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IMMUNOLOGY (foundation B) > 36. Biological threats to the body - BACTERIA > Flashcards

36. Biological threats to the body - BACTERIA Flashcards

1
Q

average size of NEUTROPHIL in diameter (prokaryote)

A

9-15 μm

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2
Q

average size of YEAST (eukaryote)

A

7 μm long

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3
Q

average size of bacterium streptococcus

A

1 μm

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4
Q

in the average human body
how many HUMAN cells
how many MICROBIAL cells

ratio

A

human cells: 30 trillion
microbial cells: 39 trillion

40:60 split

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5
Q

Bacterial cells have various different

A

SHAPES

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6
Q

which organelles are present in both PROKARYOTIC and EUKARYOTIC (3)

A

CYTOPLASM
RIBOSOMES
CELL MEMBRANE
(although no inner membranes in prokaryotes so less compartmentalisation)

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7
Q

ORGANELLES in PROKARYOTIC CELLS

A
  • FLAGELLA (protein)
    -PILLI (protein structures that stick out)
  • NUCELOID (DNA)
  • PLASMID (EXTRA chromosomal DNA)
  • CAPSULE (sticky polysaccharide)
  • CELL WALL
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8
Q

name of the PROTEIN STUCTURES that stick out of PROKARYOTES (bacteria)

A

PILLI

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9
Q

What are the 2 STRONGLY IMMUNOGENIC PROTEINS in PROKARYOTES that the IMMUNE SYSTEM TARGET

A

FLAGELLA
PILLI

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10
Q

how are FLAGELLA and PILLI (targeted by immune system) in prokaryotes PROTECTED FROM / AVOID IMMUNE RESPONSE

A

MAKE NEW VARIANTS

bacteria ALTER GENE SEQUENCES of these proteins to CHANGE the ANTIGENIC PRESENTATION of them frequently
or CHANGE DNA SEQUENCES that ENCODE them

so ANTIBODIES CANNOT RECOGNISE them after a few hours

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11
Q

how else (beside protein variants) do BACTERIA AVOID IMMUNE RESPONSE
(which structure)

A

CAPSULE (sticky polysaccharide)

difficult to ENGULF or be seen

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12
Q

what is another DIFFERENCE between PROKARYOTES and EUKAROTES

A

SIZE DIFFERENCE
Prokaryotes: BIGGER 9-15 μm
Eukaryotes: 7 μm

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13
Q

2 main TYPES of BACTERIA

A

GRAM +
GRAM -

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14
Q

how are GRAM + BACTERIA

A
  • surrounded by Lipid Bilayer membrane (SINGLE)
  • encased in a THICK rigid layer of PEPTIDOGLYCAN

makes it strong so maintains the high internal pressure

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15
Q

how are GRAM - BACTERIA

A
  • surrounded by DOUBLE LIPID BILAYER (2 lipid bilayer membranes)
  • THIN PEPTIDOGLYCAN region Between the membranes

harder to get into

(but have small porins to allow small solutes in)

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16
Q

which bacteria type has a THICK PEPTIDOGLYCAN layer

A

GRAM +

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17
Q

which bacteria type has 2 LIPID BILAYERS

A

GRAM -

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18
Q

structure of acid-fast MYCOBACTERIA

A
  • THIN PEPTIDOGLYCAN LAYER
  • extremely NARROW PORINS (more drug resistance)
  • arabinogalactan (filling space)
  • mycolic acid with acyl lipids and other surface proteins linked
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19
Q

why do MYCOBACTERIA have more DRUG RESISTANCE

A

NARROW PORINS

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20
Q

CAPSULE/GLYCOCALYX
composition?
Function?

A

POLYSACCHARIDE

  • ADHESION
  • EVASION of host immune response
  • PROTECTION

often contributes to Pathogenic Nature of Bacteria

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21
Q

CHROMOSOME:
composition?
structure?
Function?

A

-DNA
- usually a CLOSED LOOP
- can be single molecule or more

  • function: genetic coding
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22
Q

FLAGELLA
composition?
Function?

A

-PROTEIN

  • MOVEMENT
  • ADHESION

associated more frequently with RODS than cocci (shaped)

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23
Q

PILI / FIMBRIAE:
composition?
Function?

