Livestock Medicine Flashcards
How should you start your physical exam
start from a distance
-BCS
-Demeanor/behavior
-Abdominal contour
-Lameness
-Neurologic
-Neck appearance and position
-Respiratory rate
What is BCS scale for beef cattle
1-9
What is the BCS scale for dairy
1-5
What is the BCS scale for sheep and goats
1-5
What is the BCS scale for camelids
1-9 or 1-10
What results in a pear shaped abdomen in a cow
bilateral ventral abdominal distention- can be associated with pregnant animal with hydrops, urinary bladder rupture
What results in a papple shape in a cow
classic vagal indigestion look. dorsal distension on the left hand side, ventral distension on the right hand side
What results in an apple shape in a cow
more classic rumen distension, distension in the dorsal aspect bilateral
What are the 5F’s of abdominal distension
fluid
feces/food
fetus
fat
flatus (gas)
How do you tell visceral abdominal pain from parietal
visceral- caused by distension, stretching ischemia- results in “colic”
parietal- caused by inflammation of serosal surfaces- results in abnormal posturing, grunting, reluctance to move
caused by inflammation of serosal surfaces- results in abnormal posturing, grunting, reluctance to move
parietal abdominal pain
caused by distension, stretching ischemia- results in “colic”
visceral abdominal pain
Is visceral or parietal abdominal pain more common in cattle
parietal pain is much more common in cattle- have more issues with peritonitis/pleuritis than the typical SI distension disease
What is essential for a systemic hands on exam
head catch or chute for restraint
What part of the body should you save for last when doing a systemic hands on cattle exam
head should be last
What should you do on the left side of the cow when giving a physical exam
-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
What is the normal cattle heart rate
60-80bpm
-bradycardia associated with anorexia
What is the most common cause of bradycardia in cattle
empty rumen.fasted animal- vasovagal reflex
*anorexia associated bradycardia
What is the most common arrhythmia in cattle
atrial fibrillation
-primary disease process is often GI disease
-resolves when GI disease or electrolyte is fixed
How do you typically resolve atrial fibrillation arrhythmias in cattle
fix the primary problem- GI disease
or electrolyte abnormality
What is the most common clinical sign of endocarditis in cattle
lameness- septic arthritis
What is the most common cause of murmurs in cattle
Endocarditis
Pleural fluid will ________ the sound of the heart
radiate the sound of the heart
Pericardial fluid will __________ the sound of the heart
muffle the sound of the heart
T/F heart sounds on a really thiq cow will muffle heart beat
True
How should you assess the rumen in a physical exam
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
How can you check for rumen contraction/motility
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
What are the layers within the rumen
1) Free gas (dorsally)
2) Doughy coarse roughage (fiber mat)
3) Fluid, fine particles
4) Frothy semifluid
What is the fiber mat of the rumen
the doughy compressible later that you feel around for when pushing into the rumen
it is made of coarse roughage
How do you perform pinging/percussion for examining the rumen
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
What are your differentials for pings on the left side
-Pneumorectum
-Left Displaced abomasum
-empty rumen
-gas distended rumen.rumen bloat
-physometra
-pneumoperitoneum
Succussion
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
What should you do on the rear end of cow
-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)
Why should you wait to do a rectal exam on a cow till after youve listened to rumen on both sides
because you dont want to create a pneumorectum that will cause you to hear a ping when listening to the rumen
What should you assess during a rectal exam in cattle
-Presence and consistency of manure
-Pelvic bones
-Rumen: size, consistency, location
-caudal aorta
-left kidney (size, location, pain, lobulations)
-lymph nodes
-reproductive tract
What can cause a ping on the left side
-pneumoperitoneum
-pneumrectum
-RDA/RVA
-physometra
-SI distension/duodenal ping
-Cecal distension/dilatation
-Spiral colon gas
What should you do in small ruminants to check if they are in late pregnancy
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
What should you assess on the head during a cattle exam
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
What should a healthy cow’s nose be
should have a clean, shiny/wet nose
What should you look for in the ears
-If female, look for bangs tattoo/tag to see if they’ve been vaccinated against Brucella
signs of otitis
Camelids have upper incisors and canines, what are these teeth called
fighting teeth
T/F Cows have 3 upper incisors on each side
F- no upper incisors
How should you perform a bovine oral exam
-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
Diastema
space between incisors and premolars, good place to grab when doing a bovine oral exam
When do deciduous teeth in cattle erupt
starting at birth for every tooth except for molars (no deciduous molars)
“Mouthing” ruminants
examine teeth for culling decisions
-excessive wear “broken mouth” - a culling risk
How might “broken mouth” develop
trauma
feed
nutritional deficiencies
genetics
*culling risk
What are clinical signs of diseases of the dental arcade
weight loss, quidding feed, low production, metabolic diseases
“Smooth mouth” ruminants
ruminants greater than 10 years of age with no incisors present
-increased risk of maintaining weight, foraging, productivity loss within the herd
What neoplasias are seen in the mouth
-Fibrosarcoma
-Oral sarcomas
-Adenosarcomas
-Odontogenic myxomas
*invasive and poor prognosis
Dentigerous cysts
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
Hamartoma
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;;
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)
periodontal disease
How do ruminants get periodontal disease
they have hypsodont teeth which allows for the stasis of food material with malocclusion/fracture and then bacterial overgrowth
How do pigs get periodontal disease
it is highly prevalent as they have brachydont teeth through through the dental calculus
can get enamel damages
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
tooth root abscess
clinical signs: ptyalism, halitosis, soft tissue swelling, quidding, inappetence, weight loss
What species are tooth root abscesses most common in?
sheep and camelids
What are the clinical signs of tooth tooth abscess?
ptyalism, halitosis, soft tissue swelling, quidding, inappetence, weight loss
What might be a cause of mandibular or maxillary swelling associated with the jaw
tooth root abscess
How might you see submandibular lymphadenopathy
secondary to lymphoma
What kind of bacteria is associated with tooth tooth abscesses
Trueperella pyogenes
non-specific inflammation of the oral mucosa (gingiva, tongue, palate, buccal mucosa)
stomatitis
What are the causes of stomatitis
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
T/F Bovine papular stomatitis virus (BPSV) is zoonotic
True- it is zoonotic, wear gloves
What bacteria can cause stomatatis through breach of mucosa, common in lambs and calves
Necrotic stomatitis (Fusobacterium necrophorum)
What kind of animals typically get Necrotic stomatitis from Fusobacterium necrophorum
lambs and calves
-sucking bottles not cleaned properly
a parapoxvirus that causes raised papules on the hard palate, muzzle, oral mucosa, and esophagus
Bovine papular stomatitis virus (BPSV)
What kind of animals typically get Bovine papular stomatitis virus (BPSV)
young feedlot cattle (1-12 months)
T/F Bovine papular stomatitis virus (BPSV) is a lifetime condition
False- it is self-limiting in animals with immunocompetence and lesions typically regress within 3 weeks, brown spots will often remain after healing
What do you need to rule out in animals with advanced lesions from Bovine papular stomatitis virus (BPSV)
BVDV
other vesicular diseases?FAD
In Bovine papular stomatitis virus (BPSV), lesions are _________ but _______
lesions are mild but focus on prevention
it is highly contagious
in Bovine papular stomatitis virus (BPSV), calves may be ____________ or ________
calves may be asymptomatic or show reluctance to nurse
What are other names for Necrotic stomatitis
Necrotic laryngitis
Calf diphtheria
Necrobacillosis
*all refer to fusobacterium necrophorum infection from oral damage and infection
*massive edema
With Fusobacterium necrophorum infection, ___________ of the larynx can be severe leading to ___________
swelling of the larynx can be severe (insipiratory dyspnea, stidor common
“Barker calves” - tracheostomy
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
Vesicular stomatitis virus (VSV)
T/F: You do not need to report cases of vesicular stomatitis virus (VSV)
False, report cases to the state veterinarian
What is the vector for vesicular stomatitis virus
midge (arthropod)
what time of year does vesicular stomatitis virus typically occur
summer and fall
What causes contagious ecthyma
Sore Mouth/Orf
(a poxvirus- similar to BPSV)
What animals typically get vesicular stomatitis virus
cattle
horses
pigs
What animals typically get contagious ecthyma virus
sheep
goats
T/F: contagious ecthyma is a self limiting virus
True- often self limiting within 3-6 weeks
do supportive care (nursing assistance)
immunity lasts 2-3 years after clinical case
What is the classic lesion seen with contagious ecthyma?
