Rumi Neonate 2

sihirlifil's version from 2018-04-29 13:14

Endemic infxn juvenile D+ (specific dz)

Question Answer
ETEC: who affected?1-7d, peak at d3 (have receptors for attachment)
ALL at risk, esp. calves, piglets, lambs
Not as common problem in kids & crias because less environmental contam
ETEC: preventive measuresK99 bacterin: admin to pregnant cows/ewes, induces colostral Abs against K99 pilus Ag (Combo vax avail now)
Neonate ingests colostrum (blocks attachment of ETEC pili)
**ETEC: TxCan use oral antibx (targeting antibx in gut). Still monogastric
(NSAIDs? plasma transfusion?)
Cryptosporidiosis: agent? type of D+? what do?
Cryptosporidium parvum
Most common!!! Inflammatory and malabsorptive/maldigestion D+
Nutritional support critical!! Tx acidosis, significant fluid loss
Rotavirus & coronavirus: common in? found where? transmission?All livestock neonates!
Ubiquitous (estimated 77-100% on pig farms) Many adult pigs shed low ##
Fecal-oral (& resp-oral for corona)
Rotavirus & coronavirus: Tx/prevention?Nutritional support critical since long-term healing required. NEED MILK! Vax (geared for cattle but can use off-label)
Rotavirus & coronavirus: more severe?Coronavirus!!! Invades all the way down to crypts, takes longer to regenerate
Coronavirus in calves & crias: how much shedding?70% healthy cows, 24% healthy calves
Coronavirus in calves & crias: clinical picture?Enterocolitis! Destroys cells from SI TO RECTUM! Colon epithelium regen very slowly (3w)
D+ is severe, protracted, can last 2+w
Coronavirus in piglets?TGE & PEDV
Coronavirus: type? when does it start? <1m of age! Maldigestion & hypersecretory
TGE & PEDV (transmissible gastroenteritis & porcine epidemic D+ virus): mechanism?Extensive villous damage in SI & LI
Fatalities common & rapid, and in naive herd virus attacks all ages
TGE & PEDV: special CS?PIGS CAN VOMIT! even though minimal stomach dmg
If you see this pig's jejunum on necropsy, you suspect...?
PEDV: CS?In naive herds: severe D+ in all ages, V+, high mortality (100% in piglets)
PEDV: incubation? shedding?12-14h incubation (short!)
Shed up to 3-4w
PEDV: how is immunity?NO cross protection w/ TGE
Herd immunity short-lasting
Maternal Abs are protective
Management key, but low success (all in-all out, disinfecet facilities, trailers...)
Coccidiosis: agents? Who affected? CS?
Isospora & Eimeria
Piglets (1w); lambs, kids, crias (2-3w); calves (3w)… NO CROSS-SPECIES INFXN
D+, ill thrift, hypoproteinemia
Coccidiosis tx: who? how?Showing CS (D+, ill thrift) & positive fecal float or Hx/suspicious (age, low protein…)
Treat water for compliant animals (i.e. not goats- need to tx them individually w/ Albon, corid, Marquis) & 2ry probs (anemia, hypoprot, rectal prolapse, nutrition, warm…)
Coccidiosis: preventionHygiene, water/feed additives (species specificity for some drugs, toxicity for some species)
D+: Age Risk by Week

