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454 Cards in this Set
- Front
- Back
inflammation of the oral mucosa is called what? |
stomatitis
|
|
what is stomatitis?
|
inflammation of the oral mucosa
|
|
what are five clinical signs of stomatitis in the ruminant?
|
1. decreased salivation
2. depressed appetite 3. dysphagia 4. abnormal odor 5. vesicles, erosions, ulcerations |
|
what are the three basic etiologies of stomatitis in the ruminant?
|
1. chemical irritants
2. physical trauma 3. infection |
|
what are four chemical irritants that cause stomatitis in the ruminant?
|
1. oral calcium supplements (CaCl2 paste)
2. foot bath chemicals 3. dehorning paste (KOH) 4. uremia |
|
what are three types of physical trauma that cause stomatitis in the ruminant?
|
1. coarse feed
2. ingestion of plants (grass awns, bristle grass, thistles) 3. medication administration (e.g. balling gun) |
|
what are nine viral diseases that cause stomatitis in the ruminant?
|
1. vesicular stomatitis
2. MCF 3. bluetongue 4. bovine papular stomatitis 5. contagious ecthyma / orf / sore mouth 6. BVD 7. FMD 8. Rinderpest 9. Vesicular Exanthema of swine |
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what are four reportable infectious diseases that cause stomatitis in the ruminant?
|
1. vesicular stomatitis
2. FMD 3. Rinderpest 4. vesicular exanthema of swine |
|
what are five clinical signs of a foreign body in the mouth of the ruminant?
|
1. difficulty eating & drinking → weight loss & dehydration
2. excessive salivation 3. dropping of feed (quidding) 4. abnormal chewing and movement of the head 5. necrotic breath |
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how is a foreign body in the mouth of a ruminant diagnosed
|
oral exam
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what is the treatment for an oral foreign body in the mouth of a ruminant?
|
remove object; a/b if object penetrates deeply into the mucosa
|
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what agent causes Woody Tongue?
|
Actinobacillus lignieresii
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explain the epidemiology of Woody Tongue
|
- Actinobacillus lignieresii normal flora of the mouth
- breaks in the oral mucosa (coarse feed, grass awns, thistles) set up opportunistic infection |
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what are clinical signs of woody tongue? (7)
|
- inability to prehend food
- excessive salivation - tongue may protrude from the mouth - base of tongue is very hard, painful, and nodular, and may affect the shaft of the tongue - nodular lesions may be ulcerated, contain yellowish-white pus - enlarged lymph nodes of the head - small ruminants: granulomatous lesions may be observed on the lips, nose, and face |
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what is one difference in the clinical presentation of woody tongue between cattle and small ruminants?
|
in small ruminants, one may observe granulomatous lesions on the lips, nose, and face
|
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what are two ways in which woody tongue is diagnosed?
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1. clinical signs
2. pus crushed between 2 slides shows sulfur granules and gram-neg rods |
|
how is woody tongue treated?
|
- IV sodium iodide solution
- sulfas and tetracycline |
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what are five clinical signs of iodism in the ruminant being treated with sodium iodide for woody tongue or lumpy jaw?
|
1. dandruff
2. excessive tearing (epiphora) 3. coughing 4. inappetence 5. diarrhea |
|
what agent causes Lumpy Jaw?
|
Actinomyces bovis
|
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explain the epidemiology of Lumpy Jaw
|
(similar to Lumpy Jaw)
- Actinomyces bovis normal flora of the mouth - breaks in the oral mucosa (coarse feed, grass awns, thistles) set up opportunistic infection - (additionally, vs. woody tongue) may enter through diseased teeth |
|
what are three clinical signs of lumpy jaw?
|
1. osteomyelitis of the mandible, possibly the maxilla - involvement of the bone
2. hard, swollen jaw and associated lymph node enlargement with or without fistulous tracts 3. pus contains yellow sulfur granules |
|
how is lumpy jaw treated?
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1. sodium iodide IV
2. penicillin 3. curettage and flushing of draining tracts |
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after lumpy jaw has been successfully treated, how long does it take for the swelling to recede?
|
never. It is permanent osteomyelitis with bone remodeling
|
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how long does it take the rumen to adapt to new dietary conditions?
|
2 weeks
|
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what are clinical signs of traumatic pharyngitis? (8)
|
- difficulty swallowing
- increased salivation - SWELLING OF THE THROAT LATCH AREA - inhalation pneumonia - abnormal chewing - halitosis - ± dyspnea - fever, if cellulitis present |
|
what causes traumatic pharyngitis of ruminants?
|
- iatrogenic: improper use of balling gun, tubes, or dose syringes
- ingestion of sharp objects |
|
what is the prognosis of woody tongue?
|
good, if tongue softens within 48 hours of treatment
|
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how is traumatic pharyngitis diagnosed in the ruminant? (2)
|
- oral exam
- history of possible trauma to pharynx |
|
how is traumatic pharyngitis treated in ruminants?
|
- penicillin
- NSAIDS - Banamine (phenylbutazone) [or aspirin] |
|
esophageal obstruction in a large animal is called what?
|
choke
|
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what are the two basic clinical manifestations of choke and their etiologies?
|
1. intraluminal - foreign bodies (e.g. apples, boluses of dry grain)
2. extraluminal - infection or constriction form a previous episode of choke |
|
what are some causes of extraluminal choke in ruminants? (7)
|
1. cellulitis from injections
2. abscesses 3. enlarged mediastinal lymph nodes 4. tumors 5. pneumonia 6. Hypoderma lineatum larvae (bots, warbles) 7. stricture from previous episodes of choke |
|
what are four clinical signs of choke in ruminants?
|
1. increased salivation and attempts to swallow
2. may throw head from side-to-side to try to dislodge mass 3. various degrees of bloat depending on how much of esophagus is occluded (EMERGENCY) 4. staggering because of anorexia due to bloat |
|
what are the three most common sites for foreign bodies to cause choke in ruminants?
|
1. post-pharyngeal
2. thoracic inlet 3. base of heart |
|
in a ruminant, what would blood work look like in a severe case of choke and why?
|
- acidotic and dehydrated because of loss of bicarb and water with excess salivation
- hypokalemic and hyponatremic due to salivation |
|
when a ruminant has choke, what are some techniques to remove the object?
|
- rumen trocar if needed
- ± sedation with xylazine - may be able to manually massage object up to pharynx - loop a piece of wire (coat hanger) and pass down esophagus to retract object - pass a stomach tube and push the object into the rumen - rumenotomy and pass a wire loop up the esophagus - trocarize the rumen, sedate, and give 24 hours to see if it will resolve on its own |
|
after choke has been resolved, what are four indicated treatments?
|
1. a/b for prevention of aspiration pneumonia
2. NSAIDs 3. fluids as needed 4. feed a soft diet |
|
what is the prognosis for choke in ruminants?
|
- good unless damaged esophageal mucosa
- guarded 24 hours post choke - grave if it cannot be resolved |
|
when is it unsafe to treat cattle for Hypoderma infections?
|
late fall to January
|
|
what two bacteria most commonly cause liver abscesses in the ruminant?
|
1. Fusobacterium necrophorum
2. Trueperella (Arcanobacterium) (Actinomyces) pyogenes |
|
what is the prevalence of liver abscesses in feedlot cattle?
|
24 - 30%
|
|
what is the most common way in which liver abscesses in cattle are diagnosed?
|
at slaughter
|
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what are three basic etiologies for liver abscesses in ruminants?
|
1. high carb, low fiber diets
2. omphalitis 3. traumatic hepatitis |
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what is the pathogenesis of liver abscess formation in ruminants on a high carb, low fiber diet?
|
- rumen acidosis from grain overload causes rumen insults
- bacteria enter the portal circulation and are filtered out by the liver, which becomes an abscess |
|
what structure does the umbilical vein become?
|
falciform ligament
|
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what structure does the umbilical artery become?
|
round ligament of the bladder
|
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omphalitis causes liver abscesses in ruminants via which anatomical structure?
|
umbilical vein
|
|
ruminants wall off abscesses in the liver that are caused by Fusobacterium necrophorum and/or Trueperella pyogenes. How does this affect clinical signs?
|
makes clinical signs not apparent in most animals
|
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why can a liver abscess in the ruminant cause diarrhea and ascites?
|
if abscess ruptures into the caudal vena cava and cause a thrombosis, ascites and diarrhea will occur due to increased splanchnic venous pressure
|
|
a ruminant with a liver abscess will be painful where upon palpation/physical exam?
|
right posterior rib
|
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what are three sequelae to caudal vena cava thrombosis from a liver abscess in the ruminant?
|
1. sudden death from sepsis or anaphylactic shock from rupture of the abscess
2. severe dyspnea and open-mouth breathing when the abscess does not result in immediate death 3. epistaxis from pulmonary embolism |
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what are three clinical pathological signs of liver abscess in the ruminant?
|
1. neutrophilia and lymphocyte:neutrophil shift
2. hyperfibrinogenemia 3. ↑GGT and ↑AST if abscess formation is active |
|
how are liver abscesses in the ruminant treated?
|
long-term penicillin therapy
|
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what are five preventative measures for liver abscesses in the ruminant?
|
1. gradually increase grain over 3-4 week period to prevent overload
2. Tylosin (or other a/b) in feed 3. roughage at least 45% of ration 4. feed long stem hay - keeps pH of rumen higher due to remastication 5. naval dipping at birth |
|
what are five clinical signs of liver abscesses in the ruminant?