A
  • PROTEIN (narrow & shorter)
    on surface
  • ADHESION (to host)
    (- sometimes CONJUGATION, DNA UPTAKE, CELL MOVEMENT)
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24
Q

PLASMID
composition?
Function?

A
  • DNA

function: ACCESSORY GENES/ VIULENCE GENES

can confer new trains
- gives LARGER GENETIC REPERTOIRE and helps survival
(although could probably survive without)

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25
Q

LPS - LIPOPOLYSACCHARIDE
aka ENDOTOXIN
composition?
Function?

A
  • LIPID & POLYSACCHARIDE
  • OUTER MEMBRANE of GRAM - BACTERIA
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26
Q

LPS - LIPOPOLYSACCHARIDE
aka ENDOTOXIN
composition?
Function?

A
  • LIPID & POLYSACCHARIDE
  • OUTER MEMBRANE of GRAM NEGATIVE BACTERIA
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27
Q

VIRULENCE FACTOR
composition?
Function?

A
  • PROTEIN, LIPID OR CARBOHYDRATE
  • something MADE OUT OF BACTERIA that contributes to its ABILITY to CAUSE DISEASE
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28
Q

define PATHOGEN

A

An organism that CAUSES DISEASE

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29
Q

define VIRULENCE

A

the DEGREE to which a PATHOGEN can CAUSE DISEASE in the host

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30
Q

define PATHOGENICITY

A

the ABILITY of an organism to CAUSE DISEASE in a host

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31
Q

define COMMENSAL

A

part of the NORMAL MICROBIOTA

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32
Q

define OPPORTUNISTIC PATHOGEN

A

can be part of the NORMAL MICROBIOTA
BUT MAY be HARMFUL if they MOVE from
one part of the body to another or if they OVER POPULATE their niche

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33
Q

define COLONISATION

A

Refers to the state where BACTERIA are PRESENT IN/ON a HOST and are GROWING
and DIVING , BUT are doing so WITHOUT CAUSING HARM

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34
Q

define INFECTION

A

Refers to the state where BACTERIA are PRESENT IN/ON a HOST and CAUSING HARM
usually with ACUTE INFLAMMATION

35
Q

define INCUBATION PERIOD

A

the TIME it takes from EXPOSURE to the pathogen to disease SYMPTOM onset

36
Q

define TRANSMISSION

A

The PASSAGE of the pathogen/disease from ONE HOST/PLACE TO ANOTHER

37
Q

what does DISEASE depend on (4)

A
  • state of HOST
  • state of PATHOGEN
  • state of host’s MICROBIOME
  • ENVIRONMENT the host is in
38
Q

DISEASE depends on the state of the HOST eg: (6)

A
  • CO-MORBIDITIES
  • VACCINATION STATUS
  • GENETICS
  • IMMUNE STATUS
  • GENDER
  • AGE
39
Q

DISEASE depends on the state of the PATHOGEN eg: (4)

A
  • VIRULENCE FACTORS
  • SEROTYPE
    ( groups within a single species of microorganisms, such as bacteria or viruses, which share distinctive surface structures)
  • NUMBERS
  • SITE of COLONISATION
40
Q

DISEASE depends on the state of the host’s MICROBIOME eg: (4)

A
  • DIVERSITY/ABUNDANCE
  • COMPOSITION
  • presence of OPPORTUNISTIC PATHOGENS
  • NICHE OCCUPATION
41
Q

DISEASE depends on the state of the host’s ENVIRONMENT eg: (4)

A
  • SOCIO-ECONOMIC FACTORS
  • POPULATION DENSITY
  • HABITS (SMOKING/DRINKING)
  • SEASON
42
Q

5 MECHANISMS of PATHOGENICITY

A
  1. COLONISATION of host (bacteria present but not causing harm)
  2. INVASION of HOST TISSUES
  3. EVASION OF IMMUNE RESPONSE
  4. cause DAMAGE to HOST TISSUES
  5. SPREAD to NEW HOST
43
Q

what is the FIRST STEP in establishing an INTERACTION with a HOST

A

to COLONISE it

44
Q

COLONISATION of host (first step) is done through…

A

ADHERANCE

45
Q

what does ADHERANCE INVOLVE

A

SURFACE COMPONENTS of BACTERIA INTERACTING with SURFACE COMPONENTS of HOST CELLS

  • SPECIFICITY
  • TARGET TISSUES
  • SPECIFIC BACTERIAL STRAINS (can be unique to specific strains)
46
Q

