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47 Cards in this Set
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*** What are the top 5 ddx for diarrhea in calves < 21 d.? ***
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enterotoxogenic E. coli
rotavirus coronavirus Cryptosporidium parvum Salmonella spp. |
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What is meant by the term "undifferentiated diarrhea of newborn calves"?
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profuse diarrhea in any calf up to 30 d.
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What are risk factors for development of neonatal diarrhea?
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INADEQUATE COLOSTRUM INGESTION: #1
fecal contaminated calving pens nursing dirty teats unsanitary feeding utensils (nipples, bottles) group housing, continuous flow overcrowding, failure to isolate sick calves: esp. in beef units |
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What are goals for occurrence of neonatal diarrhea in dairy & beef calves?
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dairy: < 6% calf deaths from 24 hrs. to 2 m. of age
beef: < 2% calf deaths from 24 hrs. to 5 m. of age |
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What vaccines are recommended to help prevent neonatal diarrhea?
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vaccinate all pregnant females w/ ETEC (w/ purified K99 Ag), rotavirus, coronavirus
Salmonella bacterin, Clostridium perfringens type C bacteria recommended in some instances |
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enterotoxogenic E. coli
a. organism characteristics b. pathophysiology |
a. dz in calves caused by strains that adhere to enterocytes & produce enterotoxins
1º virulence factor: adhesins in pili (allow bacteria to adhere) >95% of ETEC strains have K99 adhesin (pillus Ag) produces heat stable enterotoxin (ST toxin) b. bacteria must survive destruction in abomasum -as pH ↓ to 2-3 in 1st few days of life, colibacillosis is no longer a problem -ST toxin --> SECRETORY DIARRHEA (excessive loss of Na & Cl into SI lumen), minimal damage to villi |
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enterotoxogenic E. coli
a. transmission b. risk factors c. clinical signs |
a. fecal-oral: infected dam or environment
-can survive for long periods in environment & reinfect animals b. AGE: 12 hrs. - 3 d. lack of colostral immunity, stocking density, weather, housing, calves born later in season c. yellow diarrhea w/ no tenesmus or blood, increased fecal pH |
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enterotoxogenic E. coli
a. dx b. tx c. control |
a. usually not done
-must ID specific strain of E. coli: fluorescent Ab, latex agglutination assay (detect K99 Ag) b. correct hydration: oral/IV fluids -considers ABs: ceftiofur, potentiated sulfas, amoxicillin c. vaccinate dam in late gestation w/ purified K99 Ag & make sure calf ingests good quantity of colostrum in 1st 6-12 hrs -can also give oral vaccine w/ specific anti-K99 monoclonal Abs when calf is born: more expensive than dam vaccination but effective -make sure calves are in clean environment & clean pens b’twn calves |
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rotavirus
a. organism characteristics b. transmission c. pathophysiology |
a. very stable at variety of pHs & temps
b. fecal-oral c. virus infects epi cells of SI villi -infected cells sloughed --> villus atrophy --> epi cells replaced w/ immature cells that have ↓ lactase activity -immature replacement cells can’t absorb nutrients --> MALABSORPTIVE DIARRHEA |
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rotavirus
a. clinical signs b. dx c. control |
a. CALVES 5-15 d. AFFECTED
-diarrhea, dehydration -high morbidity, low mortality -infection generally over after 24 hrs., but diarrhea continues until replacement epi cells mature & villi are restored b. FECAL EM, fluorescent Ab testing, ELISA, latex agglutination, PCR -definitive: detection of virus + characteristic histologic lesions (villus atrophy & shortening) c. good management practices: isolate new animals on arrival, handle calves before adults, isolate sick calves, disinfect hutches after each calf -vaccinate cows prior to calving to boost colostral Abs |
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coronavirus
a. organism characteristics b. transmission c. pathophysiology |
a. stable at pH > 3, unstable at temps > 45º C
b. fecal-oral, resp. over very short distances c. infects mature villus epi & crypt cells of LARGE & SMALL INTESTINE -atrophy of villi & fusion of adjacent villi in SI --> functionally immature cells emerge --> impaired electrolyte transport --> MALABSORPTIVE DIARRHEA |
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coronavirus
a. clinical signs b. dx c. control |
a. calves 4 d. - 1 mo. affected
-diarrhea w/ no blood or tenesmus: usually more severe than rotavirus +/- dehydration, depression, anorexia, hypoglycemia, resp. signs (rhinitis, sneezing, coughing) b. FECAL EM, fluorescent Ab staining of colon -histopath: villus atrophy & fusion in SI, loss of colonic ridges in LI c. vaccinate dams in late gestation to boost colostral IgG -↓ exposure to calves: use stalls, disinfect, etc. -calves eventually “grow out” of coronavirus infections |
