Smith 5 - 32 Ruminant GI Flashcards
decreased skin turgor, tear film, dry mms, sunken eyes indicate
dehydration - not hypovolaemia
normal CVP of adult horse
7-12mmhg
when to correct academia with bicarb
- pH < 7.2
- hyponatremia , hyperchloremia
- normal resp function
ruminant saliva
- 90-120mmol/L bicarb
- pH 8.2
sialoadenitis
inflamed salivary gland due to ascending infection from a traumatized duct
-abscess formation
actinobacillus lignieresii
woody tongue
- gram neg rod
- granulomatous abcscesses
- sulfur granules in pus
- Dx: biopsy and culture
- Tx: sodium iodide IV
actinomyces bovis
lumpy jaw
- gram pos filamentous
- osteomyelitis + new bone + fibrous tissue
- Tx: sodium iodide + penicillin, +/- isoniazid
bovine papular stomatitis
- parapox virus
- no vaccine
bluetongue
arthropod transmitted (culicoides) orbivirus
- cattle are reservoir host
- reproductive syndromes or hemorrhagic fever affecting upper GI
- Vx available
Incubation- 3-7 days-> transient fever (106F or higher), edema of face, lips, muzzle and ears; excessive salivation + hyperemia of oral mucosa; mucopurulent nasal discharge leaving crusts; cyanotic tongue; oral petechial hemorrhages, erosions and ulcers esp on dental pad and lip commissures
Hemorrhagic fever - vasculitis - infarctions = ulcers and cyanotic tongue - teratogen
BVDV
-pestivirus, 1b predominant in us cattle
acute-transient BVD
- postnatal cattle aged 6-24 months
- mostly no clinical signs
severe acute BVD
- disease in normal cattle 6-24mos
- diarrhea, fever, abortions
- high morbidity + death
- BVDV-2 non cytopathic strain in non-vax animals
hemorrhagic BVD
- thrombocytopenia
- highly fatal
- Bloody D+, epistaxis, petechial hemorrhages, ecchymoses, hyphema, bleeding @ injection sites or insect bites, Leukopenia
- Almost all BVDV-2 NCP
- Bone marrow infxn and specifically BVDV infection in bone marrow megakaryocytes may be important in etiology of thrombocytopenia
acute BVD immunosuppression
causes leukopenia, decreased number of B and T cells
dams infected when will deliver PI calves?
45-125 days
-non cytopathic strains only!
BVD mucosal disease
-NCP PI cow becomes infected with CP strain
- superinfection with a cytopathic strain similar to the PI NCP strain
- acute is 100% fatal
- chronic
Necrotizing erosive or ulcerative lesions involving the mouth, external nares/nasal cavity, tongue, esophagus, ruminal pillars, omasum, abomasum, intestines, cecum
Bowel contents are watery, hemorrhagic and foul smelling
Depletion of gut associated lymphoid tissue
Skin and hoof lesions
BVD Vx
goal is to limit infection, not disease
malignant catarrhal fever
- group of herpesviruses
- OHV-2 in sheep
- lymphocytic vasculitis + dysentery
- mostly fatal
- DDX mucosal disease, blue tongue
VS
- rhabdovirus, vesiculovirus
- cyclic vesicles, erosions, ulcers
- distinguish from FMD: PCR, ELISA microscopy
- old high producing cows more susceptible
FMD
- higher mortality rate in young due to myocarditis
- picornavirus, aphthovirus
- spreads rapidly
- Dx w PCR or virus isolation
- survival good but causes poor production
DDX for dysphagia
RABIES
choke complications in cattle
- dehydration
- metabolic acidosis (due to saliva loss)
- bloat
parietal pain
- travels through peripheral spinal nerves
- localizes over affected area
- reluctant to move because pressure and tension worsen it
R ping ICS9-13
abomasal torsion or RDA
ping - R paralumbar fossa to hip
cecal dilation or volvulus
L ping ICS 8-13 dorsally
LDA
ruminant indigestion
- dysfunction of the reticulorumen
- inappetance, decreased motility, abnormal feces
1) abnormal motor function
2) abnormal contents
most common sign of ruminal dysfunction
