Infectious And Metabolic Diseases Exam I

Front 1

Colostrum

Back 1

-Produced by pregnant mammal during the last bit before giving birth
-IgG form maternal serum goes into milk
--makes milk colostrum
-IgG is passed to neonate directly after birth
--provides protective antibodies
-Production ends after parturition
-If 1st milk is lost or not available to calf, calf will not get IgG

Front 2

Failure of Passive Transfer

Back 2

-Newborn does not get IgG from colostrum
-No protective immunity during first weeks of life
-Not a death sentence, but not good either
-Can be due to:
--inadequate volume of colostrum
--improper absorption of colostrum
--Inadequate concentration of IgG in colostrum

Front 3

Colostrum needs for a calf

Back 3

-Should ingest and absorb 150g to get 1g of passive transfer into neonate serum
-4L of colostrum needed for full dose
-4L colostrum in 4 hours

Front 4

Causes of Failure of Passive Transfer

Back 4

1. Poor quality colostrum
--low concentration of IgG in colostrum
2. Calf does not consume adequate volume of colostrum
3. Colostrum is improperly absorbed by the calf

Front 5

Issues with IgG concentration

Back 5

-Causes failure of passive transfer
-1st calf heifers have decreased IgG concentrations
--poor quality colostrum
-Mastitis or mammary infection can decrease quality of colostrum
-Lost 1st milk or animal pre-milks
-Premature calves may have reduced colostrum from dam, cow/mother has not finished making colostrum for that baby

Front 6

Inadequate Colostrum Volume

Back 6

-Premature calves, weak calves, or dystocias
-Natural suckling will not result in enough volume for full passive transfer
--Farmer/producer has to enforce or tube feed colostrum to get required 4 liters in 4 hours

Front 7

Colostrum Absorption

Back 7

-Special process that can only occur during the 1st 24 hours of life
-"Open gut" allows for pinocytosis of IgG by epithelial cells in gut
-Maximum absorption and transfer occurs within 4 hours
--efficiency of absorption decreases after 4 hours
--Absorption continually decreases until no absorption after 24 hours

Front 8

Diagnosis of Failure of Passive Transfer

Back 8

-Want to measure IgG in plasma
-Can do snap test for IgG in foals
-Can measure plasma total proteins with refractometer in calves
--TP more than 5.5 indicates adequate passive transfer in calves
--does not work for foals
--Need to be sure animal is not dehydrated, dehydration will concentrate proteins

Front 9

Treatment for Failure of Passive Transfer

Back 9

-Cannot give more colostrum, gut is no longer open
-Have to give plasma transfusion IV
--costs $250, too expensive for dairy calves but not for foals
-Check colostrum levels at 24 hours to be sure of failure
--at 12 hours can still be absorbing from gut

Front 10

Septicemia in Neonates portals of entry

Back 10

-Umbilicus
-penetration of GI tract, entero-invasive
-Tonsils into lymph nodes
-Prenatal infection via placentitis
--animal is born with infections

Front 11

Bacteria causing Septicemia in Foals

Back 11

-E. Coli
-Strep equi zooepidemicus
-Salmonella

Front 12

Bacteria causing Septicemia in Calves

Back 12

-E. coli
-Salmonella

Front 13

Gram- Bacteria

Back 13

-Cell wall is rich in LPS
--LPS interacts with receptors on WBCs
-Inflammatory mediators are released when LPS interacts with receptors on WBCs
--IL-1, TNF-a
--inflammatory mediators cause fever and inflammatory reactions

Front 14

Inflammation caused by Gram- bacteria

Back 14

-Inflammatory mediators are released when LPS on bacterial cell wall interacts with receptors on WBCs
-IL-1, TNF-a are released and cause fever and inflammatory reactions
-Arachadonic acid is converted into prostaglandins via COX
-Clotting cascade is activated
-Vasodilation, decreased BP, hypovolemic shock
-Damage to vasculr endothelium
-Leads to endotoxic shock and SIRS
--MASSIVE collateral damage in every organ in the body

Front 15

Signs of Septicemia

Back 15

-Fever due to pyrogenic activity of inflammatory mediators
-Hypothermia
-Scleral injection, prominent vessels and bloodshot eyes
-Proteins and WBCs in anterior chamber of the eye
--Hydropion, aqueous flare
--"starburst"
-Petechial hemorrhages in pinna of the ear (foals)
-Hyperemia in mucus membranes
-non-specific signs

Front 16

Non-specific signs of Septicemia

Back 16

-Increased HR
-Depression
-Dehydration
-Hypovolemia
-Weak pulses
-Cold extremities due to poor perfusion

Front 17

Diagnostic Testing for Septicemia

Back 17

-Fibrinogen
-WBC count
-Bacterial culture
-Acid/Base balance
-Glucose levels
-IgG concentration

Front 18

Fibrinogen and Septicemia

Back 18

-Fibrinogen is acute phase protein
-Produces in liver in response to inflammatory mediators
-increases in response to infection

Front 19

WBC count and Septicemia

Back 19

-Acute sepsis will result in leukopenia and left shift
--neutrophils are moving into tissue and site of infection
--younger neutrophils are needed and enter circulation
-Within 24 hours WBC count will increase, may have leukocytosis

Front 20

Bacterial Culture for Septicemia

Back 20

-Need to culture for confirmation of bug
-Takes a while to get response, need to start treatment before know exactly which bug
--start with broad-spectrum antibiotic
-Culture results help guide antibiotic therapy

Front 21

Acid/Base balance and Septicemia

Back 21

-Septic patients are often acidic
-Poor perfusion leads to anaerobic glycolysis and increased lactate production

Front 22

Neonates and Hypoglycemia

Back 22

-Neonates do not have any glycogen stores, are very susceptible to hypoglycemia
-Septicemia can result in hypoglycemia due to bacteria consuming glucose

Front 23

Dehydration and failure of passive transfer

Back 23

-Dehydration will cause increase in TP in serum
-In calves will appear as if calf has received sufficient colostrum
--concentration of TP can be interpreted as increased IgG in serum
-Does not actually indicate successful passive transfer!

Front 24

Treatment for Septicemia

Back 24

1. Kill bacteria: antibiotics
2. Give IV fluids: supplement fluids with glucose
--use balanced electrolyte solution (Plasmalyte)
3. Give anti-inflammatory: Flunixin meglumine (banamine)
4. Give IgG plasma infusion (usually only in foals due to cost)

Front 25

Antibiotics as treatment for Neonatal Septicemia

Back 25

-Use broad spectrum antibiotic early
-Be sure to culture to identify organism
-Foals: Penicillin, Amikacin, Gentamycin
-Calves: Ceftiofur
--more limited antibiotic use, calves are food animals

Front 26

Prognosis of Septicemia in Calves

Back 26

-Good if treated aggressively with appropriate antibiotic

Front 27

Calf Diarrhea Complex

Back 27

-"Scours"
-Enterotoxigenic E. Coli (ETEC)
-Coronavirus
-Rotavirus
-Cryptosporidium

-All act differently, but result in identical clinical signs
-Treatment for all is exactly the same
-Oftentimes more than one pathogen is involved

Front 28

Enterotoxigenic E.Coli
ETEC

Back 28

-"Classic" diarrhea
-Cholera in people
-Different from invasive strains of E. coli
-Transmitted in feces or water, fecal-oral transmission
-E. coli does damage in small intestine

Front 29

Calves and ETEC transmission

Back 29

-Manure in calving stall/pen is source of contamination
-Feces on udder of cow

Front 30

ETEC in GI tract

Back 30

-Does damage in small intestine
-Has to go through stomach (abomasum) and HCl acid barrier
--Newborn calves have neutral abomasal pH, more permissive environment
-has to attach with correct fimbriae to small intestine epithelium
--allows adhesion
-Does NOT invade GI tract, does not cause damage to mucosa
-Just sticks on surface of epithelium
-Once adhered, produces enterotoxin
-Results in secretory diarrhea, can be devastating

Front 31

Abomasal pH of calves

Back 31

-Normally abomasum is extremely acidic
-Newborn calf abomasum is neutral pH, more permissive environment
-Less than 24 hours old, neutral pH ad susceptible
-more than 24 hours old, pH drops to 2, extremely acidic and resistant environment

Front 32

ETEC enterotoxin

Back 32

-Produced once E. coli is adhered to epithelium
-Interacts with epithelial cells and stimulates Adenyl Cyclase enzyme activity
--converts ATP to cAMP
--Increased cAMP leads to secretion of Cl and H2O into intestinal lumen
-H2O and electrolytes go OUT of cell
-results in secretory diarrhea

Front 33

ETEC Important info

Back 33

-No Invasion
-No destruction
-Needs Fimbriae for adhesion
-Needs to produce enterotoxin

Front 34

ETEC clinical signs

Back 34

-Dehydration
--sunken eyes, skin tent, slow jugular vein refill or not visible
-Hypoglycemia due to anorexia
-Weakness
-Depression
-Watery diarrhea
-May not have a fever, in inflammatory response

Front 35

Treatment for ETEC

Back 35

-Fluids!
-IV fluids are rapid, more expensive, and need sterility
--better for severe dehydration
-Oral fluids are cheap, take longer to have effect
-Can give Na or glucose to stimulate H2O absorption
-Need to give H2O with additives, otherwise no benefit!
-Pepto-bismol will solidify stool and slow transit time to increase H2O reabsorption
-Give antibiotics (Ceftiofur)

Front 36

Bloody Diarrhea in Calves

Back 36

-Salmonella or Clostridium
NOT calf diarrhea complex

Front 37

Prevention of Calf Diarrhea

Back 37

1. decrease exposure
2. Increase resistance

Front 38

Decreasing Exposure to decrease Calf diarrhea

Back 38

-Decrease exposure to contaminated feces
-Calving pen sanitation is essential
--clean between calvings to prevent E. coli contamination
-Keep cow's teats manure free and clean, employ good udder sanitation
-Put calves in calf hutches
--prevents fecal contamination between calves and nose to nose contact between calves
--prevents contamination from adult calves
-Remove calf from cow as soon as possible

Front 39

Increasing Resistance to decrease calf diarrhea

Back 39

-Ensure adequate colostrum intake (4L in 4 hours)
--tube feed or bottle feed calves to get sufficient amount
-Vaccinate cow against E. coli during dry period
--cow will secrete IgG into colostrum for calf
-Passively administer antibodies (first defense for calves)

Front 40

Calving on pasture to decrease calf diarrhea

Back 40

-Eliminates concentration of manure
-makes it less likely calf will get sufficient dose of E. coli to become sick
-Hard to monitor cow for calvings or dystocias

Front 41

"First Defense" for calves

Back 41

-Colostrum supplement
-Additional passive antibodies for calf from E. coli
-Give to the calf when born

Front 42

Calf Rotavirus/Coronavirus

Back 42

-Similar clinical signs to other calf diarrhea pathogens
-Oral-fecal transmission
-Totally different pathogenesis from E. coli/ETEC

Front 43

Rotavirus/Coronoavirus Pathogenesis

Back 43

1. Calf ingests virus
2. Virus invades epithelial cells at tip of villus
3. Malabsorption due to decreased surface area
4. Destruction of lactase enzyme in brush border of epithelial cells further causes maldigestion
5. Maldigestion leads to undigested carbohydrates in colon
--pull water into colon, causes osmotic diarrhea

Front 44

Ingestion of Rotavirus/coronavirus

Back 44

-Calf ingests virus
-Virus is not susceptible to acids, can infect any calf younger than 8 weeks old
-Rotavirus goes into the small intestine
-Coronavirus goes into the small and large intestine
-Once in site, virus invades villus epithelial cells at tip of intestinal villus

Front 45

Rotavirus/Coronavirus Villus epithelial cell invasion

Back 45

-Virus invades villus epithelial cells at the tip of the intestinal villus
-Causes cells to slough off the tip of the villus
-Villus becomes shortened due to erosion of epithelial cells
-Decreases effective absorptive surface area
-Results in malabsorption due to decreased surface area

Front 46

Rotavirus/Coronavirus Malabsorption

Back 46

-Malabsorption occurs due to decreased surface area of villi
--decreased absorptive surface area

Front 47

Rotavirus/Coronavirus Maldigestion

Back 47

-Lactase enzymes live in epithelial cell brush border
-Destruction of epithelial villus tips results in destruction of lactase enzyme
-Intestine can no longer break lactose down into glucose and galactose
-undigested carbohydrates in corn ferment due to colonic bacteria
--pulls H2O into colon
--Osmotic diarrhea

Front 48

Rotavirus/Coronavirus Diarrhea

Back 48

-NOT permanent
-Cells in the intestinal crypts mature and migrate upwards, replace destroyed cells
-Takes 7-10 days
-Need to give calf supportive care during 7-10 day period for regrowth and maturation of villi

Front 49

Rotavirus/Coronavirus diarrhea treatment

Back 49

-Fluids!
--oral or IV
-Oral fluids are not absorbed as well due to villus damage and blunting

Front 50

Cryptosporidium overview

Back 50

-Can affect people
-Fecal-oral transmission

Front 51

Cryptosporidium life cycle

Back 51

-Calf ingests oocyst
-Oocyst infects the distal small intestine
-Oocyst is shed in feces and is immediately infective
-Oocysts are extremely resistant to the environment, live for a long time and are impossible to kill
-Internal cycle of oocysts also exists, internal auto-infection
--creates recurring infection that can go on for weeks
-5 day incubation period

Front 52

Cryptosporidium autoinfection

Back 52

-Oocysts can multiply in distal small intestine and re-infect host
-Can cause prolonged infections that are difficult to get rid of

Front 53

Cryptosporidium pathogenesis

Back 53

-Blunts and shortens villi leading to malabsorption and maldigestion
-Increases cAMP secretion, leading to increased Na and Cl secretion into GI lumen and water follows electrolytes

Front 54

Human Ingestion of Cryptosporidium

Back 54

-May be uncomfortable but not life-threatening to immuno-competent people
-Can be dangerous or deadly for immunocompromised individuals

Front 55

Diagnosis of Cryptosporidium

Back 55

-Fecal float with acid-fast stain
-Always test for crypto when possible
--ensures public health

Front 56

Treatment of Cryptosporidium

Back 56

-No currently approved drug treatment
--Azythromycin? not approved for use in cattle
-Give fluids and hydration support

