9-8 Rickettsia - Erlichia Flashcards
Rickettsiaceae Family Characteristics
- Size
- Gram Positive vs. Gram negative
- LPS and Peptidoglycan description
- Flagella?
- Which Stain do you use?
- Small (0.3 to 0.5 m)
- Gram negative
- LPS and Peptidoglycan present (but both minimal or no endotoxin activity)
- No flagella
- Best visualized with Giemsa stain of infected cells
A: Rickettsiaceae Division occurs through _____ ______ but is SLOW. They are ______ ______ PATHOGENS!
B: What do they require from their host? (4)
A: Rickettsiaceae Division occurs through [binary fission] but is SLOW. They are OBLIGATE INTRACELLULAR PATHOGENS!
B: They require host ATP / CoA / NAD+ / [amino acids]. After a while they can synthesize their own ATP
A: Pathogenesis of [Rickettsiaceae Family] (3)
B:
1st. Infection occurs by induction of an endocytic process that requires energy
2nd. Bacteria are initially present in membrane-bound vesicle (phagosome) but use [Phospholipase A] to enter cytoplasm
3rd: . Bacteria grow inside eukaryotic cells but location of replication varies
A: Locations of replicating bacteria vary
1. Where do [Coxiella and Ehrlichia] replicate?
- Where do [Rickettsia and Orientia] replicate?
B. Members of the genus Coxiella replicate in ________
- What does Coxiella growth require from this organelle?
- Coxiella has the ability to delay _____ fusion
A: Locations of the replicating bacteria vary
1. [Cytoplasmic vacuoles]: Coxiella and Ehrlichia
- Cytoplasm: [Rickettsia and Orientia] (they escape their initial vacuole using [phospholipase A] to enter Cytoplasm)
B. Members of the genus Coxiella replicate in Coxiella-containing vacuole (CCV)
a. Growth of Coxiella requires the low pH of this organelle
b. Coxiella delays lysosomal fusion
Which Rickettsiaceae have the ability to Spread intra- and inter-cellularly using actin polymerization? (2)
R. Rickettsii and R.Typhi Spread intra- and inter-cellularly using actin polymerization
A: [Rickettsia _______] can NOT UTILIZE [cytoplasmic projections] to move between cells like its cousins
B: What does this bacteria eventually do as a result?
C: Outside host cell, Rickettsiaceae family die quickly BUT _______ IS DIFFERENT SINCE IT IS RESISTANT TO _______! –> remains viable for years but _______ decreases as time outside host increases.
A: [Rickettsia Prowazekii] can NOT UTILIZE [cytoplasmic projections] to move between cells like its cousins
B: It just has to eventually grow until it lyses the eukaryotic cell.
C: Outside host cell, Rickettsiaceae family die quickly BUT COXIELLA IS DIFFERENT SINCE IT IS RESISTANT TO DRYING! –> remains viable for years but infectivity decreases as time outside host increases.
A: How does the [Rickettsiaceae Family] cause [Primary Vasculitis lesions] ? (3)
B: Where is [Primary Vasculitis lesion] more common? Where is MORE SERIOUS?
[Primary Vasculitis lesion]
a. Bacteria multiply in endothelial cells lining small blood vessels.
b. Endothelial Cells become swollen and necrotic
c. Thrombosis (clotting) of the vessel, leading to rupture and more necrosis —> [Primary Vasculitis lesion]
B: Skin but more serious in adrenal glands
List the general guidelines for [Rickettsiaceae Family] Tx (5)
Treatment:
1. Therapy should be instituted before seroconversion and is less effective if illness is dx later than 1st week
- Tetracycline and chloramphenicol are effective if treatment is started early given
orally and continued for 3-4 days after defervescence. - Sulfonamides enhance growth of Rickettsiae = contraindicated
- Abx do not free the body of rickettsiae, but they do suppress growth.
- Limited vaccines
Which 2 Rickettsia are in the Rocky Mountain Spotted Fever group?
B: Which is more dangerous
C: This more dangerous Rickettsia is maintained in the tick population by passage from tick to tick through
_______ _________. Small ______ and ______ may serve as a reservoir for tick infection
D: Incubation Period of this Rickettsia
Rocky Mountain Spotted Fever: Rickettsia rickettsii
Rickettsialpox: R. akari
dangerous = Rickettsia rickettsii
C: Maintained in the tick population by passage from tick to tick through transovarian transmission.
i. Small rodents and dogs may serve as a reservoir for tick infection
D: 2 to 6 days before sx onset, but may take more than 2 weeks
3 Ways to Diagnose Rickettsia rickettsii
- Positive results for [Immunoflurouescence Antibody]
Initial titer of 1:64 with 4-fold rise in antibody titer
(Antibody levels arise 2-3 weeks after onset) - Microimmunofluorescence (MIF)
- PCR with gene targets such as ompA, ompB
3 Ways to TREAT Rickettsia rickettsii
B: Which Tx is Rarely Used?
