Livestock Medicine

Question 1

How should you start your physical exam

Answer 1

start from a distance
-BCS
-Demeanor/behavior
-Abdominal contour
-Lameness
-Neurologic
-Neck appearance and position
-Respiratory rate

Question 2

What is BCS scale for beef cattle

Answer 2

1-9

Question 3

What is the BCS scale for dairy

Answer 3

1-5

Question 4

What is the BCS scale for sheep and goats

Answer 4

1-5

Question 5

What is the BCS scale for camelids

Answer 5

1-9 or 1-10

Question 6

What results in a pear shaped abdomen in a cow

Answer 6

bilateral ventral abdominal distention- can be associated with pregnant animal with hydrops, urinary bladder rupture

Question 7

What results in a papple shape in a cow

Answer 7

classic vagal indigestion look. dorsal distension on the left hand side, ventral distension on the right hand side

Question 8

What results in an apple shape in a cow

Answer 8

more classic rumen distension, distension in the dorsal aspect bilateral

Question 9

What are the 5F’s of abdominal distension

Answer 9

fluid
feces/food
fetus
fat
flatus (gas)

Question 10

How do you tell visceral abdominal pain from parietal

Answer 10

visceral- caused by distension, stretching ischemia- results in “colic”

parietal- caused by inflammation of serosal surfaces- results in abnormal posturing, grunting, reluctance to move

Question 11

caused by inflammation of serosal surfaces- results in abnormal posturing, grunting, reluctance to move

Answer 11

parietal abdominal pain

Question 12

caused by distension, stretching ischemia- results in “colic”

Answer 12

visceral abdominal pain

Question 13

Is visceral or parietal abdominal pain more common in cattle

Answer 13

parietal pain is much more common in cattle- have more issues with peritonitis/pleuritis than the typical SI distension disease

Question 14

What is essential for a systemic hands on exam

Answer 14

head catch or chute for restraint

Question 15

What part of the body should you save for last when doing a systemic hands on cattle exam

Answer 15

head should be last

Question 16

What should you do on the left side of the cow when giving a physical exam

Answer 16

-Perform this first
1) Palpate the left prescapular lymph node- run hand right off the front of scapula
2) Examine brisket- palpate for any masses, edema, etc. also palpate left lateral neck
3) Examine left forelimb
4) Heart- up under the front limb- under tricep
5) Lungs- small area of auscultation- most pneumonia is the cranioventral lung fields
make sure to always listen to the trachea
6) Ventral abdomen- umbilicus, milk vein for hemotomas or abscess, stephanophilaria fly larvae
7) Rumen - auscultate, pinging/percussion
8) Left pre-femoral LN in front of quadriceps
9) Mammary gland or prepuce/scrotum, CMT
10) left hind limb

Question 17

What is the normal cattle heart rate

Answer 17

60-80bpm
-bradycardia associated with anorexia

Question 18

What is the most common cause of bradycardia in cattle

Answer 18

empty rumen.fasted animal- vasovagal reflex
*anorexia associated bradycardia

Question 19

What is the most common arrhythmia in cattle

Answer 19

atrial fibrillation
-primary disease process is often GI disease
-resolves when GI disease or electrolyte is fixed

Question 20

How do you typically resolve atrial fibrillation arrhythmias in cattle

Answer 20

fix the primary problem- GI disease
or electrolyte abnormality

Question 21

What is the most common clinical sign of endocarditis in cattle

Answer 21

lameness- septic arthritis

Question 22

What is the most common cause of murmurs in cattle

Answer 22

Endocarditis

Question 23

Pleural fluid will ________ the sound of the heart

Answer 23

radiate the sound of the heart

Question 24

Pericardial fluid will __________ the sound of the heart

Answer 24

muffle the sound of the heart

Question 25

T/F heart sounds on a really thiq cow will muffle heart beat

Answer 25

True

Question 26

How should you assess the rumen in a physical exam

Answer 26

put your hand on the paralumbar fossa- your hand should be displaced- that is a strong rumen contraction/motility if it is moving your hand

If you hear tinkling when the rumen moves, then it is likely that there is reduced/no fiber mat in the rumen

feel around on rumen- push in with closed fist to feel for gas cap-fiber mat- fluid layers of the rumen. fiber mat is doughy, compressible player

Pinging/percussion

Question 27

How can you check for rumen contraction/motility

Answer 27

put your hand on the paralumbar fossa- your hand should be displaced- that is a strong rumen contraction/motility if it is moving your hand

Question 28

What are the layers within the rumen

Answer 28

1) Free gas (dorsally)
2) Doughy coarse roughage (fiber mat)
3) Fluid, fine particles
4) Frothy semifluid

Question 29

What is the fiber mat of the rumen

Answer 29

the doughy compressible later that you feel around for when pushing into the rumen
it is made of coarse roughage

Question 30

How do you perform pinging/percussion for examining the rumen

Answer 30

football shaped field between the elbow and the ileal wing- flick/slap along the abdomen
you make a vibration and then hear what happens after the vibration

*assessing the air-fluid interface

Normal: hear a “thud”
Abnormal: hear a “ping” resonant “tinking” in a viscous with gas distension-

can be very challenging to flick hard enough so can slap around instead- need to make enough vibration to find gas distension

Question 31

What are your differentials for pings on the left side

Answer 31

-Pneumorectum
-Left Displaced abomasum
-empty rumen
-gas distended rumen.rumen bloat
-physometra
-pneumoperitoneum

Question 32

Succussion

Answer 32

if you hear a ping, do this

displace the contents of the viscous then listening for fluid-gas interface and fluid splashing
listening for “tinkling”

-helps to differentiate lD and rumen- if there is a fiber mat in the viscous (rumen) then you should hear the splashing because the fiber mat will buffer that sounds

if you hear splashing, then less likely that it is rumen as the rumen should have a normal healthy fiber mat that prevents you from displacing the air-fluid interface

Question 33

What should you do on the rear end of cow

Answer 33

-temperature
-muscle symmetry
-pulse in caudal artery
-vulvar mucous membranes
-popliteal LNs
-Supramammary LNs
-Rectal exam (wait until after examining right hand side of animal to avoid pneumorectum)

Question 34

Why should you wait to do a rectal exam on a cow till after youve listened to rumen on both sides

Answer 34

because you dont want to create a pneumorectum that will cause you to hear a ping when listening to the rumen

Question 35

What should you assess during a rectal exam in cattle

Answer 35

-Presence and consistency of manure
-Pelvic bones
-Rumen: size, consistency, location
-caudal aorta
-left kidney (size, location, pain, lobulations)
-lymph nodes
-reproductive tract

Question 36

What can cause a ping on the left side

Answer 36

-pneumoperitoneum
-pneumrectum
-RDA/RVA
-physometra
-SI distension/duodenal ping
-Cecal distension/dilatation
-Spiral colon gas

Question 37

What should you do in small ruminants to check if they are in late pregnancy

Answer 37

ballotment- push in with the hand in the lower flank and then hold- feeling for something to swing away from you and then come back- ballot for a late pregnancy

Question 38

What should you assess on the head during a cattle exam

Answer 38

1) symmetry (ear/eye position), check for drooping, discharge (OMI)
2) Nostrils- airflow, discharge, dry,
3) Parotid LN- right under the ear (cancer eye)- cant feel unless abnormal
4) Mandibular LN
5) Cranial nerve exam
6) Ears- bangs tag (female) and discharge (otitis)
7) Eyes- discharge, color, sclera, cornea, anterior chamber, PLR
8) oral: MM and teeth, ulcerations, vesicles, buccal papillae

Question 39

What should a healthy cow’s nose be

Answer 39

should have a clean, shiny/wet nose

Question 40

What should you look for in the ears

Answer 40

-If female, look for bangs tattoo/tag to see if they’ve been vaccinated against Brucella

signs of otitis

Question 41

Camelids have upper incisors and canines, what are these teeth called

Answer 41

fighting teeth

Question 42

T/F Cows have 3 upper incisors on each side

Answer 42

F- no upper incisors

Question 43

How should you perform a bovine oral exam

Answer 43

-Visual assessment for facial symmetry
-External palpation (lymph nodes- submandibular LN) and stability of mandible and maxilla
-Intraoral exam (manual, mouth gag) - teeth, palpate, diastema, tongue

Question 44

Diastema

Answer 44

space between incisors and premolars, good place to grab when doing a bovine oral exam

Question 45

When do deciduous teeth in cattle erupt

Answer 45

starting at birth for every tooth except for molars (no deciduous molars)

Question 46

“Mouthing” ruminants

Answer 46

examine teeth for culling decisions

-excessive wear “broken mouth” - a culling risk

Question 47

How might “broken mouth” develop

Answer 47

trauma
feed
nutritional deficiencies
genetics

*culling risk

Question 48

What are clinical signs of diseases of the dental arcade

Answer 48

weight loss, quidding feed, low production, metabolic diseases

Question 49

“Smooth mouth” ruminants

Answer 49

ruminants greater than 10 years of age with no incisors present

-increased risk of maintaining weight, foraging, productivity loss within the herd

Question 50

What neoplasias are seen in the mouth

Answer 50

-Fibrosarcoma
-Oral sarcomas
-Adenosarcomas
-Odontogenic myxomas

*invasive and poor prognosis

Question 51

Dentigerous cysts

Answer 51

a congenital anomaly in younger animals due to overgrowth of mature cells

extra tooth or teeth outside the dental arcades usually within the soft tissues and musculature of the mandibular and maxillary regions

need to remove all

Question 52

Hamartoma

Answer 52

congenital anomaly in younger animals due to overgrowth of mature cells

benign growth composed of an abnormal mixture of epithelial and mesenchymal elements.

need to remove a;;

Question 53

inflammation and infection of the structures that hold a tooth within the alveoalr socket.
triggered by malocclusion/fracture -> pocketing with periodontal defects and bacterial overgrowth (anaerobes typically)

Answer 53

periodontal disease

Question 54

How do ruminants get periodontal disease

Answer 54

they have hypsodont teeth which allows for the stasis of food material with malocclusion/fracture and then bacterial overgrowth

Question 55

How do pigs get periodontal disease

Answer 55

it is highly prevalent as they have brachydont teeth through through the dental calculus
can get enamel damages

Question 56

caused by injury to the gingiva leading to an infection of the premolar and molar and abscess of the root
*most common during eruption
can lead to mandibular swelling

Answer 56

tooth root abscess

clinical signs: ptyalism, halitosis, soft tissue swelling, quidding, inappetence, weight loss

Question 57

What species are tooth root abscesses most common in?

Answer 57

sheep and camelids

Question 58

What are the clinical signs of tooth tooth abscess?

Answer 58

ptyalism, halitosis, soft tissue swelling, quidding, inappetence, weight loss

Question 59

What might be a cause of mandibular or maxillary swelling associated with the jaw

Answer 59

tooth root abscess

Question 60

How might you see submandibular lymphadenopathy

Answer 60

secondary to lymphoma

Question 61

What kind of bacteria is associated with tooth tooth abscesses

Answer 61

Trueperella pyogenes

Question 62

non-specific inflammation of the oral mucosa (gingiva, tongue, palate, buccal mucosa)

Answer 62

stomatitis

Question 63

What are the causes of stomatitis

Answer 63

1) Trauma
a) plant awn, bedding-cornhusk
b) abnormal wear/loss of cheek teeth
c) Breach of mucosa- secondary infection (Necrotic stomatitis from Fusobacterium necrophorum in lambs and calves)

2) Viral infection
a) bovine papular stomatitis virus (BPSV)
-Parapoxvirus: raised papules on hard palate, muzzle, oral mucosa, esophagus
young feedlot cattle (1-12 months), slef-limiting but ddx from other vesicular diseases
lesions will regress within 3 weeks and brown spots will remain after healing *zoonotic

Question 64

T/F Bovine papular stomatitis virus (BPSV) is zoonotic

Answer 64

True- it is zoonotic, wear gloves

Question 65

What bacteria can cause stomatatis through breach of mucosa, common in lambs and calves

Answer 65

Necrotic stomatitis (Fusobacterium necrophorum)

Question 66

What kind of animals typically get Necrotic stomatitis from Fusobacterium necrophorum

Answer 66

lambs and calves
-sucking bottles not cleaned properly

Question 67

a parapoxvirus that causes raised papules on the hard palate, muzzle, oral mucosa, and esophagus

Answer 67

Bovine papular stomatitis virus (BPSV)

Question 68

What kind of animals typically get Bovine papular stomatitis virus (BPSV)

Answer 68

young feedlot cattle (1-12 months)

Question 69

T/F Bovine papular stomatitis virus (BPSV) is a lifetime condition

Answer 69

False- it is self-limiting in animals with immunocompetence and lesions typically regress within 3 weeks, brown spots will often remain after healing

Question 70

What do you need to rule out in animals with advanced lesions from Bovine papular stomatitis virus (BPSV)

Answer 70

BVDV
other vesicular diseases?FAD

Question 71

In Bovine papular stomatitis virus (BPSV), lesions are _________ but _______

Answer 71

lesions are mild but focus on prevention
it is highly contagious

Question 72

in Bovine papular stomatitis virus (BPSV), calves may be ____________ or ________

Answer 72

calves may be asymptomatic or show reluctance to nurse

Question 73

What are other names for Necrotic stomatitis

Answer 73

Necrotic laryngitis
Calf diphtheria
Necrobacillosis

*all refer to fusobacterium necrophorum infection from oral damage and infection
*massive edema

Question 74

With Fusobacterium necrophorum infection, ___________ of the larynx can be severe leading to ___________

Answer 74

swelling of the larynx can be severe (insipiratory dyspnea, stidor common
“Barker calves” - tracheostomy

Question 75

caused by a virus in family Rhabdoviridae, lesions may be indistinguishable from FMD- report cases to state vet
infects cattle, horses, pigs
arthropod vector
clinical signs: ptyalism due to oral ulceration, inappetence, weight loss

Answer 75

Vesicular stomatitis virus (VSV)

Question 76

T/F: You do not need to report cases of vesicular stomatitis virus (VSV)

Answer 76

False, report cases to the state veterinarian

Question 77

What is the vector for vesicular stomatitis virus

Answer 77

midge (arthropod)

Question 78

what time of year does vesicular stomatitis virus typically occur

Answer 78

summer and fall

Question 79

What causes contagious ecthyma

Answer 79

Sore Mouth/Orf
(a poxvirus- similar to BPSV)

Question 80

What animals typically get vesicular stomatitis virus

Answer 80

cattle
horses
pigs

Question 81

What animals typically get contagious ecthyma virus

Answer 81

sheep
goats

Question 82

T/F: contagious ecthyma is a self limiting virus

Answer 82

True- often self limiting within 3-6 weeks
do supportive care (nursing assistance)
immunity lasts 2-3 years after clinical case

Question 83

What is the classic lesion seen with contagious ecthyma?

Answer 83

crusting at the mucocutaneous junction of the nose and mouth
-can see proliferative oral lesions

Question 84

Is contagious ecthyma zoonotic?