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1. weight loss, ↓weight gains
2. ↓milk production 3. fever and anorexia 4. painful when ambulating, lying down, pressure over the right posterior rib 5. ascites and diarrhea from thrombosis in the caudal vena cava |
|
what type of microbe comprises the majority of rumen flora?
|
gram-negative anaerobes
|
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what two things predisposes an animal to frothy bloat, and in each, what forms the froth?
|
1. diets of lush legumes or alfalfa hay - chloroplast membrane fragments produce the froth
2. high concentrate/grain diets - bacteria produce a mucoprotein slime in response to the low pH environment. |
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in free-gas bloat, what is the pathway that causes a decrease in ruminal contractions?
|
- consumption of concentrate without acclimated rumen
- increased VFAs and pH drops - when pH drops below 5.3, lactic acid is produced - ↑VFA and ↓pH inhibits cyclic contractions and ↓ eructation - hypocalcemia leads to muscular weakness, which further decreases contractions |
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what are two ways in which the esophagus can become blocked can cause free-gas bloat in ruminants?
|
1. obstruction of the esophagus
2. postural bloat - cardia is submerged below the ruminal gas cap; occurs when an animal casts itself |
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what are clinical signs of bloat?
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- distension of paralumbar fossa above the rib and tuber coxae
- distension may cause the animal to bulge on the right side, depending on severity of bloat - signs of colic: frequently getting up and down, stretched out neck, stretched out back legs - open mouth breathing, cyanosis, collapse, and death |
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in bloat, what are seven things to instruct the owner to do before you arrive?
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1. If down, put in sternal recumbency
2. keep animal moving: keeps ingesta mixed and may reduce pressure on the diaphragm 3. place a gag in the animal's mouth to ↑ saliva production 4. pass a garden hose 5. raise the front end of the animal to reduce pressure 6. drench with 1 tbsp. of soap in 1 qt. of water 7. trocarize rumen as a last resort |
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what are three things you can administer to break up the froth in frothy bloat?
|
1. poloxalene
2. mineral oil 3. dish washing soap |
|
trocarization in bloat:
- indication - where do you trocarize? - Tx for severe frothy bloat |
- if patient is in respiratory distress
- trocarize the left paralumbar fossa - emergency rumenotomy to remove froth |
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what are two ways to treat extraruminal bloat?
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- rumenotomy and suture rumen wall to skin leaving a fistula; fistula will heal over 4-6 weeks
- place a trocar in the rumen and leave in place for a month |
|
where are 3 common sites of esophageal obstruction in cattle?
|
1. post-pharynx
2. thoracic inlet 3. base of heart |
|
cows that have rabies cannot swallow and are likely to have what metabolic and electrolyte imbalances? (3)
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- acidosis
- hyponatremic - hypokalemic |
|
how do you treat traumatic pharyngitis in the ruminant?
|
- penicillin 10,000 IU BID
- NSAIDs |
|
why does frothy bloat prevent eructation
|
receptors in the cardia, when covered with water, ingesta, or foam, will inhibit eructation
|
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what is the role of ruminal
- low threshold receptors? - high threshold receptors? |
- low: cause cyclical contractions of the rumen
- high: inhibit ruminal contractions |
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at necropsy, what is pathognomonic for bloat?
|
bloat line in the esophagus
|
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what are four ways to prevent bloat?
|
1. introduce to lush pastures slowly
2. feed dry hay before putting out 3. poloxalene (non-ionic surfactant) blocks 4. feed ionophore |
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what is a major difference in clinical sign of choke versus bloat?
|
choke: they can't swallow; bloat, they can swallow
|
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why is bloat an emergency? (2)
|
- pressure on diaphragm (can't breathe)
- pressure on abdominal vessels (ischemia) |
|
what are four sequelae to infection resulting from traumatic reticuloperitonitis?
|
1. abscesses and adhesions
2. peritonitis - diffuse or localized 3. liver abscesses 4. pericarditis |
|
epidemiology of hardware disease:
- type of cattle predisposed - prevalence in small ruminants |
- dairy > beef
- rare in small ruminants because they are more discretionary eaters |
|
what are seven clinical signs of acute hardware disease?
|
1. dairy: acute ↓ milk
2. fever, anorexia, decreased rumen motility 3. pain: grunt when lying down, urinating, defecations 4. BACK IS ARCHED 5. stiff gait; abducted elbows 6. regurgitation of feed 7. acute death |
|
what are four clinical signs of chronic hardware disease?
|
1. ±fever
2. ADR cow 3. weight loss 4. walks gingerly |
|
if hardware disease involves the pericardial sac
- what does the heart sound like? - what other clinical sign? |
- heart sounds are muffled, sounds like a washing machine due to fluid-gas interface
- signs of congestive heart failure (e.g., jugular pulse) |
|
what are six methods to diagnose hardware disease?
|
1. clinical signs and rule out other things
2. grunt test/withers pinch test 3. abdominocentesis 4. radiographs 5. exploratory 6. clin path |
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what is the most common clinical pathological result of hardware disease?
|
increased fibrinogen > 500 and ↑ plasma proteins
|
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how is hardware disease treated if acute and painful?
|
surgery to remove object
|
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how is conservative management of hardware disease performed?
|
- magnet
- PPG FOR A WEEK (or other a/b) - confinement; elevate front end to relieve pressure on diaphragm - fluids and transfaunation |
|
what are three ways to prevent hardware disease?
|
1. administer magnets at 6-8 months of age
2. clean up the environment 3. magnets on feed handling equipment |
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what are four basic etiologies for simple indigestion in the ruminant?
|
1. abrupt feed changes
2. increase in amount fed or change in ingredients 3. poor quality/unbalanced feed 4. consumption of afterbirth |
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what are four examples of poor quality/unbalanced feed that could cause simple indigestion in ruminants?
|
1. moldy or heated feeds
2. frosted forages 3. partially fermented (e.g., silo opened too soon) or spoiled silage 4. too much grain |
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what are four clinical signs of simple indigestion in the ruminant?
|
1. degrees of anorexia for 1-2 days
2. decreased rumen motility with gassy pongs 3. decreased milk production 4. diarrhea within 24 hours of anorexia |
|
how does simple indigestion present epidemiologically in a herd?
|
variable number of animals affected
|
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what are three ways to treat simple indigestion in the ruminant?
|
1. oral fluids
2. transfaunation 3. wait and see what happens (simple indigestion is usually self-limiting) |
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what are two ways to prevent simple indigestion in the ruminant?
|
1. make feed changes gradually
2. feed quality feeds |
|
what are the two major causes of rumen acidosis?
|
1. excessive consumption of readily fermentable carbohydrates (e.g. breaks into feed storage)
2. animal exposed to feed without adaptation |
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what are four ways in which animals are exposed to feed without adaptation and can result in rumen acidosis?
|
1. off feed then return to full feed
2. competition at feed bunk 3. recently gave birth and put back on full feed 4. break into feed room |
|
what is the pathophysiology of dehydration caused by rumen acidosis following grain overload?
|
1. proliferation of Streptococcus bovis and production of lactate
2. lactate production reduces rumen production pH to 5 or less 3. bacteria and protozoa die off 4. Lactobacilli take over for Strep 5. rumen osmolality increases due to lactate accumulation, which pulls water into the rumen 6. rumen distends and animal dehydrates |
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after an animal has become dehydrated due to rumen acidosis, what is the pathophysiology that will eventually lead to death?
|
1. circulatory impairment, decreased renal perfusion, anuria
2. this leads to metabolic acidosis due to poor perfusion (ischemia/hypoxia) 3. both D- and L-lactate are produced in and absorbed by the rumen; only L is metabolized 4. lactate burns the rumen lining, may lead to fungal rumenitis and liver abscesses 5. gram-negative bacteria die off, causing endotoxic shock 6. rumen fluid becomes alkalotic because of putrefaction and fluid influx into rumen |
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what are five clinical signs of rumen acidosis?
|
1. depression, coma, death
2. atonic, sloshy, fluid-filled rumen 3. dehydration, ↑HR, ↑RR (i.e., hypovolemic shock) 4. staggering gait or down 5. diarrhea may develop the next day |
|
what are three ways to diagnose rumen acidosis?
|
1. History
2. tap rumen; pH < 5 3. look for live protozoa |
|
what are 9 treatments for rumen acidosis?
|
1. alkalinizing fluids IV
2. empty the rumen if early in the course fo the disease 3. systemic and oral penicillin 4. magnesium hydroxide orally if early in the course of the disease 5. mineral oil to coat the lining of the gut and ↓ absorption of endotoxin 6. NSAIDs 7. thiabendazole (TBZ) to kill fungi 8. B vitamins (bacteria usually make these) 9. TRANSFAUNATE!! |
|
how are alkalinizing fluids given with rumen acidosis?
|
IV
|
|
comment on antibiotic use for rumen acidosis
|
systemic and oral. Treats septicemia and kills Lactobacilli and Streptococci in the rumen causing the disease
|
|
what agent is used to alkalinize the rumen as a treatment for rumen acidosis?
|
magnesium hydroxide
|
|
why would mineral oil be given for rumen acidosis?
|
coats the lining of the gut to protect adsorption of endotoxin
|
|
what micronutrient is deficient with rumen acidosis?
|
B vitamins, because they are produced by ruminal bacteria
|
|
when treating rumen acidosis, how do you prevent fungi from overtaking the ruminal fluid?
|
administer TBZ (thiabendazole)
|
|
when treating rumen acidosis, what is an important step in repopulating the rumen with normal flora?