- decreased / absent / abnormal ruminal contraction sounds in the L paralumbar fossa
- abnormal L sided contour
bradycardia w/ indisgestion
- vagal
- HR 40-60
- reversed with atropine
excitatory inputs to the gastric centers
1) low threshold tension receptors in the reticulum (medial wall - influence frequency of contraction)
2) buccal receptors in the mouth (double rate of primary contractions when food is in the mouth)
3) acid receptors in the abomasum
inhibitory inputs to the gastric center
1) high threshold tension receptors (sensory nerve endings in rumen and reticulum)
2) tension receptors (abomasum)
3) chemical receptors (ret, rumen)
4) pain receptors in the body
5) direct effect on gastric centers (medulla- ex drugs)
6) hypocalcemia
ventral vagus innervates
cranial and medial reticulum, omasum, and abomasum
the dorsal vagus innervates
rumen
secondary rumen cycles are responsible for
eructation
ruminal parakeratosis
- papillae dark, enlarged, thick, clumped
- thickened cornfield layer of epithelial cells
- reaction to high concentration of VFAa
- animals on pellets / finely ground high energy diets
- increased propionate and butyrate, decrease acetate
- lower rumen pH
vagal indigestion
obstructive indigestion
- progressive distention (dorsally and ventrally L abdomen, ventrally R)
- overfilled rumen, not abomasum
- anorexia, weight loss, decreased feces
omasal transport failure
- accumulation of ingesta in reticulorumen
- omasum and abomasum empty
- inappetance with gross distention of the L flank
- Papple (L apple / R pear)
- greasy, large fiber or particles in feces
- uniform frothy rumen contents
causes of omasal transport failure
- HARDWARE (TRP)
- abscesses, adhesions, peritonitis, chronic bronchopneumonia in calves
pyloric outflow failure
- accumulation of ingesta in abomasum and omasum
- can result in Cl sequestered in abomasum (metabolic alkalosis)
- rumen contents remain stratified
causes of failure of pyloric outflow
- abomasal volvulus
- LDA / RDA
- advanced pregnancy
chronic recurrent bloat is associated with what type of obstructive indigestion
all forms
chronic recurrent bloat
- mild to mod
- waxes and wanes
- gross abdominal distention
causes of rumen tympany
- obstruction of eructations
- ruminal motor dysfunction
- chemical inhibition
trichobezoars in calves
- low roughage diet
- lick hair coats vigorously
two most common causes of obstructive indigestion
- inflammatory lesions of the reticuloomasal region
- abomasal disease that involves distention, twisting, or vascular impairment (worse prognosis)
ideal feed for cows
high quality, long length fiber
crude fiber > 18% of DM
moderate protein concentrate 20-50% of total intake
ideal VFAs
acetic > propionic > butyric acid
low nutrient forage diet, low protein
- increases pH
- poor growth / malnutrition
high concentrate diet
- decreases rumen pH
- high production and rapid growth
- risk of acidosis, milk fat depression
ideal rumen pH
5.5-7
acute rumen acidosis
- can be lethal in 24 hours
- depression, dehydration, weakness, recumbency, diarrhea
- increased HR/RR, decreased temp
- rumen accumulates fluid
- may be blind, stagger
- metabolic acidosis, decreased pH and bicarb, acidic urine
rumen microbes produce what type of lactate
L and D
how is lactate eliminated
oxidation, gluconeogenesis, renal excretion
-speed depends on hydration status, liver and muscle metabolism, and renal function
SARA
- subacute ruminal acidosis
- excess concentrate or low level roughage
- prolonged exposure, pH 5-5.5
- microbes adapt; cellulolytic decrease, lactate using increase, starch-and-glucose fermenting species increase
- feed is rapidly fermented, lactate is used so it does not accumulate
