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108 Cards in this Set

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Sarcoptic Mange

Agent
Sarcoptes scabiei var suis
Sarcoptic Mange


Epidemiology
Older Herds of
CONVENTIONAL HEALTH STATUS

ERRADICATION IS EASY

Rare in High Health or Newer Closed Herds

Associated with Reduction in
ADG and
Feed Efficiency
via Intense Puritis

POTENTIALLY ZOONOTIC
But Does NOT Colonize Humans
Sarcoptic Mange


Clinical Signs
History
Lesions Noted 3 Weeks POST CONTACT

PURITIS
Mite Burrow Opening

PAPULE ERYTHEMATOUS

Associated with Hypersensitivity →
Further Puritis and Scratching

ENCRUSTATIONS Small
Ear Canal,
Pina, Eyes,
Snout, Flank,
Abdomen

KERATINIZATION CHRONIC EXCESSIVE
Thickened Wrinkled Skin,
Sebum Crusts,
Serum - Ears, Neck, Limbs

Head Shaking

Aural Hematomas

PIN POINT HOLES (0.5 to 1 mm)
Centered in Area of Hyperemia
Pathognomic Virtually
Sarcoptic Mange


Diagnosis
SKIN SCRAPING - 50% Yield
Encrutesed Areas
Ear Canal - DEEP

KOH (10%) DIGESTION
Base of Ear Canal
High Sensitivity
Sarcoptic Mange


Treatment
TOPICAL INSECTICIDES
Registered Products

Anti Parasitic PARENTERAL
2 X For Chronic Dz
Ivermectin

Anti Parasitic PARENTERAL
2 X For Chronic Dz
Dectomax

Anti Parasitic Feed
Ivomec
Sarcoptic Mange


Control
ERRADICATION
Cull Chronic Animals (Sows)

MEDICATE
ALL Remaining Animals
Lice (Pediculosis)

Agent
Haematopinus suis
Lice (Pediculosis)

Etiology
Haematopinus suis

Species Specific

BLOOD SUCKING

Life Cycle Entirely On Host

6 mm Long
Eggs 1- 2 mm Creamy White
Lice (Pediculosis)

Epidemiology
RARE In Canada
Lice (Pediculosis)

Clinical Signs
PURITIS SEVERE
Continual Scratching

Lice
THIN SKINED AREAS
Neck,
Base of Ears,
Inner Ears,
Medial Legs,
Flanks

Eggs
White
Hair Shafts

Lice
Congregated Around Areas of Skin Damage
Greasy Pig (Exudative Epidermatitis) All Forms

Agent
Staphylococcus hyicus
Greasy Pig (Exudative Epidermatitis)

All Forms

Stage
Suckling

Nursery
Greasy Pig (Exudative Epidermatitis)

All Forms

Etiology
Dermatitis
Generalized
Focal

OPPORTUNISTIC Invasion
RESISTANCE
INCREASES with AGE

EXFOLIATIVE TOXIN
Heat Labile

Commensual Flora
Skin,
Vagina,
Preputial Diverticulum

Similar Dz in Human Neotates
Scalded Skin Syndrome (S. aureus)
Toxins SPECIES SPECIFIC
tf NOT Zoonotic
Greasy Pig (Exudative Epidermatitis)

All Forms

Epidemiology
Infection
Birth or Subsequent

Acute Outbreaks
Common Gilt Startup Herds
ie After Depopulation

ABRASIONS and SKIN WOUNDS
Important Opportunity for Colonization
ie FIGHTING
Greasy Pig (Exudative Epidermatitis)

Suckling Piglets

Clinical Signs
INFECTION ACUTE GENERALIZED

Mobidity Low

Case Fatality High

Septicemia

Dermatitis Exudative
Sebum,
Serum,
Sweat
Greasy Pig (Exudative Epidermatitis)

Nursery On

Clinical Signs
Dermatitis Exudative
FOCAL,
LOCALIZED

Discrete Lesions
Greasy Pig (Exudative Epidermatitis)

