Long lasting antibiotic preparations Should not be used if cows will not have full dry period

Frequent milking

reduce ability to proliferate

Oxytocin treatment

reduce volume of "media" reduce pathogen population

All intramammary infusions should be conducted aseptically

Clean teat ends with alcohol Insert infusion tube only as far as necessary

Fluid therapy for "toxic shock"

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Transition Period

Transition period includes final few weeks prior to parturition and the first few weeks post-parturition Hormonal changes during this time tend to suppress immune function Metabolic disorders occur primarily in early lactation Period of great stress and drastic changes in nutritional requirement Nutrient intake is increased, but energy demands are rarely met Cow exists in state of negative energy balance for a period of time during early lactation Metabolic disorders can be managed Prevention is better than treatment Cannulas on commercial mastitis treatments should only be inserted one-quarter inch into the teat end to minimize keratin removal (Courtesy of Mark Kirkpatrick)

Critical Days

Deliver a healthy calf 0 6-8 wk 10 wk No milk fever No retained placenta High peak production Fast increase in intake Limited loss of BCS No mastitis No ketosis 44 wk of lactation High fertility No fatty liver No displaced abom. No metritis -3 wk -8 wk

Metabolic disorders often occur in a predictable sequence or cascade (Courtesy of Dana Boeck)

Overconditioning

Optimal BCS for a cow at calving is 3.5-3.75 Overconditioning increases susceptibility to all metabolic disorders

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

Rapid fat mobilization to meet energy needs

Fatty Liver Syndrome

Commonly occurs within a few days of calving in excessively fat cows

Most prevalent in cows receiving too much energy or not enough protein during late lactation These cows accumulate excessive stores of internal fat Th l t i t fi t lf t

Liver fills with fat and is unable to function optimally

When feed intake decreases fat stores in the body are mobilized

Much of this fat is accumulated in liver, preventing liver from oxidizing fats for energy Body senses energy deprivation and increases rate of fat mobilization Creates vicious cycle, and increasing fat accumulation in liver Ketones (partially oxidized fats) can be released from liver, further depressing appetite

Decreased milk yields Longer period of negative energy balance

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Fatty Liver Syndrome

Cows with fatty liver exhibit decreased feed intake and drop in milk production

Rapid body weight loss Cows can go down but remain alert Symptoms of ketosis can be apparent Immune function is depressed

Treatment/Prevention

Treatment limited to treating symptoms

Response is poor

Prevention is key y

Calve at BCS of 3.5 Maintain pre-calving feed intake Balance rations for protein and energy

Account for decreases in intake

Fatty liver is highly correlated with other disorders Cows are likely to get fatty liver syndrome if they are losing weight rapidly

Avoid overfeeding Balance ration for protein and energy

Exercise Choline chloride supplementation in high-risk animals

Ketosis (Acetonemia)

Usually affects high-producing cows 10 days to 6 weeks following parturition

Incidence increases as cow approaches peak lactation

Ketosis (Acetonemia)

Ketones are formed from incomplete oxidation of mobilized fat

Body fat is mobilized in response to negative energy balance

Characterized by increased concentrations of free fatty acids and ketones in the blood and urine, decreased concentrations of glucose

In ketotic cows the liver cannot metabolize high levels of free fatty acids quickly enough High concentration of ketones tend to depress appetite, exacerbating problem further

Ketosis (Acetonemia)

Symptoms

Abrupt drop in milk production

Although percentage of fat increases

Ketosis (Acetonemia)

Treatments are designed to increase blood glucose

IV glucose (40% dextrose)

Infused glucose is quickly used by animal Feeding glucose is ineffective, as rumen microbes will convert glucose to VFA's

Depressed appetite, excessive weight loss Acetone breath Drowsiness Increased ketone bodies in blood and urine Liver glycogen levels decrease, while lipid levels increase in liver

Glucose precursors

Sodium propionate top dress

0.5 pounds/cow/day

Propylene glycol

Oral drench

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Ketosis (Acetonemia)

Treatment

Glucocorticoids

Stimulate body to convert body protein to glucose l Prolonged use may deplete protein stores and depress immune system

Ketosis (Acetonemia)

Prevention

Keep cows in optimal condition at p parturition

BCS 3.25-3.75

Niacin supplements

When fed to pre-clinical ketotic cows, their ketone levels in blood and urine decreases

Increased efficiency in lipid metabolism

Avoid abrupt ration changes Maximize dry matter intake

Six to twelve grams per day

Displaced Abomasum

Refers to repositioning of abomasal compartment from the right ventral abdominal wall

Twisting from this repositioning slows or stops flow of digesta Gas buildup leads to bloat appearance

"Pinging" detected with stethoscope by thumping the cow near the last rib and listening on the left flank

D A B C A B C D

85-90% left-sided

Right-sided more complete torsion

Abomasum = A Rumen = B C = Omasum D = Liver

75% occur within 1st 14 days postcalving Rare in heifers

Symptoms of DA

Dramatically decreased feed intake Drastic drop in milk production Pain (stand with back arched) Can diagnose by "thumping" near last rib and listening along left flank

Causes and Risk Factors

Space in abdominal cavity

Decreased feed intake Sudden ration changes

Hypocalcemia allows stagnant gut and gas buildup in abomasum High grain feeding (high VFA production) prior to proper rumen papillae development Over 2/3 of cases are preceded by a different metabolic disorder Cows with high condition scores at parturition are more prone to displacements

