Rickettsial diseases Flashcards

1
Q

Classification of Rickettsia?

A
  • small
  • gm -
  • non-motile
  • rod -to-coccoid-shaped bacterium (why you cover with broad spectrum, doesn’t just fit into one category)
  • similar to chlamydia
  • size of a large virus
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2
Q

What does it mean that Rickettsiae is an obligate intracellular bacterial parasite?

A
  • steal ATP, unable to produce sufficient energy to replicate extracellularly
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3
Q

What does cell wall of rickettsiae resemble?

How rickettsiae is transmitted?

A
  • gram - rods
  • in arthropods (insects), rickettsiae grow in gut lining, often w/o harming host, require an arthropod vector (except for Q fever)
  • human infection results from either an arthropod bite or contamination with its feces
  • circulate widely in bloodstream (bacteremia)
  • infecting endothelium of blood vessel walls (this produces clotting -> petechiae)
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4
Q

What cells do Rickettsiae infect?

A
  • endothelium of blood vessel walls
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5
Q

Pathophysiology of Rickettsial disease?

A
  • typical lesion: vasculitis, Rickettsia has a tropism for endothelial cells that line blood vessels
  • damage in endothelial lining of vessel wall where organism is found
  • damage to vessels of skin results in characteristic rash
  • edema and hemorrhage caused by increased capillary permeability
  • most Rickettsia cause rashes, high fevers, and bad HAs (always have meningitis as differential)
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6
Q

What are most of the rickettsial diseases in the U.S.?

A
  • Tickborne
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7
Q

Common presentation of rickettsial diseases?

A
  • most have fevers, arthralgia, rashes and HAs
  • some cause vasculitis (petechiae, purpura)
  • see in children
  • Hx is huge!!!!
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8
Q

What is the primary method of dx of Rickettsial disease?

A
  • Hx of insect bite
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9
Q

What is the confirmation of your clinical dx of rickettsial disease?

A
  • based on measuring immunological titers to the infecting organism, and this may take weeks to develop
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10
Q

Hx that might reveal rickettsial disease?

A
  • outdoor activities during April- Sept., particularly in areas with high uncut grass, weeds, and low brush can increase risk for tick bites
  • the include recreational pursuits
  • occupational activities that involve persons being in brushy or grassy areas that might be inhabited by ticks
  • vegetation that borders roads, trails, yards, or fields also are potential areas that might be inhabited by ticks.
  • In endemic areas (where the agents causing TBRD are present at all times), even children who play in grassy areas in backyard are at risk.
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11
Q

What would be good to know about your community?

A
  • what types of insects reside in your community

- what types of arthropod-borne diseases have been reported in your community

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12
Q

What are the Rickettsial diseases in the US?

A
  • Rocky Mountain Spotted Fever
  • Rickettsial pox
  • Endemic Flea-Borne Typhus ( Murine Typhus)
  • Epidemic Louse-Borne Typhus
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13
Q

Rocky Mountain Spotted Fever:

pathogen, geography, insect vector, and other carrier?

A
  • Rickettsia rickettsii
  • Western Hemisphere US (especially mid-Atlantic coast)
  • tick
  • rodents, dogs
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14
Q

Epidemic (louse-borne) Typhus: pathogen, geography, insect vector, and other carrier?

A
  • Rickettsia prowazakii
  • Central and NE Africa, Central and S. America
  • louse
  • Human body, flying squirrels
    (more severe typhus)
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15
Q

Endemic (murine) typhus: pathogen, geography, insect vector, and other carrier?

A
  • Ricekttsia typhi
  • small focus (US: SE gulf)
  • Flea
  • rodents
    (mild)
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16
Q

Rickettsial pox (causes an eschar): pathogen, geography, insect vector, and other carrier?

A
  • Rickettsia akari
  • U.S.
  • mite
  • mice
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17
Q

Clinical presentation of Rocky Mountain Spotted Fever?

