Waterborne Bacterial Diseases

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