# Presentation: 475464

## 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”**

## Slide 3

## 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**

## Slide 5

## 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 103****0****-105****0**
**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 pneumoniaBacterial (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

## Slide 43