All Forms

Diagnosis
Lesions First Noted
Face,
Behind Ears

MACULE Red - Brown

PUSTULE

EXUDATE
Greasy
Sebum,
Serum,
Sweat

Erythema

CRUSTS Exudative

SEPTICEMIA
Greasy Pig (Exudative Epidermatitis)

All Forms

Treatment
Antimicrobial Parenteral Penicillin

Antimicrobial Parenteral TMS

Antiseptic Shampoo Affected Areas

Skin Antiseptics Prophylaxis

Hygeine
+/- Efficacy
Pityriasis Rosea

Etiology
Inherited DERMATITIS PUSTULAR

Noninfectious

Young Swine

REGRESSION
4 Weeks
Self Limiting Without Tx

Often Confused with Ringworm
Pityriasis Rosea

Clinical Signs
EPIDERMAL COLLARETTES - Swarming

Early Distribution
ABDOMEN,
GROIN

Progression
Cranial,
Dorsal

PAPULE ERYTHEMATOUS
Centre Crater

COLLARETTE
COALESCES Mosaic Pattern

PURITIS NIET

Secondary Infections Possible
Pityriasis Rosea

Treatment
None Required
Epitheliogenesis imperfecta

Etiology
INHERITED CONGENITAL
Simple Autosomal Recessive

EMBRYONIC EPIDERMAL DIFFERENTIATION
Primary Failure
Epitheliogenesis imperfecta

Epidemiology
Sporadic

Individual Piglets in Litter

Differentiate Heat Lamp Burns
Not Present at Birth
Epitheliogenesis imperfecta

Clinical Signs
Squamous Epithelial Defects
Well Demarcated
Various Sizes

Generally
Back,
Loin,
Limbs
Epitheliogenesis imperfecta

Treatment
Open Wound Managemet

Allow Granulation
Wound Care
Keep Clean
Do NOT Put on Gunk
Melanoma


Etiology
Inherited
DUROC

Congenital
Possible

Develop in Adults
BENIGN
Generally
Progressive

Metastisis Possible
Internal Organs

Zoonatic NIET
Melanoma


Clinical Signs
Big Black Oozing Lesions
Isoimmune Thrombocytopenic Purpura

Epidemiology
Relatively Common
Purpura

Etiology
Isoimmune Thrombocytopenic ANTI PLATELET AB

Aquired in Colostrum
Isoimmune Thrombocytopenic Purpura


Epidemiology
MULTIPAROUS SOW P3 and Up

Normal at Birth

Die in TWO WAVES 1 to 3 Weeks
Early Neonatal Period Platelet Destruction
2 to 3 Weeks Megakaryocyte Suppression

Hemorrhage Percipitated by
Bruises,
Cuts,
Wounds

Most Piglets in Litter Affected

Parity One Sow Progeny NOT AFFECTED
Pathogenesis From Previous Parity
Isoimmune Thrombocytopenic Purpura


Pathogenesis
PREVIOUS GESTATION
Dam Gestates PIGLET
Containing PLATELETS of a DIFFERENT ISOTYPE

Blood Leaks
CONCEPTUS to DAM
Late Pregnacy or Farrowing

SYSTEMIC IgG Response Induced in Dam
To "Foreign" Piglet Platelet Isotype

Subsequent Parity Piglets
ABSORB ANTIPLATELET IgG AB
In COLOSTRUM
Isoimmune Thrombocytopenic Purpura


Clinical Signs
HEMORRHAGE WIDE SPREAD

Most Body Systems

Skin
Sub Cutaneous Common
Isoimmune Thrombocytopenic Purpura


Treatment
None
Isoimmune Thrombocytopenic Purpura


Control
Cull Repeat Offender Sows
Mycoplasma hyosynoviae


Arthritis

Agent
Mycoplasma hyosynoviae
Mycoplasma hyosynoviae Arthritis


Significance
Musculoskeletal Dz and Lameness

Most Significant Cause of Morbidity and Mortality

All Ages
Mycoplasma hyosynoviae Arthritis


Epidemiology
UBIQUITIOUS
TONSIL
URT

SHEDDING HIGH

SPORADIC Generally
Can be Severe on Some Farms

Transmission HORIZONTAL
Grower and Finisher Pigs > 8 Weeks In,
Naïve Gilts
Mycoplasma hyosynoviae Arthritis


