Bacteria Flashcards
Give 3 key points about the development of germ theory
- Idea of transmissible, infectious disease from C16; disease as process C19
- Lister brought Pasteur’s observations to surgery - introduced antisepsis
- Robert Koch isolated pure cultures, showed specific bacteria cause specific diseases
What are Koch’s postulates (4)
- bacterium is present in every case of the disease
- bacterium must be isolated from the disease and grown in pure culture
- specific disease must be reproduced from pure culture in healthy susceptible host
- bacterium must again be recovered
Name some new diseases that have emerged as the population has aged and our lifestyle/ environment changes (4)
food-borne infections, Legionnaires’ disease, Helicobacter ulcers, toxic shock syndrome
Diseases also re-emerge, increasingly protected by
resistance to antibiotics (TB, pneumonia, whooping cough, STIs, nosocomial infections)
Name 2 bacterial diseases that are acute and last days and 2 that can be chronic, lasting for years
Name a bacterial disease that involves a carrier
pneumonia, gastroenteritis
syphilis, TB
typhoid
How do bacterial modes of transmission compare with viral modes?
often similar but as bacteria are rarely obligate intracellular parasites and can multiply outside the host they can spread in additional ways.
Give 4 modes of horizontal bacterial transmission and give examples of each
sexual contact e.g. syphilis, gonorrhea
• via respiratory tract (air-borne droplet)
Upper: pharyngitis, scarlet fever, diphtheria
Lower: whooping cough, tuberculosis, pneumonia, plague
• contamination from own flora e.g. urinary tract infection (UTI) from GI tract
• contact with skin, eyes e.g. boils, impetigo, fasciitis, conjunctivitis, leprosy, anthrax
How can bacterial disease spread vertically (2)
give eg of each
transplacental e.g. syphilis
parturition e.g. gonorrhoea
Other than vertical and horiztonal, how else can bacterial disease spread
indirect contact:
via inanimate objects, food, water, animals, soil
Give examples of bacteria that can spread via a) inanimate objects, b) food, c) water, and d) soil
a)e.g. nosocomial infections (hospital acquired) e.g. urinary tract following catheterization, surgical wound, burn infections. Caused by ‘opportunistic’, often drug resistant, pathogens e.g. (MRSA), Pseudomonas aeruginosa
b) intoxication e.g. Staphylococcal food poisoning, botulism
infection e.g. Salmonellosis (chicken, eggs), E.coli 0157 (beef)
c) cholera, dysentery, typhoid (these are faecal-oral)
Legionnaires’ disease (air-con, respiratory)
d) via wound (spores) – tetanus, gas gangrene
Give examples of bacterial diseases being spread via animals
(Zoonoses).
Animals have disease and/or are reservoirs, can include food-borne diseases, also from livestock (e.g. brucellosis, leptospirosis, E.coli 0157), wild animals (lyme disease via ticks)
Define the following
endemic
epidemic
pandemic
• Endemic: disease that occurs regularly at low or moderate frequency, e.g. dental
caries.
• Epidemic: sudden appearance of disease, or increase above endemic level e.g.
diphtheria
• Pandemic: global epidemic e.g. cholera
What are the 3 steps taken when there is a disease outbreak
traced to source, the mode of transmission determined, and the infectious agent identified.
True or false
bacterial disease outbreaks can arise from a single origin
As bacteria can survive and replicate outside the host, point source outbreaks can arise from a single origin, even non-living e.g. food poisoning, nosocomial infections.
When was there a key outbreak of Legionnaire’s disease
How is it typically contracted
What causes it
What happened to the outbreak
1976
from air con units
the bacterium Legionella pneumophila
as the origin was identified it could be address and it was only a point source outbreak
How does a point source outbreak become continuous source outbreaks
if the source is not eradicated e.g. typhoid (carrier),
travellers’ diarrhoea, food-borne infections,
hospital-acquired Staphylococci.
Describe the continuous source outbreak in 2012 of MRSA
rapid DNA sequencing identified an ongoing outbreak of MRSA in the Special Care Baby Unit at the Rosie Maternity Hospital. Screening of healthcare workers found one carrying MRSA. DNA sequencing confirmed that this MRSA strain was the source of the outbreak. The worker was treated with antibiotics, bringing this continuous source outbreak to an end.