crusting at the mucocutaneous junction of the nose and mouth
-can see proliferative oral lesions
Is contagious ecthyma zoonotic?
yes - wear gloves
What causes Wooden Tongue
Actinobacillus lignieressi
Actinobacillus lignieressi causes
Wooden tongue
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
Actinobacillus lignieressi
T/F: Actinobacillus lignieressi is a normal oral commensal that causes disease when there is an injury to oral mucosa or skin
True
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
Actinobacillus lignieressi
What are the clinical signs seen in Actinobacillus lignieressi (Wooden Tongue)
inability to prehend food (tongue)
granuloma +/- draining tract
bloat
esophageal obstruction
Where are the soft tissue granulomas seen in Actinobacillus lignieressi infection
tongue, pharynx, esophagus, forestomach, lymph nodes
Actinobacillus lignieressi causes:
soft tissue granulomas (sulfur granules) on the tongue, pharynx, esophagus, forestomach, lymph nodes
How do you treat Actinobacillus lignieressi granulomas?
sodium iodide (20% solution) therapy
debridement/debulking
What causes lumpy jaw
Actinomyces bovis
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
Actinomyces bovis “lumpy jaw”
Why are younger cattle more prone to Actinomyces bovis infection
enamel eruption increases risk as it infects bones and teeth following injury to the oral mucosa
What are the classical signs seen in Actinomyces bovis infection
firm, painful, bony swelling, but can also cause granulomatous infectious throughout the body
-pyogranulmoatous osteomyelitis
How do you treat Actinomyces bovis
success depends on degree of osteomyeltitis: often requires iodine therapy in addition to long term antibiotics (penicillin), surgical debulking?
pharyngitis is most commonly due to
pharyngeal injury from forceful use of balling gun or drenching syringe
*lack of restraint = major risk factor
clinical signs of pharyngitis
dysphagia
hypersalivation
malodorous breath
neurologic sign
stidor/dyspnea
How might you get emphysemia dissecting facial planes
large tears in the pharynx
What is a common sequelae of pharyngitis
aspiration pneumonia
What are the causes of esophageal diseases
-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)
What are the clinical signs of esophageal obstruction
salivation
regurgitation
development of palpable cervical swelling over time
weight loss
recurrent episodes
What are the clinical signs of esophageal disease
salivation
regurgitation
bloat
crepitus within subcutaneous tissue (rupture)
nasal discharge containing feed (choke)
What are the causes of esophageal obstructions
-Indiscriminate grazing (cattle)
-Neuromuscular dysfunction (camelids)
-Megaesophagus (often idiopathic, trauma, tumors, vascular ring (congenital)
present as young adults- follow weaning)
What are the causes of esophageal dysmotility
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)
calves with megaesophagus often present with
chronic bloat +/- regurgitation
esophageal motility is necessary for
normal rumen function
How might you see excessive salivation
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)
T/F: Clinicial signs are important because they are diagnostic
False- they are important but testing is needed to identify specific viruses, especially if thy are foreign animal diseases
what are viruses that are erosive/ulcerative
bovine viral diarrhea (BVD)
malignant catarrhal fever (MCF)
Bluetongue (BT)
Rinderpest
What ate vesicular viral diseases
-Foot and mouth disease (FMD)
-Vesicular stomatitis (VS)
What are proliferative viral disease
-Bovine papular stomatitis
-Orf (soremoth, contagious ecthyma of sheep and goats)
What are the clinical signs of BVDV, bluetongue, and malignant catarrhal fever
fever
ulcerative lesions of oral tissues
lesions at mucocutaneous junction
lesions of skin/hoof junctions
depression
anorexia
How do you do confirmatory testing for viruses
Virus identification- isolation, PCR
-Serologic antibody response
-Characteristic histpathology
What are some clinical signs of BVD/Mucosal disease
-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
What causes diarrhea in mostly cattle with leukopenia, lymph node atrophy, and immunosuppression with persistent infection
BVD/ Mucosal disease (Flavivirus, Pestivirus)
What causes buccal mucosal cyanosis and erosions, coronary band and interdigital lesions, lameness, cattle are typically asymptomatic
Bluetongue (Orbivirus)
What kind of virus is BVD/Mucosal disease
flavivirus, pestivirus
T/F: diarrhea is common with bluetongue (orbivirus)
False- diarrhea is uncommon
What animals is bluetongue most common in?
sheep
T/F: bluetongue is seasonal
true- requires an arthropod vector
What causes malignant catarrhal fever (MCF)
herpesvirus (OHV-2)
What disease has erosions throughout the oral cavity (hard palate), panopthalmitis, arteritis, swollen lymph nodes, coronary band/interdigital lesions, lameness
Malignant catarrhal fever (OHV-2)
T/F: diarrhea is common with malignant catarrhal fever
false- it is uncommon
What are the signs of malignant catarrhal fever
erosions throughout the oral cavity (hard palate)
panopthalmitis
arteritis
swollen lymph nodes coronary band/interdigital lesions, lameness
T/F: malignant catarrhal fever effects herds
False- typically affects individual animals
What side is the rumen on?
