36. Biological threats to the body - BACTERIA Flashcards
average size of NEUTROPHIL in diameter (prokaryote)
9-15 μm
average size of YEAST (eukaryote)
7 μm long
average size of bacterium streptococcus
1 μm
in the average human body
how many HUMAN cells
how many MICROBIAL cells
ratio
human cells: 30 trillion
microbial cells: 39 trillion
40:60 split
Bacterial cells have various different
SHAPES
which organelles are present in both PROKARYOTIC and EUKARYOTIC (3)
CYTOPLASM
RIBOSOMES
CELL MEMBRANE
(although no inner membranes in prokaryotes so less compartmentalisation)
ORGANELLES in PROKARYOTIC CELLS
- FLAGELLA (protein)
-PILLI (protein structures that stick out) - NUCELOID (DNA)
- PLASMID (EXTRA chromosomal DNA)
- CAPSULE (sticky polysaccharide)
- CELL WALL
name of the PROTEIN STUCTURES that stick out of PROKARYOTES (bacteria)
PILLI
What are the 2 STRONGLY IMMUNOGENIC PROTEINS in PROKARYOTES that the IMMUNE SYSTEM TARGET
FLAGELLA
PILLI
how are FLAGELLA and PILLI (targeted by immune system) in prokaryotes PROTECTED FROM / AVOID IMMUNE RESPONSE
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
how else (beside protein variants) do BACTERIA AVOID IMMUNE RESPONSE
(which structure)
CAPSULE (sticky polysaccharide)
difficult to ENGULF or be seen
what is another DIFFERENCE between PROKARYOTES and EUKAROTES
SIZE DIFFERENCE
Prokaryotes: BIGGER 9-15 μm
Eukaryotes: 7 μm
2 main TYPES of BACTERIA
GRAM +
GRAM -
how are GRAM + BACTERIA
- surrounded by Lipid Bilayer membrane (SINGLE)
- encased in a THICK rigid layer of PEPTIDOGLYCAN
makes it strong so maintains the high internal pressure
how are GRAM - BACTERIA
- 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)
which bacteria type has a THICK PEPTIDOGLYCAN layer
GRAM +
which bacteria type has 2 LIPID BILAYERS
GRAM -
structure of acid-fast MYCOBACTERIA
- THIN PEPTIDOGLYCAN LAYER
- extremely NARROW PORINS (more drug resistance)
- arabinogalactan (filling space)
- mycolic acid with acyl lipids and other surface proteins linked
why do MYCOBACTERIA have more DRUG RESISTANCE
NARROW PORINS
CAPSULE/GLYCOCALYX
composition?
Function?
POLYSACCHARIDE
- ADHESION
- EVASION of host immune response
- PROTECTION
often contributes to Pathogenic Nature of Bacteria
CHROMOSOME:
composition?
structure?
Function?
-DNA
- usually a CLOSED LOOP
- can be single molecule or more
- function: genetic coding
FLAGELLA
composition?
Function?
-PROTEIN
- MOVEMENT
- ADHESION
associated more frequently with RODS than cocci (shaped)
PILI / FIMBRIAE:
composition?
Function?
- PROTEIN (narrow & shorter)
on surface - ADHESION (to host)
(- sometimes CONJUGATION, DNA UPTAKE, CELL MOVEMENT)
PLASMID
composition?
Function?
- DNA
function: ACCESSORY GENES/ VIULENCE GENES
can confer new trains
- gives LARGER GENETIC REPERTOIRE and helps survival
(although could probably survive without)
LPS - LIPOPOLYSACCHARIDE
aka ENDOTOXIN
composition?
Function?
- LIPID & POLYSACCHARIDE
- OUTER MEMBRANE of GRAM - BACTERIA
LPS - LIPOPOLYSACCHARIDE
aka ENDOTOXIN
composition?
Function?
- LIPID & POLYSACCHARIDE
- OUTER MEMBRANE of GRAM NEGATIVE BACTERIA
VIRULENCE FACTOR
composition?
Function?
