Micro Final

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pathogenicity

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ability to cause disease

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virulence

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degree or extent of pathogenicity

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Portals of entry

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- Mucous membranes.

- Skin.

- Parenteral.

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Most common portals of entry of pathogens

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Gastrointestinal and respiratory mucous membranes.

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The easiest and most frequently used portal of entry

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respiratory tract

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Incubation period for influenza virus

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18-36 hours

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Lectin

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Any protein that binds to a carbohydrate

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M protein

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Found on some cell walls, such as that of Streptococcus pyogenes, that is a strong virulence factor

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Streptokinases

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Extracellular enzymes (exoenzymes) that break down fibrin

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IgA proteases

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destroys IgA

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Siderophores

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Used by bacteria to strip iron from host iron transport proteins

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Toxemia

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Presence of toxins in the blood

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Exotoxins

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Proteins produced by some bacteria that can be either excreted or released by lysis

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Genes for most exotoxins are found where

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on plasmids or prophage DNA

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Antitoxins

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antibodies that bind to toxins

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Toxoids

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exotoxins inactivated by heat, chemicals, or other ways. Used as vaccines.

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Parts of A-B toxins

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B - binding component - gets the other part into the cell.

A - active part - does something bad to cell.

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Leukocydins

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membrane-disrupting toxins that kill white blood cells

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Hemolysins

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toxins that kill red blood cells

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Superantigens

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provoke a very intense immune response. Cause T cells to release massive amounts of cytokines.

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Cytokines

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small protein signalling molecules that stimulate or inhibit many normal cell functions. Secreted by immune system cells and carry signals locally.

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Origin of diptheria toxin

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lysogenic Corynebacteria diptheriae. Toxin found on phage DNA.

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Origin of Botulinum toxin

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Clostridium botulinum

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Origin of Tetanus toxin (tetanospasmin)

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Clostridium tetani

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Genes for the tetanus toxin are found where

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on a plasmid

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Opisthotonis

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Spastic paralysis, such as caused by tetanus

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Origin of cholera toxin

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Vibrio cholerae

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Origin of anthrax toxin

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Bacillus anthracis

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All of these important toxins are _____ toxins

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A-B

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Endotoxins

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lipid A, a part of the LPS in the outer membrane of gram-negative bacteria. Released when they lyse. Stimulate macrophages to release massive amounts of cytokines.

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Septic shock

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shock caused by bacteria

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Cytopathic effects (CPE)

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Visible effects of a viral infection on a host cell

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synctium

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Several adjacent infected cells fuse to form a large multinucleate cell

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Trichothecenes

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Fungal toxins that inhibit protein synthesis in eukaryotic cells

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Innate immunity

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Defenses that are present since birth. Always present and available to provide rapid response.

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First and second lines of defense are part of ____ immunity

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innate

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Adaptive (specific) immunity

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Involves specific recognition of a specific microbe. Third line of defense.

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B cells and T cells are part of the _____ immunity

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adaptive (specific)

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Sebum

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produced by sebaceous glands in the skin, prevents hair from drying and forms a protective film. Lowers pH

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Lysozyme

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Contained in perspiration. breaks down cell walls of gram-positive bacteria, and to a lesser extent gram-negative. Breaks the bonds in peptidoglycan.

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Types of phagocytes

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Neutrophils, eosinophils, monocytes (macrophages)

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Leukocytes

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White blood cells

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Serum

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Blood plasma without clotting factors

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Leukocytosis

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increase in number of WBCs

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Leukopenia

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Decrease in number of WBCs

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A count of more than ______ leukocytes in a microliter of blood is considered a high WBC count

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10,500 leukocytes

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A count less than _______ leukocytes in a microliter of blood is considered a low WBC count

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3,500 leukocytes

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Percentage of each type of WBC in blood

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Neutrophils - 60-70%

Basophils - 0.5-1%

Eosinophils - 2-4%

Monocytes - 3-8%

Lymphocytes - 20-25%

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Neutrophils

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Leukocytes that are highly motile, highly phagocytic, can leave the blood and enter tissues, multilobed nuclei

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Basophils

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Leukocytes that release histamine; important in inflammation and allergic reactions

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Eosinophils

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Leukocytes that are not highly phagocytic, can leave the blood, major function is to produce toxic proteins against certain parasites

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Types of agranulocytes

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Monocytes and lymphocytes (T and B cells)

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Types of granulocytes

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Neutrophils, basophils, eosinophils

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Macrophages are the mature form of

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Monocytes, they mature into them

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Types of lymphocytes

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T and B cells

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Toll-like Receptors (TLRs) recognize

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pathogenic-associated molecular patterns (PAMPs)

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Chemotaxis

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chemical attraction of phagocytes. Can be due to microbial products, components of WBCs, damaged tissue cells, complement peptides