Answer 84

yes - wear gloves

Question 85

What causes Wooden Tongue

Answer 85

Actinobacillus lignieressi

Question 86

Actinobacillus lignieressi causes

Answer 86

Wooden tongue

Question 87

a gram - pleomorphic rod aerobic, facultative anaerobic bacteria that is a normal oral commensal that causes disease through a primary injury to oral mucosa or skin, causing local cellulitis and pyogranulomatous infection
sulfur granules develop within pus. cause soft tissue granulomas on tongue, pharynx, esophagus, forestomach, and lymph nodes

Answer 87

Actinobacillus lignieressi

Question 88

T/F: Actinobacillus lignieressi is a normal oral commensal that causes disease when there is an injury to oral mucosa or skin

Answer 88

True

Question 89

What has sulfur granules that develop with the pus, causing soft tissue granulomas that can be found on the tongue, pharynx, esophagus, forestomach and lymph nodes

Answer 89

Actinobacillus lignieressi

Question 90

What are the clinical signs seen in Actinobacillus lignieressi (Wooden Tongue)

Answer 90

inability to prehend food (tongue)
granuloma +/- draining tract
bloat
esophageal obstruction

Question 91

Where are the soft tissue granulomas seen in Actinobacillus lignieressi infection

Answer 91

tongue, pharynx, esophagus, forestomach, lymph nodes

Question 92

Actinobacillus lignieressi causes:

Answer 92

soft tissue granulomas (sulfur granules) on the tongue, pharynx, esophagus, forestomach, lymph nodes

Question 93

How do you treat Actinobacillus lignieressi granulomas?

Answer 93

sodium iodide (20% solution) therapy
debridement/debulking

Question 94

What causes lumpy jaw

Answer 94

Actinomyces bovis

Question 95

a gram + filamentous, branching, anerobic bacteria
normal commensal of oral cavity and GIT
infects bones and teeth following injury to oral mucosa (course roughage, plant awns, enamel eruption increases risk)
sulfur granules in evident in pus or within infected tissue
-causes pyogranulomatous osteomyelitis: bone resorption around mandibular cheek tooth

Answer 95

Actinomyces bovis “lumpy jaw”

Question 96

Why are younger cattle more prone to Actinomyces bovis infection

Answer 96

enamel eruption increases risk as it infects bones and teeth following injury to the oral mucosa

Question 97

What are the classical signs seen in Actinomyces bovis infection

Answer 97

firm, painful, bony swelling, but can also cause granulomatous infectious throughout the body

-pyogranulmoatous osteomyelitis

Question 98

How do you treat Actinomyces bovis

Answer 98

success depends on degree of osteomyeltitis: often requires iodine therapy in addition to long term antibiotics (penicillin), surgical debulking?

Question 99

pharyngitis is most commonly due to

Answer 99

pharyngeal injury from forceful use of balling gun or drenching syringe

*lack of restraint = major risk factor

Question 100

clinical signs of pharyngitis

Answer 100

dysphagia
hypersalivation
malodorous breath
neurologic sign
stidor/dyspnea

Question 101

How might you get emphysemia dissecting facial planes

Answer 101

large tears in the pharynx

Question 102

What is a common sequelae of pharyngitis

Answer 102

aspiration pneumonia

Question 103

What are the causes of esophageal diseases

Answer 103

-Trauma: balling guns, esophageal feeder, stomach tube, diet anomaly (sugar beets)

-Infectious: mucosal lesions (BVDV), IBR, intraluminal or extraluminal compression

-Motility dysfunction (mechanical vs functional)

Question 104

What are the clinical signs of esophageal obstruction

Answer 104

salivation
regurgitation
development of palpable cervical swelling over time
weight loss
recurrent episodes

Question 105

What are the clinical signs of esophageal disease

Answer 105

salivation
regurgitation
bloat
crepitus within subcutaneous tissue (rupture)
nasal discharge containing feed (choke)

Question 106

What are the causes of esophageal obstructions

Answer 106

-Indiscriminate grazing (cattle)
-Neuromuscular dysfunction (camelids)
-Megaesophagus (often idiopathic, trauma, tumors, vascular ring (congenital)
present as young adults- follow weaning)

Question 107

What are the causes of esophageal dysmotility

Answer 107

1) Esophageal ulceration (pain)
2) pharyngeal trauma (vagus n. branches) - esophageal feeder in calves
3) thoracic mass (thymic lymphosarcoma, LN enlargement)

*Esophageal motility disorders (rare)

Question 108

calves with megaesophagus often present with

Answer 108

chronic bloat +/- regurgitation

Question 109

esophageal motility is necessary for

Answer 109

normal rumen function

Question 110

How might you see excessive salivation

Answer 110

animals may drool due to excess saliva production or may not be able to swallow the saliva

-Tooth abnorm
-Stomatitis- irritant (trauma, chemical, bacterial, viral infection
-Swallowing problems (pharynx, esophagus, neurologic)

Question 111

T/F: Clinicial signs are important because they are diagnostic

Answer 111

False- they are important but testing is needed to identify specific viruses, especially if thy are foreign animal diseases

Question 112

what are viruses that are erosive/ulcerative

Answer 112

bovine viral diarrhea (BVD)
malignant catarrhal fever (MCF)
Bluetongue (BT)
Rinderpest

Question 113

What ate vesicular viral diseases

Answer 113

-Foot and mouth disease (FMD)
-Vesicular stomatitis (VS)

Question 114

What are proliferative viral disease

Answer 114

-Bovine papular stomatitis
-Orf (soremoth, contagious ecthyma of sheep and goats)

Question 115

What are the clinical signs of BVDV, bluetongue, and malignant catarrhal fever

Answer 115

fever
ulcerative lesions of oral tissues
lesions at mucocutaneous junction
lesions of skin/hoof junctions
depression
anorexia

Question 116

How do you do confirmatory testing for viruses

Answer 116

Virus identification- isolation, PCR
-Serologic antibody response
-Characteristic histpathology

Question 117

What are some clinical signs of BVD/Mucosal disease

Answer 117

-Oral, MCJ lesions- epitheliotrophic
-Coronary band interdigital lesions-lameness
-corneal lesions
-bloody diarrhea
-linear esophageal erosions
-Peyer’s patch necrois
-immunosuppressive (lymphocytotrophic)

-Most common sign of infection is clinically normal
-Abortions

Question 118

What causes diarrhea in mostly cattle with leukopenia, lymph node atrophy, and immunosuppression with persistent infection

Answer 118

BVD/ Mucosal disease (Flavivirus, Pestivirus)

Question 119

What causes buccal mucosal cyanosis and erosions, coronary band and interdigital lesions, lameness, cattle are typically asymptomatic

Answer 119

Bluetongue (Orbivirus)

Question 120

What kind of virus is BVD/Mucosal disease

Answer 120

flavivirus, pestivirus

Question 121

T/F: diarrhea is common with bluetongue (orbivirus)

Answer 121

False- diarrhea is uncommon

Question 122

What animals is bluetongue most common in?

Answer 122

sheep

Question 123

T/F: bluetongue is seasonal

Answer 123

true- requires an arthropod vector

Question 124

What causes malignant catarrhal fever (MCF)

Answer 124

herpesvirus (OHV-2)

Question 125

What disease has erosions throughout the oral cavity (hard palate), panopthalmitis, arteritis, swollen lymph nodes, coronary band/interdigital lesions, lameness

Answer 125

Malignant catarrhal fever (OHV-2)

Question 126

T/F: diarrhea is common with malignant catarrhal fever

Answer 126

false- it is uncommon

Question 127

What are the signs of malignant catarrhal fever

Answer 127

erosions throughout the oral cavity (hard palate)
panopthalmitis
arteritis
swollen lymph nodes coronary band/interdigital lesions, lameness

Question 128

T/F: malignant catarrhal fever effects herds

Answer 128

False- typically affects individual animals

Question 129

What side is the rumen on?

Answer 129

left side

Question 130

what lies behind diaphragm, making puncture of it dangerous for the pericardial sack and diaphgram

Answer 130

reticulum

Question 131

Where does milk from the esophageal groove go to

Answer 131

reticular-omasum orifice

Question 132

what does the spiral colon do

Answer 132

where a lot of the fluid is absorbed and the pellets are formed

Question 133

What is fermented in the rumen

Answer 133

1) Carbohydrate
a) simple sugars- rapidly broken down
b) Polysarccharides- starch, amylose
c) structural carbs- cellulosa and hemicellulose

2) Proteins- manufactured by microbes. some bypass rumen and proteins are then processed by small intestine

Question 134

Where do most of the proteins get made in ruminants

Answer 134

manufactured by microbes in the rumen

Question 135

What is the end product of carbohydrate fermentation

Answer 135

-Acetate (2 carbon) -Lipogenic

-Propionate (3 carbon)- glucogenic

-Butyrate (4 carbon) - ketogenic

Question 136

What VFA is glucogenic

Answer 136

propionate (3 carbons)

Question 137

What VFA is lipogenic

Answer 137

acetate (2 carbon)

Question 138

What VFA is ketogenic

Answer 138

butyrate (4 carbon)

Question 139

T/F: the rumen is nonglandular

Answer 139

True it is nonglandular absorptive epithelium

Question 140

Where are VFAs absorbed in ruminants to be transported to the liver in the blood

Answer 140

the rumen- it is nonglandular absorptive epithelium

some do reach the abomasum

Question 141

what is the glandular portion of the ruminant stumach

Answer 141

abomasum- has cardiac, propergastric and pyloric glands

Question 142

the most important motor function in the rumen to facilitate fermentation

Answer 142

primary contractions

Question 143

motor function for eructating gas in the rumen

Answer 143

secondary contraction

Question 144

What are the motor functions of the rumen

Answer 144

1) Primary contractions
2) Secondary contractions
3) Eructation
4) Regurgitation
5) Esophageal groove
6) Control mechanisms

Question 145

How is material fermented in the rumen

Answer 145

-Inflow- feedstuffs, saliva
-Outflow- absorption, ingesta passage
-Fiber (slowly fermented
-Concentrates (starch/cereal grains that are fermented rapidly

Question 146

What is the 6 purposes of primary contractions

Answer 146

-Mixing of ingesta (maceration of fibrous feeds)
-Stratifcation of rumen contents
-Sorting of feed by particle size (selective passage of small particles)
-Aborad movement (passage of ingesta through reticulo-omasal orifice
-Enhanced VFA absorption- fluid contact with rumen wall
-Enhance contact with bacteria with feedstuffs

Question 147

What stimulates primary contractions

Answer 147

1) feeding/chewing
2) low threshold receptors that signal the rumen is mildly distended
3) Abomasal acidity signaling for more ingesta to be passed
4) Environmental cold

Question 148

what inhibits primary contractions

Answer 148

1) High VFA concentrations/acidity
2) Abomasal distension
3) High threshold receptors signaling that the rumen wall is too tight
4) Pain
5) CNS depression and systemic illness/fever

Question 149

Does environmental cold stimulate or inhibit primary rumen contractions

Answer 149

stimulate
-heat is generated and allows the animal to stay warm

Question 150

Does abomasal acidity stimulate or inhibit primary rumen contractions

Answer 150

stimulate

Question 151

does feed/chewing stimulate or inhibit primary rumen contractions

Answer 151

stimulate

Question 152

does high VFA concentrations/acidity stimulate or inhibit primary rumen contractions

Answer 152

inhibit

Question 153

Does abomasal distension stimulate or inhibit primary rumen contractions

Answer 153

inhibit

Question 154

What is the purpose of secondary contractions

Answer 154

move gas generated from fermenation to the cardia
clears the cardia
Prepares animal for eructation

Question 155

relaxation of the esophagus, close glottis and inhaling gas from stomach system creating negative thoracic pressure

Answer 155

eructation

Question 156

reticular contraction that lifts feed to the cardia, where fibrous feed is then eructated to be masticated again

Answer 156

regurgitation

Question 157

directs milk directly into the abomasum

Answer 157

esophageal groove

Question 158

What part of the stomach has shagged rug appearance to buffer the acidic VFAs

Answer 158

rumen

Question 159

virtually all disease of rumen occur when

Answer 159

normal physiology is distrubed

Question 160

What would happen if the animal cant clear the cardia

Answer 160

prevent eructation

Question 161

lower right abdominal distension is an issue with the

Answer 161

abomasum

Question 162

upper left distension in the abdomen indicates

Answer 162

possible bloat

Question 163

upper right abdominal distension indicates that there is an issue with the

Answer 163

abomasum- filled with gas (volvulus)

or cecal volvulus dominates the right side

Question 164

When do you hear abdominal pings

Answer 164

when there is gas over the smooth surfgace
-gas or fluid or gas over serosal surface

-Pneumoabdomen or left displaced abomasum fluid inside hollow viscous where gas is above and fluid is below

Question 165

common in dairy cows the abomasum is filled with gas and migrated up the left abdomen. will hear a ping there instead of the rumen

Answer 165

left displaced abomasum

Question 166

When do you hear a ruminal ping

Answer 166

when the layers of the rumen are changed so fibrous material is at the bottom, then fluid, and then gas
*textbook for rumen stasis

Question 167

RDA a _________ while abomasal volvus is a _________

Answer 167

partial obstruction ; complete obstruction

Question 168

What are problems resulting in right sides pings

Answer 168

-abomasal volvulus
-abomasal displacement (right)
-cecal dilatation
-cecal volvulus
-pneumoperitoneum
-ascending colon gas
-rectal gas

Question 169

distention of the rumen due to gas accumulation
caused by problems that disrupt the eructation gas

Answer 169

bloat

Question 170

T/F: bloat is caused by excessive gas production

Answer 170

bloat is not caused by excessive gas production but rather problems that disrupt eructation

-with normal functioning rumen, it can expel gas at any rate produced

Question 170

How is bloat caused

Answer 170

caused by problems that disrupt eructation

Question 170

What is required for normal eructation

Answer 170

1) patent esophagus
2) ability to clear the cardia
3) presence of gas in a “free” gas cap (not gas trapped in foam)
4) normal snesory and motor function to generate secondary contractions followed by normal eructation movement

Question 171

How might you get bloat

Answer 171

1) esophageal obstruction: choke- cant get gas out

2) Partial esophageal obstruction- compression, restriction or neuromuscular problem

3) Frothy gas: non eructable

4) failure of gas to clear cardia: weakness (hypocalcemia), lateral recumbancy, rumen overfill, thoracic inflammation (vagal nerve damage)

Question 172

solid feed material causing esophageal damage and inability for an animal to release gas from the rumen

Answer 172

Complete “Choke” resulting in bloat
*acute

Question 173

How might you get partial esophageal obstruction

Answer 173

-Esophageal compression (thoracic masses, pneumonia, mediastinal masses, LDA)
-Failure to relax esophagus (Tetanus)
-LDA (occasionally)

*mostly chronic, recurring bloat
-Rarely life threatening

Question 174

why should you evaluate cardiopulmonary function in bloat cases

Answer 174

it makes it so it is more difficult to breathe for the animal.

