Rickettsia, Orientia, Ehrlichia, Anaplasma and Coxiella Flashcards

1
Q

Rickettsia rickettsii causes what disease

A

Rocky Mountain Spotted Fever

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2
Q

characteristics of Rickettsia, Orientia, Ehrlichia, Anaplasma and Coxiella

A
  • Small rods
  • Gram negative (don’t stain well ) (Giemsa)
  • Typical morphology of a gram-negative -LPS, peptidoglycan missing in some
  • No flagella
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3
Q

Growth and metabolism of Rickettsia, Orientia, Ehrlichia, Anaplasma and Coxiella

A

Division occurs through binary fission
Growth is slow 8-10 h
Obligate intracellular pathogens

Use host ATP, coenzyme A, nicotinamide adenine dinucleotide and available amino acids

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4
Q

how do bacteria enter the host

A

Bacteria enter by endocytosis:
Energy-requiring
Bacteria initially in a membrane-bound vesicle

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5
Q

where do the bacteria replicate

A

either:
1. *Cytoplasmic vesicle (membrane-bound)
Phagosome (Ehrlichia, Anaplasma)
Phagolysosome-like vesicle (Coxiella)

  1. *Cytoplasm
    (Rickettsia, Orientia)
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6
Q

lysosome fusion has what effects on : Ehrlichia, Anaplasma and coxiella

A

Ehrlichia, Anaplasma: Killed if lysosomes fuse with phagosome, Prevents lysosomal fusion

Coxiella: CCV (Coxiella-containing vesicle) Phagosome fuses with endosomes
Requires low pH for growth
Delayed lysosomal fusion

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7
Q

symptoms of RMSF

A

High fever and severe headache
Rash ( Macular rash, initially involving the extremities may become petechial later on) , mental confusion, and myalgia (sore muscles)

Incubation period : 2 to 7 days, but may be upwards of two weeks

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8
Q

RMSF epidemiology

A

Transmitted by hard tick vectors
Associated with exposure to wooded areas where ticks exist – more common in summer months

most common in North Carolina and Oklahoma

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9
Q

treatment of RMSF

A

** Tetracyclines, fluoroquinolones
Chloramphenicol: higher relapse
Delayed treatment: increased likelihood of death
10-25% mortality if untreated

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10
Q

Prevention of RMSF

A
No vaccine
• Avoidance or reduction of tick contact
	Transmission requires 24-48 h exposure
• Control is virtually impossible
	 Non-feeding ticks survive as long as 4 years
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11
Q

R. rickettsii is what kind of pathogen

A
  • Intracellular, replicates in cytoplasm and spreads via actin polymerization
  • Most common rickettsial pathogen in US
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12
Q

Rickettsialpox is caused by

A

Rickettsia akari

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13
Q

Rickettsialpox: phase 1

A

Phase 1: Firm red papule at the site of the bite
Develops into vesicle, then a black eschar
Bacteria spread

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14
Q

Rickettsialpox: phase 2

A

Phase 2: 9-14 days: high fever, severe headache, chills/sweats, myalgias, photophobia, vesicular rash develops

Self-limiting after 1 week; no deaths have been reported

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15
Q

Rickettsialpox is spread by

A

Vector is bloodsucking mites, found on mice
Transovarian transmission occurs
Northern USA, Russia, Africa, and Korea

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16
Q

Transovarial transmission

A

when arthropods transmit disease-causing bacteria from parent arthropod to offspring arthropod. It allows the disease to remain in the host for generations

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17
Q

Epidemic typhus is caused by

A

Rickettsia prowazekii

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18
Q

epidemic typhus symptoms

A

Fever, headache and myalgias begin 1 to 2 weeks after exposure

Maculopapular rash
Flat red area covered with bumps
First on the trunk** and then spreads to the extremities

more fatal in pts over 40 y/o

19
Q

maculopapular rash

A

• is a type of rash characterized by a flat, red area on the skin that is covered with small confluent bumps.

The term “maculopapular” is a compound: macules are small, flat discolored spots on the surface of the skin; and papules are small, raised bumps. It is also described as erythematous, or red.