left side
what lies behind diaphragm, making puncture of it dangerous for the pericardial sack and diaphgram
reticulum
Where does milk from the esophageal groove go to
reticular-omasum orifice
what does the spiral colon do
where a lot of the fluid is absorbed and the pellets are formed
What is fermented in the rumen
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
Where do most of the proteins get made in ruminants
manufactured by microbes in the rumen
What is the end product of carbohydrate fermentation
-Acetate (2 carbon) -Lipogenic
-Propionate (3 carbon)- glucogenic
-Butyrate (4 carbon) - ketogenic
What VFA is glucogenic
propionate (3 carbons)
What VFA is lipogenic
acetate (2 carbon)
What VFA is ketogenic
butyrate (4 carbon)
T/F: the rumen is nonglandular
True it is nonglandular absorptive epithelium
Where are VFAs absorbed in ruminants to be transported to the liver in the blood
the rumen- it is nonglandular absorptive epithelium
some do reach the abomasum
what is the glandular portion of the ruminant stumach
abomasum- has cardiac, propergastric and pyloric glands
the most important motor function in the rumen to facilitate fermentation
primary contractions
motor function for eructating gas in the rumen
secondary contraction
What are the motor functions of the rumen
1) Primary contractions
2) Secondary contractions
3) Eructation
4) Regurgitation
5) Esophageal groove
6) Control mechanisms
How is material fermented in the rumen
-Inflow- feedstuffs, saliva
-Outflow- absorption, ingesta passage
-Fiber (slowly fermented
-Concentrates (starch/cereal grains that are fermented rapidly
What is the 6 purposes of primary contractions
-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
What stimulates primary contractions
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
what inhibits primary contractions
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
Does environmental cold stimulate or inhibit primary rumen contractions
stimulate
-heat is generated and allows the animal to stay warm
Does abomasal acidity stimulate or inhibit primary rumen contractions
stimulate
does feed/chewing stimulate or inhibit primary rumen contractions
stimulate
does high VFA concentrations/acidity stimulate or inhibit primary rumen contractions
inhibit
Does abomasal distension stimulate or inhibit primary rumen contractions
inhibit
What is the purpose of secondary contractions
move gas generated from fermenation to the cardia
clears the cardia
Prepares animal for eructation
relaxation of the esophagus, close glottis and inhaling gas from stomach system creating negative thoracic pressure
eructation
reticular contraction that lifts feed to the cardia, where fibrous feed is then eructated to be masticated again
regurgitation
directs milk directly into the abomasum
esophageal groove
What part of the stomach has shagged rug appearance to buffer the acidic VFAs
rumen
virtually all disease of rumen occur when
normal physiology is distrubed
What would happen if the animal cant clear the cardia
prevent eructation
lower right abdominal distension is an issue with the
abomasum
upper left distension in the abdomen indicates
possible bloat
upper right abdominal distension indicates that there is an issue with the
abomasum- filled with gas (volvulus)
or cecal volvulus dominates the right side
When do you hear abdominal pings
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
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
left displaced abomasum
When do you hear a ruminal ping
when the layers of the rumen are changed so fibrous material is at the bottom, then fluid, and then gas
*textbook for rumen stasis
RDA a _________ while abomasal volvus is a _________
partial obstruction ; complete obstruction
What are problems resulting in right sides pings
-abomasal volvulus
-abomasal displacement (right)
-cecal dilatation
-cecal volvulus
-pneumoperitoneum
-ascending colon gas
-rectal gas
distention of the rumen due to gas accumulation
caused by problems that disrupt the eructation gas
bloat
T/F: bloat is caused by excessive gas production
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
How is bloat caused
caused by problems that disrupt eructation
What is required for normal eructation
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
How might you get bloat
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)
solid feed material causing esophageal damage and inability for an animal to release gas from the rumen
Complete “Choke” resulting in bloat
*acute
How might you get partial esophageal obstruction
-Esophageal compression (thoracic masses, pneumonia, mediastinal masses, LDA)
-Failure to relax esophagus (Tetanus)
-LDA (occasionally)
*mostly chronic, recurring bloat
-Rarely life threatening
why should you evaluate cardiopulmonary function in bloat cases
it makes it so it is more difficult to breathe for the animal.
How should you evaluate bloated animals
-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
Choke is typically caused by ______________ and there is also ______________,
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
solid feed material causing choke are typically
a) pushed into the rumen
b) taken out of the mouth
taken out of the mouth
if it could pass further it would have passed normally
what are clinical signs of bloat
-labored breathing
-agitated animal
-rumen restricting diaphragm (emergency)
-froth at nose from labored breathing
T/F: bloat from partial esophageal obstruction is life threatening
False, rarely
T/F bloat from complete esophageal obstruction is life threatening
True
and damaged esophagus have long term deleterious effects
What is trocharization
tubes with a sharp stylet that is punctured through body wall into rumen. stylet is then removed to relieve excess gas from the rumen
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
Rumen fistulation
When is rumen fistulation used
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
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)
frothy bloat
How might frothy bloat form
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)
How do you relieve frothy bloat
Poloxalene (Therabloat, a surfactant) orvegetable oil - breaks down the froth
*cant relieve with stomach tube or rumen trocar
T/F: you can remove frothy bloat with stomach tube or rumen trocar
False
relieve with Poloxalene (Therabloat, a surfactant) orvegetable oil - breaks down the froth
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?
Streptococcus bovis
T/F: frothy bloat may be an emergency
True- can be in respiratory distress
If not emergency: destabilize foam with Poloxalene or veggie oil
If emergency- perform rumenotomy to
What should you do if an animal is in respiratory distress due to frothy bloat
Perform a rumenotomy
if not emegency: destabilize the foam with Poloxalene or veggie oil
How do you prevent flothy bloat from occuring in a herd
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
how can you relieve free gas bloat
can be relieved by a tibe
may be chronic/recurrent
How do you get free gas bloat
*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
What is seen in a normal rumen
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
Will a free gas bloat produce a ping
? yes i think so- fill in later
What does continuous fermentation required
-inflow- feed substrate
-outflow- finished product
-removal- inhibitory/toxic products
-control of pH
T/F you can feed meat and bone meal as feed stuffs
False- it is illegal due to pathogen spread
What is the color of normal rumen fluid
olive-brownish green
What is the odor of normal rumen fluid
aromatic- smelly
-Will be less aromatic with less fermentation
What is the consistency of normal rumen fluid
slightly viscous (gruel)
-active fermentation and some gas bubbles
What is the pH of normal rumen fluid
5.5-7
wide range due to presence/less VFAs
What should the chloride be of normal rumen fluid
<25-30 mEq/l
What should the methylene blue reduction be of normal rumen fluid
3-6 min
*determination of bacterial activity (redox)
What is the sedimentation/flotation of rumen fluid used for
Should be 4-8 minutes
Tells you the bacterial activity- how rapidly they are fermenting. light particles move to the top with active fermentation
How do you collect rumen fluid
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
What color of rumen fluid is seen in rumen acidosis with cereal grain consumption
very yellow/whitish color
What color of rumen fluid is seen in fresh forage feed
a fresh green color
What should you see in terms of protozoal activity when examining rumen fluid
Active- moving around
All sizes are present
*dead protozoa dont move around
What does a rapid sedimentation of rumen fluid tell you
if rapid (less than 3 minutes), sedimentation indicates that there is poor microflora activity
What does no sedimentation of rumen fluid tell you
there is frothy bloat or vagal indigestion
What is a normal sedimentation test time of rumen fluid
4-8 minutes
-Rapid <3 min tells poor microflora activity
-No sedimentation tells you frothy bloat or vagal indigestion
How is a new methylene blue reduction test performed on rumen fluid
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
What is likely happening if it takes longer than 6 minutes for there to be decolorization after adding new methylene blue to rumen fluid
Indicates bacterial die off- mostly common in
prolonged anorexia with indigestion or ruminal acidosis
What part of the rumen fluid does not decolorize in a new methylene blue test
the top (aerobic part)
pH of rumen fluid should be ________ but may be __________ if chronically fed gain
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
pH will tend to be higher when _________ while it will be lower when _____
higher when its longer time after feeding
Lower when its right after feeding (generation of VFAs)
If an animal is anorexic and you measure the pH to be <5.5. What is occuring
highly indicative of ruminal acidosis
pH should be higher when there hasnt been eating
Would methylene blue reduction time be higher or lower when on a pure straw diet vs one that has grain in it
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)
When does chloride rich fluid in the rumen occur
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
What does a rumen fluid chloride value of >30 mEq/L indicate
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
What is the pathogenesis of traumatic reticuloperitonitis
-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
Why does hardware disease rarely occur in sheeps and goats
because they are browsers- eat with their lips instead of their tongue
How do you prevent hardware disease
-careful farm management
-give cattle a magnet
-feed mixing truck with magnets on the outflow chute to trap steel contaminants
What cant you prevent with a reticulum magnet
aluminum needles do not stick to the steel magnet and could still cause traumatic reticuloperitonitis
What are the clinical signs traumatic reticuloperitonitis
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
What appearance does the reticulum have?
