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MID EXAM 2 > Rickettsia > Flashcards

Rickettsia Flashcards

1
Q

Shared characteristics of rickettsiae and rickettsia-like bacteria

A

1) Gram Neg
2) Intracellular organisms
3) Life cycle involves arthropods (ticks, lice, mites or flea) and mammals; humans are an accidental host
4) Zoonotic/arthrpod vectors or reservoirs are important
5) Similar clinical manifestations- fever, headache, w/ or w/o rash, that are often dificult to dx and end up being treated empirically based on clinical suspicion
6) arthropod bites are often not noticed or remembered, so know is at risk

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2
Q

Rickettsia Species Groups

A

Spotted Fever Group or Typhus Group

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3
Q

Spotted Fever Species

A

Spotted Fever Group:

1) R. rickettsii
2) R. conorii
3) R. africae
4) R. akari

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4
Q

Types of spotted Fevers

A

1) Rocky Mountain Spotted Fever (R. rickettsii)
2) Fievre Boutonneuse/MSF and African tick typhus (R. conorii & R. africae)
3) Rickettsialpox (R. akari)

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5
Q

Rocky Mountain Spotted Fever (RMSF)

A

R. Rickettsii

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6
Q

RMSF Epidemiology

A

Vector and reservoir:Dermacentor tick species (American dog tick and Rocky Mountain tick); incidence of ix inceases in the summer; endemic in US (Carolinas, Tennessee), Canada, Mexico, Central America, Brazil and Columbia

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7
Q

RMSF Pathogenesis

A

1) tick bite puts bacteria into the skin, spreads systemically
2) bacteria infect vascular endothelium, which they enter and then replicate in the cytoplasm
3) bacteria spread directly from cell to cell like the lil creeps they are, causing direct cellular injury, leading to loss of vascular integrity and resulting in edema, hemorrhage and hypotension
4) vascular injury results in consumption of platelets therefore expect to find thrombocytopenia

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8
Q

RMSF IMPORTANT clinical features

A

First: fever, anorexia and headache
Second: 3-5 days later MACULOPAPULAR rash that progresses into a PETECHIAL rash of the wrists, ankles, palms and/or soles that spreads centrally to the trunk.
Last but not least: don’t expect to find eschar at the tick bite and the cellular damage may progress to necrosis/gangrene that may require amputation

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9
Q

RMSF additional clinical features that hopefully aren’t as important, but read it anyways

A

Other organ manifestations: conjunctivits, abdominal pain, nausea, voiting, hepatosplenomegaly, meningo-encephalitis, non-cardiogenic pulm edema. There is a 20% fatality rate, esp with African Americans, those with G6PD DEFICIENCY, elderly and chronic alcoholics, so be on the lookout for these sx or pt could die due to shock/hypoTN w/in 8-15days of onset

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10
Q

RMSF lab findings

A

Leukopenia and thrombocytopenia in 30-50% of pts

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11
Q

RMSF dx and tx

A

dx: epidemiological and clinical clues should prompt empirical tx before confirming dx with serology. Tx: a mystery not discussed in notes

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12
Q

RMSF Prevention

A

avoid areas/seasons of risk (ie Tennessee in the summer Steve McQueen), use tick repellant, tuck yo lightly colored pants into your socks, and check your skin for exposure after

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13
Q

Other RMSFs - R. conorii and R. Aficae

A

R.conorii- Fièvre Boutonneuse/MSF (africa, mediterranean and middle east), R. africae- African tick bite fever (southern Africa) :
starts the same with fever, headache, myalgia but pt would have “TACHE NOIRE” a necrotic ulcerated lesion at tick bite site.
Usually not deadly, but can develop into a serious illness if other comorbidities present

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14
Q

Other RMSFs- R.akari

A

Rickettsialpox, common in urban areas with homeless. The reservoir is MICE and then a mite from the mouse bites the human, leaving an eschar at the bite site.
Then comes the fever, chills, headache and a VESICULOPAPULAR rash. (note this is the only spotted fever with a VP rash). complications and death are also rare

