Ruminant Diarrhea 3

sihirlifil's version from 2018-02-24 15:30

Winter dysentery, Cu/Co, Toxins, Misc

Question Answer
Agent of Winter dysentery

Winter dysentery: typical HxHoused dairy cattle, northern USA, HERD outbreak (unlike salmonella where only few have CS at a time), 2 week duration outbreak = quick!
HIGH MORBIDITY but low mortality :)
What age gets winter dysentery?ADULTS >4m
CS of winter dysenterySevere projectile +/- blood, mucus, malodorous (parvo-ish)
Anorexia, depression, severe drop in milk produxn, +/- colic & dehydration, fever, mild resp dz
How long do CS of winter dysentery last?2-5d (rips through entire barn by 2 weeks)
Dx of winter dysenteryPE: Dec rumen motlilty but inc borborygmi in SI
Rectal: distended SI
No oral lesions (ddx BVD, MCF)
Exclusion (parasite ova, coccidial oocysts, Salmonella cultures...)
What is the tx for winter dysentery?Rarely needed! Oral fluids & e-lytes, maybe IV if severely affected, salt block access & fresh water
Why is winter dysentery important?Lose milk for a few weeks = economic
What are the preventative strategies for winter dysentery?NONE! Herds have sustained protection for 2-3 years after natural infxn, then Abs wane/new animals introduced/new animals born --> outbreak
**Trick for rehydrating cattleBolus IV of hypertonic solution off the needle! raises serum osmolariry, they go drink a ton of water (rumen has enough volume that they can compensate for fluid shifts just by oral)
What's the difference between 1ry & 2ry Cu deficiency?Primary = low dietary Cu
Secondary = high Molybdenum, sulfates, zinc, iron (interfere with copper uptake)
CS of copper deficiencyChronic watery diarrhea, ill thrift
Changes in coat color/wool quality
Spontaneous fractures (e.g. vertebral), demyelination (enzootic swayback in SR)
How does copper deficiency usually present?Multiple animals affected, usually on pasture (High Mo or sulfates, or decreased Cu in lush, mature pasture)
Dx of Cu deficiencyDietary Cu:Mo ratio (suggested to be >4:1)
Liver Cu concentration
Serum Cu (liver biopsy more helpful)
Tx of Cu deficiencyCopper glycinate SQ
Cu sulfate, Cu oxide supplementation
Remove predisposing factor
CS of Cobalt deficiencyIll thrift, diarrhea
Normocytic normochromic (=nonregen) anemia, decr feed efficiency, anorexia
Who gets Cobalt deficiency?Sheep>cattle
Why is Co important in rumis?Necessary for formation of vitamin B12 by rumen microbes! & required for metabolism for proprionate
Tx of Cobalt deficiencyB12 injections, ensure ration has >0.1 mg/kg Co
How can metritis/mastitis cause d+?Endotoxemia
Which toxic plant causes diarrhea?Oak (acorn) (mostly cattle, large quantities consumed)
How are acorns toxic? CS? Result?Tannins hydrolyzed in rumen --> gallic acid, pyrogallol = oral, esophageal, ruminal, intestinal ulcers
Sudden death, edema, bloody-dark diarrhea.
Also toxic to renal tubules (so if trying to ddx animal with some oral lesions, D+, Hx of acorn exposure: AZOTEMIA points you more towards acorn tox)


Question Answer
Notable nematodes causing dzOstertagia, Haemonchus, Trichostrongylus, Cooperia
General lifecycleL3 infective, persist in environment from Oct-May, PPP = 3 weeks
CS of nematode infestationAnorexia, ill thrift, hypoproteinemia, diarrhea, anemia (especially haemonchus!)
Develop immunity
How does Ostertagia develop?Arrest in host during summer (too hot to live), then resume development in fall
Type I Ostertagiasis =Young cattle <18m, in their FIRST grazing season
Type II Ostertagiasis =2-4 year old cattle in their 2nd or 3rd grazing season. Larvae have encysted and synchronous recrudescence of inhibited larvae causes diarrhea & other CS
Dx of GI nematodes in cattleHx, CS, necropsy
Timing for tx of GI nematodes in cattle? WHY?Aim at 1st grazing season
Maintains refugia in older animals (=slower devp of resistance), drug withdrawals avoided (arent enteringn production cycle anytime soon), may not need to do any adult replacement animals (get them while theyre having CS)
**What's refugia? why is it important?Population of parasites NOT exposed to dewormer = MOST IMPORTANT PART OF NOT DEVELOPING RESISTANCE!
What's the tx for nematodes?Moxidectin, eprinomectin pour-on: no withdrawals, 5 weeks residual action, treat at turnout & again at 8 weeks
Ivermectin: 2-3 weeks residual action, tx at turnout & again in 6 weeks (more resistance!)
Sustained release devices: Benzimidazoles, levamisole, morantel, Ivermectin (doesnt appear to reduce development of immunity)
Resistance has been reported to:BZs, ML, LEV