a honey comb pattern
What clinical signs do the acute cases of hardware disease have
-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
What are the clinical signs of chronic localized perionitis from hardware disease
-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)
T/F: rumen pings are common with chronic localized peritonitis from hardware disease
True- gas over fluid in the rumen
How do the clinical signs differ from acute vs chronic traumatic reticuloperitonitis
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
What are the sequellae to TRP
1) uneventful recovery following treatment
2) infection of other tissues (pleuritis, pericarditis)
3) reticular wall abscessation - obstructive vagal indigestion
What diagnostics do you run if you suspect traumatic reticuloperitonitis
-Physical exam and observation
-CBC. including a fibrinogen (must)
-abdominal exploratory sx
maybe: ultrasound: abdomen and chest, abdominocentesis, radiograph of cranial abdomen
What is with Whithers pinch/scootch test used for
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
What is a sternal pressure/grunt test used for
does the cow resent pressure as it induced localized pain
-arch the back and resents the pain
How do you treat traumatic reticuloperitonitis
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
What kind of antibiotics should you use to treat traumatic reticuloperitonitis
Beta-lactam: typically facultative anaerobes
What is a result of traumatic reticulopericarditis
-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)
How might you get a jugular pulse
from right sides heart failure signs seen with traumatic reticulopericarditis
how do you get brisket edema
from right sided heart failure
-signs seen with trauamtic reticulopericarditis
What are the 4 things associated with obstructive (Vagal) indigestion syndrome
1) Omasal transport (outflow) failure
2) Pyloric transport (outflow) failure
3) obstructive indigestion-other causes (Haybelly)
4) Abomasal emptying defect of Suffolk sheep
What are the 4 key signs of obstructive (vagal) ingestion
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
T/F: Obstructive (vagal) indigestion is caused by vagal injury
False
Most cases are not due to vagus injury
it is a syndrome
What causes the Papple shape seen with obstructive (vagal) indigestion
impaired forestomach emptying. causes the rumen to move from its left sided position into an L shape
Omasal transport failure leads to
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
What could result when there is obstructive indigestion due to omasal transport failure
Rumen is overfilled
homogeneous consistency
With rumen overfilling- develop free gas bloat
occassionally cows “vomit” = large scale regurgitation (forestomach)
T/F: a papple shape is seen with obstructive indigestion
True
What are the causes of omasal transport failure (a cause of obstructive indigestion)
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
How can TRP lead to omasal transport failure
abscess of the reticular wall leads to failure to initiate primary contractions- cannot sense rumen
fill to stimulate rumen activity
Pyloric outflow failure leads to
Obstructive indigestion
cardinal signs
1) Chronic, progression abdominal distention
2) Gradual weight loss/body condition loss
3) Decrease fecal volume
4) Papple shaped abdomen
What is the pathogenesis for pyloric outflow failure, leading to obstructive indigestion
*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
How do you distinguish between omasal transport failure and pyloric outflow failure
Rumen chloride will be elevated in pyloric outflow failure due to the backing up of abomasal conts from pyloric outflow failure
What are the causes of pyloric outflow failure, leading to obstructive indigestion
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
What is the prognosis for pyloric outflow failure
poor- abomasum does not return to its normal function.
What is indigestion of late pregnancy
during late pregnancy, large fetus develops abdominal contour. fetus moves the abomasum to where abomasal flow is obstructed.
fixed with birth
T/F: acute frothy bloat can cause a “papple” abdomen
True
T/F uterine problems such as hydrops can cause “papple” abdomen
True- uterine filled up can give the appearance
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:
Type I Obstructive (Vagal) indigestion
failure of omsal transport caused by abscess or adhesion along the right (medial) side of the reticulum is classified as:
Type II Obstructive (Vagal) indigestion
T/F: Type I Obstructive (Vagal) indigestion results in papple shaped abdomen
False
abomasal impaction due to chronic or severe abomasal distension (RDA or RAV) is classified as
Type III Obstructive (Vagal) indigestion
secondary to late gestation, resolves with parturition. “Indigestion of late pregnancy” is classified as
Type IV Obstructive (Vagal) indigestion
What is abomasal emptying defect of suffolk sheep
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
What is another name for grain overload
Rumen acidosis
-acute ingestion of high carb feeds, typically grains
T/F: sheep and goats are not at risk for rumen acidosis
false- all ruminants are at risk
How might rumen acidosis occur
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)
What is the pathogenesis of rumen acidosis
-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
What isomer of lactate isnt absorbed well?
D-lactic isomer
-creates a D-lactic acidosis
What is the bacteria associated with Rumen acidosis
Strep. bovis
D lactate _____________ the osmolality of the rumen, resulting in :
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
How can rumen acidosis lead to endotoxemia
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
Hww do you get sloshy or fluid rument content
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
Rumen acidosis causes the rumen fluid to be:
pH:
Color:
Odor:
NMB:
Protozoa:
Consistency:
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
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
rumen acidosis
What will the rumen papillae look like in rumen acidosis
Hyperemic, damaged, peel off, general mucosal damage
What are the presenting problems with rumen acidosis
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
How do you treat mild cases of rumen acidosis
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
How do you treat Severe Rumen Acidosis
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
How do you treat rumen acidosis
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
What are some potential complications of rumen acidosis
-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
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
Subacute/Chronic Ruminal Acidosis (SARA)
What can subacute to Chronic Rumen acidosis lead to
-High incidence of Displaced abomasums
-Lameness; acidosis induced laminitis
-Poor milk production
-Fluctuating feed intake
-Milk fat depression
-Diarrhea
How do you diagnose subacute to chronic rumen acidosis
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
If multiple cows with a pH below __________ you can diagnose the herd with subacute to chronic rumen acidosis
below 5.5
what is haybelly
-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)
-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
Hay belly
What kinds of cows get haybelly
1) Animals eating forages with too little readily fermentable carbs
2) Overwintered beef cows
3) young weaned calved on poor forage diet
What is the pathogenesis of haybelly
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
What are the clinical signs of Haybelly
-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
In Haybelly, the rumen fluid will be
pH:
Color:
NMB:
Protozoa:
Consistency:
Sedimentation:
pH: elevated (at or above 7)
Color: Brown color
Odor:
NMB:prolonged
Protozoa: Reduced
Consistency: watery
Sedimentation: rapid
Abomasal reflux
internal vomiting,
very common in ruminant
abomasum into the rumen
Rumen vomiting
large scale regurgitation
uncommon
What causes vomiting in ruminants
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
What toxic plants cause vomiting in ruminants
azalea, rhododendron, sneezeweed (helenium), spoiled feedstuffs
Does nasogastric intubation cause vomiting
No- but orogastric does
Does orogastric intubation cause vomiting
Yes- but nasogastric intubation does not
What occurs at the caudal 20% of the C3 in camelids ?
