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Microbio > Lecture 7 > Flashcards

Lecture 7 Flashcards

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1
Q

Pathogenicity

A

The ability to cause disease

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2
Q

Virulence

A

The extent of pathogenicity

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3
Q

The Portals of Entry

A

Mucous membranes, skin, parenteral route (deposition directly into tissues beneath the skin and mucous membranes)

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4
Q

The portals of exit

A

Respiratory tract (coughing,sneezing), Gastrointestinal tract (feces, saliva) , Genitourinary tract (urine, vaginal/urethral secretions) , Skin (exfoliation) , Blood (biting arthropods, needles/syringes)

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5
Q

ID50

A

Infectious dose for 50% of the population

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6
Q

LD50

A

Lethal dose of a toxin for 50% of the population

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7
Q

Adherence

A

Adhesions/ligands bind to receptors on host cells

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8
Q

Coagulase

A

Coagulate blood

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9
Q

Kinases

A

Digest fibrin clots

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10
Q

Hyaluronidasae

A

Hydrolyses hyaluronic acid

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11
Q

Collagenase

A

Hydrolyses collagen

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12
Q

IgA proteases

A

Destroy IgA antibodies

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13
Q

Siderophores

A

Take iron from host iron-binding proteins

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14
Q

Antigenic variation

A

Alter surface proteins

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15
Q

Toxin

A

Substance that contributes to pathogenicity

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16
Q

Toxigenicity

A

Ability to produce a toxin

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17
Q

Toxemia

A

Presence of toxin in host’s blood

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18
Q

Toxoid

A

Inactivated toxin used in a vaccine

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19
Q

Antitoxin

A

Antibodies against a specific toxin

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20
Q

Exotoxins

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A

Are proteins produced inside mostly gram + bacteria as part of their growth and metabolism. They are secreted and released following lysis of the cell. They are neutralized by antitoxin and have a low LD50

21
Q

A-B Toxins (Type III toxin)

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A

These are exotoxins that have A (active) and B (binding) components. The B part binds to a host cell receptor and enters the cell. The A part alters cell function by inhibiting protein synthesis.
Ex = Corynebacterium Diphtheriae, Clostridium botulinum, C. Tetani, Vibrio cholerae

22
Q

Superantigens (Type I toxins)

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A

Cause an intense immune response due to release of cytokines from host cells CYTOKINE STORM Symptoms include fever, nausea, vomiting, diarrhea, shock, and death
Ex = Staphylococcus aureus

23
Q

Membrane-disrupting (Type II Toxins)

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A

Lyse host cells by making protein channels in the plasma membranes and disrupting the phospholipid bilayer
Ex = Streptococcus pyogenes

24
Q

Endotoxin

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A

Part of the LPS of the outer membrane (lipid A) of GRAM NEGATIVE bacteria. They are released when the bacteria dies and the cell wall breaks apart. Induce fever, are not neutralized by antitoxin, large LD50

25
Steps leading to Fever
1. Macrophage ingests a gram neg bacterium 2. The bacterium is degraded in a vacuole, releasing endotoxins that induce the macrophage to produce interleukin-1 (IL-1) 3. IL-1 is released into the bloodstream through which it travels to the hypothalamus 4. IL-1 induces hypothalamus to produce prostaglandins which reset the body’s “thermostat” to a higher temp than normal, producing the fever
26
Pathogenic properties of Fungi
Fungal waste products may cause symptoms , chronic infections provoke an allergic response
27
Pathogenic properties of protozoa
Protozoan waste products cause symptoms. Avoid host defenses by growing in phagocytes and by antigenic variation
28
Toxins produced by algae
Responsible for various types of shellfish poisoning.
29
Hypersensitivity reactions
Response to antigens (allergens) that leads to damage to self tissues. They require an initial sensitizing dose
30
Type I Hypersensitivity (Anaphylactic)
Involves IgE antibodies. Localized response causes hives (wheal/flare) or asthma (spasms of bronchial tubes) from contact with or inhaled antigens Systemic Response = antigen travels through the bloodstream throughout the body causing widespread vasodilation and in severe cases shock
31
Type II Hypersensitivity reactions (Cytotoxic)
Involves IgG or IgM antibodies and complement. Complement activation causes cell lysis or damage by macrophages
32
Hemolytic disease of the newborn
Caused when an Rh - mother carries an Rh + child. If she is exposed to the fetal blood during childbirth, she will develop Rh antibodies. If she carries another Rh + child, her antibodies can cross the placenta and agglutinate the fetal blood
33
Type III Hypersensitivity (Immune Complex)
IgG antibodies and antigens form complexes that lodge in basement membranes. This activates complement and attracts inflammatory cells such as neutrophils. Enzymes released from degranulation of inflammatory cells cause damage to endothelial cells of the basement membrane of blood vessel
34
Type IV Hypersensitivity (Cell-mediated)
Delayed type due to Td cells. Cytokines from Td cells attract macrophages and initiate tissue damage Ex = poison ivy
35
Autoimmune Disease
Loss of self tolerance. Clonal deletion during fetal development ensures self-tolerance. If autoimmune disease is present from birth it is a Primary AD, all others are Secondary ADs.
36
Histocompatibility antigens
Self antigens on all cells of the body
37
MHC
Major histocompatibility complex, genes encoding the histocompatibility antigens
38
HLA
Human Leukocyte Antigen complex, MHC genes in humans specific HLAs can make you more likely to develop an autoimmune disease
39
Transplant Reactions
Transplants may be attacked by T cells, macrophages, and complement fixing antibodies. Transplants to “privileged sites” like cartilage of the ear or the cornea (no blood supply) do not cause an immune response.
40
Autograft
Use of one’s own tissue for a transplant
41
Isograft
Use of an identical twin’s tissue for transplant
42
Allograft
Use of tissue from another person for transplant
43
Xenograft
Use of non-human tissue Ex = animal tissue , pig heart transplant
44
Graft-versus-host disease
Transplanted bone marrow that contains immunocompetent cells can attack the cells of the recipient
45
Prevention of immune response to transplant
Immunosuppression helps prevent an unwanted response, suppress IL-2
46
Congenital Immunodeficiency
Due to defective or missing genes from birth. SCID, T and B lymphocytes fail to develop in the bone marrow. Selective IgA immunodeficiency
47
Acquired Immunodeficiency
develop during one’s life due to drugs, cancers, infections. Ex of natural cause = HIV , kills off the T cells Artificial = immunosuppression drugs
48
Cancer
Cancer cells possess tumor specific antigens Tc cells recognize and Lyse cancer cells Cancer cells may lack tumor antigens or kill Tc cells
49
Immunotherapy for Cancer
Tumor necrosis factor, IL-2, and interferons may kill cancer cells Immunotoxins link poisons with a monoclonal antibody directed at a tumor antigen Vaccines that contain tumor-specific antigens can be administered

Microbio (14 decks)

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