Rickettsiae and Related Bacteria Flashcards

1
Q

Describe pathogenesis/clinical presentations of infections

A

/

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2
Q

Microbiology of Ricketsial/Orientia sp

A
  • small, gram negative obligate intracellular bacteria in pairs of rod-shaped cells with tapered ends or single coccobacilli
  • need tissue culture cell lines or embyonated eggs to culture, grow in cytoplasm, and can be readily visualized with Giemsa stain (not bacteriologic stains)
  • have efficient transport systems for ATP, amino acids, metabolites from cell but capable of independent metabolism
  • Free rickettsiae cease metabolic activity/lose infectivity within short pd. Readily inactivated >56C and by standard disinfectants
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3
Q

General clinical features of Rickettsial dz

A
  • most infections cause clinical dz. Transmitted to humans from animal reservoirs via bites of arthropod vectors. Invade vascular endothelial cells and become disseminated. Pathology due to destruction of infected host cells
  • Major clinical features: fever, headache, rash (due to focal infection causing increased vascular permeability/edema)
  • Late: Thrombosis/blockage of small blood vessels with extravasation
  • Petichial lesions= hallmark

clinical consequence to brain, kidneys, lung, heart > than those of cutaneous lesions

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4
Q

Main categories of Rickettsia diseases

A

1) Typhus group- rash first on trunk and progresses to extremities
2) Scrub typhus group-rash often absent
3) Spotted fever group: rash first on extremities, moves centripetally, and involves palms and soles

  • diagnose with antibody levels in serum
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5
Q

Epidemic Typhus etiology, epidemiology, prevention

A

-organism: Due to Rickettsia prowazekii

Epidemiology:

  • worldwide
  • human/flying squirrels = common reservoir. Transmit via feces from human body louse and squirrel ecto-parasites
  • favor crowding, poor hygiene; prevalent during wars/natural disaster

PREVENT

  • live attenuated vaccine in armed services and ppl at risk
  • insecticides to kill lice
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6
Q

Epidemic typhus clinical manifestations, prevention, treatment

A
  • Erythematous macular rash starting 1-2 weeks post inoculation on trunk and progresses to extremities
  • Bacteremia, high fever, prostration, renal failure, stupor
  • 20-70% mortality if untreated
  • life-long immunity in most cases
  • possibility of latency/lifelong persistence in some
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7
Q

Brill’s disease

A
  • from Rickettsia prowazekii
  • similar to epidemic typhus except milder, usually no rash
  • many years after primary infection as consequence of recrudescence,, usually in immigrants from Easter Europe who had typhus in WWII
  • if pts infested with lice, possibility of transmission
  • can be source of new outbreaks of epidemic typhus
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8
Q

Endemic Typhus

A
  • Rickettsia typhi
  • common reservoir: rats
  • Transmission: feces from rat fleas
  • prevalent throughout the world, particularly in ports, countries with warm climates and other locations where rat populations high
  • clinically very similar to epidemic typhus but milder (
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9
Q

Rickettsial typhus diseases

A

Epidemic typhus
Endemic typhus
Brill’s Disease

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10
Q

Scrub typhus group of diseases

A

Scrub Typhus

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11
Q

Scrub typhus

A

-Org: Orientia tsutsugamushi

Epidemiology

  • Common reservoirs: Chiggers (larval mites). bacterium can be transmitted in mites from generation to generation by transovarian transmission
  • Transmission: Chigger bite
  • high incidence in WWII and vietnam war
  • Endemic in Asia, South Pacific, Australia

Clinical:

  • similar to epidemic typhus but rash often absent/echar develops at site of chigger bite
  • short-lived immunity due to antigenic variation
  • 7% mortality (untreated)

Treat: doxycycline or chloramphenicol

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12
Q

Spotted fever group

A

Rocky Mountain Spotted Fever

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13
Q

Rocky Mountain Spotted Fever

A
  • diseases caused by Rickettsia rickettsii and antigenically related bacteria
  • various spotted fevers endemic to different areas in the world, often reflected by names
  • most important rickettsial dz in US–seen throughout with highest incidence in Mid-Atlantic, Virginia, and Carolinas
  • bacteria present in salivary secretions of ticks and mites and injected when then feed on humans
  • 95% cases between April 1 and Sept 30 when ticks active/ppl outdoors
  • > 70% pts have tick bite history
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14
Q

Rocky Mountain spotted fever etiology/epidemiology/clinical

A
  • Etiology: Rickettsia rickettsii

Epidemiology:

  • Reservoir: widespread in wild mammals, birds, ticks (transovarial)
  • Transmission: tick bite. American dog tick in East, Wood tick in West, Lonestar tick in South/SE
  • takes 4 hrs of feeding before ticks willl inoculate host w/virulent bacteria
  • Geographic distribution: North, central, South America

CLINICAL

  • 2-6 days post bite, similar to typhus except rash starts at extremities (wrists/ankles) and moves to trunk
  • macular petichial rash
  • 7% mortality if untreated

TREAT: doxycycline (except if prego/allergic)

Prevent: no vaccine; prompt tick removal

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15
Q

Ehrlichia and Anaplasma general characteristics

A
  • similar to Rickettsiae; major differences are that the host target cells are phagocytic cells instead of endothelial and they multiply in phagosomes instead of cytosol.

Clinically similar to rocky mountain spotted fever (fever, headache, often multisystem involvement) but without rash. Haematologic abnormalities include leucopenia/thrombocytopenia

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16
Q

Human Monocytotrophic Ehrlichiosis (HME) epi/clinical manifestations

A
  • caused by Ehrlichia chaffeensis, Ehrlichia awingii
  • reservoir = deer
  • transmission: bite from hard tick
  • 90% cases mid-April- late Oct
  • mostly south-central and south-eastern US
  • Clinical manifestation varies between pts but headache, fever, chills, malaise, muscle pain, nausea, vomiting, diarrhea, confusion, conjunctival injection, rash (60% kids,
17
Q

Pathogenesis of human monocytotrophic Ehrlichiosis (HME) and diagnosis

A
  • infect monocytes/macrophages and can be fatal in immunocompromised; E. ewingii disease usually less severe

LAB DIAGNOSIS

  • rapid: pcr from whole blood. most sensitive in first week of infection
  • blood smear in 1st week may show morulae (microcolonies of but) in cytoplasm of white cells in up to 20%
  • Serology: indirect immunofluorescence assay with E. chaffeensis antigen on paired serum samples to show significant rise in Ab. Take 1st sample as early as possible and 2nd 2-4 weeks later. Many times, first IgG IFA titer low or negative and 2nd shows significant increase in IgG Ab levels

Treat: Tetracycline or Doxycycline

18
Q

Human anaplasmosis (formerly human granulocytic ehrlichiosis)

A
  • Org: Anaplasma phagocytophilia

Epi:

  • emerging US infection, predominantly in NE and upper midwest
  • reservoir = deer
  • transmission from Ixodes tick

Pathogenesis/Lab Dx
-Infects virculating neutrophils but less severe than HME
- Inclusion bodies in neutrophils
Serology: (IFA): some pts develop Ab that cross-react in tests for Lyme dz

Treat: Doxycycline

19
Q

Prevention of tick-born diseases

A
  • Treat clothes with permethrin
  • Treat exposed skin with 20-30% DEET (N, N-diethyl-m-toluamide)
  • Tuck pants into boots/socks
  • Shower when you return from outdoors
  • Perform daily tick checks