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Path > 2: Rickettsial + Zoonotic > Flashcards

2: Rickettsial + Zoonotic Flashcards

1
Q

vector borne diseases: intracellular vs. extracellular + vectors

A

intracellular:
- rickettsial typhus (lice)
- rickettsial RMSF (ticks)

extracellular:
- lyme disease (ticks)
- relapsing fever (lice or ticks)
- plaque (fleas)

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2
Q

histologic hallmark of rickettsia

A

‘perivascular cuffing’ - intracellular infection of endothelial cells w/ perivascular lymphocytic infiltrate

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3
Q

general characteristics of rickettsia

A

G(-)

obligate intracellular

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4
Q

rickettsia transmission

A 
by arthropod (ticks, mites, fleas, lice) 
bite or contamination of abraded skin with arthropod feces
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5
Q

what might a patient have at the inoculation site for rickettsia?

A

eschar - dark, swollen, crusted, necrotic lesion

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6
Q

how is rickettsia diagnosed?

A
  • immunostaining of organisms
  • anti-rickettsial serology
  • exposure to vector

(not by culture - will not grow)

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7
Q

pathogenesis of rickettsia and what it causes

A

multiply mainly in small vessel endothelia - causes secondary vascular leakage:

  • rash
  • fever
  • CNS manifestations
  • small vessel vasculitis w/ microthrombi, focal ischemia, or hemorrhage
  • lyse endothelial cells (typhus) or spread cell to cell (spotted fever group)
  • may progress to hypovolemic shock w/ peripheral edema
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8
Q

perivascular cuffing

A

MAKE SURE TO STUDY PICTURES IN THE PACKETS TOO

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9
Q

what is responsible for much of the tissue damage seen in rickettsial disease?

A

NK cells produce gamma-IFN -> cytotoxic T cell response responsible for damage

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10
Q

clinical features of rickettsia

A
  • fever
  • rash
  • CNS symptoms

severe cases:

  • hypovolemic shock
  • DIC
  • pulmonary edema
  • gangrene
  • petechiae
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11
Q

which clinical feature of rickettsia is also seen in N. meningitidis G(-) sepsis and how do you differentiate the two?

A

sx of sepsis/shock - differentiate based on context

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12
Q

what other diseases are on the ddx for rickettsia?

A

-meningococcemia
-rubeola
-rubella
-ehrlichiosis
(last three are way down on the list b/c they almost never cause shock and DIC)

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13
Q

transmission of epidemic typhus and what organism causes it

A

caused by Rickettsia prowazekii

head lice mediates human to human transfer

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14
Q

forms of disease for epidemic typhus

A
  • begins with centrifugal rash
  • followed by CNS shit (apathy, dullness, stupor, some coma)
  • high fever
  • chills
  • cough
  • rash
  • severe muscle pain
  • sensitivity to light
  • delirium
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15
Q

if epidemic typhus is untreated, what is the mortality rate?

A

10-60%

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16
Q

clinical findings of mild epidemic typhus

A
  • rash

- small hemorrhages

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17
Q

clinical findings of severe epidemic typhus

A

-gangrene of finger tips, nose, earlobes, scrotum, penis, vulva

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18
Q

histologic/morphologic findings with epidemic typhus

A
  • cuff of mononuclear inflam cells around vessels
  • ecchymotic hemorrhages of affected organs
  • microthrombi
  • no necrosis of vessels
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19
Q

transmission of RMSF

A

dog or wood tick bite

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20
Q

incubation period of RMSF

A

7d

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21
Q

symptoms of RMSF

A
  • high fever for 2-3d
  • nausea
  • vomit
  • headache
  • muscle pain
  • rash appears 6d of fever (b/c lymphocytes now attacking vessels - microthrombi add to rash)
    • hemorrhagic rash extends over entire body (including PALMS AND SOLES)- spreads periphery to trunk/neck/face
  • eschar rare
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22
Q

histologic/morphologic findings with RMSF

A
  • perivascular mononuclear infiltrate
  • necrosis, fibrin extravasation, and thrombosis of small vessels and arterioles
  • severe: foci of necrotic skin (fingers, toes, elbows, earlobes, scrotum)
  • microinfarcts in brain
  • noncardiogenic pulmonary edema
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23
Q

what is the major cause of death in RMSF

A

noncardiogenic pulmonary edema

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24
Q

how to differentiate noncardiogenic pulmonary edema from cardiogenic pulmonary edema

A

non: lymphocytes in this fluid, it is an exudate
cardio: transudate! and no lymphocytes

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25
Q

area distribution of RMSF by tick

A

dog tick: east

wood tick: west

26
Q

if you get these symptoms in winter vs. summer, what is more likely: RMSF or meningitis?

A

winter: meningitis
summer: RMSF

27
Q

what causes scrub typhus and where do you find it?

A

Orientia (formerly Rickettsia) tsutsugamushi

endemic in Far East, China, India

28
Q

how is scrub typhus different from epidemic typhus?

