Pediculosis and the Treponema Flashcards
Pediculus humanus capitis
- 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
Pediculus humanus corporis
- 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
Pthirus pubis
- 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
Treponema pallidum (syphilis)- bacteriology
- 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
Pathogenesis of Treponema pallidum (syphilis)
- 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
Primary syphilis
- 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
Secondary syphilis
- 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
Latency
- 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
Tertiary syphilis
- 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
Spirochetes and pregnancy
- Spirochetes can easily cross placenta
- 40-50% miscarriage/stillbirth/neonatal death
- congenital syphilis: survivors develop severe secondary syphilis and physical abnormalities
Syphilis immunity
- immunity is incomplete
- late latency has some protection from reinfection
Diagnosis of Syphilis
- 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
Lab Diagnosis of Syphilis
- 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
Treatment of syphilis
- 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
Yaws
- 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
Pinta
- 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
Acquired Syphilis
- 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
Neurosyphilis
- 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
Congenital Syphilis
- treponemes readily cross placenta and infect fetus
- miscarriage/stillbirth/neonatal death 40-50%
- within first two years, surviving infants develop severe secondary syphilis
Syphilis and HIV
- ulcerations of syphilis facilitate HIV infection
- HIV immunosuppression accelerates syphilis course, and reduces efficacy of treatment
Primary Syphilis Exam
- 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
Secondary Syphilis Exam
- 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
Tertiary Syphilis Exam
- 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
Meningovascular syphilis
- 5-10 years after infection
- endarteritis affects small blood vessels of the meninges, brain and spinal cord
- CNS vascular insufficiency or stroke
Parenchymal neurosyphilis
- 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
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
Imaging for syphilis
- CT for gummas
- chest radiograph, angiograph for cardiovascular syphilis
- CT and MRI for neurosyphilis
Syphilis and Lumbar puncture
- for neurosyphilis or syphiis + HIV
- VDRL, cell count, protein
- PCR for evidence of past infection
Labs for Syphilis
- 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
VDRL/RPR Flocculation Assay
- Reagin + Ox Heart Extract = Aggregates
- cheap, easy
- semiquantitative: titer decreases with successful treatment
Treponeme-specific tests
- fluorescent treponemal antibody-absorption (FTA-ABS)
- quantitative VDRL/RPR
- microhemagglutination assay T pallidum (MHA-TP)
- T. pallidum hemagglutination (TPHA)
- T. pallidum particle agglutination (TPPA)
Syphilis stages and possible test results
- primary chancre- dark field+, RPR+/-, VDRL +/-
- secondary eruptions- RPR+, VDRL+, TP-PA+, AIA+, FIA+
- tertiary disease- RPR +/-, VDRL +/-, TP-PA+, AIA+, FIA+
Histology of Syphilis
- 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
T. pallidum Treatment
- 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