Borrelia Flashcards

1
Q

Zoonoses

A

Infectious diseases of other animal species that are accidentally transmitted to humans.

May be viral, bacterial or parasitic.

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2
Q

Vector

A

Arthropod that transmits infection from animal to human.

Not all zoonoses are transmitted by vectors.

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3
Q

Reservoir

A

The animal species in which the microbe is maintained in nature.

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4
Q

Lyme Disease

A
  • Caused by Borrelia burgdorferi
  • Spirochete transmitted by deer ticks (Ixodes dammini) to man during a blood meal
  • Serious public health problem in the USA (300k cases per year)
    • Esp. in regions w/ a large deer population
    • ↑ # of deer and deer ticks ⇒ ↑ incidence of Lyme
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5
Q

B. burgdorferi

Morphology and Cultivation

A
  • Loosely-coiled spirochete
  • Contains several outer surface proteinsOspA and OspB
    • May undergo antigenic variation
  • Fastidious
  • Grows best at 33°C in a complex liquid medium
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6
Q

B. burgdorferi

Reservoirs

A

Zoonotic disease w/ animal and tick reservoir.

White footed mouse ⇒ larval and nymph forms (spring)

White tailed deer ⇒ adult ticks (late summer)

Infection of humans (accidental)

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7
Q

B. burgdorferi

Transmission

A

Spirochetes transmitted by ticks that normally feed on deer and white footed mouse:

  • Lives in tick midgut until it takes a blood meal
  • Contact with mammalian blood ⇒ ∆ expression of Osps ⇒ replication ⇒ gut wall invasion ⇒ dissemination throughout the tick including salivary glands ⇒ injected into mammalian host
    • Process takes 24 to 36 hrs
  • Tick must feed for 18-24 hrs before mature spirochetes will be injected into the host
    • If ticks are removed on a daily basis, risk of transmission is low
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8
Q

B. burgdorferi

Epidemiology

A

Transmission occurs in areas with a large deer population.

Three distinct geographic regions in the US:

  • Northeast corridor ⇒ Massachusetts to Maryland
    • Highest transmission
  • Upper Midwest ⇒ Wisconsin and Minnesota
  • Northern California
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9
Q

B. burgdorferi

Clinical Infection

A

3 stages of Lyme disease:

  • Stage 1 - Early localized
    • Local spread of B. burgdorferi in the skin
    • Characteristic annular lesion @ site of tick bite (bullseye) ⇒ erythema migrans
      • Usually occurs within 2 weeks of bite
    • Fever, malaise and headache may accompany the rash
  • Stage 2 - Early disseminated
    • Local dissemination
    • Multiple smaller annular rashes
    • Other common manifestations:
      • Cranial nerve palsies
      • Meningitis
      • Conjunctivitis
      • Systemic sx such as fever, malaise, fatigue and arthralgia
  • Stage 3 - Late disseminated
    • Period of latency (months to several years)
    • ± Attacks of arthritis affecting large joints, esp. knees
      • Episodes become progressively longer
      • Small % of individuals may become chronic and progressive
    • Chronic neurologic involvement may also occur
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10
Q

B. burgdorferi

Pathogenesis

A

Pathology not due to the organism ⇒ no toxins or direct tissue damage

  • Early stagesviable bacteria/inflammation
  • Late stageimmune-mediated injury
    • Microbial persistence ⇒ immune response ⇒ bystander injury to the host
    • Affected tissues w/ inflammatory infiltrate of lymphocytes and monocytes
    • Potent inducer of IL-1 and TNF-α
    • HLA-DR4 and IgG to OspA (chronic patients)
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11
Q

B. burgdorferi

Diagnosis

A
  • Lesion > 5 cm is pathognomonic
  • Difficult to cultivate and visualize
  • Pts with Stage 1 disease frequently seronegative ⇒ dx based on clinical manifestations
  • More advanced pts ⇒ dx by two-step serological process
    • EIA or ELISA
      • Done with whole cell antigens
      • Numerous false positives with other spirochete antigens, viral infections and autoimmune diseases
      • Positive or equivocal EIA must be corroborated with an immunoblot
    • Immunoblot or Western
      • Uses proteins specific to B. burgdorferi
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12
Q