- PROTEIN, LIPID OR CARBOHYDRATE
- something MADE OUT OF BACTERIA that contributes to its ABILITY to CAUSE DISEASE
define PATHOGEN
An organism that CAUSES DISEASE
define VIRULENCE
the DEGREE to which a PATHOGEN can CAUSE DISEASE in the host
define PATHOGENICITY
the ABILITY of an organism to CAUSE DISEASE in a host
define COMMENSAL
part of the NORMAL MICROBIOTA
define OPPORTUNISTIC PATHOGEN
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
define COLONISATION
Refers to the state where BACTERIA are PRESENT IN/ON a HOST and are GROWING
and DIVING , BUT are doing so WITHOUT CAUSING HARM
define INFECTION
Refers to the state where BACTERIA are PRESENT IN/ON a HOST and CAUSING HARM
usually with ACUTE INFLAMMATION
define INCUBATION PERIOD
the TIME it takes from EXPOSURE to the pathogen to disease SYMPTOM onset
define TRANSMISSION
The PASSAGE of the pathogen/disease from ONE HOST/PLACE TO ANOTHER
what does DISEASE depend on (4)
- state of HOST
- state of PATHOGEN
- state of host’s MICROBIOME
- ENVIRONMENT the host is in
DISEASE depends on the state of the HOST eg: (6)
- CO-MORBIDITIES
- VACCINATION STATUS
- GENETICS
- IMMUNE STATUS
- GENDER
- AGE
DISEASE depends on the state of the PATHOGEN eg: (4)
- VIRULENCE FACTORS
- SEROTYPE
( groups within a single species of microorganisms, such as bacteria or viruses, which share distinctive surface structures) - NUMBERS
- SITE of COLONISATION
DISEASE depends on the state of the host’s MICROBIOME eg: (4)
- DIVERSITY/ABUNDANCE
- COMPOSITION
- presence of OPPORTUNISTIC PATHOGENS
- NICHE OCCUPATION
DISEASE depends on the state of the host’s ENVIRONMENT eg: (4)
- SOCIO-ECONOMIC FACTORS
- POPULATION DENSITY
- HABITS (SMOKING/DRINKING)
- SEASON
5 MECHANISMS of PATHOGENICITY
- COLONISATION of host (bacteria present but not causing harm)
- INVASION of HOST TISSUES
- EVASION OF IMMUNE RESPONSE
- cause DAMAGE to HOST TISSUES
- SPREAD to NEW HOST
what is the FIRST STEP in establishing an INTERACTION with a HOST
to COLONISE it
COLONISATION of host (first step) is done through…
ADHERANCE
what does ADHERANCE INVOLVE
SURFACE COMPONENTS of BACTERIA INTERACTING with SURFACE COMPONENTS of HOST CELLS
- SPECIFICITY
- TARGET TISSUES
- SPECIFIC BACTERIAL STRAINS (can be unique to specific strains)
2 MECHANISMS in ADHERANCE (colonisation).
FIRST STEP:
- NON-SPECIFIC
- REVERSIBLE
- Hydrophobic interactions, Electrostatic interaction, Atomic/Molecular Vibrations, Brownian Movement, Mechanical Trapping (cells get caught up in Biofilm Polymers and Capsule Interactions)
2 MECHANISMS in ADHERANCE (colonisation).
SECOND STEP:
- SPECIFIC
- IRREVERSIBLE
- RECEPTOR/LIGAND BINDING
EXAMPLES of BACTERIA that use COLONISATION/ADHESION
- 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
GRAM POSITIVE EXAMPLES (3)
- STREPTOCOCCUS PYOGENES
COCCI shape - STRAPHYLOCOCCUS AUREUS
COCCI shape - CLOSTRIDIUM SPOROGENES
ROD shape
GRAM NEGATIVE EXAMPLES (3)
- NEISSERIA GONORRHOEAE
DIPLO-COCCI shape - PSEUDOMONAS AERUGINOSE
ROD shape - HAEMOPHILUS INFLUENZAE
ROD shape
colonisation/adhesion examples
STREPTOCOCCUS PYOGENES (gram +)
what adhesion produced?
receptor it binds to?
attachment site?
disease?
- PROTEIN F (on surface - in peptidoglycan)
- AMINO TERMINUS of FIBRONECTIN
- in PHARYNGEAL EPITHELIUM (back of throat)
- SORE THROAT
colonisation/adhesion examples
NEISSERIA GONORRHOEAE (gram -, diplococci)
what adhesion produced?
receptor it binds to?
attachment site?
disease?
- makes a lot of different TYPE 4 PILLI (alters)
(RETRACTABLE) - bind to various types of GLUCOSAMINE-GALACTOSE CARBOHYDRATE
- URETHRAL/CERVICAL EPITHELIUM
- GONORRHEA
colonisation/adhesion examples
STRAPHYLOCOCCUS AUREUS (gram+)
what adhesion produced?
receptor it binds to?
attachment site?
disease?
