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17 Cards in this Set
- Front
- Back
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Rickettsia phys/structure
gram? shape? intra/extracellular? oxygen use? peptidoglycan layer? LPS? two groups |
gram neg rods
obligate intracellular aerobic minimal peptidoglycan (stains poorly w/gram stain) LPS has weak endotoxin activity two groups: Spotted fever Typhus group |
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Orientia phys/structure
stain? what does it lack? |
lacks peptidoglycan and LPS
visualize w/Giemsa or Giemenez stain |
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Rickettsia and Orientia both:
how do they enter cells? what dothey do once inside? won't survive unless? multiplication speed how do they get energy |
enter cells by stimulating phagocytosis
once inside, degrade phagosomal membrane using phospholipase must be released into cytoplasm or won't survive multiplication is slow are energy parasites: utilize glutamate & glutamine as carbon sources for generation of ATP, but can also parasitize host ATP by ATP/ADP exchange mech |
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How are rickettsia released?
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by exocytosis at ends of host filapodia
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orientia and Spotted fever rickettsia:
where do they grow? when are they released |
grow in cytoplasm and nucleus
released continuously from cell thru long cytoplasmic projections |
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Typhus group rickettsia
when are they released |
accumulate in cell cytoplasm until the cell membranes lyse
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what are the typhus group spp?
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R. prowazekii- causes endemic typhus worldwide, and sporadic typhus in US
R. typhii causes endemic (murine) typhus worldwide |
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R. rickettsia
R. akari |
rickettsia- spotted fever in W. hemisphere
akari- spotted fever worldwide |
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what determines distribution of rickettsia?
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distribution of the arthropod vector
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Rickettsia rickettsia
disease caused transmission principle reservoir and vector how is it maintained in the reservoir population? what are other reservoirs? |
rocky mt spotted fever
true zoonosis- tick to human transmission when tick feeds (must be exposed to tick for 24-48 hours; rickettsia are activated by the warm blood, and are released from the salivary gland, and regurgitated into bloodstream) hard ticks are the main reservoir/vector maintained in tick population by transovarian transmission |
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what does loss of ATP activity lead to?
what type of cells do r. rickettsii infect? |
loss of ATP activity (since rickettsia are energy parasites) causes shutdown of proton pumps, H2O pours into cells, dilated RER, Mito, and nuclear membrane
vascular endothelial cells |
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what does infection of vascular endothelial cells cause?
what is the primary pathologic event? |
increase in peroxides- damages host cells
decreases in key anti-oxes (thiols, G6Pdehydrog, catalse) which usu defend cells against damage oxidative damage and increased peroxidation of membrane damages endo cells further endothelial damage leads to platelet adherence, reducing platelet count in circulation sets up DIC b/c of increased coagulation time damaged endothelial cells released from walls and clog vessels occlusion of small vessels= microthrombi/microhemorrhage= petechiae and edema loss of fluid- hypovolemia, Hypotension, shock decreased perfusion- anoxic brain injury, acute renal failure leaky vessesl=accumulation of fluid in lungs, vasculitis death can result from shock, vasomotor weakness, renal failure, resp/cardiac arrest primary pathologic event = oxidative cell injury |
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RMSF: clinical disease
abrupt onset Sx rash characteristics |
abrupt: high fever, chills, headache, myalgias
rash develops after 3 or more days can go from erythematous --> maculopapular --> petechial goes from extremities to trunk |
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RMSF: internal Sx
other complications |
fulminant vasculitis- endothelial cells, and vascular sm muscle cells of kidney, heart, skin, brain, subcu tissue
complications: GI sx, resp failure encephalitis renal failure |
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RMSF diagnosis
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culture can be grown in tissue cultures and embryonated eggs
microscopy w/giemsa or giemenez stains fluoescein labeled Abs Serology (microimmunofluorescence, molecular diagnosis via PCR) |
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RMSF treatment
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tetracyclines (doxy) and fluoroquinolones (cipro)
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Rickettsia prowazekii
disease caused primary vector primary reservoir locations recrudescent disease |
epidemic typhus or louse-borne typhus
primary vector= pediculus humans (human body louse, no transovarian transmission) primary reservoir- humans (in crowded, unsanitary conditions that favor spread of louse) |