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Cryptosporidium parvum
a. organism characteristics b. transmission c. pathophysiology |
a. protozoan
thin walled oocyst: rupture in intestinal lumen --> reinfection (AUTOINFECTION) thick walled oocyst: passed in feces in sporulated form (IMMEDIATELY INFECTIVE) -sporulation w/in host is unique to Crypto b. fecal-oral, fomites, water & feed contamination c. damage to villus epi --> villus atrophy -hyperplasia of crypt epi --> impaired absorption |
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Cryptosporidium parvum
a. clinical signs b. dx c. control |
a. calves 5 d. - 1 mo. affected
-white to yellow diarrhea +/- blood, dehydration, metabolic acidosis, depression, anorexia -diarrhea typically persists for several days b. DETECTION OF OOCYSTS IN FECES: 10^5-10^7/ml feces = (+) definitive: ID of oocysts in feces OR trophozoites/schizonts in intestinal epi + characteristic histologic lesions c. good management practices: oocysts destroyed by freezing, temps > 65º C, or by drying) ZOONOTIC |
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Salmonella
a. organism characteristics b. transmission |
a. G (-) intracellular bacteria
S. dublin & S. typhimurium: most common in calves persists in environment for 14 mo.: killed by heat b. primarily fecal-oral, also airborne -animal to animal, contaminated feed (common), contaminated environment: birds, rodents |
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Salmonella
a. pathophysiology b. clinical signs |
a. bacteria invade intestinal wall & go to mesenteric lns
-produce 2 exotoxins (enterotoxin, cytotoxin) -bacteria spreads to liver & bloodstream -fever seen 24-48 hrs after initial invasion: this septicemic phase has high mortality -bacteria can then invade intestines --> MALABSORPTIVE & SECRETORY DIARRHEA b. septicemic form (common): sudden death -diarrheal form: BLOODY DIARRHEA W/ MUCOSAL SHREDS & TENESMUS -calves will be very sick: fever, poor appetite, lethargy, leucopenia |
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Salmonella
a. dx b. tx c. control |
a. FECAL CULTURE (GOLD STANDARD): involves enrichment broth & selective media (can be hard to grow)
-PCR on feces -CBC: leucopenia, neutropenia, severe L shift -serology: only used to monitor herd seroprevalence, not for individual dx b. ABs (ceftiofur), fluids, NSAIDs c. vaccination: generally provides poor protection but is sometimes done (autogenous) -good farm management practices -many strains are zoonotic -concern re: development of multiple AB resistant strains |
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What is the cause of nutritional diarrhea?
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usually d/t feeding poor quality milk replacer, esp. those that contain PLANT PROTEINS instead of milk proteins
SOY protein is a major problem in calves |
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attaching & effacing E. coli (enterohemorrhagic, verocytotoxic E. coli)
a. organism characteristics b. pathophysiology c. signs d. dx |
a. specific group of E. coli that attach intimately to & efface (detach) microvilli & enterocytes
b. produce verotoxins --> necrosis & sloughing of enterocytes c. DIARRHEA W/ BRIGHT RED BLOOD IN CALVES 15-30 d. OF AGE d. must prove that E. coli strain produces verotoxins zoonotic |
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Clostridium perfringens type C
a. pathophysiology b. signs c. dx d. control |
a. bacteria adhere to SI villi & multiply & produce β-toxin
- β-toxin inactivated by trypsin, so this is only a dz in young calves (<15 d.) b/c they have poor trypsin production --> necrotizing enteritis w/ sloughing of enterocytes, toxemia, & death b. GENERALLY SEE SUDDEN DEATH D/T HEMORRHAGE & TOXEMIA BEFORE YOU EVER SEE DIARRHEA affected animals usually growing well & have good milk intake c. characteristic lesions in intestines -isolation of bacteria from intestine & presence of β-toxin d. vaccinate cows before they calve if this is a problem |
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coccidiosis
a. etiology b. pathophysiology c. signs |
a. Eimeria zurneii & E. bovis
b. oocysts ingested from environment undergo asexual repro in SI --> mild enteritis sexual repro in LI --> SEVERE CECAL & COLONIC DAMAGE --> leakage of fluid, electrolytes, & plasma from epi prepatent period: 16-30 d. (CANNOT see coccidiosis in calves < 3 w.) c. affects JUVENILE ruminants: 3-6 mo. -low volume of bloody diarrhea w/ mucus, mucosal shreds, tenesmus, dehydration not too severe |
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coccidisosis
a. dx b. control |
a. quantitative fecal egg count: > 5000 oocysts/gram
-histopath: typhlitis & colitis w/ coccidial organisms present around sites of inflammation b. decrease stocking rates -don’t place feed directly on ground to avoid fecal contamination of feed -sustained feeding of oral anticoccidial agents: IONOPHORES (ex. monensin), decoquinate, amprolium: should get ionophores thru out life |
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What are some causes of death in calves w/ diarrhea?
