Spirochetes (Woychik) - 5/2/16 Flashcards
Spirochetes
General features:
How to visualize?
- Gram negative
- Coiled cell wall
- Motile
- Endoflagella
Best visualized by dark-field microscopy or immunofluorescent stains
3 genera cause disease in humans and animals
- Borrelia
- Lyme disease - Borrelia burgdorferi (Robin Hood)
- Relapsing fever - Borrelia recurrentis - Leptospira
- Leptospirosis - Leptospira interrogans (Surfer’s oasis) - Treponema
- Syphilis - Treponema pallidum
Left untreated, diseases caused by spirochete infections typically occur in stages, with different clinical manifestations at each stage
Borrelia burgdorferi & Lyme Disease
General info:
- Geographical distribution/seasonal?
- Reservoirs?
- Gram Stain?
- Transmission?
General info:
- Northeastern US (esp. NH and CT)
- Hiking/camping - most exposures from May through July
Mice and deer constitute main reservoirs –> Lyme disease = most common vector borne illness in US and Europe
Gram Stain: spirochetes don’t gram stain b/c they have really thin walls
Transmission: by bite of small deer tick Ixodes - requires tick attachment for 24 hours or more
Ixodes life cycle?
- White-footed mouse = main reservoir (host of tick larvae)
- White-tailed deer = obligatory host (host of adult tick)
- Tick = vector (what is transferring the bacteria)
- Humans = incidental/dead-end host
Virulence Factors?
Surface exposed lipoproteins (OspA-F) - allow attachment of B. burgdorferi to mammalian cells
Clinical Manifestations of Lyme Disease:
Three Stages?
Stage 1: Localized infection (days after tick bite)
- Erythema migrant (EM) - 7-10 days after tick bite
- EM hot to touch and causes burning sensation; sometimes it itches and is painful
Stage 2: Disseminated infection Days to weeks after tick bite)
- Flu-like symptoms–headache, fever, chills, and generalized ashiness
- Multiple skin lesions
- Bilateral Bell’s Palsy & Heart Block
Stage 3: Persistent infection (months to years after tick bite)
- Musculoskeletal pain in large joints (knees) - autoimmune arthritis, bones, muscles and tendons; neurologic manifestations and cardiac disease
- CNS issues (confusion, meningitis, subtle encephalopathy)
Lyme Disease Treatment?
ALL STAGES CURABLE W/ APPROPRIATE ANTIBIOTIC TREATMENT.
- Doxycycline for stage one
- Ceftriaxone used for later presentations
Vaccine: OspA = lipoprotein that mediates spirochete attachment to tick gut
- Vaccine prevents infection by acting on tick itself (antibodies to OpsA kill spirochete in tick gut)
Laboratory Diagnosis?
In absence of EM, CDC recommends two-test serological approach: ELISA first –> Western blot
Borrelia recurrentis & relapsing fever
Clinical manifestations?
Epidemic or endemic
Epidemic relapsing fever: transmitted by person-to-person contact by HUMAN BODY LOUSE, usually during war, poverty, or famine
- Organism released only after crushing the lice; not transmitted in saliva, excrement or transovarially
Endemic relapsing fever: transmitted by bites from infected TICKS (different than those causing Lyme disease); infected ticks are healthy and transmit trasovarially
- Reservoir: rodents and small animals (chipmunks, squirrels, rabbits)
Clinical manifestations:
- Sudden onset of fever with chills, severe headache and malaise lasting 3-6 days and ending abruptly
- Relapse occurs 7-10 days later
- Severity of symptoms and duration of illness progressively decrease with each relapse; louse-borne relapsing fever usually associated with single relapse
Leptospira interrogans and leptospirosis
General characteristics:
Transmission:
Clinical Manifestations:
- Question-mark shaped
- Endemic in tropical regions/ highest incidence in US is Hawaii
- Commonly found in rodent and dog urine which then contaminates water we swim in
- Leptospira viable in water for several weeks
Transmission:
- Indirect -> from ingestion of contaminated water or food, or swimming or bathing in contaminated water
Clinical Manifestations:
- Early infection: fever and intense headaches
- Severe infection: Weil’s disease (renal dysfunction, high creatinine, liver dysfunction and jaundice)
Treponema Pallidum and syphilis
General characteristics:
Transmission:
- STD
- Can have active lesions on fingers, breasts, lips, oral cavity, or genitals
- Both primary and secondary lesions rich in spirochetes and highly infectious
- Can invade virtually any organ in the body and the CNS
- Patient most infectious early in the disease
Transmission:
- During sex but can be transmitted through placenta or during birth, or by kissing, etc..
Syphilis clinical manifestations
Primary
- Painless genital chancre (ulcer) appearing a few weeks after inoculation (primary lesion, heals spontaneously, small blood vessels damaged –> ischemia, ~30% completely cured without treatment)
Secondary
- Disseminated stage: secondary lesions anywhere on body - maculopapular rash occurs on palms and soles weeks to months after infection
Latent
- Serologic tests positive but no clinical manifestations; 30% stay at this stage if untreated, however blood remains infectious
Late
- Slow progressing inflammatory disease affecting any organ in body
- Neurosyphilis - demyelination of dorsal/posterior columns of spinal cord –> loss of vibration sense, proprioreception
- Cardiovascular syphilis (Aortitis of ascending thoracic aorta –> aneurysm) - syphilis destroys the vast vasorum - blood vessels that supply the aorta
- Gummatous syphilis (soft growth with a firm necrotic center)
Congenital syphilis
Symptoms?
May result in fetal death and resulting miscarriage
But post-birth: Developmental abnormalities - Saber shins (anterior bowing of tibia) - Saddle-shaped nose - Congenital deafness - Teeth deformities
Laboratory Diagnosis?
Dark-field microscopy - T. palladium can be quickly and directly detected upon examination of exudate from primary, secondary, and congenital lesions by dark-field microscopy
Serologic tests - measure either nonspecific nontreponemal or specific antitreponemal antibodies
- NONTREPONEMAL TESTS: rely on observation that antibodies to a lipoid antigen present in host tissues are specifically generated upon syphilis infection (antibodies called REAGIN)
Two tests to measure presence of reagin:
1a. VDRL (general disease research laboratories)
1b. RPR (rapid plasma reagin)2. Complement Fixation-reagin in serum can fix complement in presence of cardiolipin (extracted from mammalian tissue)
Advantages: inexpensive, easy, reliable for large-scale screening
Disadvantages: false positives to other diseases
- SPECIFIC TREPONEMAL TESTS: detect T. palladium antibodies in patient serum
- Test: FTA-ABS (Fluorescent Treponema Ab) - indirect immunofluorescence; rabbit T. pallidum as antigen, test for antibody in serum
- Test: TPHA (T. pallidum hemagglutination) - RBCs treated to adsorb T. palladium on surface; RBCs then clump when mixed with antitreponemal antibodies
Treatment?
Penicillin!!!!
Jarisch-Herxheimer reaction may occur hours after treatment - dying spirochetes releasing a bunch of LPS –> cytokines –> fever, chills, etc…
