Spirochetes and Vibrios Flashcards Preview

Micro/Immuno Part 2 > Spirochetes and Vibrios > Flashcards

Flashcards in Spirochetes and Vibrios Deck (32):

spirochetes recurring themes

-wide variety of transmission methods
-cross easily into bloodstream
-primary virulence factors are for immune evasion- not immunogenic enough for a vaccine
-diagnosis is challenging-phases, treponema small, lyme no lab, eye exam is good
-little acquired antibiotic resistance-grow slowly and no plasmids
-Jarisch-Herxheimer reaction to treatment


genera of spirochete pathogens

-treponema-syphilis, yaws, pinta
-borrelia-lyme, relapsing fever


T pallidium

-small-0.25 uM diameter means invisible to light microscope
-delicate, cant survive outside host
-motile-flagellar corkscrew motion
-human restricted in nature but can induce in lab rabbits
-cannot be grown in culture
-extremely infectious sexually
-virulence based on immune evasion


t pallidum pathogenesis

-transmitted by sexual contact (acquired), blood, transplancentally (congenital)
-national plan to eliminate in US has hit bumps- MSM and SES disadvantaged


acquired T pallidium

-penetrates mucous membranes or small abrasions
-grows in BV endo, enters lymphatics and bloodstream
-CNS is invaded relatively early, though symptoms take years to develop, first CSF abnormalities, then meninges, then parenchyma of brain and spinal cord
-host raises antibodies, but they aren't useful
-surface of spirochete is nonimmunogenic
-spirochete downregulates TH1 cells


primary syphilis

-painless chancre at site of transmission 3-6 weeks later- highly infectious
-IF infiltrate at site fails to clear organism
-chancre heals 3-12 weeks


secondary syphilis

-4-10 weeks, spirochete multiplication-systemic symptoms
-fever, malaise, myalgias, arthralgias, lymphadenopathy
-mucocutaneous lesions of variable types, condylomata lata, patchy alopecia (moth eaten)
-high antibody titers


latent syphilis

-end for 2/3
-organism remains
-secondary symptoms resolve, may return intermittently over years


tertiary syphilis

-1/3 untreated, fatalities possible
-gummatous syphilis, granulomatous lesions with rubbery, necrotic center. primarily liver, bones, testes
-cardiovascular syphilis: >10 years: aneurysm of ascending aorta caused by chronic inflammation of vasa vasorum



-syphilitic meningitis-early -6mo
-meningovascular syphilis-damage to BV of meninges, brain, SC
-parenchymal neurosyphilis-tabes dorsalis- damage to SC- impaired sensation, wide based gait
-disruption of dorsal roots-loss of pain and temp sensation, areflexia
-general paresis-damage to cortical brain tissue-dementia


Argyll Robertson pupil

-hallmark of neurosyphilis
-one or both pupils fail to constrict in response to light
-bur do constrict to focus on a near object


congenital syphilis

-treponemes readily cross placenta and infect fetus
-miscarriage/stillbirth/neonatal death 40-50%
-within first two years, surviving infants develop sever secondary syphilis


prevention of syphilis

-penicillin and CONDOMS


B burgforferi bacteriology

-motile spirochete
-flat wave shape, not spiral
-stainable with giemsa, silver stain, IF, visible by standard microscopy
-tick borne, more common on east coast
-highest risk in summer, when nymphs are feeding
-small mammal reservoirs-mouse, rate perferred by nymphs, deer preferred by adults- can be in winter
-incidence increasing due to expansion of deer herds
-almost always requires 24h attachment to transmit


removing ticks

-tweezers and gloves
-bag and freeze
-doxy if patient is neither pregnant nor allergic to tetracyclines


B burgdorferi pathogenesis

-disease begins with injection of b burdoferi into host by tick, asymptomatic clearance possible
-over next 6 months, organism spreads
-erythema migrans rash (75%), anti-spirochete/autoantibodies raised
-very persistent skin infection established
-months to 1 year after infection, immune/neurological issues arise (stage 2). lyme arthritis predisposed by HLA-DR4 and HLA-DR2 genotypes and strains of bacteria
-other strains associated with neuro manifestations
-post lyme- 80% of untreated/undertreated cases report some neurological sequela
-reinfections occur



