week 7 evasion of host immune responses (adherence and inital)

what is the frst step in nacteral pathogensis

attachment to host cells colonization

why is attachment criitical for bacteria

preents removal by host defneses and allows colonization

what is coloniization

estabilishment and mulplcation of bacteira at a specifc stie

after attachement what must bacteria acquire to contnue nfection

nutrents for growth

why is iron acquiston consdered a vrulence factor

host lmt ron avablty so bactera must actelvy obtan itw

hat is the purpose of immune evason in pathogenesis

to allow persstence wthin the host

define persistence

the ability of bacteria to survive and reman n the host over tmewha

Q: What step allows bacteria to spread beyond the initial infection site?

A: Dissemination

Why is dissemination important for bacterial survival?

A: Enables infection of new tissues and increases chances of transmission

Q: What is transmission?

A: Spread of bacteria from one host to another

Q: What does “species survival outside host” refer to?

A: Survival in environment before infecting a new host (“pre-infection stage”)

Q: What determines disease symptoms?

A: Microbial factors + host immune response

Q: True or False: Disease symptoms are always caused directly by bacteria.

false often due to host response too

Q: Define virulence factors.

molecules or strateges that enable bactera to infect survive, and cause disease

are virulence factors always toxins

no can include adhesins, capsules, eznymes, immune evasson

Q: If a bacterium can attach and grow but cannot evade the immune system, what happens?

A: It will likely be cleared → no persistent infection

Q: A mutant bacterium cannot acquire iron in the host. Which stage is affected?

A: Nutrient acquisition → growth

Q: A bacteria survives well in the environment but cannot attach to host cells. What happens?

A: No infection → fails at colonization

Q: Which step is MOST directly linked to symptoms: attachment, growth, or immune evasion?

A: Trick question — symptoms result from BOTH bacterial products AND host response

Q: If bacteria spread through the bloodstream to multiple organs, which step is this?

A: Dissemination

Q: Why might a highly virulent bacterium reduce its own transmission?

A: If it kills the host too quickly, it limits spread

Q: True or False: Transmission is required for disease within a single host.

A: False (transmission is for spread between hosts, not disease within one)

Q: What stage would biofilm formation MOST directly support?

A: Persistence (immune evasion + long-term survival)

Q: If a pathogen triggers a strong immune response that damages host tissue, who is causing the damage?

A: BOTH pathogen and host (key concept!)

Q: Which step is targeted by vaccines most often?

A: Attachment or early infection stages

the steps of bacteral

1. attachment to host cells

2. nutrent acquston

3. evason of host mmune system

4. dissemination (species survivel)

5. transmission

6. speces survival OUTSDE HOST (pre-infection)

Q: During which growth phase is bacterial division at its MAX rate?

exponential log

Q: Which phase is MOST associated with adhesins and initial host interaction?

A: Early exponential phase

why are adhesins epxressed early n nfection

to establish attachment before host defenses remove bacteriawha

what process often follows adhesion durng nfecton

internaliization into host cells

Q: Which phase is associated with secretion of proteins and tissue damage?

A: Early stationary phase

Q: Why do bacteria secrete proteases during stationary phase?

A: Break down host tissue → release nutrients

Which phase is most associated with persistence and long-term survival?

stationaryt

t or f bacteria are metabolically inactive in stationary phase

false

what tiggers entry into stationary phaes

nutrient limitation or waste accumulation

what is teh role of MgA

regulates virulence genes (adhesions early phase)

what do two compnnets system like NRA/ROFA do

sense envrionment and regulat gene expression

what does Rgg do

quorum snesng and regulation of virulencen

what is ropb known for

controls expresson of secreted virulence factors

Q: List 3 environmental challenges bacteria face outside the host.

• nutrient limtation

• UV radiation

  • desiccaton (DRYNG)

why iis lack of adherence stes a problem

bacteria cant easily colonize or persist

what is the most resstant bacterial survial form

endosporewha

what conditions trigger endospore formation

envrionmental stresswha

what s matabolc dormancy

reduced metbaolc actvty to conserve energywh

why s dormancy benfal a

llows survval wthout nutrents

Q: What type of damage does UV light cause?

dna

Q: What must bacteria resist to survive oxidative stress?

A: Protein oxidation

Q: What is the advantage of forming biofilms on abiotic surfaces?

A: Protection + increased survival

Q: Give an example of an abiotic surface.

A: Medical devices, pipes, plastics

Q: How do intermediate hosts help bacteria survive?

A: Provide protection and transport

Q: Name two intermediate hosts mentioned.

A: Insects and amoeba

Q: A mutant bacterium cannot form endospores. What environment would MOST reduce its survival?

A: Extreme conditions (heat, UV, desiccation)

Q: If adhesin genes are not expressed, which step of pathogenesis fails?