What are propagated outbreaks of bacterial disease
host-to-host transmission results in ever greater numbers of infections
e.g. whooping cough, tuberculosis, gonorrhoea, dysentery, cholera, typhoid
Give an example of a bacterial disease that had point source, continuous source and propagated outbreaks
Bubonic plague, caused by Yersinia pestis, spreads from rodents (point/continuous source) to humans, in which the disease becomes pneumonic (propagated person-to-person)
Are bacteria obligate parasites?
Bacteria make ATP and protein, so generally are not obligate parasites. Rare exceptions include Chlamydia
Give a key difference between bacterial and viral replication
Unlike viruses, bacteria maintain structural integrity during replication
How do bacteria usually exist
typically unicellular and free-living, bacteria also live in complex multicellular communities (biofilms) and/or in association with eukaryotes.
do bacteria have organelles?
cell membranes?
usually no
yes - a lipid bilayer that acts as an osmotic barrier, and is the site of signal reception, transport of nutrients, and respiration. In Gram-negative bacteria this is called the ‘cytoplasmic’ or ‘inner’ membrane.
Give 2 ways bacterial cells can be motile
e.g. rotating flagella, extending/retracting pili ‘grappling hooks’
How do bacterial cells divide?
binary fission
Do bacteria have sexual reproduction
no meiosis,
but horizontal genetic transfer (HGT)
Briefly describe a typical bacterial genome
haploid, usually single & circular
+ plasmids, bacteriophage
Give 2 facts about bacterial mRNA
often polycistronic (co-linear genes), unstable
How does bacterial cell regulation differ from mammalian?
bacterial: mostly transcription initiation
mammalian: often post transcriptional
what are the different types of pathogenic bacteria (think shape)
give examples of bacteria and diseases for each
cocci (e.g. Staphylococcus, Streptococcus, Enterococcus),
rods (e.g. Salmonella, E. coli)
or curved rods (e.g. ‘comma-shaped’ Vibrio cholerae),
and are sometimes spiral e.g. Treponema (syphilis), Helicobacter (gastric ulcers)
Which bacteria produce endospores (4 examples)
where are bacteria that do this usually found
Clostridium tetani (tetanus), C. perfringens (gas gangrene, food poisoning), C. botulinum (‘botulism’ food poisoning), Bacillus anthracis (anthrax).
usually in soil
How to tell Gram positive from Gram negative bacteria
iodine-crystal violet complex is washed out of Gram-negative cells, but not Gram-positive cells.
The Gram stain reflects substantial differences in cell envelopes. Gram-positive bacteria have a thicker peptidoglycan wall, and Gram-negative bacteria have an extra (outer) membrane.
True or false
all bacteria are either Gram positive or negative
false
Some medically important bacteria do not Gram stain
(i) Mycobacteria, including Mycobacterium tuberculosis which causes TB, are called
‘acid-fast’ as they are difficult to stain/destain because of their waxy lipid coat.
(ii) Chlamydia and Mycoplasma, which cause non-gonococcal urethritis, lack a substantial cell wall. They are difficult to culture and insensitive to many antibiotics.
What is the bacterial cell wall made of
describe this material
peptidoglycan
- a huge macromolecule of alternating sugars N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM), cross-linked by short oligopeptides.
Oligopeptide crosslinks also form vertically to connect peptidoglycan sheets into a thick layer
How does the size of peptidoglycan differ between Gram positive and negative bacteria
Gram-positive peptidoglycan is 150-500 angstroms thick, the Gram-negative peptidoglycan layer is thinner.
Which bacteria have a periplasm
what is this
Gram negative
between inner and outer membranes
What does the periplasm contain
enzymes e.g. proteases, lipases, phosphatases, β-lactamases (break down lactam-ring containing antibiotics e.g. penicillin, cephalosporin) and components of transport (import, export) systems.
Where are porins found in Gram negative bacteria
outer membrane
Where is LPS found
The outer leaflet of the outer membrane contains lipopolysaccharide
(only in Gram negative)
What are the different parts of the LPS
O-antigen: highly variable, generating different antigens and therefore
serotypes. An important defence against host attack
Core polysacchride: constant sugars
Lipid A: he endotoxin released from dying bacteria, and is a major PAMP ‘alarm signal’ that triggers a wide-ranging
immune response.
Which type of bacteria tend to have polysacchride capsules
what is the point
respiratory pathogens like
Streptococcus pneumoniae and Haemophilus influenzae.
Capsule prevents drying and protects from host defences:
complement and macrophage.
