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Flashcards in Spirochetes and Vibrios Deck (37)

Recurring themes of spirochetes

-wide variety of transmission methods
-cross easily to blood stream, some also cross blood-brain barrier
-primary virulence factors are for immune evasion
-diagnosis is challenging
-once correctly diagnosed, treatment may be simple
-Jarisch-Herxheimer reaction to treatment


Spirochetes- wide variety of transmission methods

-Sexual: syphilis
-Vector: Lyme Disease, relapsin fever
-Environmental: Leptospirosis


Spirochetes- primary virulence factors are for immune evasion

-little inflammation: no Brudzinki's sign
-few exotoxins
-no vaccines


Spirochetes; Diagnosis is challenging

-wide variety of symptoms: disease develops in phase as spirochetes invade new organs; meticulous history-taking is crucial to accurate diagnosis
-T. palludum (symphilis) are too small to see by standard microscopy
-B. burgdorfi (Lyme Disease) has no good lab diagnostic
-Eye exam can be useful:
Argyll-Robertions pupil
Conjunctival suffusion, uveitis in leptospirosis


Jarisch-Herxheimer reaction to treatment

-Occurs 24 hr after antibiotic treatment
-flulike symptoms
-lasts 24-48 hrs


Genera of Spirochete Pathogens

-TreponemaL Syphilis, yaws, pinta
-Leptospira: Leptospirosis
-Borrelia: Lyme Disease, relapsin fever


T. pallidum Bacteriology

-Small: 0.25uM diameter means invisible to light microscope, need dark field
-delicate: can't survive outsite host
-motile: flagellar "corkscrew" motion
-human-restricted in nature (can infect rabbits in lab)
-cannot be grown in culture
-extremely infectious sexually
-virulence based on immune evasion


Overview of T. pallidum

-transmitted by sexual contact (aquired), blood transplacentally (congenital)
-national plan to eliminate in US has hit bumps: MSM and socioeconomically disadvantaged


Acquired T. Pallidum

-T. pallidum penetrates mucous membranes or small abrasions, grows in blood vessel endothelium, 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: specific anti-treponemal, nonspecific reagin
-But immunity is incomplete:
-surface of spirochete is nonimmunogenic
-spirochete down regulates TH1 cells


Primary syphilis

-painless chancre at site of transmission 3-6 weeks later:highly infectious
-inflammatory infilitrate at site fails to clear organism
-chancre heals 3-12 weeks


Secondary syphilis

-4-10 weeks, spriochete multiplication -> systemic symptoms
-fever, maliase, myalgias, arthralgias, lymphadenopathy
-mucocutaneous lesions of variable types, condylomata later, patchy alopecia ("moth eaten")
-high antibody titers


Latent syphilis

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


Tertiary Syphilis

-1/3 untreated, fatalities possible
-gummatous syphilis: granulomatous lesions ("gummas") with rubbery, necrotic center. Primarily liver, bones, testes
-Cardiovascular syphilis: (>10 years): aneurysm of ascending aorta causes by chronic inflammation of vasa vasorum



-syphilitic meningitis: early 6 mon
-mengingovascular syphilis: damage to blood vessels of meninges, brain, spinal cord
-parenchymal neurosyphilis:
Tabes dorsalis- damage to spinal cord-> impaired sensation, wide-based gait
Disruption of dorsal root-> loss of pain and temperature sensation, areflexia
General paresis: damage to cortical brain tissue -> dementia


Neuosyphilis signs

-Argyll-Robertson pupil: Hallmark of neurosyphilis
-one or both pupils fail to constrict in response to light
-but does constrict to focus on a near object


Congenital Syphilis

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


Treatment of Syphilis

-single injection of penicillin for primary or seconday. Slow release
-use condoms


Borrelia burgdorferi (Lyme Disease) Bacteriology

-motile spirochete- flat-wave shape, not spiral
-stainable with giema, silver stain, visible by standard microscopy
-tick borne- more common in East Coast
-highest risk in summer, when nymphs are feeding
-small mammal reservoirs for nymphs, large mammal hosts by adults
-incidence in US increasing due to expanision of deer herds
-almost always takes 24 hr attachment to transmit


Removing ticks

-tweezers, gloves
-bag and freeze
-promptly (Lyme requires 24-48 h to transmit)
-Doxycycline if the patient is neither pregnant nor allergic to tetracyclines


B. burgdorferi pathogenesis

-disease begins with injection of B. burdorferi into host by tick. Asymptomatic clearance possible
-over the next 6 mon, organism spreads, erythema migrans rash (75%), anti-spirochete/autoantibodies raised
-months to 1 yr after infection, immune and/or neurological issues arise
-lyme arthritis predisposed by HLA-DR4 and HLA-DR2 genetypes
-post-lyme: 80% of untreated/undertreated cases report some neurological sequela
-reinfections occur