- increased Propionic and Butyric, Decreased acetic a
- herd level
frothy bloat
- stable foam forms
- can distend enough to compress thoracic viscera
- uniform abdominal enlargement
- pain and resp distress
- lush legumes, wheat pasture, or high concentrate rations
- fluid is high in chloroplast membranes, soluble protein, and fine particles
- poloxalene or mineral oil via stomach tube; rumenotomy
ruminal alkalosis
- microbial fermentation is reduced
- continual saliva ingestion
- pH 7-7.5
- overfeeding np-nitrogen or fertilizer poisoning
predominant fore stomach organisms in calves
coliforms and lactobacilli
-lactose fermenting, facultative anaerobes
major adverse effects of peritoneal contamination
1) rapid clearance of bacteria leading to bacteremia/endotoxemia
2) rapid influx of protein rich fluid leading to hypovolemia / hypoproteinemia
3) deposition of fibrin, occludes lymph drainage, contributes to abdomen distention, enhances chance of abscesses
4) ileus
5) adhesion formation, might cause obstruction
causes of ascites in ruminants
severe liver dz
right sided CHF
young cattle w/ mesothelioma
what can a sharp foreign object do in cattle
1) attach to magnet
2) penetrate reticular wall = intramural inflammation
3) perforate reticulum and go into peritoneum = localized septic peritonitis
4) migrate into peritoneum and thorax or pericardium
CS of severe TRP
fever, anorexia, decreased or absence of ruminal contractions, cranial abdominal pain
-grunting or standing w back arched
CS of TRP + pericarditis
muffled heart sounds, jugular vein distention, edema of the submandibular region, brisket, and ventral abdomen
prerequisite factor for abomasal displacement
hypomotility
which DA is more common
L
-esp adult dairy cattle, early postpartum
RDA vs volvulus
-progressively more ill and dehydrated w/ volvulus
4 types of abomasal ulcers
1) non perforating
2) non perforating with severe blood loss
3) perforating with local peritonitis
4) perforating with diffuse peritonitis
type ___ abomasal ulcers erode blood vessels
2; can cause anemia, melena, hemorrhagic shock
All ruminants;
colic, then chronic low grade pain, dehydration, mucus plus blood in dark red feces, slow abdominal distention, decreased fecal output, mass palpated rectally, distended loops of intestine
intussuception
mild to severe colic, distended upper right abdomen, ping in R paralumbar fossa, distended cecum
cecal dilation and volvulus
most common intestinal tumor in cattle
adenocarcinoma
diseases caused by c. perf toxins
yellow lamb disease, lamb dysentery, necrotic enteritis, enterotoxemia
yellow lamb disease
- c perf type A
- alpha toxin causes lysis of RBCs, platelets, and leukocytes
- icterus, high temp, usually die in 6-12 hours
lamb dysentery
- c. perf type B
- not in america
- less than 1 weeks old, D+ and die
- can vax
necrotic enteritis / neonatal hemorrhagic enterotoxemia / struck
- c. perf type C
- beta toxin (usually destroyed by trypsin in intestine; colostrum inhibits trypsin)
- calves, lambs, foals, and piglets
- D+ yellow to brown and bloody
- severe dz, may have neuro signs,
overeating disease / pulpy kidney
- c. perf type D
- sheep and goats >2wks
- high grain diets
- ataxia, trembling, stiff limbs, opisthotonos, resp difficulty, convulsions, coma, death
- rarely have D+
onset of CS may be hyperglycemia, at death glucosuric
oak / acorn toxicosis
- Quercus spp
- oak tannin metabolites and volatile phenols; metabolized to gallic acid / pyrogallol
- edema, anuria, anorexic and listless
- calves have hemorrhagic D+
- uremia
winter dysentery
- coronavirus
- acute contagious explosive D+ in a herd
- BUBBLES!