|
transfaunation
|
|
what are five ways to prevent rumen acidosis?
|
1. prevent exposure to large quantities of CHOs
2. Make gradual feed changes 3. keep food in secure place 4. provide adequate feeder space to reduce competition 5. provide long-stem hay/forage |
|
why is providing long stem hay to ruminants so helpful in treating a variety of diseases of the digestive system?
|
- they chew their cud more, so they swallow more saliva, which buffers the rumen
- it is filling, so they are less tempted to overeat grain/forage |
|
what does the cow's body look like when in bloat?
|
distended left paralumbar fossa (sometimes the right if severe)
|
|
what does bloat sound like when percussed?
|
a pong resonance in the rumen
|
|
what does the rumen sound like upon auscultation with bloat?
|
decreased to absent motility; sloshy with ballottement
|
|
what is a major visual clinical sign of bloat, not involving the digestive system?
|
signs of respiratory distress
|
|
what is the most common clinical presentation of simple indigestion in a cow? (4)
|
- off feed
- depressed rumen motility - anorectic - EVERYTHING ELSE IS NORMAL |
|
how would a cow with hardware disease present differently compared to if she just had simple indigestion? (6)
|
- ± fever
- painful - positive grunt test - ↑ fibrinogen - muffled heart sounds - longer duration |
|
what does a cow's body look like when she has vagal indigestion?
|
"papple" shaped; bloat in the left paralumbar fossa; severe fluid distention on the right side
|
|
what is the basic reason that the rumen becomes distended with vagal indigestion?
|
outflow problems
|
|
what are five lesions that can cause vagal indigestion?
|
1. pleuritis or peritonitis
2. severe pneumonia 3. hardware disease 4. swelling of pharyngeal area (compress vagus nerves) 5. abomasal diseases |
|
why is vagal indigestion associated with late pregnancy in cows? (2)
|
- compression of vagus nerves by the fetus
- abnormal position of the pylorus, causing outflow failure |
|
what are five clinical sings of vagal indigestion?
|
1. papple shape
2. decreased fecal output 3. dehydration 4. anorexia 5. 30% have bradycardia |
|
what are the two syndromes associated with vagal indigestion and which is most common?
|
1. omasal transport failure (most common)
2. pyloric outflow failure |
|
greasy, pasty feces with large particle size would be compatible with which type of vagal indigestion in the cow?
|
omasal transport failure
|
|
lack of fecal production would be consistent with which type of vagal indigestion in the cow?
|
pyloric outflow failure
|
|
describe the dynamics of the forestomachs with omasal transport failure syndrome of vagal indigestion
|
- atony of the reticulorumen
- recurrent bloat - hypermotility - distention of the forestomachs |
|
describe the dynamics of the forestomachs with pyloric outflow failure syndrome of vagal indigestion. Clin path?
|
- fluid accumulates in the omasum and abomasum
- motility initially normal in the reticulum, but gets distended over time - RUMEN CHLORIDE INCREASES (internal vomiting/abomasal reflux of the abomasum into the rumen) - dehydration and HYPOCHLOREMIA along with METABOLIC ALKALOSIS |
|
what are three predisposing factors to pyloric outflow failure (vagal indigestion) in the ruminant?
|
1. abomasal volvulus
2. displaced abomasum 3. late pregnancy |
|
what are six ways to treat vagal indigestion?
|
1. IV fluids
2. a/b, NSAIDs 3. surgery (rumenotomy, rumenostomy) 4. limit feed intake; high fiber 5. transfaunation 6. if pregnant, C-section or abort |
|
what is the prognosis of vagal indigestion?
|
poor
|
|
in a cow: a ping heard in an obliquely oval region half way up the left abdominal wall, in the middle, which extends from the lung field to the costal arch or a couple inches into the left paralumbar fossa area is what?
|
LDA
|
|
in a cow: a ping heard in an obliquely oval region half way up the right abdominal wall, in the middle, which extends from the lung field to the costal arch or a couple inches into the left paralumbar fossa area is what?
|
RDA or RTA
|
|
a ping heard that extends through throughout the whole paralumbar fossa area is what? (2)
|
- left side: rumen
- right side: cecum or spiral colon |
|
when percussing over the ribs on the left side of a cow, you can hear 2 distinctly different pitched resonances, depending on location, what are you thinking?
|
LDA
|
|
how can you tell ileus in the cow versus normal?
|
- normal: pongs in the right paralumbar fossa will migrate
- ileus: the pongs will remain in a consistent location |
|
a resonating ping on both the left and right sides of a cow may indicate what?
|
peritonitis
|
|
what three conditions are associated with post-partum displaced abomasum?
|
"The 3 M's"
1. milk fever (hypocalcemia) 2. mastitis (endotoxemia) 3. metritis (endotoxemia) |
|
when does post-partum displaced abomasum usually occur?
|
usually within the first 2 weeks of freshening
|
|
besides post-parturition, what three things are associated with displaced abomasum?
|
1. high grain diets and inadequate adjustments to grain
2. high producing dairy cows, 2nd or greater lactations 3. deep-chested cows |
|
what is the pathophysiology of a displaced abomasum?
|
1. atomy of the abomasum
2. gas accumulates 3. abomasum floats and is trapped |
|
what are three things that can cause atony of the abomasum, which may lead to a DA?
|
1. increased VFAs (high grain diet)
2. hypocalcemia (milk fever) 3. endotoxins (metritis, mastitis) |
|
a "sprung rib" in a cow is often indicative of which disease?
|
displaced abomasum
|
|
what are some metabolic conditions associated with a displaced abomasum?
|
- ketonuria
- alkalosis - paradoxical aciduria (if dehydrated and hypokalemic) - hypokalemia (due to alkalemia) - hypocalcemia |
|
describe the eating behavior of a cow with a DA?
|
- anorectic
- no cud chewing |
|
on auscultation over the left side of the ribs in a cow, you hear a gurgling or tinkling sound instead of a normal rumen scratchy sound, what might you think?
|
LDA
|
|
what are four clinical signs of a right torsed abomasum that differ from a simple abomasal displacement?
|
1. signs of shock (↓CRT, cool extremities)
2. HEART RATE 100+ !!!! 3. acutely ill, painful, and dehydrated 4. abdominal distention and borborygmi are absent |
|
what is the "Liptak Test"?
|
tests for a displaced abomasum.
- stick a needle 6 inches below the ping - test pH of the fluid - pH 2-4 = abomasum - pH 5.5-8 = rumen |
|
a cow is ambulated to the VTH due to suspect LDA, but the pings are not heard upon arrival. What could be going on?
|
floating DA
|
|
what are five treatments for a displaced abomasum?
|
1. roll
2. roll and tack 3. right flank omentopexy 4. right paramedian abomasopexy 5. left flank abomasopexy |
|
what are five adjunct therapies for treatment of a displaced abomasum?
|
1. fluids
2. NSAIDs 3. calcium supplementation 4. glucose 5. treat other concurrent conditions |
|
prognosis for displaced abomasums:
- simple LDA - simple RDA - RTA - what condition lowers prognosis? |
- simple LDA: good
- simple RDA: good - RTA: poor - diarrhea prior to correction lowers prognosis |
|
what are five ways to prevent displaced abomasums?
|
1. INCREASE THE EFFECTIVE FIBER IN THE DIET AND REDUCE GRAIN
2. decrease post-partum diseases 3. prevent hypocalcemia (milk fever) 4. transition diet 5. introduce feedlot cattle to grain gradually |
|
what type of displaced abomasums can be corrected with roll and tack?
|
LDA only
|
|
what type of displaced abomasums can be corrected with right flank omentopexy?
|
all DAs
|
|
what type of displaced abomasums can be corrected with left flank abomasopexy?
|
LDAs
|
|
what type of displaced abomasums can be corrected with right paramedian abomasopexy?
|
all DAs
|
|
abomasal impaction, epidemiology:
- when? - associated with what type of feed? - etiologies |
- usually winter months
- associated with poor quality feeds - vagal indigestion, hardware, pyloric obstructions (e.g., lymphosarcoma) |
|
what are five clinical sings of abomasal impaction?
|
1. normal TPR
2. anorexia and depression 3. DISTENTION OF LOWER-RIGHT ABDOMEN 4. decreased fecal output 5. INCREASED RUMEN CHLORIDE |
|
who is most predisposed to abomasal ulcers?
|
high producing dairy cows early in lactation
|
|
what are four causes of abomasal ulcers in adult cows?
|
1. stress of calving and lactation
2. high grain diets 3. lymphosarcoma of the abomasum 4. use of NSAIDs |
|
what are two causes of abomasal ulcers in calves?
|
1. eating solid food
2. copper deficiency |
|
what are six clinical signs of abomasal ulcers in the cow?
|
1. ADR
2. off feed and ↓ milk production 3. ↓ rumen motility 4. colic 5. GI bleeding → melena, dark feces, anemia 6. acute death |
|
what are 3 ways to diagnose abomasal ulcers in the cow?
|
1. history
2. grunt test 3. fecal occult blood |
|
what are four treatments for abomasal ulcers?
|
1. more forage, less grain
2. ± protectants and antacids 3. blood transfusions 4. treat for peritonitis |
|
a cow is presented with bradycardia and a distended lower-right abdominal quadrant and a distended upper-left abdominal quadrant. Scant feces. What is the presumptive diagnosis?
|
vagal indigestion
|
|
a cow with vagal indigestion:
- what would her chloride status be? - what would her potassium status be? - what would he blood pH be? |
- hypochloremic (but increased rumen chloride)
- hypokalemic (from alkalosis) - alkalosis (from abomasal reflux) |
|
what are three reasons why postpartum cows are at increased risk of having an LDA?
