Causative Agent

Transmission

Enter the bloodstream

Release of bacterial cell wall components Endotoxin ( Lipopolysaccharide) Substance release from pathogen and damaged tissues Leukocyte Activation (macrophage & mononuclear cells) Brings transcriptional changes Exotoxins (Peptoglycans)

Regulate adhesion molecules on the vascular endothelium

Regulate Production

Pro inflammatory Cytokines (TNF, INF, IL6)

Antiinflammatory Cytokines (IL10, IL8)

Activation of complement pathway

Generate C3B

Neutrophils

Production C5A

Production C3A & C4A

Coats Pathogen Opsonization Activated Neutrophils

Arresting and Activating rolling Neutrophils in the vascular wall Decreased expression of B2 integrins in Neonatal Vascular Space Continues rolling along the vascular wall Inability to adhere to vascular endothelium Move to site of injury Does not change shape Phagocytes C3b coated organisms Inability to pass between endothelial cells

Degranulation of mast cells

Contraction of Smooth Muscle

Change Shape

Increased permeability of vascular endothelium

Pass through vessel wall Allow activated cells to move out of the vessels

Poor transmigration of Neutrophils and chemotaxis

Lack of localization of infection

Bloodstream infection

Circulation

Cross Blood Brain Barrier (BBB)

Via circumventricular vascular organs known as organum vascolosum laminae terminalis

Hypothalamic Endothelium

Arachidonic Acid Pathway PGE2

Cyclic AMP

Inhibited

Sympathetic Nervous System

Activation

Stimulate Sweat Glands Evaporation Loss

Vasoconstriction of Skin Vessels

Shivering Center Activation

Increased Muscle Heat Production Secretion of Neurotransmitter Increased Cell Metabolism Heat Production

Heat Conservation

Catalyzed by the microsomal enzyme heme oxygenase

biliverdin

Cytosolic enzyme reductase

bilirubin

Unconjugated (not soluble) Free Bound to serum Indirecyt albumin

Deposit in Skin Pigment

Oxidation Reaction HEME

Cross BBB

Travels Liver

Kernicterus

Hemoglobin Phagocytosed by Macrophages

Increased Lysis or degradation

Glucuronic Acid

Brain Damage

Conjugated (water soluble) GLOBIN Protein degraded into amino acids Catalyzed by Uridine diphosphate glucorynyl transferase (UDGPT)

Excreted from Liver

Urobilinogen

Intestinal Bacteria

Biliary duct & Cystic duct as part of bile

Stercobilinogen

Oxidized Stercobilin

Reabsorbed by Transported in the intestinal cells blood

Passed out in feces

Kidney

Urobilin

Passed out in the urine

ATP disruption (dependent resting membrane potential)

Na+ flow into neuron

K+ flow out of neuron

Increased released of Glutamate

Burst of electrical activity from the cortex Long lasting depolarization of the neuronal cell membrane

Alteration in the integrity of neuronal cell membrane

Discharges of electrochemical energy

Nerve cells fire an increased in frequency and amplitude of impulse

Continuous impulse

Increased intensity of discharges

Spread to adjacent normal neurons Blocking of normal inhibition

Perpetuate a feedback loop (threshold)

AURA (a premonitory or warning sensation; it can be visual, auditory or olfactory

Inhibitory neurons in the cortex, anterior thalamus & basal ganglia slow the neuronal firing Produce an intermittent contraction relaxation phase at the muscle fibers Continuous stimulation of impulses throughout the body Continuous muscle contraction (TONIC) Exhaustion of the epileptic neurons (CLONIC)

Building of inhibitory process

Depresses CNS