Question 175

How should you evaluate bloated animals

Answer 175

-First evaluate animal demeanor and degree of respiratory compromise

-Consider feed history

-Pass a stomach tube (Does it pass? does it relieve the bloat)

-Torcharize: to relieve life-threatening rumen distention, only if free gas

-Evaluate rumen function

Question 176

Choke is typically caused by ______________ and there is also ______________,

Answer 176

choke is typically caused by solid feed materia; and there is damage to the esophagus (long term consequences)
-will not pass further
try to retrieve the feed material back to the mouth

Question 177

solid feed material causing choke are typically
a) pushed into the rumen
b) taken out of the mouth

Answer 177

taken out of the mouth

if it could pass further it would have passed normally

Question 178

what are clinical signs of bloat

Answer 178

-labored breathing
-agitated animal
-rumen restricting diaphragm (emergency)
-froth at nose from labored breathing

Question 179

T/F: bloat from partial esophageal obstruction is life threatening

Answer 179

False, rarely

Question 180

T/F bloat from complete esophageal obstruction is life threatening

Answer 180

True
and damaged esophagus have long term deleterious effects

Question 181

What is trocharization

Answer 181

tubes with a sharp stylet that is punctured through body wall into rumen. stylet is then removed to relieve excess gas from the rumen

Question 182

used instead of trocharization when the bloat is chronic/recurrent. surgery that allows gas to be removed from the rumen while the primary problem resolves

Answer 182

Rumen fistulation

Question 183

When is rumen fistulation used

Answer 183

used instead of trocharization when the bloat is chronic/recurrent. surgery that allows gas to be removed from the rumen while the primary problem resolves

Question 184

occurs when a stable foam forms that traps gas bubbles, and prevents normal eructation
formed by:
a)bacterial slime from agents that digest grain (feedlot bloat or grain bloat)
b) Legume feeds- protein and cation content (pasture bloat) or (legume bloat)

Answer 184

frothy bloat

Question 185

How might frothy bloat form

Answer 185

a)bacterial slime from agents that digest grain (feedlot bloat or grain bloat)
b) Legume feeds (ie alfalfa)- protein and cation content (pasture bloat) or (legume bloat)

Question 186

How do you relieve frothy bloat

Answer 186

Poloxalene (Therabloat, a surfactant) orvegetable oil - breaks down the froth

*cant relieve with stomach tube or rumen trocar

Question 187

T/F: you can remove frothy bloat with stomach tube or rumen trocar

Answer 187

False

relieve with Poloxalene (Therabloat, a surfactant) orvegetable oil - breaks down the froth

Question 188

Animals on feedlots fed high grain diets will overgrow certain bacteria that allow them for form frothy bloat. What is one of the most common bacteria indicated?

Answer 188

Streptococcus bovis

Question 189

T/F: frothy bloat may be an emergency

Answer 189

True- can be in respiratory distress

If not emergency: destabilize foam with Poloxalene or veggie oil

If emergency- perform rumenotomy to

Question 190

What should you do if an animal is in respiratory distress due to frothy bloat

Answer 190

Perform a rumenotomy

if not emegency: destabilize the foam with Poloxalene or veggie oil

Question 191

How do you prevent flothy bloat from occuring in a herd

Answer 191

1) Dietary strategies (decrease intake of lush alfalfa or feed high fiber feed in addition)

2) Ionophores (change fermentation and suppress step bovis)

3) Poloxalene lick blocks

Question 192

how can you relieve free gas bloat

Answer 192

can be relieved by a tibe
may be chronic/recurrent

Question 193

How do you get free gas bloat

Answer 193

*Failure to clear the cardia

1) rumen function- hypocalcemia weakens contractions
2) animal position (lateral recumbency- milk fever, foot triming/vet procedures)
3) Weak rumen contractions or rumen stasis with some indigestions (acidosis or acute hardware)
4) abnormal rumen fermentation (feed)
5) overfilled rumen (with feed)
6) cardia obstruction- foreign body or mass

Question 194

What is seen in a normal rumen

Answer 194

rumen fills but does not distend the abdomen

different consistency can be appreciated by ballotment

fluid consistency ventrally
firm, fibrous consistency above
gas cap is small and not palpable because under transverse processes

Question 195

Will a free gas bloat produce a ping

Answer 195

? yes i think so- fill in later

Question 196

What does continuous fermentation required

Answer 196

-inflow- feed substrate
-outflow- finished product
-removal- inhibitory/toxic products
-control of pH

Question 197

T/F you can feed meat and bone meal as feed stuffs

Answer 197

False- it is illegal due to pathogen spread

Question 198

What is the color of normal rumen fluid

Answer 198

olive-brownish green

Question 199

What is the odor of normal rumen fluid

Answer 199

aromatic- smelly

-Will be less aromatic with less fermentation

Question 200

What is the consistency of normal rumen fluid

Answer 200

slightly viscous (gruel)
-active fermentation and some gas bubbles

Question 201

What is the pH of normal rumen fluid

Answer 201

5.5-7
wide range due to presence/less VFAs

Question 202

What should the chloride be of normal rumen fluid

Answer 202

<25-30 mEq/l

Question 203

What should the methylene blue reduction be of normal rumen fluid

Answer 203

3-6 min
*determination of bacterial activity (redox)

Question 204

What is the sedimentation/flotation of rumen fluid used for

Answer 204

Should be 4-8 minutes
Tells you the bacterial activity- how rapidly they are fermenting. light particles move to the top with active fermentation

Question 205

How do you collect rumen fluid

Answer 205

obtained through an orogastric tube or via percutaneous puncture with long needle in the left flank

*Best method is orogastric tube with stainer to strain out the fiber

Question 206

What color of rumen fluid is seen in rumen acidosis with cereal grain consumption

Answer 206

very yellow/whitish color

Question 207

What color of rumen fluid is seen in fresh forage feed

Answer 207

a fresh green color

Question 208

What should you see in terms of protozoal activity when examining rumen fluid

Answer 208

Active- moving around
All sizes are present

*dead protozoa dont move around

Question 209

What does a rapid sedimentation of rumen fluid tell you

Answer 209

if rapid (less than 3 minutes), sedimentation indicates that there is poor microflora activity

Question 210

What does no sedimentation of rumen fluid tell you

Answer 210

there is frothy bloat or vagal indigestion

Question 211

What is a normal sedimentation test time of rumen fluid

Answer 211

4-8 minutes

-Rapid <3 min tells poor microflora activity
-No sedimentation tells you frothy bloat or vagal indigestion

Question 212

How is a new methylene blue reduction test performed on rumen fluid

Answer 212

Add 1:12 new methylene blue to rumen fluid

wait about 3 minutes to decolorize (aerobic area on top does not decolorize)

prolonged time to decolorize indicates bacterial die off; most commonly seen in prolonged anorexia with indigestion or ruminal acidosis

3-6 min is normal

Question 213

What is likely happening if it takes longer than 6 minutes for there to be decolorization after adding new methylene blue to rumen fluid

Answer 213

Indicates bacterial die off- mostly common in
prolonged anorexia with indigestion or ruminal acidosis

Question 214

What part of the rumen fluid does not decolorize in a new methylene blue test

Answer 214

the top (aerobic part)

Question 215

pH of rumen fluid should be ________ but may be __________ if chronically fed gain

Answer 215

Should be 6-7, may be 5.5 if chronically fed grain.

Should be 7 if it is on forage only

if high, it may be normal or indicative of contamination of sample with saliva

Question 216

pH will tend to be higher when _________ while it will be lower when _____

Answer 216

higher when its longer time after feeding

Lower when its right after feeding (generation of VFAs)

Question 217

If an animal is anorexic and you measure the pH to be <5.5. What is occuring

Answer 217

highly indicative of ruminal acidosis

pH should be higher when there hasnt been eating

Question 218

Would methylene blue reduction time be higher or lower when on a pure straw diet vs one that has grain in it

Answer 218

Higher methylene blue reduction time and higher pH due to less bacterial fermentation because there are no carbohydrates

Mixed hay/grain ration will result in shorter methylene blue reduction time and lower pH (more VFAs being produced)

Question 219

When does chloride rich fluid in the rumen occur

Answer 219

only when there is abomasal reflux (internal vomitting)

abomasum generates the HCl and is moved to rumen. Chloride is poorly absorbed in the rumen

**Indicates a problem with abomasal outflow

Question 220

What does a rumen fluid chloride value of >30 mEq/L indicate

Answer 220

a problem with abomasal outflow

-HCl is produced in the abomasum and during abomasal reflux, it gets moved to the rumen where is is poorly absorbed

Question 221

What is the pathogenesis of traumatic reticuloperitonitis

Answer 221

-feed mixers/ gridners often chop up wire, nails
-wire migrates to the reticulum where is migrates through the wall into the peritoneum
-Peritonitis, abscessation at the reticulum of rumen fluid

Question 222

Why does hardware disease rarely occur in sheeps and goats

Answer 222

because they are browsers- eat with their lips instead of their tongue

Question 223

How do you prevent hardware disease

Answer 223

-careful farm management
-give cattle a magnet
-feed mixing truck with magnets on the outflow chute to trap steel contaminants

Question 224

What cant you prevent with a reticulum magnet

Answer 224

aluminum needles do not stick to the steel magnet and could still cause traumatic reticuloperitonitis

Question 225

What are the clinical signs traumatic reticuloperitonitis

Answer 225

1) fever (peritoneal inflammation)

2) Pain/arched back/extended neck/abnormal gait (anterior abdominal inflammation)

3) Rumen stasis (reflex inhibition of motility due to pain/inflammation)

4) Anorexia (inflammation and rumen stasis inhibit appetite)

5) Scant, dry feces- reduced passage of ingesta

Question 226

What appearance does the reticulum have?

Answer 226

a honey comb pattern

Question 227

What clinical signs do the acute cases of hardware disease have

Answer 227

-Fever, cranial abdominal pain, grunt
-acute onset rumen stasis
-Rapid drop in milk production
-Normal abdominal contours- but may have mild free gas bloat
-Normal rumen layering of ingesta
-Decreased bacterial fermentation

Question 228

What are the clinical signs of chronic localized perionitis from hardware disease

Answer 228

-NO FEVER, weight loss, poor production
-Prolonged rumen stasis- fiber mat sinks, fluid above
-Decreased rumen size
-Rumen pings ae common- gas over fluid in rumen
-Bacterial fermentatio is almost absent

*Some cases- new signs develop as foreign body pentrates other tissues (thorax, heart sac)

Question 229

T/F: rumen pings are common with chronic localized peritonitis from hardware disease

Answer 229

True- gas over fluid in the rumen

Question 230

How do the clinical signs differ from acute vs chronic traumatic reticuloperitonitis

Answer 230

acute case: normal layers in the rumen and body contours. Rumen stops moving, may develop mild bloat
Rumen fluid shows inactivity (mild increase pH and mild increase MBR time)

chronic: inappetance/rumen stasis, shrunken rumen, firm fibrous material sinks to the bottom of the rumen, rumen fluid shows significant inactivity
firm, scant feces, reduced passage of ingesta

Question 231

What are the sequellae to TRP

Answer 231

1) uneventful recovery following treatment
2) infection of other tissues (pleuritis, pericarditis)
3) reticular wall abscessation - obstructive vagal indigestion

Question 232

What diagnostics do you run if you suspect traumatic reticuloperitonitis

Answer 232

-Physical exam and observation
-CBC. including a fibrinogen (must)
-abdominal exploratory sx

maybe: ultrasound: abdomen and chest, abdominocentesis, radiograph of cranial abdomen

Question 233

What is with Whithers pinch/scootch test used for

Answer 233

does the cow resist dropping their head back due to anterior abdominal pain?
-Doesnt want to go into lordosis because it will be in pain

Question 234

What is a sternal pressure/grunt test used for

Answer 234

does the cow resent pressure as it induced localized pain
-arch the back and resents the pain

Question 235

How do you treat traumatic reticuloperitonitis

Answer 235

if early and heart is not affected- conservative treatment is often elected
-give magnet
-antibiotics (beta-lactams): typically facultative anaerobes
-Rumenotomy to retrieve the wire
-Transfaunate with donor rumen fluid

Question 236

What kind of antibiotics should you use to treat traumatic reticuloperitonitis

Answer 236

Beta-lactam: typically facultative anaerobes

Question 237

What is a result of traumatic reticulopericarditis

Answer 237

-Pericarditis that is restrictive to the heart
causes right sided heart failure signs and a jugular pulse
-Washing machine murmur
-Brisket edema
-Pericardium may be folled with purulent fluid or with fibrin
-Necropsy: “shappy heart” (fibrinous pericarditis)

Question 238

How might you get a jugular pulse

Answer 238

from right sides heart failure signs seen with traumatic reticulopericarditis

Question 239

how do you get brisket edema

Answer 239

from right sided heart failure
-signs seen with trauamtic reticulopericarditis

Question 240

What are the 4 things associated with obstructive (Vagal) indigestion syndrome

Answer 240

1) Omasal transport (outflow) failure
2) Pyloric transport (outflow) failure
3) obstructive indigestion-other causes (Haybelly)
4) Abomasal emptying defect of Suffolk sheep

Question 241

What are the 4 key signs of obstructive (vagal) ingestion

Answer 241

1) Chronic, progression abdominal distention
2) Gradual weight loss/body condition loss
3) Decrease fecal volume
4) Papple shaped abdomen

*Varies etiologies (syndrome)
*Most cases are not due to vagus injury

Question 242

T/F: Obstructive (vagal) indigestion is caused by vagal injury

Answer 242

False
Most cases are not due to vagus injury
it is a syndrome

Question 243

What causes the Papple shape seen with obstructive (vagal) indigestion

Answer 243

impaired forestomach emptying. causes the rumen to move from its left sided position into an L shape

Question 244

Omasal transport failure leads to

Answer 244

Obstructive indigestion (vagal indigestion)
*Behaves like omasal orifice being obstructed and causes the rumen to filled beyond capaciy as ingesta does not move through reticulo-omasal orifice. Scant feces, body condition loss,
secondary cycles continue=rumen contractions but ineffective
ingesta mixed to homogenous mass

Cardinal signs of syndrome:
1) Chronic, progression abdominal distention
2) Gradual weight loss/body condition loss
3) Decrease fecal volume
4) Papple shaped abdomen

Question 245

What could result when there is obstructive indigestion due to omasal transport failure

Answer 245

Rumen is overfilled
homogeneous consistency
With rumen overfilling- develop free gas bloat

occassionally cows “vomit” = large scale regurgitation (forestomach)

Question 246

T/F: a papple shape is seen with obstructive indigestion

Answer 246

True

Question 247

What are the causes of omasal transport failure (a cause of obstructive indigestion)

Answer 247

1) Abscess of the reticular wall- failure to initiate primary contractions- cannot sense rumen. fill to stimulate rumen activity. *Secondary to TRP

2) Obstruction of omasal orifice- rumen overfulls, primary contractions cease, mass lesions and foreign bodies caused

*Prognosis depends on cause

Question 248

How can TRP lead to omasal transport failure

Answer 248

abscess of the reticular wall leads to failure to initiate primary contractions- cannot sense rumen
fill to stimulate rumen activity

Question 249

Pyloric outflow failure leads to

Answer 249

Obstructive indigestion
cardinal signs
1) Chronic, progression abdominal distention
2) Gradual weight loss/body condition loss
3) Decrease fecal volume
4) Papple shaped abdomen

Question 250

What is the pathogenesis for pyloric outflow failure, leading to obstructive indigestion

Answer 250

*Pyloric outflow failure= behaves like the pylorus is obstructed

Ingesta does not pass out of abomasum
Abomasum distends and fluid passes back into the rumen
Papple shaped abdomen
*Rumen chloride is typically elevated

Question 251

How do you distinguish between omasal transport failure and pyloric outflow failure

Answer 251

Rumen chloride will be elevated in pyloric outflow failure due to the backing up of abomasal conts from pyloric outflow failure

Question 252

What are the causes of pyloric outflow failure, leading to obstructive indigestion

Answer 252

1) Secondary to preceding abomasal problem (abomasal displacement or abomasal volvulus)

2) Foreign bodies or feed materail cannot pass through pylorus (abomasal impaction)

*prognosis is usually poor, abomasum does not return to normal function

Question 253

What is the prognosis for pyloric outflow failure

Answer 253

poor- abomasum does not return to its normal function.

