MGI 301 Week 14 Quiz

steps of municipal water purification

water source —> coagulation —> flocculation —> sedimentation —> filtration —> disinfection —> distribution

role of biofilms in waterborne infections

bacteria attach to surfaces and each other, protected by ECM, resistant to disinfectants, can detach and spread infection

vibrio cholerae transmission

fecal-oral

vibrio cholerae environment

replicates in water

vibrio cholerae location in host

extracellular (intestinal lumen)

vibrio cholerae disease

cholera —> severe diarrhea

salmonella typhi transmission

fecal-oral

salmonella typhi environment

does not replicate in water

salmonella typhi location in host

intracellular

salmonella typhi disease

typhoid fever (systemic infection)

vibrio cholerae vs salmonella typhi key difference

v. cholerae is extracellular and causes diarrhea; s. typhi is intracellular and causes systemic diseaseh

how pathogens cause disease (molecular level)

interactions with host cells (toxins, invasion, immune evasion) disrupt normal processes —> symptoms

toxin-coregulated pili (TCP)

allow vibrio cholerae to attach to each other and surfaces; required for biofilm formation and colonization

cholera toxin mechanism

AB toxin: B binds cell, A activates cyclase —> increases cAMP —> ion (Na+, Cl-) and water secretion —> severe diarrhea

non-typhoid salmonella infection

localized infection, causes inflammation and diarrhea to promote spread

salmonella typhi infection

systemic infection, avoids inflammation, spreads to organs and hides in host

salmonella typhi carrier state

lives in gallbladder, forms biofilm, asymptomatic shedding of bacteria, can persist for years

bacterial survival and environment relationship

depends on metabolic, genetic, and structural traits that allow growth in specific conditions

steps of biofilm formation

attachment —> microcolony formation —> early biofilm —> mature biofilm (ECM) —> dispersion

biofilm vs planktonic bacteria

biofilm: attached, ECM present, slow metabolism, antibiotic resistant

planktonic: free-swimming, no ECM, faster growth, more susceptible

quorum sensing in vibrio cholerae

cell density signaling: low density = motile; high density = biofilm formation —> aids survival and infection

effects of mutations in aerobic respiration (v. cholerae)

less ATP production —> slower growth —> less competitive in intestine

why salmonella typhi has many pseudogenes

lost genes unnecessary for human-only lifestyle (i.e., environmental survival, inflammation triggers, chemotaxis)

effects of mutations, HGT, microbials, and immune response on bacteria

mutations alter genes; HGT adds virulence traits; antimicrobials select resistance; immune response selects evasion traits

role of HGT in salmonella typhi evolution

acquires pathogenicity islands, toxin genes, and virulence factors —> enables systemic infection

zoonosis

disease found primarily in animals but transmissible to humans; usually spread by direct contact or respiratory routes

enzootic

disease present endemically in certain animal populations (geographic or seasonal)

epizootic

an epidemic occurring within an animal population

vector (in disease transmission)

a live agent that transmits infectious diseases from an infected host to an uninfected host (i.e., insects, ticks)

common vectors of disease

fleas, mosquitos, ticks

how vectors benefit pathogens

allow pathogens to bypass physical barriers (like skin) and enter directly into the bloodstream

dead end host

a host in which the pathogen cannot replicate or be transmitted further

rickettsial diseases (general characteristics)

caused by obligate intracellular bacteria; transmitted by vectors (often ticks); treated with antibiotics

rickettsial disease examples

rocky mountain spotted fever, typhus, Q fever

rocky mountain spotted fever pathogen

rickettsia rickettsii

rocky mountain spotted fever vector

ticksrocky mountain spotted fever

rocky mountain spotted fever symptoms

fever, headache, severe rash, diarrhea, vomiting

how rickettsia spreads to host

injected into bloodstream —> rapidly disperses to multiple organs

typhus pathogen

rickettsia prowazekii

typhus vector

head lice

typhus reservoir

flying squirrels

why vector control prevents disease

reducing vector populations lowers transmission of vector borne pathogens

lyme disease vector

deer tick

lyme disease pathogen

borrelia burgdoferi

plague vector

fleas

plague pathogen

yersinia pestisp

plague reservoir

wild rodents (especially rats)

how plague spreads to humans

fleas transmit the pathogen from infected rodents to humans

bubonic plague

affects lymph nodes; flu-like symptoms after 3-7 days; high mortality if untreated