Neonatal Diarrhea

Question Answer
Causes of diarrhea in neonatesE. coli
#1 cause of neonatal deathDIARRHEA! Half of calf mortality on dairy farms
What is the importance of neonatal diarrhea#1 cause of neonatal death
Economic impact: $120mil/yr
Difficult to control/tx
Mechanisms of diarrheaHypersecretion (toxin stimulates secretion from crypt cells)
Malabsorption (villus tip dmg)
Exudation (incr permeability)
Risk factors: HostLow birth weight, premature, FPT
Risk factors: EnvironmentSanitation, population density, feeding system
Risk factors: agentVirulence, load
What's the approach for getting a diagnosis?Not essential to find definitive dx, most of the time just going to tx the same way
Lab data = Metabolic acidemia (not alk like adults!!) from HCO3- loss. Worse >8d old
Hyponatremia, hypochloremia, hyperkalemia
CBC: Hemoconcentration or leukopenia
What fecal dx can you do?Culture & typing
Gram stain
Electron microscopy
Antigen testing
What age is affected by E. coli?<6d (often <3d)
MAJOR cause of diarrhea in dairy & beef calves younger than 6d?Enterotoxigenic E. coli (ETEC)
Prevalence of E. coliVariable (herds, healty vs sick, geographically... some farms have probs every year)
Pathogenenic factors of ETEC? What do they do?Encapsulated
Fimbrial antigen F5 (K99): allows attachment, colonization in distal small intestine, binds to immature epithelial cells
**Why does ETEC only really affect neonates? WHat about older calves?Have binding sites for immature epithelial cells
In older calves, comorbidities with rotavirus cause villous atrophy --> immature cells migrate to villous tips so can bind there
ETEC mechanism of D+Hypersecretion of predominantly chloride, then Na+, H2O, other e-lytes follow
ETEC pathophysHeat stable toxins (predominantly STa)
Reversible binding to endothelial receptors
CS of ETECWatery diarrhea, not usually bloody (b/c hypersecretory), onset can be rapid --> weakness, collapse
Not usually febrile (not inflam, just affects Cl- channels), hypothermic if hypovolemic shock
ETEC lab dataAcidemia, decreased Na, Cl, K, glucose
Dx of ETECFecal PCR, ELISA (if really want to know for sure)
Tx of ETECSupportive. Abs not usually indicated unless septic or really weak (2ry pneumonia)
Dry cow FS vax, oral FS products in outbreak
Types of Attaching & Effacing E. coliEPEC: intimin (eae) gene
STEC: Shiga-toxin producing
EHEC: both
Attaching & Effacing: age?Calves 2-21d, can be up to 4m
Attaching & Effacing: whats the diarrhea like?Can be bloody (attachment in SI, colon, or both)
Attaching & Effacing: DxPCR (harder because atypical)
Most common viral cause of D+Rotavirus
Most common group of rotavirusA
Rotavirus: incubation? environment?Short incubation (12-24h) and stable in environment (above freezing) (prob why its so common)
Rotavirus: affects who? how long?Calves <3 weeks, peak 6 days, usually lasts 2-5d (also in foals)
Rotavirus mechanism of D+(small intestine) Malabsorptive: spares crypts, villous atrophy, cells arent there to take up fluid anymore
If you saw this in a 2-week-old calf with diarrhea, what would you be thinking?
Rotavirus (villous atrophy)
CS of rotavirusLethargy, dehydration, anorexia
Low-grade fever (some inflam)
Watery, yellow diarrhea (no blood!!)
Mixed infection common! (ETEC, Crypto)
Rotavirus: morb? mort?Morbidity HIGH but mortality low-variable
ETEC or rota: which has higher mortality?More calves die from ETEC

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