Proteins central to interaction with the host are typically exported and/or assembled on the bacterial surface e.g. toxins, adhesins, flagella.
what mustt these things cross in Gram postive and negative bacteria
In Gram-positive and Gram-negative bacteria, proteins typically cross the cell (inner) membrane using an N-terminal secretion signal and the standard secretion (Sec) pathway.
In Gram-negative bacteria, additional export pathways cross the periplasm and outer membrane
What are the 4 steps of binary fission
genome duplication, segregation, cell septation and division
How fast do lab cultures of E. coli replicate
how does this compare to in vivo infection
Laboratory cultures can double every 20-30 minutes, but doubling can take hours in an infection
Are bacteria active in stationary phase?
yes
Radical changes in physiology and gene expression enable survival and reduce susceptibility to many antibiotics.
What are most bacteria’s relationship with oxygen
Most pathogenic bacteria are facultative anaerobes, e.g. Salmonella, Staphylococcus
What does facultative anaerobe mean
able to grow with or (usually less well) without oxygen
What do facultative anaerobes use for energy when growing aerobically
use glycolysis, the citric acid cycle and oxidative phosphorylation to generate ATP from glucose
Name some bacteria that are strict anaerobes
how do they gain energy
e.g. Clostridium, Bacteroides
from fermentation (using various terminal electron acceptors e.g. nitrate, sulphate or ferric iron. Oxygen is toxic to many
Where do all bacteria find carbon and energy
from organic matter (including us)
How are bacteria usually motile
flagella
How do flagella provide motility
The long flagellar filament is rotated like a propeller by a motor anchored in the cell (inner) membrane
What direction do bacteria move in
sense chemical signals and move towards them (nutrients) or away from them (toxic chemicals) by chemotaxis, in which chemoreceptors at the ‘nose’ of the cell sense and transmit information, via a phosphorelay, to the flagellar motor switch. The switch controls the direction in which the helical propeller rotates: counter clockwise (CCW) to swim, or clockwise (CW), causing the bacterium to ‘tumble’ and randomly change direction
True or false
bacteria usually have access to lots of resources
false
Pathogenic bacteria lead lives of feast and famine
How is a bacterium usually able to switch genes on/off depending on its environment
largely determined by changes in the coupled transcription of contiguous genes
(operons), which is tightly coupled to translation and rapid mRNA turnover.
Name 2 things bacteria have adapted to sense the environment effectively
large SA:volume ratio
signal transduction systems called histidine-aspartate phosphorelay (HAP) signalling pathways
Name some signals that might make a bacterium change its gene expression
temperature, pH, amino acids, osmolarity, ‘stress’.
What is global regulation
bacteria’s ability to co-regulate expression of networks of operons (regulons)
What is quorum sensing
how do bacteria do this
cell density sensing
whereby some pathogens switch on
their armoury of virulence genes when its population reaches a specific density.
by secreting a small signal molecule and sensing its concentration -
a form of communication!
How do bacteria change their genes other than immediate physiological changes
what does this lead to
evolution
genetic change is driven by mutations in large populations of rapidly replicating cells.
This results, for example, in variation in cell surface structures e.g. Salmonella and E. coli have hundreds of O (LPS) and K (capsular polysaccharide) antigen serotypes
What are bacterial DNA rearrangements
shuffling the genome
caused by random capture and insertion of DNA elements called insertion sequences (IS)
What are insertion sequences (IS)?
e a few hundred base pairs long and enter the genome using their own recombination system
part of DNA rearrangement in bacteria
What are transposons in bacteria
genomic elements (bigger than and often including IS elements) which have picked up useful (to the pathogen!) genes encoding e.g. antibiotic/heavy metal resistance, or virulence factors e.g. toxins.
How are transposons incorporated into the bacterial genome
what does this allow
s can be incorporated into the main genome or carried by plasmids
allow bacteria further flexibility and have enabled rapid spread of antibiotic resistance and virulence genes.
What are the 3 ways for bacteria to transfer DNA
transduction
transformation
conjugation
What is transduction (bacteria)
transfer of DNA via bacteriophages
What is transformation (bacteria)
uptake of DNA from dead/ lysed bacteria
What is bacterial conjugation
direct transfer of DNA requiring contact between 2 bacteria
Give 3 historical landmarks that are important for DNA transfer in bacteria
1928: discovery of transformation in Streptococcus pneumoniae (dead capsulated bacteria ‘transformed’ live non-capsulated bacteria and killed mice).