- Cell-bound PROTEIN
- AMINO TERMINUS of FIBRONECTIN
- MUCOSAL EPITHELIUM
- can set up infection *ANYWHERE
TYPE 4 PILLI on bacteria are RETRACTABLE making them great for… (2)
example NEISSERIA GONORRHEA
- 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)
what is INVASION
MOVEMENT through Host Tissues
( get from where they are to where its going to cause disease)
what is INVASION usually DRIVEN BY
PRODUCTION of ENZYMES that ACT LOCALLY
and have an IMMEDIATE EFFECT on the LOCATION of the producing BACTERIAL CELL
within a very SHORT RANGE
examples of COMMON ENZYMES associated with INVASION (4)
- HYALURONIDASE
- COLLAGENASE
- NEUROMINIDASE
- PHOSPHOLIPASES
HYALURONIDASE enzyme in INVASION
- activity
- examples of bacteria involved (3)
- ATTACKS INTERSTITIAL CEMENT
- & DEGRADES/DEPOLYMERISES HYLURONIC ACID
of CONNECTIVE TISSUES
bacteria:
- STEPTOCOCCI
- STAPHYLOCOCCI,
- CLOSTRIDIA
COLLAGENASE enzyme in INVASION
- activity
- examples of bacteria involved (1)
- BREAKS DOWN/DISSOLVES PROTEIN COLLAGEN in basement membrane that holds tissues together
Bacteria:
CLOSTRIDIUMSPECIES
NEUROMINIDASE enzyme in INVASION
- activity
- examples of bacteria involved (2)
- DEGRADES NEURAMINIC ACID (aka Sialic Acid) of INTESTINAL MUCOSA - HOLDS EPITHELIAL CELLS TOGETHER
Bacteria:
- VIBRIO CHOLERAE
- SHIGELLA DYSENTERIAE
PHOSPHOLIPASE enzyme in INVASION
- activity
- examples of bacteria involved
- HYDROLYSE PHOSPHOLIPIDS in CELL MEMBRANES
Bacteria:
- CLOSTRIDIUM PERFRINGENS
what INVASINS does STAPHYLOCOCCI AUREUS make
- LEUKOCIDIN
- COAGULASE
what INVASIN does STREPTOCOCCUS PYOGENES make
STREPTOLYSIN
what is EVASION of HOST DEFENCES
OVERCOMING HOST PHAGOCYTIC DEFENCES
- AVOID CONTACT with phagocytes
- INHIBIT phagocyte ENGULFMENT
- SURVIVE inside the phagocyte
5 WAYS of EVASION of host defences
- EVADE COMPLEMENT
- MOLECULAR MIMICRY
- ANTIGENIC DISGUISE
- SHEDDING of bacterial ANTIGENS
- Huge VARIATION of SEROTYPES
EVASION OF HOST DEFENCES:
EVADE COMPLEMENT
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)
EVASION OF HOST DEFENCES:
MOLECULAR MIMICRY
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
EVASION OF HOST DEFENCES:
ANTIGENIC DISGUISE
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
EVASION OF HOST DEFENCES:
PERSISTANCE at SITES INACCESSIBLE to IMMUNE RESPONSE
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
EVASION OF HOST DEFENCES:
SHEDDING of BACTERIAL ANTIGENS
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
EVASION OF HOST DEFENCES:
HUGE VARIATION of SEROTYPES
SEROTYPE: groups within a single species of microorganisms eg bacteria/viruses which SHARE DISTINCTIVE SURFACE STRUCTURES
- distinguishable by ANTIBODIES
what 2 things can CAUSE DAMAGE to HOST TISSUES
production of..
- ENDOTOXINS
- EXOTOXINS
what are ENDOTOXINS (cause damage to host tissues)
LIPOPOLYSACHHARIDES
MOST COMMON PYROGEN (substance produced by bacteria that produces fever)
found in the outer membrane of Gram-NEGATIVE bacteria
what are EXOTOXINS (cause damage to host tissues)
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
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?
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
Staphylococcus enterotoxins TOXIN (superantigen) is made by which bacteria
STAPHYLOCOCCUS AUREUS
Toxic shock syndrome toxin (TSST-1) TOXIN (superantigen) is made by which bacteria
STAPHYLOCOCCUS AUREUS
Pyrogenic exotoxins (SPE) e.g. Erythrogenic toxin (scarlet fever toxin) is made by which BACTERIA
STREPTOCOCCUS PYOGENES
5 TRANSMISSION ROUTES
- 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
General concepts of ANTIBIOTICS
- 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)
ANTIBACTIA: MIC (Minimal Inhibitory Conc) & MBC (minimum Bactericidal Conc)
MIC: 1st conc of antibiotics at which there is no bacterial GROWTH
MBC: lowest conc of antibiotics where all bacteria is KILLED
things to think about when administering antibiotics
- route of admission
- metabolism / half life
- Side-effects
- Bactericidal vs Bacteriostatic
Antibiotics attack either (5)
- CELL WALL SYNTHESIS
- INHIBIT METABOLIC PATHWAY
- PROTEIN SYNTHESIS
- DNA SYNTHESIS
- RNA SYNTHESIS
Bacterial mechanisms of RESISTANCE
- 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