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Displaced Abomasum

When abomasal attachments stretch during pregnancy, this may increase risk for developing a DA Genetics of the animal may also affect the predisposition to this disorder Resting positions may affect risk for DA

Resting on left side reduces risk of LDA relative to resting on right side

Displaced Abomasum

Non-surgical treatment

Removal of gas from abomasum Rolling cow over, taking on rough trailer ride Tethering of right hind leg

87% recovery rate

Surgical treatment

Move abomasum into place and attach it surgically to body wall

Open incision or blind tack 92% recovery rate

Displaced Abomasum

Prevention

Prevent other metabolic diseases Cows should be in proper body condition at parturition Cows fed to encourage maximal intake Prevent hypocalcemia

Encourage cows to lie on left side Cows lie with hooves downhill Stall/Barn design may affect incidence

Metabolic disorders often occur in a predictable sequence or cascade (Courtesy of Dana Boeck)

Milk Fever

Hypocalcemia

Ca mobilization unable to keep up with demand

Calcium moves from blood to mammary gland Requires increased absorption of calcium from feed Requires increased resorption of calcium from bone

Milk Fever

Timing: % of cases Timing relative to calving

Associated with blood changes

Hypophosphatemia Hypermagnesemia Hyperglycemia

3% 6% 75 % 12 % 4%

Before calving At calving 1 - 24 h. after calving 25 - 48 h. after calving More than 48 h. after calving

Most cases in first 24 hours post-calving

Higher frequency in older cows Higher frequency in Jerseys

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Symptoms of Milk Fever

Stage 1: staggers, wobbly, appetite gone

Gut motility stops

Stage 2: sternal recumbency, head along g y, g flank, ears cold, muzzle dry

Pulse fast, breathing labored, occasional split pelvis

Stage 3:lateral recumbency, comatose

Nerve damage, muscle necrosis

Death follows

Cows with milk fever will typically tuck their head back against their flank (Courtesy of University of Illinois)

Milk Fever

Symptoms

No fever, ears and teats actually become hypothermic Loss of appetite

Feed remains in rumen, calcium is essential for gut motility

Associated Problems

Mastitis

Sphincter open in high-pathogen environment Neutrophil function compromised by low Ca

Increases risk of k t i I i k f ketosis

Depression of feed intake is long-term

Pulse and respiration rate increase

Dystocia

Pre-calving hypocalcemia

No uterine contractions

Milk fever is 100% fatal if untreated

After treatment, secondary problems may occur

Degeneration of muscle, nerve paralysis from laying too long Injuries from staggering and falling

Uterine prolapse

Milk Fever

Treatment

Slow infusion of calcium intravenously

Rapid delivery will cause heart to stop Some animals need second treatment 8 hours after th S i l d dt t t h ft the first treatment

Milk Fever

Incomplete first milking

Increased incidence of mastitis

Preventative feeding strategies

Limit calcium intake during dry period g yp

Not practical

Some herds regularly use oral calcium gels at calving to improve calcium status

Calcium chloride problematic Calcium propionate preferred

Can be used as stand-alone treatment, in conjunction with IV calcium, or as prevention

Limit potassium intake in forages fed to dry cows

More important

By increasing concentration of anions in diet, it becomes acidogenic

Decreases blood pH, much less susceptible to milk fever Increases calcium resorption from bone Reduces severity of hypocalcemia

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Laminitis

Separation of epidermal laminae from dermal laminae of hoof Causes in cattle include: Carbohydrate overload, metritis, ketosis, mastitis and a heritable form in Jerseys. y Foot rot or hoof damage and secondary infection can result in laminitis in cattle (Bacteroides nodosus, Fusobacterium necrophorum ) Typical Clinical Findings: Pain, lameness, abnormal stance, reluctance to move Pounding digital pulses, increased temperature of hoof wall Typical Gross Findings: Acute: Swelling of coronary band Chronic: Circumferential hoof rings, altered hoof growth, flattened sole, penetration of third phalanx through sole, depressed coronary band

Hemorrhagic Bowel Syndrome (HBS)

Newly emerging, highly fatal intestinal disease Sudden, progressive & occasionally massive hemorrhage into small intestine with formation of blood clots that cause obstruction Affected areas of intestine become necrotic Most commonl seen in adult cows early in lactation commonly ad lt co s ea l Cause of HBS is unknown Maybe associated with Clostridium perfringens type A Treatment is difficult and often unsuccessful Medical therapy: fluids, laxatives, antibiotics and anti-inflammatory drugs Surgical excision of affected bowel There is no current control measures; unsure of pathogenesis of disease

Bovine Leukosis

Bovine leukemia virus (BLV) Retrovirus that causes lymphosarcoma Infects B lymphocytes Cattle infected for life (persistent carriers) Virus transferred in blood, milk, colostrum, other bodily fluids and less likely across placenta from dam to fetus Less than 5% of cattle infected with BLV develop tumors Affects adult cattle 3-6 years old Tumors develop in lymph nodes, abomasum, heart, uterus, retrobulbar space & epidural space around spinal cord Diagnosis with serologic tests: PCR, AGID, ELISA Control: Good sanitation, test and cull or segregate valuable positive animals

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