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Microbio > Lecture 7 > Flashcards

Lecture 7 Flashcards

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

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)

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)

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)

A

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

24
Q

Endotoxin

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
Q

Steps leading to Fever

A
  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
Q

Pathogenic properties of Fungi

A

Fungal waste products may cause symptoms , chronic infections provoke an allergic response

27
Q

Pathogenic properties of protozoa

A

Protozoan waste products cause symptoms. Avoid host defenses by growing in phagocytes and by antigenic variation

28
Q

Toxins produced by algae

A

Responsible for various types of shellfish poisoning.

29
Q

Hypersensitivity reactions

A

Response to antigens (allergens) that leads to damage to self tissues. They require an initial sensitizing dose

30
Q

Type I Hypersensitivity (Anaphylactic)

A

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
Q

Type II Hypersensitivity reactions (Cytotoxic)

A

Involves IgG or IgM antibodies and complement. Complement activation causes cell lysis or damage by macrophages

32
Q

Hemolytic disease of the newborn

A

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
Q

Type III Hypersensitivity (Immune Complex)

A

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
Q

Type IV Hypersensitivity (Cell-mediated)

A

Delayed type due to Td cells. Cytokines from Td cells attract macrophages and initiate tissue damage
Ex = poison ivy

35
Q

Autoimmune Disease

A

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
Q

Histocompatibility antigens

A

Self antigens on all cells of the body

37
Q

MHC

A

Major histocompatibility complex, genes encoding the histocompatibility antigens

38
Q

HLA

A

Human Leukocyte Antigen complex, MHC genes in humans
specific HLAs can make you more likely to develop an autoimmune disease

39
Q

Transplant Reactions

A

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
Q

Autograft

A

Use of one’s own tissue for a transplant

41
Q

Isograft

A

Use of an identical twin’s tissue for transplant

42
Q

Allograft

A

Use of tissue from another person for transplant

43
Q

Xenograft

A

Use of non-human tissue
Ex = animal tissue , pig heart transplant

44
Q

Graft-versus-host disease

A

Transplanted bone marrow that contains immunocompetent cells can attack the cells of the recipient

45
Q

Prevention of immune response to transplant

A

Immunosuppression helps prevent an unwanted response, suppress IL-2

46
Q

Congenital Immunodeficiency

A

Due to defective or missing genes from birth.
SCID, T and B lymphocytes fail to develop in the bone marrow.
Selective IgA immunodeficiency

47
Q

Acquired Immunodeficiency

A

develop during one’s life due to drugs, cancers, infections.
Ex of natural cause = HIV , kills off the T cells
Artificial = immunosuppression drugs

48
Q

Cancer

A

Cancer cells possess tumor specific antigens
Tc cells recognize and Lyse cancer cells
Cancer cells may lack tumor antigens or kill Tc cells

49
Q

Immunotherapy for Cancer

A

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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