|
1. empty space from fetus
2. change in diet: increased grain 3. metabolic diseases (slows abomasal contractions) |
|
what are three metabolic diseases that lead to LDA?
|
1. ketosis
2. grain overload - high CHO diet 3. hypocalcemia |
|
what two agents cause hemorrhagic bowel syndrome in cattle?
|
1. Clostridium perfringens type A
2. Aspergillus fumigatus |
|
epidemiology of hemorrhagic bowel syndrome in cattle:
- what type of cattle? - when is it seen? - what type of feed is it associated with? - what two agents cause it? |
- dairy cattle
- usually seen within first 100 days of lactation - diets high in protein and energy content - Clostridium perfringens type A and Aspergillus fumigatus |
|
what are four clinical signs in a cow with hemorrhagic bowel syndrome and what would you find on rectal exam?
|
1. off feed, depressed, may find dead or dying
2. ↑HR and ↑RR 3. progressive abdominal distention 4. low pitched pings in the lower-right abdomen - rectal: blood clots or bloody feces; distended small bowel loops |
|
what gross pathologic lesions are associated with a cow with hemorrhagic bowel syndrome
|
blood clots in the jejunum
|
|
what is the treatment and prognosis of hemorrhagic bowel syndrome in the cow?
|
- surgery
- fluids, NSAIDs, a/b - prognosis: grave |
|
how is hemorrhagic bowel syndrome in cows prevented? (3)
|
1. gradual feed changes
2. don't feed moldy feeds (i.e. that contain Aspergillus) 3. ± vaccine |
|
what is the predisposing factor to intussusception in:
- calves? - older cows? |
- calves: tapeworms
- cows: polyps |
|
what are four clinical signs of intussusception in cattle?
|
1. colic
2. depression and anorexia 3. abdomen swells over a couple of days 4. dehydration |
|
what are two ways to diagnose intussusception in cattle?
|
1. palpation (feel a cylindrical hard loop of intestine)
2. small gas ping on right |
|
what are three treatments for intussusception in cattle?
|
1. supportive - fluids and antibiotics
2. self-correcting 3. surgery |
|
what is the prognosis of intussusception in cattle?
|
poor
|
|
what are four clinical signs of SI volvulus in ruminants?
|
1. acute onset, rapid progression
2. ↑HR and ↑RR 3. painful 4. abdomen swells quickly |
|
what are two ways to diagnose SI volvulus in ruminants?
|
1. pings on the right side
2. palpation |
|
how is SI volvulus in ruminants treated?
|
it is not; grave prognosis
|
|
what are four clinical signs of cecal dilation and torsion in the ruminant?
|
1. torsed animals will be shocky
2. anorexia, drop in milk 3. scant feces 4. signs of colic |
|
how is cecal dilation and volvulus in the ruminant diagnosed?
|
palpation
|
|
cecal dilation and torsion in ruminants: why does the cecum dilate?
|
because of ileus associated with high grain diets or metabolic diseases; torsion occurs after dilation
|
|
how is cecal dilation and torsion in the ruminant treated?
|
- oral fluids
- calcium supplementation - ↓grain - exercise - surgery to correct torsion |
|
how is cecal dilation and torsion in the ruminant prevented?
|
↑forage, ↓grain
|
|
what are six causes of rectal prolapse in food animals?
|
1. pneumonia and coughing
2. causes of persistent straining (coccidiosis, rectal tear) 3. sheep - closely docked tails 4. pigs piling on each other 5. feeding finely ground feed 6. vaginal or uterine prolapse |
|
what are four ways to treat rectal prolapse in the ruminant?
|
1. replace rectum and purse string suture (some people inject iodine to form adhesions)
2. amputation (rectal whistle - placed with an elastrator band) 3. NSAIDs 4. ± antibiotics |
|
rectal prolapse in ruminants:
- prognosis - control |
- prognosis: depends on severity; may want to recommend slaughter
- control: remove predisposing factors |
|
what breeds of cattle are predisposed to fat necrosis?
|
Channel Island breeds: Jersey and Guernsey
|
|
what are four clinical signs of fat necrosis in cattle?
|
1. usually subclinical
2. may cause intestinal obstruction 3. weight loss, anorexia, diarrhea 4. abdominal enlargement and discomfort |
|
what causes iatrogenic atresia ani?
|
palpation at day 42
|
|
how are the following atresia diseases diagnosed:
- ani? - recti? - coli? |
- ani: observe
- recti: may feel constriction in the rectum - coli: abdominal distension and lack of feces |
|
how are the following atresia diseases treated:
- ani? - recti? - coli? |
- ani: create an anus
- recti and coli: euthanasia |
|
what is the general principle for the development of neonatal diarrhea?
|
the number of infectious agents supersedes the neonate's resistance
|
|
what is the general principle for the prevention of neonatal diarrhea?
|
keeping the number of infectious agents low and the neonate's resistance high
|
|
how much colostrum should a dairy calf have and over what period of time to get good passive transfer
|
6-8 L over 24 hours
|
|
when in gestation are antibodies transferred from cow → calf fetus?
|
last 2 weeks of gestation
|
|
to provide colostral immunity, when should you vaccinate
- cows? - naïve heifers? |
- cows: 3-4 weeks before calving
- naïve heifers: 6 weeks before calving and boost at 3-4 weeks before calving |
|
why won't calves suckle teats that hang too low?
|
because they look up to find them. If they are too low, they are out of the calf's field of view?
|
|
why are gilts more likely to have FPT piglets than sows?
|
because the gilts are more likely to be immuno-naïve
|
|
ideally, how often does a beef calf suckle? A dairy calf?
|
- beef: every 2 hours
- dairy: 2x per day (or schedule set by the farm) |
|
what happens if a calf drinks too much milk (i.e. gorges themselves)?
|
since they don't have enough enzymes to process and digest the nutrients from an overload of milk, they will have osmotic diarrhea
|
|
what is an ideal temperature of a farrowing house? What two pathophysiological effects does colder temperature have on piglets that predisposes them to disease?
|
- keep at 90 °F (floor temperature)
1. cold slows mucociliary apparatus 2. cold slows peristalsis → slower clearing of infectious agents |
|
when is rotaviral/coronaviral vaccine given?
|
to the dam prior to parturition
|
|
when sacrificing a neonate to determine the causative agent of a diarrhea outbreak in the herd, which animal should you pick?
|
one that just recently got sick, so that you have a higher likelihood of isolating the infectious agent
|
|
what gross pathological samples should be collected to diagnose neonatal diarrhea?
|
1. ILEUM***
2. duodenum 3. jejunum 4. mesenteric lymph nodes 5. spiral colon 6. abomasum 7. liver 8. spleen |
|
comment on the pH of neonatal diarrhea as a function of etiologic agent
|
- bacterial will be basic because of bicarb secretion by duodenum and lack of reabsorption
- viral will be acidic because of villous atrophy → maldigestion → fermentation → lactic and VFAs |
|
how can you tell if there is villous atrophy in the SI of pigs in necropsy? (2)
|
1. look for lacteals; if they are absent or contain no chyle, there has been villous atrophy
2. may see digesta through a transparent intestinal wall because of the thinning caused by villous atrophy |
|
mucus in diarrhea leads you to which organ?
|
large intestine
|
|
colostrum intake elevates which clinical pathological value in calves?
|
ALP
|
|
Neonatal colibacillosis in the calf clin path:
- Cl? - Na? - K? - blood pH? |
- ↓Cl
- ↓Na - ↑K - acidotic |
|
why does the ETEC that infects neonatal calves not cause disease in adults?
|
because these bacteria have attachment pili that attach only to receptors in the neonatal gut
|
|
describe the gross pathology of a small intestine from a calf that dies of neonatal diarrhea from colibacillosis (ETEC)
|
- normal wall thickness
- chyle in the lymphatics - in other words, no gross lesions |
|
if neonatal calves can absorb nutrients with a colibacillosis infection, why do they still have watery (and sometimes milky) diarrhea?
|
due to the infection, the amount of milk and fluids ingested exceeds the absorptive capability of the SI and LI absorptive cells.
|
|
what type of diarrhea results from neonatal colibacillosis and why?
|
secretory. Because the ETEC enterotoxins increase intestinal secretion.
|
|
how do you treat ETEC neonatal diarrhea?
|
- oral fluids (or tube) with water, Na, Cl, K, and glucose.