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Opsonization

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coating of microbe with certain serum proteins that promote attachment of the microbe to the phagocyte

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Phagosome

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food vacuole; microbes are ingested by phagocytes in these

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Oxidative burst

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Rapid release of reactive oxygen species by a leukocyte to kill the ingested microbe

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Four signs and symptoms of inflammation

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Redness, pain, heat, swelling

(also loss of function)

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Types of acute-phase proteins

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Complement, cytokines, C-reactive protein (CRP), mannose binding lectin, fibrinogen, kinins for vasodilation

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Edema

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swelling

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margination

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The process of phagocytes sticking to the endothelium of capillaries near where they need to exit into the tissue

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Diapedesis

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Phagocytes squeezing between the epithelial cells of capillaries to get into the tissue

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Histamines

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Released by basophils, mast cells, and activated platelets. Cause vasodilation and increased permeability.

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Prostaglandins

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Components of plasma membranes, released by damaged cells. Lipids, act as hormones. Intensify the effects of histamine and kinins.

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Leukotrienes

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fatty molecules, produced from arachidonic acid by mast cells and basophils. Increase permeability of blood vessels.

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Components of complement system

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- Stimulate release of histamine.

- Attract phagocytes.

- Promote phagocytosis.

- Form membrane attack complexes (MACs).

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Interleukin-1 can act as a

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pyrogen

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Complement

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over 30 proteins produced by the liver and found circulating in the blood and within tissues.

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Names of the parts of complement

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C1 through C9

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Function of C3b

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Enhances phagocytosis by opsonization; binds to the surface of a microbe, binds antibodies to the microbe, receptors on phagocytes bind to it.

Also initiates cytolysis.

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C8 and several C9 molecules join to form a

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membrane attack complex (MAC) forms from them

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C3a and C5a work by

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binding to mast cells, causing release of histamine and other chemicals

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Three methods of complement activation

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- Classical pathway

- Alternative pathway

- Lectin pathway

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Classic pathway of complement activation

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Antibody molecules attach to an antigen.

This activates C1.

C1 activates C4 and C2.

C4 splits into C4a and C4b.

C2 splits into C2a and C2b.

C4b and C2a combine, activating C3.

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Alternative pathway of complement activation

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Doesnt involve antibodies. Involves complement proteins: Factors B, D, and P, they are attracted to microbes, together they activate C3.

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Lectin pathway of complement activation

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When macrophages digest bacteria/viruses they release chemical signals that cause the liver to produce lectins. Mannose binding lectins (MBLs) when bound activate C2 and C4, which activate C3.

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Interferons

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Class of antiviral proteins produced by certain cells after viral stimulation.

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Effect of alpha and beta interferons

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Induce neighboring cells to express genes for antiviral proteins (AVPs)

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Toll like receptors

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Found on the surface of many types of cells, including dendrites and macrophages. Detect certain elements of bacteria. Activate immune response.

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Pathogen-associated molecular patterns (PAMPs)

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Molecules that are distinguishable from host molecules and are detectable by pattern recognition receptors (PRRs) such as TLRs

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Types of antimicrobial peptides (AMPs)

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- Alpha and Beta defensins

- Dermicidin

- Thrombocidin

- Cathelicidins

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Antibodies

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Proteins synthesized in response to antigen

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Humoral immunity

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Immunity brought about by antibodies

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Types of receptors on T cells

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T cell receptors (TCRs)

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Epitope

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region on an antigen with which an antibody interacts

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Hapten

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a molecule that is by itself too small to stimulate antibody formation. Can be combined with a larger carrier molecule to stimulate an immune response.

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Antibody valence

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The number of antigen-binding sites on an antibody. Most are bivalent (2 sites)

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IgG

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Immunoglobulin.80% of all antibodies in serum. Maternal IgG can cross the placenta. Enhances the effectiveness of phagocytic cells. Bivalent monomer.

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IgM

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Immunoglobulin.Makes up 5-10% of serum antibodies. Pentamer, valence of 10. Remains in blood. Effective in aggregating antigens together. Short-lived, appears first in response to infection.

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IgA

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Immunoglobulin.About 10-15% of serum antibodies. By far most common in mucous membranes and secretions. Most abundant immunoglobulin in the body. Monomer in serum; dimer in secretory state.

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Serum IgA is a _______, while secretory IgA is a ______

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Monomer, dimer

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Colostrum

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first milk, heavy in IgA, very important for nursing baby. Mothers should breast feed until age 3.

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IgD

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Immunoglobulin.Little found in blood or lymph. Most found on surface of B cells.

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IgE

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Immunoglobulin. Very little found in blood, but binds tightly to receptors on mast cells and basophils, where it stimulates the release of histamine and other inflammatory chemicals. Important in defense against worms and allergic responses.