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septicemia
acidemia hyperkalemia prolonged malnutrition (hypoglycemia) hypothermia |
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What is the pathophysiology of dehydration assoc. w/ calf diarrhea?
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-occurs d/t ↑ loss of fluids in feces & ↓ fluid intake
-most calves don’t drink water during 1st wk of life & are dependent on milk dehydration --> ↓ plasma volume, ↓ ECF volume --> ↓ CO & ↓ O2 delivery --> HYPOVOLEMIC SHOCK |
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How can dehydration be assessed in calves?
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-eyeball recession into orbit: normal eyeball should be right up against lower lid
-skin tent in neck region -plasma protein conc.: more accurate than hematocrit |
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What are the expected demeanor, sinking of eye (mm), & skin tent (sec) values in a calf that is:
a. < 6% dehydrated b. 6-8% dehydrated c. 8-10% dehydrated d. 10-12% dehydrated e. > 12% dehydrated |
a. normal, none, none
b. depressed, 2-4 mm, 1-3 s. c. depressed, 4-6 mm, 2-5 s. d. comatose, 6-8 mm, 5-10 s. e. dead, 8-12 mm, > 10 s. |
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What is the pathogenesis of metabolic acidosis in calves w/ diarrhea?
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d/t differences in strong ion balance (hyponatremia), not bicarb loss
-significant component of acidosis d/t ↑ D-lactic acid -ruminants can’t metabolize D-lactic acid very efficiently acidosis -acidosis --> progressive CNS depression, ↓ suckle reflex, weakness, ataxia, recumbency, death -usually more severe in calves > 7 d. |
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How can metabolic acidosis be assessed?
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venous blood gas: ideal
base deficit: can be estimated from total CO2 on chem. panel TCO2 ~= blood HCO3 normal HCO3 = 27 mEq/L base deficit ~= 27 – TCO2 depression scores: based on clinical signs (used when lab work not available) |
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How are depression scores used to assess metabolic acidosis?
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based on principle that acidosis is more severe in very depressed calves & in older calves: older calves seem to mask signs of acidosis better
-only applicable to calves w/ uncomplicated diarrhea (can be wrong, esp. w/ septicemia I: alert, active, normal BD if < 8 d. = 0 mEq/L BD if > 8 d. = 7 mEq/L II: depressed, slow, lethargic BD if < 8 d. = 5 mEq/L BD if > 8 d. = 11 mEq/L III: sternal recumbency, weak suckle BD if < 8 d. = 12 mEq/L BD if > 8 d. = 16 mEq/L IV: lateral recumbency, absent suckle BD if < 8 d. = 13 mEq/L BD if > 8 d. = 20 mEq/L |
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What electrolyte abnormalities are common in calves w/ diarrhea?
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intestinal electrolyte loss, ↓ milk intake --> total body deficit in Na, Cl, & K
K conc. variable & does not reflex body stores since K+ is primarily intracellular ion -chronic diarrhea: usually HYPOkalemic -acute diarrhea: usually HYPERkalemic lower the pH, higher K conc. hyperkalemia -suspect when HR < 70 bpm (hypothermia) -if lab work unavailable & HR normal: assume hypokalemia |
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How does calf diarrhea result in a negative energy balance?
