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110 Cards in this Set
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MPS Mycoplasmal Pneumonia of Swine
Agent |
Mycoplasma hyopneumoniae
aka Enzootic pneumonia |
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MPS Mycoplasmal Pneumonia of Swine
Significance |
Major Respiratory Pathogen NA
Contributor Procine Respiratory Dz Complex PRDC |
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MPS Mycoplasmal Pneumonia of Swine
Etiology |
Culture SLOW GROWTH 4 to 8 Weeks
Dx = NIET Antimicrobial Resistance HIGH Persistence Poor Survival Environment |
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MPS Mycoplasmal Pneumonia of Swine
Epidemiology |
Incubation 2 to 3 Weeks
TRANSMISSION HORIZONTAL Sow to Piglet via Crates, Pig to Pig Nursery and Grower REGIONAL SPREAD AEROSOL 3.2 Km Season Winter Cold, Wet, Light Winds GROWER Mainly Affected > 10 WEEKS |
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MPS Mycoplasmal Pneumonia of Swine
Epidemiology Epidemic |
NAÏVE FARMS ACUTE OUTBREAKS Severe Disease
All Ages Affected Pyrexia (40 to 40.5) Anorexia, Pyrexia, Lethargy Respiratory Signs Severe Disease Extensive Lung Involvement Death Occasionally Peracute Abortion Occasionally Via Pyrexia |
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MPS Mycoplasmal Pneumonia of Swine
Epidemiology Endemic |
MOST COMMON
CHRONICALLY Infected Herds Susceptible Pig Exposed Entering GROWER via Waning Maternal AB, Shedding of Older Animals Coughing Develops 2 to 3 Weeks Post Exposure EARLY GROWER PERIOD Morbidity High Mortality Low |
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MPS Mycoplasmal Pneumonia of Swine
Clinical Signs |
COUGH NON PRODUCTIVE
if UNCOMPLICATED Dry Raspy COUGH PORDUCTIVE if CONCURRENT INFECTION SEVERITY Influenced by Mycoplasma hyopneumoniae STRAIN Pig Flow, Density, Air Quality |
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MPS Mycoplasmal Pneumonia of Swine
Pathogenesis |
COLONIZES
TRACHEAL EPI CELLS BRONCHIAL EPI CELLS CLUMPS CILIA IMPAIRS MUCOCILIARY ESCALATOR SECONDARY INVASION Mixed Bacterial and Viral Infections RESOLUTION Uncomplicated Cases INCREASED SEVERITY Concurrent RESPIRATORY PATHOGENS Leads to PRDC |
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MPS Mycoplasmal Pneumonia of Swine
Diagnosis Pathology |
BRONCHO PNEUMONIA
CRANIO VENTRAL CONSOLIDATION Cranial, "Middle", Accessory Lobes +/- Cranial Portion Caudal Lobes FIRM Meaty Lungs Red Purple CATARRHAL EXUDATE Airway Cut Surface MEDIASTINAL LYMPH NODES Enlarged, Edematous PERI-BRONCHIAL LYMPHOID HYPERPLASIA (Cuffing) Highly Suggestive Alveoli Debris and Inflammatory Cells |
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MPS Mycoplasmal Pneumonia of Swine
Diagnosis |
Fluorescent Antibody Test
ANTIGEN Lung Include CILIATED Airway Epi Immuno Histo Chemistry ANTIGEN Lung Include CILIATED Airway Epi PCR Nucleic Acid Lung, Bronchial Fluid, Trachea Serology IgG ELISA DAKO (blocking), IDEXX (indirect) |
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MPS Mycoplasmal Pneumonia of Swine
Diagnosis Serology |
IgG ELISA
DAKO (blocking), IDEXX (indirect) MEASURES EXPOSURE Interpretation Difficult Seroconversion HIGHLY VARIABLE Up to 6 WEEKS TO INDUCTION IgG Can NOT DIFFERENTIATE Natural Infection vs Vaccination Correlation Vaccine Titres and Protection NIET SPECIFICITY GOOD SENSITIVITY LOW (DAKO Better) |
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MPS Mycoplasmal Pneumonia of Swine
Diagnosis Slaughter Check |
Lung Lesion Scoring
PREVELANCE AND SEVERITY Herd Infection Probable INDIVIDUAL LESION SCORE > 5% Herd Infection Probable PREVEALENCE of INFECTED LUNGS > 20% PCR UNRELIABLE Environmental Contamination Proportion of AFFECTED LOBE Estimated Score is TOTAL for All Lobes |
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MPS Mycoplasmal Pneumonia of Swine
Control Vaccination Injection |
Sow, Nursery, Grower
REDUCES PREVALENCE and SEVERITY COLONIZATION NOT PREVENTED 2 to 3 Weeks PRIOR TO EXPECTED EXPOSURE (Typically Grower) One and Two Dose Products Available Severity, Infection Pressure, Cost MATERNAL AB INTERFERENCE tf Vaccinate AFTER 6 to 8 Weeks Age |
