VDPAM 445 Swine Topics Enteric Disease Control Dr. Alex Ramirez Veterinary Diagnostic and Production Animal Medicine Iowa State University

Neonatal Diarrhea

Neonatal Immunity Age of immunocompetency Colostral immunity Around day 70 of gestation Antigen dependent Colostral immunity IgG primarily  systemic antibodies Acquisition stops: no more produced, no more absorbed Titer in sow at farrowing = titer of pig at 4 weeks of age Lactogenic immunity IgA  local antibodies in the gut Milk origin

Neonatal Diarrhea Differential diagnosis E. coli Viral Coccidiosis K88, K99, F41, 987, etc. Viral Rota TGE Coccidiosis Clostrium spp Clostridium perfringes type C & A Clostridium difficlile

Coccidiosis

Coccidiosis Usually only a problem in farrowing or early nursery Isospora suis Minimum age = 5 days No approved treatments Marquis (15% w/w ponazuril) Antiprotozoal Oral Paste by Bayer

Clostridiums

Clostridiums Clostridium perfringens – Rot gut Toxin driven C = traditional more common A = “newer” Acute: blood Chronic: rope gut DDx = coccidiosis Prevention Vaccination Pre-farrow Feed sows BMD 14 days pre-farrow & lactation

Clostridium perfringens

Clostridiums Clostridium difficile Incidence Antibiotic use Discontinue antibiotics Re-establish normal microbial flora

Neonatal Diarrhea Treat baby pigs Environment Prevention  Sows Treat whole litter Be aggressive – dehydration Environment Temperature Moisture Prevention  Sows Vaccination Oral feedback

Post-Weaning Diarrhea (PWD)

Post Weaning Diarrhea- PWD Classic PWD caused by E. coli Often hemolytic F18 pillus antigen type is most common Pigs can be bred to be resistant: gene probe selection TGE after an outbreak can persist in the nursery and will mimic PWD Historically right after weaning, now 2-3 weeks into nursery (withdrawal of animal proteins?) SBM hypersensitivity Transition diets especially pellet  ground

Post Weaning Diarrhea- PWD Classic PWD caused by E. coli Can also have acute septicemic disease resulting in sudden death in nursery and suckling pigs Edema disease: shiga-like toxins Vascular effects CNS signs: focal encephalomalacia Acute deaths Poor doers PCR organism to check for genetic codes Pilli F18, K88, K99, 987, F41 Toxins Sta, Stb, LT, Stx2e

Post Weaning Diarrhea- PWD

Post Weaning Diarrhea- PWD Pre-disposers Chilling: cold floors, drafts Poor diet quality Ingredient quality: fish meal Pellet integrity Least cost formulations Feed changes, medication changes, simultaneous feed and medication changes Poor sanitation between groups: some plastic floors are hard to clean Feeding mats moving to disposable/biodegradable Major problem in some large systems

PWD: Therapy Enteric infection  oral medication “Nutritional” prevention via diet or water Plasma proteins (7.5% of diet) until 15#’s May break upon withdrawal; continual at lower level until 25#’s Plasma proteins in water (Solutein- APC) Zinc oxide <15# - 3,000 ppm 15-30# - 2,000 ppm Citric acid (1# per gallon of stock solution) or other organic acids Vitamins and electrolytes in water: supportive

PWD: Therapy Antibiotic therapy in feed for prevention Apralan (150 gram per ton) Mecadox (50 gram per ton) Denagard (35 gram per ton) Plus (400 grams CTC) Antibiotics in water for prevention or treatment 4-5 day treatment Spectinomycin (5 mg/#) Gentamycin (1-2 mg/#) Neomycin (2-10 mg/#) Amoxicillin, Ampicillin Antibiotics – “red butt” condition

PWD Rule-outs Carryover from farrowing Endemic TGE Coccidiosis Rotavirus Endemic TGE Plus or minus carryover from farrowing Loss of lactogenic immunity at weaning plus environmental exposure  TGE

PWD Treatments Prevention Environment Sanitation Vaccination Feed Oral F18 Feed Antibiotics Water

Ileitis (PPE, PIA)

