Swine Health & Pre-weaning Piglet Mortality / Enteric Diseases.

What are the primary behavioral and production indicators of illness in swine?

• Behavioral Changes: Decreased appetite, decreased interest/alertness, and lethargy/reduced activity.

• Production Changes: Decreased average daily gain (ADG), poor reproductive performance (small litter sizes, failure to conceive, increased days open, regular or irregular return to oestrus).

What is the normal physiological body temperature range for a pig?

• 101.5F-102.5F/(38.6C-39.1C)

What is the average preweaning mortality loss in swine herds, and what are the major causes?

12–15%. Losses are primarily caused by unsupervised farrowing leading to:

1. Crushing (overlay by sow)

2. Stillbirths

3. Starvation

4. Hypothermia/Suffocation

5. Injury

How does the farrowing crate improve piglet survival?

• Prevents crushing (reduces accidental stepping/overlaying by the sow).

• Facilitates micro-climate temperature management (sow kept cool at 22C, piglets kept warm at 30-34C.

• Allows creep feeding/electrolyte access exclusive to piglets.

• Provides a sanitary, easy-to-disinfect environment.

• Enables safe piglet processing during the critical first 72 hours.

What are the key selection criteria for breeding sows?

Ideal Body Condition Score (BCS of 3 – 3.5 out of 5), proven mothering ability, functional teats (12–14 total), and good udder/teat conformation.

What pre-farrowing protocol must be followed for sows and farrowing facilities?

• Deworming: At least 2 weeks prior to moving to the farrowing unit.

• Ectoparasite Treatment: Bath if necessary (not within 3 weeks of farrowing).

• Sow Washing: Wash with warm soapy water before entering the farrowing crate to remove organic matter and decrease piglet pathogen exposure.

• Facility Sanitation: Remove all organic matter, disinfect (e.g., quaternary ammonia compounds, sodium hypochlorite/bleach), and leave empty/idle for 5–7 days prior to stocking.

Why is early colostrum intake vital for neonatal piglets, and what is the window for absorption?

Piglets receive no transplacental immunoglobulin transfer in utero and are born with an immature immune system (7–10 day lag period to generate endogenous antibodies). Colostrum provides essential IgG and IgA for passive immunity, energy for thermoregulation, and has a laxative effect. It must be ingested within 6 hours of birth.

What are the alternatives if a sow fails to produce colostrum?

Frozen colostrum bank from other sows (hand-milked and stored; avoid repeat freeze-thaw cycles). Bovine colostrum can be used as a secondary alternative (provides nutritional support and partial protection, but is not species-specific).

Why do piglets require artificial heat sources during their first week of life?

Piglets cannot regulate their own body temperature at birth. Supplemental heat (heat lamps at proper height, dry bedding over concrete) prevents hypothermia, which directly contributes to weakness, starvation, and crushing.

What is the protocol for navel (umbilical) care, and why is it critical?

The umbilicus is a direct entry point for systemic bacteremia leading to joint ill (suppurative arthritis), meningitis, or umbilical hernias.

• Protocol: Clamp/tie and trim 1–2 inches from the abdominal wall (short enough so the piglet cannot step on it), then submerge/dip in 2–5% Tincture of Iodine until healed.

Why is iron supplementation mandatory for neonatal piglets?

• Nursing piglets rapidly develop iron deficiency anemia due to:

  1. Minimal iron reserves at birth.

  2. Extremely low iron concentrations in sow milk/colostrum.

  3. Rapid post-natal growth rate.

  • Intervention: Intramuscular iron injection within the first few days of life.

Why are needle teeth clipped in newborn piglets?

Piglets are born with 8 sharp needle/wolf teeth. Clipping prevents:

• Lacerations to the sow's teats/udder (which cause pain, nursing refusal, abnormal milk letdown, and starvation).

• Facial lacerations to littermates during competitive fighting, which create entry portals for bacterial infections.

What is the primary cause of bacterial diarrhea in piglets under 5 days of age?

Enterotoxigenic Escherichia coli (ETEC)

Which fimbrial adhesins and enterotoxins are produced by ETEC?

• Fimbriae (Adhesins): F4 (K88) and F18 (jejunum & ileum); F5 (K99), F6, and F41 (posterior jejunum & ileum).

• Heat-Labile Toxin (LT): Stimulates cyclic adenylate cyclase → Increase intracellular cAMP.

• Heat-Stable Toxin (STa / STb): Stimulates cyclic guanylate cyclase → Increase intracellular cGMP.

What pathophysiological mechanism causes ETEC diarrhea, and what are the clinical consequences?

Increased cAMP and cGMP stimulate hypersecretion of bicarbonate, sodium, and water into the intestinal lumen, causing a hypersecretory diarrhea. This leads to rapid dehydration, metabolic acidosis, hyperkalemia, and high mortality (up to 80%).

What post-mortem findings differentiate ETEC from viral causes of enteritis?

• ETEC: Intestines are distended and gas-filled; villi remain intact (NO villous atrophy); chyle is PRESENT in the mesenteric lymphatics; fecal pH > 8.0 (alkalized by bicarbonate secretion).

• Viral (TGE/Rotavirus/PEDV): Marked villous atrophy; thin-walled intestines; chyle is ABSENT; acidic fecal pH < 7.0 (malabsorptive).

What medical and preventive strategies control ETEC in swine herds?

• Treatment: Oral/parenteral antimicrobials (Ampicillin, Amoxicillin, Ceftiofur, Sulfa drugs, Aminoglycosides) plus aggressive fluid/electrolyte therapy containing glucose.

• Prevention: Maternal vaccination of sows prior to farrowing (killed fimbrial vaccines for IgG; Kohler oral milk vaccine for IgA), strict sanitation, all-in/all-out management, maintaining piglet temperatures at 30-34, and breeding for the genetic absence of the MUC4 receptor (prevents F4 fimbrial attachment).