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MPS Mycoplasmal Pneumonia of Swine
Control Antimicrobial Feed |
Prior or During PEAK EXPOSURE
DOES NOT ELIMINATE Mycoplasma hyopneumonia Controls Secondary Infections Cost Effective Grower Tiamulin Controls Secondary Infections Cost Effective Grower Chlortetracycline Controls Secondary Infections Cost Effective Grower Lincomycin Controls Secondary Infections Cost Effective Grower Tetracyclines Controls Secondary Infections Cost Effective Grower Tylosine |
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MPS Mycoplasmal Pneumonia of Swine
Treatment Antimicrobial Parenteral |
Secondary Infections Lincomycin
Secondary Infections Tylosine Secondary Infections Tetracyclines Secondary Infections Tiamulin |
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MPS Mycoplasmal Pneumonia of Swine
Control Environment |
Air Quality Improvements
AIAO ALWAYS Segregate Groups Control OTHER RESPIRATORY PATHOGENS PRRS, PCV2, SIV, Streptococcus suis, Haemophilus parasuis, etc |
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APP Actinobacillus Pleuropneumonia
All Forms Etiology |
Severe Disease Traditionally
Less Severe Western Canada Last 20 Years Biotypes I and II Typical NAD Dependent Atypical NAD Independent Culture NAD Supplied by Staph Streaks Ask FOR IT SEROTYPES 15 Count em VARYING VIRULENCE Serotypes 1, 5, 7 MOST VIRULENT and COMMON CANADA |
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APP Actinobacillus Pleuropneumonia
All Forms Epidemiology |
Transmission HORIZONTAL Primarily
Transmission AEROSOL SHORT DISTANCES INCUBATION SHORT 6 to 12 Hours SEVERITY Influenced by Serotype, Dose Herd Immune Status, Concurrent Dz |
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APP Actinobacillus Pleuropneumonia
All Forms Pathogenesis |
Colonizes
TONSIL ALVEOLAR EPI FIMBRIAL ADHESINS Facillitate Colonization Adherence Phagocytosis ALVEOLAR MACROPHAGES RTX EXOTOXINS Apx I, II, III, IV HEMOLYTIC, CYTOTOXIC INFLAMMATORY CYTOKINES SEPTIC SHOCK Peracute Death ARTERIOLAR THROMBOSIS ALVEOLAR NECROSIS Acute Lung Lesions |
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APP Actinobacillus Pleuropneumonia
Peracute Clinical Signs |
Death Peracute (3 TO 36 Hours Post Infection)
Sporadic in Pigs Tachycardia Tachypnea CYANOSIS Extremities Generalized EPISTAXIS FOAMY |
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APP Actinobacillus Pleuropneumonia
Acute Clinical Signs |
Anorexia, Pyrexia, Depression > 40
DYSPNEA COUGH AGONAL BREATHING Outcome Varies with Animal Death Acute Cardiovascular and Circulatory Collapse |
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APP Actinobacillus Pleuropneumonia
Chronic Clinical Signs |
COUGH CHRONIC
via CHRONIC PLEURITIS APPETITE REDUCED Weight Gain Impaired |
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APP Actinobacillus Pleuropneumonia
Peracute and Acute Diagnosis Pathology |
Pneumonia Severe Acute Well Demarcated
Pneumonia NECROTIZING HEMORRHAGIC Pneumonia CAUDAL LOBES (Generally) PLEURITIS FOCAL Trachea Blood Tinged Froth |
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APP Actinobacillus Pleuropneumonia
Chronic Diagnosis Pathology |
PLEURITIS
CHRONIC ADHESIONS CONSOLIDATION and NECROSIS FOCAL PULMONARY ABSCESSES BLACK FOCI FIBRIN GROUND GLASS APPEARANCE |
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APP Actinobacillus Pleuropneumonia
All Forms Diagnosis |
NECROTIZING HEMORRHAGIC PNEUMONIA
FOCAL PLEURITIS PLEURAL ADHESIONS HIGH % SLAUGHTER CHECK Culture Lung Lesions Serotyping Lung Lesions Serology ELISA Screening All Serotypes Serology ELISA INDIVIDUAL SEROTYPES 1, 5, 7 |
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APP Actinobacillus Pleuropneumonia
All Forms Control Environment |
Air Quality Improvements
AIAO ALWAYS Segregate Groups Control OTHER RESPIRATORY PATHOGENS PRRS, PCV2, SIV, Streptococcus suis, Haemophilus parasuis, etc |
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APP Actinobacillus Pleuropneumonia
All Forms Control Antimicrobial Parenteral |
