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MS II Micro/Immuno > Pediculosis and the Treponema > Flashcards

Pediculosis and the Treponema Flashcards

1
Q

Pediculus humanus capitis

A
  • site: scalp, esp behind ears
  • appearance: 1 and 2 (nits and the long bodies)
  • classic presentation: schoolgirls sharing hair accessories
  • treatment (patient): insecticidal shampoo twice 10D apart plus Nit Combing
  • treatment (environment): hot wash all clothing and linens, check family and classmates
  • special considerations: allergic reactions to louse saliva, secondary staph infection
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2
Q

Pediculus humanus corporis

A
  • site: clothing, esp seams
  • appearance: 2 (long bodies)
  • classic presentation- homeless
  • treatment (patient)- refer for services; improve hygiene
  • treatment environment- discard clothing or wash plus insecticide treatment
  • special considerations: can transmit typhus, trench fever, relapsing fever
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3
Q

Pthirus pubis

A
  • site: pubic hair
  • appearance: 3 (short bodies- crabs)
  • classic presentation: sexually promiscuous
  • treatment (patient): shave pubic hair or coat with vaseline
  • treatment (environment): hot wash all clothing and linens, check partners and children
  • special considerations: marker for other STDs, condoms not protective
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4
Q

Treponema pallidum (syphilis)- bacteriology

A
  • spirochetes are motile: flagellar corkscrew motion
  • not culturable
  • very slow growing
  • treponema are too slender to Gram stain
  • too delicate to survive outside a host
  • small- 0.25 uM diameter means invisible to light microscope
  • extremely infectious sexually
  • virulence based on immune evasion
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5
Q

Pathogenesis of Treponema pallidum (syphilis)

A
  • transmits by intimate contact- sexually (acquired): very low infectious dose (~57), transplacental (congenital), rarely- blood-blood
  • infects endothelium of small blood vessels
  • triphasic infection
  • pathogenesis does not seem to invovle toxins, primarily immune evasion
  • national plan to eliminate in US has hit bumps: working among whites, women, not among MSM, slower among minorities
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6
Q

Primary syphilis

A
  • weeks: initial replication at site of infection, forms an ulcer, chancre, initiates bacteremia
  • 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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7
Q

Secondary syphilis

A
  • months: macropapular rash on palms and soles, moist papules on skin and mucous membranes
  • highly infectious moist lesions on genitals “condylomata lata” patchy alopecia, may be constitutional symptoms of low fever, malaise, anorexia, weight loss, headache, myalgia, lymphadenopathy
  • 4-10 weeks-> spirochete multiplication -> systemic symptoms
  • high antibody titers
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8
Q

Latency

A
  • 1/3 resolve, 1/3 enter latency (years)
  • early latency- symptoms come and go, patients remains infectious
  • late latency- symptoms absent, not infectious
  • organism remains
  • secondary symptoms resolve, may return intermittently over years
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9
Q

Tertiary syphilis

A
  • remaining 1/3 enter tertiary syphilis, fatalities possible
  • granulomas “gummas”: granulomatous lesions with rubbery, necrotic center. Primarily in liver, bones, tests
  • CNS involvement- early meningitis (6 mo): low inflammation; late neurosyphilis- meningovascular syphilis and parenchymas neurosyphilis (Tabes dorsalis, general paresis)
  • cardiovascular syphilis: >10 years aneurysm, ascending inflammation of vasa vasorum
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10
Q

Spirochetes and pregnancy

A
  • Spirochetes can easily cross placenta
  • 40-50% miscarriage/stillbirth/neonatal death
  • congenital syphilis: survivors develop severe secondary syphilis and physical abnormalities
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11
Q