A
  • acute onset of nonspecific sxs: ex - fever, severe HA, myalgia, and prostration
  • rash appears 2-6 days later, merciless that frequently progress to petechiae (wood tick or dog tick)
  • ***Rash usually appears first on hands and feet and then moves inward to the trunk
  • 90% of kids have rash
  • rash may be of short duration
  • localized to a particular region of the body
  • rash completely absent or atypical in up to 20% of RMSF cases
  • DDX: syphillis (RPR), hand, foot, and mouth, meningitis
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18
Q

What can the rashes turn into in Rocky mountain spotted fever if left untx?

A
  • can become necrotic tissue, looks like DIC, TTP
  • if don’t tx aggressively -> can lead to death
  • transmits bacteria in 6-10 hours after bite so early dx is key
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19
Q

Work up for RMSF?

A
  • CBC: thrombocytopenia
  • chemistry panel: hyponatremia, elev AST, hyperbilirubemia
  • may need spinal tap to study CSF and rule out meningococcus
    LP: mild increase WBC, low glucose
    ** tip off: AST elevated
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20
Q

DDX of RMSF?

A
  • difficult
  • 40% of pts don’t recall tick bite
  • rash may be confused with that of measles, typhoid, ehrlichiosis, or most impt: meningococcemia
  • need blood cultures and exam of CSF
  • mortality: 70% in elderly (myocarditis)
    can be fatal in kids too if left untx
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21
Q

Tx for RMSF?

A
  • delay in tx can lead to severe disease and fatal outcome
  • is susceptible to tetracycline-class abx:
    Doxy- DOC
    in pregnancy: chloramphenicol (dangerous AEs)
  • optimal duration of therapy hasn’t been established
  • current recommendations for RMSF are tx for at least 3 days after fever subsides, and until evidence of clinical improvement is noted, which is typically for a minimum course of 5-7 days
  • severe of complicated disease might require longer tx courses
22
Q

When does Epidemic Louse-Born Typhus occur?

A
  • caused by Rickettsia prowazekii, parasite of body louse
  • in US -> flying squirrels are an extra human reservoir
  • crowded, unsanitary, famine, war
  • considered bioterrorism agent
23
Q

Sxs and signs of Epidemic louse-borne typhus?

A
  • prodromal malaise, cough, HA, arthralgias, and CP (pleuritic chest pain) during incubation period of 10-14 days
  • abrupt onset of chills, high fever, and flu like sxs progressing to delirium and stupor (looks like flu that progressed to pneumonia)
24
Q

Lab findings in Epidemic Louse Borne typhus?

A
  • CBC: thrombocytopenia
  • CMP: elevated liver enzymes, proteinuria, and hematuria (leaky kidneys, not filtering very well)
  • CXR: patchy consolidation (could also be mycoplasma or fungal)
25
Q

What is Brill-Zinsser Disease?

A
  • R. prowazekii can survive in lymphoid tissues after primary infection, and years later, produce recrudescence of disease
  • this phenomenon can serve as pt source for future outbreaks
  • more gradual onset than primary, fever, and rash are of shorter duration, and the disease is milder and rarely fatal (main concern: contagious)
26
Q

Tx of Epidemic louse-borne typhus?

A
  • doxy

- chloramphenicol

27
Q

MOA of Doxy?

A
  • protein synthesis inhibitor at 30s subunit

side effects: discoloration of teeth, and stunted bone growth

28
Q

Chloramphenicol MOA andAEs?

A

MOA: protein synth. inhibitor at 50S

  • gray baby syndrome
  • aplastic anemia
  • hemolytic anemia
29
Q

Endemic (murine) typhus signs and sxs?

A
  • Rickettsia typhi
  • transmitted from rat to rat via the rat flea (same flea as bubonic plague)
  • urban
  • gradual onset, less severe sxs, and shorter duration of illness than epidemic typhus
30
Q

labs, Dx, and Tx of endemic (murine) typhus?

A
  • same as epidemic louse-borne typhus
    labs: CBC: thrombocytopenia
    CMP: elev liver enzymes, proteinuria and hematuria (ineffective kidney filtration)
  • CXR: patchy
    tx: doxy and chloramphenicol
31
Q

What would be a pro to getting endemic (murine) typhus?