Front 57

Bovine Viral Diarrhea Virus
BVDV

Back 57

-Very common in cows
--70% of cows have antibodies with no clinical signs
-Can cause abortion storms, respiratory issues, diarrhea
-Pestivirus, related to hog cholera
-Wide genetic diversity of virus
-Animal to animal transmission
-Shed in any and all bodily secretions of any infected animal
--blood, nasal secretions, uterine secretions

Front 58

Type I BVD

Back 58

-Very common, 70% of cattle have been exposed and have antibodies
-Milder case, short viremia
-Generally asymptomatic infection, May not see fever
--mild illness
-Animal will have antibodies
-Most common type of BVD
-Can cause immunosuppression
--plays a role in bovine respiratory diseases
--opportunistic pathogens are able to set up shop in the respiratory tract

Front 59

Type II BVD

Back 59

-Fatal! Causes death!
-High fever

Front 60

BVD in Pregnant cows

Back 60

-Both types of BVD can cross the placenta and cause abortion
-Previously exposed and resistant cows are safe, will not get viremia and there will be no effect on the fetus
-Susceptible cows are not safe, viremia can cross placenta and damage the fetus

Front 61

BVD effects on fetus based on time of infection

Back 61

-0-60 days gestation: early embryonic death
-60-180 days gestation: abortion, fetus dies
--congenital defects, damage during organ development
--eye and cataract issues, micro-opthalmia
--short snout
--cerebellar hypolasia
-post 180 days: abortion, fetus dies
--weak calf with BVD viremia
--no birth defects, organogenesis is complete by the time of infection

Front 62

Non-cytopathic BVD

Back 62

-Specific strain of BVD
-Virulent to the host
-Infection between 50 and 125 days of gestation results in persistently infected calves (PI calf)
-Virus is shed in HUGE amounts in all secretions from PI calf

Front 63

PI calf

Back 63

-Calf infected with BVD in-utero between 50 and 125 days of gestation
-Infection during timeframe when calf's immune system is developing
-Calf recognizes virus as "self" and does not illicit an immune response
-Calf becomes persistent shedder, "BVD factory"
--HUGE reservoir for BVD on the farm
-Calf is born looking normal but is always infected with BVD

Front 64

Metabolism of PI calf

Back 64

-Non-cytopathic BVD takes big toll on animal's metabolism
-Energy is put towards making viral proteins
-Unthrifty calves that get chronic infections
-50% of PI calf population dies every year
-Some survive past calf-bearing age and get pregnant
--produce PI calf

Front 65

Musocal BVD

Back 65

-PI calf is exposed to cytopathic form of BVD
-Fatal disease
-Severe ulcerations on all mucus membranes
--feet, ulcers on hard palate, blunted oral papillae

Front 66

When to test for BVD

Back 66

-Outbreak of fever and diarrhea
-Screening for replacement heifers
--do not want to bring in BVD or a PI calf!
-Suspect PI calf on farm
--need to find the source of the outbreak

Front 67

BVD Diagnosis

Back 67

-Animal will not have antibodies in acute stage of disease, have to find and identify the virus
--PCR on whole blood buffy coat
-IN convalescent stage, can test for antibodies but will not find viral particles
--does not give definitive cause for disease episode
--antibodies only indicate presence of an infection at some point, not recent infection
--Ab could be present from earlier infection or from vaccine
-Paired serum samples: use to determine acute disease
--look for seroconversion over time
-Serology is a lot cheaper than PCR!

Front 68

Finding a BVD PI calf

Back 68

-Animal will not produce antibodies, Ab screening is not effective
-Have to look for presence of virus and viral particles
-PCR buffy coat, have to do at least 2x to determine PI shedder
-Skin biopsy: stain for histopathology
--viral particles accumulate in skin
--cheap, preferred method
--take skin from ear (ear punch)

Front 69

Clostridial myositis in Ruminants

Back 69

-Blackleg
-Malignant edema

Front 70

Clostridium infections general thoughts

Back 70

-Infectious, but not contagious
--no contamination between animals
--will cause an infection in an animla
-Gram+, spore-forming rods
-All are potent exotoxin producers, gives pathogenicity
--form toxin to be pathogenic
-All over in environment and normal GI flora
-Cause disease in special circumstances
--at specific times
--based on specific risk factors

Front 71

Clostridium pathogenesis

Back 71

-Toxins of different organisms vary in way they gain entry to the circulation

1. Ingestion of pre-formed toxin
2. Absorption from GI tract after abnormal proliferation of organism in alimentary tract
3. Ingestion of causative organism, distribution to tissue with sporulation in areas of local infection
--anaerobic environment in tissues allows sporulation

Front 72

Blackleg

Back 72

-Clostridial myositis in ruminants
-Clostridium chauvoei
-Affects cattle mostly (beef), sometimes sheep
-rare in goats

Front 73

Blackleg Pathogenesis

Back 73

1. Ingestion of contaminated feed
2. Clostridium chauvoei spreads to muscles, sporulates and proliferates when muscle is traumatized
--any condition that causes anaerobic environment
--transport, herding, shearing, docking, umbilicus, lambing, fighting
3. Toxins are produced
4. Severe necrotizing myositis and systemic toxemia

Front 74

Blackleg Clinical Findings

Back 74

-Sudden death is common
-Severe lameness
-Swelling of the upper limb
-Initially limb is hot, painful to palpation
--eventually becomes cool, painless, discolored, dry
-Atypical lesions on tongue, heart, diaphragm, brisket, and udder can occur, crepitus in muscle
-Signs of toxemia are present
--depression, anorexia, rumen stasis, fever, tachycardia, cool extremities, prolonged CRT, poor perfusion
-Injected/toxic mucus membranes

Front 75

Blackleg Diagnosis

Back 75

-Diagnose based on clinical signs and history of trauma
-May be able to see or feel gas in tissues
-Pre-mortem: needle aspirate with direct smear/culture
--fluorescent antibody testing
--look for gram- rods on smear
-Post-mortem: necropsy examination
--darm muscles, sanguineous fluid with gas, rancid odor

Front 76

Blackleg Treatment

Back 76

-Surgical debridement/fasciotomy
--introduce O2 to the muscle, stop anaerobic growth!
-High doses of penicillin, kills clostridium
-Antiserum is poor value

Front 77

Malignant Edema

Back 77

-Clostridium septicum
-Affects sheep, goats, and pigs
-Usually occurs during fighting between goats
--trauma to head results in myopathy

Front 78

Malignant Edema Pathogenesis

Back 78

-Clostridium septicum enters body via wound
--can be surgical or accidental wound
-Ports of entry can also include umbilicus, genital tract, vaccination, or veinupuncture
--OB wounds are a common source
-Anaerobic environment of wound allows sporulation, with sporulation toxin is produced

Front 79

Malignant Edema Clinical Findings

Back 79

-Sudden death
-Acute onset of fever and signs of toxemia
-Inflammation and swelling at the side of the wound
--Heat, edema, pain, subcutaneous emphysema

Front 80

Malignant Edema Diagnosis

Back 80

-Same as for blackleg, diagnose based on clinical signs and history of wound
-Look for bacteria on histopathology slide

Front 81

Malignant Edema treatment

Back 81

-Irrigate wound, debride, and allow O2 into tissue
--O2 will kill anaerobic bacteria and stop toxin production
-Irrigate wound with H2O2, antiseptic and O2 introduction

Front 82

Clostridial Myositis in Horses

Back 82

-Caused by various clostridial species
--clostridium chauvoei
--clostridium septicum
--Clostridium sordelli
--Clostridium novyi type B
--Clostridium perfringens type A
--Clostridium carnis

Front 83

Clostridial Myositis in Horses Pathogenesis

Back 83

-Clostridial bacteria comes in through IM injection or penetrating wound
--Allows for direct spore deposition into the tissue
-If conditions are suitable, bacteria converts to vegetative sporulation state and toxins are produced
--need anaerobic conditions
-Can also occur without a wound
--spores enter through GI tract and circulation to muscles and blunt trauma causes anaerobic state and allows toxin production
-End result is severe necrotizing myositis and systemic toxemia
--if signs of toxemia are present, bad news! too late!

Front 84

Clostridial Myositis in Horses Diagnosis

Back 84

-Diagnosis based on clinical signs and history or a wound
-CBC is not specific
--shows stress/toxic leukogram (neutrophilia)
--hemoconcentration
-Chemistry profile shows increased CK and AST, increased muscle enzymes present
-Aspirates of affected tissues

Front 85

Clostridial Myositis in horses Treatment

Back 85

-Aggressive antimicrobial therapy (penicillin)
-Aggressive surgical debridement
-O2 therapy (questionable efficacy)
-Give specific anti-toxin when possible
-Supportive care
--fluids, analgesia, anti-inflammatory agents
--avoid laminitis, dehydration, electrolyte imbalances
-Prognosis is fair to guarded

Front 86

Vaccination for Clostridial myositis in Ruminants

Back 86

-Vaccination is very effective
--SQ administration
--monovalent, bivalent, or multivalent bacterin toxins
-Start vaccine 3-6 months of age, give 2x 4 weeks apart
-Need annual booster, part of annual protocol
--cattle: spring/summer
--sheep: before lambing or shearing

Front 87

Vaccination for Clostridial myositis in Horses

Back 87

-Vaccination is not common in horses
-More of a rare disease in horses

Front 88

Prevention/Control of Clostridial Myositis

Back 88

-Proper care of wounds
--debride, systemic antimicrobials, etc.
-Avoid unsanitary or unnecessary surgical or obstetrical procedures
-Avoid IM injection of irritating drugs, especially in horses
--anthelmintics
--anti-inflamatory drugs (Banamine IV only!)

Front 89

What to do with Clostridial Myositis outbreak

Back 89

-Most likely to occur in beef cattle
-Vaccinate, or booster vaccination to all unaffected animals
-Prophylactic treatment with Penicillin to all unaffected animals at risk
-Carcasses of dead animals should be destroyed
--burn, deep burial
--avoid contamination!!
-Educate farmers, farm managers, etc.

Front 90

Clostridial Hepatitis in Ruminants

Back 90

-Black disease: infectious necrotic hepatitis
-Bacillary Hemoglobinuria

Front 91

Black Disease

Back 91

-Clostridial Hepatitis in Ruminants
-NOT blackleg
-Clostridium novyi type B
-Affects all ruminants, especially cattle

Front 92

Black Disease Pathophysiology

Back 92

-Portal of entry: intestinal mucosa
-From intestine clostridium novyi disseminates to liver
-In liver, local anaerobic conditions allow germination of spores and production of toxins
-Causes necrosis of liver
-Fluke migration through liver will provide anaerobic environment needed for sporulation

Front 93

Black Disease Clinical Findings

Back 93

-Sudden death
-Depression, anorexia
-Fever
-Respiratory distress
-Normal urine

Front 94

Black Disease Diagnosis

Back 94

-Pre-mortem: almost never identified pre-mortem due to rapid disease progression
-Post-mortem:
--liver tissues in advanced state of decomposition
--migrating fluke channels in liver
--swollen, congested liver
--hemorrhages in subcutaneous tissues, abdominal cavity, thoracic cavity, pericardial sac
-Urine is NORMAL
-Gram stain of liver can confirm diagnosis

Front 95

Black Disease Treatment

Back 95

-Rare, disease progresses so quickly most animals are found dead
-Antimicrobials have limited value, usually given too late
-No commercially available anti-toxin

Front 96

Black Disease Prevention

Back 96

-Vaccination!! Vaccinate for Black disease!!!
-Prevention of liver flukes in endemic regions

Front 97

Bacillary Hemoglobinuria

Back 97

-"Red water"
-Clostridium haemolitycum
-Affects all ruminants

Front 98

Bacillary Hemoglobinuria Pathophysiology

Back 98

-Ingested spores spread to the liver and may stay latent for a long time
-Injury to liver causes anaerobic conditions
--fluke migration, liver biopsy
-Anaerobic conditions allow for sporulation and release of toxins
-Toxins cause hepatic necrosis and intravascular hemolysis
--will get hemoglobinuria, urine will be color of port wine

Front 99

Bacillary Hemoglobinuria Clinical Findings

Back 99

-Sudden death in animals that were completely normal 24 hours before
-Depression, reluctance to move, anorexia
-Fever, tachypnea, tachycardia
-Icterus
-Hemoglobinuria, port-wine urine
-Blood-tinged froth form nostrils and mouth
-Rectal bleeding and bloody feces

Front 100

Bacillary Hemoglobinuria DDx

Back 100

-Copper toxicosis
-Also causes intravascular hemoglobinuria

Front 101

Bacillary Hemoglobinuria Diagnosis

Back 101

-Pre-mortem: clinical findings and absence of vaccination history
--important to rule out copper toxicity
-Post-mortem:
--carcass in advanced state of decomposition
--icterus
--subcutaneous and petechial/ecchymotic hemorrhages
--blood-tinged fluid in thoracic, abdominal, and pericardial cavities
--Dark red urine in the bladder
--Gram stain of liver or culture of liver should confirm diagnosis

Front 102

Bacillary Hemoglobinuria Treatment

Back 102

-Rare due to rapid progression of disease
-High doses of systemic antibiotics (Penicillin)
-Supportive care
--IV fluids
--blood transfusion

Front 103

Bacillary Hemoglobinuria Prevention

Back 103

-Same as Black Disease
-VACCINATION
-Prevent liver flukes in endemic regions

Front 104

Enterocolitis associated with Clostridium in Horses

Back 104

-Clostridium difficile
-Clostridium perfringens type A and C
-Can cause severe enterocolitis
-Should not affect healthy animals
--animals on systemic antimicrobials will be affected due to decreased or modified microflora
--C. difficile out-competes deficient microflora and takes over

Front 105

Clostridial Enterocolitis in Horses Pathogenesis
C. difficile

Back 105

-C. difficile is ingested and proliferates in the GI tract
--proliferation is favored by decreased competition by normal flora
-Produces 2 types of toxins
-Toxin A: secretory, causes pronounced inflammation
-Toxin B: mostly secretory

Front 106

Clostridial Enterocolitis in Horses Pathogenesis
C. perfringens

Back 106

-Organism is common in GI tract, all over
-Can overgrow due to decreased competition by normal flora
-Overgrowth leads to release of toxins within the intestines
-Toxins cause necrosis and release of toxins into circulation
-Secretory diarrhea and systemic disease result

