Rickettsia (Woychik) - 5/2/16 Flashcards
Rickettsia Classification:
General Characteristics:
Transmission:
Clinical Symptoms:
Lab Identification:
Treatment:
Rickettsia
- Spotted Fever Group: Rickettsia rickettsia
- Typhus Group: Rickettsia prowazekii
Characteristics:
- Obligate intracellular bacteria (unable to produce NAD+ and CoA so they need eukaryotic cells)
- Coccobacillary
- Gram staining - poor but slightly gram (-)
Transmission:
- Transmitted to humans by arthropod vectors (fleas, lice, mites, ticks)
- Seasonal and geographical distribution of diseases caused by these organisms dependent on habitat of vector (e.g., fleas found worldwide as are diseases caused by them; ticks - more specific)
- Organisms need host to survive
Clinical Symptoms:
- Headache and fever early in Rickettsial infection
- Vasculitis = unique symptom + bump rash
- Diagnosis based on serology and PCR since culture is extremely difficult; however, serological diagnosis problematic due to high level of cross reactivity between species
- Weil Felix Test (diagnostic tool) - agglutination test that tests for cross-reactivity between Rickettsia and Proteus vulgaris
Treatment: doxycycline or other tetracyclines (bind to 30S ribosomal subunit - block elongation step)
Rickettsia rickettsia
General Characteristics:
Obligate intracellular
Poor gram staining (use giemsa stain to visualize)
CoA and NAD+ necessary for growth and provided by host
Rickettsia rickettsia
Transmission:
Via derma center tick bites
Tick is both vector and reservoir (*not same tick that causes Lyme disease)
Rickettsia rickettsia
Pathogenesis:
1) Rickettsia rickettsia attach to receptors on host vascular endothelial cells via outer membrane proteins OmpA or OmpB
2) Induce phagocytosis
3) Escape from phagosome into host cytosol and proliferate
4) Proliferation in cytosol –> leads to cell damage –> increased vascular permeability
5) Spread to adjacent cells through host cell actin-mediated propulsion
6) Characteristic petechial rash (manifesto of networks of contiguously infected cells)
Rickettsia rickettsia
Clinical manifestation
Rocky Mountain Spotted Fever
Incubation period: 2-14 days
Disease begins with:
- Fever
- Severe headache
- Rash (starts at extremities and moves centrally)
- Myalgia (severe muscle pains)
Rickettsia akari & rickettsialpox
Transmission:
Clinical Characteristics:
Transmission - to humans through mouse mite
Target cells - macrophages/monocytes, NOT endothelial cells
Clinical Characteristics of rickettsialpox:
- At site of mite bite, a primary papule forms, ulcerates, and forms dark ESCHAR (clinical hallmark - present 100% of the time)
- Fever develops + rash (but NOT ON PALMS AND SOLES as with RMSF)
Rickettsia prowazekii & louse-borne typhus
General Characteristics:
Transmission:
Clinical Manifestations:
Obligate intracellular w/ poor gram staining
Require CoA and NAD+ from eukaryotes
Outbreaks historically have paralleled times of war, natural disasters (floods/earthquakes) –> clothing is not changed, hot water bathing is infrequent, crowding is common
Transmission:
Lice become infected upon taking a blood meal from persons infected with R. prowazekii
–> R. prowazekii enters louse gut epithelial cells
–> R. prowazekii replicates until cells burst
–> Large numbers of dormant, extracellular form of R. prowazekii in louse feces on skin and clothes
–> scratching introduces Rickettsia into blood
Clinical Manifestions:
Rash starts at trunk and spreads outwards toward extremities (opposite of RMSF); spares face, palms, and soles
- Severe headache, fever, myalgia
Rickettsia typhii & murine typhus
General Characteristics:
Transmission:
Clinical Manifestations:
Found worldwide - but esp. prevalent in tropical and subtropical seaboard regions (e.g., South Texas and Southern California)
Transmission:
Rat = reservoir, rat flea = vector –> transmits disease from rat to rat and occasionally rat to human (infected flea feces into flea bite wound)
Cat fleas = also vectors (primary source of US cases)
Ehrliche and Anaplasma?
Human Monocytic Ehrlichiosis (HME)?
Cause of recently discovered TICK borne zoonoses
Unlike most Rickettsia, infection does NOT occur through endothelial cells:
- Ehrlichia - monocytes and macrophages
- Anaplasma - neutrophils
Multiply within cytoplasmic membrane-bound vesicles that look like inclusion bodies but are referred to as MORULA
Cell walls are thin b/c they lack peptidoglycan and LPS
HME: mammalian host = white tailed deer
Symptoms: fever, headache, myalgia, LEUKOPENIA, THROMBOCYTOPENIA (uncommon in RMSF or Lyme disease)
Coxiella burnetii
Characteristics:
Transmission:
Clinical Presentation:
Treatment:
Gram negative
Obligate intracellular organism
Transmission:
- Via ticks or other arthropods whose bite infects animals
- Reservoir: sheep, goats, and cattle
- Infected animals shed organisms in urine, feces, milk, and especially birth products such as placenta
Coxiella forms SPORES that can survive digestive system and be excreted in animal feces –> aerosol transmission to humans
Clinical Presentation:
- fever, NO RASH, hepatitis
Treatment is usually not needed - usually goes away in two weeks but can cause endocarditis in immunocompromised patients (rare)
Differential Diagnosis:
- Rash
- Leukopenia/Neutropenia
- Morale
- Vasculitis
- RMSF, HME, HGA
- Leukopenia = HME, neutropenia = HGA; either is uncommon in RMSF
- Morale - occasionally in neutrophils of patients with HGA, but not with RMSF
- Vasculitis: hallmark of RMSF