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Infection. 2006 Dr. Nasser Rizk. Infection. Invasion and multiplication of microorganisms inside body producing S&S and immune response. Severity of infection depends on : 1- Pathogenicity 2- number 3- host defenses Transmission of infection needs:

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Dr. Nasser Rizk

  • Invasion and multiplication of microorganisms inside body producing S&S and immune response.
  • Severity of infection depends on :

1- Pathogenicity 2- number 3- host defenses

  • Transmission of infection needs:

1- Causative agent 2- reservoir 3-port of transmission 4-susceptible host

risk factors
Risk Factors
  • 1-Weak defense mechanisms
  • 2- Enviromemental factors
  • 3- Developmental factors
  • -----------------------
  • Weak Defense mechanisms:
  • Immunodeficiency or Immunocompromise
  • Impaired WBCs and low level of T and B cells (immunodeficiency)
  • May be congenital (before or at birth) or acquired (after birth)
  • body’s ability to recognize and fight pathogens is impaired
risk factors continued
Risk Factors (continued)
  • Conditions which suppress immune Response:

1-Diabetes mellitus

2 –Renal failure

3- Liver cirrhosis

4- Steroids

5-Immunosuppresive drugs (transplantation)

6- Chemotherapy.

Acquired immune suppression in:

stress malnutrition infections


2 enviromemental factors
2- Enviromemental factors
  • Conditions weaken a person immune defense are:

1- Poor hygiene

2- Malnutrition

3- Inadequate barriers

4- Stressors

5- Chronic diseases

6- Inadequate treatment

7-Inadeqaute immunization

Dust facilities transport of pathogens,

e.g., Aspergillus, (lung)

3 developmental factors
3- Developmental factors
  • Children and old age at high risk.
  • Children : immune system is not fully developed (6 months)
  • most common: respiratory infections
  • Exposure to communicable diseases is high in care- centers and schools.
  • Old age: decline in immune system
  • DM and atherosclerosis: weak delivery of nutrients by impaired blood flow to organs
components of the chain of infection
Components of the chain of infection
  • Agents:
  • Bacteria, Viruses,
  • Fungi, Parasites, Mycoplasma,
  • Ricketessia, Chlamydia
  • Reservoir:
  • Microbes can survive
  • E.g., humans, animals , etc
components continued
Components (continued)
  • Portal of exit (entry):
  • infectious agent leave (enter) the organism
  • Respiratory, genitourinary, GIT, skin, Mucus membranes, and placenta.
  • Secretions as : blood, sputum, emesis, stools, urine, wound drainage and genital secretions act as portal.

Mode of transmission

Means from portal of exit to host

4 modes: chart 3

Vector- born: flea, mosquito (tropical)

Chart 3

stages of infection
Stages of infection
  • 1- Incubation:

replication, transmission.

  • 2-Prodromal stage:

vague complaint, transmission.

  • 3- Acute illness:

microbes destroy host cells, affecting systems.

  • 4- Convalescent stage:

body defense take over the microbe, healing.

pathophysiologic changes
Pathophysiologic changes
  • Characteristic changes:

Prodromal stage

1- Fever

2- Muscle aches

3- Headache

4- Lethargy

Acute stages:

Moe specific symptoms

  • A major reactive defense mechanism against infective agents.
  • It may result from:

1- tissue injury 2- infection 3- allergy

  • Stages:
  • 1- Vascular 2- Cellular


arterioles constrict then dilate--------edema


inflamm. Cells release histamine---edema

Which dilute microbes

signs and symptoms of inflammation
Signs and Symptoms of Inflammation
  • Redness
  • Heat
  • Pain
  • Edema
  • Loss of function
five classic local signs of acute inflammation
These were known





Loss of function

by the Romans





Functio laesa

Five classic local signs of acute inflammation

Added Later

five classic local signs of acute inflammation1
Five classic local signs of acute inflammation
  • The major components responsible for these local signs are
    • Heat - vasodilatation
    • Redness - vasodilatation
    • Swelling - vascular permeability
    • Pain - mediator release/pmn’s
    • Loss of function - mediator release/pmn’s
Alerts !!
  • 1- Localized infections:
  • produce rapid inflammatory response
  • Obvious symptoms and signs
  • 2- Disseminated infections:
  • Slow inflammatory response
  • Long time for treatment
  • Acute - minutes to days
    • Characterized by fluid and protein
    • PMN’s
  • Chronic - weeks to years
    • Lymphocytes and macrophages
  • ACUTE Inf - PMN’s (Polymorphonuclear Cells)
  • CHRONIC Inf - Mononuclear Cells