pneumonic plague

infects lungs; spread by inhalation or progression from other forms

septicemic plague

bacteria spread in bloodstream; rapid onset and often fatal before diagnosis

tetanus pathogen

clostridium tetani

clostridium tetani characteristics

strict anaerobe, spore-forming bacterium found in soil

tetanus reservoir

soil (anaerobic environments)h

how tetanus infection occurs

spores enter deep puncture wounds —> germinate in low-oxygen conditions

tetanus disease mechanism

production of tetanus toxin —> causes spastic paralysis

tetanus prevention

toxoid vaccine

common infection sites of s. aureus

skin (SSTIs), blood (bacteremia/sepsis), bone/joint (osteomyelitis, septic arthritis), ear (otitis media), wounds (localized infections)

hemolysins (staphylococcus virulence factor)

cytolytic toxins that lyse RBCs

leukocidins (staphylococcus virulence factor)

kill WBCs —> helps bacteria evade immune system

coagulase (staphylococcus virulence factor)

forms fibrin clot around bacteria —> hides from immune system

capsule (staphylococcus virulence factor)

prevents phagocytosis by immune cells

protein A (staphylococcus virulence factor)

interferes with antibodies

catalase (staphylococcus virulence factor)

breaks down hydrogen peroxide —> helps bacterial survival

toxic shock syndrome

caused by a superantigen toxin leading to massive immune activation, widespread inflammation, and life-threatening effects

gram stain of s. aureus

gram positive bacteria in chains

STDs

infections spread through direct sexual contact (gonorrhea, syphillis)

syphilis pathogen

treponema pallidum (spirochete)

gonorrhea pathogen

neisseria gonorrhoeae (gram negative diplococcus)

how gonorrhea escapes adaptive immunity

antigenic variation (changes pili), high mutation rate, HGT —> immune system cannot recognize it —> reinfection possible

primary syphilis

painless chancre (sore) at entry site; appears 2 weeks-2 months after infection

secondary syphilis

rash and systemic spread; may enter latent phase

tertiary syphilis

long term damage to skin, bones, and nervous system; can cause blindness and disfigurement

food preservation - refrigeration

slows enzyme activity and metabolism —> slows bacterial growth

food preservation - acidity

low pH disrupts enzymes and cell processes

food preservation - drying

removes water needed for growth

food preservation - salt/preservatives

causes osmotic stress or chemical damage

food preservation - radiation

damages dna

food preservation - heat (pasteurization/canning)

denatures proteins and kills bacteria

food preservation - fermentation

produces acids —> inhibits microbial growth

listeria monocytogenes - food industry threat

can grow in the fridge, has a 20-40% fatality rate, and causes systemic infection

temperature range of growth

determines if bacteria can grow during storage

DRT

time to kill 90% of bacteria at a given temp; longer DRT = more heat resistant

oxygen requirements

facultative anaerobes survive in more environments —> higher risk

sanitization resistance

biofilm-forming bacteria persist on surfaces —> harder to remove

pH tolerance

wider tolerance = can survive in more food types

foodborne intoxication

disease from preformed toxin in food; bacteria may be dead; fast symptoms

foodborne infection

disease from live bacteria growing in host; slower onset

cooking + infection vs intoxication

cooking kills bacteria and prevents infection; heat-stable toxins remain and intoxication still occurs

gene expression adaptation - foodborne

bacteria adjust to gene expression to survive in new environments (food —> host)

SEA (staphylococcal enterotoxin A)

heat stable toxin made in food; superantigen —> inflammation —> intoxication

shiga toxin

AB toxin made in host; inhibits protein synthesis —> cell death —> infection

SEA vs shiga (key difference)

SEA = preformed, heat stable, intoxication

shiga = produced in host, requires live bacteria

ETEC (enterotoxigenic E. coli)

extracellular intestinal pathogen; toxin-mediated diarrhea; usually mild

listeria monocytogenes (pathogenesis)

intracellular systemic pathogen; no toxin; immune response causes damage

listeriolysin O (LLO)

breaks phagosome —> allows listeria to enter cytosol and replicate

intoxication vs infection (data clues)

intoxication = rapid, toxin present, bacteria absent

infection = delayed, bacteria present, growth required

serotype

classification based on surface antigens

serotype vs genotype

serotypes reflect underlying genetic differences

pulsed field gel electrophoresis

separates large dna fragments —> creates band patternd