Peracute and Acute Only Penicillin G
Peracute and Acute Only Tetracyclines |
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APP Actinobacillus Pleuropneumonia
All Forms Control Antimicrobial Feed |
Amoxicillin
Tiamulin Tilmicosin |
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APP Actinobacillus Pleuropneumonia
All Forms Control Antimicrobial Water |
Amoxicillin
Tiamulin Tilmicosin |
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APP Actinobacillus Pleuropneumonia
All Forms Control Vaccination Injection |
BREEDING HERD
Nursery, Grower, Finisher Protection from CLINICAL Dz +/- Does NOT PREVENT INFECTION Variable Value Rarely Used Western Canada (Except Pre Entry Acclimation Subunit and Killed Products Serotype Specific All Have (1,5, 7) |
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SIV Swine Influenza
All Forms Significance |
Zoonotic Potential
Mixed Infections MAY Lead to Reassortment with Human, Avian and Swine Viruses Possible Pandemic Strains - ok enough from Chicken Little Transmission Has Been Docmented Swine to Human Human to Swine (More Common) ala 1918 Pig Influenza Die Off Swine Worker Vaccination for Seasonal Influenza Minimize Opportunities for Reassortment Pig Influenza Viruses Have RECEPTORS in BOTH GI and RESPIRATORY TRACTS Spanish Flu 1918 Avian H1N1 Asian Flu 1957 - 1958 Avian H2N2 Pig Mixing Vessel Hong Kong Flu 1968 - 1969 Avian H3N2 Pig Mixing Vessel |
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SIV Swine Influenza
All Forms Agent |
Type A Influenza Virus Orthomyxoviridae
Multiple Strains (H1,2,3 and N1,2,3) |
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SIV Swine Influenza
All Forms Etiology |
8 SEGMENTS SS RNA
SHIFT (Segment Reassortment Between Strains) = Rapid Change DRIFT (Point Mutations) = Slow Change Surface Glycoprotein AG H (Hemagglutinin) Virus Attachment, RBC Agglutination N (Neurominidase) Viral Release from Infected Cells CLASSIC SWINE H1N1 Exclusive Strain NA 1930 to 1998 Stable Genotype Due to Abundant Naïve Pigs EUROPEAN H1N1 Uniquely Highly Pathogenic 1930 to 1998 TRIPLE REASSORTED H3N2 After 1998 A Big SMOZZLE Genes from HUMAN, SWINE and AVIAN Viruses THREE CLUSTERS Linked to HUMAN STRAIN Multiple Strains Emerging tf Must Sequence Farm's Strain(s) to Know What it Is |
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SIV Swine Influenza
All Forms Epidemiology |
HIGHLY INFECTIOUS Respiratory Disease
Transmission Horizontal DIRECT CONTACT Pig to Pig Via Nasopharyngeal Secretions AIRBORNE Hog Dense Regions Passive Immunity Protects Against Dz DOES NOT Prevent Infection or Shedding Morbidity High - 100% Mortality Low SHORT INCUBATION 1 to 3 Days |
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SIV Swine Influenza
Classic Swine H1N1 Clinical Signs |
COUGING
EXPLOSIVE - Sudden Onset PAROXYMAL SEAL BARK - Highly Suggestive Dyspnea Pyrexia PROSTRATION Piling HIGH MORBIDITY 100% LOW MORTALITY Rapid Recovery 5 to 7 Day Clinical Course |
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SIV Swine Influenza
Modern Reassorted Strains Clinical Signs |
Less Severe Dz is Possible
POTENTIALLY SUBTLE VARIABLE ALL AGES AFFECTED Herd Presentation Varies Strain, Age, Immunity Concurrent Dz (PRRS, MH, etc) |
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SIV Swine Influenza
All Forms Pathogenesis |
RAPID REPLICATION
Respiratory Tract, Lungs, Nasal Mucosa Tonsil, Lymph Nodes BRONCHIOLAR EPITHELIUM Highly Specific Trophism EPITHELIAL CELL NECROSIS Inflammation Cytokines TNF, IL-1 EXUDATE Accumulation Degenerate Mucosal Cells and Neuts RAPID CLEARANCE of Virus |
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SIV Swine Influenza
All Forms Diagnosis Pathology |
Viral Replication
Respiratory Tract ONLY CONJUNCTIVITIS NASAL DISCHARGE CONSOLIDATION CRANIAL and MIDDLE Lobes Purple Firm Pneumonia Bronchial / Interstitial Cranio Ventral +/- Hyper Inflation EXUDATE Blood Tinged, Fibrinous EDEMA Interlobular |
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SIV Swine Influenza
All Forms Diagnosis Histopathology |
BRONCHITIS / BRONCHIOLITIS NECROTIZING