20
Q

epidemiology of Epidemic typhus

A
  • Present in Central, South America, Africa

* Disease associated with unsanitary conditions; peaks in winter

21
Q

Epidemic typhus vector and resevoir

A

Transmission by body louse - Organisms are present in the feces of the infected lice (lice die after 2-3 weeks therefore no transvarian transmission)

Reservoirs include humans and flying squirrels

22
Q

treatment of Epidemic typhus

A

Tetracycline or chloramphenicol

Louse control

Vaccine available for high risk population

23
Q

Brill-Zinsser

A

aka Recrudescent Typhus or Brill’s disease

Relapse of louse-borne typhus
Appears 10-40 years after the primary attack

Milder and less often fatal
Partial immunity may still be present

Rickettsia persist for many years in the lymph nodes

Humans themselves are thus the reservoir

24
Q

R. prowazekii characteristics

A

Intracellular, replicates in cytoplasm, no actin polymerization

25
Murine Typhus (Endemic Typhus) is caused by
R. typhi
26
murine typhus vectors and resevoirs
Rat flea, cat flea vectors Rodents are reservoirs 50-100 cases annually in U.S. Found in temperate and subtropical coastal areas (texas, hawaii)
27
murine typhus is treated with
Tetracycline, doxycycline, chloramphenicol
28
murine typhus symptoms
Incubation period 1-2 weeks Abrupt fever, severe headache, chills, myalgia, nausea Rash in 50% of cases—late--maculopapular on trunk
29
Scrub Typhus cause
Orientia tsutsugamushi
30
scrub typhus symptoms
Fever, headache, maculopapular rash after 5 days, lymphadenopathy 50 to 80% develop initial lesion: Necrotic eschar at site of bite
31
scrub typhus epidemiology
Found in the Far East (Southwest Pacific, Southeast Asia, and Japan) Mites are the vectors and reservoir. Passaged to progeny via infected ova.
32
scrub typhus treatment
Fever responds to tetracycline, doxycycline or chloramphenicol Untreated: fever disappears within 2-3 weeks
33
Ehrlichiosis two diseases
Human anaplasmosis (HA): Anaplasma phagocytophilum Ehrlichia ewingii Human monocyte ehrlichiosis (HME)-- Ehrlichia chaffeensis
34
common symptoms of HA and HME
both: flu-like illness, high fever, headache, myalgias. onset 1-2 weeks after tick bite Leukopenia, thrombocytopenia, and elevated serum transaminases develop in majority of patients Mortality low but >50% require hospitalization
35
differences between HA and HME
HME - sometimes late onset rash, primarily monocytes, mononuclear phagocytes HA: granulocytes primarily infected (neutrophils, eosinohils, basophils)
36
common areas of Ehrlichiosis:
Most common in the summer Most common in Midwest, south states HME: Midwest, coastal Atlantic HA: Upper midwest, northeast Atlantic
37
Ehrlichiosis is spread by
Transmitted by ticks: Lone star, western black legged ticks (deer and mice reservoirs) Transovarial transmission inefficient Transmission within about 6 hours
38
Ehrlichiae structure
lack peptidoglycan and LPS 2 morphologic forms: small elementary bodies and larger reticulate bodies. Elementary bodies assemble morulae Prevent lysosomal fusion, Growth until cell lysis
39
Ehrlichiae treatment
Doxycycline should be used Rifampin: pregnant women Chloramphenicol, penicillins, macrolides not effective Vaccines not available
40
Q-Fever is caused by
Coxiella burnetii
41
Q-fever symptoms
• Most human infections are NOT apparent: No rash • A mild, dry, hacking cough and pneumonia sometimes present. • 9 to 20 days: abrupt onset of fever, chills, and headache. • Chronic Q fever: subacute endocarditis Fatalities are rare
42
Q-fever transmission
* Transmission from animals to humans by inhalation of dust * Carried by mammals such as cattle, sheep, and goats * World-wide distribution
43
Q-fever phase 1 and 2
Phase I: intact LPS | Phase II: missing outermost O-antigen of LPS
44
Treatment and prevention of Q-fever
* Tetracycline (doxycycline) or combination for chronic infections * Vaccines have been developed--for unexposed