Pathogenesis
Intranasal Infection

SEPTICEMIA
Persists 8 to 10 Days

LOCALIZATION Joints

Persistent Infection
Some Joints

Synovial Membranes
EDEMA
HYPEREMIA

VILLOUS HYPERTROPHY
via Increased Volume Synovial Fluid
Mycoplasma hyosynoviae Arthritis


Diagnosis

Pathology
Villous Hypertrophy
DDx ES

Synovial Membrane
EDEMA,
HYPEREMIA

ARTICULAR CARTILAGE NORMAL
Generally
tf Differentiate ES
Mycoplasma hyosynoviae Arthritis


Clinical Signs
Arthritis
ONE OR MORE JOINTS
NO Tail Bite

PAIN

Reluctance to Rise

Recumbancy

Lameness
Weight Bearning
Non Weight Bearing

Joint Swelling Rarely Observed
Mycoplasma hyosynoviae Arthritis


Diagnosis
Culture
Joint Aspirate
Necropsy

PCR
Joint Aspirate
Necropsy

Penicillin Response
Poor is Suggestive
Mycoplasma hyosynoviae Arthritis


Treatment
Early Recognition and Tx Imperative

Antimicrobial Parenteral Tiamulin

Antimicrobial Parenteral Tylosine

Antimicrobial Parenteral Lincomycin

Anti Inflammatory Predef

Anti Inflammatory Flunixin meglamine

Anti Inflammatory Ketoprofen
OCD Osteochondrosis Dessicans

Significance
Major Cause of Lamness ADULT PIGS

Non Infectious

Degenerative Generalized Condition
Epiphyseal Cartilage
OCD Osteochondrosis Dessicans

Stage
Finisher Late

Adult
OCD Osteochondrosis Dessicans

Etiology
MULTIFACTORIAL

HIGH GROWTH RATE
Modern Genetics
Deposit More Body Weight
Prior to Skeletal Maturity (18 Month)

ABNORMALITIES BREED and CONFORMATION
Broad Hams,
Short Hind Legs,
Sloping Pasterns

MECHANICAL STRESSES COMPRESSION - JOINT OVERLOADING
Overcrowding,
Breeding,
Fighting,
Slippery Floors
OCD Osteochondrosis Dessicans

Age
Month 4 to 18
OCD Osteochondrosis Dessicans

Clinical Signs
LAMENESS
Weight Bearing to Non Weight Bearing

Reluctance to Rise
Recumbancy

LAMENESS
Shifting Weight from Leg to Leg
Chronic,
Progressive
One or More Limbs

PAIN
Inflammation,
Increased Joint Fluid,
Swelling
OCD Osteochondrosis Dessicans

Clinical Signs

Location
Medial Articular Surfaces Most Likely Affected

ARTICULAR CARTILAGE
Stifle,
Elbow,
Hock,
Shoulder

GROWTH PLATES
Distal Ulna,
Distal Femur,
Femoral Head,
Humeral Head,
Ischiatic Tuberosity

EPIPHYSIOLYSIS
Glenoid Cavity,
Capital Femoral Epiphysis
OCD Osteochondrosis Dessicans

Pathogenesis
ENDOCHONDRIAL OSSIFICATION Disrupted

CARTILAGE RESORPTION

CALCIFICATION

ARTICULAR CARTILAGE THICKENS
Underlying Chondrocytes Deprived of Nutrition

CHONDROCYTE NECROSIS

MECHANICAL STRESSES and TRAUMA
Produce CRACKS and FISSURES on Articular Surface

SYNOVITIS
via SYNOVIAL FLUID Leakage

FLAP or FRAGMENT on Articular Surface
and Voila - OCD and
If it Breaks Off - A Joint Mouse
OCD Osteochondrosis Dessicans