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One B cell can have roughly ______ antibodies on its surface

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100,000 antibodies

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T-independent antigen

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Antigen that can activate B cells without added stimulation of helper T cells. Usually polysaccharides or lipopolysaccharides. Weaker response; no memory cells formed.

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Process of activation by T-dependent antigen

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Antibody on the B cell surface binds to the antigen. Antigen is internalized and cleaved. Portions displays on B cell surface in MHC class II. MHC recognized by TCR on helper T cell, which become activated and produces cytokines, which in turn activate the B cell.

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MHC class II

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Major histocompatability complex class II.

Found on B cell surfaces.

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Clonal selection/Clonal deletion

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B cells that respond to self epitopes are removed

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Plasma cells

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Some B cells become these when activated. Secrete antibody.

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Affinity

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strength of an antibody's attachment to antigen

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Ways in which antibodies work against pathogens

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- Agglutination.

- Opsonization.

- Neutralization.

- Antibody-dependent cell-mediated cytotoxicity.

- Activation of complement.

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Agglutination

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Antibodies bind to multiple antigens and clump them together. IgM most effective.

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Antibody-dependent cell-mediated cytotoxicity

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Target cell (often a worm) is coated, and immune system cells gather and team up in its destruction.

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Neutralization by antibodies

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IgG inactivates viruses by binding to them and blocking their attachment to host cells. Can also bind to toxins and block their enzymatic activity.

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M cells

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Microfold cells, found over Peyer's patches in digestive tract. Take up antigens from the lumen and transfer them to lymphocytes.

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GALT

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gut associated lymphoidal tissue

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80% of the weight of the immune system is

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Plasma cells producing IgA

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Antigen presenting cells (APCs)

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Process antigen and present it to T cells. Include activated macrophages and dendritic cells.

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Classes of T cells

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- Helper T cells (Th)

- Cytotoxic T cells (Tc)

- Regulatory T cells (Treg)

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Function of helper T cells

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Recognize specific antigen presented in MHC class II by APCs. Stimulates the APCs to more efficiently phagocytize and present antigen.

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Activated Th cells proliferate and form two populations:

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- Th1 cells release cytokines that activate cellular immunity.

- Th2 cells produce cytokines that stimulate B cells.

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Cytotoxic T cells

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When activated, kills cells that present a specific antigen in MHC Class I (found on all cells in body).

Also kills tumor cells.

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Perforin

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pore-forming protein that Tc cells secrete to kill doomed cells.

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Granzymes

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Secreted by Tc cells, enter the doomed cell and induce apoptosis.

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Dendritic cells are fairly poor at _______, but good at ________

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Poor at phagocytizing, but good at presenting antigens

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Naturak Killer cells

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Agranulocytes, can destroy virus-infected cells and tumor cells, can attack parasites, not immunologically specific. Kills cells that are not displaying the correct MHC class I.

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Interleukins (IL)

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Cytokines that communicate between WBCs

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Chemokines

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Cytokines that act as chemical attractants for chemotaxis

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Immunological memory - primary response (first exposure to antigen), peaks

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peaks in about 10-17 days, then declines gradually

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Immunological memory - secondary response (second exposure to antigen), peaks

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peaks in 2-7 days, lasts many days

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naturally acquired active immunity

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Person becomes ill and the recovers.

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Naturally acquired passive immunity

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Natural transfer of antibodies from mother to infant. IgG across placenta. IgA in milk.

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Artificially acquired active immunity

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Vaccination; immunization. Introduction of weakened antigen.

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Artificially acquired passive immunity

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Injection of antibodies from an animal or person that is already immune to the disease.

Antiserum. Short-lived.

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Variolation

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A technique long used in China, where scabs from infected person were crushed and blown into the nose of another.

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Edward Jenner

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Discovered from milk maids the effectiveness of vaccination.

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Vaccination

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Activates a primary immune response, leading to the formation of antibodies and memory cells. Later encounters with the pathogen will result in a swift, intense secondary response.

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Attenuated vaccines

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Live vaccines. The virus is still alive and can reproduce, but it cant cause disease anymore. Induces both humoral and cellular immunity.

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Inactivated killed vaccines

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The pathogen has been killed, usually by formalin or phenol. Safer than live vaccines, but induces mostly only humoral immunity.

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Subunit vaccines

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Antigenic fragments of microbe used to vaccinate.

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Toxoid vaccines

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Inactivated toxins. Serum antibodies against a toxin.

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Conjugated vaccines

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Polysaccharide capsular molecules combined with proteins such as diptheria or tetanus toxoid.

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Adjuvant

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substance that enhances the immune response of antigen. Only accepted one in US right now is aluminum hydroxide.

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Diseases caused by fusobacterium

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Periodontal disease, Lemierre's syndrome, and topical skin ulcers.