Syphilis immunity

A
  • immunity is incomplete

- late latency has some protection from reinfection

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12
Q

Diagnosis of Syphilis

A
  • exam: chancre, rash, condylomata lata, patchy alopecia, CNS symptoms including meningitis, gummas, cardiovascular symptoms, Argyll-Robertson pupil (one or both pupils fails to constrict in response to light, but does constrict to focus on a near object)
  • must contain complete history of symptoms- may extend over years with varied symptoms arriving and departing
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13
Q

Lab Diagnosis of Syphilis

A
  • microscopy- scab lesions for darkfield microscopy or IF, biopsy gummas for histology with silver or IF
  • serology- reagin: nonspecific antibodies detecteable by flocculation tests with cardiolipin (VDRL or RPR)
  • positivity decreases with treatment. False positives and negatives (prozone phenomenon) may occur; positives may be confirmed by specific tests
  • specific antibodies: detectable by IF or hemagglutination, remain positive for life (Ie, tests exposure, not current disease
  • then do full panel of STD tests
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14
Q

Treatment of syphilis

A
  • antibiotics are indicated: penicillin
  • single injection of benzathine penicillin G for primary or secondary syphilis. Slow release enhances effectiveness. No known resistence
  • alternate: long-term doxycycline, erythromycin, ceftriaxone, much less effective- follow up with repeat reagin tests
  • patient should expect flulike symptoms for 24h after tretment (Jarisch-Herxheimer reaction)
  • patient education- condoms
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15
Q

Yaws

A
  • Treponema pertenue
  • tropical disease of Africa, Asia, Souther America and Oceania, overcrowding and poor sanitation
  • spread by direct contact with cutaneous lesions
  • three-phase disease like syphilis, but without neuro- or cardio- involvement
  • tests with reagin-positive
  • treat w/ penicillin G
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16
Q

Pinta

A
  • treponema carateum
  • even rarer than Yaws, Central and South America
  • no constitutional symptoms, just hypo- and hyper-pigmented skin plaques
  • probably spread by direct contact
  • skin lesions, primarily young adults, probably passed by direct contact
  • tests reagin-positive
  • treat w/ penicillin G
  • human restricted
17
Q

Acquired Syphilis

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, and nonspecific reagin
  • but immunity is complete: -surface of spirochete is nonimmunogenic, spirochete down-regulates TH1 cells
18
Q

Neurosyphilis

A
  • syphilitic meningitis: early (6 mo)
  • meningovascular syphilis: damage to blood vessels of meninges, brain, spinal cord
  • parenchymal neurosyphilis:
  • tabes dorsalis: damage to spinal cord- loss of sensation, widened gate
  • disruption of dorsal roots- lots of pain
  • general paresis- damage to cortical brain and dementia
19
Q

Congenital Syphilis

A
  • treponemes readily cross placenta and infect fetus
  • miscarriage/stillbirth/neonatal death 40-50%
  • within first two years, surviving infants develop severe secondary syphilis
20
Q

Syphilis and HIV

A
  • ulcerations of syphilis facilitate HIV infection

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

21
Q

Primary Syphilis Exam

A
  • the great imitator
  • time course of symptoms: primary syphilis -3 weeks
  • chancres are raised, red, firm, buttonlike structure up to several cm, heal in 4-8 weeks, not painful unless superinfected
  • site many be genital or other intimate; local lymph node swells with invasion
22
Q

Secondary Syphilis Exam

A
  • secondary syphilis: begins 4-10 weeks after primary, peaks 3-4 months after infection
  • may be subtle
  • first-round rash is bilaterally symmetrical, with generalized nontender lymphadenopathy, round pink spots 5-10mm
  • second batch of lesions appears days or weeks later, palms and soles, become necrotic
  • patchy alopecia
  • condylomata lata: reddish-brown papular lesions on the penis or anogenital area, can coalesce into large elevated plaques up to 2-3 cm in diameter, lesions usually progress from red, painful, and vesicular to gun metal grey
  • sometimes confused with venereal warts
  • mild constitutional symptoms: malaise, headache, anorexia, nausea, aching pains in the bones and fatigue, fever and neck stiffness
  • syphilitic meningitis
23
Q