Treatment
Cull Best for Welfare of Animal

Anti Inflamatory Labled Isoflupredone (Predef)

Anti Inflamatory Not so Labled (ie Go to Jail) Dexamethasone

Euthanize
Unrelenting Pain,
Unable to Walk Onto Truck (Be Damn Sure It Can Walk Off),
Non Ambulatory
OCD Osteochondrosis Dessicans

Control
MECHANICAL STRESS PREVENT

Flooring
Non Slip,
Slatted

Pen Density Reduce

Fighting Reduce

Competition Reduce
Humpy Back Pigs


Etiology
SPORADIC
Increasing Significance Western Canada

IN UTERO PATHOGENESIS
Gets the Little Piggly Scientists Excited

Prognosis Poor

Etiology Unknown

Pathogenesis Unknown
Humpy Back Pigs


Stage
Suckling

Nursery
Humpy Back Pigs


Age
Weeks 1 to 12
Humpy Back Pigs


Clinical Signs
LORDOSIS
Thoracic Spine

KYPHOSIS
Lumbar Spine

WEIGHT GAIN IMPAIRED
Unthrifty,
Initially Good Body Condition

DUMBO EARS
Large,
Pulled Caudo Ventrally

Wide Chested
Humpy Back Pigs

Diagnosis

Pathology
RIB FRACTURES at Birth
Single or Multiple,
Bony Callus

ARTERITIS
NECROTIZING or Lymphocytic

PERIARTERITIS
NECROTIZING or Lymphocytic

MYOSITIS Skeletal Muscle
Lymphocytic
Humpy Back Pigs


Treatment
Euthanize
Humpy Back Pigs


Control
NIET
Biotin Deficiency

Etiology
B Vitamin Required for Horn Integrity

CEREAL GRAINS are LOW in AVAILABLE BIOTIN
Biotin Deficiency

Clinical Signs
Hoof Cracks
TRANSVERSE

Foot Pads
Cracking,
Bleeding
Biotin Deficiency

Pathogenesis
MULTIFACTORIAL


BIOTIN SUPPLEMENTATION

Increases Compressive STRENGTH and HARDNESS
of Hoof Side Wall

SOFTENS HEEL BULB
Increased Cushioning,
Better Weight Distribution
Biotin Deficiency Treatment
NIET

Existing Lesions
CANNOT be Healed with Biotin Supplementation
Biotin Deficiency

Control
BIOTIN SUPPLEMENTATION

Helps Prevent NEW Lesion Development

Grower Finisher Diets 50 to 100 μg/kg,

Sow and Gilt Diets 150 to 750+ μg/kg
Bacterial Polyarthritis

Significance
MOST COMMON Cause

INFECTIOUS Lameness
Bacterial Polyarthritis

Etiology
MANY OPPORTUNISTIC BACTERIA
Strep suis,
Strep equisimilis,
Staph hyicus,
Staph aureus,
E. coli,
Arcanobacterium pyogenese,
etc
Bacterial Polyarthritis

Epidemiology
PASSIVE IMMUNITY
Insufficiency
Gilt Litter,
Large Litters,
Late Born Piglets

Gender MALE
+/- Castration

HYGEINE or Sanitation Poor
Processing Equipment,
Syringes,
Needles

INJURIES and WOUNDS
Teeth Clipping,
Tail Docking,
Abrasions,
Fighting

TAIL BITING

SKIN WOUNDS

FIGHTING
Bacterial Polyarthritis

Pathogenesis
BACTEREMIA
Localization in Joint

Increased Joint Fluid

Synovial Hyperemia

Periarthritis Fibrinous

ABSCESSATION

SEQUELLA
Septicemia,
Menignitis,
Endocarditis,
etc
Bacterial Polyarthritis

Clinical Signs
Lameness ONE OR MORE JOINTS
Hock,
Elbow,
Pasten,
Carpus

Joint Swelling
Hot,
Red

Pain

Lameness
Weight Bearing to Non Weight Bearing

Differentiate Bursitis
Small Swellings
Generally Associated with Hock or Elbow Joint
Bacterial Polyarthritis