- necrosis and hemorrhage of crypt epithelium
- incubation 2-8 days; takes 2 weeks to run through whole herd
- most recover spontaneously
salmonella in ruminants
- increasing in prevalence in dairy cows
- B, C, D, E, K
- D1 DUBLIN MOST COMMON
- fever and D+, watery to mucoid with fibrin and blood
- acute PLE
dry gangrene
may occur after salmonella infection in calves; legs, ears and tails are affected
salmonella abortion
1) bacteremia in the dam causes infected placenta/fetus
2) bacteremia, endotoxemia, fever release PGF2a - lyse CL
salmonella tx in cattle
florfenicol, ceftiofur
- tms po in calves <3 weeks
- NSAIDs
- fluids
abx not allowed in cattle
- metro
- nitrofurazone
johnes disease (MAP)
- intracellular pathogen, survives in macrophage by preventing maturation and acidification of the phagocytic vacuole
MAP portal of entry
ileum
tonsils maybe
what is necessary to clear MAP infection
macrophages activated by TH-1, IFN-gamma
CS copper deficiency in ruminants
- D+, decreased gain, unthrifty appearance, anemia, coat color changes, spontaneous fractures, lameness (epiphysitis), and ataxia (demyelination)
minimum recommended copper
4-10 ppm (mg/kg) - cattle
5ppm for sheep
ovine while liver disease
Co deficiency
- ill thrift, weight loss, serous ocular discharge, photosensitization
Co deficiency
- nonspecific signs
- ill thrift, pica, anemia, lacrimation
- B12 may appear falsely elevated but is actually deficient
- inefficient propionate metabolism
3 largest salivary glands in ruminants
parotid, mandibular, sublingual
hard, painful, nodular ulcerated lesions at base of tongue
actinobacillus lignieresii / woody tongue
Tx = sodium iodide
excessive tearing, coughing, inappetence, diarrhea, dandruff = CS of?
Iodinism - stop treatment!
causative agent of lumpy jaw
actinomyces bovis
also tx with Na iodide
which BVDV is most common in the US?
BVDV-1a,b and BVDV-2
BVDV-1b accounts for 78% of PI’s
DNA poxvirus of the parapoxvirus subgroup
Dz of sheep and goats that is zoonotic. Wild ruminants and camelids also affected.
2-14 day incubation period; tends to be more severe in goats with Boers more likely to have severe generalized infxns with proliferative dermatitis, arthritis and lymphadenopathy
Endotheliotropic virus that creates proliferative lesions in the skin of the lips, nostrils, oral mucosa, teats + occasionally the vulva. Crusting, proliferative lesions of the mucocutaneous junctions of the mouth and nose. Can see lesions on coronary band, tongue, interdigitally, conjunctiva, external genitalia, udder or teats.
Papular->vesicular->pustular-> proliferative, coalescing and scabbed lesions
Reluctant to nurse, eat, walk or be nursed dependent on location
Runs course in 6 weeks typically
Orf
BVDV infection at 0-45 days of gestation will cause
abortion
BVDV infection at 45-125 days of gestation will cause
a PI!
BVDV infection at 100-150 days of gestation will cause
Congenital Defects: cerebellar hypoplasia, hypomyelinogenesis, hydrancephaly, alopecia, cataracts, optic neuritis, brachygnathism, hydrocephalus, microencephaly, thymic aplasia, hypotrichosis, pulmonary hypoplasia, growth retardation
Dx of BVDV PI’s
Direct antigen detection by IHC, ACE or immunofluorescence with ear notch tissue sample
Acutely infected and PI animals can be differentiated based on location of viral antigen in skin
Virus isolation is gold standard - RT-PCR can be used on multiple samples in other acutely infected animals (serum, nasal swab, tissue)
low threshold tension receptors
- are in the reticulum, medial wall
- sense mild distention and tension generated during contractions
- excite gastric centers
- cause increased rumen motility
high threshold tension receptors
- are in the reticulum and cranial rumen sac
- sense bloat and severe ruminal distention
- inhibit gastric centers
- cause decreased rumen motility
rumen indigestion: primary cycle disturbances
- inhibition of gastric centers
- high threshold receptor activation
- abomasal distention
- VFAs increased in retic and rumen, acidosis, toxins
- pain
- hypocalcemia
- central depression (medulla)
rumen indigestion: secondary cycle disturbances
- eructation obstruction (choke)
- ruminal motor dysfunction (frothy bloat)
- chemical inhibition (DA, vagus nerve damage dt inflammation, ruminal stasis)
TRP may occur with _____ deficiency
phosphorous (pica)
fever can be used to differentiate indigestion from ?