Sporadic infx juvenile D+

Question Answer
Difference btw sporadic vs endemicWider age range
Blood, mucosa, fibrin in feces + systemic involvement
Greater fatality rate
Much variation in virulence
Less frequently show endemic patterns
Sporadic D+ e.g.GI parasites
Clostridial enteritis (enterotoxemia)
Clostridial enteritis (enterotox): agent? when’s it a problem?C. difficile (horses) & C. perfringens A, C, D, B, E (all livestock, multiple ages)
Frequently fatal inflamm D+, spores in environment, normal flora
Clostridia: CS?Rapid debilitation & shock
Colic, bloat
Hge D+
Death w/ no external signs
Clostridia: caveat for Dx?C. perf A overgrows rapidly in cadaver’s GI tract, must sample quickly
Calf comes in for necropsy and you see this… suspect?
C. perfringens
Hge GI contents. Gram stain lots of large G(+) rods
C. perfringens: tx?Antitoxin (PO, SQ)
Antibx (PO, parenteral, both): PPG, oxytet
NPO 24h, gradual restart small feedings and monitor bloat
**Which antibx for C. perf?Oxytet systemically secretes into GI tract (enterohepatic circ) if more than a few weeks old. PPG works when still in monogastric stage
Clostridia: preventionGradual intro of rich feeds, pasture turnout, grain
Minimize separation time of neonates & dams
Cold milk if on lamb bar (bucket w/ nipples)
Clostridia: vax?Toxoids: C. perf C & D; C. perf A
Nothing avail for C. diff
(remember antitox is for neutralizing! not preventing)
Salmonellosis: agent? which serotypes?
S.enterica subsp. enterica (26 serogroups A-Z)
B (typhimurium), C (infantis), D (Dublin), E most common in livestock
Dublin common in dairy
Lots of virulence variation, all spp susceptible, any age, but hits neonates hardest
Neonatal salmonellosis: from where? in who? CS?Subclinical carriers & environment
Dairy>Beef (dairy replacement calves in beef herds), 2-3m old (colostral Abs waning, starting to wean = stress)
CS: peracute septicemia, acute enteritis, resp dz component… & dead
What is point-source contamination?(Epidemiology) Contam colostrum or milk on dairies: track animals getting sick, notice sudden spike, find the point in time where contam is happening in the process, go back and get a handle on that milk handling/processing step. Pasteurize, disinfect, make sure calf feeders/nipples/etc are clean
How does contagious spread occur?(Epidemiology) Continued propagation, carriers
How is salmonella transmitted?Primarily fecal-oral, shed in every fluid but mostly manure (can get mastitis from fecal contam)
Salmonella: characteristics?G(-) rod. Has endotoxin, exotoxin (secretory, cytotoxic)
Intracellular, invasive
Engulfed by WBCs but not killed efficiently
Salmonella: mechanisms for dz?Secretory (toxins)
Inflammatory (PG-induced)
Salmonella: CSFever
D+: variable volume +/- blood, fibrin, mucosa
Respiratory dz
Salmonella: TxProblematic! Fluid & e-lyte support, Plasma (PLE), NSAIDs, gastroprotectants
Salmonella: do we use antibx?Controversial… often don’t help with outcome. REALLY want C&S data
What’s the conundrum here?
Resistant to everything except enrofloxacin… but can’t use for calves :/
Salmonella: PreventionStress plays huge role! Closed herd, quarantine new purchases. Don’t overcrowd, get it mixed into feed (it’s opportunistic)
Salmonella: Specific preventive measures?Vax often doesn’t help (depends how well it matches the strain)
(Autogenous bacterin: very serotype-specific, short-lived)
Common antigens e.g. Siderophore-receptor proteins
MLV? (e.g. swine vax)