Treatment
Antimicrobial Parenteral Antibiogram, Response to Tx

Antimicrobial Parenteral Penicillin G

Antimicrobial Parenteral Lincomycin

Antimicrobial Parenteral TMS

Antimicrobial Parenteral Ceftiofur

Antimicrobial Parenteral
Generally 4 to 5 Consecutive Days Tx

Antimicrobial Parenteral
Monitor For Pain - 10 Days to Abate Swelling

Anti Inflammatory Parenteral Labled Isoflupredone (Predef)

Anti Inflammatory Parenteral Not so Labled (ie Go to Jail) Dexamethasone

Anti Inflammatory Parenteral Flunixin meglamine

Anti Inflammatory Parenteral Ketoprofen

Early Recognition and Tx Essential

Euthanize Chronic
Bacterial Polyarthritis

Control
PASSIVE ANTIBODY TRANSFER Enhance
Pseudorabies (Aujesky's Dz)

All Forms

Agent
Herpesviridae Broad Host Range
Pseudorabies (Aujesky's Dz)

All Forms

Etiology
NATURAL HOST Only Pigs
Subclinical and Latent Infections Common
LATENT INFECTIONS
Sensory Ganglia (Months)
Tonsil (Weeks)

FATAL INFECTIONS
Dead End Hosts
Many Other Species

INTENSE PRURITIS
Dead End Hosts
Mad Itch

Host Susceptability HIGH
SHEEP,
GOATS,
CATTLE,
CATS

Host Susceptability Moderate
Dogs,
Raccons,
Skunks

Host Susceptability
Low
Rats,
Mice,
Horses
Pseudorabies (Aujesky's Dz)

All Forms

Epidemiology
Persistence Environment - Moderate
2 Weeks

Susceptable Many Disinfectants

Shedding Recovered Animals Large Amount
2 Weeks

Recrudescence and Shedding Periods of Stress
Rapid Spread
NAÏVE FARMS ACUTE OUTBREAKS
7 Days or Less

Transmission HORIZONTAL
Oral Secretions,
Nasal Secretions,
Fomites,
+/- Aerosol

Transmission VERTICAL
Transplacental,
Milk,
Vaginal Mucosa,
Semen
Pseudorabies (Aujesky's Dz)

All Forms

Clinical Signs
SEVERITY DECREASES with AGE

Respiratory Dz Increases with Age

Neurologic Dz Decreases with Age
Pseudorabies (Aujesky's Dz)

Sow

Clinical Signs
NON CLINICAL

RESPIRATORY SIGNS MOST OFTEN
Cough
Sneezing
Nasal Discharge

Early Embryonic Death Trimester 1

Abortion Trimester 2 and 3

Stillbirth Trimester 2 and 3

Mummies Trimester 2 and 3

Weak Piglets Trimester 2 and 3

Congenital Trimester 2 and 3
Pseudorabies (Aujesky's Dz)

Suckling Piglets

Clinical Signs
NEUROLOGIC Dz Predominates

DEATH PERACUTE 24 to 36 Hours

Depression

Pyrexia

Emesis

Diarrhea

Tremors

Hypersalivation

Incoordination

Convulsions

Dog Sitting

Coma

MORBIDITY 100%

MORTALITY 90% DDx TGE, FMD
Pseudorabies (Aujesky's Dz)

Nursery

Clinical Signs
Death Acute

Depression Less Severe than Suckling Pigs


Cough

Sneezing

Nasal Discharge

Tremors Less Severe than Suckling Pigs

Hypersalivation Less Severe than Suckling Pigs

Incoordination Less Severe than Suckling Pigs

Convulsions Less Severe than Suckling Pigs

Dog Sitting Less Severe than Suckling Pigs

Coma Less Severe than Suckling Pigs

MORBIDITY High

MORTALITY Moderate
Pseudorabies (Aujesky's Dz)