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15
Q

Typhus Species

A

1) R. prowazekii
2) R.typhi
3) Orienta tsutsugamushi

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16
Q

Epidemic/Louse Borne Typhus

A

caused by ole R. prowazekii

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17
Q

Louse Typhus/R.prow Epidemiology

A

Found in crowded, unsanitary conditions esp those caused by war, famine and natural disasters, ex: refugee camps.
Esp during fall/winter, and in cold climates where clothes are washed less often.
Vector: body lice, reservoir: humans and even flying squirrels

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18
Q

LTy/R.prow Pathogenesis

A

Louse poops on you while drinking your blood (super rude), this irriates you and your skin (obvs) so you scratch it and the bacteria into you. and get this… bacteria then goes on to kill the louse1-3 weeks later by gut obstruction.

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19
Q

LTy/R.prow Clinical features

A

Abrupt onset of the usual fever, chills, myalgia, and headache. Pt real sick.
Then, 3-5 days after the fever, MACULOPAPULAR rash that starts on the trunk and spreads to the extremities (spares face, palms and soles).
Fever for about 2 weeks, but pts may take between 2-3 months to fully recover.
Fun fact: can establish latency and relapse can occur years later with coinciding immunosuppression

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20
Q

LTy/R.prow dx

A

Based on clinical and epi clues, confirmed by serology not old school Weil-Felix test.

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21
Q

LTy/R.prow tx

A

Doxycycline (other countries are into chloramphenicol)

22
Q

Endemic/Murine Typhus

A

caused by R. typhi

23
Q

MTy/R.ty Epidemiology

A

Reservoir: rats, cats and opossums. Vector: Fleas

-usually a traveller’s disease, though ix seen in SoCal and Texas

24
Q

MTy/R.ty Pathogenesis

A

Fleas carry the ix lifelong, flea bites and poops on human, human scratches bite/poop, and wound is inoculated with species.
R. typhi targets endothelial tissue, damages the cell by lysis and releases bacteria from the cell to do more damage

25
Q

MTy/R.ty Clinical features

A

Abrupt onset of fever, severe headache, chills, nausea
Sometimes this rash appears immediately or it may develop over time, MACULOPAPULAR but may also be PETECHIAL and is found equally on trunk and limbs (so its a combo of LTy and RMSF sx)

26
Q

Other MTy/R.ty clinical features

A

Cough and chest radiograph abnormalities, sx mild and resolve in a week unless you’re old or immunocompromised. Lab features are similar to that of RMSF- leucopenia and thrombocytopenia

27
Q

MTy/R.ty dx and tx

A

Clinical suspicion, confirmation by serology, tx with doxy

28
Q

Scrub typhus

A

caused by… Orienta tsutsugumushi aka CHIGGERS!

29
Q

STy/Otsutsu Epidemiology

A

Reservoir: rodents, other small mammals, and chiggers
Vector: larval stage of trombiculoid mites aka chiggers
Humans are accidental hosts, usually the infected are travellers, military personnel or inhabitants of China, Japan, Korea, pakistan, India, and Australia

30
Q

STy/Otsutsu Pathogenesis

A

Mite bites host, inoculates the site, a papule forms that develops into an eschar. Lymphadenopathy may develop before systemic sx

31
Q

STy/Otsutsu Clinical features

A

Suden onset of fever, headache and myalgias
Eschar at bite site in 50% of ppl
REGIONAL LYMPHADENOPATHY
3-5 days later, maculopapular TRUNCAL rash may develop
**if accompanied by delerium or DEAFNESS and other sx add up, Scrub typhus better be on your differential

32
Q

STy/Otsutsu dx and tx

A

dx with serology or PCR, tx with doxy

33
Q

Q Fever

A

Caused by the Cox, Coxiella burnetii

34
Q

Q Fever / Cox bacteria, why is this in the rickettsia packet?

A

bc it’s a pleomorphic gram neg coccobacillus that was originally classified as a rickettsia, but its actually more related to Legionella and Francisella.

