Swine Respiratory Pathogens

Primary vs. opportunistic swine pathogens

Primary pathogens cause disease alone

Opportunistic bacteria require prior defense damage or stress

Four mechanisms primary pathogens use to enable secondary infection

Damage mucociliary apparatus

Induce immunosuppression

Alter cytokine responses

Impair macrophage function

Most frequently isolated pathogen in ISU-VDL pneumonia cases

Porcine reproductive and respiratory syndrome virus (PRRSV)

Three principles of herd-level PRDC control

Reduce pathogen load

Minimize negative environmental/stress influences

Maximize pig resistance

What are the 3 main primary pathogens of PRDC?

IAV

PRRSV

Mycoplasma hyopneumoniae

Influenza A Virus (IAV) — Persistence Category

Short-cycle: clears in ~7 days

Influenza A Virus (IAV) — Primary Transmission

Direct contact (oronasal secretions) or aerosol within barns

Influenza A Virus (IAV) — Primary Replication Site

Lower respiratory tract epithelium with minimal systemic spread

Deep lung infection

Influenza A Virus (IAV) — Key Factors for Disease

Fully susceptible/seronegative population (nursery pigs or naive older pigs)

Waning maternal antibodies

Co infection worsens disease

Antigenic diversity

Influenza A Virus (IAV) — Virulence Mechanism

HA receptor binding

Reassortment/drift

Host cytokine storm drives pathology (secondary inflammation)

Influenza A Virus (IAV) — Vaccine Limitation

Inactivated vaccines reduce lung disease but do not block nasal shedding or transmission

IAV is analogous to what bovine respiratory disease?

BHV-1/IBR

PRRSV — Persistence Category

Long-cycle: persists in tonsils and lymphoid tissue for up to 100-165 days

PRRSV — Transmission

Direct and long distance aerosol

Fomites

Semen

Transplacental in 3rd trimester

PRRSV — Required Receptor

CD163 on monocyte/macrophage-lineage cells

PRRSV — Primary Sites of Replication

Pulmonary alveolar/intravascular macrophages

Lymphoid tissue macrophages

Fetal thymus/tonsil

PRRSV — Key Factors for Disease

Naive herd/strain mismatch

Young age

Concurrent LPS/co-infection

Host genetics

PRRSV — Virulence Mechanism

Macrophage infection and bystander apoptosis

Type I IFN blockade

Delayed adaptive immunity

PRRSV — Mechanism Impairing Bacterial Clearance

Direct macrophage killing (necrosis/bystander apoptosis) and impaired macrophage bactericidal function

PRRSV — Key Herd-Level Control Methods

Gilt acclimatization

Load-close-expose herd closure

All-in/all-out flow

Strict biosecurity

PRRSV is analogous to what bovine respiratory disease?

BVDV

Mycoplasma hyopneumoniae — Persistence Category

Long cycle

Mycoplasma hyopneumoniae — Transmission

Nose to nose (slow/inefficient)

Long distance aerosol

Mycoplasma hyopneumoniae — Site of Replication

Cilia of ciliated respiratory epithelium in trachea, bronchi, and bronchioles

Mycoplasma hyopneumoniae — Key Factors for Disease

Inoculum size

Strain virulence

Co-infection

Naive replacement gilts

Mycoplasma hyopneumoniae — Virulence Mechanism

Adhesins (P97 family) bind cilia causing ciliostasis, cilia loss, and cytokine dysregulation

IL-10 immune suppression

Mycoplasma hyopneumoniae — Antibiotic Limitations

Inherently resistant to beta-lactams because it lacks a cell wall

Actinobacillus pleuropneumoniae (APP) — Persistence Category

Long cycle

Actinobacillus pleuropneumoniae (APP) — Transmission

Direct/short distance aerosol

Sow to piglet

Actinobacillus pleuropneumoniae (APP) — Primary Colonization Site

Palatine tonsil crypts

Moves to alveoli when respiratory defenses fail

Blood borne

Actinobacillus pleuropneumoniae (APP) — Key Factors for Disease

Ciliary damage from M. hyopneumoniae or viral co-infections

Overcrowding, poor ventilation

Naive/high health status

Actinobacillus pleuropneumoniae (APP) — Dominant Virulence Factors

ApxI/II/III/IV pore-forming RTX exotoxins

Anti-phagocytic capsule

Endotoxic LPS

Neurotoxins

Actinobacillus suis — Persistence Category

Commensal

Actinobacillus suis — Site of Replication

Upper resp tract (tonsil)

Actinobacillus suis primarily affects...