- [Doxycycline - Tetracycline]
- Chloramphenicol
- Fluoroquinolones (RARELY USED FOR THIS)
How do you Prevent [Rickettsia Rickettsii] Infection? (3)
Since there is no Vaccine,
1) Avoid Tick Contact and remove them frequently
2) These Ticks can live for 4 years without feeding
A: What bacteria causes Rickettsialpox? Describe the dz
B:
- What animal is the [Vector AND Reservoir] for this bacteria?
- Transovarian transmission?
- Where is it found? (4)
A: Spotted Fever group: Rickettsialpox
- Disease: Mild disease with a rash resembling that of varicella
- Cause: Rickettsia akari
B:
1. Vector AND Reservoir is [blood sucking mites from mice]
- Transovarian transmission occurs
- Found in [northern USA] / Russia / Africa / Korea
Describe The Clinical Manifestations of [Rickettsia Akari]
A: Phase 1 (3)
B: Phase 2- list sx -(6)
C: How does this resolve?
a. Phase 1
i. A firm red papule appears at the site of the bite
ii. Papule develops into deep-seated vesicle then black eschar
iii. Bacteria spread systemically
b. Phase 2
i. After 9-14 days, [high fever/sweats], severe headache, myalgia, photophobia
ii. A vesicular rash develops (small, blister like lesions filled with clear fluid).
C. Self-limiting after 1 week; no deaths have been reported
A: [Rickettsia Prowazekii] is transmitted by what 2 organisms?
B: Transovarian Transmission?
C: How is this bacteria transmitted?
D: 2 Reservoirs
(body LICE)
- Pediculus humanus corporis
- Pediculus humanus capitis
B: These Lice die 2-3 weeks = NO TRANSOVARIAN TRANSMISSION
C: [Rickettsia Prowazekii] remain viable in [lice feces], even when Lice are dead —> transmission occurs when human scratches [lice feces] into a Lice bite
D: Reservoirs = Humans and [Flying Squirrels]
<p>Macular </p>
<p>flat lesions detected because of a change in color or texture</p>
<p>Papular</p>
<p>lesions, which are <strong>raised</strong> and well <strong>circumscribed</strong></p>
- Describe symptom course for [Rickettsia Prowazekii]
- How do you diagnose this bacteria in lab?
- Two tx
- [Fever / HA / (Maculopapular Rash)/ myalgia] begin 1-2 weeks after bite and Fever last 2 weeks
- Diagnose with MIF
3.
- [Doxycycline - Tetracycline]
- Chloramphenicol
What is [Brill’s Recrudescent Typhus disease] caused by ?
A: Description (2)
B: B. Rickettsia persist for many years in the ____ ____ of an individual without any symptoms
[Brill’s Recrudescent Typhus disease] = [Rickettsia Prowazekii]
A:
- Relapse of louse-borne typhus appearing 10-40 years after the primary attack
- Milder and less often fatal; partial immunity may still be present
B. Rickettsia persist for many years in the lymph nodes of an individual without any symptoms
d. Humans themselves are thus the reservoir of the Rickettsia of epidemic typhus
What are the 4 bacterial organisms that are LACTOSE NEGATIVE?
“Shig and Sal Protested Yogurt”
- Shigella
- Salmonella
- Proteus Mirabilis
- Yersenia Enterocolitica
Rickettsia Typhi
A: Vector
B: RESERVOIR
C: Where is it found
D: Incubation
E: Sx (3)
Rickettsia Typhi
A: [Cat or Rat Flea] = Vector
B: Rodents = RESERVOIR
C: Found in subtropical costal areas during warm months
D: Incubation = 1-2 weeks and sx are abrupt
E:
-[MaculoPapular Rash] STARTING on chest/abdomen but can [spread to palms/soles]
- Myalgia
- Nausea
Rickettsia Typhi
A: How to Diagnose
B: Tx (2)
Positive IFA
iii. Significant titers detectable within 1-2 weeks
B:
- [DOXY-tetracycline]
- Chloramphenicol
A: What causes [Scrub Typhus]
B:
- Vector
- Reservoir
C: Sx (4)
D: tx (3)
A: Orientia tsutsugamushi
B: Mites that invest rodents are the [Vector/Reservoirs] mostly in Asia
C:
- Resemble [Epidemic Typhus - Rickettsia Prowazekii] clinically
- initial lesion: necrotic eschar at bite site on extremities
- [Generalized lymphadenopathy] and [Lymphocytosis]
- Potential Severe Cardiac/Cerebral involvement
D: Tx
- Fever SELF RESOLVES after 2-3 weeks but can be treated with
- [DOXY-tetracycline] or
- chloramphenicol
A: Human monocyte ehrlichiosis (HME) is caused by ____
B: vector
C: Reservoir (2)
D: Location (2)
A: Human monocyte ehrlichiosis (HME) = [Ehrlichia
chaffeensis]
B: HME vector is Lone Star tick (Amblyomma Americanum);
C:
1) white-tailed deer
2) domestic dog
D: Found in SE U.S. and South Central
A: Human anaplasmosis (HA) is caused by _______ or _______
B: Vector
C: Reservoirs (3)
D: Location (2)
E: What distinguishes this from HME?