1944: DNA demonstrated to be the component responsible for transformation
1952: only DNA is introduced during transduction of bacterial cells by bacteriophage
What are the key events in bacterial pathogenesis? (3)
• colonization of epithelia/mucous membranes. This can involve stable adhesion on an epithelial surface and/or entry into host cells
• multiplication requires the ability to evade or survive the hosts defences.
This can lead to spread, locally or to distant sites
• transmission to a new host
These key events differ in sequence and mechanism in different bacteria.
What does the pathology of bacterial disease arise from
from host cell malfunction or death caused directly by toxins or bacterial invasion, and/or indirectly arising from the host response to the bacterial infection.
Give 3 facts about virulence genes
- are specialised. Not constitutively expressed, but switched on in response to host environmental signals. Often co-regulated by the same signals - global regulation.
- are often carried on extrachromosomal plasmids and bacteriophage, and/or grouped on pathogenicity islands (PAI) in the chromosome.
- encode proteins or other molecules that are exported to the bacterial cell surface, secreted into the environment, or delivered into host cells.
Where are bacterial genes for infection usually found
on pathogenicity islands (NOT randomly distributed in the genome)
How have pathogenicity islands evolved
by integration of transposons, plasmids and bacteriophage and incorporation of transformed DNA (pathogenicity islands typically have a G+C content that differs from the surrounding chromosomal DNA).
Name 2 Salmonella pathogenicity islands
What do they do
SPI-1 and SPI-2
determine, respectively, entry into non-phagocytic cells and survival in macrophages.
These increase dissemination of virulence traits and facilitate virulence gene co-regulation
For which bacteria is cell motility important in colonisation
e.g. enabling bacteria such as Vibrio cholerae and Helicobacter pylori to move through mucus.
Give 2 uses of flagella in bacterial colonisation
Many bacteria swim through liquids by means of rotary flagella.
Some bacteria also use flagella to ‘swarm’, moving rapidly across surfaces (e.g. urinary tract epithelium) as a coordinated population.
What do cell surface adhesins allow
enable bacteria to attach stably to host cells or extracellular matrix, via carbohydrate or glycolipid receptors
Where are bacterial adhesins usually found
give an example
assembled on the tips of long rigid pili (or fimbriae) projecting from the bacterial cell.
eg P-pilus adhesin of uropathogenic E.coli which binds a kidney receptor.
How are UTIs usually caused
by uropathogenic E. coli (UPEC) from the
host’s own colon flora by ascending infection.
Which types of people tend to get UTIs
women (shorter urethra)
catheter users
Which bacterium is associated with UTIs following catheter use?
Proteus (highly motile)
what is cystitis and what can it lead to
bladder infection
can ascend to kidney (pyelonephritis)
What can proteus infections of the urinary tract lead to
kidney stones (Proteus cleaves urea to ammonia by producing urease)
How does cystitis lead to kidney stones? (5)
Cell motility aids ascent of urinary tract
Common (type 1) pili bind bladder cells
Pap (P-pili) bind to receptors on the kidney
Damage by pore-forming toxin (haemolysin) and inflammation (LPS)
In Proteus infections, urease cleaves urea to ammonia causing kidney stones
Give an example of long term colonisation of the urinary tract
UPEC can cause recurrent UTIs
During acute infection, superficial epithelial cells undergo ‘exfoliation’, allowing UPEC to invade underlying epithelial cells where they persist as quiescent reservoirs, protected from antibiotic treatment. Quiescent UPEC can then resurge and enter the bladder lumen, causing further acute infection
Name 2 bacteria which adhere to host epithelial cells extremely tightly
enteropathogenic E.coli (EPEC) and enterohaemorrhagic E.coli (EHEC) causing intestinal disease
How do EPEC and EHEC adhere to epithelial cells
Interaction with the host cell cytoskeleton induces ‘pedestal’ formation by the host.
The bacterium uses specialized needles to deliver (‘inject’) proteins into the host cell, including a specific receptor (translocated intimin receptor, Tir).
Binding of the bacterial surface protein intimin to Tir subverts host cell signal transduction and promotes actin polymerisation
Which protein does EHEC inject into epithelial cells to cause actin polymerisation and pedestal formation
Tir (translocated intimin receptor)
this interacts with intimin on the bacterial surface to subvert host cell signaling
Give 3 examples of bacteria forming biofilms
- plaque-forming Streptococcus mutans and other bacteria on teeth (glucan formed from food sugar, acid leads to demineralisation i.e. caries)
- Staphylococci which colonise catheters e.g. in the urinary tract
- Pseudomonas aeruginosa which can colonise contact lenses, causing conjunctivitis
What is Pseudomonas aeruginosa
How does it cause damage
how are its genes encoding virulence factors and biofilm formation controlled
Gram negative opportunistic pathogen
Damage is direct (toxins etc) and indirect (inflammation).
co-regulated by quorum sensing.