Question 254

What is indigestion of late pregnancy

Answer 254

during late pregnancy, large fetus develops abdominal contour. fetus moves the abomasum to where abomasal flow is obstructed.
fixed with birth

Question 255

T/F: acute frothy bloat can cause a “papple” abdomen

Answer 255

True

Question 256

T/F uterine problems such as hydrops can cause “papple” abdomen

Answer 256

True- uterine filled up can give the appearance

Question 257

failure to eructate due to damage to the proximal vagus nerve resulting in acute rumen stasis and free gas bloat
- Signs: acute, severe pneumonia, pharyngeal or esophageal trauma
Classified as:

Answer 257

Type I Obstructive (Vagal) indigestion

Question 258

failure of omsal transport caused by abscess or adhesion along the right (medial) side of the reticulum is classified as:

Answer 258

Type II Obstructive (Vagal) indigestion

Question 259

T/F: Type I Obstructive (Vagal) indigestion results in papple shaped abdomen

Answer 259

False

Question 260

abomasal impaction due to chronic or severe abomasal distension (RDA or RAV) is classified as

Answer 260

Type III Obstructive (Vagal) indigestion

Question 261

secondary to late gestation, resolves with parturition. “Indigestion of late pregnancy” is classified as

Answer 261

Type IV Obstructive (Vagal) indigestion

Question 262

What is abomasal emptying defect of suffolk sheep

Answer 262

abomasum fail to transport ingestion leading to chronic weight loss

-Similar to obstructive indigested

-No observed preceding cause (genetic?)

Increased rumen chloride

abdominal distention not profound

*No longer around

Question 263

What is another name for grain overload

Answer 263

Rumen acidosis
-acute ingestion of high carb feeds, typically grains

Question 264

T/F: sheep and goats are not at risk for rumen acidosis

Answer 264

false- all ruminants are at risk

Question 265

How might rumen acidosis occur

Answer 265

Acute ingestion of high carbohydrate feeds, typically grains
-Too rapid movement from forage to grain at feedlot
-Mixing or grinding errors at dairies
-Individual animal gets into the grain bin (small ruminants)

Question 266

What is the pathogenesis of rumen acidosis

Answer 266

-CHO rapidly fermented by bacteria (Strep bovis) producing D and L lactate
-L isomer is utilized by D isomer persists creating a D-lactic acidosis
-Rumen pH drops to 5 or below
-Other bacteria die off while Strep bovis thrives until severe where it dies

-D lactate increases osmolality of the rumen and draws in water
-Dehydration, electrolyte imbalance, systemic acidosis result
-Acid environment may permanently damage the rumen wall
-Absoprtion of endotoxin

Question 267

What isomer of lactate isnt absorbed well?

Answer 267

D-lactic isomer
-creates a D-lactic acidosis

Question 268

What is the bacteria associated with Rumen acidosis

Answer 268

Strep. bovis

Question 269

D lactate _____________ the osmolality of the rumen, resulting in :

Answer 269

it increases the osmolality of the rumen, draws the water in.
leads to dehydration, electrolyte imbalance and systemic acidosis

acid environment damages the rumen wall and absorption of endotoxin

Question 270

How can rumen acidosis lead to endotoxemia

Answer 270

it increases the osmolality of the rumen, draws the water in.
leads to dehydration, electrolyte imbalance and systemic acidosis

acid environment damages the rumen wall and absorption of endotoxin

Question 271

Hww do you get sloshy or fluid rument content

Answer 271

Increased D-lactate from increased fermentation of soluble carbohydrates
makes it hyperosmolar which draws fluid into the rumen resulting in sloshy or fluidy rumen content and systemic dehydration

Question 272

Rumen acidosis causes the rumen fluid to be:
pH:
Color:
Odor:
NMB:
Protozoa:
Consistency:

Answer 272

pH: low
Color: yellow, brown
Odor: sweet odor
NMB: early-rapid from hyperactive bacteria ; later-prologned
Protozoa: dead of absent
Consistency: sloshy and low fiber

Question 273

Why might the rumen fluid to be
pH: low
Color: yellow, brown
Odor: sweet odor
NMB: early-rapid; later-prologned
Protozoa: dead of absent
Consistency: sloshy and low fiber

Answer 273

rumen acidosis

Question 274

What will the rumen papillae look like in rumen acidosis

Answer 274

Hyperemic, damaged, peel off, general mucosal damage

Question 275

What are the presenting problems with rumen acidosis

Answer 275

depends on the severity and the chronicity

severe cases: shock, acidosis, bloat, dehydration, anorexia, decreased milk prod, high HR and RR, depressed to obtunded, splashy rumen, rumen stasis- sometimes free gas bloat, ileus

Milder cases: diarrhea, inappetence, transient rumen stasis, feces- fluid, malodorous, grain particles

Question 276

How do you treat mild cases of rumen acidosis

Answer 276

1) IV Fluids- hemodynamic support
2) Kingman tube- drain rumen
3) Banamine- anti-endotoxin
4) Rumen alkalinizers (Mg hydroxide)
5) Transfaunation (nx gi flora)
6) Parenteral antibiotics
7) Held off feed, including water until the rumen as emptied itself and motility is gained

Question 277

How do you treat Severe Rumen Acidosis

Answer 277

1) rumenotomy- evacuate rumen ocntents
2) Laxatives
3) Parenteral calcium (for hypocalcemia)
4) IV fluids: hypertonic saline and then balanced electrolyte solutions- add bicarbonate if pH is very low and potassium (once acid base status is restored)
5) Flunixin meglumine (Banamine) to decrease endotoxin and inflammation
6) B vitamins
7) Parenteral antibiotics

Question 278

How do you treat rumen acidosis

Answer 278

Mild
1) IV Fluids- hemodynamic support
2) Kingman tube- drain rumen
3) Banamine- anti-endotoxin
4) Rumen alkalinizers (Mg hydroxide)
5) Transfaunation (nx gi flora)
6) Parenteral antibiotics
7) Held off feed, including water until the rumen as emptied itself and motility is gained

Severe:
1) rumenotomy- evacuate rumen ocntents
2) Laxatives
3) Parenteral calcium (for hypocalcemia)
4) IV fluids: hypertonic saline and then balanced electrolyte solutions- add bicarbonate if pH is very low and potassium (once acid base status is restored)
5) Flunixin meglumine (Banamine) to decrease endotoxin and inflammation
6) B vitamins
7) Parenteral antibiotics

Question 279

What are some potential complications of rumen acidosis

Answer 279

-Polioencephalomalacia
-Laminitis
-Liver abscesses
-Caudal vena-caval syndrome

Long term:
-Pneumonia: aspiration
-Pulmonary arterial abscesses (hematogenous infection and pulmonary bleeding)
-Poor weight gain due to rumen wall fibrosis and inability to digest

Question 280

most common in dairy cows or feedlot steers fed energy rich TMR
cause an opportunistic infection of embolic bacterial showers- liver abscesses and caudal vena caval syndrome and endocarditis
-Chronic rumenitis (less VFA absorption)
-Perakeratosis of rumen mucosa

Answer 280

Subacute/Chronic Ruminal Acidosis (SARA)

Question 281

What can subacute to Chronic Rumen acidosis lead to

Answer 281

-High incidence of Displaced abomasums
-Lameness; acidosis induced laminitis
-Poor milk production
-Fluctuating feed intake
-Milk fat depression
-Diarrhea

Question 282

How do you diagnose subacute to chronic rumen acidosis

Answer 282

Diagnose herd by smapling several cows for rumen pH (Ruminal aspirate 2-4 h post feeding if fed grain, 6-8 post feeding if fed TMR
Multiple cows with pH is below 5.5 diagnostic

Question 283

If multiple cows with a pH below __________ you can diagnose the herd with subacute to chronic rumen acidosis

Answer 283

below 5.5

Question 284

what is haybelly

Answer 284

-consumption of forages with too little readily fermentable carbohydrates
-overwintered beef cows
-young weaned calves on poor forage diet
-equates to protein/energy malnutrition
-Form of obstructive indigestion (caused by fermentation)

Question 285

-consumption of forages with too little readily fermentable carbohydrates
-overwintered beef cows
-young weaned calves on poor forage diet
-equates to protein/energy malnutrition
-Form of obstructive indigestion
-become stunted- recumbent

Answer 285

Hay belly

Question 286

What kinds of cows get haybelly

Answer 286

1) Animals eating forages with too little readily fermentable carbs
2) Overwintered beef cows
3) young weaned calved on poor forage diet

Question 287

What is the pathogenesis of haybelly

Answer 287

1) Overconsumption of poor fermented diet: decreased availability of soluble CHO leading to decreased fermentation rate, reduced VFA, increased pH, rumen retention of feed material and decreased population of fermenting bacteria -> rumen overfills

2) Excess accumulation of rumen contents- decreased primary cycle activity -> rumen stasis with large accumulation of fibrous feed -> chronic recurrent bloat

Question 288

What are the clinical signs of Haybelly

Answer 288

-Body condition loss
-Abdominal distension (papple shape)
-Firm.doughy rumen consistency throughout the left abdomen
-scant, dry feces
-normal vital signs
-gradually progressive weakness
-recurrent bloat

Question 289

In Haybelly, the rumen fluid will be
pH:
Color:
NMB:
Protozoa:
Consistency:
Sedimentation:

Answer 289

pH: elevated (at or above 7)
Color: Brown color
Odor:
NMB:prolonged
Protozoa: Reduced
Consistency: watery
Sedimentation: rapid

Question 290

Abomasal reflux

Answer 290

internal vomiting,
very common in ruminant
abomasum into the rumen

Question 291

Rumen vomiting

Answer 291

large scale regurgitation
uncommon

Question 292

What causes vomiting in ruminants

Answer 292

1) Rumen overfilling (obstructive -vagal-indigesting)
2) Feed-toxic plants:azalea, rhododendron, sneezeweed (helenium), spoiled feedstuffs
3) Orogastric intubation- gag reflex (not nasogastric intubation)
4) Lateral recumbency- as rumen fills, there can be vomiting- milk fever, general anesthesia, restraint procedures

Question 293

What toxic plants cause vomiting in ruminants

Answer 293

azalea, rhododendron, sneezeweed (helenium), spoiled feedstuffs

Question 294

Does nasogastric intubation cause vomiting

Answer 294

No- but orogastric does

Question 295

Does orogastric intubation cause vomiting

Answer 295

Yes- but nasogastric intubation does not

Question 296

What occurs at the caudal 20% of the C3 in camelids ?

Answer 296

HCl secretion from the gastric glands

Question 297

Abomasal ulcers are multifactorial. what are some etiologies

Answer 297

-Viral infections (BVDV-MD, MCF)
-Bacterial infection (C.perfringens type A- calves stress)
-Reduced perfusion (relative to udder, fetus)
-Lymphoma (tumor -> bleeding)
-Abrasive roughage (trauma)

Question 298

Where do you see abomasal ulcers in adults

Answer 298

ulcers commonly in the fundic region

Question 299

Where do you see abomasal ulcers in calves

Answer 299

ulcers are commonly in the pyloric antrum

Question 300

What are some risk factors for adult cattle developing abomasal ulcers

Answer 300

-High energy, finely ground diets (low pH)
-Fresh cows 30-40DIM (negative energy balance, periparturient diseases)
-LDA (especially chronic)
-Cows in peak milk (udder perfusion relative to abomasum)*
-NSAID use: prostaglandins important to mucosa layer

Question 301

What are some risk factors for calves developing abomasal ulcers

Answer 301

-mineral deficiencies (Copper)
-Trichobezoars
-Consuming sand, bedding
-Feeding large volumes of milk in 2 feedings/day

Question 302

Abomasal ulcers that are asymptomatic and cause mild to moderate anorexia. have failure to consume grain, bruxism, decreased rumen motility, poor weight gain (calves)
mild decrease in PCV and TP
positive fecal occult blood test

Answer 302

Type I abomasal ulcer

Question 303

What are the different types of abomasal ulcers

Answer 303

Type I: asymptomatic and cause mild to moderate anorexia. have failure to consume grain, bruxism, decreased rumen motility, poor weight gain (calves)
mild decrease in PCV and TP, positive fecal occult blood test

Type II: non-perforating, hemorrhage- moderate to severe anorexia, decreased rumen motility, bruxism, pale mucous membranes, tachycardia, melena (if severe). Moderate to severe decrease in PCV and TP. positive fecal occult blood test

Type III: perforating, local peritonitis. total anorexia, absent rumen motility, tachycardia, fever, cranial abdominal pain (ddc TRP), colic- hyperfibrinogenemia, leukopenia, mild-moderate peritoneal effusion (exudate)

Type IV: perforating, diffuse peritonitis- causing total anorexia, absent rumen motility, tachycardia, fever, severe dehydration/shock, recumebent, severe pain/colic. shows hypergibrinogenemia, severe leukopenia and severe peritoneal effusion (septic exudate)

Question 304

abomasal ulcers where non-perforating, hemorrhage causing moderate to severe anorexia, decreased rumen motility, bruxism, pale mucous membranes, tachycardia, melena (if severe). Moderate to severe decrease in PCV and TP. positive fecal occult blood test

Answer 304

Type II abomasal ulcer (non-perforating, hemorrhage)

Question 305

abomasal ulcers where perforating, local peritonitis. total anorexia, absent rumen motility, tachycardia, fever, cranial abdominal pain (ddc TRP), colic- hyperfibrinogenemia, leukopenia, mild-moderate peritoneal effusion (exudate)

Answer 305

Type III abomasal ulcer- perforating, local peritonitis

Question 306

abomasal ulcers where perforating, diffuse peritonitis- causing total anorexia, absent rumen motility, tachycardia, fever, severe dehydration/shock, recumebent, severe pain/colic. shows hypergibrinogenemia, severe leukopenia and severe peritoneal effusion (septic exudate)

Answer 306

Type IV: abomasal ulcer: perforating, diffuse peritonitis

Question 307

peptic ulcers in camelids that most commonly occur at the pylorus and into the cranial duodenum.
risk factors: stress, high grain diet, nsaids, concurrent disease, ileus
signs: variable- hyporexia/anorexia, mild colic (legs extended at cush), recumbency (acute perforation)