2 MECHANISMS in ADHERANCE (colonisation).
FIRST STEP:

A
  1. NON-SPECIFIC
  • REVERSIBLE
  • Hydrophobic interactions, Electrostatic interaction, Atomic/Molecular Vibrations, Brownian Movement, Mechanical Trapping (cells get caught up in Biofilm Polymers and Capsule Interactions)
47
Q

2 MECHANISMS in ADHERANCE (colonisation).
SECOND STEP:

A
  1. SPECIFIC
  • IRREVERSIBLE
  • RECEPTOR/LIGAND BINDING
48
Q

EXAMPLES of BACTERIA that use COLONISATION/ADHESION

A
  • Streptococcus pyogenes
  • Streptococcus mutans
  • Streptococcus salivarius
  • Streptococcus pneumoniae
  • Staphylococcus aureus
  • Neisseria gonorrhoeae
  • Enterotoxigenic E. coli
  • Uropathogenic E. coli
  • Uropathogenic E. coli
  • Bordetella pertussis
  • Vibrio cholerae
  • Treponema pallidum
  • Mycoplasma
49
Q

GRAM POSITIVE EXAMPLES (3)

A
  • STREPTOCOCCUS PYOGENES
    COCCI shape
  • STRAPHYLOCOCCUS AUREUS
    COCCI shape
  • CLOSTRIDIUM SPOROGENES
    ROD shape
50
Q

GRAM NEGATIVE EXAMPLES (3)

A
  • NEISSERIA GONORRHOEAE
    DIPLO-COCCI shape
  • PSEUDOMONAS AERUGINOSE
    ROD shape
  • HAEMOPHILUS INFLUENZAE
    ROD shape
51
Q

colonisation/adhesion examples

STREPTOCOCCUS PYOGENES (gram +)

what adhesion produced?
receptor it binds to?
attachment site?
disease?

A
  • PROTEIN F (on surface - in peptidoglycan)
  • AMINO TERMINUS of FIBRONECTIN
  • in PHARYNGEAL EPITHELIUM (back of throat)
  • SORE THROAT
52
Q

colonisation/adhesion examples

NEISSERIA GONORRHOEAE (gram -, diplococci)

what adhesion produced?
receptor it binds to?
attachment site?
disease?

A
  • makes a lot of different TYPE 4 PILLI (alters)
    (RETRACTABLE)
  • bind to various types of GLUCOSAMINE-GALACTOSE CARBOHYDRATE
  • URETHRAL/CERVICAL EPITHELIUM
  • GONORRHEA
53
Q

colonisation/adhesion examples

STRAPHYLOCOCCUS AUREUS (gram+)

what adhesion produced?
receptor it binds to?
attachment site?
disease?

A
  • Cell-bound PROTEIN
  • AMINO TERMINUS of FIBRONECTIN
  • MUCOSAL EPITHELIUM
  • can set up infection *ANYWHERE
54
Q

TYPE 4 PILLI on bacteria are RETRACTABLE making them great for… (2)

example NEISSERIA GONORRHEA

A
  • allowing MOVEMENT of their bacteria ALONG THE SURFACE
  • BINDING DNA and PULLING it INTO a BACTERIAL CELL
    (these bacteria are good at taking up foreign DNA)
55
Q

what is INVASION

A

MOVEMENT through Host Tissues
( get from where they are to where its going to cause disease)

56
Q

what is INVASION usually DRIVEN BY

A

PRODUCTION of ENZYMES that ACT LOCALLY

and have an IMMEDIATE EFFECT on the LOCATION of the producing BACTERIAL CELL
within a very SHORT RANGE

57
Q

examples of COMMON ENZYMES associated with INVASION (4)

