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HLSC 124 - Microbiology for Health Professionals > Chapter 15 - Microbial Mechanisms of Pathogenicity > Flashcards

Chapter 15 - Microbial Mechanisms of Pathogenicity Flashcards

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1
Q

Pathogenicity

A

-the ability to cause disease

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2
Q

Virulence

A

-the degree/extent of pathogenicity

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3
Q

Portals of Entry

A

-how a pathogen enters its host
-mucous membranes, skin, direct deposition

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4
Q

Mucous Membranes

A

-a portal of entry
-line many pathways in the body
-most enter through respiratory and GI tract

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5
Q

Respiratory Tract (Mucous Membranes)

A

-easiest to enter
-enter by inhalation through nose or mouth in droplets
-ie. common cold, pneumonia, TB, influenza, measles

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6
Q

Gastrointestinal (GI) Tract (Mucous Membranes)

A

-enter via food, water, contaminated fingers
-most bacteria destroyed by HCl and stomach/small intestine enzymes
-ie. food poisoning, E. coli, Hep A, Typhoid fever, Shigellosis
-these pathogens are eliminated in feces and then transmitted

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7
Q

Genitourinary (GU) Tract (Mucous Membranes)

A

-sexually contracted pathogens
-ie. any STDs/STIs

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8
Q

Conjuctiva/Eye (Mucous Membranes)

A

-lines the eyelids and covers white of the eyeballs
-ie. measles, conjunctivitis, trachoma

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9
Q

Skin

A

-a portal of entry
-natural defence, largest organ
-unbroken skin is impenetrable by most organisms
-enter via broken skin, hair follicles, sebaceous glands
-ie. S. aureus, fungal agents (nail infection)

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10
Q

Parenteral Route

A

-a portal of entry
-depositing into the tissues beneath the skin when penetrated or injured
-punctures, wounds, insect bites, surgery, dry skin splitting
-ie. malaria, lyme disease, HIV, tetanus

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11
Q

Adherence

A

-how pathogens attach themselves to host cells/tissues
-establishes the infection
-a route for invasion

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12
Q

Adhesins/Ligands

A

-attachment between pathogen and host that involves the binding of adhesins to surface receptors on host cells

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13
Q

Host Receptors

A

-are complex sugars
-ie. mannose fucore

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14
Q

Glycoprotein Adhesins

A

-carb + protein on pathogen
-specific structure
-bind to host receptor

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15
Q

Lipoprotein Adhesin

A

-lipid + protein on pathogen
-specific structure
-bind to host receptor

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16
Q

Adhesin Location

A

-on glycocalyx/capsule, flagella, fimbriae, M protein, mycolic acid, opa protein

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17
Q

Capsule

A

-blocks/evades phagocytosis (1st line of defense)
-ie. S. mutans (tooth decay)

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18
Q

Creation of Dental Plaque

A

-S. mutans uses enzyme glucosyltransferase to digest sucrose into glucose and fructose
-glucose uses the same enzyme to make glucan and then plaque
-fructose uses the same enzyme to make the acid that degenerates the tooth structure

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19
Q

Fimbriae

A

-adhesins on fimbriae adhere only to specific kinds of cells
-ie. E. coli, N. gonorrhoea, bacteria on skin

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20
Q

M Protein

A

-found on cell surface and fimbriae
-heat and acid resistant
-used for attachment and evading phagocytosis
-increases virulence
-ie. S. pyogenes

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21
Q

Mycolic Acid

A

-waxy lipid
-makes up the cell wall of Mycobacterium sp.
-resists phagocytosis

22
Q

Exoenzymes

A

-aids on virulence
-chemicals that can digest materials between cells, digest blood clots

23
Q

Coagulase

A

-coagulate (clot) the fibrinogen in blood
-fibrinogen (produced by liver) is converted to fibrin to form the threads of a blood clot
-clot may protect from phagocytosis and isolate it
-ie. Staphylococcus aureus

24
Q

Kinase

A

-break down fibrin and digest clots
-isolate the infection
-ie. S. pyogenes

25
Q

Hyaluronidase

A

-hydrolyzes hyaluronic acid that holds connective tissue cells together
-allows bacteria to invade deeper
-ie. tissue blackening in C. perfringens (gangrene)
-ie. S. pyogenes (flesh eating disease)

26
Q

Collagenase

A

-facilitates the spread of gas gangrene
-breaks down collagen protein
-ie. C. perfringens