MUST HAVE Airway Epithelium Degeneration and Necrosis ALVEOLI FILLED with EXUDATE (Desquamated Cells and Neuts) Also Bronchi, Bronchioli Atelectasis BRONCHIO INTERSTIIAL PNEMONIA |
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SIV Swine Influenza
All Forms Diagnosis Immuno Histo Chemistry |
AG Detection Type A
(tf ALL SPECIES) Lung, Nasal Swabs < 8 DAYS ONLY > 8 Days = False Negative |
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SIV Swine Influenza
All Forms Diagnosis PCR |
Nucleic Acid
Lung, Nasal Swabs < 8 DAYS ONLY > 8 Days = False Negative |
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SIV Swine Influenza
All Forms Diagnosis Serology |
HI (Paired Samples)
ELISA SENSITIVITY VARIES via Specific Strain Used in Assay HOMOLOGOUS STRAINS = HIGHER TITRES Stain Specific Assays Can be Developed GENETIC ANALYSIS or SEQUENCING +ve = USEFULL INFROMMATION ie Determine Usefullness of Commerial Vaccines -ve = LITTLE INFROMATION |
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SIV Swine Influenza
All Forms Diagnosis Time Line |
24 Hours Post Infection
Peak Fever 48 Hours Post Infection Peak Excretion (Good TIME to SAMPLE) Coughing Starts 6 to 8 Days Post Infection Viral Clearance 10 to 14 Days Post Infection Seroconversion Coughing Stops |
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SIV Swine Influenza
All Forms Treatment |
SUPPORTIVE Care ONLY
Antimicrobial Parenteral SECONDARY BACTERIAL Infections Control Concurrent Dz Antimicrobial Feed SECONDARY BACTERIAL Infections Control Concurrent Dz AIR QUALITY Improve NH3, Dust Sannitation Improve |
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SIV Swine Influenza
All Forms Control Vaccination Injection |
H1N1 (All), H3N2 (Most)
+/- Efficaccy Bivalent Killed Bacterins Generally Effective CLASSIC H1N1 VARIABLE H3N2 Rapid Shift in Genome AUTOGENOUS EFFECTIVE tf Try Early Sows Pre Farrowing Piglets Weaning or Post Weaning |
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PRCV Porcine Respiratory Corona Virus
Etiology |
EVOLVED FROM TGE
Genetic Mutation Trophism for Lung Instead of GIT |
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PRCV Porcine Respiratory Corona Virus
Clinical Signs |
ASYMTOMATIC
SUBCLINICAL INTERSTITIAL PNEUMONIA DIFFUSE MILD VIREMIA Parenchymal Organs Lymph Nodes |
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PRCV Porcine Respiratory Corona Virus
Significance |
Partial Protection from TGE
Masks Clincal Dz Reduced Incidence of TGE Worldwide CROSS REACTIONS Serologic Testing Serum Neutralization tf Use Competitive ELISA to Differentiate TGE/PRCV |
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PRDC Porcine Respiratory Dz Complex
Etiology |
Multifactorial
ala Bovine Shipping Fever Virus Mycoplasma 2˚ Bacteria Bacteria Mycoplasma hyopneumoniae, Pasteurella multocida, Actinobacillus pleuropneumonia, Streptococcus suis, Haemophilus parasuis, Actinobacillus suis Viruses Swine Influenza Virus, PRRS, PRCV, PCV2 Parasites Acaris suum |
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PRDC Porcine Respiratory Dz Complex
Diagnosis |
IDENTIFICATION PRIMARY and SECONDARY PATHOGENS
CRITICAL Detailed History and Clinical Workup Pathology Gross and Histology Early Cases and Untreated Serology Multiple Assays Serial Studies Culture PCR Immuno Histo Chemistry |
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Streptococcus suis
All Forms Significance |
Emerging Disease Livestock Intensification
Stress Percipitated 35 SEROTYPES Identified by Capsular Proteins TYPE 2 Most Common ZOONOTIC |
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Streptococcus suis
All Forms Epidemiology |
UPPER RESPIRATORY TRACT Infection
NORMAL INHABITANT EARLY COLONIZER Also Found Genital Tract Alimentary Tract RESERVOIRS VECTORS Many DOMESTIC SPECIES Persistence Environment LENGTHY Manure > 100 Days Multiple Serotypes and or Strains On Farm VIRULENCE VARIES with SEROTYPE Transmission HORIZONTAL Sow to Piglet via GENITAL TRACT via RESPIRATORY via Alimentary PIG to PIG Nurseries On CARRIERS SOWS NEAR 100% |
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Streptococcus suis