Gower and Finisher

Clinical Signs
RESPIRATORY Dz Predominates
Cough
Sneezing
Nasal Discharge

NEUROLOGIC Dz SPORADIC

Morbidity High

Mortality Low
Pseudorabies (Aujesky's Dz)

All Forms

Pathogenesis
NASOPHARYNX Epithelium Primary Replicaton

TONSIL Primary Replicaton

LYMPH NODES Spreads to Regional LN

BRAIN and SPINAL CORD Reaches via Nerves

SYSTEMIC DISTRIBUTION Follows Brief Viremia

LUNG Localizes

PLACENTA Localizes
tf Transplacental Infection
Pseudorabies (Aujesky's Dz)

All Forms

Diagnosis

Pathology
Gross Lesions
Often Subtle,
Not Pathognomic

Keratoconjuctivitis

RHINITIS FIBRINONECROTIC DDx Atrophic, IBR (Catarrhal)

TONSILAR (PALLANTINE) EPITHELIAL NECROSIS
Very Suggestive in Young Pigs

Meningial Congestion

Lymph Nodes (URT, Oral Cavity)
Enlarged,
Hemorrhagic

Liver Necrosis Disseminated Focal

Spleen Necrosis Disseminated Focal
Pseudorabies (Aujesky's Dz)

All Forms

Diagnosis

Histopathology
INTRA NUCLEAR INCLUSION BODIES BASOPHILIC

Mengoenchephalomyelitis NON SUPPURATIVE
Pseudorabies (Aujesky's Dz)

All Forms

Diagnosis

Alarm Bells
TONSILAR NECROSIS SUCKLING PIGLETS

NEUROLOGIC SIGNS SUCKLING PIGLETS

HIGH MORTALITY and FEVER SUCKLING PIGLETS

DEATH of OTHER LIVESTOCK or Pets

Simultaneous and Severe Dz REPRODUCTIVE,
RESPIRATORY,
NEUROLOGIC
Pseudorabies (Aujesky's Dz)

All Forms

Control
REPORTABLE

Contact CFIA

Do NOT Leave Farm
CSF Classical Swine Fever (Hog Cholera)


Agent
Classical Swine Fever Virus Pestivirus
CSF Classical Swine Fever (Hog Cholera)


Etiology
Pestivirus (RNA) Related to
BVD,
Border Dz

Natural Host Pigs Only

HIGHLY CONTAGIOUS

SEVERITY VARIES
Serotype Virulence,
Host Determinants
CSF Classical Swine Fever (Hog Cholera)


Epidemiology
RESISTANCE
Salting and Curing,
Survives in Meat for Months to Years (Frozen)

RESISTANCE
Environment - Moderate
2 Weeks

RESERVOIRS FERRAL PIG

Global Distribution
Including Central America, South America
Excluding Canada, USofA

Transmission Horizontal
BLACK MARKET MEAT TRADE,
AIR AND SEA PORTS - GARBAGE, CONTAMINATED MEAT PRODUCTS

Virulence STRAIN VARIATION GREAT

Virulence EARLY RECOGNITION UNLIKELY
Mild and Moderate Strains,
tf Potential for Wide Distribution
CSF Classical Swine Fever (Hog Cholera)


Clinical Signs
Depression

Prostation Piling APPEAR CHILLED

PYREXIA HIGH 41 to 42

DIARRHEA WATERY Severe

Emesis

SKIN LESIONS

Hyperemia

Cyanosis

Hemorrhage Petechial - Ecchymotic

INCOORDINATION

HYPEREFLEXIA GOOSE STEPPING
DDx Vit B Deficiency

Paresis Caudal

Convulsions

Death 10 to 20 Days
CSF Classical Swine Fever (Hog Cholera)