Misc causes of juvenile D+

Question Answer
Overeating: how does it cause D+?Heavy milking dam
Prot & fat > digestive enzyme levels (+/- surface area for absorption) --> colon
How does osmotic D+ (overeating) D+ present?‘Happy & crappy!’ Still growing well, make sure to keep them hydrated
Where do undigestible nutrients come from?Sucrose, high fructose corn syrup (not absorbed by intestine)
Sand, bedding (hungry animals eat it!) --> physical irritation of gut lining
Some milk replacers
Grain --> excess VFAs in gut
“Dummy”calf – causes of this?Born to dams fed low protein diets w/added stress of parturition
Perinatal hypoxia (following dystocia from fetal/maternal mismatch or breech)
Selenium deficiency
Infx dz (fetal infxns)
“Dummy” CS?Weak at birth, no/weak/uncoordinated suckle response
“Dummy” tx/preventionColostrum 24h, then milk (tube, indwelling NE feeding tube) small quantities at a time (reduce risk rumen putrefaction)
Supplement O2
Supportive: warm, vit/min supplements, etc
R/O infxn (BVDV status, ABG, Selenium status of dam & neo)
Prevent next season
Neonatal Respiratory Distress Syndrome (NRDS): what happens?Progressive resp failure due to inadequate surfactant production + structurally immature lung + highly compliant chest wall --> Predisposition for airway collapse (surfactant produced by Type II pneumocytes in last 24h before birth, so if premature/C-section might not have enough)
NRDS: Dx testsRads: mixed interstitial & alveolar pattern (pulmonary atelectasis)
ABG: persistant hypoxemia, progressive hypercapnia
Lecithin:sphingomyelin ratios <2
More than 1 risk factor present: very early gestational age, induced parturition, C-section
Persistent tachypnea
No evidence of SIRS at birth (normal CBC, fibrinogen)
Congenital cardiac dz r/o
NRDS: TxIdeal = IPPV & recombinant surfactant
Practical: nasal O2 insufflation, maintain energy lvls (tend to live if survive 3-5d)
Neonatal Acute Lung Injury & Acute Respiratory Distress (NALI-ARD): caused by? what happens?Acute onset, ineffective O2 exchange caused by inflam process
1ry pulmonary infxn (viral, bact) (IBR/ BHV-1, salmonella, Manheimia hemolytica, Pasturella multocida, Histophilus somni); SIRS (septicemia, trauma, burns)
NALI-ARD: PredispositionsFPT
Adverse enviro conditions
High pathogen load
NALI-ARD: Tx1ry problem, supportive care
Septicemia: caused by?Mostly G(-) infxn (E. coli, salmonella)
Septicemia: CS?(Same as for adults)
Injected sclera, abnorm muc mb, cold extremities, neutropenia + LS, high fibrinogen, hypoglycemia
Septicemia: TxCheck passive transfer status (guarded prog)
Antibx: IV (but not ceftiofur…)
IV fluids
Plasma or whole blood
GI protectants
Abomasitis: risk factors?(Sporadic)
Intermittent feeding large volumes
Dietary changes
C. perf A
Cu deficiency
Abomasitis: CS?Acute gas distention of abomasum
Colic, restlessness
No relief w/ stomach tube
Metabolic acidosis, depression, shock
Abomasitis: TxDecompression (avoid torsion & rupture)
R flank laparotomy (if torsed)
Fluid therapy (hydration, e-lyte abnorm, acid-base)
Antibx: Penicillin, Oxytet
C & D antitoxin PO/SQ
Difficult to stop/reverse
Abomasitis: preventionVax agains C. perf (TOXOID!)? correct mineral def’s?
** Ruminal bloat: caused by?Rumen putrefaction (tubing milk, overeating, esoph groove dysfxn)
2ry bloat (complication of bronchopneumonia)
** Rumen putrefaction: CS?Recurrent bloat, poor growth, D+, rough hair coat
** Rumen putrefaction: TxRumen lavage
Tetracycline/Penicillin PO
Stop tubing milk!
** Rumen putrefaction: PreventionChange feeding protocol (nipple rather than bucket to close groove, smaller more freq meals, warm milk)
Calf starter (promote rumen devp’t)
Limit separation time, encourage neos to stand, adequate shelter
** 2ry bloat: Pathophys
2ry bloat: TxFix 1ry problem (pneumonia)
Intermitten tubing/temporary fistula or trochar
Stomach/abomasal/C3 ulcers: presentation? risks?Relatively common, rarely CS unless perforation (like TRP)
Risks: weather change, C. perf, Cu def’y, diet change, hairballs, mycotic infxn
Stomach ulcers: CS?Bruxism, expiratory grunt, drooling, painful & distended abd, melena/occult blood positive
Abomasal ulcers: Defensive factors?Local blood flow
Mucus prodxn
Mucosal cell resistance (protein, P4, preg)
Abomasal ulcers: Aggressive factors?Hyperacidity: Low Ca2+, Histamine, stress
Trauma: parasites, virus
Cu def’y
C. perf A
If ulcer perforates…?Peritonitis, septic shock, quick down spiral
Abomasal ulcer: txGI protectants (Kaopectate, sucralfate)
C. perf C & D antitox
Rumen fluid, grass hay
Antibx PO
Avoid NSAIDs (Opioids for pain)
Long recovery! work on prevention strategies (monitor trace min status in dams, minimize diet change, feed less vol more often…)

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