- IV fluids with bicarb and glucose |
|
in a calf with neonatal colibacillosis, why is IV glucose given (along with bicarb)? (2)
|
- they may be hyperglycemic
- glucose causes insulin release, which reduces hyperkalemia |
|
at what age does enteric colibacillosis occur?
|
1-4 days
|
|
what causes enteric colibacillosis, what predisposes them to infection, and how is it prevented?
|
- in neonates 1-4 days old, ETEC with attachment pili (K99, K88, F41)
- predisposed: FPT and/or contaminated environment (e.g., dirty birthing area) - prevention: proper colostrum intake, birth in clean environment, vaccination of dam with pili antigen before parturition, oral monoclonal antibody |
|
what type of rotavirus causes illness in:
- calves - small ruminants? - piglets? - humans? |
- calves: type A
- small ruminants: type B - piglets: A, B, C, and E - humans: type A |
|
when does rotaviral diarrhea occur in
- calves - pigs - small ruminants |
- calves: 4-14 days
- pigs: 1-6 weeks (most around weaning) - small ruminants: 4-14 days |
|
what is the pathophysiology of rotaviral diarrhea?
|
- viruses infect SI mucosa in the tips of the villi
- malabsorption and lack of digestive enzymes leads to fermentation of digesta in large intestine - this leads to osmotic diarrhea |
|
describe the SI on gross pathology of rotaviral diarrhea
|
- lack of lymphatics
- moderate distention - may see digesta through the walls due to villous atrophy and thinning of the mucosa |
|
describe the diarrhea caused by rotavirus
- severity - type - what determines severity |
- absent or mild; severe when there is a 2ndary infection
- malabsorptive - dependent on immunity and exposure |
|
how is rotaviral diarrhea definitively diagnosed?
|
EM, FA of mid-ILEUM
|
|
why is rotaviral diarrhea treated with fluid therapy?
|
enhances absorption and supports the large intestine, which is hyperosmolar from malabsorption
|
|
how is rotaviral diarrhea prevented?
|
reduce exposure, reduce stress, ±vaccine
|
|
transmissible gastroenteritis in swine:
- morbidity and mortality - causative agent - age |
- high morbidity and mortality
- coronavirus - neonates less than 2 weeks of age; postweaning age; growers, finishers, and adults |
|
what are clinical signs of TGE in neonatal swine? (6)
|
- profuse white to yellow diarrhea
- very wet tails - dehydration - vomiting - excessive thirst - DEATH |
|
how do clinical signs of TGE in post-weaned pigs compare with clinical signs in neonatal swine?
|
similar clinical signs, but recovery unless unusually stressed. These become carrier animals
|
|
in herds of swine with endemic TGE, who are the carriers?
|
post-weaning age pigs
|
|
what are clinical signs of TGE in grower, finisher, and adult pigs? (4)
|
- anorexia
- vomiting - fever - ± diarrhea |
|
what type of diarrhea is caused by TGE in swine?
|
malabsorptive
|
|
how does the SI appear grossly in a necropsy of a piglet that had TGE?
|
- fluid distention with jejunal and ileal "thinning"
- no visible lymphatics in mesentery in the area of "thinning" |
|
what are three ways to prevent TGE in neonates?
|
- increase temp of farrowing house to 90 °F
- provide electrolyte (Gatorade) - ± vaccination (expensive) |
|
what are some non-swine carriers of TGE virus?
|
BIRDS, dogs, cats, flies
|
|
if TGE vaccination is used, how is it administered?
|
parenterally and orally (sows, gilts, piglets)
|
|
why do you see flecks of blood in coronaviral diarrhea of calves, but not usually in rotaviral diarrhea?
|
because coronaviral diarrhea is much more severe
|
|
epidemiology of coronavirus in calves
- who sheds the virus and when is the virus shed? - prevalence? - morbidity/mortality? |
- asymptomatic cows shed the virus, especially round parturition
- almost 100% prevalence of antibodies - moderate (10-15%) morbidity and moderate (5-10%) mortality |
|
what is the age of calves affected by coronaviral diarrhea?
|
5 - 30 days old
|
|
what is the major clinical sign of coronavirus in calves?
|
diarrhea consisting of feces containing mucus, milk curds and ± BLOOD
|
|
what type of diarrhea is caused by coronavirus in calves?
|
malabsorptive
|
|
what part of the GI tract does coronavirus affect in
- piglets? - calves? |
- piglets: SI only
- calves: SI and large intestine |
|
how is coronavirus of calves definitively diagnosed?
|
EM, FA of ILEUM AND COLON
|
|
how is coronavirus of calves treated?
|
fluid therapy
|
|
what is the most common cause of hemorrhagic enteritis in food animals?
|
Clostridium perfringens type C ("clostridial scours")
|
|
what age pigs are affected by clostridial scours?
|
1-14 days; 1-5 day old piglets most severely affected
|
|
What predisposes a litter of piglets to clostridial scours that are otherwise managed with good husbandry?
|
gilt litters, because gilts can confer less immunity to their litters
|
|
what is the pathognomonic lesion for clostridial scours in neonatal piglets?
|
subserosal and luminal bleeding in the SI, and occasionally the cecum and LI; also, intestinal emphysema
|
|
describe the epidemiological curve of clostridial scours in swine
|
sporadic
|
|
during a swine clostridial scours outbreak, how is it treated?
|
- give antitoxin orally to piglets; give oral and/or parenteral penicillin to piglets
|
|
how are clostridial scours in swine prevented?
|
give the Clostridium perfringens type C bacterin to dams prior to parturition. Clean the sows prior to farrowing
|
|
how is clostridial scours in swine (Clostridium perfringens type C) diagnosed in swine?
|
jejunal smear
|
|
what three bacteria cause enterotoxemia in ruminants and the disease associated with them?
|
1. Clostridium perfringens type C - hemorrhagic enteritis
2. C. perfringens type B - lamb dysentery 3. C. perfringens type D - overeating disease |
|
what are clinical signs of Clostridium perfringens type C infection in neonatal ruminants? (6)
|
- diarrhea
- dysentery - colic - opisthotonus - tetany - may die before development of diarrhea |
|
how is enterotoxemia in ruminants prevented?
|
vaccination
|
|
how is enterotoxemia in ruminants treated?
|
antiserum, penicillin, fluids
|
|
what are pathological findings of Clostridium perfringens type C infection in neonatal ruminants?
|
- hemorrhagic inflammation of the jejunum, ileum, and lymph nodes
- large numbers of Gram + rods in the intestine |
|
what type of enteric cells are attacked by
- rotavirus? - coronavirus? |
- rotavirus: tips of the villi epithelium
- coronavirus: undifferentiated epithelial cells, fibroblasts and endothelial cells note that intestinal crypt cells are spared |
|
what enteric disease commonly attacks ruminants that are the best doers and kills them acutely?
|
Clostridium perfringens type D enterotoxemia; "pulpy kidney disease"; "overeating disease"
|
|
what are clinical signs of Clostridium perfringens type D enterotoxemia in ruminants?
|
- most common presentation is sudden death
- neurologic signs - renal damage, hyperglycemia, hypertension, edema - glucosuria in sheep, but not cattle |
|
what is the causative agent of Pulpy Kidney Disease?
|
Clostridium perfringens type D
|
|
what are gross path lesions of Clostridium perfringens type D enterotoxemia in ruminants?
|
pleural and pericardial fluid with petechial hemorrhages on the serosal surface of intestine, diaphragm, endocardium, and pericardium, along with fibrin
|
|
When do you vaccinate for Clostridium perfringens (enterotoxemia)
- in dams? - cattle? - calves? - lambs? |
- dams prior to parturition
- cattle ≤ 2 years 1-2x per year - calves at 8 to 12 weeks of age and upon entering feedlot - lambs at 2 weeks prior to weaning and upon entering a feedlot |
|
One of a pair of lambs dies of pneumonia; the other sibling is healthy and has his mother's milk all to himself. One morning, farmer Rasputin comes out to find the lamb dead. The lamb seemed fine yesterday and has been happy and healthy. What could have killed this lamb in the gastroenterological area of diseases?
|
Clostridium perfringens type D enterotoxemia; "pulpy kidney disease"; "overeating disease".
|
|
what agent causes lamb dysentery?
|
Clostridium perfringens type B
|
|
what is a big difference between the shed oocysts of cryptosporidium and coccidia?
|
crypto are infectious immediately after shedding; coccidia needs to complete part of its life cycle in the environment
|
|
why might a carefully well-managed farm that has never had cryptosporidium problems before, suddenly have an outbreak?
|
because the oocysts are hardy and build up in the environment. Since oocyst dose correlates with clinical signs, asymptomatic carriers may be gradually adding to the oocyst burden on the land until the critical concentration has built up
|
|
cryptosporidiosis:
- age of calves - clinical signs - histopath lesions |
- calves 1-3 weeks
- tenesmus, non-bloody diarrhea, anorexia, weight loss, and depression; 2ndary infections can complicate - lesions: in the distal SI, find organisms attached to the brush borders of the villi |
|
what are two ways that cryptosporidiosis diagnosed?
|
1. fecal flotation
2. see organisms in the SI brush border |
|
what are two ways that cryptosporidiosis prevented?
|
1. sanitation (bleach)
2. move calves away from outbreak areas |
|
what are three ways that cryptosporidiosis treated?
|
1. fluids
2. vitamin A supplementation 3. supportive care |
|
what neonatal disease of calves is zoonotic?
|
cryptosporidium
|
|
how can coccidia in cattle lead to pneumonia?
|
coccidiosis → diarrhea → stress → pneumonia
|
|
what predisposes a ruminant to coccidiosis?
|
crowded, unsanitary conditions and during periods of stress (movement to feedlot, weaning, through sale barn)
|
|
where on the property usually contains the highest concentration of coccidia oocysts?
|
near watering areas or other marshy areas that cattle frequently visit
|
|
what is the youngest that a ruminant can be to show patent coccidiosis?
|
3-4 weeks and older
|
|
describe the characteristics of the diarrhea in calves, lambs, and kids with coccidiosis.
|
- may have mucus and strands of mucosa ± blood
- usually no blood in lambs and kids |
|
besides diarrhea, what are other clinical signs of coccidiosis in ruminants?
|
- dehydration
- emaciation - weak and listless - rough hair-coats - tenesmus → rectal prolapse |
|
what is the primary determinant of how severe coccidial diarrhea will be in ruminants?
|
the number of oocysts ingested
|
|
what classification of diarrhea is caused by coccidiosis?