Front 107

Clostridial Enterocolitis in horses Risk Factors

Back 107

-Administration of systemic antimicrobials
--certain types are worse than others
--can be geographic
-Mares of foals on antimicrobials
-Hospitalization and nosocomial infections
--anesthesia, antimicrobials, resistant strains in hospitals
-Diets rich in protein
--increases carbohydrates in small intestine, increases chance for bacterial multiplication

Front 108

Clostridial enterocolitis in Horses Clinical Findings

Back 108

-Affects foals and adult horses
-Will have abdominal pain and diarrhea, colic
-Foals may have signs of septicemia, gas/fluid distended intestines
-Profuse watery diarrhea
--may be hemorrhagic or mucoid/necrotic
-Other signs are secondary to diarrhea

Front 109

Clostridial Enterocolitis in Horses Diagnosis

Back 109

-Toxigenic clostridia isolated from feces or tissues
--bacterial culture or direct smear
-Identification of toxin is essential to form diagnosis
-Commercially available kits exist for ELISA and PCR

Front 110

Clostridial Enterocolitis in horses Treatment

Back 110

-Oral metronidazole
--C. difficile is resistant to metronidazole in some areas (CA)
-Broad-spectrum systemic antimicrobials if neonate or immunosuppressed adult
-Antitoxin for C. perfringens in foals, keep off milk feeding for 24 hours
--reduce substrates for C. difficile
-Supportive care
--fluids, plasma, anti-inflammatory drugs, anti-endotoxemic drugs
-Can also give yeast, biosponge, activated charcoal, etc. to bind toxins present

Front 111

Diseases caused by Clostridium perfringens toxins

Back 111

-Enterotoxemia
-Yellow Lamb Disease
-Lamb disentery
-Necrotic entertitis

Front 112

Clostridium perfringens

Back 112

-Gram+ rod
-anaerobic bacteria
-spore-forming
-Normal inhabitant of soil
-Commensal intestinal organism of animals
--in the intestinal tract of most animals

Front 113

Clostridium perfringens biotypes

Back 113

-Type A: alpha toxin
-Type B: alpha, beta, and epsilon toxins
--beta toxin predominates
-Type C: alpha and beta toxins
--beta toxin predominates
-Type D: alpha and epsilon toxins
--epsilon toxin predominates
-Type E: alpha and iota toxins in equal amounts

Front 114

Clostridium perfringens type A

Back 114

-"Yellow lamb disease"
-Alpha toxin predominates
-Toxin is phospholipase, causes lysis of RBCs, platelets, and leukocytes
-Causes endothelial damage of blood vessels
--makes blood vessels more permeable, leads to edema
-Causes necrosis of villous tips of small intestine
--blunts villi and leads to malabsorption
-Mostly affects lambs
-Intravascular hemolysis leads to hemoglobinemia and hemoglobinuria

Front 115

Clostridium perfringens Type A Clinical Signs

Back 115

-Yellow lamb disease
-Icterus
-Anemia due to widespread hemolysis
-weakness
-hemoglobinuria and hemoglobinemia
-High fever
-Death in 6-12 hours of onset

Front 116

Clostridium perfringens type A DDx

Back 116

-Other causes of hemolytic disease in small ruminants
-Copper toxicosis
-leptospirosis (geographic distribution)
-Bacillary hemoglobinuria

Front 117

Clostridium perfringens type A Diagnosis

Back 117

-Difficult to confirm diagnosis, usually presumptive diagnosis
-Commensal organism, exists in host regardless
-May find gram+ rods in impression smears from small intestinal mucosa
-More than 1 lamb will usually be affected

Front 118

Diseases caused by C. perfringens type A

Back 118

-Yellow lamb disease
-Ruminal and abomasal tympany in neonatal calves
-Abomasal ulcers in neonatal calves
-Hemorrhagic bowel syndrome in adult cattle

common cause of disease in food animals

Front 119

Clostridium perfringens type B

Back 119

-"Lamb dysentery," diarrhea with fresh blood
-Beta toxin is major toxin, responsible for most clinical signs
--alpha and epsilon toxins also play a role

Front 120

Clostridium perfringens type B clinical signs

Back 120

-Occurs in lambs less than 1 week old
-depression
-yellow diarrhea progresses to dark brown from presence of blood
-No icterus, less alpha toxin and therefore no intravascular hemolysis
-Death

Front 121

Clostridium perfringens type B diagnosis

Back 121

-Post-mortem exam:
-ulcers in small intestine and throughout the GI tract
-sloughing of GI mucosa
-Severe dehydration

Front 122

Clostridium perfringens type B prevention

Back 122

-Use type B toxin cavvine
-cross protection of types C and D vaccine

Front 123

CDT vaccine

Back 123

-Clostridium toxins type C and D and tetanus

Front 124

Clostridium perfringens type C

Back 124

-"Necrotic enteritis" or "Neonatal hemorrhagic enterotoxemia"
-Beta toxin is major toxin
--alpha toxin is minor toxin
-Affects neonates of all species
--calves, lambs, foals, piglets

Front 125

Clostridium perfringens type C pathophysiology

Back 125

-Probably multi-factorial causes
-Ingestion of protein-rich diet allows rapid growth of C. perfringens
-Beta-toxin results in necrosis and invasion of deeper intestinal layers, causes diarrhea
--profuse diarrhea
--toxins can cross into bloodstream and cause viremia
-Death is caused by severe diarrhea and bacteremia/toxemia
--dehydration

Front 126

Clostridium perfringens type C Clinical Signs

Back 126

-Explosive diarrhea, yellow or hemorrhagic diarrhea
-Gray/red streaks of necrotic mucosa may be present in stools
-Acute abdominal pain
-Dehydration
-Anemia
-Weakness
-Acute death

Front 127

Clostridium perfringens type C Epidemiology

Back 127

-C. perfringens C is in environment
-animals can ingest via feeding or housing on drylot
--pick up toxin from environment
-Neonates ingest type C organisms during first few days of colostrum feeding
-in foals disease is associated with housing or stalls on drylot

Front 128

Clostridium perfringens type C DDx

Back 128

-Salmonellosis
-Coccidiosis if animal is old enough
--20-21 day incubation period

Front 129

Clostridium perfringens type C necropsy findings

Back 129

-Necrosis of mucosa of small intestine
-Intraluminal blood
-Hemorrhagic mesenteric lymph nodes
-Necrotic villi tips are covered with many large gram+ rods
--blunted villi with gram+ rods

Front 130

Clostridium perfringens type D

Back 130

-"enterotoxemia" or "overeating disease" or "pulpy kidney disease"
-Usually affects the biggest, fattest lambs
--will have increased protein in the diet from efficient eating, more protein for C. perfringens D to eat
-Epsilon toxin is major toxin
--alpha toxin is minor toxin
-Affects lambs mostly
--less important in calves and kids

Front 131

Clostridium perfringens type D Clinical signs

Back 131

-Sudden death of a well-fed rapidly growing animal
--can be VERY acute, disease runs course in 30-90 min
-Ataxia, trembling, stiff limbs
-Opisthotonus, convulsions
-Coma
-Hyperglycemia and glucosuria
-Neonatal sings are due to epsilon toxin

Front 132

Clostridium perfringens type D pathophysiology

Back 132

-Over-nutrition provides substrate for rapid proliferation of type D organisms
--heavy grain feeding
-Type D organisms produce epsilon toxin

Front 133

C. perfringens type D in body

Back 133

-Commensal organism, normally present in body
-overgrowth Kept in check by:
--acidic environment of abomasum
--Continuous peristalsis, continued emptying of contents
--low amounts of fermentable substrates in intestines

Front 134

C. perfringens type D Epsilon toxin pathophysiology

Back 134

-Increases intestinal permeability
-Increases vessel permeability everywhere in the body
--Leads to massive edema, even in brain
-Edema in lungs, kidney, brain
--leads to rapid deterioration and death
-Causes massive hepatic glycogen release
--leads to hyperglycemia and glucosuria

Front 135

Diagnosis of diseases caused by Clostridium perfringens

Back 135

-C. perfringens is often isolated from clinically normal animals
--bacterium also proliferates quickly after organism dies
--Isolation from necropsied animal is not sufficient on own for Dx
-Need to see toxin in gut contents
-History and clinical signs:
--unvaccinated animal
--group of animal affected
--neurologic signs
-Can isolate C. perfringens toxins via PCR or ELISA
--isolates should come from freshly dead animals
-Collect samples of gut contents and freeze!

Front 136

C. perfringens treatment

Back 136

-usually none possible, too acute

Front 137

C. perfringens Outbreak control

Back 137

-Give C and D antitoxin and oral antibiotics to all susceptible animals in the group
-Adjust diet to minimize substrates
--avoid high-protein high-carbohydrate diet
-Vaccinate all other susceptible animals in the group
--CDT vaccine
-Vaccine for A and B types are not available, but may have cross-protection with types C and D

Front 138

Salmonella enterica

Back 138

-Most common type of salmonella
-Over 2460 serotypes
--based on O and H flagellar antigens

1. Specific to human host
2. Specific to animal hosts
3. unadapted serotypes that cause disease in humans and animals

Front 139

Cattle Salmonella serotypes

Back 139

-B: S. typhimurium, S. agona
-C: S. newport, S. montevideo, S. kentucky
-E: S. anatum
-K: S. cerro

Western U.S.: group D, S. dublin

Front 140

Horse Salmonella serotypes

Back 140

-S. typhimurium
-S. newport
-S. Infantis
-S. Norwich
-S. Anatum
-S. Javiana

Front 141

Morbidity in Salmonella cases

Back 141

-Morbidity is high in groups of calves/foals
-Young animals
-Fresh cows
-Hospitalized animals

Front 142

Mortality in Salmonella cases

Back 142

-High mortality in all cases
--can reach 100% if left untreated
-Higher mortality in neonates

Front 143

Salmonellosis risk factors

Back 143

-Virulence of the serotype
-Dose of inoculum
--higher dose, bigger infection
-Degree of immunity or previous exposure
--exposed cows have some immunity
--immunocompromised animals are at higher risk
-Transportation, parturition, concurrent disease, anesthesia, surgery
-Systemic antimicrobials reduce risk of competition in GI tract
-Food deprivation puts stress on GI system, decreases peristalsis

Front 144

Secondary risk factors contributing to Salmonellosis

Back 144

-Free stall housing in cattle
--contributes to fecal-oral contamination
-Contaminated ration components
--contaminated prior to feeding cows
--contaminated by cows themselves
-Birds/rodents can shed salmonella and act as vectors
--can die and contaminate mangers or feed
-Spreading manure on crops then used for feed

Front 145

Salmonella Pathogenesis

Back 145

1. Salmonella is ingested, fecal-oral contamination
2. Salmonella attach to and destroy enterocytes
--inflammatory diarrhea
--maldigestion and malabsorption also contribute to diarrhea and protein loss
3. Bacterium gain access to submucosa or distal small intestine and colon
--can go hidden or undetected, protected from immune system
4. Salmonella enters lymphatics and causes bacteremia in neonates
--young animals are particularly susceptible

Front 146

Salmonella in Cattle

Back 146

1. Calves 2-6 weeks old:
--calf-raising farms
--veal calves through sale barns
--group housing of calves, mingling calves
2. Adult cows:
--usually sporadic cases
--outbreaks are possible in fresh cow pens with free-stall management
--contaminated maternity pens

Front 147

Acute Enteric Salmonella

Back 147

-Affects young and adults
-High fever is 1st sign
-abdominal pain, severe profuse watery diarrhea
--can be very watery, may see strands of mucosa
--diarrhea smells BAD
-Fever often goes away when diarrhea starts
-Severe depression, progresses to recumbency
--hypovolemia, acid/base disturbance, electrolyte disturbances
-Complete anorexia, and off-feed
-Tachycardia, tachypnea
-Congested mucus membranes with scleral injection
--injected mucus membranes
-Severe dehydration
-Abortion is possible, occurs a few weeks after outbreak in calves

Front 148

Septicemic Salmonella Clinical Signs

Back 148

-Usually in neonates
-Profound depression, dullness, high fever
-signs of toxemia (scleral injection)
-Dyspnea
-Dehydration, sunken eyes
-Neurological signs
-Death in 24-48 hours
-Sometimes animals are found dead without prior signs
--no time to develop diarrhea
--high dose of virulent strain at young age, causes multi-organ failure

Front 149

Salmonella complications in calves

Back 149

-Osteomyelitis/physitis
--can occur after several weeks
-Polyarthritis in carpi, tarsi, fetlocks, and stifle joints
-Encephalitis or meningitis
-Dry gangrene of distal extremities, loss of feet or ears
-Pneumonia

Front 150

Salmonella in Horses: animals at risk

Back 150

-Any stressed animal
--immunocompromised, working, stressed
-Foals (especially in breeding barns)
-Weanlings
-Broodmares
-Racehorses and performance horses
-Post-surgical cases, especially colics
-Any hospitalized horse
-Off-feed
-Systemic anti-microbials

Front 151

Acute enteritis from Salmonella in the Horse

Back 151

-Most common form of salmonella in horses
-Affects all ages
-24-48 hours:
--depression, fever, abdominal pain, tachycardia, toxic mucus membranes
-Diarrhea: watery and projectile, leads to dehydration and electrolyte imbalance, foul odor
--associated toxemia
-May lead to phlebitis or laminitis in adults
-Some cases never develop diarrhea

Front 152

Salmonella Septicemia in Horses

Back 152

-Same as for neonatal calves
-Arthritis, physitis
-Pneumonia
-Meningitis
-Nephritis
-Death within 24 hours is not rare

Front 153

Salmonella clinical findings in the Horse

Back 153

-Colic with or without diarrhea
-Large number of colic cases that come into referring hospitals are positive for salmonella

Front 154

Anterior enteritis Clinical signs in the horse

Back 154

-Enteritis in the small intestines of the horse
-Inflammation of the anterior portion of small intestine
--ileus
-Will get persistent reflux in large volumes
--may have gross blood or fluid with occult blood
--may culture salmonella from gastric reflux
-Rarely caused by salmonella
-Fever
-Leukopenia
-Variable abdominal pain

Front 155

Anterior enteritis Laboratory findings

Back 155

-Leukopenia associated with severe neutropenia and degenerative toxic left shift
--all cells are called out to the intestine
-Hyponatremia, hypochloremia
-Hypokalemia in adults, hyperkalemia in calves
--old animal are anorexic
--young animals in acidosis try to exchange excess H for K, H out of cells and K into cells
-Azotemia (pre-renal or renal with dehydration)
-Acidosis, losing HCO3- in diarrhea
-Hyponatremia

Front 156

Salmonella Bacterial Culture for Diagnosis

Back 156

-For definitive etiological diagnosis
-Can culture from feces, blood, milk, gastric reflux, other body fluids and tissues
-May have false negatives, need to do many cultures
-Needs 48 hours for presumptive Dx, takes a long time
-Biochemical confirmation of genotype and antibiogram may need additional 24-48 hours

Front 157

Salmonella PCR diagnosis

Back 157

-Highly sensitive and specific
-Short turnaround
-Expensive!

