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MICROPARA LEC > BACTERIAL MECHANISMS OF PATHOGENICITY > Flashcards

BACTERIAL MECHANISMS OF PATHOGENICITY Flashcards

Lesson 6

1
Q

the ability to cause disease by overcoming host defenses

A

pathogenicity

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2
Q

the degree of pathogenicity

A

virulence

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3
Q

PORTALS OF ENTRY

A

Mucous Membranes
- respiratory tract
- gastrointestinal tract
- genitourinary tract
- conjunctiva

Skin
Parenteral Route

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4
Q
  • epithelium lining the respiratory tract, GIT,GUT, and conjunctiva
  • mostly through:
    1. GIT
    2. respiratory tract– easiest and most frequent
A

MUCOUS MEMBRANES

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5
Q
  • unbroken skin – impenetrable by most microorganisms
  • e.g.,:
  • through openings in the skin e.g., hair follicles and sweat gland ducts
  • hookworm –bore through intact skin
  • fungi – grow on keratin in skin or infect skin itself
A

SKIN

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6
Q
  • direct deposition into tissues beneath the skin or into mucous membranes
    whenpenetrated orinjured
  • e.g., punctures, injections, bites, cuts, wounds, surgery, and splitting of the
    skin or mucous membrane due to swelling or drying
A

PARENTERAL

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7
Q

NUMBER OF INVADING MICROBES

A
  • ID50
  • LD50
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8
Q

ADHERENCE FACTORS

A

Streptococcus mutans
Actinomyces
Enteropathogenic Escherichia coli
Neisseriae gonerrhoeae
Treponema pallidum
Staphylococcus aureus
Streptococcus pyogenes

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9
Q

– bind surface receptors (usually mannose) on the cells of certain host tissues

A

Adhesins/Ligands

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10
Q

converts fibrinogen to fibrin that coagulates the blood to protect bacteria from phagocytosis and defenses
e.g. Staphylococcus

A

Coagulase

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11
Q

breaks down fibrin and digests clots

  • Fibrinolysin/streptokinase –produced by Streptococcus pyogenes
A

Kinase

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12
Q

hydrolyzes hyaluronic acid, which holds together cells in connective tissues

e.g. streptococci and Clostridium perfringens

A

Hyaluronidase

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13
Q

breaks down collagen in connective tissues
e.g. Clostridium perfringens

A

Collagenase

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14
Q

destroys IgA
e.g. Neisseria gonorrhoeae and Neisseria meningitidis

A

IgA protease

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15
Q
  • prevents phagocytic cells from adhering to the bacterium
  • can induce antibody production and subsequent opsonization
  • Some Killers Have Pretty Nice Capsules
A

CAPSULE

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16
Q
  • a heat-resistant and acid-resistant protein produced by Streptococcus pyogenes
  • mediates attachment of bacterium to host epithelial cells and helps resist phagocytosis
A

M PROTEIN

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17
Q
  • waxy lipid that makes up the cell wall of Mycobacterium tuberculosis
  • resists digestion by phagocytes, and allow bacterial multiplication inside phagocytes
A

MYCOLIC ACID

18
Q

an aggregate of interactive bacteria attached to a solid surface or to each other and
encased in an exopolysaccharide matrix

A

BIOFILMS

19
Q

BIOFILMS

A
  1. Enhance adherence
  2. Resist disinfectants and antibiotics
  3. Resist phagocytosis
    * Phagocytes do not move through
    the viscous carbohydrates of biofilms.
    * The EPS of Pseudomonas aeruginosa kills phagocytes.
  4. Shield antigens
20
Q
  • process bywhich pathogenscanalter surfaceantigens
  • By the time the body mounts an adaptive immune response against a
    pathogen, the pathogen has already altered its antigens and is unaffected
    by the antibodies.
  • e.g. Neisseria gonorrhoeae, Borrelia recurrentis
A

ANTIGENIC VARIATION

21
Q
  • M.tuberculosis, L. monocytogenes, Brucella species, Legionella species
  • live and grow in the hostile environment within PMNs, macrophages, or
    monocytes
  • may avoid entry into phagolysosomes and live within the cytosol of the
    phagocyte
  • maypreventphagosome–lysosomefusionandlive within the phagosome
  • may be resistant to lysosomal enzymes and survive within the
    phagolysosome
  • can live within nonphagocytic cells
A

INTRACELLULAR PATHOGENICITY

22
Q
  • take the iron awayfromiron-transport proteins (e.g. lactoferrin, transferrin,
    ferritin, hemoglobin) by binding the iron even more tightly
  • iron-siderophore complexes are taken up by siderophore receptors on the
    bacterial surface into the bacterium
A