35
Q

Q fever Cox pathogenesis

A

Bacteria infects machrophages and survives/replicates w/in the phagolysosome of these cells.
It then sporulates and thses sprores survive extracellularly and in the env’t in extreme temps and dryness.
Fucking spores then contaminate the env’t and become AEROSOLIZED allowing for airborne trasmission
Worst of all- it only takes 1 organism to cause disease

36
Q

Q fever/ Cox Epi

A

Ubiquitous, it’s everywhere, but especially a disease of livestock/farmers
Reservoir: cattle, sheep, goats, dogs, cats. Spores shed in their urine/feces/milk or when ix tends to reactivate in pregnant animals and then is spread via aerosolized spores or fluids to the person who births that baby. So keep a lookout for this in farm workers, meat packers, vetrinarians, etc.

37
Q

Q fever/ Cox Clinical features

A

Animals are usually w/o sx, but human disease severity is dependent on the inhaled dose. Only 50% get sx and it is categorized as either ACUTE or CHRONIC

38
Q

Acute Q Fever

A

Atypical pneumonia and hepatitis

39
Q

Chronic Q Fever

A

Culture negative endocarditis, subacute presentation, osteomyelitis; more common in immunocompromised

40
Q

Q Fever dx and tx

A

clinical suspicon (have you birthed a baby cow recently), serology

acute: doxy reduces time of resolution
chronic: doxy +rifampin or cipro for at least 18 months

41
Q

Ehrlichioses- Why is this in the ricketssiae packet?

A

Again, another tickborne obligate intracellular bacteria

But these bacteria survive and multiply w/in intracytoplasmic vesicles called morulae (clusters of bacteria)

42
Q

Two Clinical presentations of Ehrlichiosis

A

1) Human Monocytic Ehrlichiosis (HME)

2) Human Granulocytic Anaplasmosis) HGA

43
Q

Ehrlichioses Pathology (same for HME and HGA)

A

1) tick bite inoculates skin with bacteria, it spreads lymphatically
2) target cells are leukocytes in the blood, bone marrow and reticuloendothelial system
3) internalized by target cells and then survives and and multiplies w/in cytoplasmic vacuoles (MORULAE)
4) results in leucopenia and thrombocytopenia
5) organisms have a direct cytopathic effect that interferes with the immune response

44
Q

HME Epidemiology

A

caused by Ehrlichia chaffeensis
vector: Amblyomma americanum (lone star ticks), which are not so surprisingly found in south central, southeastern and mid-atlantic states.
Reservoir: White tailed deer and humans

45
Q

HGA Epidemiology

A

caused by Anaplasma phagocytophilum
vector: Ixodes ticks which may also transmit LYMEs and babesiois in US (think Cape Cod), Europe and Asia
Reservoir: rodients and small mammals

46
Q

HME and HGE shared epi

A

ix is related to occupational and recreational exposure to ticks
incidence highest summer thru fall
men more commonly infected than women

47
Q

E. ewingii

A

canine pathogen that is similar to HME bacteria, but infects neutrophils like HMA, that mostly occurs in immunocompromised hosts with fewer complications and no fatalities

48
Q

HME clinical features

A

1) fever, chills, headache, and malaise
2) maculopapular rash in 30%
3) nausea, vomiting and then may develop into severe illness like multi organ failure, meningitis or death esp in those with HIV
class ex: HIV+ goes on vacay in Cape Cod and returns with fever, headache and rash, delayed dx results in meningitis.

49
Q

HGA Clinical features

A

1) fever, blah, headache, blah, malaise, nausea
2) Rash is real uncommon and so is CNS involvement (no cape cod, meningitis story)
3) But you can expect to see peripheral neuropathies- facial palsy, brachial plexopathy
- - death rare

50
Q

HME & HGA lab findings

A

Leucopenia, thrombocytopenia and increased liver enzymes

51
Q

HME & HGA dx and tx

A

Suspicion! then do a blood smear, wichis more sensitive with HGA than HME and unlike all the other rickets, PCR is more sensitive for dx than serology
tx is still doxy

MID EXAM 2 (11 decks)

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