Front 158

Salmonella DDx in Cattle
Acute Enteric Form

Back 158

1. Calves:
--cryptosporidiosis
--coccidiosis
--BVD
--rotavirus/coronavirus
--E. coli
--C. perfringens
2. Adults:
--Winter dysentery
--BVD (usually not a large group of animals)
--toxins

Front 159

Salmonella DDx in Cattle
Septicemic Form

Back 159

-E. coli

Front 160

Salmonella DDx in Horse
Septicemic Form

Back 160

-E. coli
-Actinobacillus equuili

Front 161

Salmonella DDx in Horse
Acute Enteric Form

Back 161

1. Foals:
--C. perfringens
--C. difficile
--Rotavirus
2. Adults:
--Potomac Horse Fever
--Clostridial diarrhea (C. perfringens or C. difficile)
--NSAID toxicity
--Peritonitis
--Toxins

Front 162

Salmonella Treatment General Goals

Back 162

1. Replace fluid and electrolyte losses
--give volume! animal needs fluids!
--8-10% dehydration is close to death
2. Correct acid/base abnormalities
--kidney can usually manage electrolyte and acid/base disturbances
3. Limit inflammatory cascade
4. Control bacteria

Front 163

Salmonella Treatment for Cattle
Fluid Therapy

Back 163

-IV fluids if not nursing or drinking
--Usually animal is acidotic, use normosol-R, LRS, or isotonic bicarbonates
-Need replacement fluids, maintenance fluids (1-3 ml/kg/hr), and ongoing losses (1-4L per day)
-Need to do blood gas to determine mMol bicarbonate
-Can give oral fluids to calf that is up and nursing or adult with mild to moderate dehydration
--do not give electrolytes and milk at the same time

Front 164

Salmonella Treatment for Cattle
Hypoproteinemia

Back 164

-Plasma
-Hetastarch
-Whole blood, proteins and IgG

Front 165

Salmonella Treatment for Cattle
Inflammatory Cascade

Back 165

-Flunixin meglumine
-0.3 mg/kg IV
-Not proven to help cattle
-Need to be careful with anorexic and dehydrated animals
-Limited by what can legally be given t the animal

Front 166

Salmonella Treatment for Cattle
Anti-diarrheal agents

Back 166

-Bismuth subsalicylate
-questionable efficacy
--has to go through rumen, not sure if retains efficacy through rumen

Front 167

Salmonella Treatment for Cattle
Nutritional Support

Back 167

1. Calves:
--with suckling reflex, decrease volume but keep feeding milk
--no suckling, supplement IV fluids with dextrose or use TPN
2. Adults:
--supplement IV fluids with dextrose, force-feed, consider PPN/TPN

Front 168

Salmonella Treatment for Cattle
Antibiotic Therapy

Back 168

-IN neonates only! bacteremia/septicemia is common
-No antimicrobial is labeled for treatment of salmonellosis in cattle
--extra-label use
--follow label dose as much as possible
-Susceptibility pattern is very important
-Ceftiofur: FOLLOW LABEL DOSE
-Ampicillin, amoxicillin, TMS, tetracycline
-Aminoglycosides

Front 169

Salmonella Treatment for Horse
IV fluids

Back 169

-Adult horses need large volumes
--50-150L per day
-Tailor fluids to correct acid/base and electrolyte imbalances
-Address hypoproteinemia also, can give plasma or hetastarch

Front 170

Salmonella Treatment for Horse
Limit Inflammatory Cascade

Back 170

-Flunixin meglumine (0.3 mg/kg)
-Polymixin B: binds endotoxins
--need to monitor kidney function
-Pentoxifyllin: inhibits TNF production
--increases secretion of prostacyclin and IL-10
-Plasma

Front 171

Salmonella Treatment for Horse
Antibiotics

Back 171

-Only in foals with possibility of bacteremia
-Must do sensitivities on all isolates
-Resistance genes are carried on plasmids that are readily transferred
--Will be resistant to commonly used drugs
-Inappropriate antibiotics will kill normal flora and may allow salmonella to grow

Front 172

Salmonella Treatment for Horse
Diarrhea and Nutritional Support

Back 172

-Bismuth subsalicylate
--no effect in 48-72 hours, stop!
--will darken feces
-Biosponge, targets and binds toxins in GI tract
-Same nutritional support as for cattle

Front 173

Salmonella Control Measures during epidemic/outbreak

Back 173

-Isolate cases early
-Clean contaminated areas well
-Record epidemiological information
-Detect carriers
-Do not use prophylactic antibiotics

Front 174

Bluetongue

Back 174

-Viral disease of domestic and wild ruminants
-Major disease worldwide
-Acute
-Non-contagious
-Sheep are most severely affected
--usually inapparent in cattle and goats
-Arthropod borne disease, needs vector for transmission
-Numerous different serotypes in US and world

Front 175

Global Importance of Bluetongue

Back 175

-Disease of high importance!
-List A disease
-In specific geographic regions of the world based on presence of vector
--Africa, Asia, North America, Europe, South America, Caribbean, Australia
-Rare or absent in northern latitudes
--spreading northwards with time
-As vector spreads, disease spreads

Front 176

Bluetongue Virus
BTV

Back 176

-Orbivirus, double-stranded RNA virus
--Reoviridae
-May infect domestic or wild ruminants
-Cattle and wild ruminants act as silent reservoirs
--virus can persist for months to years without causing clinical presentation
-Makes control difficult

Front 177

Bluetongue Virus in USA

Back 177

-Present across most of the US except in northeast
--not common in hotter areas
--present in diagonal line from northwest to southeast
-Most common in late summer and early fall
--vector activity is greatest
-Disease occurs when a new strain or naive animal is introduced to a region

Front 178

Bluetongue Virus in Bighorn basin WY

Back 178

-Recent outbreak of serotype 17
-Geographic/topographical constraints on area previously prevented vector infiltration
--protective geographic barrier
-Warmer than average summer allowed vector migration and introduction of new serotype

Front 179

Bluetongue Virus Genetic variability

Back 179

-LOTS of genetic variability, lots of different strains/serotypes
--at least 24 worldwide
-Genetic drift of original gene segments and reassortment of gene segments within vector or host
-US serotypes: 10, 11, 13, 17

Front 180

Culicoides sonorensis

Back 180

-Vector of Bluetongue disease
-Biting midge
-Everything of disease depends on the vector

Front 181

Bluetongue Pathogenesis

Back 181

-Inoculation of virus usually occurs during feeding
--biting midge gets into host mouth
-Initial virus replication in local lymph nodes
-Progression to full viremia, spreads systemically then goes back out to mucosal surfaces
-Virus attacks epithelial and mucosal surfaces
--tongue, mouth, esophagus, rumen, skin
-Incubation period in sheep is 7-10 days
-Viremia can be detected in sheep for 11-54 days
--animal may look cured, no clinical signs, but will still be viremic

Front 182

Bluetongue Clinical Signs
Sheep

Back 182

-Only in sheep! Cattle are sub-clinical
-Severe clinical signs in sheep of all ages
-Fever
-Leukopenia
-Oral mucosal ulceration
-Swelling of lips, gums, tongue
-Salivation and profuse nasal discharge due to pain on swallowing
-Lameness/stiffness due to coronitis and myositis
--hot, swollen coronary bands
-Teratogenic, causes abortions, stillbirths, weak lambs
-Less than 10% mortality, more than 50% morbidity
--LOTS of animals will be sick, but few actually die

Front 183

Bluetongue Clinical Signs
Cattle

Back 183

-Usually subclinical, no disease signs
-NEVER clinical in goats
-When clinical disease occurs, signs can be severe
--fever
--leukopenia
--oral mucosal ulceration
--swelling of lips, gums, tongue
-Lameness/stiffness due to coronitis and myositis
-Teratogenic, causes abortions, stillbirths, and weak calves
-"Burnt muzzle" appearance due to hyperemia and crusting
-Salivation and profuse nasal discharge
-In severe cases can cause skin sloughing, swolline udder, teat ulcerations
-Mortality is less than 1%, morbidity less than 10%
--LOW morbidity and low mortality

Front 184

Bluetongue Clinical Signs
Goats

Back 184

-Subclinical
-Cases are usually very mild
-Mild depression
-Fever
-Temporary anorexia
-Hyperemia of oral and nasal mucosa

Front 185

Bluetongue Diagnosis

Back 185

-Dx most often by clinical signs alone
-Can isolate virus from blood, most definitive
--isolate from blood, semen, spleen, aborted fetal tissue
-Virus presence is helpful for detecting long-term presence of infectious virus
-Virus is detected in experimentally infected sheep for 11-54 days
--clinical for a few weeks, then viremic for 2 months

Front 186

Bluetongue PCR

Back 186

-PCR is available for diagnosis
-Highly sensitive and specific test
-Only determines the presence of the genetic material belonging to the virus
--does not indicate active infection, can detect viral particles without the disease being present
-Viral particles have been identified in sheep for 100 days after infection

Front 187

Bluetongue Serology

Back 187

-AGID, ELISA, COmplement fixation
-Indicates exposure, immune system reaction to the pathogen
--Does not indicate active infection
-Antibodies to BTV can persist for 2 years
-Antibody cross-reactivity to other orbiviruses can occur

Front 188

Bluetongue Differential Diagnoses

Back 188

-Vesicular diseases
--FMD, Vesicular stomatitis, Rinderpest, Malignant catarrhal fever, Bovine papular stomatitis
-Photosensitization

Front 189

Bluetongue Treatment

Back 189

-No known cure
-Have to let virus run its course
--low mortality is helpful
-Treatment is mostly supportive care
--analgesics/NSAIDs
--Antibiotics to prevent secondary bacterial infections
--Nutritional and fluid support if needed

Front 190

Bluetongue Prevention

Back 190

1. Control culicoides vector! Difficult to do
-Reducing vector breeding grounds can be helpful
--no standing water or mud
-Bring animals in at dusk, high activity time for flies
2. Vaccinate
-difficult due to complex immune response
-vaccine may not contain serotype local to region
-Vaccine can be teratogenic or abortogenic
3. Natural immunity
-Provides the strongest protection
-Serotype-specific and lasts 2 years

Front 191

Tetanus

Back 191

-Sustained muscle contraction without relaxation
-Usually refers to disease caused by Clostridium tetani infection
-World-wide distribution
-Can occur in any domestic animal or person
-Susceptibility varies by species
--Horses are much more susceptible than dogs and cats

Front 192

C. tetani

Back 192

-Spore-forming gram+ anaerobic rod
-Produces 3 endotoxins
--tetanospasmin
--tetanolysin
--nonspasmogenic toxin
-Spores are resistant to degradation and all over in the environment
--in soil, intestines, feces, everywhere in the world
-Anaerobic environment is needed for infection
--punture wounds are perfect

Front 193

Tetanus Pathophysiology

Back 193

-Spores + damaged tissue + anaerobic environment = germination
-in 4-8 hours vegetative form of bacteria forms neurotoxin
-Neurotoxin disseminates via blood and lymphatics
-Toxin binds at the end-plates of peripheral motor neurons and is internalized
-Retrograde transport of the toxin to spinal cord gray matter
-Toxin exists neuronal cell bodies, binds to inhibitory interneurons (Renshaw Cells)
--cleaves cell membrane proteins needed for release of inhibitory NT (GABA in brainstem, or Glycine in spinal cord)
-Loss of inhibition from interneuron leads to sustained contractions and extensor rigidity
--seizures autonomic dysfunction
-Toxin can be bound for 3 weeks

Front 194

Tetanus Clinical Signs

Back 194

-Spastic paralysis
-Range from severe to mild
-May be diffuse or focal
--depends on toxin load
--Focal signs are rare, only in small animals
-Usually occur within 5-10 days of wound becoming infected
--can range from 2 days to 2 months

Front 195

Tetanus Mild Signs

Back 195

-Stiff gait and posture, "sawhorse stance"
-Extensor muscles are more affected
-Elevated tail
-Altered facial expression "Risus sardonicus"
--contraction of all facial muscles
-Jaws are clamped shut and impossible to open
--"lockjaw"
-Hyperesthesia, sensitive to touch

Front 196

Tetanus Clinical signs in the Horse

Back 196

-Erect, caudally directed ears
-Elevated upper eyelid
-Spasmodically protruding 3rd eyelid
-Flared nostrils
-Retracted lips

Front 197

Tetanus Severe Signs

Back 197

-Intractable abdominal pain
-Inability to talk or total recumbency
-Recumbency is bad news
-Extensor ridgidity of all limbs, opisthotonus, severe trismus
-Seizures
-Death from respiratory failure
--involvement of diaphragm and intercostal muscles

Front 198

Tetanus Diagnosis

Back 198

-Clinical Diagnosis, do not need bacterial or toxin confirmation
-In early/mild cases can elicit muscle spasms via stimulation
--auditory, ocular, tactile stimulation
-May need to do a wound culture for treatment of other contaminating bacteria
-No characteristic clinicopathologic or post-mortem lesions

Front 199

Tetanus Differential Diagnoses

Back 199

-Electrolyte abnormalities
--hypocalcemia, hyperkalemia, hypomagnesemia
-Acute laminitis
-Myopathies
-Meningitis
-Colic
-Equine Motor Neuron Disease, shivers, severe neck pain