|
malabsorptive, due to destruction of enterocytes
|
|
how is coccidiosis diagnosed in ruminants? (3)
|
- fecal. MAY BE POSITIVE OR NEGATIVE
- necropsy: lesions in LI for cattle, SI for sheep and goats - histopath: visualization of organism |
|
where does coccidiosis cause lesions in:
- goats? - sheep? - cattle? |
- goats: SI
- sheep: SI - cattle: LI (and SI) |
|
what are two drugs used to treat coccidiosis in ruminants?
|
1. amprolium
2. sulfaquinoxaline |
|
what are some non-pharmaceutical techniques for preventing coccidiosis?
|
- avoid wet environments, such as areas around water toughs and ponds
- sanitation |
|
what are four feed additives used to prevent coccidiosis?
|
1. amprolium
2. decoquinate 3. monensin 4. lasalocid |
|
when does coccidiosis in lambs and kids most commonly occur?
|
weaning
|
|
why do sheep and goats usually not have bloody diarrhea with coccidiosis, whereas it is more common in cattle?
|
because in goats and sheep, infection is in SI, whereas infection is in both the SI and LI of cattle.
|
|
at what age is coccidiosis in pigs usually seen?
|
7-11 days of age (range is 5 days to 3 weeks)
|
|
describe the characteristics of the diarrhea in pigs with coccidiosis.
|
yellow-tan to gray, pasty; becomes watery later on, leading to dehydration and unthriftiness
|
|
in a kids and lambs with diarrhea, how do you rule out worms as the causative agent?
|
kids and lambs don't usually get diarrhea with worms (DUH!)
|
|
describe the epidemiological curve and economic importance of coccidiosis in pigs?
|
sporadic, but economically important due to poor growth
|
|
how do you treat coccidiosis in pigs?
|
- increase the temperature of the nursery
- give electrolytes - there is no accepted coccidiostat, in contrast to ruminants |
|
at what time of year does coccidiosis in swine most commonly occur?
|
late summer and fall, due to a build-up of organisms
|
|
how is coccidiosis in swine prevented?
|
hygiene, disinfection (bleach or ammonia), all-in/all-out
|
|
what is the causative agent for swine dysentery?
|
Brachyspira (Serpulina, Treponema) hyodysenteriae
|
|
you necropsy some nursery pigs because they had mild diarrhea that caused reduced weight gains. What infectious agent would you suspect?
|
rotavirus
|
|
you are looking at some 10-day-old dairy calves that have diarrhea. The diarrhea is watery, but the calves appear bright and alert. What is your list of differentials?
|
rotavirus, cryptosporidiosis
|
|
what is the best means to control enterotoxemia in lambs less than 7 days of age?
|
vaccinate the dam, pre-partum, with Clostridium perfringens types C&D bacterin.
|
|
some grower/finisher pigs have severe bloody diarrhea, what are 4 differentials?
|
1. Salmonella choleraesuis
2. Swine dysentery (Brachyspira hyodysenteriae) 3. Whipworms (Trichuris suis) 4. African Swine Fever (afsavirus) |
|
what is the causative agent for Bloody Scours/Black Scours in pigs?
|
Brachyspira (Serpulina, Treponema) hyodysenteriae (aka Swine Dysentery)
|
|
Swine dysentery shedding of Brachyspira bacteria: how long does it occur in
- carrier pigs? - vectors and non-swine reservoir hosts? |
- carrier pigs: 90 days
- others: 30 days |
|
what non-swine reservoir hosts and vectors carry Brachyspira hyodysenteriae (Swine Dysentery)
|
birds, rodents, dogs, and flies
|
|
what are 3 common ways in which swine dysentery (Brachyspira hyodysenteriae) is brought into a herd of swine?
|
1. fomites such as trucks and dirty boots, clothing
2. carrier pigs 3. reservoir hosts such as birds (droppings) and dogs |
|
how long can Brachyspira hyodysenteriae live in lagoon water? Why is this important?
|
- 2 months
- because reusing lagoon water to clean the floors may spread the disease and continue the outbreak |
|
describe the gross pathological lesions caused by swine dysentery
|
- confined to the large intestine, cecum, and spiral colon
- mucofibrinous enteritis - multi-focal areas of petechial to paint brush hemorrhages on the mucosal surfaces |
|
what age group is most commonly affected by swine dysentery?
|
post-nursery age groups (growers and finishers)
|
|
why are grower/finisher pigs with swine dysentery chronic poor-doers?
|
mucofibrinous enteritis reduces capacity for absorption
|
|
what type of diarrhea is caused by swine dysentery?
|
malabsorptive, due to destruction of enterocytes
|
|
how is swine dysentery diagnosed?
|
gross path and culture
|
|
how is swine dysentery prevented?
|
vaccinate, hygiene, and biosecurity (note, reportable in some states)
|
|
what is the usual cause of a Salmonella outbreak on a pig farm?
|
stress
|
|
Why are Salmonella outbreaks in pig farms usually associated with stress?
|
Because Salmonella choleraesuis is host-adapted and an outbreak is triggered by stress.
|
|
what is the morbidity and mortality of Salmonellosis in pig farms?
|
both high
|
|
what are two sources of Salmonella in pig farms?
|
1. carrier animals
2. feedstuffs (high-protein supplements such as non-ruminant blood meal and Ca:P bone meal) |
|
describe the diarrhea associated with salmonellosis in pigs
|
watery, yellow diarrhea, often with necrotic debris, and may be BLOODY
|
|
what are clinical signs of salmonellosis in pigs?
|
- diarrhea ± bloody
- febrile, anorectic due to septicemia - may see pneumonia - POOR GROWTH - ± rectal strictures |
|
what type of diarrhea is caused by salmonellosis in swine?
|
- malabsorptive from intestinal damage
- secretory due to inflammatory products |
|
how is swine salmonellosis diagnosed
- via culture? - via necropsy? |
- culture guts, lymph nodes, and gall bladder
- necropsy: inflamed and thickened ileum and colon with fibrinous adhesions, mucosal hemorrhages, and button ulcers; lymphadenitis |
|
what are the gross pathological lesions associated with salmonellosis in swine?
|
inflamed and thickened ileum and colon (SMALL AND LARGE INTESTINE) with fibrinous adhesions, mucosal hemorrhages, and button ulcers; lymphadenitis
|
|
how is salmonellosis in swine treated?
|
antibiotics and supportive care
|
|
how is salmonellosis in swine prevented?
|
- closed herds
- live, avirulent live culture vaccine of S. choleraesuis intranasally or in water |
|
what Salmonella serovars cause salmonellosis in swine?
|
1. S. choleraesuis
2. S. typhimurium |
|
what age pigs are most commonly affected by salmonellosis?
|
nursery and grower
|
|
which Salmonella serovar is host-adapted in cattle?
|
S. dublin
|
|
how is salmonella acquired in cattle?
|
- environment due to hardiness of bacteria
- manure from rodents, birds, and infected cattle - S. dublin recrudescence and shed in milk - contaminated feed and in water through runoff |
|
what type of diarrhea is caused by salmonellosis in cattle?
|
- malabsorptive from intestinal damage
- secretory due to prostaglandin from enterotoxins |
|
what is the typical age of a salmonella outbreak in a herd of cattle?
|
10 days - 3 months, but all ages can be affected
|
|
what are clinical signs of salmonellosis in cattle?
|
- enteritis (diarrhea)
- fever - inappetence - depression - dehydration |
|
describe the diarrhea associated with salmonellosis in cattle
|
initially it is watery, but as the disease progresses, may contain shreds of mucosa, fibrin casts, or FRNAK BLOOD. Putrid, foul odor.
|
|
what circumstances lead to disease in cattle caused by Salmonella dublin.
|
usually from stress of calving, which leads to immunosuppression
|
|
why would a cow with salmonellosis abort?
|
systemic infection
|
|
what are four gross pathological lesions of salmonellosis in cattle?
|
1. FIBRIN TAGS on the intestines along with excessive peritoneal fluid
2. mesenteric lymph nodes often large and hemorrhagic 3. bowel contents may contain mucus, blood, fibrin tags, and fluid feces 4. fibrin and mucosal casts are often found in both the SI and LI |
|
a cow presents with a retained placenta and has dropped 100-150 pounds in the past few days. What is high on the DDx list?
|
salmonellosis
|
|
if you suspect salmonellosis in cattle, what tissues should be cultured?
|
feces, lymph nodes, bile, and portions of affected GI tract
|
|
how is salmonellosis in cattle treated?
|
- fluids (oral and/or IV)
- parenteral Ceftiofur, TMS (or a/b based on C/S testing) - NSAIDs: Banamine |
|
how is salmonellosis in cattle prevented?
|
- clean the environment
- proper nutrition - reduce stress - ± vaccine |
|
What causes porcine proliferative enteritis?
|
Lawsonia intracellularis
|
|
what age pigs are most commonly affected by proliferative enteritis (Lawsonia intracellularis)?
|
grower and finishing pigs (6-20 weeks)
|
|
what are the clinical signs associated with proliferative enteritis in pigs?
|
- watery to mucoid hemorrhagic diarrhea
- POOR GROWTH, chronic wasting - sudden death with intestinal hemorrhage in breeding age animals |
|
what are the gross pathological lesions associated with proliferative enteritis (Lawsonia intracellularis) in swine?
|
- "garden hose gut" - proliferative thickening of the SI, LI, ileum, cecum, and upper spiral colon
- the proliferation is caused by granulation tissue (i.e., intracellular bacterial infection) |
|
how is swine proliferative enteritis diagnosed in the lab?