Acute Clinical Signs |
CONVULSIONS Acute
Death ACUTE Septicimia, POLYSEROSITIS, MENINGITIS OPISTHOTONOUS Acute Paddling Acute |
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Streptococcus suis
All Forms Clinical Signs |
WEEKS 5 to 10 PRIMARY ONSET
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Streptococcus suis
Chronic Clinical Signs |
ARTHRITIS
Poly Chronic Cyanosis Feet, Tails Left Sided Endocarditis Infarction Peripheral Tissue Pneumonia Broncho Pneumonia Chronic VALVULAR ENDOCARDITIS Chronic |
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Streptococcus suis
Peracute Clinical Signs |
Death PERACUTE
Good Condition |
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Streptococcus suis
Meningitis Pathogenesis |
ENDOTHELIAL INVASION
Blood Brain Barrier Local Inflammation Cytokine Production INCREASED PERMEABILITY of BBB TRANSEDOTHELIAL MIGRATION Neutrophils Monocytes LEAKAGE Plasma Proteins Into Subarachnoid Space CEREBRAL EDEMA Increased Intracranial Pressure Impaired Circulation |
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Streptococcus suis
Sepsis Pathogenesis |
TONSILAR and / or NASAL CAVITY
INVASION HUMORAL IMMUNITY INEFFECTIVE Association with Blood Monocytes Encapsulation Resists Phagocytotic Killing tf Serotype (Capsule) IMPORTANT BACTEREMIA CYTOKINES RELEASED TNf, IL-1, IL-6, IL-8 SEPTIC SHOCK Peracute Death |
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Streptococcus suis
All Forms Diagnosis Pathology |
Cerebellar Vermis Protrusion
Meningial Exudates Subtle Endocarditis Vegatative Pulmonary Edema Hepatic Congestion Chronic Passive Suppurative Bronchopneumonias |
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Streptococcus suis
All Forms Diagnosis |
Clinical Signs
CONVULSIONS Most Suggestive CULTURE Brain, Joints, Parenchymal Organs Lung = NIET SEROTYPES Brain, Joints, Parenchymal Organs Lung = NIET Serology Limited |
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Streptococcus suis
All Forms Treatment |
PROMPT
Recognition and Tx Essential for Meningitis ANTIBIOGRAM MONITORING Resistance Patterns Tetracyclines Most Strains Resistant Antimicrobial Parenteral Bacteriacidal = BEST B-Lactams Antimicrobial Parenteral Bacteriacidal = BEST TMS Anti Inflammatories Parenteral Convulsions Isoflupredone (Predef) Anti Inflammatories Parenteral Convulsions Dexamethazone |
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Streptococcus suis
All Forms Control |
Antimicrobial Water
1st Week, Repeat 2nd Week Penicillin G Most Common PERCIPITATION STRESS FACTORS Control Overcrowding, Ventilation, Sanitation, Temperature, Mixing, Ages Vaccination Injection GENERALLY INEFFECTIVE Vaccination Injection Capsular Specific AB Facilitate Opsonization and Phagocytosis Vaccination Injection Must Be SEROTYPE (CAPSULE) SPECIFIC Vaccination Injection Commerial and Autogenous Do NOT Produce Sufficient Serum IgG Vaccination Injection Multiple Injections Required 4 to 6 Per Pig |
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Streptococcus suis
Zoonosis Significance |
Rare but SEVERE Dz
TYPE 2 Most Common MENINGITIS Septicemia / Bacteremia Endocarditis Cellulitis Arthritis DEAFNESS 50 to 65% of Meningitis Direct Contact with Pigs Most Common Entry through SKIN WOUNDS Hand Washing Effective Disinfectants Effective |
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Glasser's Disease (Porcine Polyserositis and Arthritis)
All Forms Agent |
Haemophilus parasuis
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Glasser's Disease (Porcine Polyserositis and Arthritis)
All Forms Etiology |
Emerging Disease
Has Become Significant Pathogen in Last Decade OUTBREAKS (Naïve Farms) ACUTE EXPLOSIVE SEROTYPES 15 - 4, 5 and 13 Most Common NA SEROTYPES Most Pathogenic UNTYPABLE Normal URT Some Serovars Virulence 5 and 13 Death in 96 Hours 4 Severe Polyserositis and Arthritis |
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Glasser's Disease (Porcine Polyserositis and Arthritis)
All Forms Epidemiology |
EARLY COLONIZATION
