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

Chapter 15 - Microbial Mechanisms of Pathogenicity Flashcards

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
Hyaluronidase
-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
Collagenase
-facilitates the spread of gas gangrene -breaks down collagen protein -ie. C. perfringens
27
IgA Proteases
-destroy the antibodies produced by body against pathogens -antitoxin -ie. N gonorrhoeae, N. meningitis
28
Damaging Host Cells
4 ways: 1. using host's nutrients 2. causing direct damage 3. producing toxins
29
Toxin
-poisonous substances that contribute to pathogenicity
30
Toxigenicity
-capacity/ability of a microorganism to produce toxins
31
Toxemia
-presence of toxins in the hosts blood
32
Exotoxins
-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
Toxoid
-inactivated toxin used in vaccines -stimulate antitoxin production to produce immunity -ie. DTaP
34
A-B (exo)Toxins
-first type to be studies -consist of an A and B part (both polypeptides) -ie. Diphtheria, Botulism, Tetanus, Cholera
35
A Part
-active enzyme component -produces the signs and symptoms
36
B Part
-binding component -binds to receptor on the host cell
37
C. Diptheriae
-A-B exotoxin -A shuts down protein synthesis -results in cell death and diphtheria symptoms (pseudomembrane)
38
C. Botulinum
-A-B exotoxin -B binds and brings A in -accesses neuromuscular junction to inhibit AcH action -results in flaccid paralysis
39
C. tetani
-A-B exotoxin -tetanospasmin -Blocks GABA at NMJ -results in lock jaw, opsithtonos (back spasm) -leads to spinal fracture and respiratory failure
40
V. Cholerae
-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
Membrane Disrupting (exo)Toxins
-cause lysis of host cells by disrupting plasma membrane bilayer -some form protein channels in the bilayer
42
Leukocidins
-membrane disrupting exotoxin -kill leukocytes -form protein channels -produced by Streptococci or Staphylococci
43
Hemolysins
-membrane disrupting exotoxin -destroy erythrocytes -form protein channels -produced by Streptococci and Staphylococci
44
Superantigens
-antigens that provoke an intense immune response -non-self-entities -body reacts to toxin -ie. Staphylococcal agents of food poisoning, TSS
45
Action of Superantigens
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
Cytokines
-small protein molecules -regulate immune responses -mediate cell-to-cell communication
47
Endotoxins
-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
Endotoxin Symptoms
-fever -nausea -vomiting -diarrhea -septic shock -can induce miscarriage
49
Fever
-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
Fever: Chill Stage
-shivering -IL-1 is working at max
51
Fever: Crisis Stage
-IL-1 reducing in the blood -sweating
52
Shock
-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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