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neonatal ruminants have limited energy stores
anorexia, malabsorption --> energy deficit assume negative energy balance in any neonate w/ diarrhea check glucose w/ portable glucometer & supplement if needed in fluids or bolus (50% dextrose) |
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oral electrolytes
a. uses b. pros c. cons d. result when given alone |
a. replace fluid losses, correct acid-base & electrolyte abnormalities, & provide nutritional support
b. quick & easy to give, don't require catheter c. need to give milk also: oral electrolytes don’t have enough energy d. slow but sustained resuscitation |
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What are the goals of IV fluid administration in tx of calf diarrhea?
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replace fluid deficit: body wt (kg) x % dehydration = L of replacement fluid needed
-max flow rate: 80 ml/kg/hr correct acidosis: is sodium bicarb indicated? |
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LRS
a. uses b. cons |
a. correct dehydration & electrolyte abnormalities (rarely used anymore)
b. WEAK alkalinizing agent: lactate must be metabolized by liver: not recommended for calves w/ severe acidemia -hard to give on farm (requires catheter, restraint, monitoring) |
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isotonic sodium bicarb
a. uses b. pros c. cons |
a. should be used to correct severe acidemia (pH < 7.2, base deficit < -15 mEq/L)
STRONG alkalinizing agent b. easy to make by mixing baking soda w/ sterile water at 13 g/L c. requires IV catheter, restraint, monitoring |
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How do you determine the liters of isotonic bicarb required to correct severe acidemia in a calf w/ diarrhea?
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MEq sodium bicarb to correct deficit = weight (kg) x 0.5 x base deficit
1 gram sodium bicarb contains 12 mEq of bicarbonate grams bicarb required = (weight (kg) x 0.5 x base deficit)/12 13 g baking soda/L water liters of isotonic sodium bicarb required = grams bicarb required / 13 |
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hypertonic saline
a. uses b. results when given alone c. results when given w/ oral electrolytes d. pros e. cons |
a. initiates water movement from GI tract into ECF
tx of choice for hyperkalemia: drives K+ into cells give 4 ml/kg over 4 min. period b. transient resuscitation c. rapid & sustained resuscitation d. can be done cheaply & w/o IV catheter e. does NOT correct acidemia |
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How is dextrose used in tx of calves w/ diarrhea?
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only non-alkalinizing fluid used in neonates
add 50-100 mL of 50% dextrose to LRS or isotonic sodium bicarb to make a mildly hypertonic sol’n |
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What type of fluids are indicated in a calf that is < 8% dehydrated, has a suckle, & is standing?
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oral electrolytes
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What type of fluids are indicated in a calf that is ≥ 8% dehydrated, has a suckle, & is standing?
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IV hypertonic saline + oral electrolytes
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What fluid therapy should be given to a calf w/ diarrhea that is < 6% dehydrated, has no suckle, & is standing?
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oral electrolytes
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What fluid therapy should be given to a calf w/ diarrhea that is ≥ 6% dehydrated, has no suckle, & is standing?
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IV hypertonic saline + oral electrolytes
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What fluid therapy should be given to a calf w/ diarrhea that has no suckle & is not standing?
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IV sodium bicarb (isotonic) + oral electrolytes
hydration status, depression score, &/or blood gas results used to determine quantity of fluid needed |
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When & which ABs are used to tx diarrhea in calves?
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most all calves w/ diarrhea get ABs
indicated anytime calf has diarrhea AND a fever, concurrent infection elsewhere, ↓ suckle reflex, blood or mucosal shreds in feces, or documented FPT commonly used: parenteral ceftiofur, amoxicillin, ampicillin others: oral amoxicillin or Clavamox, potentiated sulfonamides |
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What are some ancillary treatments used for calves w/ diarrhea?
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NSAIDs (flunixin) can be used, esp. if possible septicemia exists (ex. fever)
+/- vitamin B & fat soluble vitamins: colostrum deprived calves or calves w/ chronic diarrhea NOT recommended: intestinal protectants, motility modifiers, probiotics |
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What are the benefits of raising dairy calves in hutches?
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calves raised in isolation: limits spread of pathogens b’twn animals
allows control of environment that calf is raised in allows close monitoring of calves, inc. daily milk, food, & water intake |
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What are the rules for raising dairy calves in hutches?
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generally separated from dam & placed into hutches w/in 12 hrs of birth
raised in hutches for 6-8 wks until weaned & well started on solid food hutches should be outside in clean environment should be separated by at least width of hutch must be moved b’twn calves old bedding should be discarded b’twn calves ground where old hutch was should be left empty for 1-2 m. before new hutch placed there farms should own 15% more hutches than they anticipate using should be placed in area where labor passes frequently |