Young/newly populated herds lacking immunity

Actinobacillus suis causes what type of illness?

Mimics Actinobacillus pleuropneumoniae (APP) acute fibrinohemorrhagic pleuropneumonia

Actinobacillus suis — Virulence Mechanism

Apx-like toxins

Adhesins

Glaesserella (Haemophilus) parasuis — Persistence category

Commensal of the normal upper respiratory tract microbiota, colonizing piglets after birth

Glaesserella (Haemophilus) parasuis — Classic Clinical Presentation

Fibrinous polyserositis, polyarthritis, and meningitis following systemic bacterial spread

Glaesserella (Haemophilus) parasuis — Transmission

Sow to piglet intact soon after birth

Mixing/co-mingling

Glaesserella (Haemophilus) parasuis — Site of Replication

Nasal mucosa -> blood -> serial surfaces, joints, meninges

Glaesserella parasuis — Key Triggers for Invasive Disease

Waning maternal immunity, strain mixing, weaning stress, and viral co-infections (PRRSV/PCV2/IAV)

Glaesserella (Haemophilus) parasuis — Virulence Mechanism

Capsule/LOS/VtaA8/9 autotransporters resist macrophage killing -> endothelial invasion -> systemic spread

Pasteurella multocida - Transmission

Nose to nose

Vertical

Occasional aerosol

Pasteurella multocida — Site of Replication

Nasal cavity/tonsil -> lung (pneumonia) or turbinates (atrophic rhinitis)

Pasteurella multocida — Key Factors for Disease

Coinfection

Pasteurella multocida — Virulence Mechanism

PMT toxin - remodels turbinate bone

Capsule and LPS

Pasteurella multocida — Role in Progressive Atrophic Rhinitis (PAR)

Toxigenic strains produce PMT toxin, which stimulates osteoclasts and degrades turbinate bone.

Pasteurella multocida — Common Co-factor for PAR

Prior Bordetella bronchiseptica infection damaging nasal mucosa and facilitating colonization

Pasteurella multocida pneumonia — Diagnostic Significance

Most common secondary bacterial pathogen in PRDC, requiring primary viral/Mycoplasma damage

Streptococcus suis — Persistence Category

Commensal

Streptococcus suis — Transmission

Sow to piglet (vaginal or respiratory) at birth

Aerosol/direct contact

Streptococcus suis — Site of Replication

Tonsil, nasal cavity, genital tract -> blood -> CNS, joints, serosae, heart valves

Streptococcus suis — Key Factors for Disease

Weaning stress

Mixing

PRRSV/PRV/influenza co-infection

Streptococcus suis — Key Virulence Factors

Capsular polysaccharide (CPS), which resists leukocyte phagocytosis

Endothelial invasion and cytokine storm

Streptococcus suis — Clinical Manifestations

Septicemia, meningitis, polyarthritis, endocarditis, and sudden death

Streptococcus suis — Zoonotic Importance

Major cause of adult bacterial meningitis in Southeast Asia; occupational risk via pork/wounds

Commensal Swine Pathogens — General Control Strategy

Manage stress, ventilation, and viral co-infections rather than attempting pathogen elimination

What list of stressors are common across commensal respiratory infections?

Weaning

Mixing

Naive health status

Poor ventilation/temp swings

Viral co-infection

What is the PRDC "gateway" pathogen?

PRRSV

Strep suis most often co-infects with...

PRRSV