B. burgdorferia Exam

-patient usually does not recall tick bite- get history of outdoor activity, note season and geographic location
-stage 1: erythema migrans expanding rash(es) at or near bite site, bull-s eye appearance in minority
-rash aroud a still-attached tick is likely to be hypersensitivity, not Lyme
-Flulike constitutional symptoms, fatique, muscle ache, regional lymphadenopthy, low fever
-coinfection with erlichia or babesioa: high fever


Chronic Lyme Disease

-Stage 3
-subacute encephalopathy
-chronic progressive encephalomyelitis
-late axonal neuropathies
-patient may recall earler episodes of Bell palsy, aseptic meningits


B. burgdorferi Lab Diagnosis

-Serology, ELISA and IFA can confirm exposure but not until 6-8 weeks later
-vaccinated will be seropositive
-seropositively remains longterm
-urine antigen testing is in the pipeline


B. burgdorferi Treatment

-treat patients who present with erythema migrans
-attempt empiric treatment of patients who are seropositive with other suggestive symptoms/history unless pregnant.
-treat 10/20 days with doxycycline unless pregnant or allergic
-Jarisch-Herxheimer reaction


B. burgdorferi Prevention

-Avoidance- protective clothing, DEET, avoid woodsy areas, tick collars on pets
-inspection: daily close inspection of whole family (including pets) for ticks during outdoor season
-prophylaxis with doxycycline may be recommended in some geographic areas


Vibrios- shape

-curved, gram- rods
-mostly ocean-dwelling
-several are halophiles (like salt water)


Vibros- causes of infection

-primarily cause fecal oral gastroenteritis
-can also infect wounds contaminated by seawater or ocean debris
-also peptic ulcers


Specialized virulence factors of vibrios

-gasoenteritis and peptic ulcers require specialized virulence factors for survival in the GI


Vibrio chloerae Bacteriology

-curved, comma-shaped motile gram(-) rod
-strains aerobic, facultatively anaerobic
-microscopic discovery of Robert Koch
-has been causing human epidemics for at least a millenium
-epidemic in London in 1854: Broad street pump
-2 reservoirs: humans and plankton ecosystem of Indian ocean


V. cholerae pathogenesis

-transmitted by fecal oral route
-shed by asymptomatic carriers in incubation or convalescence
-travels to untreated water or undercooked shellfish
-usually killed by stomach acid: high infectious dose (1000-1,000,000 IUs), people on antacids or with gastrectomy are most susceptible
-surviving bacteria reach small intestine, secrete mucinase to clear path to brush border, attach and colonize
-growing bacteria secrete chlorea toxin (enterotoxin): choleragen
-A-B subunit structure
-B binds the ganglioside receptor GM1 on intestinal lining


Persistant activation of V. chlorae

-B binds to receptor and A cause persistent activation of adenylate cyclase, leads to loss of water and ions
-blocks absorption by microvilli while also promoting secretion from crypt
-leads to massive watery diarrhea
-toxin and other virulence factors carried by lysogenic bacteriophage CTX
-local-acting, little penetration of gut wasll
-morbidity and death result from dehydration and electrolyte imbalance
-surviving patients run the self-limited course in 7 days


Exam of V. chlorae

-Rice water stool
-no pain, blood or neutrophils in stool
-acidosis and hypokalemia from loss of bicarbonate and potassium
-dehydration leading to cardiac and renal failure, 40% untreated mortality
-look for dehyration in hand skin


Treatment of V. cholerae

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


Helicobacter pylori bacteriology

-discovered in 1983
-curved gram(-) rods
-very similar to Campylobacter, but strongly Urease (+)
-causes peptic ulcer disease, associated with mucosa- associated lymphoid tissue (MALT) lymphomas, gastric lymphoma, adenocarcinoma of the stomach


Pathogenesis of H. pylori

-transmission mode is known, probably person to person
-bacteria attach to mucus-secreting cells of stomach
-break down urea into ammonia w/ urease virulence factor
-ammonia neutralizes stomach pH, allowing bacterial growth and irritating stomach lining
-organisms appears to create a niche in the lining where it multiples
-appears to upregulate caspases, causing apoptosis in nearby cells
-irritation predisposes to gastrisis, peptic ulcer, gastric cancer, and MALT llymphoma


H. pylori Diagnosis

-culture is very difficult, and not useful
-"Urea breath" test" : patient ingests radiolabeled urea, if infected, exhales radiolabeled carbon dioxide
-antigen present in stool, tests for it are becoming available but expensive


Treatment of H. pylori

-reduce irritation with bismuth salts (Pepto Bismol)
-proton pump inhibitors
-kill bacteria with metronidazole+ amoxicillin or tetracycline for 10-14 days
-reinfection may occur