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17 Cards in this Set
- Front
- Back
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ddx for scours in neonates (piglets not yet weaned)
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E. coli
C. perfringens type C C. perfringens type A C. difficile TGE coccidiosis rotavirus |
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When doing diagnostic investigation of scours, what types of samples are needed?
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demand untreated live piglets in early stages of dz
-pathogen/Ag lost quickly d/t overgrowth (Clostridials) or post-mortem autolysis (TGE) post all freshly dead piglets submit piglets from several litters get tissues from all age groups affected: may be multiple pathogens involved samples -multiple sections of fresh SI -swabs of SI -multiple sections of SI & LI in formalin -impression smears -SI & LI fluid w/ formalin remember, mixed infections are common! |
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E. coli
a. epidemiology b. pathogenesis c. signs |
a. age of onset: 0-5 wks ubiquitous: most common cause of neonatal scours
gilt immunity poorest: gilt litter piglets scour 1st & worst b. secretory scours pill for adherence: K88, K99, 987P toxins: LT, ST c. most severe in piglets suckling gilts or poor milking sows: insufficient/intermittent IgA supply syndrome reoccurs if producer fails to (re)-vaccinate before farrowing affected piglets NOT stunted at weaning does not cause just scours in any older age groups |
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E. coli
a. dx b. tx c. prevention |
a. gross lesions: lacteals full, fluid filled SI, initially watery clear scours, scours pasty if very dehydrated, alkaline fecal pH
culture: intestinal swab histopath: NO LESIONS b. anti-Gram (-) ABs: penicillin (IM to suckling piglets) rapid response: resistant to many ABs, change if no response in 1-2 d. tx whole herd for 3 d. c. sanitation vaccinate sows before each farrowing: ensure vaccine contains proper pillus type & toxoid feed baby pig scours to sows & gilts 5-3 wks. pre-farrowing: if commercial vaccines don’t work |
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C. perfringens type C: peracute form
a. signs b. gross lesions c. dx d. tx |
a. death in largest piglets, 24-48 hrs old
bloody diarrhea is rare: toxin kills piglets before they can excrete blood b. necrotizing/hemorrhagic enteritis: pathognomonic lacteals empty c. gross lesions, anaerobic culture, PCR (toxin), histopath d. none: found dead |
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C. perfringens type C: chronic form
a. signs b. dx c. tx d. prevention |
a. diarrhea in piglets 5-7 d.
acid fecal pH stunted into nursery no other age groups affected b. gross lesions (tightly adherent low fibrinonecrotic membrane), culture, PCR (toxin), histopath, impression smear c. ABs ineffective once scours start d. gilt & sow vaccination at 5 & 3 wks pre-farrowing w/ type C toxoid oral/SQ type C antitoxin: AT BIRTH to prevent peracute form sanitation |
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C. perfringens type A
a. pathogenesis b. signs c. control |
a. type A toxins cause less mucosal damage than type C --> ↑ gut permeability, acid gut pH
b. scours in piglets 3-10 d. old piglets look like they’re wasting away survivors stunted going into nursery c. sow vaccination pre-farrowing w/ killed autogenous C. perfringens type A ABs: tx each piglet w/ tylosin IM at birth sanitaiton |
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C. difficile
a. pathogenesis b. signs c. gross lesions |
a. type A & B toxins essential --> mucosal damage --> malabsorption --> acid gut pH
**associated w/ preventive AB use at processing** b. scours: birth – 7 d. pasty to watery yellow feces, colonic contents stunted into nursery c. mesocolon edema, colonic diphtheritic membrane |
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C. difficile
a. dx b. tx c. prevention |
a. anaerobic culture (fecal swab, colon contents), impression smear, lesions in spiral colon (NOT SI), PCR (toxins)
c. sanitation end routine “preventive” or “growth promoting” AB use in piglets at birth or early lactation |
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TGE
a. etiology b. transmission c. lesions |
a. coronavirus
b. environmentally stable; spread via feces, pigs, fomites, aerosol in winter c. malabsorptive diarrhea large volume of fluid in gut acid pH, lacteals empty THIN gut wall, no pseudomembrane |
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TGE
a. signs: acute form b. signs: chronic form |
a. explosive diarrhea & epidemic spread in naïve herds
-all ages scouring & off feed -many pigs also vomiting, depressed -high morbidity in older pigs -survivors stunted -sows hard to breed back after weaning b. common outcome after TGE infection enters PRCV immune herds --> partial immunity vs. TGE scours seen 1st in naïve younger parity sow or gilt litters scours starts in pigs 3-5 d. after weaning/entering nursery piglets stunted persists for months |
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TGE
a. dx: acute form b. dx: chronic form c. tx |
a. clinical signs
b. HARD to dx live pigs in early stages: fresh frozen section FA TGE SN: can't differentiate PRCV Abs c. supportive: electrolytes in water, ABs, heat, early weaning |
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TGE
a. prevention: acute form b. prevention: chronic form |
a. biosecurity
purchase TGE (-) stock b. depopulate, clean, disinfect, & DRY all farrowing & nursery rooms ensure herd wide infection during outbreaks: feed back scours, piglet intestines purchase 4 months of gilts, expose them, close the herd sanitation |
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coccidiosis
a. etiology b. signs c. lesions |
a. Isospora suis
b. no bloody scours! no scours in piglets < 6 d. uncommon onset after 10 d.: post-weaning onset is possible piglets stunted c. malabsorptive diarrhea acid pH loosely adherent thick pseudomembrane |
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coccidiosis
a. dx b. tx c. prevention |
a. impression smear
fecal float: frequent false (-) b. ABs to tx 2º bacterial infection (may see clinical benefit) c. sanitation coccidiostats orally 3 d. prior to scour |
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rotavirus
a. pathogenesis b. signs c. lesions |
a. environmentally resistant
destroys only enterocytes only at villi tips --> malabsorptive diarrhea (acid pH if uncomplicated) E. coli co-infection common b. scours in piglets > 7 d. to 2 wks post-weaning mild stunting possible no other ages affected c. watery diarrhea in SI, often w/ “flecks” in fluid usually pasty scours |
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rotavirus
a. dx b. tx c. control |
a. histopath suggestive (destruction of villus tips only), EM on gut fluid
b. supportive w/ broad spectrum ABs c. sanitation oral feed-back of piglet scours vaccination: immunity is serotype specific |