SIDEROPHORES: USING THE HOST’s
NUTRIENTS

23
Q
  • e.g., E. coli, Shigella, Salmonella, Neisseria gonorrhoeae
  • can induce host epithelial cells to engulf them similarly to phagocytosis
  • cause cells to rupture
A

DIRECT DAMAGE

24
Q
  • poisonous substances that are produced by certain microorganisms
  • often the primary factor contributing to pathogenicity
A

TOXINS

25
Q

capacity to produce toxins

A

Toxigenicity

26
Q

presence of toxins in the blood

A

Toxemia

27
Q

caused by the presence of a toxin; not by microbial growth

A

Intoxication

28
Q

2 types of toxins:

A
  • Endotoxins
  • Exotoxins
29
Q
  • part of bacterial cells, not a metabolic product
  • released during bacterial multiplication and when gram-(-) bacteria undergo lysis
  • lipid A portion of LPS in the outer membrane
  • producedbygram-(-) bacteria
  • general and universal effects (fever, weakness, generalized aches, leukopenia,
    hypoglycemia, disseminated intravascular coagulation [DIC], sometimes shock
    andevendeath)
  • do not promote the formation of effective antitoxins (which actually enhance the
    effect of toxins)
A

ENDOTOXINS

30
Q
  • a sensitive test to identify the presence of endotoxins in drugs, medical
    devices, and body fluids
  • a.k.a. LimulusAmebocyte Lysate (LAL)Assay
  • The hemolymph (blood) of the horseshoe crab, Limulus polyphemus,
    contains white blood cells called amebocytes, which have large amounts
    of aprotein (lysate) that causes clotting.
  • In the presence of endotoxin, amebocytes in the crab hemolymph lyse
    andliberate clotting proteins.
  • Agel-clot (precipitate) is a positive test for the presence of endotoxin.
A

BACTERIAL ENDOTOXIN TEST

31
Q
  • producedinside a bacterium aspart of growth andmetabolism
  • secreted into the outside medium orreleased following lysis
  • proteins
  • producedbygram-(+) orgram-(-) bacteria
  • highly specific effects
  • among the most lethal substances known
  • soluble in body fluids and can easily diffuse into the blood and are rapidly
    transported
  • carried by genes on bacterial plasmids or phages
A

EXOTOXINS

32
Q
  • E.g.,:
  • Botulism
  • Staphylococcal foodpoisoning
  • Antitoxins– antibodies that provide immunity to exotoxins.
  • Toxoids
  • exotoxins inactivated by heat or by formaldehyde, iodine, or other
    chemicals
  • used as vaccines to induce immunity (antitoxin production), but not cause
    disease
  • e.g. diphtheria, tetanus
A

EXOTOXINS

33
Q

NAMING EXOTOXINS

A

Based on type of cells attacked:
Based on disease caused:
Based on bacterial source:

34
Q

TYPES OF EXOTOXINS

A

A-B TOXINS
MEMBRANE-DISRUPTING TOXINS
SUPERANTIGENS

35
Q
  • 2 polypeptides
  • A: enzyme component (toxic)
  • B: binding component
  • e.g. Corynebacterium diphtheriae
A

A-B TOXINS

36
Q

cause lysis of host cells by disrupting
their plasma membranes forms protein channels (e.g. Staphylococcus aureus) and
disrupts the phospholipid bilayer
(e.g. perfringens)

A

MEMBRANE DISRUPTING TOXINS

37
Q

kill phagocytes by forming protein channels

A

Leukocidins

38
Q

kill erythrocytes by forming protein channels

A

Hemolysins

39
Q

produced by streptococci

A

Streptolysins

40
Q

produced by Listerian monocytogens

A

Membrane-attack complexes (MAC’s)

41
Q
  • antigens that provoke a very intense immuneresponse
  • bacterial proteins that combine with a protein on macrophages
  • results in proliferation ofT cells and overproduction of cytokines
  • produce S/Sx e.g.,: fever, nausea, vomiting, diarrhea, sometimes shock and even
    death
  • e.g., staphylococcal enterotoxin, toxic shock syndrome toxin
A

SUPERANTIGENS

42
Q
  • Rfactors–resistance to antibiotics
  • Virulence factors e.g., tetanus neurotoxin, heat-labile enterotoxin,
    staphylococcal enterotoxin D, dextransucrase produced by Streptococcus
    mutans, adhesins and coagulase produced by Staphylococcus aureus, and
    fimbria of enteropathogenic strains of E. coli
A

PLASMIDS

MICROPARA LEC (6 decks)

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