How do clinical features of the Epidemic form of Transmissible Gastroenteritis (TGE) differ from the Endemic form?

• Epidemic Form: Occurs in seronegative herds. Rapid spread across all age groups. Sows show anorexia, agalactia, and abortions. Mortality approaches 100% in piglets under 3 weeks of age.

• Endemic Form: Occurs in partially immune/seropositive herds. Slow spread. Sows show no signs. Signs are restricted to piglets 1–2 weeks post-weaning with low mortality (10–20%).

What is the primary pathogenesis and hallmark necropsy lesion of TGE and Porcine Epidemic Diarrhea Virus (PEDV)?

Both are Coronaviruses that infect and destroy mature small intestinal villous enterocytes (jejunum/ileum), causing acute cell necrosis and severe villous atrophy. This results in malabsorptive/maldigestive diarrhea (fecal pH <7.0). Necropsy reveals translucent, thin-walled intestines containing curds of undigested milk and an absence of chyle in mesenteric lacteals.

How can a herd manager eliminate TGE during an epidemic outbreak?

1. Stop all herd additions for 4–6 months.

2. Perform whole-herd feedback: feed minced infected piglet intestines (autogenous virus) to all sows due to farrow in $>2$ weeks to stimulate uniform IgA lactogenic immunity.

3. Enforce strict all-in/all-out production.

4. Introduce sentinel seronegative pigs 2 months after signs resolve to monitor seroconversion.

What are the key features of Rotavirus infection in swine?

• Ubiquitous viral infection (100% seroprevalence in many herds); Group A causes >90% of cases. Replicates in villous enterocytes causing malabsorptive diarrhea (watery to creamy, yellow-to-white) predominantly in piglets 3–5 weeks of age. Morbidity and mortality are generally low unless secondary bacterial co-infections occur.

What are the characteristics of Porcine Epidemic Diarrhea Virus (PEDV)?

Alphacoronavirus transmitted via fecal-oral, fomite, and aerosol routes (can travel up to 10 miles). Causes severe malabsorptive diarrhea and vomiting with up to 100% mortality in neonates. Clinically indistinguishable from TGE; requires RT-PCR or immunohistochemistry for definitive diagnosis. Controlled via strict biosecurity and controlled oral feedback to pregnant gilts/sows at 57–60 days gestation.

What are the key distinctions between Clostridium perfringens Type C and Type A in swine?

• Primary Toxins: Type C produces Alpha and Beta beta toxins, while Type A produces Alpha toxin only.

• Primary Pathology: Type C causes acute hemorrhagic and necrotic enteritis, whereas Type A causes milder necrotizing enteritis.

• Age Affected: Type C affects piglets <7 days old (peaking at day 3), while Type A affects piglets within 48 hours of birth.

• Fecal Characteristics: Type C features hemorrhagic (bloody) to dark reddish-brown feces with tissue shreds, whereas Type A features pinkish, mucoid feces.

• Mortality: Type C reaches up to 100% mortality in naïve litters, whereas Type A mortality is low with most piglets recovering slowly.

• Necropsy Lesions: Type C shows an intensely hemorrhagic small intestine with gas bubbles in the intestinal wall, while Type A displays mild-to-moderate mucosal inflammation.

How is Clostridium perfringens Type C controlled and prevented?

• Prophylaxis: Administration of equine antitoxin immediately at birth (provides protection up to 3 weeks) or oral ampicillin/amoxicillin for the first 3 days of life.

• Prevention: Vaccinate pregnant sows with Type C toxoid mid-gestation and 2–3 weeks prior to farrowing to confer passive colostral protection.

What is the primary protozoal pathogen causing diarrhea in nursing piglets, and what is the typical age of onset?

Cystoisospora suis (formerly Isospora suis). Clinical signs typically appear in piglets 7 to 9 days of age (range: 5–15 days). Note: Coccidiosis is NOT a cause of diarrhea in piglets under 5 days old.

What are the clinical signs and diagnostic findings of Porcine Coccidiosis?

• Clinical Signs: Yellowish to grayish, loose, pasty-to-watery diarrhea; high morbidity with low-to-moderate mortality; unresponsive to antimicrobial therapy.

• Diagnosis: Fecal flotation or mucosal smears demonstrating oocysts (peak shedding occurs 2–3 days after clinical onset); histopathology showing villous atrophy and merozoites within mucosal enterocytes.

How is Cystoisospora suis controlled on a swine farm?

• Traditional coccidiostats and antibiotics (Amprolium, Trimethoprim/Sulfa) have questionable efficacy once diarrhea starts. Control relies on thorough sanitation of farrowing pens (removing organic debris, steam cleaning, and applying effective disinfectants between farrowings) along with rodent and insect control.

A piglet less than five days of age is having diarrhea, what are some differential diagnoses?

ETEC, C. perfringens Type C or A, TGE, PEDV.

A piglet seven to forth-teen days of age is having diarrhea, what are some differential diagnoses?

• Cystoisospora suis (Coccidiosis), Rotavirus.

Briefly outline the pathophysiology for ETEC and Viral (TGE,PEDV,Rota).

• ETEC = Hypersecretory diarrhea (Villi intact, Chyle present, Fecal pH >8.

• Viral (TGE/PEDV/Rota) = Malabsorptive diarrhea (Villous atrophy, Chyle absent, Fecal pH <7.

A pig is experiencing hemorrhagic diarrhea with gas bubbles in the small intestinal wall, state the possible diagnosis.

Clostridium perfringens Type C.

An 8 day old piglet is experiencing bloody diarrhea and is unresponsive to antibiotics, state the diagnosis.

Cystoisospora suis