Pathogenesis
Trophism Varies with Virulence

Oral Nasal Infection

TONSILAR EPITHELIAM Replication

TONSILAR NECROSIS

VIREMIA via Spread to Regional Lymph Nodes

LYMPHOID DEPLETION
tf Susceptable to Secondary Infection

LEUKOPENIA SEVERE

THROMBOCYTOPENIA SEVERE

HEMORRHAGE PETECHIAL - Ecchymotic

TRANSPLACENTAL INFECTION
Abortion,
Mummies,
Stillbirths,
Congenital Infections,
Congenital Tremors
DDx Circa Virus
CSF Classical Swine Fever (Hog Cholera)

Diagnosis

Pathology
Lesions Vary with Strain Virulence

LYMPHADENOPATHY
GASTRO-HEPATIC (betcha never seen one),
Submandibular,
Systemic

HEMORRHAGE PETECHIAL AND ECCHYMOTIC
Lymphnodes,
Kidneys,
Epiglottis,
Gall Bladder

SPENOMEGALY

SPLENIC INFARCTS
DDx
Lepto,
PDNS

LARGE INTESTINE INFLAMMATION FIBRINOUS HEMORRHAGIC
DDx Swine Dysentary

Cecum BUTTON ULCERS

Colon BUTTON ULCERS

ENCEPHALITIS NON SUPPURATIVE
Pathognomic Almost
CSF Classical Swine Fever (Hog Cholera)


Diagnosis

Alarm Bells
FEVER and PILING

TONSILAR NECROSIS MILD

LYMPHADENOPATHY HEMORRHAGIC
PETECHIATION EXTENSIVE
SYSTEMIC
Any Age of Pig
CSF Classical Swine Fever (Hog Cholera)

Diagnosis

Must Dos
Collect Blood (EDTA) for LEUKOGRAM

SUBMIT BRAIN (Even if Captive Bolt)
Those Pathologists are Oh So Clever
CSF Classical Swine Fever (Hog Cholera)


Control
REPORTABLE

Contact CFIA

Do NOT Leave Farm
ASF African Swine Fever

Agent
African Swine Fever Virus Asfarviridae
ASF African Swine Fever

Etiology
Asfarviridae

Highly Contagious

DENDRITIC CELL DESTRUCTION
Virulent Forms
SWINE UNABLE to PRODUCE STERILIZING AB (Serum Neutralization)
ASF African Swine Fever

Epidemiology
Vectors SOFT TICKS

Reservoirs SOFT TICKS

Inapparent Infection Established
TICKS AND AFRICAN FERRAL SWINE
Warthog,
Bushpig,
Giant Forest Pig
ASF African Swine Fever

Clinical Signs
More Severe than Classical Swine Fever

Vary With Strain

Depression

Prostation Piling APPEAR CHILLED

PYREXIA HIGH 41 to 42

DIARRHEA WATERY Severe

Emesis

SKIN LESIONS
Hyperemia
Cyanosis
Hemorrhage Petechial - Ecchymotic

Death 7 to 10 Days
ASF African Swine Fever

Pathogenesis
Oral Exposure
Garbage,
Swill

Tick Bite

ENDOTHELIAL CELL DAMAGE

VASCULAR DAMAGE
CONSUMPTION COAGULOPATHY (DIC)
Severe Hemorrhage and Edema Everywhere

Highly Virulent Strains
Destruction of Dendritic Cells →
Leukopenia →
FAILURE OF IMMUNE RESPONSE →
Death

Lower Virulence Strains
Fewer Dendritic Cells Destroyed →
Partial Immune Response →
NO SERUM NEUTRALIZING AB
ASF African Swine Fever

Diagnosis

Pathology
More Severe than Classical Swine Fever

Lesions Vary with Strain Virulence

LYMPHADENOPATHY
GASTRO-HEPATIC (betcha never seen one),
Submandibular,
Systemic

HEMORRHAGE PETECHIAL AND ECCHYMOTIC
Lymphnodes,
Kidneys,
Epiglottis,
Gall Bladder