B. burgdorferi

Treatment

A
  • Doxycycline or Amoxicillin PO vs IV
    • Duration of therapy is guided by clinical course
    • Usually 2-4 weeks
  • Treating stage 1 or 2 prevents stage 3
  • Re-infection is possible
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13
Q

Post-Treatment

Lyme Disease Syndrome

A
  • 10-20% of treated pts have prolonged sx
    • Fatigue
    • Muscle and joint pain
    • Cognitive issues
  • May be d/t tissue damage not continued presence of organism
  • No e/o to support long term abx tx
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14
Q

Chronic Lyme Disease

A

Persistent pain, fatigue, cognitive sx in the absence of clinical and serological e/o infection w/ B. bergdorferi

Not recognized by the IDSA

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15
Q

B. burgdorferi

Prevention

A

Cover all exposed skin areas and/or use repellent when in tick infected areas

Check for ticks and remove daily

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16
Q

Relapsing Fever

Overview

A
  • Periodic episodes of pyrexia with septicemia and apyrexia
    • Two forms: epidemic vs endemic
  • Caused by several species of Borrelia ⇒ B. recurrentis, B. hermsii, B. turicatae
  • Transmitted to man by:
    • Soft bodied ticks (Ornithodoros) ⇒ Tick Borne
    • Human louse (Pediculus humanus corporis or Pediculus humanus capitis) ⇒ Louse Borne
17
Q

Epidemic

Relapsing Fever

A

Louse Borne Relapsing Fever

  • Caused by Borrelia recurrentis
  • Reservoir host is unknown
  • Transmitted to man and spread from man to man by the body or head louse
  • Usu. occurs during times of breakdown of public health infrastructure, war, natural disasters etc.
    • Common in Sudan, Somalia, and Ethiopia
    • Virtually non-existent in the USA
18
Q

Endemic

Relapsing Fever

A

Tick Borne Relapsing Fever

  • Caused by B. hermsii and B. turicatae
  • Transmitted from infected animals ⇒ tick ⇒ man
    • Animal reservoirs are wild rodents and other forest animals
    • Vector is the Ornithodorus species (soft tick)
    • Borrelia may be passed trans-ovarily to subsequent generations in the tick
  • Occurs primarily in the Western US, Grand Canyon, state and national parks
  • Occurs most often in summer
19
Q

Relapsing Fever

Virulence Factors

A
  • Antigenic variation of the infecting strain
  • New variants are responsible for relapses
  • Ab is not protective for new strains
20
Q

Relapsing Fever

Pathogenesis and Clinical Disease

A
  • Infection is initiated by entry of organisms by bite or crushing of the insect vector
  • Spirochetemia develops ⇒ febrile period (~ 7 days)
    • Various organs of the reticuloendothelial system may become infected
      • Heptatosplenomegaly
      • Hepatic necrosis
      • Cardiac failure
      • Cerebral hemorrhage
  • Disappearance of Borrelia from the blood streamfever remission (3-10 days)
  • Reappearance of fever and Borrelia with new antigenic typesrelapse
    • Antigenic variation critical to pathogenesis of the organism
    • Relapses are usually limited to 3 or 4
21
Q

Relapsing Fever

Diagnosis

A
  • Visualize the organism in blood during febrile period
    • Direct staining of blood smears by Giemsa or Wright procedures
    • Darkfield microscopy (uncommon)
  • Serology by EIA or immunoblot
    • Methods are not standardized
    • Serum samples should be sent to the CDC
22
Q

Relapsing Fever

Treatment and Prevention

A
  • Tx w/ Tetracycline or Erythromycin
    • Endemic form - 5% mortality
    • Epidemic form - 40% mortality
  • Preventative measures include delousing, de-ticking and control