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Microbiology/Immunology > Spirochetes and Vibrios > Flashcards

Spirochetes and Vibrios Flashcards

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Biology 101 flashcards
1
Q

Recurring themes of spirochetes

A
  • 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
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2
Q

Spirochetes- wide variety of transmission methods

A
  • Sexual: syphilis
  • Vector: Lyme Disease, relapsin fever
  • Environmental: Leptospirosis
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3
Q

Spirochetes- primary virulence factors are for immune evasion

A
  • little inflammation: no Brudzinki’s sign
  • few exotoxins
  • no vaccines
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4
Q

Spirochetes; Diagnosis is challenging

A

-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

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5
Q

Jarisch-Herxheimer reaction to treatment

A
  • Occurs 24 hr after antibiotic treatment
  • flulike symptoms
  • lasts 24-48 hrs
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6
Q

Genera of Spirochete Pathogens

A
  • TreponemaL Syphilis, yaws, pinta
  • Leptospira: Leptospirosis
  • Borrelia: Lyme Disease, relapsin fever
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7
Q

T. pallidum Bacteriology

A
  • 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
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8
Q

Overview of T. pallidum

A
  • transmitted by sexual contact (aquired), blood transplacentally (congenital)
  • national plan to eliminate in US has hit bumps: MSM and socioeconomically disadvantaged
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9
Q

Acquired T. Pallidum

A
  • 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
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10
Q

Primary syphilis

A
  • 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
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11
Q

Secondary syphilis

A
  • 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
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12
Q

Latent syphilis

A
  • end for 2/3
  • organism remains
  • secondary symptoms resolve, may reutrn intermittently over years
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13
Q

Tertiary Syphilis

A
  • 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
  • Neurosyphilis
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14
Q

Neurosyphilis

A

-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

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15
Q

Neuosyphilis signs

A
  • 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
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16
Q

Congenital Syphilis

A
  • treponemes readily corss placenta and infect fetus
  • misscarriage/stillbirth/neonatal death 40-50%
  • within first two years, surviving infants develop severe secondary syphilis
17
Q

Treatment of Syphilis

A
  • single injection of penicillin for primary or seconday. Slow release
  • use condoms
18
Q

Borrelia burgdorferi (Lyme Disease) Bacteriology

A
  • 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
19
Q

Removing ticks

A
  • tweezers, gloves
  • bag and freeze
  • promptly (Lyme requires 24-48 h to transmit)
  • Doxycycline if the patient is neither pregnant nor allergic to tetracyclines
20
Q

B. burgdorferi pathogenesis

A
  • 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
21
Q

B. burgdorferia Exam

A
  • 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
22
Q

Chronic Lyme Disease

A
  • Stage 3
  • arthritis
  • subacute encephalopathy
  • chronic progressive encephalomyelitis
  • late axonal neuropathies
  • fibromyalgia
  • patient may recall earler episodes of Bell palsy, aseptic meningits
23
Q

B. burgdorferi Lab Diagnosis

A
  • 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
24
Q

B. burgdorferi Treatment

A
  • 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
25
Q

B. burgdorferi Prevention

A
  • 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
26
Q

Vibrios- shape

A
  • curved, gram- rods
  • mostly ocean-dwelling
  • several are halophiles (like salt water)
27
Q

Vibros- causes of infection

A
  • primarily cause fecal oral gastroenteritis
  • can also infect wounds contaminated by seawater or ocean debris
  • also peptic ulcers
28
Q

Specialized virulence factors of vibrios

A

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

29
Q

Vibrio chloerae Bacteriology

A
  • 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
30
Q

V. cholerae pathogenesis

A
  • 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
31
Q

Persistant activation of V. chlorae

A
  • 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
32
Q

Exam of V. chlorae

A
  • 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
33
Q

Treatment of V. cholerae

A
  • rehydrate and rebalance electrolytes
  • treat with a short course of tetracycline, doxycline, or furazolidone after IV rehydration to shorten course and reduce shedding
34
Q

Helicobacter pylori bacteriology

A
  • 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
35
Q

Pathogenesis of H. pylori

A
  • 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
36
Q

H. pylori Diagnosis

A
  • 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
37
Q

Treatment of H. pylori

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

Microbiology/Immunology (46 decks)

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