Answer 307

C3 ulcers in camelids

Question 308

C3 ulcers in camelids

Answer 308

peptic ulcers in camelids that most commonly occur at the pylorus and into the cranial duodenum.
risk factors: stress, high grain diet, nsaids, concurrent disease, ileus
signs: variable- hyporexia/anorexia, mild colic (legs extended at cush), recumbency (acute perforation)

Question 309

a neoplasia within the abomasum that may/may not be associated with BLV- causes disruption of mucosal integrity and ulcer development

Answer 309

lymphosarcoma

Question 310

5% of BLV infected cows

Answer 310

develop lymphosarcoma in the abomasum

Question 311

How do you treat/prevent abomasal/C3 ulcers

Answer 311

1) Diet change: remove silage, high moisture corn for at least 14 days
2) Coating agents (Kaopectate )
3) Pantprazole (PPI) and Ranitidine (oral H2 antagonist)
4) Transfusion (severe anemia)
5) Aminocaproic acid to maintain clots
6) Antibiotics (periotnitis)- poor prognosis

Question 312

Kaopectate is a _______ use to treat _________

Answer 312

coating agent used to treat abomasal/C3 ulcers

Question 313

What is a coating agent that you can use to treat abomasal/C3 ulcers

Answer 313

Kaopectate

Question 314

What should you give to reduce the acidity in treating abomasal/C3 ulcers

Answer 314

Pantoprazole (proton pump inhibitor)
Ranitidine (oral in preruminants): H2 antagonist

Question 315

Pantoprazole is a _______ used to ___________

Answer 315

proton pump inhibitor used to reduce acidity in treating abomasal/C3 ulcers

Question 316

Ranitidine is a _______ used to ___________

Answer 316

H2 antagonist used to reduce acidity and helps to treat abomasal/C3 ulcers

Question 317

Aminocaproic acid is used to:

Answer 317

maintain clots in abomasal/C3 ulcers

Question 318

What causes abomasal tympany

Answer 318

Clostridium perfringens type A
-a commensal that when overgrown increases alpha toxin and phospholipase causing the lysis of RBCs, leukocytes, endothelial damage and the necrosis of the intestinal mucosa

Question 319

What is the pathogenesis of Clostridial Abomasitis

Answer 319

Clostridium perfringens type A, a commensal that when overgrown increases alpha toxin and phospholipase causing the lysis of RBCs, leukocytes, endothelial damage and the necrosis of the intestinal mucosa

*Typically calves 2-6 weeks, beef calves, and lambs that are mild-fed and rapidly growing

Question 320

Clostridial Abomasitis typically affects

Answer 320

Typically calves 2-6 weeks, beef calves, and lambs that are mild-fed and rapidly growing

poor milk hygiene, large volume feeding

MR with high CHO/protein, increasing % TS

Question 321

Clostridial Abomasitis

Answer 321

Clostridium perfringens type A, a commensal that when overgrown increases alpha toxin and phospholipase causing the lysis of RBCs, leukocytes, endothelial damage and the necrosis of the intestinal mucosa

*Typically calves 2-6 weeks, beef calves, and lambs that are mild-fed and rapidly growing

Signs: acute bilateral bloat, anorexia, rapidly progressive dehydration and shock, succussible fluid and variable pings throughout the ventral abdomen

Question 322

How do you diagnose Clostridial Abomasitis

Answer 322

ultrasound
fecal/abomasal fluid smear (GP rod overgrowth)

Question 323

How do you treat Clostridial Abomasitis

Answer 323

treatment: relieve distension, Penicillin, IVF/supportive care, antitoxin? -debatable (cross protection)

Prevention: vaccine (Type A toxoid) has unknown efficacy)

Question 324

What do Suffolk sheep have

Answer 324

abomasal motility disorder resulting in abomasal impactions

Question 325

Primary abomasal impaction is caused by

Answer 325

some sort of fibrous feed with dehydration, pica, sand, rocks, idiopathic

Question 326

Secondary causes of abomasal impaction are more common. What are their causes

Answer 326

1) Pyloric outflow obstruction
2) Vagal nerve injury
3) Adhesions (calves with peritonitis from ulcer
4) LSA

Question 327

What is the most common displacement

Answer 327

Left Displaced Abomasum

Question 328

What is the peak occurence of abomasal dispalcement

Answer 328

Peak occurence is 1st 6 weeks of lactation
Any DIM, (bulls and calves)

-RDA is often later in lactation (adults)

Question 329

What kind of abomasal displacement for preweaned calves typically get

Answer 329

RDAs

Question 330

What is likely the cause of abomasal displacement

Answer 330

*Multifactorial
-Excess production of VFA (silage, HMC)
-GI stasis caused by metabolic or infectious disease
-Decreased feed intake around calving
-Deep body capacity (modern dairy cow genetic selection)
-Factors lead to abomasal stasis, gas, reduced rumen fill

Question 331

What are the risk factors for development of LDA

Answer 331

-Hypocalcemia (ileus and last of motility)
-High concentrate diet
-Low forage diet
-Finely ground feed
-Low rumen fill (less forage)
-Infectious/inflammatory disease (post parturient) such as mastitis, ketosis, metritis/RP, indigestion- reduce rumen fill and increase risk of endotoxemia

Question 332

What are the clinical signs of LDA

Answer 332

*Acute decrease in milk production (30-50%)
-Decreased appetite for TMR/silage
-Rumen monitors (bolus): indicate decreased rumination time before dx of a ping
-Tympanic resonance “ping” on left
Ballottement -> succession on the left (mild)
atrial fib

Question 333

How do you tell the rumen from a DA

Answer 333

-Location (DAs can be variable
-rectal (rumen fill tells you its not a rumen ping with it being empty)
-US
-Bloodwork
-Tube test (if passed through esophagus and you listen to ping, if it sounds the same after blowing into tube. if it doesnt then the ping is from something else besides rumen)

Question 334

What are the physical exam findings of a right displaced abomasum/volvulus

Answer 334

dull, moderate to severely dehydrated
tachycardia
rumen hypomotility
rtmpanic resonance “ping” on the right- extend to 8th or 9th ICS
Ballotement -> succession on R (often large)
RDA/RVA palpable on rectum
Aciduria
Arrhythmias

Question 335

RDA usually results in _____________

Answer 335

damage to the vagal nerves (lie on the lesser curvature

comprised vessels is a surgical emergency

Question 336

with ruminant GI obstructive disease you see a _____chloremic, ______kalemic metabolic _________

Answer 336

hypochloremic (low Cl-)
hypokalemic (low K+)
metabolic alkalosis

Question 337

Does LDA result in mild or severe changes on blood work)

Answer 337

mild to moderate change

*partial obstruction

Question 338

Does RDA result in mild or severe changes in bloodwork

Answer 338

severe changes in blood work
*complete obstruction

Question 339

What does RVA result in

Answer 339

tissue necrosis and shock (mixed acid base)

Question 340

What is abomasal reflux

Answer 340

-hydrochloremic acid retention into the forestomach (mechanical/function)

caused by partial/complete obstruction (DA, LSA) and ileus (indigestion, pain)

causes dehydration, increased rumen HcL >30mEq), metabolic acidosis

Question 341

What is a potential sequelae to abomasal reflux

Answer 341

metabolic alkalosis will tend to decrease bone resportion (iCa) and hypocalcemia in fresh cows may be subclinical

Question 342

What is paradoxical acuduria

Answer 342

when you have a ruminant with hypochloremic metabolic alkalosis

-kidney wants to save Na+ (correct dehydration)
Cl- is low so bicarbonate is reabsorbed)
-H+ will be exchanged for Na+ because K+ is low (distal tubule)

*Both processes potentiate aciduria and systemic alkalosis

Question 343

Paradoxical aciduria is a result of the kidney wanting to ________ so H+ is exchanged for ______ because ______ is low in the distal tubule

Answer 343

Kidney wants to save Na+ to correct the dehydration, Cl- is low so bicarbonate is reabsorbed (anion), H+ will be exchanged for Na+ because K+ is low (distal tubule)
Both processes potentiate aciduria and systemic alkalosis

Question 344

How do you treat LDA

Answer 344

1) Rolling (most successful in calves)
2) Rolling and blind tack (toggle pin abomasopexy)
3) Right flank omentopexy or pyloro-omentopexy
4) Right paramedian abomasopexy (preferred if ulcers)
5) Left flank abomasopexy

Question 345

How do you treat RDA/RVA

Answer 345

right flank omentopexy or pylor-omentopexy

Question 346

How do you perform Roll for blind toggle/tack

Answer 346

1) cast cow on the right and roll into dorsal recumbency
2) Percussion used to confirm the abomasum location
3) Trocar and suture push rod to introduce toggle suture
4) Roll cow to left side before getting her up

*High chance of failure but very cheap to perform, can develop peritonitis

Question 347

Right Paramedian Abomasopexy (LDA)

Answer 347

cast cow on the right and roll into dorsal recumbency
surgical approach to abomasopexy
preferred approach if there is a concern of abomasal ulcers

Question 348

What is the best approach to fix a LDA if there is concern of abomasal ulcers

Answer 348

Right Paramedian Abomasopexy

Question 349

What are some complications of displaced abomasum correction

Answer 349

1) reoccurence (most common with blind toggle
2) Abomasal fistula- develop secondary to abomasopexy
associated with intraluminal suture placement- unintentinal (surgical) or intentional (blind)
-abomasal contents leak and incision line breaks down -> mucosa prolapse
severe hemorrhage can development

tx: intensive supprotive care, surgical resection

prognosis: depends on size of fistula, but considered guarded

Question 350

Abomasal ulcers vary in their clinical presentation and prognosis by the __________

Answer 350

degree of hemorrhage and perionitis

Question 351

pyloric outflow obstruction (mechanical and functional) in ruminants causes

Answer 351

characteristic changes in acid base status
Hypochloremic, hypokalemic metabolic alkalosis

Question 352

LDA development is multifactorial however factors associate with _______________, ________________, and _______________ increase the risk of abomasal atony and gas production

Answer 352

diet,
concurrent disease,
lactation status

Question 353

Diagnosis of an RDA requires

Answer 353

immediate surgical intervention

Question 354

Intestinal accidents (cecal distension or volvulus, intussusception- small intestine, mesenteric volvulus, and intestinal incarceration)
are __________ common than abomasal issues

Answer 354

less

Question 355

What might cause hemorrhagic bowel syndrome (HBS)

Answer 355

Clostridium perfringens Type A in adult dairy cattle

blood clots and acts as an obstruction

Question 356

What are the physical signs used to diagnose GI obstruction

Answer 356

1) Abdominal distension
2) Colic- stretching or damge to the mesentery
3) Hydration status
4) Fecal changes

Question 357

What is colic normally accredited to in cattle

Answer 357

-Urinary problem (ie obstruction)

-Uterine (ie torsion)

*Unusual to get the GI diseases that cause colic but it can happen

Question 358

How do you treat GI obstruction

Answer 358

fluid imbalances
ideally fluid composition based on measured values but commonly need to provide fluids without measurements
important to understand the most common fluid electrolyte imbalances

-Chlorie-rich fluid sequestion, dehydration and metabolic alkalosis with hypochloremia and hypokalemia

Question 359

What are the blood biochemical changes of GI obstructive disorders

Answer 359

1) Decreased Cl-: abomasal secretion, sequestration

2) Increased HCO3 (metabolic alkalosis)- varies with changes in Cl-, strong ions

3) Decreased K+ (alkalosis- redistribution, GI loss, decreased consumption, and renal loss)

4) Increased creatine, Increased plasma protein (dehydration, pre-renal azotemia)

5) Decreased Ca2+ (decreased absorption, alkalosis-decreased ionized)

6) Decreased Na+ (sequestration, ongoing losses, decreased intake)

7) Increased PO4 (GI vs renal excretion, variably elevated)

8) Ketosis- depends on glucose demands

Question 360

What dictates the degree of fluid change in GI obstructions

Answer 360

Site of obstruction (proximal is more profound vs distal)

Duration of obstruction- acute vs chronic

Extent or degree of obstruction- partial vs complete

Strangulation of bowel- inflammatory mediators

Question 361

Ileus with gram - infections of mammary gland or uterus can

Answer 361

produce a hypochloremic, hypokalemic metabolic alkalosis

Question 362

Why do baby ruminants not follow the pattern of alkalotic blood biochemical change

Answer 362

they are not ruminants yet

Question 363

Does rectal prolapse occur more frequently in fat or skinnier animals

Answer 363

fat- perineal/perirectal fat loosens up the connection

Question 364

Why might you commonly get rectal prolapse in sheep

Answer 364

Lax perirectal musculature due to docking the sheep’s tail too short

Question 365

What are factors that increase the incidence of rectal prolapse

Answer 365

1) fat animals- perineal/perirectal fat

2) Lax perirectal musculature from tail docking too short

3) Tenesmus, increased abdominal pressure from pneumonia (coughing), urinary irritation/obstruction

Question 366

What might result in tenesmus and subsequent rectal prolapse

Answer 366

*Increased abdominal pressure from 1) pneumonia (coughing)
2) Urinary irritation/obstruction in castrated males
3) Enteritis/coocidiosis

Question 367

What should you do when you assess rectal prolapse

Answer 367

-Evaluate size of prolapse
-Tissue integrity- viable vs necrotic
-Conservative treatment: replace prolapse, suture in place (pursestring suture) or create adhesions to retain tissue (Perirectal sclerosing agent)
must also mitigate tenesmus,
-tissue removal: use aprolapse ring- strangulate tissue and surgical removal

Question 368

a congenital anomaly where there is failure to connect rectum to the anal orifice

Answer 368

atresia ani

Question 369

a symptomatic congenital anomaly except for when the ventral hernial sac prominently is observed and may lead to entrapment

Answer 369

Umbilical herniation

Question 370

a congenital anomaly where there is the failure to form the patent spiral colon
clinical signs include no feces, progressive abdominal distension, decreasing appetite and increasing depression over several days

Answer 370

Atresia coli

Question 371

Crypt cells _____ then migrate to the __________

Answer 371

divide and then slowly migrate towards to villus

Question 372

What digestive enzymes do enterocytes have

Answer 372

lactase
maltase
peptidases

Question 373

How long does it take for the enterocytes to migrate from the crypt to the tip of the villus

Answer 373

5 to 7 days to replenish themselves

Question 374

Mucosa in the intestine acts as a

Answer 374

barrier against bacteria, viruses, antigens, toxins, endotoxin (LPS), and chemicals

Question 375

How might liver problems contribute to wider spread of normal pathogens in the GI lumen

Answer 375

Kuppfer cells (macrophages) clear portal venous bacterian and viruses. Hepatocytes detoxify noxious chemicals

*Protection of other organ systems from toxins, bacterial invasion
prevent gut origin bacteria from translocating to other organs

Question 376

What is a pathogen that causes secretory diarrhea

Answer 376

Enterotoxigenic E coli (ETEC) in ruminants - k99

Question 377

At what age does secretory diarrhea from ETEC-k99 typically affect neonates

Answer 377

Less than 7 days, sometimes up to 10 days

next generation of enterocytes in the GI do not have the k99 receptor

Question 378

T/F: ETEC k99 only affects neonatal ruminants and swine

Answer 378

true

Question 379

What kind of diarrhea does ETEC cause

Answer 379

Secretory

Question 380

What is the pathogenesis of ETEC

Answer 380

-Attach to enterocyte receptors
-Hijack normal cellular activity via enterotoxin to, activate cAMP to open Cl- channels to release Cl- into lumen. causing loss of Na, H20 and HCO3-

