pathological diagnosis of mycoplasmosis in swine swine mycoplasma pneumonia workshop fda / cvm march...
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Pathological Diagnosis of Mycoplasmosis in Swine
Swine Mycoplasma Pneumonia Workshop
FDA / CVM
March 6,7 of 2002
Kansas City, MO
Kent Schwartz
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Swine Pneumonia: Early Years• “Normal” for pigs to cough / scratch
• Enzootic (Mycoplasma + Pasteurella)
• Ascarid Migration
• 1918: H1N1 Swine Influenza
• Atrophic rhinitis (Bordetella and Pasteurella)
• Small farms / “home remedies”
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Mechanization: Trend to Confinement and Larger Herds
• M hyo, SIV, ascarids, AR
• More science, agents, diagnostics– PRV, Actinobacillus pleuropneumonia– Pasteurella multocida with M hyo
• Age of therapeutics (antimicrobials)
• “Vaccination” products
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Era of Altered Ecology/New Agents
• Segregated rearing / larger populations / Altered herd immunity / altered ecology
• M hyo, SIV, App remain• Bacterial “Opportunists” Emerge
– Hemophilus parasuis, Streptococcus suis– Actinobacillus suis, Salmonella sp. others
• “New” agents; respiratory and systemic– PRRSV, PCV, SIV H3N2, PRCV
• Porcine Respiratory Disease Complex (PRDC) is a multifactorial culmination
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“Immune Confusion” • Respiratory Tract: mixing vessel for:
– Systemic diseases (PRRSV, PCV, bacteria) – Respiratory agents (SIV, bacteria) – M hyo
• “Herd immunity” is variable for agents– Sow herd “stability” influences maternal
immunity– Piglet infection status variable and sequential– Immune status is variable
• Many permutations of agents involved • Many permutations in sequence of
infections and sequence may matter
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M hyo remains Central and Primary
• Infection is common; not easily eliminated• Infection persists for months• Alters mechanical clearance of debris• Inflammation / immune-mediated damage• Altered, nonproductive immune response• “Immunologically privileged” site of
infection so clearance is compromised • Provides sites for opportunists• Synergy with other lung pathogens
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Clinical Disease: M hyo alone
• Mild malaise
• No fever
• Cough: nonproductive / chronic
• Moderate morbidity / no mortality
• Altered growth performance– ADG– Feed efficiency
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Enzootic pneumonia=M hyo + bacteria
• M hyo facilitates bacterial infections• Cough, malaise and anorexia• Moderate fevers 1030-1050
• Expiratory dyspnea / “thump”• Variable morbidity and mortality• Stunting, chronic pneumonia, death• Strategic interventions (medication or
vaccination) can influence outcome and/or subsequent disease severity
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PRDC = Enzootic pneumonia + virus(M hyo + bacteria + virus)
• Severe depression, high fever, anorexia
• Expiratory dyspnea (thump)
• Rapid loss of condition
• Medication less efficacious
• High morbidity and frequently high mortality (5-20%)
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Gross Pathology:
• Bronchopneumonia– Cranioventral, firm, exudate in airways
• Interstitial pneumonia– Diffuse, mottled, lobular distribution– Edema fluid in airways
• Both can occur simultaneously: common in field cases of PRDC
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Normal Lung: Gross
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Actinobacillus pleuropneumniae
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Bronchogenic pneumoniaBacterial (B. bronchiseptica)
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Interstitial pneumonia(Viral, bacterial septicemia)
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M hyo: mild and “early”
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Early / mild M hyo.