Where do P aeruginosa biofilms form
in the lungs of individuals with cystic fibrosis
What is a critical component of chronic P. aeruginosa biofilm lung infections
the copious production of alginate polysaccharide ‘slime’. This protects bacteria in the biofilm from the host immune response and antimicrobials
What makes opportunistic bacteria like P aeruginosa particularly dangerous
often multidrug resistant due to multiple efflux pumps in the cell envelope
What are the 2 ways bacteria can force entry into non-phagocytic cells, e.g. intestinal epithelial cells rather than remaining on the surface
what do both mechanisms have in common
zipper mechanism
trigger mechanism
both induce changes in (‘remodel’) the host cell cytoskeleton by binding actin directly and/or subversion of host signal transduction.
What is the zipper mechanism used by bacteria to gain access to a non-phagocytic cell
Receptor mediated endocytosis e.g. by Listeria.
Here, bacterial ‘invasins’ mimic eukaryotic ligands e.g. fibronectin, a component of the host extracellular matrix that binds integrins. This causes cytoskeletal rearrangement to internalise the bacteria
What is the trigger mechanism used by bacteria to enter non-phagocytic cells
Subversion of host cells by bacterial effector proteins, some binding to actin, that are delivered directly into the target host cell through bacterial needles e.g. by Salmonella
These effector (invasion) proteins mimic eukaryotic cell proteins e.g. in actin binding and polymerisation (SipA and SipC) or signalling pathways (SptP). In Salmonella, genes encoding effectors (and needle) are on a pathogenicity island (SPI-1)
Name 2 pyogenic cocci
Staphylococcus and Streptococcus
How do Staphylococcus and Streptococcus spread through tissue
by using batteries of enzymes to spread through tissues, e.g. collagenase to break down connective tissue, coagulase to induce fibrin clot formation, staphylokinase to break down blood clots (opposite effect to coagulase), and DNAse to break down DNA in pus
How does Listeria spread in the body
enters cell in a vacuole via zipper mechanism
Inside the cell, it lyses the vacuole to enter the cytosol
Here it replicates and manipulates the cytoskeleton to become motile (actin comet tail) to spread into neighbouring cells in another vacuole
repeat
What are actin comet tails
a form of cytoskeletal rearrangement - actin polymerisation
induced by the pathogen, this time at one end (pole) of the bacterial cell granting it motility
What is a key difference between the behaviour of listeria and salmonella in the cell
listeria lyses its vacuole before beginning intracellular movement and replication
salmonella stays in its entry vacuole to replicate
What causes typhoid
which cells does it replicate in
salmonella typhi
macrophages - stays in entry vacuole so is not destroyed. this allows it to be spread locally and throughout the body by the host defense system.
Which diseases does chlamydia trachomatis cause
i) trachoma, the most prevalent form of infectious blindness in the developing world.
(ii) non-gonococcal urethritis, a common sexually transmitted infection, is often asymptomatic, many ‘silent’ carriers. However, can cause acute prostatitis (inflammation triggered by e.g. chlamydial LPS) and chronic infection can lead to pelvic inflammatory disease and infertility.
How big is the chlamydia genome
1.04 Mbp encoding ~900 genes (cf. Salmonella: 4.85 Mbp, ~4450 genes),
Why can the chlamydia genome be so small
has lost many metabolic enzymes and pathways and is adapted to obligate intracellularity, scavenging essential metabolites from the hostcell.
What are the 2 forms of the chlamydia bacterium in its lifecycle
infectious elementary body (EB), which has low metabolic activity and cannot replicate,
and
reticulate body (RB) that replicates inside host cells.
What are the 4 key stages of the chlamydia life cycle
- EB attaches to host epithelial cell and induces uptake in endosome.
- EB in the endosome differentiates to the metabolically active RB, which replicates. The RB-containing vacuole segregates from the normal endosome maturation pathway and becomes a protective, nutrient-rich vacuole or ‘inclusion
- The RBs then produce both EBs and RBs.