Question 381

What is loss into the lumen with secretory diarrhea

Answer 381

Cl- loss and following loss of:
Na+
H20
HCO3-

Question 382

What will the pH of purely ETEC diarrhea be

Answer 382

neutral ph: 7.4 to alkaline because of the loss of bicarbonate into the lumen

Question 383

What kind of diarrhea is Rotavirus

Answer 383

Malabsorptive Diarrhea

Question 384

What kind of diarrhea is Coronavirus

Answer 384

Malabsorptive diarrhea

Question 385

What kind of diarrhea is caused by Cryptosporidium

Answer 385

Malabsorptive Diarrhea

Question 386

Does coronavirus typically infect older animals or younger animals

Answer 386

older animals

Question 387

__________ is a virus of ruminants, swine, and horses that is ubiquitous and causes disease when concentrated

Answer 387

Rotavirus

Question 388

What are some common causes of malabsoportive diarrhea

Answer 388

-Rotavirus
-Coronavirus
-Cryptosprodium

Question 389

transmissible gastroenteritis virus (TGE) and porcine epidemic diarrhea virus are kinds of

Answer 389

coronaviruses

Question 390

What kind of species can get cryptosporidium

Answer 390

ruminants and crias
-typically dairy calves

Question 391

TGE is a diarrhea disease that also has

Answer 391

vomiting

Question 392

What is the pathogenesis of rotavirus

Answer 392

-Attacks the mature enterocytes on the villus tips.
-Virus then enters these cells and replicates
-Viral particle load gets so large that it ruptures, releasing more viruses to infect other mature enterocytes
-Villi smooth muscle contracts when the epithelium is lost
-Viruses pass out in the feces to find another host
-MALABSORPTIVE DIARRHEA

Question 393

What is the protective mechanism when the epithelium is lost due to Rotavirus infection

Answer 393

the villi smooth muscle contracts to limit the surface area potential for pathogens to be translocated

Question 394

What is the pathogenesis of coronavirus

Question 395

What part of the enterocytes does coronavirus target

Answer 395

at the tips and maturing enterocytes and on the villi
-Viral particle load gets so large that it ruptures, releasing more viruses to infect other mature enterocytes
MALABSORPTIVE DIARRHEA
More mucosal loss, more villous blunting and malabsorption/maldigestion
*More milk nutrients into the colon and more fermentation in the large intestine- more inflammatory infiltrate because a greater cell loss and more severe diarrhea

Question 396

is coronavirus or rotavirus infection more severe

Answer 396

Coronaviral

*More villous blunting and malabsorption/maldigestion
*more milk nutrients into the colon leading to more fermentation. more inflammatory influltrate leading to greater cell loss and more severe diarrhea

Question 397

What part of the intestines does rotavirus hit the hardest

Answer 397

the small intestine- lesions evident from duodenum down to the ileum

Question 398

How does malabsorptive diarrhea lead to metabolic acidosis

Answer 398

VFAs are generated via fermentation of undigested nutrients- osmotically active
-Pull water into colon lumen, resulting in diarrhea
-Colonic bacteria make both D and L isomers which D isnt metabolized by the liver as well and the metabolic acidosis is harder to correct
-Fecal pH tends to be acidic

Question 399

What is the pH of the feces when malabsorptive diarrhea is occuring

Answer 399

Acidic -organic acids produced in the large colon

Question 400

What does rotavirus diarrhea look like

Answer 400

yellow or white watery diarrhea
-feces may bubble once passed, owing to continued fermentation and liberation of gas bubbles.
looks like cooking pancakes

Question 401

Is the primary pathologic process in rotavirus due to malabsorption or inflammation

Answer 401

malabsorption

-there is some inflammation as the cells are disturbed but malabsorptive causes most of the tissues

Question 402

What is the pathogenesis of Cryptosporidiosis

Answer 402

Infects small intestinal cells in an endocytic vacuole under the luminal membrane of enterocytes
-Disrupts the function of the brush border causing maldigestion and malabsorption of nutrients
-Triggers cell-mediated immune response inducing cytokine release which causes
-Villous blunting- worsens malabsorption
-Inflammatory changes in gut wall

Question 403

What part of the intestine does cryptosporidiosis impact

Answer 403

jejunum and ileum is hit
-lesions can extend orad into duodenum and aborad into the colon

Question 404

What are the causes inflammatory diarrhea

Answer 404

1) Clostridial enteritis (Clostridium perfringens/over eating disease/ intestional clostridiosis) *Any age, any animal

2) Salmonellosis (S. enterica >2000 serotypes) *Any age, any animal

Question 405

What are the more pathogenic strains to the intestine of Clostridium perfringens

Answer 405

Type C and D - less prevalent in normal gut flora but more pathogenic

Type A- more abundant part of normal flora but pathogenic strains exist

Question 406

What allows C. perfringens to proliferate in the intestines

Answer 406

high starch, sugar, or protein content in the small intestine
“Overeating disease” - rich diet, higher content of intestinal starch, sugar, and protein - exotonix production

Question 407

What is the pathogenesis of Clostridial Enteritis

Answer 407

1) Ingestion of lots of spores or ingestion of lots of starch/sugar/protein (milk, protein supplements like soybean meal or lush grass) this allows substrate for proliferation of C. perfringens

2) Typically type C produce potent exotoxins (phospholipase and beta toxin) that destroy all enterocyte cell types
Bloody contents in diarrhea

Question 408

Why is the intestine of a neonate an ideal spot for C. perfringens type C

Answer 408

-Anaerobic environment
-Not a lot of competitive microflora established yet
-Warm
-Lots of nutrients (milk)

Question 409

How does Clostridium perfringens type C differ from type D when it comes to clostridial enteritis

Answer 409

C. perfringens type D acts differently as its episilon toxin is absorbed and acts on distant organs to cause nedothelial cell death and edema of multiple tissues and organs

C. perfringens type C results in cranberry contents of cranberry crap. critters crash. alpha and beta toxins kill enterocytes

Question 410

C. perfringens type D causes

Answer 410

Edema and endothelial damage through epsilon toxin increasing vascular permeability of distant organs through endothelial damage

edema of brain can cause terminal opisthotonus and convulsions

pulpy kidney

Question 411

What is the pathogenesis of Salmonellosis

Answer 411

-Invade gut wall
-Triggers massive inflammatory response
-sheds LPS during cell division and death amplifying the local inflammation
* Profound PLE and endotoxemia
*Sometimes bloody diarrhea

Question 412

What part of the intestine does salmonella infect

Answer 412

Enterocolitis- small intestine, cecum, and large intestine can be infected

Question 413

What kind of diarrhea cause also causes profound PLE

Answer 413

Salmonellosis

Question 414

When does ETEC K99 typically affect calves

Answer 414

0 to 5-7 days

Question 415

When does Salmonella typically affect calfs

Answer 415

5-14 days, anytime

Question 416

When does Rotavirus typically affect calfs

Answer 416

5-14 days

Question 417

When does coronavirus typically affect calfs

Answer 417

1 week to 1 month

Question 418

When does Cryptosporidium typically affect calfs

Answer 418

1 to 4 weeks (5-28 days)

Question 419

When does Giardia typically affect calfs

Answer 419

2 weeks to 2month

Question 420

When does BVDV typically affect calfs

Answer 420

first month, anytime

Question 421

When does coccidia (Eimeria) typically affect calfs

Answer 421

after the first month

Question 422

If the signalment is an ill neonate, what do you need to rule out, even if it is not mentioned as the chief complaint

Answer 422

Diarrhea

Question 423

What are proctitis, vulvitis, and perineal dermatitis all consistant with?

Answer 423

Diarrhea

Question 424

How might vulvitis affect the findings of a free catch urinalysis

Answer 424

might have bacteria and WBC from the vulva instead of the urine

Question 425

What are the clinical signs of neonates with diarrhea
*Know this

Answer 425

1) Diarrhea
2) Dehydration
3) Metabolic acidosis
4) Reduction in appetite
5) Hypothermia

Less consistent, not every case
6) Septicemia/ endotoxemia
7) Electrolyte imbalance

Question 426

What are some clinical signs of calves with diarrhea

Answer 426

-Weakness or recumbency
-Skin tent persist >2sec
-Orbital recession
-Dry mouth
-Tachycardia from hypovolemia

Question 427

How do you measure dehydration in ruminants

Answer 427

Measure the eyeball recession
Multiple by 2
The resulting value is the % of the body fluid that was lost

Question 428

A calf has a gap between the lower palpebral edge to corneal surface that is estimated to be at 5mm. How dehydrated are they

Answer 428

10% dehydrated

Question 429

Metabolic acidosis seen in diarrhea causes

Answer 429

poor cardiovascular performance
recumbency and inability to stand, ataxic, drunken gait, incoordination

Question 430

How do you know how much bicarbonate to give to address the metabolic acidosis caused by diarrhea

Answer 430

look at their clinical signs assessing metabolic acidosis if they are in lateral recumbency and no suckle reflex and cold oral cavity you should give 20mEq/L.
However, ifthey only show weak symptoms you might give less

Question 431

What kind of diarrheas are septicmeia/endotoxemia more common in

Answer 431

inflammatory diarrheas as mucosal loss and gut wall inflammation increase the uptake of the bacteria and toxins into the portal blood. If translocation is excessive, it overpowers liver iltering

Question 432

How do you tell the difference between septicemia and endotoxemia

Answer 432

it is very difficult to do on the basis of clinical signs. you need a blood culture to tell the difference

Question 433

in cases of neonatal diarrhea when are Na and Cl concentrations impacted

Answer 433

okay for 1-2days

Low Na,Cl in ECF 3-4days (milk has low amounts)

there can be mixing errors in oral electrolyte replaces when excess salt force fed

Question 434

Acidosis may trigger and efflux of ___________ from the ___________ causing potentially life threatening condition

Answer 434

efflux of potassium (and H+) from the intracellular fluid causing concurrent potentially life threatening hyperkalemia and bradycardia

Question 435

What is the SHADES mneumonic for neonatal diarrhea

Answer 435

Septicemia
Hypoglycemia
Acidosis
Dehydration
Electrolyte imbalance
Suffocation (birth hypoxia)

Question 436

What is your #1 priority when dealing with diarrhea in a neonate

Answer 436

Fluid therapy- restore normal hydration status, replete lost electrolytes, correct any hypoglycemia, and correct metabolic acidosis

Question 437

How many liters of fluids should you give a calf that is 40kg and 10% dehydrated
(determined as there was 5mm recession of globe (10% dehydrated)

Answer 437

Fluid deficit: 40 x 0.1 = 4L of fluid deficit

*if recumbent give IV fluids

Question 438

How do you determine normal maintenance fluid needs

Answer 438

70ml/kg/day
(or 3-4ml/kg/hour which is 72ml/kg/day)

ex: 40kg x 70ml/kg/day =2800ml

Question 439

70ml/kg/day

Answer 439

Maintenance fluid needs

Question 440

How can you estimate the ongoing fluid losses (volume of diarrhea)

Answer 440

Weight the animal daily to tract it.

Question 441

How will fluids be given to the diarrheic neonate

Answer 441

Standing + intact suckle response -> do oran rehydration therapy (ORT)

Recumbent/weak, poor suckle response or severe dehydration -> do IV fluid therapy to resuscitate then ORT until diarrhea resolves

*Subcutaneous/IP fluids: may not be well-perfused if severely dehydrated

Question 442

Why might you not give subcutaneous or intraperitoneal fluids for diarrheic neonate

Answer 442

-Might cause damage
-Hypoperfused tissue to the subcutis when dehydrated

Question 443

What does adding glucose/glycine to fluids do

Answer 443

they are co-transported with sodium from the gut lumen across the brush border. this enhances sodium absorption from the gut and water will follow
Dextrose is the D-isomer of glucose.
also helps correct any hypoglycemia that may exist

Question 444

What is the D-isomer of glucose called

Answer 444

Dextrose
added to fluids to enhance sodium and water reabsorption through co-transportation

Question 445

WHat are the ingredients in oral rehydration therapy

Answer 445

-Water
-Na+
-Cl-
-K+
-glucose
-NAHCO3/sodium acetate to become bicarbonate in liver

Question 446

Oral Rehydration therapy

Answer 446

use when the animal has intact suckle response and standing
-Nipple bottle or esophageal feeding tube
-Must feed them milk to try to meet caloric nutrient needs
-Aim for 10% of bodyweight in milk to maintain (40kg- do 4L)
-dont mix ORT with milk
-bicarb will impair milk clot formation in abomasum (needs acid and Ca2+)
-Alternate milk/ORT q6-8h
-“milk in morning, lytes at night”

Question 447

Why shouldnt you mix ORT with milk,
what should you do instead?

Answer 447

Bicarb will impair milk clot formation (needs acid and Ca2+)

Alternate milk/ORT q6-8h “milk in morning, lytes at night”

Question 448

How do you determine how much Na bicarbonate a calf needs to correct its metabolic acidosis

Answer 448

Bodyweight (kg) x 0.5L/kg x base deficit mEq/L (estimated)
0.5 for neonates
0.3 for adults

ex: 20mEq/L x 0.5L/kg x 40kg - 400mEq of bicarbonate needed to correct acidosis

give as 1/3 or 1/2 and then re-assess

Question 449

What might grossly tell you that a patient is acidotic

Answer 449

bradycardia in a patient that you think would be tachycardic

(hypovolemia normally increases heart rate) but efflux of K+ decreases the heart rate

Question 450

When should you use antimicrobial drugs in neonatal diarrhea

Answer 450

-If signs of inflammatory diarrhea
-If signs of septicemia/toxemia
-if failure of passive transfer is suspected or documented
-If ETEC infection is strongly suspected (oral antibiotic)

Question 451

If you have a neonate with diarrhea and showing signs of sepsis/endotoxemia
What antimicrobial should you use

Answer 451

-Ampicillin or ceftiofur: reasonable gram - spectrum, safe

Question 452

Why are aminoglycosides not a good choice for the treatment of neonates with diarrhea

Answer 452

nephrotoxic- dehydration increases the risk and prolonged renal residues. not a good choice

Question 453

Why should you never use fluoroquinolones on food animals

Answer 453

legal restrictions on food animals. cartilage toxicity risk- also no

Question 454

Why shouldnt you use oxytetracycline for the treatment of neonatal diarrhea

Answer 454

they are bacteriostatic, you want a bactericidal agent because the neonate immune system isnt good

Question 455

Why do you want a parenteral antimicrobial for the treatment of patients with systemic sepsis

Answer 455

because an injectable is fast to get high plasma levels of antimicrobials

Question 456

What are the clinical signs of sepsis or endotoxemia, warranting antimicrobial use

Answer 456

fever
scleral injection
petechiation
blood or mucosal tags in feces
increased fibrinogen concentration
inflammatory leukogram

Question 457

When are oral antibiotics indicated for use in calves with diarrhea

Answer 457

for ETEC candidates (under 1 week of age)

use oral ampicillin, amoxicillin, sulfonamide, or trimethoprim-sulfa

Question 458

How should you treat clostridial enteritis

Answer 458

may want to treat both orally and systemically with penicillin

Question 459

Should you use oral antimicrobials for the treatment of salmonellosis

Answer 459

antimicrobial resistance, might not be indicated
depends on serovar and factors

Question 460

If you have a 2-3 week old neonate that you suspect coccidiosis and show signs of inflammatoy diarrhea, what antimicrobial should you use to treat?