A
  • makes you immune to epidemic louse-bourne typhus which is much more severe
32
Q

Transmission of Rickettsialpox?

A

Rickettsia akari

- transmitted to humans via mites that ride on mice

33
Q

signs and sxs of Rickettsialpox?

A
  • mild, self-limited, febrile illness that starts with an initial localized red skin bump
  • bump turns into a blister and days later: fever and HA develop, and other vesicles appear over body
34
Q

Tx of Rickettsial pox

A

responds well to Doxy

- get sticky mouse traps

35
Q

What is cause of Q fever?

A
  • Coxiella burnetii
36
Q

What is Coxiella burnetii?

A
  • gram - intracellular organism

- Coxiella burnetti (formerly known as rickettsia, but now considered a proteobacteria)

37
Q

What does Coxiella burnetii infect?

A
  • infects cattle (usually spread by milking), sheep and goats
  • in man = Q fever
  • highly resistant spore stage that is transmitted to humans when animal tissue is aerosolized or ingestion of contaminated milk
  • doesn’t need vector
38
Q

Signs and sxs of Q fever?

A
  • begins suddenly with fever, sever HA, cough, and other flu like sxs
  • ***pneumonia develops in about 50% of pts
  • **Hepatitis is frequent enough that combo of pneumonia and hepatitis suggest Q fever
  • Q fever is acute disease: recovery is expected even in absence of abx therapy
    chronic Q fever: endocarditis: culture will be negative, high risk pts: heart valve disease, valve replacement
39
Q

lab findings in Q fever

A
  • CBC: may have leukocytosis
  • CMP: elev. LFTs
  • CXR: may be more prominent than what physical signs suggest - patchy pulmonary infiltrates (like mycoplasma)
  • echo: rule out endocarditis
40
Q

DDX with Q fever?

A
  • Viral, mycoplasma, and bacterial pneumonitis, legionnaire disease, kawasaki disease, tb, psittacosis.

** think Q fever in cases of unexplained fevers with negative blood cultures in association with embolic or cardiac disease especially with suspicious history, no rash hepatitis, and pneumonia presentation

41
Q

Tx and prognosis of Q fever?

A
  • doxy
    Hydroxychloroquine and doxy for endocarditis
  • even when untx: mortality rate is low unless endocarditis develops
42
Q

Lyme disease?

A
  • spirochete, but tick transmitted disease
  • corkscrew shaped, but larger than Treponema
  • Borrelia burgdorferi
43
Q

Where is lyme disease seen?

A
  • NE, midwest and NW US
  • Ixodes tick
  • takes 24 hours to transfer infection
  • similar to syphilis (can have chancre but it won’t be painful)
  • can disseminate to heart, CNS, joints, CN 7 palsy, fatigue, can develop chronic arthritis
  • ddx: think lupus
44
Q

Signs and Symptoms of lyme disease?

A
  • recognize sxs in person who has been exposed to ticks in area endemic to lyme disease
  • Erythema migrans, bull’s eye
  • Ha or stiff neck
  • arthralgias, arthritis, myalgias, arthritis is often chronic and recurrent
45
Q

Dx of lyme disease

A
    • Erythema migrans, bull’s eye, leading edge of rash bx
  • culture is really difficult, usually use levels of antiBorrelia burgdorferi abs to help make dx
  • ELISA and western immunoblotting
46
Q

Tx of Lyme disease?

A
  • doxy or PCN family abx are currently most effective ab for treating the disease
  • is vaccination available but withdrawn in 2002 due to poor sales
47
Q

When should you be thinking a rickettsial disease?

A
  • high fevers, arthralgia, and rashes
48
Q

RMSF rash?

A
  • starts at wrists, ankles, sole and palms and spread to the trunk
49
Q

Lyme disease differentiation?

A
  • bulls eye: erythema chronicum migrans
50
Q

Rickettsialpox skin findings?

A
  • red skin bump turns into blister