- The host cell lyses to release EBs that go on to infect more host cells
How is damage caused in chlamydia infections
by cell lysis and inflammation triggered by chlamydial LPS
How do chlamydia EBs induce uptake into host cells
Involves rearrangement of host actin cytoskeleton by chlamydial effector Tarp (translocated actin recruiting phosphoprotein) injected into host cell using virulence needle (similar to EPEC, Salmonella).
Name 5 of the physical and chemical barriers to bacterial survival and multiplication (not immune system)
skin mucous lysozymes gastric acid/ bile salts iron limitation resident microflora
How does the skin protect against bacterial survival and multiplication
- dry acidic, cool, high salt (limit growth)
* sloughing cells (remove bacteria)
How do mucous membranes protect against bacterial survival and multiplication (4)
- cilia (pulmonary airway)
- eyelid blinking, urine flow, GI tract motility
- mucin layer (physical barrier, traps bacteria)
- tight junctions (limit invasion between cells)
How do lysozymes protect against bacterial survival and multiplication
• in tears – splits bacterial peptidoglycan
Which 2 chemical barriers inhibit growth of bacteria in the body
gastric acid/ bile salts
Fe limitation via sequestration by lactoferrin and transferrin
How do resident microflora protect against bacterial infection
some sites densely occupied e.g. colon can have1011/ml.
Inhibits colonization by occupancy, toxic waste (pH) and chemicals (e.g. fatty acids, bacteriocins).
What are the early immune responses to bacterial infection (3)
• acute inflammation
• complement - alternative pathway activation by bacteria
(e.g. LPS)
• macrophages etc bind bacteria via lectins.
Kill in phagolysosome
Give 8 things that happen in the induced immune response to bacterial infection
- enhanced inflammation
- classical pathway of complement activation
- Ig production - CD4/MHCII/Th2
- IgG opsonization- Fc-mediated phagocytic killing
- Ig neutralization of toxins
- IgA at mucosa - blocks colonisation
- MHCII/Th1 activates macrophages;
- CTLs in some cases
Name bacteria that infect the following areas:
a) oral cavity
b) upper resp tract
c) skin
d) large intestine
e) urethra/ vagina
a) lactobacillus
b) Strep, corynebacterium, neisseria
c) staphylococcus, epidermidis
d) bacteriodes, E. coli
e) lactobacillus
Give 2 ways the body can make a hostile environment for pathogens
lack of essential iron
gastric acid
How do bacteria overcome the body’s attempt at making the environment hostile by reducing iron
Include examples
bind iron at high affinity (much higher than host) e.g. by secreting iron-binding siderophores and reimporting them loaded into the cell, e.g. green fluorescent pyoverdin secreted by the opportunistic pathogen Pseudomonas aeruginosa and equibactin produced by Streptococcus equi
How can bacteria overcome the hostile acidic gastric environment
Pathogens like Shigella (dysentery), and Helicobacter (ulcers) can resist
low pH by pumping H+ out of their cell and/or producing NH3 by urease action.
How can bacteria prevent macrophage uptake (4)
(i) Paralyse the macrophage by subverting its functions
(ii) Inhibit chemotaxis
(iii) Resist phagocytosis by shielding with antiphagocytic capsules
(iv) Kill macrophages with secreted cytolysins
How can bacteria paralyse the macrophage by subverting its functions
give examples
disrupting intracellular trafficking and signal transduction by injecting (needles again) anti-phagocytic proteins into the macrophage, e.g. Yersinia injects multiple effectors including YopT, a protease that targets small GTPases to disrupt the cytoskeleton, and YopP, an acetyl transferase that inhibits signaling, triggering apoptosis
How does Yersinia inhibit macrophage function (2)
injects multiple effectors including YopT, a protease that targets small GTPases to disrupt the cytoskeleton, and YopP, an acetyl transferase that inhibits signaling, triggering apoptosis
How can bacteria inhibit macrophage chemotaxis
Cleave complement C5a with C5a peptidase.
What are bacterial capsules commonly made of
which bacteria tend to have them
how can capsules help a bacterium avoid phagocytosis (3)
Capsules are commonly made of polysaccharide,
e.g. by bacteria causing pneumonia (e.g. Streptococcus pneumoniae)
- steric hindrance i.e. physical block
- non-immunogenic polysaccharide e.g. sialic acid
- lack affinity for complement factor B: C3b not formed
How can bacteria kill macrophages
with secreted cytolysins
What are cytolysins
pore-forming toxins that disrupt cell functions, cause apoptosis, and destroy cell
membrane integrity