HCl secretion from the gastric glands
Abomasal ulcers are multifactorial. what are some etiologies
-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)
Where do you see abomasal ulcers in adults
ulcers commonly in the fundic region
Where do you see abomasal ulcers in calves
ulcers are commonly in the pyloric antrum
What are some risk factors for adult cattle developing abomasal ulcers
-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
What are some risk factors for calves developing abomasal ulcers
-mineral deficiencies (Copper)
-Trichobezoars
-Consuming sand, bedding
-Feeding large volumes of milk in 2 feedings/day
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
Type I abomasal ulcer
What are the different types of abomasal ulcers
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)
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
Type II abomasal ulcer (non-perforating, hemorrhage)
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)
Type III abomasal ulcer- perforating, local peritonitis
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)
Type IV: abomasal ulcer: perforating, diffuse peritonitis
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)
C3 ulcers in camelids
C3 ulcers in camelids
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)
a neoplasia within the abomasum that may/may not be associated with BLV- causes disruption of mucosal integrity and ulcer development
lymphosarcoma
5% of BLV infected cows
develop lymphosarcoma in the abomasum
How do you treat/prevent abomasal/C3 ulcers
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
Kaopectate is a _______ use to treat _________
coating agent used to treat abomasal/C3 ulcers
What is a coating agent that you can use to treat abomasal/C3 ulcers
Kaopectate
What should you give to reduce the acidity in treating abomasal/C3 ulcers
Pantoprazole (proton pump inhibitor)
Ranitidine (oral in preruminants): H2 antagonist
Pantoprazole is a _______ used to ___________
proton pump inhibitor used to reduce acidity in treating abomasal/C3 ulcers
Ranitidine is a _______ used to ___________
H2 antagonist used to reduce acidity and helps to treat abomasal/C3 ulcers
Aminocaproic acid is used to:
maintain clots in abomasal/C3 ulcers
What causes abomasal tympany
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
What is the pathogenesis of Clostridial Abomasitis
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
Clostridial Abomasitis typically affects
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
Clostridial Abomasitis
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
How do you diagnose Clostridial Abomasitis
ultrasound
fecal/abomasal fluid smear (GP rod overgrowth)
How do you treat Clostridial Abomasitis
treatment: relieve distension, Penicillin, IVF/supportive care, antitoxin? -debatable (cross protection)
Prevention: vaccine (Type A toxoid) has unknown efficacy)
What do Suffolk sheep have
abomasal motility disorder resulting in abomasal impactions
Primary abomasal impaction is caused by
some sort of fibrous feed with dehydration, pica, sand, rocks, idiopathic
Secondary causes of abomasal impaction are more common. What are their causes
1) Pyloric outflow obstruction
2) Vagal nerve injury
3) Adhesions (calves with peritonitis from ulcer
4) LSA
What is the most common displacement
Left Displaced Abomasum
What is the peak occurence of abomasal dispalcement
Peak occurence is 1st 6 weeks of lactation
Any DIM, (bulls and calves)
-RDA is often later in lactation (adults)
What kind of abomasal displacement for preweaned calves typically get
RDAs
What is likely the cause of abomasal displacement
*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
What are the risk factors for development of LDA
-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
What are the clinical signs of LDA
*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
How do you tell the rumen from a DA
-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)
What are the physical exam findings of a right displaced abomasum/volvulus
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
RDA usually results in _____________
damage to the vagal nerves (lie on the lesser curvature
comprised vessels is a surgical emergency
with ruminant GI obstructive disease you see a _____chloremic, ______kalemic metabolic _________
hypochloremic (low Cl-)
hypokalemic (low K+)
metabolic alkalosis
Does LDA result in mild or severe changes on blood work)
mild to moderate change
*partial obstruction
Does RDA result in mild or severe changes in bloodwork
severe changes in blood work
*complete obstruction
What does RVA result in
tissue necrosis and shock (mixed acid base)
What is abomasal reflux
-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
What is a potential sequelae to abomasal reflux
metabolic alkalosis will tend to decrease bone resportion (iCa) and hypocalcemia in fresh cows may be subclinical
What is paradoxical acuduria
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
Paradoxical aciduria is a result of the kidney wanting to ________ so H+ is exchanged for ______ because ______ is low in the distal tubule
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
How do you treat LDA
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
How do you treat RDA/RVA
right flank omentopexy or pylor-omentopexy
How do you perform Roll for blind toggle/tack
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
Right Paramedian Abomasopexy (LDA)
cast cow on the right and roll into dorsal recumbency
surgical approach to abomasopexy
preferred approach if there is a concern of abomasal ulcers
What is the best approach to fix a LDA if there is concern of abomasal ulcers
Right Paramedian Abomasopexy
What are some complications of displaced abomasum correction
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
Abomasal ulcers vary in their clinical presentation and prognosis by the __________
degree of hemorrhage and perionitis
pyloric outflow obstruction (mechanical and functional) in ruminants causes
characteristic changes in acid base status
Hypochloremic, hypokalemic metabolic alkalosis
LDA development is multifactorial however factors associate with _______________, ________________, and _______________ increase the risk of abomasal atony and gas production
diet,
concurrent disease,
lactation status
Diagnosis of an RDA requires
immediate surgical intervention
Intestinal accidents (cecal distension or volvulus, intussusception- small intestine, mesenteric volvulus, and intestinal incarceration)
are __________ common than abomasal issues
less
What might cause hemorrhagic bowel syndrome (HBS)
Clostridium perfringens Type A in adult dairy cattle
blood clots and acts as an obstruction
What are the physical signs used to diagnose GI obstruction
1) Abdominal distension
2) Colic- stretching or damge to the mesentery
3) Hydration status
4) Fecal changes
What is colic normally accredited to in cattle
-Urinary problem (ie obstruction)
-Uterine (ie torsion)
*Unusual to get the GI diseases that cause colic but it can happen
How do you treat GI obstruction
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
What are the blood biochemical changes of GI obstructive disorders
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
What dictates the degree of fluid change in GI obstructions
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
Ileus with gram - infections of mammary gland or uterus can
produce a hypochloremic, hypokalemic metabolic alkalosis
Why do baby ruminants not follow the pattern of alkalotic blood biochemical change
they are not ruminants yet
Does rectal prolapse occur more frequently in fat or skinnier animals
fat- perineal/perirectal fat loosens up the connection
Why might you commonly get rectal prolapse in sheep
Lax perirectal musculature due to docking the sheep’s tail too short
What are factors that increase the incidence of rectal prolapse
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
What might result in tenesmus and subsequent rectal prolapse
*Increased abdominal pressure from 1) pneumonia (coughing)
2) Urinary irritation/obstruction in castrated males
3) Enteritis/coocidiosis
What should you do when you assess rectal prolapse
-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
a congenital anomaly where there is failure to connect rectum to the anal orifice
atresia ani
