Term
| Defense again infective organisms |
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Definition
1-/ Scavenger cells such as neutropils arrive early at the site of infection but survive only a few days.
2-/ The complement system circulating proteins attach the microbial invaders, leading to their destruction.
3-/ Macrophages engulf foreign matter and signal other immune cell to attach invaders.
4-/ Macrophage display antigens from ingested invaders, which activate helper T cells.
5-/ Helper T cells multiply and activate B cells and macrophages.
6-/ B cells divided and form plasma cells which produce antibodies.
7-/ Antibodies bind to invaders, either destroying them or making them more vulnerable to macrophages
8-/ Killer T cells form and destroy foreign invaders.
9-/ Regulatory T cells slow or stop the immune response once the foreign invader is defeated.
10-/ Some B and T cell becomes memory cells which can quickly mount a defense if the same invader attach again. |
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Term
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Definition
| Macrophages, Mast cells, Neutrophils, Dendritic cells |
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Term
| Characteristics of Innate Immune Response |
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Definition
• Immediately available
•No selection
•No memory
•Response to common structureson invading organisms: PAMPs
• PRRs |
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Term
| Characteristics of Adaptive immune Response |
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Definition
•T and B lymphocytes
•Antigen recognition
•Clonal selection of Ab-producing B cells
•4-7 days for full reponse |
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Term
| Defense against bacterial infection— |
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Definition
| Pathogen Recognition, Antibody Recognition, Opsonization, Complement Activation, Engulfment |
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Term
| Bacterium Opsonization is done by: |
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Definition
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Term
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Definition
| Pathogen-Associated Molecular Paterns |
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Term
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Definition
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Term
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Definition
| Pattern recogn.Receptors [PRRs], leading to adherence |
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Term
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Definition
| Function is to Tag bacteria |
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Term
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Definition
| Two types, Toll-Like Receptors [TLRs]) and Dectins |
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Term
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Definition
| lipids and lipoproteins on gram negative (LPS) and gram positive bacteria (Lipoteichoic acid), and viral/microbial RNA or DNA. |
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Term
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Definition
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Term
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Definition
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Term
| Intracellular PRRs: RLRs and NLRs recognize |
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Definition
oligonucleotides of viral
pathogens as well as stress signals—Damage-associated molecular patterns(DAMPS) |
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Term
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Definition
-T-helper immune response and antibody production
-activate secretion of Mannose Binding Lectins (MBLs) (opsonins) |
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Term
| Innate immune responses can activate adaptive immune responses |
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Definition
Breakdown of bacteria in phagosomes releases peptides that are used forantibody production through the Major Histocompatibility Complex II
(MHCII) |
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Term
| TLRs 3, 7, 8 and 9 recognize |
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Definition
oligonucleotides of
viruses/bacteria, are located in endosomes, and initiate
IFN-α response |
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Term
| Bacterial Virulence and Infectivity : |
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Definition
Bacteria must have iron to multiply
– Siderophores (iron receptors)
Presence of polysaccharide capsules
Suppression of complement activation
Bacterial proliferation rates can surpass protective response |
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Term
| Acute inflammatory response to infection |
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Definition
—presentation of PAMPs to PRRs.Eradication of the pathogen
Reversible collateral tissue damage
Resolution/repair phase
Restoration of normal tissue homeostasis. |
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Term
| Chronic inflammatory disease |
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Definition
Nonimmune pathophysiologic process
Production of damage-associated molecularpatterns (DAMPs).
Amplification by cytokines and chemokines. Non-resolving inflammation
Tissue damage
The inflammatory response –More DAMPS
Positive feedback loop. |
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Term
| Tissue responses to invading organisms: |
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Definition
Vasodilation, Vascular
Leakiness, and Exudation |
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Term
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Definition
-Functions to activate and assist inflammatory cells
-Causes dilation of blood vessels, pain, smooth muscle contraction, vascularpermeability, and leukocyte chemotaxis |
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Term
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Definition
| bradykinin (Factor XII+connective tiss enzymes—Kallikreinformation—Kininogen to Kinin ) |
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Term
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Definition
| Movement o motile cells or organism or part of one. |
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Term
| Complement C5a and C3a cause |
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Definition
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Term
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Definition
| Histamine, cytokines TNFα, IL’s, Leukotrienes, Plateletactivating factor, prostaglandins |
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Term
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Definition
| Mass of cells or substance that has speeded out of blood vessel or an organ. |
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Term
| Serous exudate –Watery exudate: |
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Definition
| indicates early inflammation |
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Term
| Fibrinous exudate –Thick, clotted exudate |
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Definition
| indicates more advanced inflammation |
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Term
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Definition
| indicates a bacterial infection— Leukocyte emigration |
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Term
| Hemorrhagic exudate – Exudate contains blood |
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Definition
| indicates bleeding through damaged vascular wall |
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Term
| Coagulation (clotting) system: |
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Definition
-Forms a fibrinous meshwork at an injured or inflamed site
-Prevents the spread of infection
-Keeps microorganisms and foreign bodies at the site of greatest --inflammatory cell activity
-Forms a clot that stops bleeding
-Provides a framework for repair and healing
-Main substance is fibrin |
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Term
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Definition
-Inflammation lasting 2 weeks or longer
-Often related to an unsuccessful acute inflammatory response |
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Term
| Other causes of chronic inflammation |
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Definition
-High lipid and wax content of a microorganism
-Ability to survive inside the macrophage
-Toxins
-Chemicals, particulate matter, or physical irritants |
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Term
| Characteristics of Chronic Inflammation |
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Definition