|
PCR or immunofluorescence
|
|
what are two DDx for grower/finisher age swine with poor growth and watery-to-mucoid, hemorrhagic diarrhea, and chronic wasting?
|
- proliferative enteritis (Lawsonia intracellularis)
- swine dysentery (Brachyspira hyodysenteriae) |
|
how is porcine proliferative enteritis treated and prevented?
|
- a/b in feed
- vaccine |
|
a pig presents with bloody, tarry feces, grinding teeth, and the farmer notices the pig will eat one day and the next day or two, will not eat. Today, he vomited up dark stuff that looks like coffee grounds. What is high on the DDx list?
|
gastric ulcers
|
|
what is the main causative agent of gastric ulcers in swine?
|
stress
|
|
what are four dietary factors that can cause ulcers in swine?
|
1. finely ground grain
2. Vitamin E and Selenium deficiency 3. copper toxicity 4. irregular feedings (i.e., pig expects meal at certain time of day, produces stomach acid, but does not get food → ulcerated mucosa) |
|
where in the stomach do gastric ulcers usually occur in swine?
|
in the pars esophageal part of the stomach
|
|
what are five ways to treat gastric ulcers in swine?
|
1. aluminum hydroxides and magnesium silicate
2. reduce stress 3. Tagamet 4. oats/alfalfa hay 5. Omeprazole |
|
what are three ways to prevent gastric ulcers in swine?
|
1. adequate Vitamin E and Se
2. reduce stress 3. consistent feeding intervals and increase coarseness of feed |
|
what are the two biotypes of BVDV?
|
cytopathic and non-cytopathic
|
|
BVD: which biotype can
- cause clinical disease in young or older cattle? - cause abortion or fetal malformations? - cause a PI calf? - cause the mucosal form of the disease? |
- either
- either - only non-cytopathic can cause persistently infected calves - both types are required in a PI animal to cause the mucosal form |
|
which BVD biotype is most common?
|
non-cytopathic
|
|
how is BVDV shed?
|
by infected animals in virtually all secretions, excretions, aborted fetuses, and uterine fluids
|
|
what are the 5 syndromes of BVD?
|
1. subclinical infection - most common
2. classic or acute BVD - associated with stress and ↑ exposure 3. infection of naïve pregnant cattle - infertility, abortion/resorption/repeat breeder, PI calves 4. mucosal disease - PI calves with both biotypes 5. BVD Type II - viral septicemia, pulmonary hemorrhage, edema |
|
what are clinical signs of Subclinical BVD (the most common form)? How long does the disease last?
|
- anorexia, fever, serous nasal discharge, leukopenia (like the "common cold")
- recover in 10 days unless complicated infection |
|
what is the most common cause of the classic/acute form of BVD?
|
in a feedlot situation, due to increased stress and exposure
|
|
what are the two primary target organ systems of the classic/acute form of BVD?
|
1. GI - acute gastroenteritis
2. respiratory - pneumonia |
|
what are four clinical signs related to the acute gastroenteritis caused the by the classic/acute form of BVD?
|
1. watery diarrhea ± blood
2. fever (104 - 106 °F) 3. no rumen motility and splashy gut sounds 4. oral mucosal lesions with BLUNTING OF THE ORAL PAPILLAE |
|
how long does it typically take feedlot cattle, with uncomplicated classic/acute BVD, to recover from the infection?
|
10 days
|
|
what are 6 fetal anomalies associated with BVD infection of a naïve cow/heifer?
|
1. cerebellar hypoplasia
2. dysmyelinogenesis 3. lenticular cataracts 4. microphthalmia 5. hydranencephaly 6. hydrocephalus |
|
at what days of pregnancy will infection of an immuno-naïve cow/heifer with BVD result in a PI calf?
|
80-120 days
|
|
calves PI with BVD:
- appearance - typical CBC - how often do they shed virus? - serological testing - mortality and survival rate |
- they can be stunted, poor-doers or can look normal
- leukopenic - they are constantly viremic and shed virus - they will be negative on serological testing - 50% die before 2 years; 10% live to breeding age |
|
what happens if an immuno-naïve cow/heifer is infected with BVD after 150 days of gestation?
|
- fetus dies and is aborted
- or survives and is seropositive at birth |
|
Mucosal form of BVD
- who gets this disease? - at what age does it typically occur? - what is required for infection to occur? |
- only persistently infected, immuno-tolerant animals can get this disease
- occurs between 6-18 months of age due to decline of maternal antibody - PI calf must encounter a cytopathic virus and seroconvert for this to happen (naturally, mutation, MLV vaccine) |
|
what are three ways in which a PI calf, which is by definition, infected with the non-cytopathic form of BVD, encounter the cytopathic form that leads to mucosal disease?
|
1. naturally
2. mutation of virus (most common) 3. MLV vaccine |
|
what are the symptoms of the mucosal form of BVD? (6)
|
- diarrhea and extensive oral lesions
- mucopurulent ocular-nasal discharge - nasal mucosa crusty with a thick layer of dry, purulent discharge - lameness - coronitis and interdigital ulcers - non-responsive to antibiotics - death |
|
What are clinical signs of Type II BVD? (5)
|
1. very high fever of 106-107 °F
2. anorexia, ↓milk production 3. respiratory distress 4. death in 48 hours 5. ±diarrhea |
|
Type II BVD
- mucosal lesions (compared to Type I) - which age group has highest mortality rate? |
- no mucosal lesions
- calves > adults |
|
what are three gross pathological lesions of BVD?
|
- blunted oral papillae
- ulcerations in the esophagus - necrosis of the Peyer's patches |
|
what causes diarrhea in cattle with BVD?
|
necrosis of Peyer's patches
|
|
what are four diagnostic methods used for BVD?
|
- serology
- VI from serum, WBC, and secretions - IHC from ear notch test - IFA |
|
how is BVD treated?
|
- supportive: prophylactic a/b and NSAIDs
- mucosal disease: euthanasia |
|
what are 2 advantages and 2 disadvantages of killed BVD vaccine
|
- advantages: safe for all groups of cattle; may provide antigenic diversity
- disadvantages: expensive; need yearly boosters (2 shots initially) |
|
what are 3 advantages and 2 disadvantages of the MLV BVD vaccine?
|
- advantages: inexpensive, quick vaccine response, long-lasting immunity
- disadvantages: immunosuppression, can't give to pregnant cows |
|
what causes vaccine complications in a killed BVD vaccine? What are two complications?
|
- caused when the vaccine is contaminated with non-attenuated viruses
1. can cause disease in pregnant animals and nursing calves 2. can cause PI calves to seroconvert, causing mucosal disease |
|
what agent causes winter dysentery in cattle?
|
coronavirus
|
|
what age group of cattle is affected by winter dysentery?
|
adults
|
|
winter dysentery in cattle:
- clinical signs - course - treatment |
- explosive light tan/brown diarrhea ± blood; ADR; ↓ milk, AFEBRILE
- rapid onset; course of about 2 weeks - supportive, oral fluids, kaolin |
|
what agent causes Jones disease?
|
Mycobacterium paratuberculosis
|
|
Mycobacterium paratuberculosis, the causative agent of Johne's disease:
- staining - culture characteristics - intra- or extracellular? |
- acid fast
- grows very slowly in culture medium - intracellular organism (→ granulomatous inflammation) |
|
what is the typical age range for clinical Johne's disease
- in cattle? - in small ruminants? |
- cattle: 2-5 years old (reported 4 months - 15 years)
- small ruminants: 1 year or older |
|
when are cattle infected with Johne's disease?
|
calves < 3-4 months old
|
|
what are four ways that Johne's disease can be transmitted to calves?
|
1. fecal-oral
2. in utero 3. colostrum/milk from stressed dam 4. contaminated water such as ponds |
|
what are the clinical signs of Johne's disease in cattle
|
- chronic weight loss despite a healthy appetite
- intermittent to persistent diarrhea - ± fever - advanced cases: debilitation, dehydration, weakness, ventral edema, anemia, death. |
|
what is the duration of Johne's disease?
|
2 weeks to 3-6 months
|
|
why does Johne's disease occur more often in dairy cattle than in beef cattle?
|
close contact and fecal material build-up of organism
|
|
what causes a Johne's positive cow to start having diarrhea?
|
stress: lactation, parturition, mastitis, 2ndary bacterial infection
|
|
what plasma protein abnormality is common with Johne's disease?
|
hyperproteinemia with hypoalbuminemia
|
|
characterize the diarrhea associated with Johne's disease in cattle
|
watery, not bloody
|
|
what is a big difference in clinical presentation of Johne's disease of small ruminants versus cattle?
|
small ruminants typically do not have diarrhea during the course of the disease; if they do, they are going to die soon.
|
|
You are out at farmer Owarzczewski's farm and he's got a cow that freshened 3 weeks ago, never tightened up and has watery diarrhea all of the time. She has a very healthy appetite. What is at the top of your DDx list?
|
Johne's disease
|
|
what type of diarrhea is caused by Johne's disease?
|
malabsorptive
|
|
what pathophysiological process is the thing that kills ruminants with Johne's disease?
|
protein losing enteropathy (from granulomatous enteritis) leading to hypoproteinemia and wasting
|
|
what are the gross pathological lesions of Johne's disease?
|
- intestines, especially ILEUM, are thickened, edematous, and corrugated
- lesions in small ruminants are not as distinct as in cattle - granulomatous lymph nodes; caseated in small ruminants |
|
after infection with Mycobacterium paratuberculosis, when do ruminants begin shedding the organism?