Nasal Cavity Healthy Pigs VIRULENCE VARIES with SEROTYPE CROSS PROTECTION POOR Amoung Serotypes INCUBATION ULTRA SHORT 12 - 24 Hours PI MULTIPLE SEROTYPES May Infect a Single Pig |
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Glasser's Disease (Porcine Polyserositis and Arthritis)
Peracute Clinical Signs |
Death PERACUTE
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Glasser's Disease (Porcine Polyserositis and Arthritis)
Acute Clinical Signs |
Convulsions
Recumbancy Joint Swelling and Pain Pyrexia High 40.5 to 42 Anorexia Depression CYANOSIS Edema |
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Glasser's Disease (Porcine Polyserositis and Arthritis)
Chronic Clinical Signs |
Lameness
Coughing Dyspnea WEIGHT LOSS Passive Immunity Wanes |
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Glasser's Disease (Porcine Polyserositis and Arthritis)
All Forms Pathogenesis |
COLONIZES
Nasal Cavity Trachea PURULENT RHINITIS Focal Loss of Cilia Inflammation of Nasal and Tracheal Mucosa SEPTICEMIA Follows Epithelial Invasion PHAGOCYTOSIS IMPEDED BY CAPSULE POLYSEROSITIS FIBRINOSUPPURATIVE DIC Peracute |
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Glasser's Disease (Porcine Polyserositis and Arthritis)
All Forms Diagnosis Pathology |
FIBRINOSUPPURATIVE
Exudates (Bread and Butter Lesions) SEROSAL SURFACE Inflammation Single or Multiple, Peritoneum, Pericardium, Pleura, Articular Surfaces, Meninges Septicemia Occasionally WITHOUT Serosal Inflammation Cellulitis Occasionally WITHOUT Serosal Inflammation Meningitis Occasionally WITHOUT Serosal Inflammation |
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Glasser's Disease (Porcine Polyserositis and Arthritis)
All Forms Diagnosis History |
Mixing Stock,
New Arrivals Especially High Health Herds |
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Glasser's Disease (Porcine Polyserositis and Arthritis)
All Forms Diagnosis CULTURE |
CAN BE DIFFICULT
Fastidious Nature Treated Animals NIET SUBMIT UNTREATED PIGS Best Fresh or Frozen Samples Requirements CO2 Enrichment, Choclate or Blood Agar, Staphylococcal Streak |
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Glasser's Disease (Porcine Polyserositis and Arthritis)
All Forms Diagnosis SEROTYPING |
Capsular AG
Helps Deterimine Virulence of Isolates Many NON Typable SEROTYPE SPECIFIC ELISA Can be Developed for Herd Investigation |
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Glasser's Disease (Porcine Polyserositis and Arthritis)
All Forms Diagnosis PCR (ERIC) |
DNA Finger Printing
Useful to Select Strains for Autogenous Vaccination Genetic Relationships of Multiple Strains Virulence Evaluation NIET |
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Glasser's Disease (Porcine Polyserositis and Arthritis)
All Forms Treatment |
Antimicrobial
Resistance Patterns Change Antimicrobial Generally Sensitive B-Lactams Tetracyclines TMS Antimicrobial Parenteral Early Tx Essential for Sick Animals Prognosis Guarded Antimicrobial Water Prophylaxis Caution Re Lameness, Illness Antimicrobial Feed Prophylaxis Caution Re Lameness, Illness |
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Glasser's Disease (Porcine Polyserositis and Arthritis)
All Forms Control Vaccination Injection |
CROSS PROTECTION
POOR AMOUNG SEROTYPES COMMERCIAL SEROTYPES VARY WITH PRODUCT (4 or 4 and 5) AUTOGENOUS EFFECTIVE SEROTYPES of IMPORTANCE for FARM Maternal AB Important for Young Pigs Protects Against Dz NOT Colonization |
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Swine Erysipelas
All Forms Agent |
Erysipelothrix rhusiopathiae
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Swine Erysipelas
All Forms Etiology |
Servovars 26
Swine Serovars 80% 1 (main) and 2 CARRIERS 30% to 50% of Healthy Swine Tonsil, Lymph Nodes Also Isolated Sheep, Turkeys Fish (tf +/- Feed Contamination) ZOONOTIC POTENTIAL Erysipeloid Skin Lesions DDx Strep Cellulitis Meat Plant, Leather, Rendering |
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Swine Erysipelas
All Forms Epidemiology |
Persistence Environment RESISTANT to DRYING
