Bacterial Structures Flashcards
Al bacterial cells must possess
cell membrane, genome, ribosomes, intracellular macromolecules, almost always a cell wall
Extrachromosomal elements (ECE)
plasmids or prophages may be present
Describe a bacterial ribosome
70S (50S + 30S)
What are 3 cell surface structures that may or may not be present on bacteria
Flagella, Pili, Capsules
dipococci
pair of cocci
streptococci
chain of cocci
staphylococci
cluster of cocci
antimicrobics may alter
cell morphology (shape and arrangement)
Flagella or antigen ____
H
Flagella is composed of
polypeptides - different than pili
Plain flagella
extend from the cell surface into the environment for motility
Endoflagella of spirochetes
internal structure that allow them to perform a corkscrew movement
Flagella function to
provide motility in liquid and some surface translocation
What allows flagella to propel?
sensory system control via chemotaxis
Virulence factor of flagella
motility with chemotaxis
H-antigen
flagella
Pili are composed of
polypeptide chain - different than flagella
Normal pili and sex pili
extend out from the cell surface into the environment
Pili functions to
aid in adherence to host, antiphagocytic, involved in surface translocation (pili type IV)
Sex pilus function
conjugation (spread of antibiotic resistance)
Another name for capsules
glycocalyx, exopolysaccharide (EPS), slime layer
Capsule is composed of
complex polysaccharides, simple sugar, or D-glutamic acid
O antigen
LPS
K antigen
capsule formed from simple sugar, complex polysaccharide, or D-glutamic acid
Biofilm
complex, 3-D structure, microcolony of bacteria or yeast, enmeshed in a mucoid exopolysaccharide film
Biofilm composition
exopolysaccharides and in some cases proteins (amyloid fibers)
Phenotypic changes of bacteria in biofilms
non-motile, persist even with antimicrobials, multi-drug resistant
the activation of biofilm formation involves
quorum sensing: sensing the density of the population and switching gene expression
Re-seeding from biofilm
some cells in the biofilm revert back to normal, therefore even if anti-microbials have been used the infection may return
How are cells released from a biofilm and when?
when the amyloid structural protein is broken down by D-A.A. when the situation dictates it
Biofilms function
adherence to host tissue and surfaces (surface colonization), protection against antibiotics and desiccation (Drying out)
surface colonization of biofilms allow them to
thrive in a moving environment
K antigen
capsular antigen
O antigen
LPS
Do gram positive bacteria have capsules?
They may or may NOT have capsules
Do gram negative bacteria have capsules?
They may or may NOT, O antigen + and K antigen - if no capsule, O antigen + and K antigen + is capsule differs from LPS, O antigen + and K antigen - if capsule is an extension of LPS
S-Layers
layer lying directly on cell walls, rigid layer with pores of fixed diameter
S-Layers are composed of
protein or glycoprotein
S-Layers function
resistance to C3b binding (resists complement mediated killing), prevents phagocytosis by PMNs
Translocation
passage through human cells to access new sites
Genera capable of Translocation
H. flu, S. pyrogenes, M. tuberculosis
Paracellular translocation
passage between cells to enter tissues
The ability to slide on solid surfaces is associated with
biofilm formation at least with Mycobacterium smegmatis
Polypeptides embedded in the lipid bilayer are stabilized by
divalent cations (Ca and Mg) and hydrophobic interactions with fatty acid moiety of phospholipids
Which genera of bacteria DO CONTAIN sterols?
Mycoplasma, helicobacter, ehrlichia, Anaplasma spp.
Cell membrane characteristics
permeable for transport, specific transport mechanisms for secretion of proteins (6 types), respiratory components, biosynthetic pathways, sensory and osmoregulatory mechanisms and chemotaxis
Type III transport system (injectosomes)
conserved multiprotein system that pathogenic gram-NEGATIVE bacteria use to insert protein toxins into cells
Respiratory components found in the cell membrane
ETC, ATP synthase, generating proton motive force
Cell membrane contains components for biosynthesis of
cell wall, cellular replication (septal ring)
The cell wall regulates osmotic pressure, such that the bacterial cell is ____________ compared to the environment
hypertonic
Chemotaxis mechanisms lie within the
cell membrane
The peptidoglycan layer in the gram positive cell wall is much ______ than the gram negative cell wall
thicker
Describe the peptidoglycan layer of the cell wall of gram-positive cells
thick peptidoglycan layer, covalently linked polysaccharides, lipoteichoic acid extend through the peptidoglycan layer, no outer LPS layer
Describe the peptidoglycan layer of the cell wall of gram-negative cells
thin peptidoglycan layer, no covantely linked polysaccharides or LA extending through, contains an outer layer of LPS, located within the periplasm
Cell wall function
maintain cell shape, shield from environment, virulence and toxicity factors
What portion of the cell wall is important in maintaining cell shape and providing mechanical strength
peptidoglycan layer
What portion of the cell wall determines the gram staining
peptidoglycan layer
Peptidoglycan layer composition
woven network of NAG and NAM (N-acetylmuramic acid and N-acetylglucosamine)
Lysozyme
cleaves the amino sugar bonds (NAM, NAG) of the peptidoglycan layer, lysing the bacteria
Where is lysozyme found
saliva and tears
Peptide stems allow for
(amino acid side chains) weaving/covalent linking of the NAM and NAG molecules of the peptidoglycan layer
Peptide side chains of NAM and NAG must contain
D-A.A.