Front 200

Tetanus Treatment

Back 200

1. Supportive care
-quiet environment where the horse can rest
2. Muscular relaxation
3. Treat infection
4. Neutralization of unbound toxin
5. Establish active immunity

Front 201

Supportive care for Tetanus patients

Back 201

-Provide quiet environment where horse can rest
-Dark lights, deep bedding, good footing
-Cotton in ears
-Sedation
-Nutritional and hydration support
-Many animals die from fractures during recovery

Front 202

Muscle relaxation for Tetanus patients

Back 202

-Drugs:
--acepromazine
--barbituates
--chloral hydrate
--methocarbamol
--diazepam
-Usually start with acepromazine, then add diazepam or xylazine

Front 203

Treatment of the Infection in a tetanus patient

Back 203

-Debride and lavage any wounds
--allows O2 into the wound
-Consider local inflitration or lavage with procaine penicillin
-Systemic penicillin
--K-Pen IV
--Procaine penicillin G IM

Front 204

Neutralization of unbound toxin in Tetanus patients

Back 204

-Use equine-origin tetanus anti-toxin
--Binds toxin in blood stream
-Cannot reverse clinical signs, but prevents future binding of toxin

Front 205

Establishing Immunity in Tetanus Patient

Back 205

-Natural infection does not confer adequate immunity
-Need to vaccinate with tetanus toxoid immediately
--can give antitoxin and vaccine at the same time, do not cross-react
-Prevent with vaccine
-Small animals have HUGE innate immunity to tetanus toxin

Front 206

Tetanus Prognosis

Back 206

-Survival rates are relatively low (25-41% survival)
-Affected animals may survive if provided excellent supportive care
-Poor prognosis:
--dysphagia
--dyspnea of respiratory muscles
--recumbency

Front 207

Tetanus Prevention

Back 207

-Adequate vaccination with toxoid and appropriate wound care
--Core vaccine for large animals!
-Use tetanus anti-toxin to provide passive immunity when horse is at risk and has not been adequately vaccinated
--unvaccinated horse with wound
--foal born to unvaccinated mare that needs surgery

Front 208

C. Botulinum

Back 208

-Gram+ anaerobic spore-forming rod
-Neurotoxin is the most potent and lethal toxin known
--has never been successfully used as bioterrorism agent but potential exists!
-Natural infection occurs in people and animals
-8 serotypes
--antigenically different toxins have the same effect
--Types A, B, and C cause botulism in horses in USA
--Type B is most common

Front 209

Botulism Epidemiology

Back 209

-Types A and B: moldy forage
--round bale hay, silage
--common in soil, gets into forage
-Type C: carrion
--dead animal is rolled into haybale, contaminates

Front 210

Botulism Ways for Infection

Back 210

1. Ingestion of pre-formed toxin (most common)
2. Ingestion of spores
--spores germinate and elaborate toxin in GI tract
--Toxicoinfectious botulism or "shaker foal" syndrome
--Immature GI tract is more susceptible
3. Wound botulism, toxin gets into anaerobic environment
--Castration sites
--umbilical hernia repairs
--deep puncture wounds

Front 211

Botulism Pathophysiology

Back 211

-Neurotoxin acts on pre-synaptic motor neuron
--cleaves fusion proteins
--prevents release of ACh from pre-synaptic terminal
-Stays in pre-synaptic terminal motor endplate
-Muscles do not contract at all

Front 212

Botulism Clinical Signs

Back 212

-Progressive symmetrical myasthenia/muscle weakness
-Shuffling gait
-Muscle tremors
-Frequent and/or prolonged recumbency
-Flaccid paralysis, can no longer stand
-Dysphagia, weak tongue tone and inability to swallow
-Mydriasis, weak eyelid tone
-Ileus, colic
-Death due to respiratory failure

Front 213

Botulism Diagnosis

Back 213

-Usually clinical diagnosis
-Tongue Stress Test:
--subjective assessment of horse's tongue strength and ability to retract tongue
-Grain test: objective assessment of ability to eat
--normal horse should finish 8 oz of sweet feed on floor in less than 2 min
--Will see LOTS of chewing without any swallowing

Front 214

Botulism lab diagnosis

Back 214

-Identify the botulinum neurotoxin
--can do mouse bio-assay, look for signs of botulism in an injected mouse
--Definitive diagnosis, but usually unsuccessful
-Identify C. botulinum on PCR
--supportive diagnosis
-No specific clinicopathologic or post-mortem changes

Front 215

Botulism Differential Diagnoses

Back 215

-Equine Motor neuron Disease
-Equine protozoal myeloencephalitis
-Neuroborreliosis
-Electrolyte derangements
-Myopathies
-Esophageal obstruction
-GI disease
-Laminitis
-Easily mistaken for colic, has similar signs

Front 216

Botulism treatment with Antitoxin

Back 216

-Immediate objective is to neutralize the circulating neurotoxin with specific antitoxin ASAP
--Each hour delay results in reduced survival!
--only 1 dose is needed, provides passive protection for 60 days +
-Does not neutralize bound toxin, just prevents from getting worse
-Commercial sources exist

Front 217

Botulism treatment

Back 217

1. Antitoxin
2. Stall rest, minimal manipulation of horse
--decrease physical activity
3. Antimicrobial drugs for secondary complications
4. Avoid drugs that potentiate neuromuscular weakness
5. Excellent nursing care is needed

Front 218

Supportive care for Botulism

Back 218

-Excellent nursing care is mandatory
-Nutritional and hydrational support
--Enteral feeding via nasogastric tube
--Can give PPN or TPN, but expensive
-Deep, dry bedding with good footing

Front 219

Botulism prognosis

Back 219

-Usually fatal unless treated ASAP with antitoxin
-Recumbency and hypoventilation are poor prognostic indicators
-Foals have better survival than adults
-Dysphagia resolves 7-14 days after anti-toxin treatment
--takes a long time to resolve, have to feed horse for duration
-Return to full strength takes more than a month
--CAN have full recovery, takes time and is expensive

Front 220

Botulism Prevention

Back 220

-Toxoid is safe, highly efficacious if administered properly
--vaccinate for Type B toxin
-Only vaccination available is type B toxin
--not protective against A and C
--need initial series of 3, 1 month apart and annual revaccination

Front 221

Summary of Tetanus and Botulism

Back 221

-Same genus, 2 very different diseases
--tetanus= muscle spasticity
--botulism= muscle flaccidity
-Due to action of toxin on neuromuscular transmission
--tetanus: loss of inhibition of LMN, causes overreactivity
--botulism: failure of LMN to release ACh causes inactivity
-Treatment is similar, preventative principles apply
-Antitoxin and supportive care
-Toxoid immunization

Front 222

Equine Infectious Anemia
EIA

Back 222

-"Swamp fever"
-Virus, retrovirus
--genetically related to AIDS virus
-Carried by mosquitoes and horseflies
-Most infections occur in "bug season," late summer and early fall
-Affects horses, donkeys, mules of all ages, breeds, and gender
-Mostly in south and SE USA
-Endemic in Americas, parts of Europe, Middle east, far east, Russia, South Africa

Front 223

Equine Infectious Anemia (EIA) Rates

Back 223

-Low morbidity, less than 2.5% in USA
-In Latin America, morbidity is 90%
--much more common
-Mortality is 50% in USA
-Less than 300 new cases since 2003
-Trend is towards fewer and fewer cases each year

Front 224

Equine Infectious Anemia (EIA) Transmission

Back 224

-Transmitted via blood
--intrauterine
--blood transfer
--blood transfusions
-Unsanitary veterinary practices
-Blood sucking vectors

Front 225

EIA Vector

Back 225

-Horsefly is #1 vector
--has large mouth, ingests a large volume of blood
--painful sucker, has interrupted feedings
-Mosquito: does little damage and does not take much blood

Front 226

EIA Pathogenesis

Back 226

-Virus is spread to horse via blood
--risk of transmission is greatest when infected horse is ill
--blood levels of virus are highest
-Horse is viremic once infected, remains viremic for life
-Viremia stimulates B and T cell response
-EIA virus multiplies in macrophages throughout the body
--localizes in lymph nodes, spleen, liver, and kidney
-Seroconversion occurs in 16-90 days
--easy to get false negative

Front 227

EIA affected organs

Back 227

-Localizes in lymoh nodes, spleen, liver, kidney
-Damages vascular intima of small vessels
--results in edema
-Causes inflammatory changes in organs, esp. liver
-Causes immune-mediated hemolytic anemia and thrombocytopenia

Front 228

Acute EIA

Back 228

-Sudden onset of disease at full-force
-Causes high fever, anemia due to breakdown of RBCs, weakness, swelling of lower abdomen and legs, weak pulse, irregular heartbeat
-Sudden death
-1ml of blood contains enough virus to infect 1 million horses
--VERY infectious!

Front 229

Subacute EIA

Back 229

-Slower, less severe disease progression
-Recurrent fever, weight loss, enlarged spleen, anemia, swelling of lower chest, abdominal wall, penile sheath, legs
-1ml of blood contains enough virus to infect 10,000 horses

Front 230

Chronic/Inapparent EIA

Back 230

-Horse tires easily, unsuitable for work
-Recurrent fever and anemia
-Can relapse to subacute or acute form of disease
--can relapse several years after original attack
-Not super viremic, but possible (1/6 million)
-May or may not result in death

Front 231

EIA clinical signs

Back 231

-Depression
-Weakness
-Weight loss
-Fever spikes, up to 105 F
-Tachycardia
-Icterus due to hemolytic anemia
-Edema of ventral abdomen, prepuce, legs, conjunctiva
--edema due to vasculitis
-Petechial hemorrhages of mucous membranes
--tongue and conjunctiva especially
--due to thrombocytopenia

Front 232

EIA clinical course

Back 232

-get better or die!
-Relapses usually occur during periods of stress
-In wild horses, 30% of horses are chronically infected with EIA but appear normal

Front 233

EIA diagnosis

Back 233

-Clinical Signs
-Antibody testing
--Coggins test

Front 234

Coggins Test

Back 234

-Used for diagnosis of EIA
--Most widely accepted procedure for EIA diagnosis
-Detects antibody against viral p26 antigen
--AGID test
-False-positive results are rare
--may occur with foals with colostral Ab, 6-9 months old
-False negative results are related to faulty interpretation by technician, low levels of antibody in test serum
--may occur during first 30-45 days of infection

Front 235

EIA Competitive ELISA

Back 235

-More sensitive test
--has occasional fasle + result, may be too sensitive
-Detects antibody against p26 antigen of EIA virus
-Test results can come back within minutes, much faster
-Positive tests must be confirmed using AGID test

Front 236

EIA prevalence

Back 236

-LOW prevalence
-Still exists, but low levels

Front 237

Who to test for EIA

Back 237

1. Equids in exhibitions or competitive events
2. Equids moved between states
3. Equids changing ownership
4. Equids entering horse auctions or sales markets

Front 238

EIA differential Diagnoses

Back 238

1. Other causes of anemia
--immune-mediated
--red maple leaf toxicity
--anemia of chronic disease
--babesia
2. Other causes of vasculitis
--purpura hemorrhagica
--equine viral arteritis

Front 239

EIA treatment

Back 239

-None! no cure!
-No way to eliminate the virus
-Provide rest and supportive care
-Suggest euthanasia

Front 240

EIA prevention

Back 240

-No effective treatment, no vaccine, no cure
-Good management can reduce potential of infection
-Good hygiene
-Insect control
-Test and identify carriers
--euthanize carriers?
--lifelong quarrantine is only other option, less acceptable

Front 241

EIA positive horses

Back 241

-ALWAYS pose unnecessary health risk to other horses
-Even if no signs of illness, are still viremic for life
-Insects cannot be totally controlled or managed, infection will likely be spread
-Best way to eradicate disease is to euthanize carriers
-Permanently identify carriers via branding
--if kept alive, need to be quarantined forever at least 200 yards away from other animals

Front 242

EIA eradication

Back 242

-Difficult due to illegal horses running wild
-have to identify carriers via testing

Front 243

Equine Viral Arteritis
EVA

Back 243

-Contagious Respiratory disease
-Affects equids
-Cause characteristic inflammatory lesions
-Lesions are induced by virus in the smaller blood vessels
--Especially affects arterioles of the acutely infected animal
-Can cause abortion storms

Front 244

Equine Viral Arteritis (EVA) Etiology

Back 244

-Small enveloped RNA virus (Equine arteritis virus)
-Restricted to equids, does not affect humans
-All strains of virus are potentially abortigenic, always assume it can cause abortions

Front 245

Equine Viral Arteritis (EVA) distribution

Back 245

-Present in many horse populations throughout the world
--NOT present in Japan or Iceland
-Infection can vary widely between horses and between regions
-More often found on standardbreds and some warmbloods

Front 246

Clinical Response t Equine Viral Arteritis (EVA)

Back 246

-Most cases are subclinical
-Morbidity rate can differ between different outbreaks
--highest morbidity is reported in large groups of horses that are housed closely together
-Fever
-Anorexia and depression
-Leukopenia
-Limb edema, most pronounced in lower hind limbs but can involve all 4
-Serous to mucoid nasal discharge
-Supraorbital or periorbital edema
-Conjunctivitis
-Epiphora. unilateral or bilateral
-Photophobia, most often in cases with severe conjunctivitis
-Edema of the scrotum/prepuce or mammary glands
-Abortion
-Interstitial pneumonia or pneumoenteritis

Front 247

Equine Viral Arteritis Prognosis

Back 247

-Most horses make complete clinical recoveries, even without any treatment
-Mortality is infrequent, only really occurs in neonatal foals
--foals are usually congenitally infected with the virus
--get fulminating interstitial pneumonia withn 48-96 hours of birth

Front 248

Equine Viral Arteritis Abortions

Back 248

-Abortion late in acute phase or early in convalescent phase
-Rates vary from 10-60%
-Exposure to pregnant mares late in gestation may not result in abortion
--foal will be congenitally infected with virus, die from fulminating interstitial pneumonia soon after birth

Front 249

Equine Viral Arteritis (EVA) Transmission

Back 249

-Aerosol transmission is most significant
-Venereal dissemination on breeding farms by an acutely infected stallion
-Congenital transmission in-utero from dam to foal

Front 250

Equine Viral Arteritis (EVA) viral reservoir

Back 250

-Natural reservoir in stallions
--may persist for weeks, months, years, or lifetime of stallion
-ONLY the stallion is the carrier

Front 251

Equine Viral Arteritis Immunity

Back 251

-Strong and durable immunity follows natural infection
-Foals born from seropositive dams are passively protected against clinical disease
-Vaccination Immunization is successful for preventing carrier state in stallions

Front 252

Equine Viral Arteritis Lab Diagnosis

Back 252

-Virus isolation
-Specific antibody response from paired titers (3-4 weeks apart)
--acute and convalescent titers)
-Can take nasopharyngeal swabs or conjunctival swab and blood samples for testing

Front 253

Equine Viral Arteritis Titers in Stallions

Back 253

-Carrier state has never been confirmed in a seronegative stallion
-Only stallions with titer of 1:4 or greater, without vaccination history are considered carriers
-Test semen!!