A: Human anaplasmosis (HA), caused by
- [Anaplasma phagocytophilum]
- [Ehrlichia ewingii]
B: Human anaplasmosis vector is [Ixodes tick]
C: reservoirs include chipmunks, mice,
voles
D: Found in NORTHERN / CENTRAL US
E:
- Infection primarily of bone marrow myeloid cells (neutrophils
- Inclusion bodies / Morulae detected in granulocytes
<p>Why is [Ehrlichia eWingii] significant? </p>
<p>Because of cross-reactivity with E. chaffeensis, diseases caused by E. ewingii (causes dz in DOGS) may be underestimated.</p>
Ehrlichiosis
a. Clinically similar to________ but with no _____
B: Sx (5)
C: This dangerous?
D: Pathology (3)
Ehrlichiosis
Clinical features and Pathology
a. Clinically similar to Rocky Mountain Spotted Fever
Typically no rash.
B. [Fever /chills],
- myalgia,
- nausea/ vomiting
- Weight loss
- [Leukopenia, thrombocytopenia, and elevated serum transaminases]
e. Mortality in less than 5% of patients
f. Ehrlichiae infect circulating leukocytes where they multiply within membrane—-> bound inclusions (morulae)
g. Prevent fusion of lysosome with Ehrlichia inclusion
h. Growth until cell lysis
A: How do you diagnose Ehrlichiosis? (3)
B: Tx (2)
C: Which abx are NOT EFFECTIVE?
A: Ehrlichiosis
1. [Morulae in WBC]
- IFA: INC in antibody titer after 2 weeks = Confirmation
- PCR
B: Tx
a) [DOXY-Tetracycline]
b) Rifampin for pregnant woman
C: DO NOT USE
X: PCN
X: CHLORAMPHENICOL
X: MACROLIDES
A: WHAT BACTERIA CAUSES Q-FEVER?
B: Transmission (2)
C: What are these bacteria’s host? (3)
D: What’s the catch with sx onset of this disease?
A: [Coxiella Burnetii]
B: Transmitted to humans BY INHALATION OF [SLAUGHTERHOUSE AEROSOL] OR DUST CONTAMINATED WITH [Coxiella Burnetii]
C: Naturally carried in cows and sheep; but are specifically found in TICKS
D: Most human infections are NOT apparent and can take 9-20 days after inhalation to appear.
A: Sx of Q-Fever (3)
B: What bacteria causes Q-Fever
C: 4 Reasons this bacteria actually causes Dz
A: Sx
- [mild dry hacking cough]
- [POTENTIAL patchy interstitial PNA]
- NO RASH!!!!!!
B: [Coxiella Burnetii]
C:
a. primarily replicates in phagosome because it requires low pH
b. forms endospores and thus is resistant to drying
c. Phase variation of LPS correlates with more and less virulent forms
d. High antibody titers lead to formation of immune complexes
<p>Diagnosis for [Coxiella Burnetii]<br></br>
A: Serology<br></br>
-IgM titer of \_\_\_\_<br></br>
-IgG titer of \_\_\_\_\_\_<br></br>
- \_\_\_\_\_ fold rise in Ab titer<br></br>
- IgG titer positive after \_\_\_\_ weeks</p>
<p>OR USE \_\_\_\_\_</p>
<p>a. Serology<br></br>
i. IgM titer of 1:50<br></br>
ii. IgG titer of 1:200<br></br>
iii. 4-fold rise in antibody titer<br></br>
iv. IgG titer positive after 12 weeks</p>
<p>OR USE PCR</p>
<p>How do you treat [Coxiella Burnetii] ?<br></br>
A: acute infection</p>
<p>B: Chronic Infection</p>
<p>C: Vaccines?</p>
<p>How do you treat [Coxiella Burnetii] ?<br></br>
a. [DOXY-tetracycline] for acute infections</p>
<p>b. [Combination of antibiotics] for chronic infections</p>
<p>c. Vaccines have been developed</p>