|
immediately
|
|
what are 3 non-invasive tests used to diagnose Johne's disease?
|
1. culture (takes 1-4 months)
2. AGID (45% sensitivity) 3. ELISA - most sensitive - note: nothing is very accurate for subclinical animals - sensitivity increases when animals are shedding large numbers of organisms during diarrhea |
|
what are 6 ways to prevent Johne's disease?
|
1. cull daughters
2. pasteurize colostrum 3. pasture rest for manure contamination 4. ± vaccine in critical cases; requires approval from state vet because it will cause a positive TB test. Given at 35 days of age. 5. replacements from certified free herds 6. prevent run-off from adult herd into water sources |
|
how is Johne's disease definitively diagnosed?
|
- isolation of M. paratuberculosis from gut, lymph node, or rectal scraping, followed by histopath
|
|
what are two drugs to treat Johne's disease? How successful are they?
|
- rifampin and isoniazid - extra-label
- relapse after treatment stops |
|
in the horse, the term used to describe the molars in the maxilla being abaxial to the mandibular teeth
|
anisognathous
|
|
what is the dental formula for equine deciduous teeth?
|
dI3/3, dC0/0, dP3/3, dM0/0 = 24
|
|
what is the dental formula for equine permanent teeth?
|
I3/3, C1/1, P3(4)/3, M3/3 = 40-42
|
|
the first permanent premolar of the horse is called what?
|
wolf tooth
|
|
how can the wolf tooth cause problems in the horse?
|
bit interference
|
|
what are "caps" on horses teeth?
|
remnants of a deciduous tooth attached to a permanent tooth
|
|
why are "caps" on horse's teeth problematic?
|
they cause root impaction and deformation of the underlying bone ("jaw bumps")
|
|
what are five primary clinical signs of oral cavity disease in the horse?
|
1. fetid odor
2. reluctance to eat 3. abnormal eating behavior such as tilting head 4. head shaking 5. quidding |
|
what are five sequelae of oral cavity disease in the horse?
|
1. weight loss
2. sinusitis 3. fetid odor from the nostril 4. choke 5. colic |
|
what are four types of oral speculums used in horses?
|
1. McPherson - adjustable
2. graphite 3. coil/spring - use very quickly or with sedation 4. wedge - need sedation |
|
what are three abnormalities you may see on exam of a horse's oral cavity?
|
1. defects such as cracks, holes, and missing teeth
2. feed accumulation 3. gingival recession or erosion |
|
what is a dental pick used for in a horse?
|
to probe the centers of the teeth and to remove debris
|
|
what tooth defects in the horse do you find with digital palpation?
|
points and erosions
|
|
what are four abnormalities related to dental problems in an oral radiograph of the horse?
|
1. cracks in the teeth (DV most useful)
2. alveolar reaction (cavity) 3. fluid lines in the sinus 4. lysis of the lamina dura dentes |
|
what are "cascades" of horses teeth?
|
malocclusion of the incisors, where the teeth form a wavy occlusal line instead of flat
|
|
what is the term used when the premolars and molars of horses' teeth do not occlude in a straight line?
|
wave mouth
|
|
what is step mouth in the horse?
|
when there is a missing tooth and overgrowth of the opposite tooth due to lack of an occlusal surface
|
|
what is brachygnathia?
|
seen in young horses (not long after birth) where the maxilla overgrows the mandible and the teeth don't occlude.
|
|
how is brachygnathism in horses treated?
|
there is no cure, but regular tooth care to prevent overgrowth; ± braces
|
|
on which teeth does dental calculus accumulate most in the horse? What kind of diet is associated with calculus?
|
- canines
- grain diet |
|
what is the usual cause of a diastema between horse teeth? Why is a diastema bad?
|
- usually associated with a bad tooth fracture
- food can migrate down and cause infection |
|
caused by a congenital defect or a bad cavity, when the occlusal surface of a horse's tooth is open down too low, sometimes to the root cavity
|
open infundibulum
|
|
what is a dentigerous cyst in the horse?
|
a tooth growing in the ear
|
|
what are four diseases of the equine esophagus?
|
1. choke
2. laceration 3. esophageal diverticulum (pulsion or traction) 4. stricture |
|
what forms the cranial sphincter of the equine esophagus?
|
cricopharyngeus muscle
|
|
what part of the equine esophagus is striated muscle?
|
proximal 2/3rd
|
|
what nerve and artery lies adjacent to the esophagus in the horse?
|
carotid artery and vagus nerve
|
|
what are 8 clinical signs of choke in the horse?
|
1. feed in nasal discharge
2. salivation 3. retching/stretching of neck and head 4. coughing 5. enlargement in cervical esophagus 6. cellulitis or emphysema from rupture or laceration of esophagus 7. aspiration pneumonia 8. dehydration |
|
how would choke show up on a lateral radiograph of the horse's neck?
|
an enlarged cervical esophagus with a food bolus or foreign body
|
|
what are four typical locations of choke in the horse?
|
1. post-pharyngeal
2. thoracic inlet 3. heart base 4. cardia of the stomach |
|
what is the best way to pinpoint the location of choke in the horse radiographically?
|
barium contrast agent
|
|
what are the clin path results of choke in the horse? (CBC, chem)
|
- CBC: dehydration
- metabolic alkalosis, ↓K, ↓Na, ↓Cl |
|
what are some general methods to treat choke in the horse?
|
1. withhold food and water (immediately) and wait and see ± sedation
2. endoscopy 3. pass a stomach tube |
|
what drugs are used to treat choke in the horse?
|
- tranquilization: acepromazine
- sedation: xylazine or detomidine - muscle relaxant: lidocaine or N-butylscopolammonium chloride (Buscopan) - muscle stimulant: Oxytocin |
|
how is a refractory case of choke treated in the horse?
|
- general anesthesia with intubation
- lower head to allow drainage - continuous lavage - loop instrument, hand, or esophagostomy to remove object |
|
what are five complications of choke in the horse?
|
1. dehydration
2. electrolyte imbalance 3. inhalation pneumonia 4. stricture 5. diverticulum |
|
what is a pulsion esophageal diverticulum?
|
food mass or object pushes though the muscle layer, leaving a defect in the muscle with a bulging mucosa
|
|
what is a traction esophageal diverticulum?
|
contracting mucosa, muscle, or adventitia pulls the esophageal wall, creating an open area that can't contract
|
|
what are 9 behavioral signs of colic in the horse?
|
1. depression
2. frequent recumbency 3. head turned back toward the flank 4. Flehmen behavior with the lips 5. pawing at the abdomen or ground 6. sitting like a dog 7. head-butting flank 8. stretching 9. uncontrollable pain (horse is freaking out) |
|
if a horse has missing skin on its face and looks depressed, what may be happening
|
the horse was thrashing from colic. Now it is in shock or acidotic
|
|
what is the incidence rate for colic in horses?
|
4.2 per 100 horse-years
|
|
what time of year do horses colic the most?
|
spring
|
|
what is the case fatality fate for colic in horses?
|
7-11%
|
|
what are the two leading causes of death in the horse?
|
1. old age
2. colic |
|
since colic in horses is sporadic, how is a risk factor defined for a particular factor?
|
the odds ratio that the incidence of colic will increase in a group of horses exposed to that factor
|
|
what is the most common cause of colic in horses that are
- weanlings? - neonates? - > 12 years old? - stallions? |
- weanlings: ileocecal intussusception
- neonatal foals: meconium impaction - > 12 years: lipoma - stallions: inguinal hernia |
|
what horse breeds are predisposed to inguinal hernias?
|
standardbred, saddlebred, warmblood
|
|
what are 6 environmental/management risk factors for colic in horses?
|
1. lack of water/dehydration
2. abrupt decrease in activity 3. electrolyte imbalance 4. medications - NSAIDs 5. sand or gravel exposure (pica) 6. poor dentition |
|
what are four parasites that can cause colic in horses?
|
1. large strongyles
2. small strongyles 3. tapeworms 4. ascarids |
|
ascarid obstruction in horses
- age groups - where is the obstruction? - when does it occur? |
- foals and weanlings
- small intestine - occurs after administration of anthelmintic |
|
what two types of lesions do tapeworms cause in horses, that may make them colic?
|
1. ileocecal intussusception
2. cecocecal intussusception |
|
what is the leading risk factor for colic in horses?
|
hay change
|
|
what are the top six risk factors for colic in horses?
|
1. HAY CHANGE
2. diet change 3. previous colic 4. weather change 5. housing change 6. anthelmintic |
|
what is the leading dietary risk factor that leads to colic in horses?
|
too much concentrate/grain/oats/bran in the feed (i.e., too many CHOs)
|
|
what are five risk factors for colon obstruction/distention in the horse?
|
1. cribbing or wind sucking
2. increasing hours stabled 3. recent change in regular exercise 4. anthelmintic not given in past 12 months 5. history of travel in past 24 hours |
|
what are three things that aerophagia can cause in the horse (colic)
|
1. SI incarceration in the epiploic foramen
2. large colon simple obstruction 3. gastric ulcers |
|
what are five things that cause enteroliths in horses?
|
1. alfalfa hay
2. high mineral content of ingesta 3. alkaline ingesta 4. aquaporin genetic defect 5. foreign body |
|
what are three risk factors for large colon impaction in horses?
|
1. confinement (stall/hospital)
2. anthelmintic administration 3. long distance shipping |