Peptidoglycan layer functions
prevents cell bursting from osmotic forces, gives cell shape
Which bacteria lack peptidoglycan
Mycoplasma, Rickettsia, Ehrlichia, Anaplasma
Outer cell membrane is
a lipid bilayer with phospholipid as the inner leaflet and LPS as the outer leaflet
Periplasm
found outside the cell membrane of gram negative bacteria and contains the peptidoglycan layer
Periplasm function
- OSMOTIC PROTECTION
nutrient uptake from OM to CM, chemotaxis, degradative enzymes, osmoregulation
Are Gram-negative bacterium more or less susceptible to cell-wall active agents?
less; only 1 layer of peptidoglycan which is hidden in the periplasm beneath the outer membrane
Outer Membrane functions
- SHIELDS AGAINST ENVIRONMENTAL CHANGES,
virulence and toxicity factors, antigenic components, receptors for antibodies and sex pilus, anchors external structures of bacteria
Outer Membrane prevents entrance of
dyes, detergents, hydrolytic enzymes (lysozome)
Outer membrane composition
lipopolysaccharide, phospholipid, proteins
The outer leaflet of the outer membrane lipid bilayer
LPS
The inner leaflet of the outer membrane lipid bilayer
phospholipid
Porins
Outer membrane proteins that form aqueous channels to allow hydrophilic substances pass through the OM
LPS constituents
Lipid A + core + O-antigenic chain
Lipid A is composed of
fatty acid + disaccharide, phosphate groups, fatty acids, LPS toxicity is associated with Lipid A
Core is composed of
oligosaccharides, sugars, ketodeoxyoctulonate [KDO] - common in enteric bacteria
Terminal Polysaccharide
O antigen
Terminal Polysaccharide is composed of
sugars, a unit repeating, highly specific and highly variable
Terminal polysaccharide variation
each strain of bacteria possesses a chemically distinct O-antigen
Lipooligosaccharide (LOS) is composed of
Lipid A + extended core
Lipooligosaccharide (LOS) is
synthesized in place of LPS in Neisseriameningitidis and N. gonorrhoeae, and H. flu and H. ducreyi
Lipooligosaccharide (LOS)
lacks O-antienic chain
LPS functions
structural component of OM, pyrogen, complement pathway, hageman factor, release of endogenous mediators
LPS acts as a pyrogen by producing
induction of IL-1 which acts on the hypothalamus, or DIRECTLY acting on the hypothalamus
LPS activates __________ complement pathway
alternative
LPS activates ___________ factor
Hageman (factor XII)
LPS induces the release of endogenous mediators:
TNF-alpha, IL-1, IL-6, arachidonic metabolites, bradykinin, histamines, NO, free radicals
LPS structure is
heat stable unless with strong oxidizers
LPS does not form
toxoids, due to to heat stability
How would one detoxify LPS?
burning or oxidation
LPS may potentially cause
SIRS; with macrophages, PMNs, and endothelial cells as effector cells
Bacterial endospore-formers
Clostridium and Bacillus
Activation of the SIRS pathway occurs via
infection (esp gram-negative bacteria) or non-infectious etiology
How does LPS activate SIRS immune response
LPS binds LBP, LBP-LPS complex binds membrane-bound CD14 on PMNs, macrophages, and monocytes to and activates TLR; complex interacts with soluble CD14 which causes endothelial leakiness (hypotension, edema)
ARDS (acute respiratory distress syndrome) is a common feature of _________, not _________
distributive shock, not systemic inflammatory response syndrome
Endogenous mediators released by activation of TLR result in
temperature > 38 or < 36
HR >90
RR >20
Leukocytosis >12,000 or leukopenia <4000
The clinical definition of SIRS is
TWO or MORE symptoms: temperature > 38 or < 36 HR >90 RR >20 Leukocytosis >12,000 or leukopenia <4000
SIRS consists of
ONE or MORE
Systemic inflammation/ “hyperinflammatory state”
Activation of coagulation
Inhibition of fibrinolysis
Why does activation of coagulation occur in SIRS?