-pt usually doesn't recall tick bite, get history of outdoor activity, note season and geographic location
-stage 1- erythema migrans expanding rashes at or near bite site, bulls eye appearance in a minority
-rash around still attached tick is likely to be hypersensitivity, not Lyme
-flu like constitutional symptoms, fatigue, muscle ache, regional lymphadenopathy, low fever
-coinfection with erlichia or babesioa-high fever


stage 3

-chronic lyme
-subacute encephalopathy
-chronic progressive encephalomyelitis
-late axonal neuropathies
-may recall earlier episodes of bell palsy or aseptic meningitis


lab for lyme

-serology, ELISA, and IFA can confirm exposure to b burgdorferi, but not until 6-8 weeks later
-patients who received briefly available vaccine will be seropositive
-seropositivity remains long term, not useful for testing the cure or comparing acute w/ convalescent sera
-urine antigen testing is in pipeline



-empiric is ok if have history/seropositive/not preg
-treat pts with erythrema migrans
-10-20 days with doxy unless preg or allergic
-if symptoms are equivocal, may observe rash 2-3 days, erythema migrans will expand
-or treat and look for Jarisch Herxheimer reaction


lyme prevention

-protective clothing, deet, avoid woodsy areas, tick collars
-prophylaxis with doxy in some geographic areas


vibrio recurring themes

-curved, gram neg rods
-mostly ocean dwelling
-several are halophiles
-primarily cause fecal-oral gastroenteritis
-can also infect wounds contaminated by seawater or ocean debris
-also peptic ulcers
-gastroenteritis and peptic ulcers require specialized virulence factors for survival in the GI


V cholerae bacteriology

-curved, comma shaped, motile gram neg rod
-stains aerobic, facultatively anaerobic
-microscopic discovery of Robert Koch
-has been causing human epidemics for at least a millennium
-epidemic in london in 1854: john snow and the broad street pump
-2 reservoirs-humans and plankton ecosystem of indian ocean


V cholerae pathogenesis

-transmitted fecal oral
-shed by asymptomatic carriers in incubation of convalescence
-travels to untreated water or undercooked shellfish
-usually killed by stomach acid
-high ID50- 1000-1 mil
-people on antacids or with gastrectomy are more susceptible
-surviving bacteria reach small intestine, secrete mucinase to clear path to brush border, attach and colonize


V cholerae pathogenesis 2

-growing bacteria secrete cholera toxin (enterotoxin)-cholderagen
-AB subunit structure
-persistent activation of adenylate cyclase, loss of water and ions
-blocks absorption by microvilli while also promoting secretion from crypt
-massive watery diarrhea
-toxin and virulence factors carried by lysogenic phage CTX


V cholerae pathogenesis 3

-local acting, little penetration of the gut wall
-morbidity and death result from dehydration and electrolyte imbalance, severe cases may kill in hours
-surviving patients run the self limited course in 7 days


v cholerae diagnosis

-mild dehydration-3-5% down from normal body weight, excessive thirst
-moderate-5-8%, hypotension, tachycardia, weakness, fatigue, prolonged skin tenting, acidosis
-severe-10%, glassy/sunken eyes, sunken fontanelles in infants, pulse weak/thready/absent, wrinkled skin, can't wake up, coma
-difficult to catch in child


V cholerae treatment

-rehydrate and rebalance electrolytes
-treat with short course tetracycline, doxy, or furazolidone after IV rehydration to shorten course and reduce shedding


H pylori

-discovered in 1893
-curved gram neg rods
-similar to campylobacter, but strongly urease pos
-causes peptic ulcer disease, associated with mucosa associated lymphoid tissue (MALT) lymphomas, gastric lymphoma, adenocarcinoma of stomach


h pylori pathogenesis

-transmission mode unknown, probably person to person within households
-bacteria attach to mucous secreting cells of stomach with flagella virulence factor
-break down urea to ammonia with urease virulence factor
-ammonia neutralizes stomach pH, allowing bacterial growth and irritating stomach lining
-organism appears to create a niche in the lining where it multiplies, leads to immune infiltrate
-appears to upregulate caspases, causing apoptosis in nearby cells
-irritation predisposes to gastritis, peptic ulcer, gastric cancer and MALT lymphoma


H pylori diagnosis

-culture is difficult and not useful
-urea breath-drink radioactive urea and breath pos co2 if pos
-antigen present in stool-tests are becoming available but are expensive


h pylori treatment

-reduce irritation/ pain/ help ulcers heal with bismuth salts and proton pump inhibitors
-kill bacteria with one of three triple therapies:
-omeprazole amox and clarithrymycin for 10 days
-bismuth subsalicyclate, metronidazole, tetra for 14
-lansoprazole, amox, clarithromycin for 10
-reinfection may occur