Ileitis Caused by Lawsonia intracellularis Porcine Proliferative Enteropathy (PPE) Three main forms PIA: porcine intestinal adenomatosis Ileal villi develop secondary and tertiary branches  thickening of the ileal mucosa Necrotic form: fibrinonecrotic membrane forms on ileal mucosa, may extend to colon Acute hemorrhagic form  sudden death Most common in gilts and sows

Ileitis Clinical signs Poor doing pig Mal-absorption Protein losing enteropathy Diarrhea: orange tinge suggestive of partially digested blood, over blood with acute hemorrhagic form Many times soft or loose stools are over interpreted Increase number of cull or light weight pigs

Ileitis Lesions

Ileitis: Treatment Antibiotics that work: Tylan, CTC, Lincomycin, Denagard (Tiamulin), Mecadox Acute hemorrhagic form in older finishers/gilts/sows Inject with Tylan (10 mg/# SID) Inject with Lincomycin (5 mg/# SID) Follow-up with 100 gram/ton Tylan in the feed for 2-3 weeks Outbreak in growing pigs Inject severe cases with Tylan (dose as above) Water soluble Tylan Water soluble Denegard

Ileitis Control MLV product from BI Timing and handling of vaccine is critical Oral administration via medicator Administer vaccine over 4 hour period No feed medication for 3 days prior to vaccination Starter pack - binds chlorine in water and colors water blue Monitoring stools is commonly done to “titrate” antibiotic control programs

Ileitis Treatment Vaccination Prevention though antibiotics Feed Water Don’t forget market-ready pigs!

Don’t Forget PCV2  Diarrhea similar to Ileitis

Swine Dysentery

Swine Dysentery Brachyspira hyodysenteriae Characteristics Mucohemorrhagic diarrhea Marked inflammation Large intestine only (cecum and/or colon) Grow finishing pigs (usually >50 lbs) Spirochetal colitis  B. pilosicoli

Swine Dysentary Prevention Treatment Negative replacement stock Wean < 21 days Rodent control Treatment Medication Feed: Mecadox, Lincocin, Denegard Sanitation

Salmonellosis

Salmonellosis Primarily Salmonella cholerasuis Salmonella typhimurium can cause diarrhea Wide variety of organisms can be food borne pathogens Often stress/environment induced Clinical signs Severe lethargy (very sick): +/- fever Purple discoloration of ears and belly = septicemia Diarrhea: +/- blood Pneumonia

Salmonellosis Lesions Diagnosis via culture Splenomegaly Inflamed intestine Pneumonia – interstitial (wet lungs) Button ulcers on mucosal surface: primarily in colon Hemorrhagic lymph nodes Especially gastro-hepatic Other signs of septicemia Diagnosis via culture

Salmonellosis

Salmonellosis: Treatment Injectables Naxcel (per label), Spectinomycin (ELU), Nuflor (ELU) Water medication Neomycin, Gentamycin, Spectinomycin (ELU) Respiratory - Nuflor Feed medication Mecadox (50 gram/ton) Neomycin and Terramycin (200 gram/ton of each) Many other options in foreign countries including quinolones

Salmonellosis Control Vaccination S. cholerasuis +/- S. typhimurium MLV’s are effective Oral IN IM Killed vaccines have poor efficacy Environment is the primary focus: sanitation

Salmonellosis Treatment Vaccination Antibiotics Prevention – Feed Treatment Water Injectable Feed Sanitation

Hemorrhagic Bowel Syndrome (HBS)

Hemorrhagic Bowel Syndrome Definition of syndrome: consistent clinical signs and/or lesions but cause unknown Older (>150#) finishing pigs found dead +/- bloated abdomen Post-mortem lesions Uniform hemorrhagic appearance of entire gut or small intestines only Lumen content hemorrhagic and not clotting No palpable volvulus of the mesenteric root

Hemorrhagic Bowel Syndrome

Hemorrhagic Bowel Syndrome Current thinking is that torsion or volvulus is primary problem: resolve in agonal state More common in deep bellied pigs? Control via feed grade medication? 100 grams per ton of tetracycline with or without 30 grams per ton of BMD (Bacitracin Methylene Disalicylate) Added fiber to the diet Usually sporadic incidence (<1%) so hard to justify therapy costs