Answer 460

oral sulfadimethoxine

Question 461

Scenario: neonate had diarrhea and
-fever0
blood or tissue in feces
-Scleral injection
-Signs of pneumonia and umbilical infection
should you treat with an antimicrobiall?

Answer 461

Yes- make sure it is parenterally
-Ampicillin or ceftiofur (reasonable gram - spectrum and safe

Question 462

Scenario: if you have a neonate that has diarrhea and is under 1 week of age. Is antimicrobial use indicated

Answer 462

yes- it is indicated. likely ETEC
give ORAL antimicrobials
-Oral ampicillin, amoxicillin, sulfonamide, and trimethoprim-sulfa

Question 463

NSAIDs can be ______toxic if the animal is _______

Answer 463

nephrotoxic if dehydrated

*make sure hydration status is restored
*monitor for anorexia, bruxism, melena:abomasal/gastric ulcers can all occur

Question 464

T/F: Flunixin Meglumine and Meloxicam are indicated for the treatment of neonatal diarrhea

Answer 464

True- reduce discomfort, reduce inflammatory changes in the gut wall and reduce synthesis of components of the systemic inflammatory cascade

Make sure they are well hydrated or they can be nephrotoxic
also monitor anorexia, bruxism, and melena for abomasal/gastric ulcers

Question 465

What is Kaolin-pectin used for

Answer 465

bind bacterial-origins toxins and reduce their translocation across the damaged gut mucosa
may also coat and protect any ulcerated mucosa

Question 466

What is bismuth subsalicylate used for

Answer 466

bind bacterial-origins toxins and reduce their translocation across the damaged gut mucosa
may also coat and protect any ulcerated mucosa (Kaolin pectin is better at this)

Question 467

What is ditriotahedral smectite (Biopsonge) used for

Answer 467

bind bacterial-origins toxins and reduce their translocation across the damaged gut mucosa
may also coat and protect any ulcerated mucosa

Question 468

What is used in prophylaxis against gastric ulcers in foals

Answer 468

Proton pump inhibitors (omeperazole)
Histamine-2receptor blockers (ranitidine, famotidine)

Question 469

yeast metabolities and oligosaccharides that can be used to help resolve diarrhea in neonates
aim to promote the growth of beneficial gut bacteria that are not living organisms

Answer 469

Pre-biotics

Question 470

Contain a probiotic and prebiotic

Answer 470

synbiotics

Question 471

directly fed microbials such as Lactobacillus, Bacillus, enterococccus, and bididobacterium that may limit the growth and activity of pathogenic bacteria

Answer 471

Pro-biotics

Question 472

T/F oral administration of small volumes of rumen fluid from a donor ruminant may be beneficial even to the pre-ruminant neonate

Answer 472

True

Question 473

What should you do for nursing care for neonates having diarrhea

Answer 473

-Isolate from healthy animals
-Supplement heat
-Dry and out the wind
-Treat scalded skin
-Monitor for corneal ulcers

Question 474

Recumbent, depressed neonates may have a _____________ which makes them more at risk for corean scratches and ulcers

Answer 474

subnormeal corneal reflex

Question 475

What is the normal incidence of diarrhea in the herd

Answer 475

5% (dont want to be losing more than 5%)

Question 476

What diarrhea causes in neonates are considered endemic in most livestock ruminants

Answer 476

ETEC
Cryptosporidium
Coronavirus
Rotavirus

Question 477

________ of infectious agent greatly influences outcome and the degree of clinical disease

Answer 477

Dose
more severe diseases and also neonates serve as amplifiers for the diseases

Question 478

IgG in colostrum must be ingested within the

Answer 478

first 12-24 hours of life to be absorbed across the neonatal intestine

Question 479

What kind of neonates are at higher risk for developing infectious diarrhea?

Answer 479

Neonates born to 1st time mothers (heifers)
-less attentive to nursing needs of newborn
-Dystocia can induce swelling of the face, jaws, and/or tongue- once born have limited capacity to suckle

Question 480

Why do calves born to heifers have an increased risk of diarrhea

Answer 480

Neonates born to 1st time mothers (heifers)
-less attentive to nursing needs of newborn
-Dystocia can induce swelling of the face, jaws, and/or tongue- once born have limited capacity to suckle

*Need to ensure that the calf gets colostrum

Question 481

When does the gut close, making the timing of colostrum very important

Answer 481

Within 24-30 hours

make sure the calf gets colostrum by 12-24 hours

Question 482

How might dairy cows and goats have difficulty providing colostrum

Answer 482

-Poor maternal instrincts
-Large, pendulous udders and teats

Calves are provides colostrum in bottle and pulled from mother. humans responsible for this
make sure as colostrum is good culture media and equipment can be an excellent fomite

Question 483

When should you test serum or plasma of neonate to assess passive transfer

Answer 483

Must be done within 30-48 hours

> 800mg/dl: foals
1000mg/dl: crias
5.5g/dl total protein correlates to IgG of >1000mg/dl in calves, lambs, and kids

Question 484

How do you assess that antibodies were absorbed in passive transfer in calves, lambs, and kids

Answer 484

You can use a less expensive serum total protein if the neonate is hydrated***
Want >5.5g/dl- correlates to IgG >1000mg/dl

Question 485

What does a calve with >5.5g/dl serum total protein indicated

*Note: this animal is well hydrated

Answer 485

there is adequate passive transfer of antibodies
correlates to IgG >1000 mg/dl

Question 486

Single radial immunodiffusion (SRID)

Answer 486

quantitatively meausres serum IgG. for foals and crisu measurement of igG is considered best means of assessing passive transfer status.
>800mg/dl for foals
>1000mg/dl for crias

Question 487

T/F: the serum total protein concentration is considered accurate for use in calves, foals, and crias

Answer 487

False: only for use in calves, lambs, and kids

Foals and crias- need to measure IgG specifically using single radial immunodiffusion

Question 488

Is vaccination of pregnant dams with ETEC vaccine efficacious

Answer 488

yes it is effective against ETEC- because antibodies are in the gut near the time of infection- antibodies block the K99 pilus attachment

Question 489

Are toxoids (inactivated exotoxin) vaccines intended to protect against exotoxins in neonates effective

Answer 489

they are considered effective but sometimes the large milk meals can provide the genotypes of Clostridia the growth media that their proliferation and exotoxin production can overwhelm any antibody titers imparted to the neonate by colostrum

-Need to manage the animals properly
the dose of agent can be higher than the antibodies present

Question 490

Is the rotavirus vaccination effective against neonatal rotaviral diarrhea

Answer 490

not as effective as ETEC or clostridial

Colostral antibodies will wane in neonate before the susceptibility periods of rotavirus (several weeks of age)/ also strain on the farm may not be specific to the strain of the vaccine

Question 491

Is the coronavirus vaccine effective against neonatal coronavirus diarrhea

Answer 491

not as effective as ETEC or clostridial

Colostral antibodies will wane in neonate before the susceptibility periods of rotavirus (several weeks of age)/ also strain on the farm may not be specific to the strain of the vaccine

Question 492

What is the most single critical factor in environmental management for neonates raised with their dams

Answer 492

udder hygiene

Question 493

What are some critical environmental factors for preventing neonatal diarrhea

Answer 493

1) Udder hygiene of dams
2) Maternity area needs to be clean
3) Isolate diarrheic neonates instantly
4) Handle healthy neonates first and then sick ones last
5) Strict biosecurity measures
6) Rotate or increase # bedding sites
7) Rotate or increase # feeding sites
8) Clean and re-bed shelters
9) Get them sun exposure and hides from the wind
10) avoid moisture
11) Lower the stocking density
12) dont get feed mixed with waste (ie equipment used to feed vs clean)

Question 494

If neonates become ill within the first week of life. What two things should you assess

Answer 494

1) passive transfer (colostrum)
2) maternity area hygiene

Question 495

What are agents are less likely to be an endemic cause of diarrhea on a farm but lead to a greater case fatality rate, even with adequate treatment

Answer 495

-Clostridiosis (Clostridial Enteritis, Enterotoxemia)- triggered by feed change or babies ingesting a massive milk feed “Hunkered down”
-Salmonellosis
-Bovine Viral Diarrhea Virus (BVDV)

Question 496

When should you give C. perfringens type c and d toxoids?

Answer 496

Dam: during pregnancy to increase the clostridial titers for the neonates

Young ruminants: 8 weeks of age and give at 2-3 weeks for booster

Question 497

What might increase the shedding of salmonella

Answer 497

Psychological stressor
-parturition, heavy lactation or severe illness, warm weather

Question 498

T/F: Salmonella immunization is effective

Answer 498

False- very serotype specific immunity
short lived
salmonella can hide inside cells so it requires cell mediated immunity for optimal protection

no current vax offers reliable cross protection against strains

-Maybe if serotype dublin is an issue you can manage that herd specifically with it

Question 499

Is there a lot of antimicrobial resistance with salmonella

Answer 499

Yes need a culture and susceptibility
-can likely change over time as you create a selective pressure for the salmonella

Question 500

What is the source for BVD exposure

Answer 500

1) Persistently infected animals- those that become infected as fetuses (mom got it during pregnancy and the fetal immune system sees virus as self- sheds huge amounts of virus during its lifetime in all body secretions)

2) Acutely infected animals can shed the virus for several days

Question 501

What are the clinical signs of acute infection with BVD

Answer 501

Depend on host- viral strain interaction
-Can be entirely subclinical
Signs
-High fever (104-106)
-Lethargy
-Profuse diarrhea
-Virus is immunosuppressive
-Lymphoid tissues are attacked (Peyers patches, tonsils)
-Lymphopenia common
*Secondary bacterial infections are common

Question 502

How do you diagnose acute infection with BVD

Answer 502

acutely infected animals are viremic- can isolate virus from bloodstream, detect antigen or DNA in blood, skin samples

Can detect antibody increase, acute and convalescent titers)

Gross lesions at necropsy and IFA on tissues

Question 503

How do you prevent BVD

Answer 503

-Identify PIs (viral detection tests) and euthanize

-Vaccinate: MLV superior

-Do not vax pregnant as it could result in baby that is PI (fetal infection occurs before discrimination of self vs nonself

Question 504

sporozoan parasites that are host species specific spread through fecal-oral transmission
adults shed low numbers but diseased shed billions

Answer 504

Coccidia (Eimeria and Isospora spp)

Question 505

How long does it take for coccidia oocysts to sporulate in the environment

Answer 505

takes 2-5 days to sporulate to become infective.

oocysts are not motile

Question 506

What determines the disease severity of coccidia infection

Answer 506

Directly proportional to the number of sporulated oocysts they ingest

Question 507

What is the pathogenesis of coccidia

Answer 507

Denudes so much mucosa as there is little discrimination in what enterocyte they attack. They can invade cecum and colonic cells as well
Massive inflammation- inflammatory ileitis, typhlitis (cecal inflammation) and colitis
one oocyst can destroy 1 million intestinal cells

*Protein losing entropathy

Question 508

T/F: there is little inflammation for coccidiosis infection

Answer 508

False- severe inflammation
little discrimination on what enterocytes they attack

Question 509

What might trigger the clinical disease of coccidiosis

Answer 509

Dose of infective oocysts- influences my fecal/oral transmission, stocking rate, and moisture in environment

Virulence of coccidial species

Stress triggered by
1) weaning
2)processing/ handling
3) bad weather
4) Shipping
5) Introduction of new animal
6) confinement
7) concurrent infections

Question 510

What are the clinical signs of coccidiosis

Answer 510

-Diarrhea: red to rust color in severe cases

+/- mucus membrane pallor from anemia

Tenesmus- straining to defecate

Rectal prolapse

Question 511

What is the difficulty of using fecal flotation to diagnose coccidiosis

Answer 511

if recently ingested oocysts they might not be shedding oocysts

may see in healthy animals- low numbers

Question 512

Are you going to treat animals with coccidiosis?

Answer 512

Yes- use sulfonamide antibiotics (Sulfamethazine and sulfadimethoxine)
-amprolium
-IV or oral fluids to rehydrate
-NSAIDs for inflammation
-Blood or plasma transfusion for severe cases of high $ value
-Ionophores
-Decoquinate

Question 513

What is Amprolium used for

Answer 513

diluted with water
thiamine analog for the -static effect of coccidiosis

Question 514

What is Decoquinate (Deccox) used for

Answer 514

It disrupts the energy metabolism of coccidia in cattle, sheep, and goats

Question 515

What is Monensin (Rumensin) used for

Answer 515

coccidiostatic agent (Ionophore) approved for goats and cattle
improves feed efficiency and wait gain

Question 516

What is Lasalocid (Bovatec) used for

Answer 516

coccidiostatic agent (Ionophore) approved for sheep and cattle
improves feed efficiency and wait gain

Question 517

What species are ionophores like Monensin or Lasalocid toxic in?