A
  • HYALURONIDASE
  • COLLAGENASE
  • NEUROMINIDASE
  • PHOSPHOLIPASES
58
Q

HYALURONIDASE enzyme in INVASION

  • activity
  • examples of bacteria involved (3)
A
  • ATTACKS INTERSTITIAL CEMENT
  • & DEGRADES/DEPOLYMERISES HYLURONIC ACID

of CONNECTIVE TISSUES

bacteria:
- STEPTOCOCCI
- STAPHYLOCOCCI,
- CLOSTRIDIA

59
Q

COLLAGENASE enzyme in INVASION

  • activity
  • examples of bacteria involved (1)
A
  • BREAKS DOWN/DISSOLVES PROTEIN COLLAGEN in basement membrane that holds tissues together

Bacteria:
CLOSTRIDIUMSPECIES

60
Q

NEUROMINIDASE enzyme in INVASION

  • activity
  • examples of bacteria involved (2)
A
  • DEGRADES NEURAMINIC ACID (aka Sialic Acid) of INTESTINAL MUCOSA - HOLDS EPITHELIAL CELLS TOGETHER

Bacteria:
- VIBRIO CHOLERAE
- SHIGELLA DYSENTERIAE

61
Q

PHOSPHOLIPASE enzyme in INVASION

  • activity
  • examples of bacteria involved
A
  • HYDROLYSE PHOSPHOLIPIDS in CELL MEMBRANES

Bacteria:
- CLOSTRIDIUM PERFRINGENS

62
Q

what INVASINS does STAPHYLOCOCCI AUREUS make

A
  • LEUKOCIDIN
  • COAGULASE
63
Q

what INVASIN does STREPTOCOCCUS PYOGENES make

A

STREPTOLYSIN

64
Q

what is EVASION of HOST DEFENCES

A

OVERCOMING HOST PHAGOCYTIC DEFENCES

  • AVOID CONTACT with phagocytes
  • INHIBIT phagocyte ENGULFMENT
  • SURVIVE inside the phagocyte
65
Q

5 WAYS of EVASION of host defences

A
  • EVADE COMPLEMENT
  • MOLECULAR MIMICRY
  • ANTIGENIC DISGUISE
  • SHEDDING of bacterial ANTIGENS
  • Huge VARIATION of SEROTYPES
66
Q

EVASION OF HOST DEFENCES:
EVADE COMPLEMENT

A

1 role of CAPSULES is to protect from complement activation - hide bacterial components

or inhibit formation of C3b complex on their surface (no membrane attack complex)

67
Q

EVASION OF HOST DEFENCES:
MOLECULAR MIMICRY

A

BACTERIAL ANTIGEN is SIMILAR to NORMAL HOST ANTIGEN - IMMUNE RESPONSE IS WEAK

  • bacteria can use this strategy to COAT THEMSELVES with HOST PROTEINS eg fibrin,fibronectin,antibody molecules for protection
  • some DEVELOP MOLECULES SIMILAR to SIALIC ACID / HYALURONIC ACID similar to to EUKARYOTES
68
Q

EVASION OF HOST DEFENCES:
ANTIGENIC DISGUISE

A

by the time immune system recognises SURFACE PROTEIN it has CHANGED
- CHANGE FREQUENTLY

  • GENES ENCODING SURFACE PROTEINS eg Pilli, Flagella etc. have variable regions of DNA that can undergo QUICK MUTATIONS
  • or carry a repertoire of genes that can be RECOMBINED
  • enables PROTEIN SEQUENCES to be CHANGES at a very HIGH RATE and frequently
69
Q

EVASION OF HOST DEFENCES:
PERSISTANCE at SITES INACCESSIBLE to IMMUNE RESPONSE

A

staying in areas where immune response is less effective eg.

  • INTRACELLULAR (without allowing microbial antigen expression on cell surface)
  • LUMINAL SURFACE of GI TRACT
  • luminal surface of ORAL CAVITY
  • luminal surface of URINARY TRACT
  • LUMEN of SALIVARY GLANDS
  • lumen of MAMMARY GLANDS
  • lumen of KIDNEY TUBULES
70
Q

EVASION OF HOST DEFENCES:
SHEDDING of BACTERIAL ANTIGENS

A

when bacteria MOVE from one area to another it SHEDS PILLI

IMMUNE SYSTEM ATTACKS the bits that have SHED and NOT the BACTERIAL CELL itself

71
Q

EVASION OF HOST DEFENCES:
HUGE VARIATION of SEROTYPES

A

SEROTYPE: groups within a single species of microorganisms eg bacteria/viruses which SHARE DISTINCTIVE SURFACE STRUCTURES

  • distinguishable by ANTIBODIES
72
Q

what 2 things can CAUSE DAMAGE to HOST TISSUES

A

production of..