a symptomatic congenital anomaly except for when the ventral hernial sac prominently is observed and may lead to entrapment
Umbilical herniation
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
Atresia coli
Crypt cells _____ then migrate to the __________
divide and then slowly migrate towards to villus
What digestive enzymes do enterocytes have
lactase
maltase
peptidases
How long does it take for the enterocytes to migrate from the crypt to the tip of the villus
5 to 7 days to replenish themselves
Mucosa in the intestine acts as a
barrier against bacteria, viruses, antigens, toxins, endotoxin (LPS), and chemicals
How might liver problems contribute to wider spread of normal pathogens in the GI lumen
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
What is a pathogen that causes secretory diarrhea
Enterotoxigenic E coli (ETEC) in ruminants - k99
At what age does secretory diarrhea from ETEC-k99 typically affect neonates
Less than 7 days, sometimes up to 10 days
next generation of enterocytes in the GI do not have the k99 receptor
T/F: ETEC k99 only affects neonatal ruminants and swine
true
What kind of diarrhea does ETEC cause
Secretory
What is the pathogenesis of ETEC
-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-
What is loss into the lumen with secretory diarrhea
Cl- loss and following loss of:
Na+
H20
HCO3-
What will the pH of purely ETEC diarrhea be
neutral ph: 7.4 to alkaline because of the loss of bicarbonate into the lumen
What kind of diarrhea is Rotavirus
Malabsorptive Diarrhea
What kind of diarrhea is Coronavirus
Malabsorptive diarrhea
What kind of diarrhea is caused by Cryptosporidium
Malabsorptive Diarrhea
Does coronavirus typically infect older animals or younger animals
older animals
__________ is a virus of ruminants, swine, and horses that is ubiquitous and causes disease when concentrated
Rotavirus
What are some common causes of malabsoportive diarrhea
-Rotavirus
-Coronavirus
-Cryptosprodium
transmissible gastroenteritis virus (TGE) and porcine epidemic diarrhea virus are kinds of
coronaviruses
What kind of species can get cryptosporidium
ruminants and crias
-typically dairy calves
TGE is a diarrhea disease that also has
vomiting
What is the pathogenesis of rotavirus
-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
What is the protective mechanism when the epithelium is lost due to Rotavirus infection
the villi smooth muscle contracts to limit the surface area potential for pathogens to be translocated
What is the pathogenesis of coronavirus
What part of the enterocytes does coronavirus target
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
is coronavirus or rotavirus infection more severe
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
What part of the intestines does rotavirus hit the hardest
the small intestine- lesions evident from duodenum down to the ileum
How does malabsorptive diarrhea lead to metabolic acidosis
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
What is the pH of the feces when malabsorptive diarrhea is occuring
Acidic -organic acids produced in the large colon
What does rotavirus diarrhea look like
yellow or white watery diarrhea
-feces may bubble once passed, owing to continued fermentation and liberation of gas bubbles.
looks like cooking pancakes
Is the primary pathologic process in rotavirus due to malabsorption or inflammation
malabsorption
-there is some inflammation as the cells are disturbed but malabsorptive causes most of the tissues
What is the pathogenesis of Cryptosporidiosis
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
What part of the intestine does cryptosporidiosis impact
jejunum and ileum is hit
-lesions can extend orad into duodenum and aborad into the colon
What are the causes inflammatory diarrhea
1) Clostridial enteritis (Clostridium perfringens/over eating disease/ intestional clostridiosis) *Any age, any animal
2) Salmonellosis (S. enterica >2000 serotypes) *Any age, any animal
What are the more pathogenic strains to the intestine of Clostridium perfringens
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
What allows C. perfringens to proliferate in the intestines
high starch, sugar, or protein content in the small intestine
“Overeating disease” - rich diet, higher content of intestinal starch, sugar, and protein - exotonix production
What is the pathogenesis of Clostridial Enteritis
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
Why is the intestine of a neonate an ideal spot for C. perfringens type C
-Anaerobic environment
-Not a lot of competitive microflora established yet
-Warm
-Lots of nutrients (milk)
How does Clostridium perfringens type C differ from type D when it comes to clostridial enteritis
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
C. perfringens type D causes
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
What is the pathogenesis of Salmonellosis
-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
What part of the intestine does salmonella infect
Enterocolitis- small intestine, cecum, and large intestine can be infected
What kind of diarrhea cause also causes profound PLE
Salmonellosis
When does ETEC K99 typically affect calves
0 to 5-7 days
When does Salmonella typically affect calfs
5-14 days, anytime
When does Rotavirus typically affect calfs
5-14 days
When does coronavirus typically affect calfs
1 week to 1 month
When does Cryptosporidium typically affect calfs
1 to 4 weeks (5-28 days)
When does Giardia typically affect calfs
2 weeks to 2month
When does BVDV typically affect calfs
first month, anytime
When does coccidia (Eimeria) typically affect calfs
after the first month
If the signalment is an ill neonate, what do you need to rule out, even if it is not mentioned as the chief complaint
Diarrhea
What are proctitis, vulvitis, and perineal dermatitis all consistant with?
Diarrhea
How might vulvitis affect the findings of a free catch urinalysis
might have bacteria and WBC from the vulva instead of the urine
What are the clinical signs of neonates with diarrhea
*Know this
1) Diarrhea
2) Dehydration
3) Metabolic acidosis
4) Reduction in appetite
5) Hypothermia
Less consistent, not every case
6) Septicemia/ endotoxemia
7) Electrolyte imbalance
What are some clinical signs of calves with diarrhea
-Weakness or recumbency
-Skin tent persist >2sec
-Orbital recession
-Dry mouth
-Tachycardia from hypovolemia
How do you measure dehydration in ruminants
Measure the eyeball recession
Multiple by 2
The resulting value is the % of the body fluid that was lost
A calf has a gap between the lower palpebral edge to corneal surface that is estimated to be at 5mm. How dehydrated are they
10% dehydrated
Metabolic acidosis seen in diarrhea causes
poor cardiovascular performance
recumbency and inability to stand, ataxic, drunken gait, incoordination
How do you know how much bicarbonate to give to address the metabolic acidosis caused by diarrhea
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
What kind of diarrheas are septicmeia/endotoxemia more common in
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
How do you tell the difference between septicemia and endotoxemia
it is very difficult to do on the basis of clinical signs. you need a blood culture to tell the difference
in cases of neonatal diarrhea when are Na and Cl concentrations impacted
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
Acidosis may trigger and efflux of ___________ from the ___________ causing potentially life threatening condition
efflux of potassium (and H+) from the intracellular fluid causing concurrent potentially life threatening hyperkalemia and bradycardia
What is the SHADES mneumonic for neonatal diarrhea
Septicemia
Hypoglycemia
Acidosis
Dehydration
Electrolyte imbalance
Suffocation (birth hypoxia)
What is your #1 priority when dealing with diarrhea in a neonate
Fluid therapy- restore normal hydration status, replete lost electrolytes, correct any hypoglycemia, and correct metabolic acidosis
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)
Fluid deficit: 40 x 0.1 = 4L of fluid deficit
*if recumbent give IV fluids
How do you determine normal maintenance fluid needs
70ml/kg/day
(or 3-4ml/kg/hour which is 72ml/kg/day)
ex: 40kg x 70ml/kg/day =2800ml
70ml/kg/day
Maintenance fluid needs
How can you estimate the ongoing fluid losses (volume of diarrhea)
Weight the animal daily to tract it.