Dense infiltration of lymphocytes and macrophages
Granuloma formation
Epithelioid cell formation
Giant cell formation |
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Term
| Systemic Manifestations of Inflammation - Fever |
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Definition
-Caused by exogenous and endogenous pyrogens
-Act directly on the hypothalamus |
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Term
| Systemic Manifestations of Inflammation-Leukocytosis |
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Definition
| Increased numbers of circulating leukocytes |
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Term
Systemic Manifestations of Inflammation-Increased plasma protein synthesis
•Acute-phase reactants |
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Definition
C-reactive protein, fibrinogen,
haptoglobin, amyloid, ceruloplasmin,etc. |
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Term
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Definition
– Presence of bacteria in the blood due to a failure of the
body’s defense mechanisms
– Characteristic of gram-negative bacteria
– Toxins released in the blood cause the release of vasoactive peptides and cytokines that produce widespread
vasodilation |
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Term
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Definition
Enzymes released during growth causing specific responses (Choleratoxin, Botulinum toxin, Hemolysis, Diphtheria toxin, Pertussis toxin
-Immunogenic
-Antitoxin production |
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Term
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Definition
Lipopolysaccharides contained in the cell walls of gram-negative organisms
Pyrogenic effects |
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Term
| Anaphylatoxins Strong chemotactic factors are: |
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Definition
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Term
| Countermeasures for chronic, refractory wounds and infections—diabetic wounds |
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Definition
| Hyperbaric Oxygen therapy |
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Term
| Drug Therapy Countermeasures-Antimicrobials |
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Definition
-Inhibit synthesis of cell wall
– Damage cytoplasmic membrane
– Alter metabolism of nucleic acids
– Inhibit protein synthesis
– Modify energy metabolism |
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Term
| Fungal Infection and Injury |
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Definition
-Large microorganisms with thick cell walls
-Eukaryotes
-Exist as single-celled yeasts, multi-cellular molds, or both Pathogenicity
-Adapt to host environment
-Wide temperature variations, digest keratin, low
oxygen
-Suppress the immune defenses |
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Term
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Definition
Diseases caused by fungi
Superficial, deep, or opportunistic |
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Term
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Definition
-The diseases they produce are called tineas (ringworm)
Tinea capitis, tinea pedis, and tinea cruris |
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Term
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Definition
| life threatening and commonly opportunistic |
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Term
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Definition
—Infective Proteins; Transmissible neurodegenerative diseases
PrPsc and PdPc;
Creutzfeldt-Jakob disease;
BSE—bovine spongiform encephalopathy (mad cow disease) |
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Term
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Definition
slightly larger than virus; intracellular infection;
capsule; contain RNA and DNA same as bacteria; prokaryotes; no need forintermediate host |
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Term
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Definition
| similar to chlamydia except for need for intermediatehost, e.g., ticks |
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Term
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Definition
| prokaryotes; independently replicating; no peptidoglycan cell wall |
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Term
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Definition
| prokaryotes; similar to gram negative bacteria |
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Term
| Gram- Positive Bacteria Cell Wall Structure and Variation |
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Definition
-The cell wall is composed of thick layer of murein through which antibiotics , nutrients and was products can diffuse.
-It has lipoteichoic acid in the outer leaflet of the cytoplasmic membrane.
-The hydrophilic molecules side chains of this molecules are involved in bacteria adherence, feeding and evasion of the host immune system. |
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Term
| Gram Negative Cell Wall Structure and Variation |
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Definition
-It has thinner murein layer, and it is surrounded by a second, outer lipid bilayer membrane.
-Hydrophilic molecules cross this outer membrane through channels of pore proteins (porins)
-It has LPS in the outer membrane, and LPS is a major antigen for the immune response to gram negative organism. |
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Term
| Mycobacteria Cell Wall Structure and Variation |
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Definition
-It has the causative agent of tuberculosis and Leprosy.
-It is analogous to Gram Negative bacteria.
-The main differences between mycobacteria and Gram Negative bacteria is that in Mycobacteria, the two leaflets of the outer membrane are asymmetric in size and composition.
-The inner leaflet of the outer membrane is composed of arabinogalactant and mycolic acids, whereas the outer leaflet is composed of extractable phospholipids. |
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Term
Bacteria reproduce asexually by celldivision; they exchange DNA
through the process of : |
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Definition
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Term
| ―Sexual‖ RecombinationF+ to F- bacteria is called: |
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Definition
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Term
Bacteria harbor circular DNA
structures that independently
replicate and can be passed to other cells; these are called: |
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Definition
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Term
partial DNA transfer
through bacterial transduction by |
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Definition
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Term
| Infant botulism results from : |
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Definition
| the absorption of heat-labile neurotoxin produced in situ by ingested Clostridium botulinum |
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Term
| Clinical manifestations of infant botulism are owing to: |
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Definition
| progressive neuromuscular blockade, initially of muscles innervated by cranial nerves and later of the trunk, extremities and diaphragm |
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Term
Clostridium botulinum is an age-limited neuromuscular disease that is distinct from classic botulism in that the
toxin is : |
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Definition
| elaborated by the organism in the infant’s intestinal lumen and is then absorbed. |
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Term
| The most potent neurotoxin known is: |
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Definition
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Term
| Infant botulism results from : |
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Definition
| the in vivo production of toxin by Clostridium botulinum after it hascolonized the infant's gut. |
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Term
| The known ubiquitous distribution of C. botulinum is |
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Definition
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Term
| Stages of Infection In tems of the infective organism |
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Definition
Colonization
Invasion
Multiplication
Spread |
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Term
| Stages of Infection In terms of the disease state: |
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Definition
Infection initiation—Incubation period
Prodromal
Acute
Convalescent
Resolution |
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