  • After introduction of infectious agent
  • Elevated temperature helps to fight infection
  • Many organisms can’t survive
  • Diaphoresis is the method of cooling down
  • Improve immune system rspone.
  • Body’s response to introduction of pathogens; WBCs increases
  • Neutrophils count increases, with increase immature cells “bands”, but not function
  • Neutrophils, monocytes, and macrophages begin phagocytosis of dead tissues and bacteria
  • They identify the foreign antigen and kill the microbe
  • Elevated count of WBCs is common; N in acute stages and Monocytes during resolution or chronic stages
chronic inflammation
Chronic inflammation
  • Infection longer than 2 weeks
  • May occur after acute Inflammation
  • Permanganate scarring and loss of function may occur
  • E.g., Mycobacterium tuberculosis
  • Medical history
  • Examination
  • Investigations-tests
  • WBCs and CBC (first test)
  • ESR: increased, inflammatory response
  • Gram stain, silver stains
  • Culture- sensitivity tests
  • MRI to locate infection sites
  • Chest X-ray (lung)
  • Gallium scan for abscess detection
  • Vary widely
  • Use vaccines----1ry immune response
  • Drugs when appropriate
  • Supportive therapy
  • Antibiotics, antiviral, antifungal-----
  • Overuse of medication----resistance
  • Proper prevention of epidemic and pandemic transmission.
acute inflammation
Acute inflammation
  • The immediate and early response to injury
  • The point? Get the pmn’s to the site as fast as possible
  • Vasodilatation
  • Endothelial permeability
  • Extravasation of pmn’s
acute inflammation major components
Acute inflammation major components
  • Vasodilatation
  • Endothelial permeability
  • Extravasation of pmn’s
vascular changes you need to know this
Vascular changes you need to know this
  • Vasodilation (forget the few seconds of vasoconstriction)
  • Exudation of protein rich fluid
  • Blood stasis
  • Margination
  • Emigration/Transmigration
vascular changes you need to know this1
Vascular changes you need to know this
  • Vasodilation (forget the few seconds of vasoconstriction)
  • Exudation of protein rich fluid
  • Blood stasis
  • Margination
  • Emigration/Transmigration
vascular permeability
Vascular permeability
  • Vasodilation, increased blood flow
  • Increased intravascular hydrostatic pressure
  • Transudate - ultrafiltrate blood plasma (contains little protein)
    • Again, this is very transient and just gets the process started. Think Acute Inflammation, think EXUDATE
  • Increased vascular permeability
vascular permeability1
Vascular permeability
  • Exudate - (protein-rich with pmn’s)
    • Exudate is the characteristic fluid of acute inflammation
  • Intravascular osmotic pressure decreases
  • Osmotic pressure of interstitial fluid increases
  • Outflow of water and ions - edema
how do endothelial cells become leaky
How do endothelial cellsbecome leaky?
  • Endothelial cell contraction
  • Junctional retraction
  • Direct endothelial injury (immediate sustained response)
  • Leukocyte-dependent endothelial injury
  • Increased transcytosis of fluid
direct endothelial injury immediate sustained response
Direct endothelial injury (immediate sustained response)
  • Endothelial cell necrosis and detachment
  • Result of severe injury or burn
  • Occurs immediately and lasts until vessel repaired
leukocyte dependent endothelial injury
Leukocyte-dependent endothelial injury
  • Occurs at sites of leukocyte accumulation
  • Due to leukocyte activation which releases proteolytic enzymes and toxic oxygen
leukocyte cellular events
Leukocyte Cellular Events
  • Margination and Rolling
  • Adhesion and Transmigration
  • Migration into interstitial tissue
  • Normal flow - RBC’s and WBC’s flow in the center of the vessel
  • A cell poor plasma is flowing adjacent to endothelium
  • As blood flow slows, WBC’s collect along the endothelium
  • This is “Margination”
endothelial activation
Endothelial Activation
  • The underlying stimulus causes release of mediators which activate the endothelium causing selectins and other mediators to be moved quickly to the surface
  • Selectins bind selected sugars
    • Selected + Lectins (sugars) = Selectins
  • Some selectins are present on endothelial cells (E-Selectin)
  • Some selectins are present on leukocytes (L-Selectin)
  • Some selectins are present on platelets (P-Selectin)
  • Movement toward the site of injury along a chemical gradient
    • Chemotactic Factors include
      • Complement components
      • Arachadonic Acid (AA) metabolites
      • Soluble bacterial products
      • Chemokines
leukocyte activation
Leukocyte Activation
  • Chemokines also “activate” PMN’s
    • AA metabolite production
    • Degranulation and Secretion of lysosomal enzymes
    • Oxidative burst
    • Modulation of adhesion molecules
phagocytosis degranulation
Phagocytosis & Degranulation
  • Phagocytosis (to eat and destroy)
    • Attach
    • Engulf
    • Kill
  • Degranulation and the oxidative burst destroy the engulfed particle
leukocyte induced tissue injury
Leukocyte-induced tissue injury
  • Lysosomal enzymes are released into the extracellular space during phagocytosis causing cell injury and matrix degradation
  • Activated leukocytes release reactive oxygen species and products of arachidonic acid metabolism which can injure tissue and endothelial cells
  • These events underlie many human diseases (e.g. Rheumatoid arthritis)

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