SUSCEPTABLE DISINFECTANTS Persistence TISSUE (Frozen, Chilled, Carcasses, Feces) MONTHS ALL AGES AFFECTED Acutely Infected Swine SHED PROFUSELY PASSIVE AB PROTECTIVE MATERNAL AB INTERFERENCE May Interfere with Vaccine Induced Active Immunity 90% of Sows Develop Dz 1 Week Pre Farrowing tf High Maternal AB tf Vaccinate AFTER 6 to 8 Weeks Age |
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Swine Erysipelas
Peracute / Acute Clinical Signs |
DEATH PERACUTE
Often Initial Manifistation PYREXIA 41 to 42.5 Depression RELUCTANCE TO MOVE Shifting Weight from Leg to Leg DIAMOND SKIN DZ Localized Hyperemia → Edema (Good Time to Culture) → Piloerection → Cyanosis → Ischemic Necrosis (Too Late to Culture) Acute Ischemic Necrosis Wide Spread Severe Dz |
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Swine Erysipelas
Chronic Arthritis Clinical Signs |
SYNOVITIS
Acutely (4 to 10 Days) Non Suppurative SYNOVIAL PROLIFERATION Fibrinous Exudation Articular Cartilage - Pannus Formation FIBROSIS and DESTRUCTION 3 to 8 Months Lameness Weight Bearing to Non Weigh Bearing |
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Swine Erysipelas
Chronic Endocarditis Pathogenesis |
Vasculitis
MYOCARDIAL INFACRTS BACTERIAL EMBOLI Fibrin Deposition Destruction of Valvular Endocardium ENDOCARDITIS VEGETATIVE VALVULAR |
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Swine Erysipelas
Chronic Endocarditis Clinical Signs |
Death Acute
Cardiac Insufficiency Exercise Intolerance Cyanosis Peripheral Tissue Dyspnea |
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Swine Erysipelas
All Forms Pathogenesis |
INCUBATION
SHORT (36 Hours) ENDOTHELIAL SWELLING (Early Edema) Monocyte Adherence VASCULITIS Systemic THROMBOSIS FIBRINOUS NECROSIS DIAPEDESIS SEPTICEMIA PERACUTE DEATH LOCALIZATION Chronic SKIN, JOINTS, HEART |
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Swine Erysipelas
All Forms Diagnosis Pathology |
VILLONODULAR HYPERTROPHY
Finisher VASCULITIS THROMBOSIS DERMATITIS NECROTIZING (+/- Pale Centre) ENDOCARDITIS VALVULAR Chronic NON SUPPURATIVE ARTHRITIS Chronic Fibrosing Hips, Elbow, Stifle SEPTICEMIA Parenchymal Organs Epicardium Petechial and Ecchymotic Hemorrhage Spleen Enlarged, Congested Kidney Petechial Hemorrhage Liver Turkey Egg Millary Foci |
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Swine Erysipelas
All Forms Diagnosis Culture |
Peracute / Acute
SYSTEMIC SITES Live Animal LN, Liver, Spleen ACUTE SKIN LESIONS (Pink or White NOT Purple) Junctional Biopsy BLOOD CULTURE EDTA Serum Several Septicemic Animals Arthritis Difficult Best = VILLONODULAR SYNOVIAL TISSUE Synovial Fluid Endocarditis Best Yield Culture Lesion |
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Swine Erysipelas
All Forms Treatment |
Antimicrobial Parenteral
Required for OVERT DZ Penicillin G Most Common Tetracyclines RAPID Recovery 12 to 24 Hours for Downers Diagnostic Antimicrobial Water Variable Success Acute Outbreaks +/- Intake via Reluctance to Move Tetracyclines Amoxicillin |
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Swine Erysipelas
All Forms Control |
HYGIENE and SANITATION
Infected Pigs SHED PROFUSELY SUSCEPTIBLE to DISINFECTANTS |
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Swine Erysipelas
All Forms Control Vaccination Injection BREEDING HERD |
Killed Bacterins
Pre Breeding Pre Farrowing |
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Swine Erysipelas
All Forms Control Vaccination Injection FEEDING HERD |
Killed Bacterins
BoosteredVaccination Nursery Early Grower Recommended in Face of Outbreak Poor Efficacy Chronic Dz |
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Swine Erysipelas
All Forms Control Vaccination Oral |
Water System
Live Avirulent NOT Recommended Acute Outbreak |
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Actinobacillus suis
All Forms Etiology |
Endemic
Sporadic Dz Mimics ES and APP |
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Actinobacillus suis
All Forms Epidemiology |
Carriers
Healthy Sows VAGINA Transmission Vertical Possible During Farrowing Transmission Horizontal Main Carriers Healthy Pigs of ANY Age Nasal Cavities Tonsil EARLY COLONIZATION Upper Respiratory Tract Neonates MORTALITY SEPTICEMIA Suckling Pigs Weaned Pigs SEVERITY DECREASES with Age |