SPENOMEGALY

SPLENIC INFARCTS
DDx
Lepto,
PDNS

LARGE INTESTINE INFLAMMATION FIBRINOUS HEMORRHAGIC
DDx Swine Dysentary

Cecum BUTTON ULCERS

Colon BUTTON ULCERS

ENCEPHALITIS NON SUPPURATIVE
Pathognomic Almost
ASF African Swine Fever

Diagnosis

Pathology

Unique
HYDROTHORAX

PULMONARY EDEMA

HYDROPERICARDIUM

ASCITES

HEMOPERITONEUM

SPLENOMEGALY MARKED
(Careful when Rolling em Over - Sploosh)
ASF African Swine Fever

Diagnosis

Alarm Bells
FEVER and PILING

SPLENOMEGALY MEGA MEGALY
RED BLACK
FRIABLE

LYMPHADENOPATHY HEMORRHAGIC GREATLY ENLARGED
RENAL LN,
GASTROHEPATIC LN
ASF African Swine Fever

Diagnosis

Must Dos
Collect Blood (EDTA) for LEUKOGRAM
ASF African Swine Fever

Control
REPORTABLE

Contact CFIA

Do NOT Leave Farm
FMD Foot and Mouth Disease

Agent
Foot and Mouth Disease Virus Picoviridae
FMD Foot and Mouth Disease

Etiology
DISTINCT STRAINS Seven
Subtypes > 60

Specific Swine Trophism
Some Strains ie 01-Taiwan
Do Not Infect Cattle

CROSS PROTECTION NIET
tf Act Like 7 Different Dz
FMD Foot and Mouth Disease

Epidemiology
AMPLIFIER HOSTS
Swine Shed Massively via Aerosol Secretions

SHORT TERM SHEDDERS Swine are (so says Yoda)

SUSCEPTABLE Swine are Not Very

Morbidity High

Mortality Low

Mortality High Up to 50% Piglets

Transmission Horizontal
DIRECT CONTACT (95% Cases),
INFECTED ANIMAL PRODUCTS (Biggest Risk to NA)
Meat,
Milk,
Offal
Fomites,
Aerosols Long Distance (We Will Fight on the Beaches - We Will Never Surrender)

Transmission Vertical
INFECTED ANIMAL PRODUCTS (Biggest Risk to NA)
Semen,
Ova



MEAT and BYPRODUCTS

Reduction of pH in Muscle Post Mortom
Kills Virus

No pH Reduction
Glands,
Bone Marrow
tf Virus Survives (to - 20)
FMD Foot and Mouth Disease

Pathogenesis
Incubation Short 1 to 2 Days

Replication
Epithelium,
Mucosa,
Myocardium

VIREMIA MARKED 3 to 5 Days

VESICLES POINTS of MECHANICAL ABRASION
SNOUT,
MOUTH,
TONGUE,
FEET,
DEWCLAWS,
OVER JOINTS,
PRESSURE POINTS,
TEATS

CARRIERS NOT PIGS
Unlike those Beastly Cattle and Sheep
FMD Foot and Mouth Disease

Clinical Signs
Pyrexia

Morbidity High

Mortality Low

PAIN

LAMENESS ACUTE
Reluctance to Move

Claw Loss

SALIVATION

Chomping

ABORTION

Stillbirth

Congenital Infections
Death Peracute Piglets
via Severe Myocardial Necrosis
FMD Foot and Mouth Disease

Diagnosis

Differentials
Exotics (FMD, VES, SVD) and
Enzootic (VS) Vesicular Dz
are
CLINICALLY INDISTINGUISHABLE

FMD
Pigs,
Cattle,
Sheep,
Goats

SVD Swine Vesicular Dz
Pigs,
Humans

VES Vesicular Exanthema of Swine
Pigs, Rare NA (1956)

VS Vesicular Stomatitis
Pigs,
Horses,
Cattle
Indiginous to NA Summer Occurance via Insect Vectors