TRP or rumenitis
gram + cocci and rods on gram stain of rumen fluid indicate ?
grain overload
rumen fluid chloride > 30 mEq/L indicates ?
abomasal reflux
risk factors for hemorrhagic bowel syndrome
o Feeding silage or total mixed ration
o Dairy farms with >100 cows
o High-intensity milk production
MgOH
contraindicated in obstruction or ileus
decreases potassium absorption
increases ruminal pH, decreases ruminal microbial activity, and causes sedation and metabolic alkalosis
most effective treatment for abomasal hypomotility
erythromycin
best clin path Dx for TRP
Haptoglobin + SAA
(better than fibrinogem)
TRP Tx
- magnet, abx, confinement
- if not better in 3 days, rumenotomy
- prevent by administering magnets to all at 6-8 months of age
CS of peritonitis
- reluctance to move
- lack of “rectal sweep”
johne’s eclipse phase
If disease not eliminated, the constant presence of MAP antigen in the intestinal and gut associated lymphoid tissue incites a chronic inflammatory response=granuloma formation with MAP laden macrophages, epitheloid cells, lymphocytes and multinucleate giant cells
§ This period called the eclipse phase where there is no detectable fecal shedding of MAP, or Ab production in serum
o Eventually, host cell-mediated immune response cannot contain infection.
§ Dangerous as animal subclinical but shedding disease through herd
o Disease spreads-MAP go to extraintestinal sites via blood or lymphatics=transplacental infection or direct shedding in milk or colostrum
johnes in other ruminants
may not have diarrhea
have weight loss, submandibular oedema, goats can become anaemic. Can have concurrent parasite burden
johnes immune based testing
ELISA
serum or milk in cattle
most sens / spec
Low sensitivity to detect low fecal/asymptomatic shedders
johnes organism tests
Fecal culture and PCR. Advantage to Ab tests include: detection earlier in disease course, allow quantification of the degree of fecal shedding , definitively ID MAP in the herd at the time of initial diagnosis BUT they are expensive (PCR) and time consuming if culture (1-2 months)
In goats- use same tests as cattle (serum ELISA, fecal culture and PCR). In sheep-testing for Ab less reliable and organism detection tests (culture and PCR on feces) is recommended
johnes Tx plan
Typical treatment plan: rifampin (10mg/kg PO Q24) and isoniazid (10-20mg/kg PO Q24). Gentamicin can be used in the initial 5-10days of treatment to hasten remission. Add in monensin for cattle (inhibits MAP growth in vitro)
rectal prolapses
Type 1) mucosal prolapse only involving mucosa and submucosa of rectum
Type 2) full thickness of rectum
Type 3) complete prolapse plus intussusception of peritoneal rectum or small colon
Type 4) intussusception of peritoneal rectum or small colon-not complete prolapse of rectum
Treat types 1 and 2 conservatively-epidural, sedation, replace prolapse and purstring
Types 3 and 4 may require celiotomy
copper deficiency
Diarrhea, decreased weight gain, ill-thrifty, anemia, coat colour changes, reduced wool quality, anemia, spontaneous fractures, lameness, demyelinization (enzootic ataxia or swayback), infertility
primary - low in diet
secondary - due to high Mb, sulfates, zinc, ca, or fe
what disinfectant is effective against crypto
formaldehyde
_______ concentration provides the most sensitive indicator of energy balance, particularly in the last 2 weeks of gestation.
Plasma NEFA
_________ concentration is useful for monitoring the energy status of dry cows in the last month of gestation, when rapid changes in energy-balance status may not be detectable from changes in body-condition score.
Plasma NEFA
________ concentrations start to increase 3 days before parturition and remain elevated for the first 9 days of lactation.
Plasma NEFA
High plasma ___ concentrations are associated with reduced milk production, increased incidence of clinical ketosis and LDA, and reduced fertility. Th
BHB
Plasma/serum _______ concentrations are affected by energy and glucose balance and are a less sensitive indicator of energy balance than plasma NEFA.
BHB
e gold-standard test for hyperketonemia (subclinical ketosis) is _______ which is more stable after collection than plasma/serum acetone or acetoacetate concentrations.
plasma / serum BHB
Prepartum concentrations are relatively stable before parturition, but increase rapidly after parturition to peak at around 9 days in milk, after which time ____ concentration gradually declines
BHB
Subclinical ketosis may start at serum BHB concentrations above ____mmol/L.