Front 254

Equine Viral Arteritis Prevention

Back 254

-Vaccinate! highly attenuated modified live virus product
--Safe and effective in stallions and non-pregnant mares

Front 255

Equine Viral Arteritis Economic Significance

Back 255

-Economic losses:
--outbreaks of abortion or foal death
--decreased commercial value of carrier stallions
--no export for carrier stallions or infected semen
--Disruption of training schedule and reduced race entries/cancellations

Front 256

Types of Salmonella Infections in Cattle

Back 256

-Clinically normal carrier without fecal shedding
-Carrier with fecal shedding
--common source of infection for others
-Shedder with clinical disease
-"Pass through"
--cow is not infected, but ingests bacteria and passes bacteria through GI tract without any impact
-Chronic salmonella infections

Front 257

Salmonella Prevalence in cattle

Back 257

-Affects both dairy and beef cattle
-More common in dairy cattle
-Percent of positive operations has increased over past 20 years
-Proportion of cows testing positive has also increased

Front 258

Types of Salmonella in Cattle

Back 258

-not all salmonella are created equal
--some cause morbidity but little mortality
--some cause both morbidity and mortality
--some affect adults, some affect calves
-Typhimurium has most affect in calves
-Newport has most affect on adults

Front 259

Salmonella Outbreaks

Back 259

-If an adult is affected, obvious clinical cases are usually less than 10% of the herd
-80-100% of fresh cows may be affected
-Even if small number of clinical cases, almost all of herd could be shedding
-Usually 3 week disease course
--infected can shed for months

Front 260

Today's Livestock Production Systems

Back 260

-Complex systems
-Highly interconnected
-Rapidly changing
--infrastructure changes
--fewer critical control points
-Unstable system from an infectious disease point
--disease can rapidly spread throughout the entire system
-LOTS of chances for interaction between livestock
-Lots of people moving between many farms

Front 261

Salmonella Strain Prevalence

Back 261

-Typhimurium is always present in medium levels
-Newport came on the scene in 2000
-Similar distribution of strains
--concentrated where the cows and calves are

Front 262

How does Salmonella get to the farm

Back 262

1. Replacement animals
--most important source of infection
2. Calves
3. Vehicles and equipment
4. Feed and forages (hard to test)
5. Water
6. Visitors
7. Birds, pests, wildlife, cats, dogs

Front 263

Salmonella Categories of Risk

Back 263

-High, medium, low
-Groups of Animals
-Areas on the farm
-Activities
-People

Front 264

Evaluation for Salmonella

Back 264

1. Biosecurity and heard health
2. Hygiene

Front 265

Herd-based risk factors for Salmonella

Back 265

-Frestalls with recycled water flush system
--NEVER flush with cows in the pens
-"Open" herds, bringing in replacements
-Lack of quarrantine and/or isolation facilities
-Rendered product use
-Certain feeding strategies
-Concurrent diseases
-Inadequate calf-feeding (colostrum and cleaning)
-Barn cats (and dogs)
-Wildlife

Front 266

Individual animal-based risk factors for Salmonella

Back 266

-Age
-Stage of lactation
-Starvation and nutritional deficiencies
-Concurrent diseases
-Poor Ig levels
-Transport, other stresses
-Manure access

Front 267

Keeping Salmonella Out

Back 267

-Key to biosecurity: Pathogens are spread by People, Pathogens, and Fomites
-No such thing as "zero risk"
-Movement of animals, people, and equipment is essential on most operations, hard to isolate
-Quarrantine alone is not usually sufficient
-Control, not prevention is key! review and control traffic flow
-Salmonella is a disease of management

Front 268

Salmonella Vaccines

Back 268

-No good vaccine
-Can give commercial bacterin
-Maximizing health through good preventative programs and management is best approach
--good nutrition and hygiene

Front 269

Potential for Salmonella Infection/Disease

Back 269

-Depends on:
--types and numbers of pathogenic organisms present
--ability of pathogen to survive or multiply outside of host
--potential for contact with susceptible host

Front 270

Salmonella Outside of the host

Back 270

-Can divide and multiply outside of the host!
-Need to prevent accumulation
-Protect vulnerable animals
--calves
--dry cows about to give birth
--sick cows

Front 271

Whole Herd Prevention of Salmonella: Hygiene

Back 271

-Manure contamination is major risk for infection!
-Improved hygiene can be initiated immediately within minimal expense to the farmer
-No "magic bullet"
-Need to frequently clean and disinfect high-risk areas
--sick and fresh pens, water troughs, feed bunks, areas of high traffic
-Clean contaminated water sources

Front 272

Whole Herd Prevention of Salmonella: Animal and People

Back 272

-Introducing animals is a major risk factor for infection
-Pay attention to biosecurity!
-Restrict visitor access to animals
--only what is necessary
-Concurrent infection with BVD is associated with increased risk of salmonella
--immunosuppressive contributing factor

Front 273

Control strategy for animal movement

Back 273

-Animal History
-Pre-purchase testing
-Quarrantine for 14 days if possible
-re-test at parturition
-Challenges: cost, intermittent shedding, sensitivity of culture, space for quarrantine

Front 274

Salmonella Risk from Visitors

Back 274

-Direct animal contact on the farm is highest risk
-Limited animal contact is medium risk
-Visiting other farms with no animal contact is medium risk
-No farm or animal contact is least amount of risk
-Anyone who has been on another farm should sanitize boots at a minimum

Front 275

Feeding techniques to prevent Salmonella

Back 275

-Protect bulk feeds from wildlife or contamination with manure
-Store feed in cool, dry, shaded area
-Do not use same equipment for manure and for feed delivery
-Clean feed bunks regularly to prevent excessive build-up of spoiled feed material or manure
-Monitor dry-matter intake

Front 276

Calf Housing to prevent Salmonella

Back 276

-Should be comfortable
-Lots of space
-Hygiene
-Individual hutches are better
-Location is important
-Clean and disinfect regularly
-In calf-barns prevent nose-to-nose contact and ensure good ventillation

Front 277

Calf feeding to prevent Salmonella

Back 277

-Need to make sure calf gets enough high-quality colostrum 4 hours after birth
-High quality milk replacer, 22% crude protein 20% fat
-Dried milk solids are the best
--avoid soybean or fish-based milk replacers
-Properly clean and sanitize feeding equipment between calves
--remove biofilms
-Do not feed waste milk from sick cows to calves unless it can be pasteurized

Front 278

Colostrum Administration

Back 278

8-10% of calf body weight
-4 quarts over 4 hours
-2 quarts at 12 hours of birth
-The earlier the better!
--100% IgG absorbed at birth
--11% IgG absorbed at 24 hours

Front 279

Heifers and Salmonella Prevention

Back 279

-Move animals in groups to minimize stress
-Avoid co-mingling of groups from different age groups
-Single contract heifer rearing is ideal

Front 280

Fresh Cows and Salmonella Prevention

Back 280

-Maintenance of environment for transition cows should be a priority!
-Always separate sick cows and fresh cows
-Clean maternity pen between occupants
-Maintain dry bedding at all times

Front 281

Sick cows and Salmonella

Back 281

-Keep sick cows away from fresh cows
-Keep water troughs separate
-Give supportive treatment
-Limit antibiotics
-Vet should visit healthy animals 1st, sick animals last

Front 282

Protecting Human health from Salmonella

Back 282

-Promote best management practices
-Raw milk consumption
-Manure contamination
-Clean protective clothing
-People feeding calves have increased risk of infection

Front 283

Veterinary Biosecurity for Salmonella

Back 283

-Wash and disinfect boots!
-Have pair of boots for each of the major herds
-Clean and disinfect ant equipment used
-Use gloves
-Wash hands
-Keep truck clean

Front 284

Requirements for Success with Salmonella

Back 284

1. written plans
2. Good leadership with clear, consistent advice
3. Defined well-marked restricted areas
4. Specfic plans for animal health and purchase
5. Good sanitation and disinfection
6. Control of animal, people, and other traffic
7. buy-in at all levels

Front 285

BVD Vaccines

Back 285

-Modified Live virus vaccine
-Killed vaccine

Front 286

BVD Modified Live Virus Vaccine

Back 286

-Creates a viral infection in the host
-Attenuated so it does not cause disease
-Antibody response AND cell-mediated immunity response
-Longer-lived protection
--more than a year
-only need 1 injection to stimulate protective immunity
-Can get febrile response or elicit sickness
--fever, malaise, illness associated with vaccine
-Animal becomes viremic
--if animal is pregnant, can cross placenta and cause abortion
--ABORTOGENIC
-Give primary vaccination at 6 months of age
--give second vaccination pre-breeding at 14 months

Front 287

BVD Killed Vaccine

Back 287

-Only antibody response
-Shorter duration of protection (6 months)
-Have to give primary and booster injection to stimulate anamnestic response
--requires 2 injections per year
-Less likely to cause fever, malaise, etc.
-Safe during pregnancy

Front 288

Acute Diarrhea in Adult Cows

Back 288

-BVD
-Clostridium
-Salmonella
-Winter dysentery

Front 289

Chronic Diarrhea in Adult Cows

Back 289

-Parasitism (esp. ostertagia)
-Johne's Disease

Front 290

Johne's Disease

Back 290

-Chronic enteric infection of many species
--goats, cows, sheep, camelids
--non-domesitcated ruminant species
-Occurs all over the USA
-Caused by Mycobacterium Avium paratuberculosis (MAP)
-Few herds are MAP free in US
-Hard to control due to long eclipse period and inapparent shedder phase

Front 291

Mycobacterium Avium paratuberculosis

Back 291

-Causes Johne's disease
-Cousin to Tuberculosis in humans
-LONG incubation period, 2-4 years
-Fecal-oral transmission, excreted in feces of infected cattle
-Young calves are particularly susceptible
--infection usually occurs in first few weeks of life
-Intracellular pathogen

Front 292

Mycobacterium bovis

Back 292

-Causes tuberculosis in Cattle

Front 293

Mycobacterium

Back 293

-All are acid-fast
--associated with lipid-rich cell wall
-Cell wall provides resistance to environment
-Bacteria survive in ponds, soil, manure for a year or more in environment
-Very slow-growing
--Can take 4 months in culture
--Long incubation period in animal, 2-4 years before clinical signs

Front 294

Mycobacterium Avium Paratuberculosis Pathogenesis

Back 294

1. Bacteria is pooped out and ingested by susceptible animal
2. Bacteria enters small intestine initially
--penetrates small intestinal wall
3. Phagocytosed by macrophages but not digested
--prevents lysosomes from fusing with the phagosome
4. Macrophages sends out cytokines, causes inflammatory response
--causes granuloma formation in intestine

Front 295

Mycobacterium Avium paratuberculosis in Phagosome

Back 295

-Prevents lysosomes from fusing with the phagosome
-Survives in macrophage

Front 296

Johne's pathogenesis

Back 296

-Chronic, granulomatous infiltration into intestine
-Thickened intestinal wall, leads to malabsorption
-Inflammatory leads to leakage of protein into bowl lumen
--Protein losing enteropathy
-Hypoproteinemia due to albumin loss
--Peripheral edema in ventral parts of the body (submandibular edema)

Front 297

Johne's Clinical Signs

Back 297

-Do not appear for 2-3 years
-Weight loss due to malabsorption
--leads to emaciation
-Osmotic diarrhea due to thickened villi, poor absorption
-Submandibular edema, brisket edema
-No fever
-Usually have a good appetite

Front 298

Johne's Diarrhea

Back 298

-"pipestream" diarrhea
-Comes out like a hose
-Watery green diarrhea
-NO blood
-Cow is still eating well!