Gastric Ulcers

Gastric Ulcers Pigs will start to develop erosions of the non-glandular portion of the stomach within 24-48 hours of feed removal Out of feed Sick due to something else: pneumonia Erosion can vary from superficial to complete penetrating Acute cases Pig found dead with large blood clot in stomach Anemia – very pale

Gastric Ulcers Subacute cases Chronic cases Lesion Pig found dead or live but very sick with blood in small intestine but no inflammation of intestine Chronic cases Gaunt pig with black, tarry looking stool Pale appearance - Anemia Lesion Non-glandular portion of stomach where esophagus enters is eroded (pitted, indented) Normally this surface is slightly elevated from rest of stomach mucosa

Gastric Ulcers

Gastric Ulcers Peritonitis with perforation Pre-disposers Local or generalized Pre-disposers Other diseases that caused reduced appetite: mainly respiratory Feed not available: plugged feeder, late deliveries Fine grind to corn (<500-700 microns) Pellet diets Common end stage cause of finisher mortality

Other Diseases

Additional Information: Whipworms – outdoor production, pet pigs Ascarids – outdoor production, pet pigs Rectal stricture – congenital, 2ndary to salmonellosis Rectal prolapse – several techniques to repair but not a high yield procedure

Whipworms Trichuris suis Antihelminitcs – NOT Ivomec! Worms are visible in large intestine and cecum Must look closely or use a magnifying lens Ileal-cecal junction if good are to look Clinical signs Diarrhea +/- blood Poor doing pigs Pre-disposers Dirt lot environment Low protein diets Antihelminitcs – NOT Ivomec!

Whipworms

Ascarids: Roundworms Ascaris suum Little or no consequence in confined pigs Lack of exposure to feces Sows in gestation stalls and farrowing crates Pigs on wire and cement slat floors Continuous problem in pasture raised pigs 21 cycle Clinical signs and lesions Poor doing pigs Liver scars (milk spots) Petechia on lungs in acute cases (larval migration)

Ascarids: Roundworms

Ascarids: Roundworms Pigs will develop immunity Common scenario Liver scars will resolve in 4-8 weeks Common scenario Replacement gilts raised in confinement have no immunity Moved to heavily contaminated, outside dirt lots to kept them cycling Larva start marching through the lung 7-10 days later  acute outbreak of respiratory disease

Internal Parasite Treatment Mandatory? Many confinement herds only deworm sows 3-4 weeks pre-farrowing or at farrowing Many herds deworm young pigs that have had no chance for exposure to roundworms: wire flooring Avermectins at weaning (okay for mange) Banminth (pyrantel) continuously in the nursery diets With outdoor pigs, recognize risk for whipworm infestation Deworm pigs several times with fenbendazol (Safe-Guard) in the feed: 9-10 and 16-18 weeks of age Double strength levamisole in water

Rectal Stricture Sequelae to: Clinical appearance Lesions Salmonellosis Rectal prolapse Clinical appearance “Air belly”; severe distension of abdomen Cachexia Lesions Stricture in rectum Enlarged spiral colon (megacolon); +/- peritonitis

Rectal Stricture

Rectal Prolapse Primarily prolapse of mucosa Pre-disposers Variable degrees Polyp on one side Complete circle Pre-disposers Genetics Increased abdominal pressure Coughing Chilling  piling

Rectal Prolapse

Rectal Prolapse Repair Purse string: tissue still fresh, sows Replace prolapse, suture around the anus, leave an approximately ¾ inch (one finger width) opening to enable defecation Rectal ring: tissue already necrotic Various sizes, choose largest that will fit Hold ring with clamp and position so that the “slot” in the ring is at the anus Use elastrator band or umbilical tape to secure the ring Trim excess tissue so that pen mates don’t bother

Rectal Prolapse Repair

Acknowledgements I would like to recognize others for their significant contributions to this presentation: Dr. Brad Thacker Dr. Locke Karriker Dr. Pat Halbur Dr. Butch Baker

Questions ?