Unit 1 - Pediculosis and Treponema Flashcards

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1
Q

what are Pediculus humanus capitis? classic presentation? treatment?

A

hair lice (appearance is thin and cylindrical)

  • mostly in schoolgirls that share hair accessories
  • treat with insecticidal shampoo twice 10 days apart (to kill any nits that have hatched) plus nit combing
  • hot wash all clothes/linen, and check family/classmates for spread
  • there can be allergic reactions to louse saliva, and possible secondary Staph infections
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2
Q

what are Pediculus humanus corporis? classic presentation? treatment?

A

body lice (appearance is thin and cylindrical)

  • mostly in homeless people who don’t bath properly
  • refer for services to improve hygeine
  • discard clothing, or wash plus insecticide treatment
  • may transmit typhus, trench fever, and relapsing fever
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3
Q

what are Pthirus pubis? classic presentation? treatment?

A

pubic hair lice (look like crabs)

  • in sexually promiscuous people
  • shave pubic hair or coat with Vaseline
  • hot-wash all clothing and linens, check partner and children (as crabs can spread easily)
  • these are markers for other STDs, and aren’t preventable with condoms
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4
Q

where does syphilis fall in the tree of bacteria?

A

Spirochetes include: Treponema, Borrelia, and Leptospira

-Treponemia include: Syphilis, Yaws, and Pinta

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5
Q

Treponema pallidum (syphilis) bacteriology

A
  • 0.25uM diamter (invisible to light microscope, so need darkfield; too slender to Gram stain)
  • spirochetes (motile in flagellar corkscrew motion)
  • not culturable (delicate, and can’t survive outside host)
  • human-restricted in nature, but can infect rabbits in lab
  • extremely infectious sexually, since virulence based on immune evasion
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6
Q

Treponema pallidum (syphilis) pathogenesis

A

transmitted by sex, transplacentally, rarely blood-blood

  • infects endothelium of small blood vessels, enters lymphatics, bloodstream
  • CNS invaded early, but symptoms take years to develop
  • -first CNS abnormalities, then meninges, then parenchyma of brain/spinal cord
  • host raises ineffective Ab (specific anti-treponema, unspecific reagin, but surface of spirochete is non-immunogenic and down-regulates Th1 cells)
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7
Q

what are the 3 phases of syphilis infection?

A

primary (weeks): initial replication at site of infection, forming chancre that initiates bacteremia
-highly infectious, inflammatory infiltrate at site fails to clear organism
-disappears in 3-12 weeks
secondary (months): macropapular rash on palms/soles, moist papules on skin and mucus membranes, highly infectious moist lesions on genitals
-high antibody titers
-1/3 resolve, 1/3 enter latency, 1/3 enter tertiary
tertiary (years): get gummas granulomas (liver, bones, testes) and CNS involvement
-early meningitis (~6 mo) low inflammation
-late neurosyphilis (meningovascular syphilis and parenchymal neurosyphilis)

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8
Q

explain syphilis latency

A

1/3 of secondary syphilis patients

  • early latency: symptoms come/go, patient remains infectious
  • late latency: symptoms absent, not infectious
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9
Q

congenital syphilis

A

treponemes easily cross placenta

  • 40-50% miscarriage/stillbirth/neonatal death
  • survivors develop severe secondary syphilis and physical abnormalities
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10
Q

relationship between syphilis and HIV

A

ulcerations of syphilis facilitate HIV infection

-HIV immunosuppression accelerates syphilis course, and reduces efficacy of treatment

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11
Q

diagnosing primary syphilis

A

“the great imitator” (can hide behind other infections)

