Chapter 15 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

portals of entry

A
mucous membrane
  -gastrointestinal tract 
  -respiratory tract 
  - genitourinary tract 
skin
parenteral route
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4
Q

preferred portal of entry

A

organisms can enter more than one way but many do not cause disease unless they enter the preferred portal of entry

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5
Q

numbers of invading microbes

A
  • ID50- infectious dose of 50% of test population
  • LD50- lethal dose (of a toxin) for 50% of the test population
  • wide variation from one kind of pathogen to another
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6
Q

Bacillus Anthracis

A

portal of enter

  • skin- (ID50)- 10-50 endospores
  • inhalation (ID50)- 10,000-20,000 endospores
  • ingestion (ID50)- 250,000-1,000,000 endospores
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7
Q

Adherence/ ligands

A
  • bind to receptors on host cells
  • attachment is necessary step in pathogenicity; non-pathogens can have attachment molecules
  • adhesions located on cells glycocalyx, pili, fimbriae or flagella
  • adhesions made of glycoproteins and lipoproteins
  • receptors on host cells are usually sugars
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8
Q

adherence examples

A
  • glycocalyx: Streptocouccs mutans
  • Fimbriae: Escherichia coli
  • M protein: Streptococcus pyogenes
  • Opa protein : Neisseria gonorrhoeae
  • Tapered end: Treponema
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9
Q

Biofilms (adherence)

A
  • communities of microbes that live together in masses on a surface
    • produce extracellular products such as polysaccharides to hold the microbes together
    • biofilms are much more organized than appear
      • channels for nutrients and oxygen to penetrate
      • cell to cell communication-quorum sensing
      • 1000x more resistant to biocides than individual cells because of the extracellular materials
      • very important in pathogenicity
      • 65% of infections may involve biofilms; catheters commonly involved
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10
Q

Extracellular enzymes (factors that make pathogens invasive: enzymes)

A

help bacteria invade tissues (exoenzymes)

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11
Q

Coagulase (factors that make pathogens invasive: Enzymes)

A

Coagulate (clot) fibrinogen of blood

-Staphylococcus aureus may produce; helps wall of boils

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12
Q

Kinases (factors that make pathogens invasive: enzymes)

A

digest fibrin clots

-some Staphylococcus and Streptococcus produce

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13
Q

Hyaluronidase (factors that make pathogens invasive: enzymes)

A
  • hydrolyses hyaluronic acid which holds certain cells of the body together
    • gas gangrene caused by Clostridium
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14
Q

Collagenase (Factors that make pathogens invasive: enzymes)

A
hydrolyzes collagen (forms the connective tissue of muscles)
    -several species of Clostridium which are involved in gas gangrene
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15
Q

IgA proteases (factors that make pathogens invasive)

A

enzymes produced by the bacteria which destroy IgA antibodies that would attack the bacteria

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16
Q

Siderophores (factors that make pathogens invasive)

A

take iron from iron-binding proteins and make available for bacteria

17
Q

Antigenic variation (factors that make pathogens invasive)

A

pathogen alters surface proteins so that the host antibodies aren’t effective
- influenzavirus; Neisseria gonorrhoeae

18
Q

Capsules (factors that make pathogens invasive)

A

they help the bacterial cell avoid being engulfed by certain immune cells

- host immune cells engulf invading bacteria (phagocytosis) and destroy them inside the immune cell    - capsule prevents the immune cell from attaching and engulfing bacteria
19
Q

invasions (penetration into the host cell)

A
  • produced by certain microbes when they come in contact with host cell membrane
    • E. coli strains and Salmonella strains
    • cause cell membrane to “ruffle” which is due to cytoskeleton being disrupted
    • bacteria can enter cell
20
Q

toxin

A

substances that contribute to pathogenicity

21
Q

toxigenicity

A

ability to produce a toxin

22
Q

toxemia

A

presence of toxin in the host’s blood

23
Q

toxoid

A

inactivated toxin used in a vaccine

24
Q

antitoxin

A

antibodies against a specific toxin

25
Q

exotoxin

A
  • source: gram +
  • relation to microbe: By-products of growing cell
  • chemistry: protein
  • fever- no
  • neutralized by antitoxin- yes
  • LD50- small (bad that its a small amount)
  • specific for a structure or function in host cell
  • genes for toxin may be introduced into bacterial cell by a lysogenic phage; only those strains with lysogenic phage produce the toxin
26
Q

3 types of Exotoxins

A
  1. A-B toxins - most common type
    - two types: A-enzyme component, B- attachment component
    ex: diphtheria toxin
  2. Membrane-disrupting toxins
    - lyse hosts cell by:
    • making protein channels in pm
      • ex: leukocidins- kill phagocytic white BC & hemolysins- kill RBC
    • disrupting phospholipid bilayer
  3. Superantigens
    - cause an intense immune response due to release of cytokines from host cells
    - fever, nausea, vomiting, diarrhea, shock and death
    - ex: staphylococcal food poisoning exotoxin
27
Q

endotoxins

A
  • source: gram -
  • relation to microbe- present in LPS of outer membrane
  • chemistry- lipid
  • fever- yes
  • neutralized by antitoxin- no
  • LD50- relatively large

-mechanism by which endotoxin in the gram neg cell causes a fever response in humans. macrophage is a type of WBC

28
Q

endotoxin (figure slide 24)

A
  • fever response (pyrogenic response)
    • gram neg bacterium ingested by macrophage
    • bacteria degraded in vacuole inside macrophage and the lipopolysaccharide (LPS) layer of cell wall is released; this causes the macrophage to release interleukin- 1 (IL-1)
  • IL-1 is carried by blood to hypothalamus of brain (controls body temp)
  • IL-1 causes hypothalamus to reset the body temp to higher temp –> fever
29
Q

endotoxins cont.

A
  • not destroyed by autoclaving temp
  • can have dead bacterial cells and still have LPS from cell wall which will cause fever response
  • drugs, injection materials and medical devices need to be LPS free
  • LAL test- limulus amoebocyte lysate test- rapid test detect the presence of LAL in pharmaceutical products
30
Q

cytopathic effects of viruses

A
  • vary with the type of virus
  • may stop cell division
  • may produce inclusion bodies
  • may cause cells to fuse together to produce large cell with multiple nuclei
  • may affect cells so that they no longer stop dividing when they touch each other (contact inhibition) and keep on dividing to form a mass of cells
31
Q

pathogenic properties of fungi

A
  • fungal waste products may cause symptoms
  • chronic infections provoke an allergic response
  • tichothecene toxins produced by molds growing in a house or on grain inhibit protein synthesis
    • ingesting the toxins causes chills, fever, nausea and vomiting
    • Fusarium; Stachybotrys
32
Q

aflatoxin

A

toxins produced by some Aspergillus growing under specific conditions; toxic if eaten

33
Q

mycotoxins

A

neurotoxins; may be quite potent

34
Q

portals of exit

A
  • respiratory tract
    • coughing and sneezing
  • gastrointestinal tract
    • feces and saliva
  • genitourinary tract
    • urine and vaginal secretions
  • skin
  • blood
    • biting arthropods and needles or syringes