A: Attachment → colonization

Q: A bacterium is alive but not dividing and highly resistant to stress. What state is it in?

A: Metabolic dormancy

Q: Why might virulence factors be upregulated in stationary phase instead of exponential phase?

A: Nutrient limitation → need to extract nutrients from host

Q: True or False: Biofilms are only important inside the host.

false mportant outsde

Q: A bacteria senses cell density and then activates toxin production. What system is this?

A: Quorum sensing (Rgg-related)

Q: Which is more important for transmission: exponential growth or survival outside host?

A: Trick — BOTH (growth for numbers, survival for spread)

Q: What is a biofilm?

A: A multicellular community of bacteria embedded in a protective matrix

Q: What is the biofilm matrix made of?

extracellular matrix

Q: Can biofilms be composed of multiple species?

A: Yes (single-species or mixed-species)

Q: How do biofilm bacteria differ from planktonic (liquid) bacteria?

A: Different gene expression, physiology, and increased stress tolerance

Q: True or False: Biofilm bacteria behave the same as free-living bacteria.

A: False

Q: Why are biofilms resistant to antibiotics?

A: Matrix protection + slow growth + altered gene expression

Q: Why are biofilms resistant to the immune system?

A: Physical barrier + reduced immune access + altered bacterial state

Q: What is the FIRST step of biofilm formation?

A: Adhesion (attachment to surface)

Q: What happens after adhesion?

A: Aggregation (cells stick together)

Q: What forms after aggregation?

mature boflm

Q: Is biofilm formation random or regulated?

A: Highly regulated process

Q: What happens in the final stage of the biofilm cycle?

A: Dispersal (cells leave to colonize new sites)

Q: What is the purpose of dispersal?

A: Spread infection / colonize new environments

biofilm sequence

Adhesion → Aggregation → Biofilm maturation → Dispersal

Q: Instead of dispersal, what can some bacteria do under starvation?

A: Fruiting body formation

Q: What is a fruiting body?

A: Structured survival form produced under nutrient limitation

Q: Name 3 infections associated with biofilms.

• Dental plaque / periodontal disease

• Endocarditis

• Medical device infections

Q: What lung disease is strongly associated with biofilms?

A: Cystic fibrosis (CF) lung infections

Q: What type of microscopy is used to visualize biofilms in 3D?

A: Confocal microscopy

Q: Why are antibiotics less effective against biofilms even if the bacteria are not genetically resistant?

A: Physical barrier + metabolic dormancy + altered gene expression

Q: A mutation prevents bacteria from producing EPS matrix. What happens?

A: Biofilm formation is impaired

Q: Which step of biofilm formation is MOST similar to initial pathogenesis?

Adhesion

Q: True or False: Dispersal reduces bacterial survival.

A: False (it promotes spread and transmission)

Q: Why might slow-growing cells in a biofilm survive antibiotics better?

A: Many antibiotics target actively dividing cells

Q: A patient has a chronic infection that doesn’t respond to antibiotics. What is a likely cause?

A: Biofilm formation

Q: What is the biggest advantage of mixed-species biofilms?

A: Cooperation → enhanced survival and resistance

Q: If bacteria in a biofilm suddenly detach and spread, what stage is occurring?

A: Dispersal

Q: Why are biofilms considered a “community” behavior?

A: Cells communicate and coordinate gene expression (quorum sensing)

Q: What type of bacterium is Pseudomonas aeruginosa?

A: Gram-negative opportunistic pathogen

Q: Why are burn patients highly susceptible to P. aeruginosa?

A: Loss of skin barrier + weakened immune defense

Q: Which disease is P. aeruginosa MOST associated with in the lungs?

A: Cystic fibrosis infections

Q: List 3 other infections caused by P. aeruginosa.

• Skin (burns, chronic wounds)

• UTIs

• Endocarditis

Q: Where is P. aeruginosa commonly found in the environment?

A: Soil, water, plants

Q: What is a key diagnostic feature on King’s medium?

A: Blue/green or yellow pigment production

Q: What are key identifying features of P. aeruginosa?

• Gram-negative rod

• Motile

• Can grow at 42°C

Q: What major lifestyle switch occurs in P. aeruginosa biofilm formation?

A: Switch from motile (free-living) → sessile (biofilm)

Q: What happens to motility genes during biofilm formation?

A: Turned OFF

Q: What is turned ON during biofilm formation?

A: Biofilm matrix production + community genes

Q: What regulates this transition?

quorum sensing

Q: What is the correct order of the biofilm cycle?

• Attachment (reversible)

• Irreversible adhesion

• Microcolony formation

• Maturation

• Dispersal

Q: What happens during initial attachment?

A: Weak, reversible binding to surface

Q: What happens during irreversible adhesion?

A: Strong attachment + gene expression changes