Tertiary Syphilis Exam

A
  • 3-10 years after infection, years of inflammation
  • gumma: bone: deep boring pain worse at night. Skin: hyperpigmented circle. Often on lower leg, asymmetric, few grouped close
  • liver- jaundice
  • cardiovascular syphilis: aorta or other major arterial scarring; diastolic murmur with a tambour quality secondary to aortic dilation with valvular insufficiency
24
Q

Meningovascular syphilis

A
  • 5-10 years after infection
  • endarteritis affects small blood vessels of the meninges, brain and spinal cord
  • CNS vascular insufficiency or stroke
25
Q

Parenchymal neurosyphilis

A
  • 15-20 years after primary infection
  • parenchymal CNS invasion by T. pallidum
  • general paretic syphilis: widespread parenchymal invasion that causes individual cell death and brain atrophy
  • Tabes dorsalis: damage to the sensory nerves in dorsal roots, ataxia and loss of pain sensation, proprioception, deep tendon reflexes, deep ulcers of the feet
  • dementia
26
Q

Argyll-Robertson pupil

A
  • Hallmark of neurosyphilis
  • one or both pupils fail to constrict in response to light
  • but does constrict to focus on a near object
27
Q

Imaging for syphilis

A
  • CT for gummas
  • chest radiograph, angiograph for cardiovascular syphilis
  • CT and MRI for neurosyphilis
28
Q

Syphilis and Lumbar puncture

A
  • for neurosyphilis or syphiis + HIV
  • VDRL, cell count, protein
  • PCR for evidence of past infection
29
Q

Labs for Syphilis

A
  • won’t culture too small to Gram stain
  • swab moist cutaneous lesions for darkfield microscopy or IF
  • for neurosyphilis, use CSF for tests, specific but not sensitive
  • serology- first nontreponemal serology screening using Veneral Disease Research Laboratory (VDRL), rapid plasma reagin (RPR), or ICE syphilis recombinant antigen test
30
Q

VDRL/RPR Flocculation Assay

A
  • Reagin + Ox Heart Extract = Aggregates
  • cheap, easy
  • semiquantitative: titer decreases with successful treatment
31
Q

Treponeme-specific tests

A
  • fluorescent treponemal antibody-absorption (FTA-ABS)
  • quantitative VDRL/RPR
  • microhemagglutination assay T pallidum (MHA-TP)
  • T. pallidum hemagglutination (TPHA)
  • T. pallidum particle agglutination (TPPA)
32
Q

Syphilis stages and possible test results

A
  • primary chancre- dark field+, RPR+/-, VDRL +/-
  • secondary eruptions- RPR+, VDRL+, TP-PA+, AIA+, FIA+
  • tertiary disease- RPR +/-, VDRL +/-, TP-PA+, AIA+, FIA+
33
Q

Histology of Syphilis

A
  • endarteritis caused by binding of spirochetes to endothelial cells mediated by host fibronectin
  • plasma- cell-rich infiltrate: delayed hypersensitivity to T. pallidum, leads eventually to gummatous ulcerations/necrosis
34
Q

T. pallidum Treatment

A
  • penicillin (Benzathine penicillin G)
  • full panel of STD tests
  • kills bacteria over weeks of slow release, no known resistance
  • tertiary neuro/cardio damage may not heal
  • congenital: treat mother by 5th month of gestation w/ penicillin. If allergic, use inpatient oral desensitization procedure and treat with penicillin
  • alts tetracycline/doxycycline, erythromycin, and ceftriaxone, much less effective
  • Jarisch-Herxheimer reaction: 8-24 h after start of treatment, many patients have flulike symptoms and/or exacerbation of rash. Resolves within 24 hours
  • follow-up bloodwork is necessary, particulary if HIV+, nonpenicillin treatment

MS II Micro/Immuno (8 decks)

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