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MHD #3 > Rickettsia, Orientia, Ehrlichia, Anaplasma and Coxiella > Flashcards

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
Q

Murine Typhus (Endemic Typhus) is caused by

A

R. typhi

26
Q

murine typhus vectors and resevoirs

A

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
Q

murine typhus is treated with

A

Tetracycline, doxycycline, chloramphenicol

28
Q

murine typhus symptoms

A

Incubation period 1-2 weeks
Abrupt fever, severe headache, chills, myalgia, nausea
Rash in 50% of cases—late–maculopapular on trunk

29
Q

Scrub Typhus cause

A

Orientia tsutsugamushi

30
Q

scrub typhus symptoms

A

Fever, headache, maculopapular rash after 5 days, lymphadenopathy

50 to 80% develop initial lesion: Necrotic eschar at site of bite

31
Q

scrub typhus epidemiology

A

Found in the Far East (Southwest Pacific, Southeast Asia, and Japan)

Mites are the vectors and reservoir. Passaged to progeny via infected ova.

32
Q

scrub typhus treatment

A

Fever responds to tetracycline, doxycycline or chloramphenicol

Untreated: fever disappears within 2-3 weeks

33
Q

Ehrlichiosis two diseases

A

Human anaplasmosis (HA): Anaplasma phagocytophilum Ehrlichia ewingii

Human monocyte ehrlichiosis (HME)– Ehrlichia chaffeensis

34
Q

common symptoms of HA and HME

A

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
Q

differences between HA and HME

A

HME - sometimes late onset rash, primarily monocytes, mononuclear phagocytes

HA: granulocytes primarily infected (neutrophils, eosinohils, basophils)

36
Q

common areas of Ehrlichiosis:

A

Most common in the summer
Most common in Midwest, south states
HME: Midwest, coastal Atlantic
HA: Upper midwest, northeast Atlantic

37
Q

Ehrlichiosis is spread by

A

Transmitted by ticks: Lone star, western black legged ticks (deer and mice reservoirs)

Transovarial transmission inefficient

Transmission within about 6 hours

38
Q

Ehrlichiae structure

A

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
Q

Ehrlichiae treatment

A

Doxycycline should be used

Rifampin: pregnant women
Chloramphenicol, penicillins, macrolides not effective

Vaccines not available

40
Q

Q-Fever is caused by

A

Coxiella burnetii

41
Q

Q-fever symptoms

A

• 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

Q-fever transmission

A
  • Transmission from animals to humans by inhalation of dust
  • Carried by mammals such as cattle, sheep, and goats
  • World-wide distribution
43
Q

Q-fever phase 1 and 2

A

Phase I: intact LPS

Phase II: missing outermost O-antigen of LPS

44
Q

Treatment and prevention of Q-fever

A
  • Tetracycline (doxycycline) or combination for chronic infections
  • Vaccines have been developed–for unexposed

MHD #3 (11 decks)

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