How will fluids be given to the diarrheic neonate
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
Why might you not give subcutaneous or intraperitoneal fluids for diarrheic neonate
-Might cause damage
-Hypoperfused tissue to the subcutis when dehydrated
What does adding glucose/glycine to fluids do
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
What is the D-isomer of glucose called
Dextrose
added to fluids to enhance sodium and water reabsorption through co-transportation
WHat are the ingredients in oral rehydration therapy
-Water
-Na+
-Cl-
-K+
-glucose
-NAHCO3/sodium acetate to become bicarbonate in liver
Oral Rehydration therapy
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”
Why shouldnt you mix ORT with milk,
what should you do instead?
Bicarb will impair milk clot formation (needs acid and Ca2+)
Alternate milk/ORT q6-8h “milk in morning, lytes at night”
How do you determine how much Na bicarbonate a calf needs to correct its metabolic acidosis
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
What might grossly tell you that a patient is acidotic
bradycardia in a patient that you think would be tachycardic
(hypovolemia normally increases heart rate) but efflux of K+ decreases the heart rate
When should you use antimicrobial drugs in neonatal diarrhea
-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)
If you have a neonate with diarrhea and showing signs of sepsis/endotoxemia
What antimicrobial should you use
-Ampicillin or ceftiofur: reasonable gram - spectrum, safe
Why are aminoglycosides not a good choice for the treatment of neonates with diarrhea
nephrotoxic- dehydration increases the risk and prolonged renal residues. not a good choice
Why should you never use fluoroquinolones on food animals
legal restrictions on food animals. cartilage toxicity risk- also no
Why shouldnt you use oxytetracycline for the treatment of neonatal diarrhea
they are bacteriostatic, you want a bactericidal agent because the neonate immune system isnt good
Why do you want a parenteral antimicrobial for the treatment of patients with systemic sepsis
because an injectable is fast to get high plasma levels of antimicrobials
What are the clinical signs of sepsis or endotoxemia, warranting antimicrobial use
fever
scleral injection
petechiation
blood or mucosal tags in feces
increased fibrinogen concentration
inflammatory leukogram
When are oral antibiotics indicated for use in calves with diarrhea
for ETEC candidates (under 1 week of age)
use oral ampicillin, amoxicillin, sulfonamide, or trimethoprim-sulfa
How should you treat clostridial enteritis
may want to treat both orally and systemically with penicillin
Should you use oral antimicrobials for the treatment of salmonellosis
antimicrobial resistance, might not be indicated
depends on serovar and factors
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?
oral sulfadimethoxine
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?
Yes- make sure it is parenterally
-Ampicillin or ceftiofur (reasonable gram - spectrum and safe
Scenario: if you have a neonate that has diarrhea and is under 1 week of age. Is antimicrobial use indicated
yes- it is indicated. likely ETEC
give ORAL antimicrobials
-Oral ampicillin, amoxicillin, sulfonamide, and trimethoprim-sulfa
NSAIDs can be ______toxic if the animal is _______
nephrotoxic if dehydrated
*make sure hydration status is restored
*monitor for anorexia, bruxism, melena:abomasal/gastric ulcers can all occur
T/F: Flunixin Meglumine and Meloxicam are indicated for the treatment of neonatal diarrhea
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
What is Kaolin-pectin used for
bind bacterial-origins toxins and reduce their translocation across the damaged gut mucosa
may also coat and protect any ulcerated mucosa
What is bismuth subsalicylate used for
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)
What is ditriotahedral smectite (Biopsonge) used for
bind bacterial-origins toxins and reduce their translocation across the damaged gut mucosa
may also coat and protect any ulcerated mucosa
What is used in prophylaxis against gastric ulcers in foals
Proton pump inhibitors (omeperazole)
Histamine-2receptor blockers (ranitidine, famotidine)
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
Pre-biotics
Contain a probiotic and prebiotic
synbiotics
directly fed microbials such as Lactobacillus, Bacillus, enterococccus, and bididobacterium that may limit the growth and activity of pathogenic bacteria
Pro-biotics
T/F oral administration of small volumes of rumen fluid from a donor ruminant may be beneficial even to the pre-ruminant neonate
True
What should you do for nursing care for neonates having diarrhea
-Isolate from healthy animals
-Supplement heat
-Dry and out the wind
-Treat scalded skin
-Monitor for corneal ulcers
Recumbent, depressed neonates may have a _____________ which makes them more at risk for corean scratches and ulcers
subnormeal corneal reflex
What is the normal incidence of diarrhea in the herd
5% (dont want to be losing more than 5%)
What diarrhea causes in neonates are considered endemic in most livestock ruminants
ETEC
Cryptosporidium
Coronavirus
Rotavirus
________ of infectious agent greatly influences outcome and the degree of clinical disease
Dose
more severe diseases and also neonates serve as amplifiers for the diseases
IgG in colostrum must be ingested within the
first 12-24 hours of life to be absorbed across the neonatal intestine
What kind of neonates are at higher risk for developing infectious diarrhea?
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
Why do calves born to heifers have an increased risk of diarrhea
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
When does the gut close, making the timing of colostrum very important
Within 24-30 hours
make sure the calf gets colostrum by 12-24 hours
How might dairy cows and goats have difficulty providing colostrum
-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
When should you test serum or plasma of neonate to assess passive transfer
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
How do you assess that antibodies were absorbed in passive transfer in calves, lambs, and kids
You can use a less expensive serum total protein if the neonate is hydrated***
Want >5.5g/dl- correlates to IgG >1000mg/dl
What does a calve with >5.5g/dl serum total protein indicated
*Note: this animal is well hydrated
there is adequate passive transfer of antibodies
correlates to IgG >1000 mg/dl
Single radial immunodiffusion (SRID)
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
T/F: the serum total protein concentration is considered accurate for use in calves, foals, and crias
False: only for use in calves, lambs, and kids
Foals and crias- need to measure IgG specifically using single radial immunodiffusion
Is vaccination of pregnant dams with ETEC vaccine efficacious
yes it is effective against ETEC- because antibodies are in the gut near the time of infection- antibodies block the K99 pilus attachment
Are toxoids (inactivated exotoxin) vaccines intended to protect against exotoxins in neonates effective
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
Is the rotavirus vaccination effective against neonatal rotaviral diarrhea
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
Is the coronavirus vaccine effective against neonatal coronavirus diarrhea
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
What is the most single critical factor in environmental management for neonates raised with their dams
udder hygiene
What are some critical environmental factors for preventing neonatal diarrhea
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)
If neonates become ill within the first week of life. What two things should you assess
1) passive transfer (colostrum)
2) maternity area hygiene
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
-Clostridiosis (Clostridial Enteritis, Enterotoxemia)- triggered by feed change or babies ingesting a massive milk feed “Hunkered down”
-Salmonellosis
-Bovine Viral Diarrhea Virus (BVDV)
When should you give C. perfringens type c and d toxoids?