  • ENDOTOXINS
  • EXOTOXINS
73
Q

what are ENDOTOXINS (cause damage to host tissues)

A

LIPOPOLYSACHHARIDES

MOST COMMON PYROGEN (substance produced by bacteria that produces fever)

found in the outer membrane of Gram-NEGATIVE bacteria

74
Q

what are EXOTOXINS (cause damage to host tissues)

A

usually PROTEINS

  • most DENATURED by HEAT
  • CATALYTICALLY ACTIVE
  • HIGH BIOLOGICAL ACTIVITY
  • SPECIFICITY of action (impact a particular tissue/cell type)
  • many INTRACELLULAR acting TOXINS have A-B STRUCTURE
    (either 1 A, 1 B subunit, or 1 A, 5 Bs)

a toxin SECRETED by bacteria

75
Q

TOXINS: Staphylococcus enterotoxins, Toxic shock syndrome toxin (TSST-1), Pyrogenic exotoxins (SPE) e.g. Erythrogenic toxin (scarlet fever
toxin)*
are examples of…
what do they do?

A

SUPER ANTIGENS
- ACTIVATE T CELL RECEPTORS which respond in an odd way without normal display by MHC class II

  • cause SEVERE IMMUNE RESPONSE
    uncontrolled activation
76
Q

Staphylococcus enterotoxins TOXIN (superantigen) is made by which bacteria

A

STAPHYLOCOCCUS AUREUS

77
Q

Toxic shock syndrome toxin (TSST-1) TOXIN (superantigen) is made by which bacteria

A

STAPHYLOCOCCUS AUREUS

78
Q

Pyrogenic exotoxins (SPE) e.g. Erythrogenic toxin (scarlet fever toxin) is made by which BACTERIA

A

STREPTOCOCCUS PYOGENES

79
Q

5 TRANSMISSION ROUTES

A
  • AIRBORNE
    droplet, nuclei or dust
  • CONTACT
    usually skin
  • VEHICLE
    food, water, biological products (blood,urine) fomites (inanimate/lifeless objects eg tissues,bedding, clothing)
  • VECTOR-BORNE
    eg mosquitos, tick bites
  • NOSOCOMIAL
    hospital acquired
80
Q

General concepts of ANTIBIOTICS

A
  • SELECTIVE toxicity
  • must SURVIVE their route of administration
  • HALF-LIVES long enough to have activity in the body
  • Broad and Narrow spectrum
  • BACTERIDICAL (kill bacteria) & BACTERIOSTATIC (inhibit growth)
  • Combinations:
    Synergism (more than the sum of the effect s of when drug given alone),
    Antagonism (less than)
    Indifference (equal)
81
Q

ANTIBACTIA: MIC (Minimal Inhibitory Conc) & MBC (minimum Bactericidal Conc)

A

MIC: 1st conc of antibiotics at which there is no bacterial GROWTH

MBC: lowest conc of antibiotics where all bacteria is KILLED

82
Q

things to think about when administering antibiotics

A
  • route of admission
  • metabolism / half life
  • Side-effects
  • Bactericidal vs Bacteriostatic
83
Q

Antibiotics attack either (5)

A
  • CELL WALL SYNTHESIS
  • INHIBIT METABOLIC PATHWAY
  • PROTEIN SYNTHESIS
  • DNA SYNTHESIS
  • RNA SYNTHESIS
84
Q

Bacterial mechanisms of RESISTANCE

A
  • Impermeability
  • Destruction
  • Modification
    adding acetyl-transferases, adenyl-transferases, phospho-transferases
  • Drug target modification
  • production of additional drug target, usually with altered sensitivity
  • Overproduction of drug target

these can be carried on Stable or Mobile Genetic Elements

IMMUNOLOGY (foundation B) (7 decks)

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