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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. Swine Pneumonia: Early Years. “Normal” for pigs to cough / scratch Enzootic (Mycoplasma + Pasteurella) Ascarid Migration

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pathological diagnosis of mycoplasmosis in swine

Pathological Diagnosis of Mycoplasmosis in Swine

Swine Mycoplasma Pneumonia Workshop


March 6,7 of 2002

Kansas City, MO

Kent Schwartz

swine pneumonia early years
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”
mechanization trend to confinement and larger herds
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
era of altered ecology new agents
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
  • Porcine Respiratory Disease Complex (PRDC) is a multifactorial culmination
immune confusion
“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
m hyo remains central and primary
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
clinical disease m hyo alone
Clinical Disease: M hyo alone
  • Mild malaise
  • No fever
  • Cough: nonproductive / chronic
  • Moderate morbidity / no mortality
  • Altered growth performance
    • ADG
    • Feed efficiency
enzootic pneumonia m hyo bacteria
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
prdc enzootic pneumonia virus m hyo bacteria virus
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%)
gross pathology
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
m hyo gross diagnosis
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
histopathology basics
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.
histopathology is fallible
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….”
m hyo histopathological diagnosis
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
what else can look like m hyo
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
key points pathological diagnosis
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
etiologic diagnosis requires
Etiologic diagnosis requires:
  • Demonstration of specific agent
    • M hyo isolation is not routine
  • Demonstration of specific antigen
  • Demonstration of specific agent nucleic acid
    • PCR and PCR based assays
  • Serology confirms antibody but is NOT a definitive etiologic diagnosis
diagnosis of swine pneumonia
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
an accurate and useful field diagnosis uses all available information
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
summary m hyo in swine
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
summary m hyo in swine42
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