  • time course is 3 weeks
  • chancres are red, firm, buttonlike, and not painful unless super-infected
  • -disappears in 4-12 weeks
  • site may be genital or other intimate spot
  • local lymph nodes swell with invasion
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12
Q

diagnosing secondary syphilis

A

4-10 weeks after primary, peaks 3-4 mo after infection

  • subtle, round rash bilaterally symmetrical with nontender lymphadenopathy, round pink spots
  • lesions weeks later on palms/soles become necrotic
  • patchy alopecia
  • condylomata lata cause reddish-brown papular lesions on anogenital area, that coalesce into elevated plaques
  • -progress from red to gunmetal
  • -may be confused with warts
  • may have constitutional symptoms like low fever, malaise, anorexia, weight loss, headache, myalgia, lympadenopathy
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13
Q

diagnosing tertiary syphilis

A

3-10 years after infection, years of inflammation

  • gumma: granulomatous lesions with rubbery necrotic center
  • -bone: deep, boring pain worse at night
  • -skin: hyperpigmented circle, often grouped close together on leg
  • liver: jaundice
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14
Q

cardiovascular syphilis

A

tertiary (>10 years): aneurysm of ascending aorta caused by chronic inflammation of vasa vasorum
-aorta or other major arterial scarring; diastolic murmur with tambour quality, secondary to aortic dilation with valvular insufficiency

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15
Q

what’s included in tertiary late neurosyphilis?

A
  • meningovascular syphilis 5-10 years after infection
  • -endarteritis affects small blood vessels of meninges, brain, spinal cord
  • -CNS vascular insufficiency or stroke
  • parenchymal neurosyphilis 15-20 years after primary infection
  • -tabes dorsalis - damage to sensory nerves in dorsal roots ataxia, and loss of pain sensation, proprioreception, DTR, deep ulcers on feet
  • general paresis - widespread parenchymal invasion that causes individual cell death and brain atrophy
  • dementia
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16
Q

what is the Argyll-Robertson pupil?

A

hallmark of neurosyphilis (tertiary)

-one or both pupils fail to constrict in response to light, but they do constrict to focus on a nearby object

17
Q

how can one exam for syphilis?

A
  1. imaging
    - CT for gummas, chest radiograph and angiograph for cardiovascular syphilis, CT and MRI for neurosyphilis
  2. lumbar puncture for neurosyphilis or syphilis+HIV
    - VDRL, cell point, protein
    - PCR for past infection
18
Q

labs for syphilis?

A

won’t culture, too small to Gram stain, so can only use darkfield
-serology with rapid plasma reagin (RPR), venereal disease research laboratory (VDRL), or ICE syphilis recombinant antigen test

19
Q

what does it mean that syphilis has specific Ab?

A

detectable by IF or hemagglutination, but remain positive for life (tests exposure, not current infection)

20
Q

histology diagnosis of syphilis

A
  1. endareritis caused by binding spirochetes to endothelial cells mediated by host fibronectin
  2. plasma-cell rich infiltrate: delayed hypersensitivity to syphilis leads to gummas
21
Q

Syphilis treatment

A
  1. full panel of STD tests
  2. penicillin (single injection of benzathine penicillin G for primary/secondary syphilis, as slow release enhances effectiveness)
    - no known resistance, but tertiary neuro/cardio damage may not heal
    - if congenital: treat mother by 5th month, and if allergic, use inpatient oral desensitization with penicillin
  3. alternative doxycycline, erythromycin, ceftriaxone are much less effective so followup with repeat reagin tests
22
Q

explain the Jarisch-Herxheimer reaction

A

8-24 hours after starting syphilis treatment, there are flulike symptoms and/or rash that resolve in 24 hours

23
Q

what kind of RPR and VDRL results to yaws and pinta give?

A

positive for both

24
Q

Treponema pertenue - yaws

-what it is, where, and how

A

in tropical areas of Africa, Asia, South America, and Oceania

  • a few thousand cases/yr, mostly peds
  • due to overcrowding and poor sanitation; transmitted by direct contact with skin lesions
  • multiple stages like syphilis, but without neuro or cardio involvement
  • treat with penicillin (G)
25
Q

Treponema carateum - pinta

-what it is, where, and how

A

Central/South america

  • similar to Yaws, but no constitutional symptoms
  • hypo and hyper-pigmented skin plaques, primarily young adults through direct contact
  • entirely human-restricted
  • treat with penicillin (G)