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Actinobacillus suis
Peracute / Acute Clinical Signs |
SEPTICEMIA
Multiple Piglets in Litter Suckling, Early Nursery DEATH PERACUTE Grower, Finisher, Adults (Less Common) |
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Actinobacillus suis
Chronic Clinical Signs |
Suckling, Early Nursery
ENDOCARDITIS Mimics Strep suis, Erysipelas SKIN LESIONS Mimics Erysipelas (Occasionally Diamond) Arthritis Pododermatitis Grower, Finisher, Adults (Less Common) PNEUMONIA FOCAL NECROTIZING Mimics APP SKIN LESIONS Mimics Erysipelas, PDNS |
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Actinobacillus suis
All Forms Pathogenesis |
SEPTIC EMBOLI
Systemic Dissemination VASCULAR HEMORRAGE NECROSIS |
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Actinobacillus suis
All Forms Diagnosis Pathology |
SEPTICEMIA
Serofibrinous Effusions Petechial and Ecchymotic Hemorrhages Pleuritis Pericarditis Milary Abscesses Multi Focal White Foci PNEUMONIA Embolic NECROTIZING HEMORRHAGIC SKIN LESIONS Ischemic and Necrotic ENDOCARDITIS Valvular ARTHRITIS |
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Actinobacillus suis
All Forms Diagnosis |
Culture
ESSENTIAL for Confirmation Clinical Signs Pathology Non Specific Serology NIET Immuno Histo Chemistry NIET PCR NIET |
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Actinobacillus suis
All Forms Treatment |
Antimicrobial Parenteral
Penicillin G Tetracyclines Antimicrobial Feed Penicillin G Tetracyclines Antimicrobial Water Penicillin G Tetracyclines |
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Actinobacillus suis
All Forms Control |
Vaccination Injection Commercial NOT Available
Vaccination Injection Autogenous VARIABLE Efficacy |
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PDNS Procine Dermatitis and Nephropathy Syndrome
Epidemiology |
Associated with PCVD and PCVAD Outbreaks
Sporadic in Canada UNTIL 2004 Increased Prevalence via PCVD Differentiate ERYSIPELAS (Skin Lesions), CLASSIC SWINE FEVER (Kidney Lesions), SEPTICEMIAS |
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PDNS Procine Dermatitis and Nephropathy Syndrome
Etiology |
Suggested
PCV2, PRRS, Pasteurella multocida, Streptococcus sp., LPS via Gram -ve, Non Infectious, Environmental Factors |
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PDNS Procine Dermatitis and Nephropathy Syndrome
Pathogenesis |
VASCULITIS Systemic
NECROTIZING SKIN and KIDNEY HYPERSENSITIVITY TYPE 3 IMMUNE COMPLEX DEPOSITION Vascular and Glomerular Capillary Endothelium NEPHRITIS GLOMERULAR |
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PDNS Procine Dermatitis and Nephropathy Syndrome
Clinical Signs |
OLDER Animals Typically
Grower, Finisher, Young Breeding Stock SEVERE to MILD Dz DEATH PERACUTE Pyrexia SKIN LESIONS CYANOTIC DEEPLY SO Smaller, Flat, NO Central Pallor Lameness Anorexia Weight Loss SPONTANEOUS RECOVERY Over Several Weeks Mild Dz |
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PDNS Procine Dermatitis and Nephropathy Syndrome
Diagnosis Pathology Skin |
RED / PURPLE
Round / IRREGULAR COALESCE to Patches NOT Diamond Not Pink or White NO Piloerection Usually Darker than Erysipelas INITIALLY HIND QUARTERS, LIMBS, ABDOMEN Then Spread Cranially Heal over Time (3 to 4 Weeks) |
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PDNS Procine Dermatitis and Nephropathy Syndrome
Diagnosis Pathology Kidney |
ENLARGED
MOTTLED PETECHIAL HEMORRHAGE Subcasular on Cortex Turkey Egg Millary Foci (DDx Lepto, CSF) |
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PDNS Procine Dermatitis and Nephropathy Syndrome
Diagnosis Pathology Systemic |
SEROUS EFFUSIONS
Body Cavities, SC Edema PETECHIAL-ECCHYMOTIC HEMORRHAGES Diffuse LN Enlarged |
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PDNS Procine Dermatitis and Nephropathy Syndrome
Treatment |
NIET
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PDNS Procine Dermatitis and Nephropathy Syndrome
Control |
NIET
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