1.0
3 stages of milk fever
Three progressively worse stages including early signs such as restlessness, muscle fasciculation over shoulder and neck, cool skin, anorexia, rumen atony with mild bloat, and insecure gait. More advanced stages with general muscle weakness leading to sternal recumbency with head resting on the chest, mental depression, dilated pupils, weak heartbeat und pulse, increased heart rate, dry muzzle, dry feces, and hypothermia. Last stage characterized by lateral recumbency, severe obtundation, severe rumen bloat, barely audible heart, tachycardia, circulatory collapse, coma, and death.
milk fever usually occurs
48 hours after calving hypo cal
DCAD: Diets high in cations, especially potassium and sodium, tend to _____ milk fever
induce
DCAD: Diets high in anions, primarily chloride and sulfur, can_____ the milk-fever incidence.
reduce
When the dietary cation concentration is increased and these cations are absorbed from the digestive tract, they tend to _______ the plasma strong ion difference (SID), thereby creating a metabolic (or strong ion) _______.
increase alkalosis
Conversely, dietary anions absorbed from the gut _____ the SID, which causes metabolic ______.
decrease acidosis
The feeding of diets containing an excess of anions relative to cations, thus with a low DCAD, will result in ?
metabolic acidosis.
How does a low DCAD diet help cows resist milk fever?
Two PTH-dependent functions, bone resorption and renal production of 1,25-(OH)2D, are enhanced in cows fed diets with added anions, and thus a low DCAD, which increases their resistance to milk fever and hypocalcemia.
DCAD4 =
(Na + K) - (Cl + S)
how to lower DCAD
lower K add Cl or S anionic salt
ideal urine pH of cows on DCAD
6-7
major precursor for gluconeogenesis in cattle
proprionate and AAs
cobalt deficiency
failure to metabolize proprionic acid in the TCA cycle —> ketosis
wasting ketosis
most common lose appetite over 2-4 days, off grain first, then silage, then hay TPR normal ketone breath firm dry feces, constipated decreased milk yield, fat
nervous ketosis
signs are usually bizarre and begin quite suddenly delirium rather than of frenzy Walking in circles Straddling or crossing of the legs Head pushing or leaning Apparent blindness Aimless movements and wandering Vigorous licking of the skin and inanimate objects Depraved appetite Hyperesthesia may be evident, with the animal bellowing on being pinched or stroked. Moderate tremor and tetany may be present, and there is usually an incoordinate gait. The nervous signs usually occur in short episodes that last for 1 or 2 hours and may recur at intervals of about 8 to 12 hours.
Possibly the most relevant biochemical index of the liver fat percentage is the
plasma NEFA : cholesterol ratio A high plasma NEFA : cholesterol concentration therefore is thought to indicate a high liver fat percentage. An increased concentration of plasma total bilirubin is also associated with increased liver fat percentage;
primary ketosis occurs when
4 - 8 weeks post calving, peak lactation
watery mouth
NO DIARRHEA Affected lambs are normal at birth but become sick at 24 to 48 hours and up to 72 hours old. The disease is characterized by dullness, lethargy, a complete failure to suck, and excessive mucoid saliva around and drooling from the mouth. As the disease pro- gresses there is hypothermia, failure to pass feces, cold extremities, depression to the point of coma, anorexia, and, in the late stages, abdominal distension and recum- bency, but rarely diarrhea. The alimentary tract is full of fluid, and the lamb rattles when it is shaken. Some lambs are hypothermic, but the temperature is normal at the onset of the condition and falls to subnormal as the disease progresses. Progress is rapid, with death 6 to 24 hours after the first signs of illness.
—High-level grain diets, immediately postpartum, dairy cows, inactivity —Acetonemia in cow within days after parturition, inappetence, feces soft and amount variable (usually reduced) —ketonuria —Excellent response following surgical correction
LDA
—Usually 2–4 weeks postpartum —Anorexia, scant feces, reduced milk production, moderate dehydration, rumen sluggish, fluid-filled viscus under right costal arch, ping over large area; tense viscus palpable per rectum in right lower quadrant, progressive and commonly results in volvulus —Alkalosis, hypochloremia, hypokalemia
RDA Surgery is immediately indicated. Prognosis good if treated early. Need to differentiate from volvulus at sx time.
