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Infection
2006Dr. Nasser Rizk
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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:1- Causative agent 2- reservoir 3-port of transmission
4-susceptible host
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Risk Factors
• 1-Weak defense mechanisms• 2- Enviromemental factors• 3- Developmental factors• -----------------------• Weak Defense mechanisms:1. Immunodeficiency or Immunocompromise2. Impaired WBCs and low level of T and B cells
(immunodeficiency)3. May be congenital (before or at birth) or
acquired (after birth)4. body’s ability to recognize and fight pathogens
is impaired
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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 pregnancy
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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)
conditions
Poor hygiene
Chronic diseases
Inadequate immunization
Treatment
stressors
Inadequate barrier
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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
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Components of the chain of infection
• Agents: • Bacteria, Viruses, • Fungi, Parasites,
Mycoplasma, • Ricketessia, Chlamydia
• Reservoir:• Microbes can survive• E.g., humans, animals , etc
6 components
Causative agents
Reservoir
Portal of Exit
Mode of Transmission
Portal of Entry
Susceptible host
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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 transmissionMeans from portal of exit to host4 modes: chart 3Vector- born: flea, mosquito
(tropical)
Mode of transmission
Contact Droplet Airborne Enteric
Chart 3
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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.
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Pathophysiologic changes• Characteristic changes:Prodromal stage1- Fever2- Muscle aches3- Headache4- LethargyAcute stages:Moe specific symptoms
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Inflammation• A major reactive defense mechanism
against infective agents. • It may result from: 1- tissue injury 2- infection 3- allergy• Stages:• 1- Vascular 2- CellularVascular: arterioles constrict then dilate--------edemaCellular: inflamm. Cells release histamine---edemaWhich dilute microbes
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Signs and Symptoms of Inflammation
• Redness
• Heat
• Pain
• Edema
• Loss of function
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Five classic local signs of acute inflammation
These were known– Heat– Redness– Swelling– Pain– Loss of function
by the Romans– Calor– Rubor– Tumor– Dolor– Functio laesa
Added Later
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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
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Alerts!!
• 1- Localized infections:
• produce rapid inflammatory response
• Obvious symptoms and signs
• 2- Disseminated infections:
• Slow inflammatory response
• Long time for treatment
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• 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
Inflammation
EXUDATE
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Fever
• 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.
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Leukocytosis• 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
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Chronic inflammation
• Infection longer than 2 weeks
• May occur after acute Inflammation
• Permanganate scarring and loss of function may occur
• E.g., Mycobacterium tuberculosis
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Diagnosis• 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
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TreatmentTreatment• 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.
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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
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Acute inflammation major components
• Vasodilatation
• Endothelial permeability
• Extravasation of pmn’s
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Vascular changes you need to know this
• Vasodilation (forget the few seconds of vasoconstriction)
• Exudation of protein rich fluid
• Blood stasis
• Margination
• Emigration/Transmigration
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Vascular changes you need to know this
• Vasodilation (forget the few seconds of vasoconstriction)
• Exudation of protein rich fluid
• Blood stasis
• Margination
• Emigration/Transmigration
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Fig 2.1 Graphic of
Acute Inflammation
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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
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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
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Fig 2.2 Graphic
of Vascular Changes
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How do endothelial cellsbecome leaky?
• Endothelial cell contraction
• Junctional retraction
• Direct endothelial injury (immediate sustained response)
• Leukocyte-dependent endothelial injury
• Increased transcytosis of fluid
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Direct endothelial injury (immediate sustained response)
• Endothelial cell necrosis and detachment• Result of severe injury or burn• Occurs immediately and lasts until vessel
repaired
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• Occurs at sites of leukocyte accumulation
• Due to leukocyte activation which releases proteolytic enzymes and toxic oxygen
Leukocyte-dependent endothelial injury
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Leukocyte Cellular Events
• Margination and Rolling
• Adhesion and Transmigration
• Migration into interstitial tissue
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Fig 2.4
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Margination
• 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”
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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
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Selectins
• 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)
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Chemotaxis
• Movement toward the site of injury along a chemical gradient– Chemotactic Factors include
• Complement components• Arachadonic Acid (AA) metabolites• Soluble bacterial products• Chemokines
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Leukocyte Activation
• Chemokines also “activate” PMN’s– AA metabolite production– Degranulation and Secretion of lysosomal
enzymes– Oxidative burst– Modulation of adhesion molecules
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Phagocytosis & Degranulation
• Phagocytosis (to eat and destroy)– Attach– Engulf– Kill
• Degranulation and the oxidative burst destroy the engulfed particle
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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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Normal Lung
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Pneumonia
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Pneumonia
Another picture of the same thing…At a higher power!