LPS activation of Hageman Factor XII, activates clotting system and fibrinolysis, followed by inhibition of fibrinolysis by plasminogen activator inhibitor
plasminogen activator inhibitor
causes inhibition of fibrinolysis during SIRS
DIC Disseminated Intravascular Coagulation
results from accumulation of undissolved thrombin in the microcirculation
DIC may lead to
multi organ failure and purpuric skin lesions
Survival of the hyper inflammatory state is followed by
hypo inflammatory state “immunoparalysis”
Hypoinflammatory state is manifested by
loss of delayed hypersensitivity
failure to clear primary infection
development of secondary infection
reactivated dormant viruses
Sepsis is defined by
the presence of BOTH:
- A proven infection
- Presence of 2 or more SIRS manifestations
Severe sepsis is defined by
the presence of BOTH:
- Sepsis
- Organ Failure
Septic Shock is defined by
the presence of BOTH:
- Severe sepsis
- refractory hypotension (40-50/30-40)
Shock is defined by
inadequate perfusion of tissues
3 Types of shock
cardiogenic, vascular obstructive, hypovolemic
Distributive shock is a type of
hypovolemic shock
Distributive shock consists of
endothelial cell dysfunction (leakiness), loss of vascular resistance –> hypotension, coagulopathy/DIC, septic cardiomyopathy –> reduced CO (reversible)
Septic cardiomyopathy is induced by
LPS, C5A, IL-1beta, TNF-alpha, IL-6
Clinical manifestations of distributive shock
fever or hypothermia, chills, leukopenia or leukocytosis, high HR and RR, DIC, hypotension shock and DIC can lead to MOF or MOD
Therapy for early Sepsis - sepsis resuscitation bundle
Measure serum lactate, obtain blood specimen for culture, administer broad-spectrum antibiotics, if hypotensive administer fluids or vasopressin, achieve O2 saturation
Therapy for early Sepsis - sepsis management bundle
corticosteroids, tight glycemic control
Failed sepsis therapies
anti-TLR4 (eritoran tatrasodium) and drotecogin alfa (activated, recombinant protein C)
Detecting LPS in pharmaceutical industry
Limulus amebocyte lysate test, mAb anti-LPS
endotoxin v exotoxin - chromosome encoded?
endotoxin only chromosome encoded, exotoxin may be encoded by chromosome or plasmid
endotoxin v exotoxin - required for survival?
endotoxin - yes; exotoxin - no
endotoxin v exotoxin - composition?
endotoxin - sugar-phosphate-fatty acids
exotoxin - protein
endotoxin v exotoxin - number encoded by bacteria?
endotoxin - more than 1 structural form
exotoxin - one specific form
endotoxin v exotoxin - toxoid?
endotoxin - NO, heat stable
exotoxin - YES, heat labile
endotoxin v exotoxin - receptor?
endotoxin - general PAR receptor
exotoxin - specific toxin receptor
endotoxin v exotoxin - mechanism?
endotoxin - systemic reaction > SIRS > DS
exotoxin - host cell reaction of altered function, lysis, molecule mimicry
endotoxin v exotoxin - pyrogens
endotoxin - exogenous (direct through BBB) and endogenous pyrogen (IL-1, TNF-alpha)
exotoxin - no
endotoxin v exotoxin - presence in human blood
endotoxin - sepsis
exotoxin - toxemia
name the main components of the gram-positive cell wall
peptidoglycan, teichoic acid, lipoteichoic acid (in outer CM leaflet)
Peptidoglycan in gram positive bacteria
extensively cross-linked (muramic side chains) and present in large amounts
Lipoteichoic acid structure
glycerol-PO4 or ribitol-PO4 covalently linked to glycolipid, noncovalently linked to outer leaflet of CM, extending through the peptidoglycan to the external environment
What is the primary factor in the adhesion of Strep pyrogenes to fibronectin on pharyngeal epithelial cells
Lipoteichoic acid
Teichoic acid structure
glycerol-PO4 or ribitol-PO4 covalently linked to peptidoglycan, extending through the peptidoglycan to the external environment
Teichoic acids medical importance
peptidoglycan + teichoic acid can produce endotoxin-like shock in patients with staph. aureus by interacting with C-reactive protein and activating the alternative complement pathway
How can DIC and DS occur with pathogens lacking LPS?
PARS recognition of PAMPS, releasing endogenous mediators that cause SIRS
NOD1 and NOD2
internal PAR, NOD2 deficiency is related to Crohn’s
TLR
extracellular PAR, bind peptidoglycan, teichoic acid, N-f-met-leu-phe, CpG, LPS
Spores
a complete but inactive cell in a protective shell, forms inside mother cell which dies
Most bacteria __________ form spores
DO NOT
Spores are formed in order for bacteria to
survive adverse conditions until environmental conditions are favorable
bacterial endospores have increased
longevity, resistance to heat/temp, resistance to desiccation, resistance to chemical agent
What 2 genera of bacteria are spore-forming
bacillus and clostridium
Small colony variants
growth-deficient variants that fem colonies, due in part to deficiencies in energy metabolism, possess enhances resistance to antibiotics, recurrent infections
small colony variants are formed by
Staphylococcus aureus, pseudomonas aeruginosa, E. coli and UTIs
Small colony variants are associated with chronic, recurrent infections of
heart,lung, bones, urinary tract
Biofilm and SCV are phenotypic switching, meaning
they can revert back to their previous form and re-seed