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108 Cards in this Set
- Front
- Back
|
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 |