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
What might increase the shedding of salmonella
Psychological stressor
-parturition, heavy lactation or severe illness, warm weather
T/F: Salmonella immunization is effective
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
Is there a lot of antimicrobial resistance with salmonella
Yes need a culture and susceptibility
-can likely change over time as you create a selective pressure for the salmonella
What is the source for BVD exposure
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
What are the clinical signs of acute infection with BVD
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
How do you diagnose acute infection with BVD
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
How do you prevent BVD
-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
sporozoan parasites that are host species specific spread through fecal-oral transmission
adults shed low numbers but diseased shed billions
Coccidia (Eimeria and Isospora spp)
How long does it take for coccidia oocysts to sporulate in the environment
takes 2-5 days to sporulate to become infective.
oocysts are not motile
What determines the disease severity of coccidia infection
Directly proportional to the number of sporulated oocysts they ingest
What is the pathogenesis of coccidia
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
T/F: there is little inflammation for coccidiosis infection
False- severe inflammation
little discrimination on what enterocytes they attack
What might trigger the clinical disease of coccidiosis
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
What are the clinical signs of coccidiosis
-Diarrhea: red to rust color in severe cases
+/- mucus membrane pallor from anemia
Tenesmus- straining to defecate
Rectal prolapse
What is the difficulty of using fecal flotation to diagnose coccidiosis
if recently ingested oocysts they might not be shedding oocysts
may see in healthy animals- low numbers
Are you going to treat animals with coccidiosis?
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
What is Amprolium used for
diluted with water
thiamine analog for the -static effect of coccidiosis
What is Decoquinate (Deccox) used for
It disrupts the energy metabolism of coccidia in cattle, sheep, and goats
What is Monensin (Rumensin) used for
coccidiostatic agent (Ionophore) approved for goats and cattle
improves feed efficiency and wait gain
What is Lasalocid (Bovatec) used for
coccidiostatic agent (Ionophore) approved for sheep and cattle
improves feed efficiency and wait gain
What species are ionophores like Monensin or Lasalocid toxic in?
Horses and camelids do not use
What are two ionophores used to treat coccidia through static actions
Monensin (Rumensin)- goat and cattle
Lasalocid (Bovatec)- sheep and cattle
Haemonchus contortus infection results in
Anemia, hypoproteinemia
*doesnt cause diarrhea
Ostertagia (Teladorsagia) cause
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
Teladorsagia cirumcincta
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
What is the infective larval stage of Ostertagia
L3
Type I ostertagiosis
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
What causes moroccan leather lesions
Nodular abomasitis from type I ostertagia
-protein losing gastropathy via imparied protein digestion (less HCl) and diarrhea occurs
Type II Ostetagiasis
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
when does hypobiosis of type II ostertagiasis occur
during the late fall and winter in the northern states
Do you see higher numbers of eggs in the feces with Type I or Type II Ostertagia
Type I
Does type I or II ostertagia cause acute abomasitis and massive destruction of gastric glands
Type II after hypobiosis is done from the emerging of L4s
How do you diagnose Type II Ostertagiasis if there are little to none eggs in the feces
-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
What abomasal lumen pH is consistent with Type II Ostertagiasis
pH >5
In the south, what allows the L4 to undergo hypobiosis in type II ostertagiasis
heat - once in fall this allows the L4 to emerge and cause acute abomasitis
How do you treat ostertagiasis
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
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
Winter Dysentery
What are the clinical signs of Winter Dysentery
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
How is winter dysentery brought on the farm?
Vets, milking machine repair personel, visistors, rodents and birds, fomites
*Biosecurity is very important
How do you diagnose Winter Dysentery
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
T/F: cows with winter dysentery are febrile
False
Chronic granulomatous enterocolitis and protein losing enteropathy caused by Mycobacterium avium ssp. paratuberculosis
Johne’s Disease
What animals does Johne’s disease impact
Adult cattle, sheep, goats, camelids
When is Johne’s Disease infection established?
Neonate but the disease is seein in the adult (Chronic, granulomatous enterocolitis, )
What is the pathogenesis of Johne’s disease
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)
Is Johne’s disease more common in beef or dairy cattle
dairy cattle
due to the management methods of dairy breeds as you concentrate feces, you concentrate pathogens
The vast majority of Johne’s disease infections occur in neonates via colostrum/milk or contaminated environment but how else can this be passed?
transplacental transmission
When do most Johne’s clinical signs seen
2-6 years of age
*larger the infective dose, the earlier the signs develop in the infected animal. reports as young as 13 months
When are Johne’s disease serologic tests normally positive
once the adult animal is showing signs of weight loss and diarrhea the antibody titer levels are typically high enough
What are the clinical signs of Johne’s disease in cattle
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
What is significant about Johne’s disease in sheep, goats, and camelids
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
How do you diagnose Johne’s disease
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
Serologic testing for Johne’s
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
How long does it take to culture Johne’s disease
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
What is a pass-through fecal positive test for Johne’s
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
T/F: adults can get infected with Johne’s disease
false- only neonates
How long should you allow to clear MAP in the tract when you suspect a pass-through fecal positive for Johnes disease
allow 2-4 months to pass, thereby enabling those innocent noninfected pass through cases to clear MAP from their GI tracts. Then test again
What are the findings of johnes disease on necropsy
thickened ileum and corrugated
mesenteric and ileocecal lymph nodes are enlarged and edematous
What are the findings of Johnes disease on histopath
clumps of acid-fast bacilli within macrophages
What tissues should you submit if you suspect Johnes disease
submit a piece of bowel, make sure to get several cm of ileum in it and ileocecal lymph nodes, located within the ileocecal fold
What is the treatment for Johnes disease
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
testing in parallel
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
How should you control for Johnes disease
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
Please provide six specific functions/effects of primary contractions of the ruminant stomach.
*Know this
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
Please list all seven conditions that can cause a ‘ping’ in the right side of a cow’s abdomen.
*Know this
Abomasal volvulus
Abomasal displacement (right)
Cecal dilatation
Cecal volvulus
Pneumoperitoneum
Ascending colon gas
Rectal gas
Please list four different functional causes of ruminal bloat.
*Know this
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)
Please provide four specific observations/measurements you will make during a cowside rumen fluid analysis.
*Know this
-Color
-Odor
-pH
-Methylene Blue Reduction
-Consistency/viscousity
-Sediment/flotation
-Protozoal activity
-Chloride content
What are the 5 clinical signs of TRP and what causes them
*know this
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
What are two factors in the pathophysiology of ruminal lactic acidosis. For each, provide a specific effect or consequence of that item.
*Know this
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
Please provide two findings that will specifically distinguish rumen acidosis from indigestion due to poorly digestible fiber (hay belly).
*Know this
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
What do BVD, Blue tongue, and MCF all have in common
they all cause:
-fever
-ulcerative lesions of oral tissue
-lesions at mucocutaneous junction
-lesions of skin/hoof junctions
-depression
-anorexia
How do you you distinguish BVD from blue tongue and from MCF
*Know this well
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
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
it causes diarrhea and a leukopenia
What are the clinical sequelae of BVD *Know this
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
Please list six factors that can predispose to development of left displacement of the abomasum in cattle.
*Know this
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
urine is acidic pH while systemic alkalosis is present
paradoxical aciduria
Please briefly define abomasal reflux, what causes it, and what its effects are.
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.
Please list three types of abomasal ulcer, and briefly describe how they will be distinguished from one another.
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
Please list fblood biochemical changes that commonly accompany various gastrointestinal obstructive disorders in ruminants.
Decreased Cl-
Decreased K+
Increased HCO3 (metabolic alkalosis)
Increased creatine (dehydration, pre-renal azotemia)
Ketosis
Decreased Ca++
Decreased Na+
Increased PO4-
Increased plasma protein
Please list and briefly describe three different congenital disorders that affect the bovine gastrointestinal tract.
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.
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?
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.
30 kg and 8% dehydrated. What is the calculated fluid deficit, in liters, for this calf?
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.