Answer 517

Horses and camelids do not use

Question 518

What are two ionophores used to treat coccidia through static actions

Answer 518

Monensin (Rumensin)- goat and cattle
Lasalocid (Bovatec)- sheep and cattle

Question 519

Haemonchus contortus infection results in

Answer 519

Anemia, hypoproteinemia

*doesnt cause diarrhea

Question 520

Ostertagia (Teladorsagia) cause

Answer 520

abomasal inflammation and C3 compartment in camelids

inflammatory damage to the acid-secreting organ that initiates protein digestion causing
1) inflammatory protein losses
2) Maldigestion of protein

Question 521

Teladorsagia cirumcincta

Answer 521

a parasite of sheep and goats that cause
abomasal inflammation
inflammatory damage to the acid-secreting organ that initiates protein digestion causing
1) inflammatory protein losses
2) Maldigestion of protein

same as Ostertagia in cattle

Question 522

What is the infective larval stage of Ostertagia

Answer 522

L3

Question 523

Type I ostertagiosis

Answer 523

where the lifecycle is completed
abomasal damage occurs during larval (L4) development
Larvae then molt to adults that lay eggs (detected on fecal flotation)

*Target the parietal glands

Diseased animals showing heavy fecal egg counts as a result of Ostertagia laying eggs

typically weaned calves on pasture during months of moderate weather

signs: diarrhea, ill thrift, edema (protein loss), anorexia

Question 524

What causes moroccan leather lesions

Answer 524

Nodular abomasitis from type I ostertagia

-protein losing gastropathy via imparied protein digestion (less HCl) and diarrhea occurs

Question 525

Type II Ostetagiasis

Answer 525

Calves ingest # infective L3s on pasture but some adverse environmental signal tells the L4s to go into hypobiosis (hibernation in the host) typically during late fall and winter

Signal of environment tells L4 ostertagia that conditions are now favorable. all can emerge at once leading to massive destruction of gastric glands acutely

Question 526

when does hypobiosis of type II ostertagiasis occur

Answer 526

during the late fall and winter in the northern states

Question 527

Do you see higher numbers of eggs in the feces with Type I or Type II Ostertagia

Answer 527

Type I

Question 528

Does type I or II ostertagia cause acute abomasitis and massive destruction of gastric glands

Answer 528

Type II after hypobiosis is done from the emerging of L4s

Question 529

How do you diagnose Type II Ostertagiasis if there are little to none eggs in the feces

Answer 529

-Diarrhea, anorexia, hypoproteinemia
-young ruminants at the proper time of year
-Abomasal lumen pH is abnormally high (ph>5)
Damaged abomasal wall leaks pepsinogen so you good look at plasma levels

Question 530

What abomasal lumen pH is consistent with Type II Ostertagiasis

Answer 530

pH >5

Question 531

In the south, what allows the L4 to undergo hypobiosis in type II ostertagiasis

Answer 531

heat - once in fall this allows the L4 to emerge and cause acute abomasitis

Question 532

How do you treat ostertagiasis

Answer 532

1) Benzimadazoles (Fenbendazole, albendazole, oxfendazole)

2) Macrocyclic lactones (ivermectin, doramectin and maxidectin)

For type II only modern macrocyclic lactones and benzimidazoles are effective
for type I you could use any anthelminthics as long as theres no issue with resistance

Supportive care: NSAIDs, plasma if severe

Question 533

a disease of lactating heifers and adult dairy cattle that are confined in the barns during the winter. Rapidly spreading outbreak of diarrhea that is normally self-limiting within 1-2
caused by a coronavirus

Answer 533

Winter Dysentery

Question 534

What are the clinical signs of Winter Dysentery

Answer 534

Diarrhea +/- blood
Afebrile
Rapid drop in milk production
Self limiting within 1-2 weeks
(Colon mucosa has a far longer regeneration time for mucosa than crypt cells of small intestine- submucosa stays exposed for a longer time and triggers a more severe inflammatory response

Question 535

How is winter dysentery brought on the farm?

Answer 535

Vets, milking machine repair personel, visistors, rodents and birds, fomites
*Biosecurity is very important

Question 536

How do you diagnose Winter Dysentery

Answer 536

clinical signs coupled with low mortality

diagnosis is achieved by process of elimination as the differentials include BVDV. salmonellosis, grain overload on herd level and parasites

Question 537

T/F: cows with winter dysentery are febrile

Answer 537

False

Question 538

Chronic granulomatous enterocolitis and protein losing enteropathy caused by Mycobacterium avium ssp. paratuberculosis

Answer 538

Johne’s Disease

Question 539

What animals does Johne’s disease impact

Answer 539

Adult cattle, sheep, goats, camelids

Question 540

When is Johne’s Disease infection established?

Answer 540

Neonate but the disease is seein in the adult (Chronic, granulomatous enterocolitis, )

Question 541

What is the pathogenesis of Johne’s disease

Answer 541

1) infection established early in life at the ileocecal junction
2) Macrophages engulf but cannot kill resulting in granulomatous enteritis and chronic insidious infection.
3) The intestinal wall thickens due to the influx of inflammatory cells but cant clear the infection
4) once enteritis is severe enough, wasting disease, malabsorption, and diarrhea begin to be evident
-Protein loss (edema)

Question 542

Is Johne’s disease more common in beef or dairy cattle

Answer 542

dairy cattle
due to the management methods of dairy breeds as you concentrate feces, you concentrate pathogens

Question 543

The vast majority of Johne’s disease infections occur in neonates via colostrum/milk or contaminated environment but how else can this be passed?

Answer 543

transplacental transmission

Question 544

When do most Johne’s clinical signs seen

Answer 544

2-6 years of age
*larger the infective dose, the earlier the signs develop in the infected animal. reports as young as 13 months

Question 545

When are Johne’s disease serologic tests normally positive

Answer 545

once the adult animal is showing signs of weight loss and diarrhea the antibody titer levels are typically high enough

Question 546

What are the clinical signs of Johne’s disease in cattle

Answer 546

1) Afebrile
2) good appetite
3) Gradual weight loss
4) Pipestream diarrhea
5) Emaciated, lethargy, weakness and apathy
6) Hypoalbuminemia leading to edema
7) Chronic diarrhea

Question 547

What is significant about Johne’s disease in sheep, goats, and camelids

Answer 547

Most comon sign is wasting disease
they do not develop chronic diarrhea like cattle do. Their feces may appear as normal pellets or soft piles

Small ruminant and camelid colon does a better job at makring formed feces even whe granulomatous enterocloitis spreads to involve more and more of the gut

can have diarrhea but is often terminal as animal is suffering from emaciation and profound weakness

Question 548

How do you diagnose Johne’s disease

Answer 548

1) Serologic testing- like agar-gel immunodiffusion or ELISA- immune response gradually builds in response to slow spread of MAP infection in gut wall. cant detect early infection very well in subclinically infected.

2) Fecal culture: gold standard for cattle but takes 3-6 months. Not too sensitive early in the course ofdisease. may not shed much

3) Necropsy: Classic bovine lesion is thickened ileu, meseneteric and ileocecal lymph nodes are enlarged and edematous

Question 549

Serologic testing for Johne’s

Answer 549

Serologic testing- like agar-gel immunodiffusion or ELISA- immune response gradually builds in response to slow spread of MAP infection in gut wall. cant detect early infection very well in subclinically infected

Question 550

How long does it take to culture Johne’s disease

Answer 550

gold standar but it takes 4+ weeks but up to 3-6 months.
Culture is not snesitive early in the course of disease due to low-level of intermittent shedding

Question 551

What is a pass-through fecal positive test for Johne’s

Answer 551

when map passes through the gut of an adult that ate the contaminated feed or was in contact with the feces. Adults are resistant to developing infection. Adult herdmate is not actively infected and not truly diseased .
Diagnosis of JD is in a herd. you have to expect that some pass through positives will exist, particarly if there is heavy infection of feed. change hygiene measures to fix this

takes 2-4 months

Question 552

T/F: adults can get infected with Johne’s disease

Answer 552

false- only neonates

Question 553

How long should you allow to clear MAP in the tract when you suspect a pass-through fecal positive for Johnes disease

Answer 553

allow 2-4 months to pass, thereby enabling those innocent noninfected pass through cases to clear MAP from their GI tracts. Then test again

Question 554

What are the findings of johnes disease on necropsy

Answer 554

thickened ileum and corrugated
mesenteric and ileocecal lymph nodes are enlarged and edematous

Question 555

What are the findings of Johnes disease on histopath

Answer 555

clumps of acid-fast bacilli within macrophages

Question 556

What tissues should you submit if you suspect Johnes disease

Answer 556

submit a piece of bowel, make sure to get several cm of ileum in it and ileocecal lymph nodes, located within the ileocecal fold

Question 557

What is the treatment for Johnes disease

Answer 557

no good options
euthanize cachetic/weak animals

identify and cull or isolated infected animals- repeated serology on flock or herd: testing in parallel: fecal culture or PCR and serology simultaneously, cull if either test is positive

isolate neonates from contact with adult feces

feed neonates pasteurized colostrum and milk or colostrum and milk from seronegative dams

improve measures to separate feces and feed: reduce environmental contamination with feces from adults

Question 558

testing in parallel

Answer 558

submitting two diagnostic tests for a disease simultaneously and considering the animal to be positive if either test comes back posotive. Maximizes sensitivity and maximizes the chances of finding truly diseased animals
done with johnes disease

Question 559

How should you control for Johnes disease

Answer 559

1) identify and cull or isolated infected animals
2) repeated serology on flock or herd: testing in parallel: fecal culture or PCR and serology simultaneously, cull if either test is positive
3) isolate neonates from contact with adult feces
4) feed neonates pasteurized colostrum and milk or colostrum and milk from seronegative dams
5) improve measures to separate feces and feed: reduce environmental contamination with feces from adults

Question 560

Please provide six specific functions/effects of primary contractions of the ruminant stomach.

*Know this

Answer 560

1) Mixing of ingesta - maceration of fibrous feeds
2) Stratification of rumen contents
3) Sorting of feed by particles - selective passage of small particles
4) Aborad movement - passage of ingesta through reticuloomasal orifice
5) Enhanced VFA absorption - fluid contact with rumen wall
6) Enhance contact of bacteria with feed stuffs

Question 561

Please list all seven conditions that can cause a ‘ping’ in the right side of a cow’s abdomen.

*Know this

Answer 561

Abomasal volvulus
Abomasal displacement (right)
Cecal dilatation
Cecal volvulus
Pneumoperitoneum
Ascending colon gas
Rectal gas

Question 562

Please list four different functional causes of ruminal bloat.

*Know this

Answer 562

1) Esophageal obstruction: choke
2) Partial esophageal obstruction: compression, restriction or neuromuscular problem
3) Frothy gas: non-eructable
4) Failure to clear cardia: rumen weakness (hypocalcemia), lateral recumbancy, rumen overfill, thoracic inflammation (vagal nerve damage)

Question 563

Please provide four specific observations/measurements you will make during a cowside rumen fluid analysis.

*Know this

Answer 563

-Color
-Odor
-pH
-Methylene Blue Reduction
-Consistency/viscousity
-Sediment/flotation
-Protozoal activity
-Chloride content

Question 564

What are the 5 clinical signs of TRP and what causes them

*know this

Answer 564

1) Pain/Arched back/Extended neck/Abnormal gait: anterior abdominal inflammation
2) Fever: peritoneal inflammation
3) Rumen stasis: reflex inhibition of motility due to pain/inflammation
4) Anorexia: inflammation and rumen stasis inhibit appetite
5) Scant, dry feces: reduces passage of ingesta

Question 565

What are two factors in the pathophysiology of ruminal lactic acidosis. For each, provide a specific effect or consequence of that item.

*Know this

Answer 565

Overconsumption of grain

Increased availability of soluble CHO —> increased fermentation rate —> increased VFA —> decreased pH —> rumen stasis —> increased population of lactate-producing bacteria —> increased lactate accumulation —> die-off of pH sensitive bacteria

Hyperosmolality of rumen contents

Increased lactate —> hyperosmolality —> increased fluid to rumen —> “sloshy” or “fluidy” rumen content —> systemic dehydration

Question 566

Please provide two findings that will specifically distinguish rumen acidosis from indigestion due to poorly digestible fiber (hay belly).

*Know this

Answer 566

pH: acidosis is low, hay belly is high

Rumen consistency: acidosis is liquid while haybelly is doughy

Onset: acidosis is acute while haybelly is chronic

Diet: acidosis is low fiber while haybelly is poor forage

Feces: acidosis is malodorous why haybelly is scant/dry

Question 567

What do BVD, Blue tongue, and MCF all have in common

Answer 567

they all cause:
-fever
-ulcerative lesions of oral tissue
-lesions at mucocutaneous junction
-lesions of skin/hoof junctions
-depression
-anorexia

Question 568

How do you you distinguish BVD from blue tongue and from MCF
*Know this well

Answer 568

all cause fever, ulcerative lesions of oral tissue and lesions at mucocutaneous junction and skin/hoof junctions, depression and anorexia, however,

BVD: mostly cattle, diarrhea, leukopenia

Blue tongue: mostly sheep, seasonal, diarrhea is uncommon

MCF: individual animals, panopthalmitis, swollen lymph nodes, and diarrhea is uncommon

Question 569

BVD, blue tongue, and MCF all cause all cause fever, ulcerative lesions of oral tissue and lesions at mucocutaneous junction and skin/hoof junctions, depression and anorexia, however, what does BDV cause that blue tongue and MCF typically doesnt

Answer 569

it causes diarrhea and a leukopenia

Question 570

What are the clinical sequelae of BVD *Know this

Answer 570

BVD can cause the following clinical sequelae:
Diarrhea (+/- blood in feces)
Fever
Depression
Oral ulcers
Abortion
Infertility
Fetal deformity
Coronary band lesions
Lymphoid depletion - decreased lymph nodes

Question 571

Please list six factors that can predispose to development of left displacement of the abomasum in cattle.
*Know this

Answer 571

All of the following can lead to abomasal atony and gas accumulation.

Hypocalcemia
High concentrate diet
Low forage diet
Finely ground feed
Low rumen fill
Intercurrent infectious/inflammatory disease

Question 572

urine is acidic pH while systemic alkalosis is present

Answer 572

paradoxical aciduria

Question 573

Please briefly define abomasal reflux, what causes it, and what its effects are.

Answer 573

Definition: flow of chloride-rich abomasal fluid back into rumen.

Causes: abomasal or lower bowel (intestinal) motility/flow disturbance.

Effects: dehydration, hypochloremia, metabolic alkalosis, hypokalemia.

Question 574

Please list three types of abomasal ulcer, and briefly describe how they will be distinguished from one another.

Answer 574

Asymptomatic : no signs

Multiple chronic bleeding : melena, decreasing PCV and plasma protein

Acute major bleeding : acute onset hypovolemia, anemia, weakness

Small perforating : localized abdominal pain, anorexia, fever, scant feces

Large perforating: sudden onset generalized peritonitis, rapid progression to shock, death

Question 575

Please list fblood biochemical changes that commonly accompany various gastrointestinal obstructive disorders in ruminants.

Answer 575

Decreased Cl-
Decreased K+
Increased HCO3 (metabolic alkalosis)
Increased creatine (dehydration, pre-renal azotemia)
Ketosis
Decreased Ca++
Decreased Na+
Increased PO4-
Increased plasma protein

Question 576

Please list and briefly describe three different congenital disorders that affect the bovine gastrointestinal tract.

Answer 576

Umbilical herniation: asymptomatic except for ventral hernial sac prominently observed - may lead to entrapment.

Atresia coli: failure to form patent spiral colon; clinical signs include no feces, progressive abdominal distention, decreasing appetite and increasing depression over several days.

Atresia ani: failure to connect rectum to anal orifice.

Question 577

You are evaluating a 30 kg, 12 day-old Jersey calf that has a 24-hour history of yellow, watery diarrhea. The calf is obtunded and unable to stand.

You measure this calf’s eyeball recession to be 4 millimeters, meaning that the corneal surface of the eye is sunken away (recessed from) the medial canthus of the eyelid by 4 mm.

Using the formula provided in the course notes, what is the estimated percentage of dehydration for this calf?

Answer 577

8%
Estimating the percentage of dehydration guides the volume of fluids given during fluid therapy, a.k.a. fluid resuscitation. To use eyeball recession to estimate the % dehydration in ruminants, first measure the distance of recession of the globe (eyeball) away from the medial canthus. Express that distance in millimeters, and multiply that distance by 2.

4 mm of recession x 2 = 8% dehydration.

Question 578

30 kg and 8% dehydrated. What is the calculated fluid deficit, in liters, for this calf?

Answer 578

Calculating the fluid deficit tells us how much fluid volume is “missing” from this animal because of losses in diarrhea. In other words, it is an estimate of how much fluids we need to give to return the patient to its normal hydration status, based on current examination findings.

Deficit = body weight (in kg) x estimated % dehydration (expressed as a decimal).

So for this Jersey calf: 30 kg x 0.08 = 2.4 liters.