Pathogenesis of Pertussis (Whooping cough or 100 days cough)

Transmission by Droplets of Bordetella pertussis (Causative Agent) The Bordetella adheres to epithelial surface Multiply or Colonize The Gram Negative Bacteria Coco Bacilli Produces toxins and substances that irritate surface cells Dermonecrotic Toxin Vascular Smooth Muscle Contraction and Ischemic Necrosis Damage to epithelial Cells Adenylate cyclase toxin Increase cAMP Intracellularly
Impairs the bactericidal effects of immune effector cells

Filamentous Hemagutinin Mediates Adhesion to Ciliated Epithelial Cells Increase Adhesion of bacteria to the epithelial cells Damage the cells Pretactin- Proteins that enhances adhesion

Pertussis Toxin

Tracheal Cytotoxin Inhibit the DNA synthesis of Cilia Promotes Ciliastasis Causes Respiratory epithelial damage

Activates the Human T lymphocytes Lymphocytosis in the blood

Promotes sensitization to histamine Signs and symptoms of Hypersensitivity

Absence of Fever

Fimbriae- doesnt affect the adhesion

Destroyed Mucociliary Clearance Increase Accumulation of mucus in the respiratory tract

Pertussis Toxinblock immune effectors cells function

CYA is activated by calmodulin, it catalyzes the production of excessive amount of cAMP from ATP. Irritates the pulmonary irritatnt receptors Violent Cough

FHA is thought to be the major colonizing factor for B. pertussis as it promotes attachment to the upper respiratory tract and the trachea

Produces Mucous Plugs

Seizures

Impaire gas exchange in the aveoli

Produce alveolar collapse in some parts Atelectasis

Decrease Oxygen to the brain

Hypoxemia

Acidosis

3 stages of Pertussis 1.) Catarrhal stage 2.) Paroxysmal Stage 3.) Convalescent Stage