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SIV can be cranioventral
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Lesion is not pathognomonic
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Enzootic: Mhyo + P. multocida
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PRDC: Enzootic + viral(M hyo + P. multocida + PRRSV)
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PRDC: Mhyo + P. multocida + PRRSV
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Enzootic: Can resolve over time
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Enzootic: Resolution takes time
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M hyo: Gross Diagnosis
• Early: 10 days-4 weeks – Cranioventral, lobular, red, firmness
• Active: 2-6 weeks– Clearly demarcated, grayish, atelectasis– Airways prominent with mucopus
• Resolution: 5-20 weeks – Gray fissures of atelectasis– Distorted lobe structure of normal lung tissue
• A population will have animals at all stages of disease with variable severity
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Histopathology: Basics• Bronchopneumonia
– Extends from small airways– Bronchiolitis with exudate and debris– Adjacent alveoli, interstitium
• Interstitial pneumonia– extends from alveolar septae– can involve small airways
• Both often present in chronic disease or in mixed infections.
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Histopathology is Fallible• Agents and agent combinations
outnumber possible responses
• Chronic lesions are less specific
• “Classic” lesions only with single agents at some stages of disease
• Few lesions are pathognomonic or “etiologically specific”
• “Lesions are compatible with….”
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M hyo: Histopathological Diagnosis
• Early: 10 days-4 weeks – peribronchiolar lymphohistiocytic
inflammation; scattered neutrophils
• Active: 2-12 weeks– mucopus, atelectasis
• Resolution: 5-20 weeks – BALT hyperplasia
• A population will have animals at all stages of disease with variation in lesion severity
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What else can “look” like M hyo ?
• Chronic persistence of antigen/agent– Lymphoid hyperplasia / airway cuffs– Subacute SIV = Early M hyo– Ascarid migration; resolving– Chronic bacterial pneumonia– Chronic viral pneumonia
• It is often difficult to demonstrate organisms in chronic lesions
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Mh IHC
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M. hyopneumoniae: IFA
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M. hyopneumoniae: Histopathology
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M hyo: BALT hyperplasia
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Key Points: Pathological Diagnosis
• Gross lesions are “compatible with but not specific for” M hyo
• Microscopic lesions are “compatible with but are not specific for” M hyo
• Sensitivity and Specificity of pathology??• Most field cases are mixed infections
– M hyo, bacteria, viruses• Time for resolution varies with:
– Severity and extent of initial lesion– Presence of concurrent pathogens
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Etiologic diagnosis requires:• Demonstration of specific agent
– M hyo isolation is not routine
• Demonstration of specific antigen– IHC, FAT, ELISA
• Demonstration of specific agent nucleic acid– PCR and PCR based assays
• Serology confirms antibody but is NOT a definitive etiologic diagnosis
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Diagnosis of Swine Pneumonia• Research / Infection models
– controlled infection, controlled specimen collection, and standardized evaluations
– Predictable outcomes / valid measures
• Field Cases: variability is uncontrolled– Descriptive pathology has limitations– Demonstrate agents: specimen dependant
• age, stage, specimens, interventions
– Interpret results in the context of clinical signs, history and population dynamics
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An accurate and useful field diagnosis uses all available information
• Clinical signs, history, diagnostic records• Production records• Compatible gross lesions• Compatible microscopic lesions• Identify agents with appropriate tests
– Primary agents, secondary agents– Define epidemiology in the population
• Serologic: cross-sectional or longitudinal– In population, infection and immunity status
varies so need statistical sampling techniques
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Mixed agents, duration, population variability makes definitive diagnosis a challenge
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Diagnostic profiles change over time
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Summary: M hyo in swine• M hyo is common in swine populations• M hyo alone is mild disease with cough,
suppression of growth and feed efficiency• M hyo duration of effect (3-20 weeks)
creates opportunities for co-infections• Not all are affected equally/simultaneously• Enzootic pneumonia is M hyo + bacteria• PRDC is M hyo + bacteria + viruses
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Summary: M hyo in swine• Takes time for lesions to develop / resolve• Pathology is useful to describe severity• Variability of lesion severity in populations • Most field cases are mixed infections• Field measures of current interventions
– Reduced prevalence of clinical pneumonia– Reduced lesion prevalence and severity– Reduced medication cost, treatments– Less variation in growth rate
• Control of M hyo disease severity often does mitigate severity of other endemic diseases
• Infection models are useful to evaluate M hyo intervention strategies and disease interactions
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