Front 299

Affect of Johne's disease on Intestinal Villi

Back 299

-Initial infection:
--few organisms invade through villus epithelial cells
-Late infection:
--granulomatous response
--macrophages, TONS of organisms present
-Takes years to go from early infection to full-blown infection
-Can see on post-mortem exam
-Enlarged lymph nodes in intestines

Front 300

Johne's infection containment

Back 300

-is NOT contained to intestine
-Can spread to udder and come out in milk
-Can spread to uterus and infect growing fetus

Front 301

Johne's disease in Goats

Back 301

-Do not develop watery diarrhea
--will get to "dog poop" consistency
-Will have weight loss and low blood protein

Front 302

Johne's Disease based on Age

Back 302

-Fecal-oral transimission
-Calves are probably infected early in life, young calves are more susceptible
--number of MAP required to infect an animal vs. age increases
--yearlings are not nearly as susceptible
-Immune system grows, animal can prevent infection
-Open gut is most susceptible timeframe

Front 303

Johne's Fecal Shedding in an Infected Animal

Back 303

-Calf is infected in first few days of life
-During 1st year, no MAP in feces
--clinically normal calf
-During 2nd year, no MAP in feces, no clinical signs
-Around 3 years, start to see MAP in feces
--still no clinical signs (normal milk production, normal body weight, normal fecal consistency)
--Asymptomatic shedder
-Eventually starts to shed BILLIONS of MAP in feces
--starts to develop clinical signs
--Will also have MAP go into milk and to fetus

Front 304

Eclipse phase

Back 304

-No signs of disease and no fecal shedding
-Only way to identify is to do surgery and biopsy intestine
-Cannot tell on ultrasound

Front 305

MAP as intracellular pathogen

Back 305

-Does not illicit a good immune response!
-Hard to detect
-Antibodies in serum increase after fecal shedding starts

Front 306

Johne's/MAP Organism Detection

Back 306

-Look for organism of animal's response to organism
-Look for organism in feces
-Can culture, can take 8 weeks to 6 months to grow
--hard to grow MAP on culture
-Can PCR
-Serology: ELISA test to detect antibodies
--cheapest solution
--can do on milk

Front 307

MAP organism detection in a clinical animal

Back 307

-Should have MAP in feces
-Will have serum antibodies
-Can do ELISA or any other diagnostic test

Front 308

MAP organism detection in Johne's in herd

Back 308

-Want to find infected cows and get rid of them before they do damage on the farm
-ELISA has low sensitivity to detect early infections
-PCR is faster, detects viral particles early
--not cost effective on a herd basis
--medically best choice, but not financially best option

Front 309

MAP organism detection on Eclipse phase cows

Back 309

-Can't find them!
-Could do surgical biopsy on lymph nodes, but not really cost-effective

Front 310

MAP organism detection when buying in Springing Heifers

Back 310

-Want to screen to not introduce Johne's into herd
-Will not be able to test individual animals
--no serum antibodies or MAP in feces
--no good screening
-Have to know where the animal came from
--test older cows in herd where they came from

Front 311

Johne's Prevention

Back 311

-Do not buy in cows! Maintain a closed herd
-If buying in cows, screen herd of origin

Front 312

Johne's Control

Back 312

-Eradicate or just control?
--Depends on what you are doing with your cows
-Reduce exposure, prevent transmission
--keep calving pens clean
--clean udder before suckling or prevent suckling
-Test and cull infected animals
-Vaccinate to increase resistance

Front 313

Johne's Vaccination

Back 313

-Not too widely used
-Causes cross-reaction with TB testing
--will cause false positives for TB
-Dangerous at injection site, can cause granulomas
--dangerous for the farmer and accidental injection!
-Not approved by certain states
-Not 100% effective, will decrease disease but will not prevent infection
-Inject into brisket, so if granuloma forms is not in crucial area

Front 314

Johne's in the eyes for Farmers

Back 314

-Not always obvious
-Does not always progress to a clinical stage on production farms
--cows do not stick around long enough to show clinical signs
-Focus efforts on young calves!

Front 315

Johne's and Manure spreading

Back 315

-MAP is focused in manure, manure is then spread on pasture, pasture is then chopped and fed to animals
-ONLY spread manure onto crops that will not be grazed or harvested for immediate use!

Front 316

Chrone's Disease and Johne's Disease

Back 316

-MAP is source of interest
-Incidence at Chrone's disease in people has increased in people at same rate of Johne's disease in cows
-Multifactorial disease with genetic component
-Is MAP a trigger for Chrone's disease?
--Compromised bowel allows for MAP to colonize in intestine?

Front 317

Johne's Treatment

Back 317

-Antimycobacterial drug exists
-Can extend the life of a cow, but will not cure infection
--reduces clinical signs
-Used for valuable cows that have valuable genetics

Front 318

Johne's Differential Diagnoses

Back 318

1. Renal Amyloidosis: protein losing nephropathy
2. Copper deficiency: not a herd problem
--results in diarrhea
--will have bleached hair coat
3. Fat necrosis: calcified and hardened mesenteric fat around bowel
--only liquid part of feces can get through
4. Vena Cava thrombosis: liver abscesses cause vena cava occlusion
--will result in distention in caudal part of the cow
5. Heart failure: traumatic pericarditis, venous distention in caudal part of the cow

None are as common as Johne's Disease

Front 319

Viral Encephalitides

Back 319

-Eastern Equine Encephalomyelitis
-Western Equine Encephalomyelitis
-Venezuelan Equine Encephalomyelitis
-"Sleeping sickness"
-Infectious disease affecting horses
-Characterized by signs of deranged consciousness, motor irritation, and paralysis

Front 320

Encephalitis Etiology

Back 320

-RNA alpha virus
-Togaviridae family
-EEE, WEE, and VEE are all immunologically different
-Vary in terms of virulence
-Clinical disease is similar with all 3

Front 321

Encephalitis Epidemiology

Back 321

-Only occurs in the Americas
-Most common in USA in southern costal states
-VEE is mostly in Central and South America
--NOT common in USA
--One outbreak in 1971
-Outbreaks of VEE can affect humans

Front 322

VEE Epidemiology

Back 322

-Outbreaks in US have been rare
-Major outbreak from 1969-1972 spread to Texas
--1,500 horses dies

Front 323

EEE Epidemiology

Back 323

-Mostly on the eastern USA
-5 cases in humans per year
-Most equine cases occur in southern states (FL, LA)

Front 324

WEE Epidemiology

Back 324

-Mostly in western USA
-usually about 19 cases per year
--less than 1 case per year in last 10 years

Front 325

Humans and EEE

Back 325

-5-10 cases reported in humans per year
--more than 200 cases from 1964 to present
-Many are fatal
-In general human cases are rare, transmission cycle takes place in swamps and few humans live in swamps
-Most cases in FL, GA, MA, NJ
--more common in coastal areas and freshwater swamps
-Humans can get the disease, but do not get it from horses
-Highest risk from late July to September

Front 326

EEE Transmission

Back 326

-Any bird acts are reservoir
-Vectors: inescts (mosquitoes)

Front 327

Viral Encephalitides

Back 327

-Occurrence is usually due to high activity of virus in mosquitoes
-Usually widespread mortalities in horses before disease occurs in humans
--Horses live outside, in swamp areas have increased exposure to mosquitoes
--also have more surface area, more area to bite

Front 328

EEE vs WEE vs VEE

Back 328

-EEE and WEE are not infectious in horses
--Horse is dead-end host
--will not spread to another horse or to a human
-VEE: horse is viremic and could potentially be infectious
--spreads virus via vectors to other horses and humans

Front 329

VEE Pathogenesis

Back 329

1. Infected mosquito bites horse
2. Virus proliferates in regional lymph nodes
3. Virema

Front 330

VEE Inapparent Infection

Back 330

-Mild fever and leukopenia
-Don't even know the horse has an issue

Front 331

VEE Generalized Illness

Back 331

-Anorexia, depression, fever, leukopenia

Front 332

Encephalomyelitis from Viremia

Back 332

-Once occurs, horse is dead within days
-Signs occur within 5 days post-infection

Front 333

Clinical signs of Encephalitic form

Back 333

-High fever
-Anorexia
-Changes in behavior
-Blindness
-Pruritus
-Cranial nerve deficits (sagging lip, nystagmus, dysphagia)
-Ataxia, paresis
-Seizures
-Respiratory arrest (potentially terminal)

Front 334

Post-mortem findings of Encephalitis

Back 334

-No gross lesions present
-Histologically will see diffuse meningoencephalitis
--perivascular infiltrate will be present

Front 335

Encephalitis Diagnosis

Back 335

-Clinical Signs (acute onset)
-Presence of vector (locale and season)
-Post-mortem findings
-Lack of vaccination
-CSF will have increased protein and increased WBCs
-Virus Isolation can be done on fresh, refrigerated, or frozen brain

Front 336

Encephalitis Differential Diagnoses

Back 336

-Hepatoencephalopathy (will have icterus and increased liver enzymes)
-Leukoencephalitis (corn is the source, herd issue)
-West Nile Disease
-Brain Abscess (asymmetrical signs will be present)
-Botulism (no cerebral signs, just weakness)
-Rabies (always a tough rule-out)
-Equine Protozoal Myelitis (rare cerebral signs)
-Herpes Myelitis
-Head Trauma

Front 337

Encephalitis Treatment

Back 337

-If recumbent, prognosis is POOR

Front 338

Encephalitis Prevention

Back 338

-No eradication program exists due to reservoir persistence
-Control mosquitoes
-Vaccinate with bivalent/trivalent killed vaccine
-In outbreak situation can vaccinate to give boost

Front 339

Polioencephalomalacia

Back 339

-"Polio" or PEN
-group of diseases that are lumped together
-Important disease of small ruminants
-Causes neurologic disease
-PEM: histologic lesion of the brain
--softening/necrosis of the regions of the gray matter of the brain
-Not an actual diagnosis

Front 340

Polio Etiologies

Back 340

1. Primary thiamin deficiency
-Ruminants produce own thiamin in rumen
2. Altered thiamin metabolism
-production of thiaminases by rumen microflora
-Ingestion of thiaminases (fern)
-Excessive sulfur consumption
3. Salt toxicity
4. Lead poisoning (necrosis of gray matter of the brain)

Front 341

Polio Pathogenesis

Back 341

-Thiamin: important co-factor for function of ATP pump
-ATP pump controls osmolality of the cell
-Insufficient thiamin results in ATP pump dysfunction
-ATP pump dysfunction leads to accumulation of ions within the cell
--water follows ions, accumualtes in cell, causes cell swelling
-Occurs all over the body
-In the brain, swelling results in clinical signs
--pressure necrosis of the gray matter in the brain

Front 342

Thiamin Production

Back 342

-Ruminants depend on rumen for production of thiamin
--have to produce daily, long-term storage is impossible
-If animal goes off-feed, thiamin is not produced
--disruption/change in normal rumen microflora
--Abnormal microflora cannot produce thiamin as they should

Front 343

Thiaminases

Back 343

-bacteria contain thiaminases
--destroy thiamin
--Bacteria present in rumen during lactic acidosis can produce thiaminases
-Plant thiaminases
--bracken fern
--horse tail
--animals will not eat on own

Front 344

Sulfur and Polioencephalomalacia

Back 344

-Sulfur and sulfates can be in high concentrations in drinking water, forages, molasses
-In rumen, sulfur is metabolized to sulfide
--Sulfide is TOXIC
-Sulfide decreases rumen thiamin production

Front 345

Polio Epidemiology

Back 345

-All ruminants can be affected
-Mostly prevalent in groups of animals
--feedlot cattle (due to feeding?)
-Market lambs and kids
-Any ruminant that has grain overload or goes off-feed
--any situation where rumen microflora is disrupted

Front 346

Feedlot Cattle and Polio

Back 346

-Due to diet changes?
-Rumen-acidifying high-energy diets on feed-lot
-Try to gradually change diet when moved to feed-lot
-No adaptation, bacterial microflora is thrown off

Front 347

Early Clinical Signs of Polio

Back 347

-Isolation from herd/flock
-Anorexia
-Hypermetric gait/ataxia
-Animal may appear blind, walk with head erect
-Excitable, may appear aggressive
-Hyperesthesia, muscle tremors, lip twitching
-Diarrhea (not in all cases)

Front 348

Late clinical signs of Polio

Back 348

-Cortical blindness
--no menace response, PLR and palpebral reflexes are intact
--eyes are not actually blind, but cannot send info to brain sometimes
-Dorsomedial or dorsolateral strabismus
-Nystagmus (abnormal movement of the eye)
-Miosis (constricted pupils)
-Repetitive chewing, grinding teeth
-Head pressing
-Opisthotonus
-Convulsions
-Death

Front 349

Polio Differential Diagnoses

Back 349

-Listeriosis
-TEME in cattle
-Nervous coccidiosis
-Enterotoxemia type D
-Vitamin A deficiency
-Lead poisoning
-Ethylene glycol poisoning
-Salt poisoning
-Rabies

Front 350

Polio Diagnosis

Back 350

-Can make tentative diagnosis based on clinical signs, history, and response to treatment
--give thiamin, should respond
-NO pre-mortem diagnostic test to confirm Polio
-Only confirmation is histology of the brain
--fluoresces under UV light
-CBC, biochemistry, and CSF are non-specific
-Need to figure out why animals are getting polio, find cause!

Front 351

Sulfur Toxicosis confirmation

Back 351

-Test feed and water supplies
-Feed should be less than 4,000 ppm
-Water should be less than 1,000 ppm
-Measure hydrogen sulfides in rumen gas cap
--should be less than 1,000 ppm
--more academic than practical

Front 352

Polio Treatment

Back 352

-Give thiamin! lots of it!
-No matter what the cause, most cases will respond to thiamin
-10 mg/kg dose
--initial dose IV is best
--follow with 10 mg/kg every 4-6 hours for several days
-Assess cerebral edema, try to get water out of brain
--steroids, mannitol, furosemide, diazepam
-Supportive treatment

Front 353

Polio Prognosis

Back 353

-Mortality is near 100% with comatose animals
-Animals that can still walk have better prognosis
-Response to treatment should occur within 12-24 hours
-Vision should return within 48 hours
--animals not showing improvement after 48 hours have poor prognosis
-Residual blindness or other cranial nerve deficits occur

Front 354

Polio Prevention

Back 354

-Based on the cause
-Diet or introduction of new diet
-Water source and feed sources
-Supplement feed or fluids with thiamin
--especially for animals suffering grain overload or chronically anorectic animals

Front 355

Bracken Fern Toxicity

Back 355

-IN horses
-Caused by ingestion of bracken fern
-Fern contains thiaminases, results in thiamin deficiency
-Can also cause bone-marrow depression in ruminants

Front 356

Bracken Fern Toxicity Clinical Signs

Back 356

-Appears suddenly, after animal has eaten a lot of bracken fern
--can eat a lot in one event, or little bits over long time
-Weight loss
-tremors and muscle fasciculations
-Recumbecy
-Colic
-Death within days to weeks if left untreated

-Will probably think of other causes first, if nothing else fits go to bracken fern

Front 357

Bracken Fern Toxicity Treatment

Back 357

-Horse will have low levels of Thiamin
-Will respond to large doses of thiamin
-Treat with Thiamin!

