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Pathological Diagnosis of Mycoplasmosis in Swine PowerPoint PPT Presentation


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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

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

  • 1918: H1N1 Swine Influenza

  • Atrophic rhinitis (Bordetella and Pasteurella)

  • Small farms / “home remedies”


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

  • 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


“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

  • 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

  • Mild malaise

  • No fever

  • Cough: nonproductive / chronic

  • Moderate morbidity / no mortality

  • Altered growth performance

    • ADG

    • Feed efficiency


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)

  • 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:

  • 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


Normal Lung: Gross


Actinobacillus pleuropneumniae


Bronchogenic pneumoniaBacterial (B. bronchiseptica)


Interstitial pneumonia(Viral, bacterial septicemia)


M hyo: mild and “early”


Early / mild M hyo.


SIV can be cranioventral


Lesion is not pathognomonic


Enzootic: Mhyo + P. multocida


PRDC: Enzootic + viral(M hyo + P. multocida + PRRSV)


PRDC: Mhyo + P. multocida + PRRSV


Enzootic: Can resolve over time


Enzootic: Resolution takes time


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

  • 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

  • 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

  • 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 ?

  • 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


Mh IHC


M. hyopneumoniae: IFA


M. hyopneumoniae: Histopathology


M hyo: BALT hyperplasia


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:

  • 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


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

  • 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


Mixed agents, duration, population variability makes definitive diagnosis a challenge


Diagnostic profiles change over time


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 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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