Bacteria IV: Rickettsial diseases Flashcards
intracellular vector-borne diseases
- typhus (lice)
- rocky mountain spotted fever (ticks)
- Erlichiosis-> ticks
Extracellular vector-borne diseases
lyme disease (ticks) relapsing fever (lice or ticks) plague (fleas)
what does rickettsia infect?
intracellular infection of endothelial cells with perivascular lymphocytic infiltrate (perivascular cuffing)
rickettsia characteristics
small, G-, obligate intercellular bacteria
- ticks
- dark, swollen, crusted lesion
how do you diagnose rickettsial disease?
immunostaining or serology or exposure to vector
where does rickettsia multiple?
small vessel endothelial
triad related to rickettsia diseases?
rash, fever, CNS manifestations (headache, seizures)
-small vessel vasculitis with microthrombi, ischemia and hemorrhage
what does the typhus group do to endothelial cells?
lysis
what does the spotted fever group do to endothelial cells?
spread cell to cell
does rickettsia have toxins?
No endotoxins, no exotoxins
- LPS non-toxic
- small vessel damage: thrombosis and hemorrhage
what are the first cells to come in for rickettsial diseases?
1st-> Natural killer cells-> produce gamma-interferon
2nd-> cytotoxic T cells mediated immune responses responsible for much of the tissue damage seen
clinical features from rickettsia
fever, rash, CNS symptoms
-severe cases: hypovolemic shock, DIC, pulmonary edema
treatment for rickettsia
doxycycline
typhus group of rickettsia
R. bellii
R. canadensis
other group of rickettsia
R. prowazekii
R. typhi
R. prowazekii: Epidemic typhus
head lice
- centrifugal rash, CNS involvement (apathy, dullness, stupor, coma)
- high fever, chills, cough, rash, severe muscle pain, sensitivity to light, delirium
murine typhus
related syndrome to epidemic typhus
-high density population and poor hygiene
clinical findings R. prowazekii: Epidemic typhus
mild rash, small hemorrhages
severe: gangrene of tips of fingers, nose, earlobes, scrotum, penis, vulva
R. prowazekii: Epidemic typhus morphology
cuff of mononuclear inflammatory cells around vessels
ecchymotic hemorrhages of affected organs
microthrombi
no necrosis of vessels
rocky mountain spotted fever group
R. rickettsia, tick bite
incubation time 7 days
-fever (high 2-3 weeks), N&V, headache, muscle pain
when does the rash appear for rocky mountain spotted fever
day 6 of fever
extends over all body, INCLUDING palms, soles
-begins in periphery (palms wrists, soles)-> then to trunk, face and neck
rocky mountain spotted fever morphology
perivascular mononuclear infiltrate
necrosis, fibrin extravasation and thrombosis of small blood vessels and arterioles
-severe cases-> foci of necrotic skin, fingers, toes, elbows, ears, scrotum
what is the major death from rocky mountain spotted fever
noncardiogenic pulmonary edema
Scrub typhus
Orienta (rickettsia tsutsugamushi)
- rash transitory or absent
- transmitted by mites
Ehrilichiosis
similar to RSMF -rash rare -(infects)Neutrophils or monocytes -cytoplasmic inclusions-> shaped like mullberries ticks
Lyme disease (Borrelia burgdorferi)
tick of white tailed deer
-shift antigenic markers to avoid antibody production
what is the primary stage of Lyme disease?
local infectio
-skin rash shows vasodilation with dense perivascular inflammatory infiltrates of mononuclear leukocytes
what is the secondary stage of Lyme disease?
spread, Late (months)
- bacteremia disseminates the spirochetes to many with focal necrosis, hemorrhages
- joint disease
- muscle pain, cardiac arrhythmias, meningitis, cranial nerve involvement
what is the tertiary stage of Lyme disease?
multisystem chronic inflammation disease
- local lesion progresses to bacteremia and chronic inflammatory lesions in distant organ
- manifestations include chronic arthritis, polyneuropathy and encephalitis, skeletal muscle involvement
what toll like receptor does LPS bind to in Lyme disease?
TLR2 of macrophages
why does the bull’s eye (target) rash appear in lyme disease?
spreading erythematous margins and a blanching center
- erythema chronicum migrans
- fever and constitutional symptoms may occur at this point
lyme disease pathogenesis
focal necrosis, hemorrhages and DIC
-rash shows vasodilation with dense perivascular inflammatory infiltrates of mononuclear leukocytes (lymphoplasmacytic cell infiltrate)
how does lyme disease resemble rheumatoid arthritis
synovial hyperplasia
lymphocytes, plasma cells
proliferative arteritis
relapsing fever (Borrelia recurrentis)
lice
1-2 week latent period, shaking, chills, fever, headache, fatigue
-successive attacks results from ability of organism to expressive new surface antigen
Plague, Yersinia Pestis
G- bacillus
-Sylvatic cycle (organism cycle in rodents)
Plague, Yersinia Pestis pathogenesis
rapid proliferation in lymphoid tissues
- injection of YOP’s, yersinia outer proteins
- inactivation molecules that regulate actin polymerization, inhibits secretion of inflammatory cytokines
- necrosis of tissue and blood vessels
- swelling of lymphoid tissue, striking leukocytosis, septicemia/DIC
what constitutes minor plague symptoms?
lymphadenopathy and constitutional symptoms
what constitutes bubonic plague symptoms?
prominent lymphadenopathy, most common
what constitutes pneumonic plague symptoms?
hemorrhagic, necrotizing pneumonia primary or secondary to bubonic infections
-septicemia-> rapidly fatal