27
Q

IgA Proteases

A

-destroy the antibodies produced by body against pathogens
-antitoxin
-ie. N gonorrhoeae, N. meningitis

28
Q

Damaging Host Cells

A

4 ways:
1. using host’s nutrients
2. causing direct damage
3. producing toxins

29
Q

Toxin

A

-poisonous substances that contribute to pathogenicity

30
Q

Toxigenicity

A

-capacity/ability of a microorganism to produce toxins

31
Q

Toxemia

A

-presence of toxins in the hosts blood

32
Q

Exotoxins

A

-exo = outside
-secreted into the outside of the cells that produce them
-produced mostly by gram negative bacteria
-produced as part of growth
-proteins in nature
-circulate through body fluids
-create SPECIFIC signs and symptoms
-work by destroying parts of the host cell or inhibiting functions
-no fever
-neutralized by IgA Molecules
-3 types of exotoxins

33
Q

Toxoid

A

-inactivated toxin used in vaccines
-stimulate antitoxin production to produce immunity
-ie. DTaP

34
Q

A-B (exo)Toxins

A

-first type to be studies
-consist of an A and B part (both polypeptides)
-ie. Diphtheria, Botulism, Tetanus, Cholera

35
Q

A Part

A

-active enzyme component
-produces the signs and symptoms

36
Q

B Part

A

-binding component
-binds to receptor on the host cell

37
Q

C. Diptheriae

A

-A-B exotoxin
-A shuts down protein synthesis
-results in cell death and diphtheria symptoms (pseudomembrane)

38
Q

C. Botulinum

A

-A-B exotoxin
-B binds and brings A in
-accesses neuromuscular junction to inhibit AcH action
-results in flaccid paralysis

39
Q

C. tetani

A

-A-B exotoxin
-tetanospasmin
-Blocks GABA at NMJ
-results in lock jaw, opsithtonos (back spasm)
-leads to spinal fracture and respiratory failure

40
Q

V. Cholerae

A

-A-B exotoxin
-vebriotoxin
-B then A
-GI tract cells turn into little pumps and trigger cAMP second messenger system
-results in rice water stool

41
Q

Membrane Disrupting (exo)Toxins

A

-cause lysis of host cells by disrupting plasma membrane bilayer
-some form protein channels in the bilayer

42
Q

Leukocidins

A

-membrane disrupting exotoxin
-kill leukocytes
-form protein channels
-produced by Streptococci or Staphylococci

43
Q

Hemolysins

A

-membrane disrupting exotoxin
-destroy erythrocytes
-form protein channels
-produced by Streptococci and Staphylococci

44
Q

Superantigens

A

-antigens that provoke an intense immune response
-non-self-entities
-body reacts to toxin
-ie. Staphylococcal agents of food poisoning, TSS

45
Q

Action of Superantigens

A
  1. Body tries to provoke intense immune response
  2. T cells released and produce cytokines
  3. Circulate in blood and reach vital organs
  4. Affect GI tract and kidneys
    Symptoms: nausea, vomiting, diarrhea, shock, sometimes death
46
Q

Cytokines

A

-small protein molecules
-regulate immune responses
-mediate cell-to-cell communication

47
Q

Endotoxins

A

-endo = within
-endotoxins are part of bacterial cells
-not a metabolic produce
-part of the outer portion of the cell wall on gram negative bacteria
-Lipid A is the endotoxin
-liberated when the bacteria die and the cell wall lyses
-stimulate macrophages to release cytokines in high concentrations (toxic)
-activation of blood clotting proteins
-no antibodies produced

48
Q

Endotoxin Symptoms

A

-fever
-nausea
-vomiting
-diarrhea
-septic shock
-can induce miscarriage

49
Q

Fever

A

-lysosomes release enzymes into the vesicle
-bacteria is digested
-LPS part of the cell wall remains and triggers IL-1 release
-IL-1 circulates in the blood and reaches the brain, causing the hypothalamus to secrete prostaglandins
-body temp is reset to higher degree

50
Q

Fever: Chill Stage

A

-shivering
-IL-1 is working at max

51
Q

Fever: Crisis Stage

A

-IL-1 reducing in the blood
-sweating

52
Q

Shock

A

-any life-threatening decrease in BP
-same mechanism of fever (cytokine release by macrophages)
-LPS triggers release of TNF (tumor necrosis factor) aka Cachetin
-TNF travels to vital organs through blood and disturbs their permeability
-BP drops immensely
-vital organs start to shut down

HLSC 124 - Microbiology for Health Professionals (18 decks)

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