PATHOPHYSIOLOGY

Predisposing Factors: Age Sex

Precipitating Factors: Post infection to

Campylobacter jejuni Poor Hygiene Stress Diet Lifestyle

Campylobacter jejuni

Enters the body by the use of multifenestrated cells or other mechanisms

Innate immune response results in the uptake of the pathogens by immature antigen presenting cells

Migration to lymph nodes, a mature, differentiated antigen presenting cell can present in major histocompatibility complex molecules and activate CD4 T cells that recognize antigens from the infectious pathogen.

Antibodies will be produced, leading to activation of the complement system and phagocytosis of the bacteria

B cells can be activated as well by newly activated Th2 cells. This produces a cell mediated and humoral response against the pathogen

Pathogen and host have homologous or identical amino acid sequences, antigens in its capsule are shared with nerves

Immune responses directed against the capsular components produce antibodies that cross-react with myelin

Molecular mimicry

Lymphocytes and macrophages circulate in the blood and eventually find myelin

Defects in the propagation of electrical nerve impulses, with eventual conduction block

lymphocytic infiltration of spinal roots and peripheral nerves, followed by macrophage-mediated, multifocal stripping of myelin and axonal damage.

If Treated: If not treated:

Acute progressive ascending weakness

lower limbs upper limbs hyporeflexia

Dull aching pains of lower back, flank, proximal legs

Guillain-Barré syndrome

Sensory changesParesthesias or numbness in feet/hands

Cranial nerve involvementFacial droop

Dysarthria Dysphagia Difficulty with

protruding tongue

Plasma Exchange intravenous

immune globulin (IVIG)/

Physical therapy and exercise

medication

Good prognosis

Extensive axonal destruction

Weakening of the diaphragm and the respiratory muscles

Ascending weakness progresses

Respiratory distress syndrome

Respiratory arrest

Shock

DEATH

BAD PROGNOSIS