—dairy cow, a few days following parturition or may have had LDA for several days —Complete anorexia, rumen stasis, almost no milk yield, ketonuria initially but may have more later
fatty liver / fat cow syndrome ketonemia and increased liver enzymes
—Single case Dairy cow, early lactation, inappetence, feces may be scant Severe cases have history of mild abdominal pain —Systemically normal Rumen only slightly hypotonic, highpitched ping on percussion over right upper flank
Cecal dilatation or cecocolic volvulus
papple shaped abdomen indicates
vagal indigestion
Abdomen usually gaunt; occasionally distended left paralumbar fossa because; ping on percussion over upper aspects of ribs 9–12
LDA
Older calves (2–4 months); right lower flank distended; fluid-splashing sounds; painful grunt on deep palpation Confirm by laparotomy and abomasotomy
abomasal trichobezoars
Marked distension of left abdomen, less of right; very tense distended left paralumbar fossa, dull resonance on percussion; pass stomach tube and attempt to relieve gas or froth
acute ruminal tympany
Marked distension of left abdomen, less of right “papple-shaped” abdomen; fluctuating rumen on palpation; excessive rumen activity or complete atony; large L-shaped rumen on rectal examination; pass large-bore stomach tube to remove contents to aid in diagnosis
vagal indigestion
Moderate distension of left flank, less of right; rumen contents are doughy or fluctuate; fluid-splashing sounds may be audible on ballottement; rumen static and systemic acidosis; rumen pH below 5
acute ruminal acidosis
Right flank and paralumbar fossa normal to severely distended; ping; rectal palpation of fluctuating or tense viscus in right lower quadrant
RDA and abomasal volvulus
Right lower flank normal to moderately distended; doughy viscus palpable caudal to costal arch; rectal palpation feel doughy viscus in right lower quadrant
abomasal impaction
Right flank may be normal or moderately distended; ping present in right paralumbar fossa; palpate movable blind end cecum on rectal examination (cecal dilatation) or multiple loops of distended large intestine (cecocolic volvulus); confirm by laparotomy
Cecal dilatation and cecocolic volvulus
Gradual enlargement of lower half of abdomen in late gestation; flaccid uterus; fetus and placentomes are easily palpable per rectum
hydrops amnion
Gradual distension of lower half of abdomen in late gestation; palpable uterus rectally, cannot palpate placentomes or fetus
hydrops allantois
History of dystocia or recent birth of one calf, twin in uterus and emphysematous; diagnosis obvious on vaginal and rectal examination
fetal emphysema
causes of reduced or absent rumen protozoon activity
Ruminal acidosis (lactic acid inactivates protozoa); primary starvation lasting more than 2–3 days; ingestion of lead, arsenic, and other poisonous substances
Calf usually under 10 days of age, progressive distension of abdomen, bright and alert for first few days then becomes depressed, no feces only thick mucus from rectum, surgery indicated but only a minority have a successful lactation as a firstcalf heifer, potential genetic component in Holstein Friesian cattle
atresia coli
Calf - May have history of diarrhea, now scant bloodstained feces, depressed, will not suck or drink, dehydrated, contour of abdomen may appear normal or slightly distended, fluid-splashing sounds and small ping may be audible, bloodstained peritoneal fluid, presurgical diagnosis often difficult, surgery necessary
intussusception
Chronic wasting disease of adult sheep; diarrhea not a distinct clinical f inding. Common cause of emaciation in ewes, although cases can occur in 10- to 15-month-old sheep in high-prevalence f locks.
johnes
goats: Chronic progressive intractable diarrhea and emaciation extending over several weeks and months. Generally, a higher prevalence in milch compared with fiber breeds.
johnes
Outbreaks of diarrhea, ill-thrift, and deaths in young deer (8–15 months) or latent infection that causes sporadic cases with weight loss and terminal diarrhea in older deer.
johnes
Currently there are four recognized species of the genus Pestivirus:
BVDV1 BVDV2 border disease classical swine fever / hog cholera
—Mostly young cattle 6 months to 2 years, can be adults —Many in group affected —Persistent diarrhea, without smell, mucus. or blood —Decreased appetite, bottle jaw, very thin
ostertagiasis