Front 358

Thromboembolic Meningoencephalitis

Back 358

-TEME "sleeper calves syndrome"
-Mostly affects feed-lot cattle
-Fulminant neurologic disease that comes from septicemia
-Caused by Histophilus somni

Front 359

Histophilus somni

Back 359

-gram- non-spore forming coccobacillus
-Agent responsible for Thrmboembolic meningoencephalitis (TEME)
-Can cause penumonia, arthritis, mastitis, urogenital tract infections and abortion, myocarditis, or conjunctivits
-in one outbreak, may see all clinical issues

Front 360

TEME epidemiology

Back 360

-High prevalence in feedlot cattle
-Occurence of clinical disease is low
-Outbreaks of neurological signs occurs most commonly in winter months, or after shipment
-Transmission through asymptomatic carriers of H. somni

Front 361

TEME Pathogenesis

Back 361

-transmission through aerosolization, into respiratory tract
-Once in body, bacteria causes septicemia
--Disseminates to other organs
--CNS, joint, heart are affected
-Causes thrombosis of small arteries and veins in the CNS
--brainstem and spinal cord mostly
-Can also affect the lungs and heart

Front 362

TEME clinical signs

Back 362

-Multiple animals are usually affected
-Respiratory disease may come before neurologic signs
--7-14 days before
-High fever
-Ataxia/weakness, animal appears drunk
-Sings of brainstem dysfunction (nystagmus, strabismus, head tilt)
-Hard lung sounds from previous pneumonia
-Closed to semi-closed eyelids due to severe conjunctivitis
-Retinal hemorrhages

Front 363

TEME Diagnosis

Back 363

-Presumptive diagnosis based on signalment, history, and clinical signs
-Hard to definitively diagnose pre-mortem
-CBC and chem are not specific
-CSF cytology will have increased WBCs, increased TP, xanthochromia (discoloration of CSF), increased RBCs
-Will be able to grow H. somni on selective cultures
-final diagnosis is often based on post-mortem exam
--hemorrhagic infarcts in brain and/or spinal cord

Front 364

Xanthochromia

Back 364

-Discoloration of CSF
-Due to micro-bleeding in spine or brain areas

Front 365

TEME Treatment

Back 365

-Attempt in animals that are still standing
-Macrolides
-Oxytetracycline
-Penicillin
-Treat clinical signs associated with swelling with NSAIDs
-Supportive treatment

Front 366

TEME Prevention

Back 366

-Vaccine is available and is protective
--should be used in feed-lot cattle

Front 367

Listeriosis

Back 367

-still should have menace, unless very advanced
-Cranial nerve deficits are unilateral
--head tilt, circling, droopy ears
-Hard to differentiate to begin with, but eventually becomes clear over a few days

Front 368

Scrapie and BSE

Back 368

-Transmissible Spongiform Encephalopathies
-Scrapie: neurodegenerative disease of sheep and goats
-BSE: neurodegenerative disease of cattle
-Public Health concern v-CJD
--appeared to be a variant of bovine form

Front 369

Transmissible Spongiform Encephalopathies

Back 369

-All have common appearance of the brain parenchyma
-Brain tissue looks like a spongy
--multiple vacuoles
--reactive astrocytes
--gliosis
-"holes in the brain"

Front 370

Known TSEs in different Species

Back 370

-Sheep: Scrapie (oldest recognized)
-Goats: Scrapie
-Cattle: BSE
-Cats: Feline spongiform encephalopathy
-Mink: transmissible mink encephalopathy
-Mule deer: CWD
-Elk: CWD

Front 371

TSE in Humans

Back 371

-CJD
-Kuru
-Gerstmann-straussier syndrome
-Fatal familial insomnia
-Alpers syndrome

Front 372

TSE Infective Agent

Back 372

-Protein infective agent
-"misbehaving protein"
--recruits other proteins to also become bad proteins
-Normal alpha helical protein transforms into b-pleated sheet
--difficult to degrade
--able to aggregate other prion proteins
--get accumulation of un-degradable proteins in the cell
-Prion accumulations are basically a space-occupying lesion
-Protein is in every cell in body

Front 373

TSE Lesions

Back 373

-Sponge-like lesions
-Protein accumulates, gets trapped in vacuoles
-During processing, protein in vacuoles is washed away and all that remains is the space where they accumulated

Front 374

Scrapie Clinical Signs

Back 374

-Neurodegenerative disease in sheep and goats
-behavioral changes
-Abnormal posture and gait
-Muscle tremors
-Intense, incessant, pruritus
--itches ALL THE TIME, rub wherever they can
--rub off wool down to skin
-Incoordination and ataxia
-Death

Front 375

Scrapie Epidemiology

Back 375

-48 month incubation period
--shows up in sheep 2.5-4.5 years old
-Morbidity is low (20-40%
-Mortality is high (100%)
-Suffolk sheep has highest incidence, but all breeds are susceptible
-Goat infection is pretty rare

Front 376

Scrapie Modes of Transmission

Back 376

-Horizontal:
--feces
--placenta
--body fluids
--environmental contamination (very stable in environment)
-Vertical:
--prenatal
--post-natal

Front 377

Scrapie Diagnosis

Back 377

-Clinical signs and histopathologic lesions
-Can do tissue innoculation
--not practical due to long incubation periods

Front 378

Scrapie Differential Diagnoses

Back 378

-Scabies/mange
-Viral encephalitides
-Neurotoxins
-Pregnancy toxemia

Front 379

Scrapie Control

Back 379

-REPORTABLE DISEASE!! Must report!
-Old protocol:
--cull all infected sheep from flock
--cull all relations to infected sheep
--42 month surveillance of remaining animals
-Consequences too severe, no one would report!

Front 380

Scrape New Developments in Control

Back 380

-Antemortem detection of prions
--biopsy the eyelid
-Can do PCR on blood to check codon 171 of PrP
--most susceptible place in the PrP protein

Front 381

Codon 171 of PrP protein

Back 381

-Check to determine susceptibility of the sheep
-Arginine/Arginine (R/R) is resistant, no scrapie
-Arginine/glutamine (R/Q) is rarely susceptible
-Gluramine/glutamine (Q/Q) is very susceptible!

-Look for R/R/ rams

Front 382

Scrapie Voluntary Control

Back 382

-Voluntary scrapie flock certification program
-Based on monitoring and movement restrictions

Front 383

Scrapie Genetic based eradication program

Back 383

-Mandatory animal identification
--herd of origin
-Clean-up plans are not as severe
--genetically test animals in infected flocks
--indemnity program is available

Front 384

BSE Clinical Signs

Back 384

-Neurodegenerative disease in cattle
-Alteration of mental status (nervousness, aggression, apprehension)
-Alteration of posture and movement ( tremor, ataxia, falling down, paresis)
-Alteration of sensation (head shyness, hyperasthesia to touch and sound)
-Decreased milk production
-Loss of body condition despite continued appetitie
-Signalment: Cows between 3 and 5 years old

Front 385

BSE Epidemic Timeline

Back 385

-Disease identified and isolated
-New slaughter policy, no sheep into cow feed
-v-CJD identified 10 years later
-EU bans export of Brittish beef
-Cattle over 30 months old destroyed
-Peak number of cases in 1992

Front 386

BSE Worldwide

Back 386

-183,442 cases reported worldwide
--180,000 cases in England alone
-Some low level of endogenous disease exists around the world

Front 387

Control measures for BSE in British Cattle

Back 387

-Ruminant derived protein removed from cattle feed
-red meat consumption declined
-50% of dairy cattle culled and destroyed at expense of EU
-British been industry was devastated, even though most cases were reported in dairy cattle
-More of a political issue, not veterinary issue

Front 388

BSE outbreaks in USA

Back 388

-Handful of cases
-One case in 2003 caused 58 countries to ban import of US beef
-Over-response to "clear the air"

Front 389

BSE control in USA

Back 389

-Non-ambulatory/downer cows not allowed in feed chain
-Cows with neurologic signs are tested and carcasses held until test results are confirmed negative
-No skull, brain, spinal cord from animals over 30 months old allowed in food supply
-No tonsils and intestines from all cattle allowed in food supply
-LATEST: monitor

Front 390

BSE reports in USA

Back 390

-Last case was in 2012
-Sporadic BSE cases in California dairy cattle
-in Canada, 20 cases total
-USA, 4 cases total

Front 391

v-CJD

Back 391

-New variant form of Creutzfeldt-Jakobs Disease
-Younger age of patient onset, 29 years old
-Longer course of disease, lasted 12 months
-Lack of typical EEG pattern
-Different presenting complaints:
--psychiatric problems and ataxia
-Neuropathology was similar to Kuru
--Florid plaques

Front 392

v-CJD Epidemiology

Back 392

-National surveillance initiated in May 1990
-1400 cases of normal CJD
-176 cases of v-CJD

Front 393

v-CJD links to BSE

Back 393

-New emerging diseases occured at the same time
-Molecular similarities to prion proteins in BSE and v-CJD
-same "fingerprint"
-LOTS of people were at risk during BSE outbreak
--only 177 deaths so far

Front 394

Decreasing concern for BSE outbreaks

Back 394

-Less ruminant-derived protein sources used
-Feeding ruminant offal to cattle is banned
-No new cases expected after 2005
-Increased surveillance

Front 395

West Nile Encephalitis

Back 395

-Infection of the brain
-Caused by West Nile Virus (Flavivirus)
-COmmonly found in Africa, West Asia, Middle East
-Horses seem to be more susceptible than other domestic animals

Front 396

West Nile Virus Origin

Back 396

-Eastern hemisphere
-Did not come into western hemisphere until 1999
-Has expanded westwards since

Front 397

West Nile Virus Infection

Back 397

-Occurs via bite from an infectious mosquito vector
-Virus is in mosquito salivary glands
-Mosquito bites and feeds on horses, virus is injected into blood system
-Virus multiplies in horse and may cause illness
-Mosquitoes become infected via feeding on infected birds or other infected animals

Front 398

West Nile Virus Pathology

Back 398

1. Horse is bitten by mosquito and virus is injected into horse
2. Virus multiples in bloodstream
3. Virus crosses BBB, causes inflammation of the brain

Front 399

Clinical Signs of West Nile Virus

Back 399

-Flu-like signs
-Horse will seem mildly anorexic and depressed
-Fine and coarse muscle and skin fasciculation/twitching
--localized areas of twitching
-Hyperesthesia, hypersensitivity to touch and sounds
-Changes in mentation
-Drowsiness
-Propulsive walking, driving or pushing forward
-Spinal signs, asymmetrical weakness
-Multiple cranial nerve deficits

Front 400

West Nile Virus Epidemiology

Back 400

-Mortality rate for horses with clinical signs is 33%
--1/3 of affected horses will most likely die
-40% of horses that survive acute illness will have residual effects
--gait abnormalities
-Biggest year for infections was 2002, has decreased since

Front 401

West Nile Virus Transmission between Animals

Back 401

-No documented evidence of person-to-person transmission
-No evidence of animal-to-person transmission
-No Documented evidence of horse-to-horse transmission
-HORSES ARE DEAD-END HOSTS

Front 402

West Nile Virus Vaccination

Back 402

-Vaccination exists
-Primary method of reducing risk of infection
-Vaccine will reduce risk of infection, but clinical disease is not fully prevented
-Vaccination is recommended for all horses in North America where disease occurs

Front 403

West Nile Virus Infection Prognosis

Back 403

-Most horses recover from infection (80%)
-Down horses are 78x more likely to die
-Unvaccinated horses are 2x more likely to die
-Treat with supportive care

Front 404

Increased West Nile Virus Activity in 2012

Back 404

-700 human cases of West Nile Virus confirmed in 2012

Front 405

ORF

Back 405

-Contagious ecthyma/ Contagious pustular dermatitis/ Soremouth
-Highly contagious
-Mildly zoonotic
-Viral disease affecting mostly sheep and goats
-One of most common skin diseases of sheep and goats
-Present almost everywhere in the world where sheep and goats are raised
-"Backyard disease"
-High morbidity, low mortality
--Exposed animals will get sick but probably will not die

Front 406

ORF etiologic agent

Back 406

-Pox virus
-Virus is present worldwide
-Can remain in the environment for years
--once on the premises, virus will stick around
-Transmitted via direct contact or fomite
-Virus is shed in scabs
--Scabs contaminate the environment and can be carried from farm to farm
-Scabs are contagious!

Front 407

ORF Pathogenesis

Back 407

-Virus enters sheep/goat through minor abrasions
-Virus causes lesions that begin as pustules, eventually become thick, wart-like crusts
-Incubation period is 4-7 days, 1 week from exposure to clinical signs
-Lesions usually resolve in 3-4 weeks
-Most often seen in young lambs and kids due to lack of immunity
--Can occur in adults also, but disease will be sporadic and not as severe
--Adults are usually already exposed

Front 408

ORF Clinical Signs

Back 408

-Proliferative and ulcerative lesions on the lips, eyelids, oral cavity, feet, teats, and genitalia
-Looks like a dirty, snotty sheep/goat nose
-Mouth and face are most commonly affected
-Animals can become very painful
-Complications can arise from crusts
--pain in mouth causes anorexia and weight loss
--Lameness due to painful feet lesions
--Mastitis can result from nursing lambs/kids
-In severe cases, crusts can advance to granulation tissue

Front 409

ORF Diagnosis

Back 409

-Diagnosed based on clinical signs
--especially in a flock with previous history of ORF infection, or addition of new animals
-Definitive diagnosis: Virus identification in tissues (lesions, saliva, scabs)
--virus isolation, fluorescent antibody testing on inoculated cell cultures, electron microscopy
-Tissue biopsy and histopathology can give Dx

Front 410

ORF Treatment

Back 410

-Disease tends to be self-limiting
-only requires treatment in severe cases
-No known cure, treatment is supportive care only
--analgesics/NSAIDs
--Antibiotics to prevent secondary bacterial infection
--Nutritional and fluid support if needed
-DO NOT REMOVE CRUSTS, May delay wound healing or increase scarring
-Crusts provide protection for body's immune reactions

Front 411

ORF Prevention

Back 411

-Maintain closed herd/flock
-Isolate all affected animals
-Isolate any new animals for replacement
-Importing previously infected animals is dangerous! Do not do!
-Vaccination is effective, but virulent live virus
--will contaminate premises
-No colostral immunity, all neonates are susceptible

Front 412

ORF Vaccine

Back 412

-Effective vaccine
-Virulent live virus vaccine
-Will contaminate premises, and disease will contaminate premises
-NEVER VACCINATE UNINFECTED HERD/FLOCK
-Immunity from vaccine or disease can last several years

Front 413

ORF DDx

Back 413

-Vesicular Diseases
--Foot and Mouth Disease
--Vesicular Stomatitis
--Rinderpest
--Malignant Catarrhal Fever
--Bovine Papular Stomatitis
-Papillomavirus/warts
-Photosensitization

Front 414

ORF Disinfectants

Back 414

-Iodine based disinfectants
-Formaldehyde (Caustic, and inactivated by organic material
-Cl based disinfectants
-70% ethanol has NO virucidal activity
-REALLY hard to disinfect! worth the effort?