A
  • resembles typhus but transmitted by mites
  • transitory or no rash
  • may be prominent lymphadenopathy
29
Q

compare/contrast ehrlichiosis and RMSF

A

similar, but ehrlichiosis has:

  • no eschar
  • rash rare (b/c infects neutrophils/monocytes instead of endothelial cells)
  • characteristic cytoplasmic inclusions (morulae)
  • transmission by ticks
30
Q

describe the morulae of ehrlichiosis

A

masses of bacteria that look like mulberries in shape

31
Q

transmission of lyme disease (borrelia burgdorferi)

A

spirochetes transmitted to man by tick bites from animals or lice (man to man)
-white-tailed deer tick

32
Q

how is borrelia burgdorferi able to persist in the body?

A

shift antigenic markers to avoid host production of Ab’s
-get local rxn when organism first injected, but then can persist and spread - chronic problems + can cause tertiary problems down the road (CNS, heart, joint)

33
Q

area distribution of lyme disease

A

wisconsin/minnesota + northeast coast US

-near boundary waters

34
Q

what two bugs should you think of when someone has recently traveled by boundary waters?

A

giardia and lyme disease

35
Q

describe lyme disease multisystem chronic inflammatory disorder

A

local lesion progresses to bacteremia and chronic inflammatory lesions in distant organs
-primary/secondary/tertiary disease

36
Q

what is much of the pathology thought to be due to in lyme disease?

A

secondary to immune response against bug:

-binding of bacteria LPS to TLR2** of macrophages

37
Q

lyme disease prevention?

A

OspA vaccine commercially available for high risk groups

vector avoidance

38
Q

treatment for lyme disease

A

doxycycline

39
Q

describe primary lyme disease

A
  • skin rash (target lesion/Bull’s eye rash) w/ vasodilation and dense perivascular inflammatory infiltrates of mononuclear leukocytes
  • rash has spreading erythematous margins and blanching center (erythema chronicum migrans)
  • fever and constitutional symptoms
  • resembles rickettsial illnesses such as RMSF
40
Q

describe secondary lyme disease

A
  • months later
  • bacteremic dissemination fo spirochetes
  • joint disease
  • muscle pain
  • cardiac arrhythmias
  • meningitis
  • CN involvement
41
Q

describe tertiary lyme disease

A
  • years later
  • CNS
  • cardiac
  • skeletal
42
Q

describe progression of lyme disease from primary to secondary to tertiary in general terms

A

local primary rxn -> disseminated rash -> tertiary localized, chronic rash

43
Q

pathology of lyme disease

A
  • focal necrosis, hemorrhages, DIC
  • skin rash w/ dense perivasular mononuclear infiltrate
  • lymphoplasmacytic cell infiltrate!!! (only syph and lyme)
44
Q

describe arthritis of lyme disease

A

resembles early rheumatoid arthritis:

  • synovial hyperplasia
  • lymphocytes, plasma cells
  • proliferative arteritis
45
Q

transmission of relapsing fever (borrelia recurrentis) and area distribution

A
  • spirochete transmitted by human lice or rodent ticks to humans
  • throughout world
  • epidemics in Africa, E Europe, Russia
46
Q

latent period of relapsing fever

A

1-2w of shaking chills, fever, headache, fatigue

47
Q

what causes the successive attacks (epochs) of relapsing fever?

A
  • ability of the dude to express new surface Ag’s

- with each wave of attack, body must make new Ab’s

48
Q

what is fatal relapsing fever accompanied by?

A

massive hepatosplenomegaly

49
Q

organism and transmission of plague

A
  • yersinia pestis
  • arthropod bite (fleas!)
  • man an accidental victim of ‘sylvatic cycle’ b/w fleas and wild animals
50
Q

pathologic mechanisms of plague

A
  • rapid proliferation within lymphoid tissues**
  • “injection” of YOPS (yersinia outer proteins)
  • necrosis of tissue and blood vessels
  • swelling of lymphoid tissues (buboes)
  • striking leukocytosis
  • septicemia/DIC -> Death
51
Q

describe the function of YOPS in plague

A
  • inactivates molecules that regulate actin polymerization

- inhibits secretion of inflammatory cytokines

52
Q

symptoms of minor plague

A
  • lymphadenopathy

- constitutional symptoms

53
Q

symptoms of bubonic plague

A

-prominent lymphadenopathy (buboes)

54
Q

symptoms of pneumonic plague

A

-hemorrhagic, necrotizing pneumonia primary or secondary to bubonic infections

55
Q

most common form of plague?

A

bubonic plague

56
Q

can you get sepsis from plague?

A

yes, and it is rapidly fatal

but rare in US

57
Q

mortality of plague untreated and treated + what is treatment

A

untreated: 50-90%
treated: 15%

doxycycline for the win!

58
Q

what is the primary immune response to intracellular dudes?

A

cytotoxic T cells

59
Q

what symptoms will you get from all disease that cause microthrombi in the brain?

A
  • obtundation
  • headache
  • seizures
60
Q

besides Rickettsia, what other diseases also cause microthrombi in CNS?

A
  • malaria
  • TTP
  • eclampsia
61
Q

flowchart of rickettsial pathogenesis

A

intracellular dude gets in-> endothelium activated + perivascular lymphocytes -> microthrombi + microhemorrhages

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