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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.? ***
enterotoxogenic E. coli
rotavirus
coronavirus
Cryptosporidium parvum
Salmonella spp.
What is meant by the term "undifferentiated diarrhea of newborn calves"?
profuse diarrhea in any calf up to 30 d.
What are risk factors for development of neonatal diarrhea?
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
What are goals for occurrence of neonatal diarrhea in dairy & beef calves?
dairy: < 6% calf deaths from 24 hrs. to 2 m. of age
beef: < 2% calf deaths from 24 hrs. to 5 m. of age
What vaccines are recommended to help prevent neonatal diarrhea?
vaccinate all pregnant females w/ ETEC (w/ purified K99 Ag), rotavirus, coronavirus
Salmonella bacterin, Clostridium perfringens type C bacteria recommended in some instances
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
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
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
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
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
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
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
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
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
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
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
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
What is the cause of nutritional diarrhea?
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
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
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
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
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
What are some causes of death in calves w/ diarrhea?
septicemia
acidemia
hyperkalemia
prolonged malnutrition (hypoglycemia)
hypothermia
What is the pathophysiology of dehydration assoc. w/ calf diarrhea?
-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
How can dehydration be assessed in calves?
-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
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.
What is the pathogenesis of metabolic acidosis in calves w/ diarrhea?
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.
How can metabolic acidosis be assessed?
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)
How are depression scores used to assess metabolic acidosis?
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
What electrolyte abnormalities are common in calves w/ diarrhea?
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
How does calf diarrhea result in a negative energy balance?
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)
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
What are the goals of IV fluid administration in tx of calf diarrhea?
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?
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)
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
How do you determine the liters of isotonic bicarb required to correct severe acidemia in a calf w/ diarrhea?
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
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
How is dextrose used in tx of calves w/ diarrhea?
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
What type of fluids are indicated in a calf that is < 8% dehydrated, has a suckle, & is standing?
oral electrolytes
What type of fluids are indicated in a calf that is ≥ 8% dehydrated, has a suckle, & is standing?
IV hypertonic saline + oral electrolytes
What fluid therapy should be given to a calf w/ diarrhea that is < 6% dehydrated, has no suckle, & is standing?
oral electrolytes
What fluid therapy should be given to a calf w/ diarrhea that is ≥ 6% dehydrated, has no suckle, & is standing?
IV hypertonic saline + oral electrolytes
What fluid therapy should be given to a calf w/ diarrhea that has no suckle & is not standing?
IV sodium bicarb (isotonic) + oral electrolytes

hydration status, depression score, &/or blood gas results used to determine quantity of fluid needed
When & which ABs are used to tx diarrhea in calves?
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
What are some ancillary treatments used for calves w/ diarrhea?
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
What are the benefits of raising dairy calves in hutches?
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
What are the rules for raising dairy calves in hutches?
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