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Rickettsiae
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Rickettsiae
Structure
 Clinical Manifestations
 Pathogenesis
 Epidemiology
 Diagnosis
 Control

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Rickettsiae
bacteria which are obligate intracellular
parasites
 spread by arthropod vectors



lice, fleas, mites and ticks
The rickettsial diseases of man are usually
broken down according to the arthropod
vector
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Genera

Rickettsia (11 species) obligate
intracellular parasites which do not multiply
within vacuoles and do not parasitize white blood cells.
Orientia: spread by chiggers, parallel evolution
 Ehrlichia (2 species) 
 obligate
intracellular parasites which do not multiply
within vacuoles but do parasitize white blood cells.

Coxiella (1 species)- obligate
intracellular parasite which grows in vacuoles
of host cells.
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Ticks

Soft Tick
 Ehrlichosis
 E. chaffeensis

Hard Tick
 Rocky Mountain
spotted fever
 Wild rodents
 R. rickettsia
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Lone Star Tick
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Louse

Typhus
R
prowazekii
 Humans, squirrel fleas flying
squirrels

Trench fever
R
quintana
 Humans
Head Louse
Body Louse
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Flea




Vector for Murine
typhus
caused by R typhi
Reservoir
Wild rodents
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C burnetii
C.burnetii differs from other rickettsia in
that it is enclosed in a persistent vacuole
during growth and division. Six to ten
daughter cells will form within a host cell
before the cell ruptures and releases
them.
 No arthropod vector
 Q fever

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Prevention

Avoid tick - infested areas
 wear
protective clothing and use repellants.
 Ticks are difficult to eradicate as they can
survive for 4 years without feeding

Remove ticks carefully
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Ehrlichia Intracellular growth
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Ehrlichia Growth Cycle
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Rickettsia conorii Growth
Gram negative short rods
 Transverse Binary Fission
 Multiple in cytoplasm
 Long filaments under poor
nutritional conditions,

 undergo
rapid and multiple division
into the typical short rod forms
when fresh nutrient is added.
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Rickettsia conorii
Immediately after division, the
rickettsia engage in extensive
movements through the
cytoplasm of the cell.
 Attach to “tail” of host actin
filaments
 actin provides propulsion

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
Metabolism
In dilute buffered salt solutions, isolated rickettsia
are unstable, losing both metabolic activity and
infectivity for animal cells. If, the medium is
enriched with potassium, serum albumin and
sucrose, the isolated organisms can survive for
many hours. If ATP is added to the solution, the
organisms metabolize and consume oxygen. The
basis for the obligate parasitism of these cells is
that they require the rich cytoplasm to stabilize an
unusually permeable cell membrane.
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Rickettsial Clinical Manifestations

Entry
 Ticks,

Spread
 Blood

fleas, lice, mites
stream & lymphatics
Disease
 encephalitis,
pneumonitis, rash,
nausea, vomiting, renal failure

Exit none
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Rickettsia Pathogenicity
Symptoms: Fever, chills, headache,
myalgias, rash
Rash: hemorrhages in the skin.
Develops after 3 days
Not seen in 10% of cases
Incubation 2-14 days after tick bite
[average 7days] Patient may not
recall painless tick bite.
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Rash of Rocky Mountain Spotted
Fever
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Hyperplasia

Hyperplasia of endothelial cells and localized
thrombus formation lead to obstruction of blood
flow, with escape of RBC's into the surrounding
tissue. Inflammatory cells also accumulate about
affected segments of blood vessels.
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Angitis

Angitis appears to account for some of the
more prominent clinical manifestations,
such as petechial rash, stupor and terminal
shock. Death is ascribed to damage of
endothelial cells, resulting in leakage of
plasma, decrease in blood volume, and
shock.
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Complications
Gastro-intestinal symptoms, respiratory
failure, encephalitis, renal failure.
Mortality is high when the disease progresses.
This is usually due to the late development
of the rash and the difficulty of diagnosing
the disease
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Human Monocytic Ehrelichiosis

Since 1964, more than 400
confirmed cases of HME, and
170 cases of HGE have been
reported, including some from
northern California. Many were
first thought to be Rocky
Mountain Spotted Fever.
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Clinical Manifestations: Q Fever
Entry: aerosol from infected
placenta of sheep goats cattle
 Spread: blood stream
 Disease

 Pneumonitis
endocarditis,
granulomas

no Exit
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Rickettsialpox
R. akari - Clinical infection is biphasic
 First phase



a vesicle develops at the mite bite site and the
organisms multiply ; within one week they have
spread systemically.
Second phase
 fever,
severe headache and chills, sweats, myalgias
and photophobia
 After 2-3 days a papulo-vesicular rash forms and
spreads over the body.
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Chemotherapy
The drugs of choice for the treatment of
rickettsial diseases are chloramphenicol and
tetracycline.
Each of these is highly toxic, especially in
children, and must be used with care.
 The sulfonamides stimulate rickettsial
growth and thus are contraindicated in the
treatment of these diseases.

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Rocky Mountain Spotted Fever
Incidence
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RMSF in USA
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Incidence of Epidemic Typhus
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Epidemic Typhus in USA
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Pathogenicity

Transmission
 to

man, via the arthropod saliva, through a bite.
Arthropod vectors
 rickettsia
multiply in the epithelium of the intestinal
tract;
 they are excreted in the feces, but occasionally gain
access to the arthropods salivary glands.

Mammalian host
 found
in the endothelium of the small blood vessels, of
the brain,skin and heart.
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Transovarian Cycle
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Endotoxin

It is assumed that the observed clinical
manifestations of a rickettsial infection are
due to production of an endotoxin, although
this endotoxin is quite different in
physiological effects from that produced by
members of the Enterobacteriaceae.
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Evidence of Endotoxon
IV-injected rickettsia cause rapid death in
experimental animals.
 UV-irradiation of rickettsia diminishes
infectivity without reducing toxicity.
 anti-rickettsial drugs do not prevent rapid death
in experimental animals.
 Antiserum specific for cell wall antigens of the
rickettsia prevents the toxic effect.

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Lab Diagnosis
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Laboratory diagnosis
Presumptive of rickettsial-like organisms in
tissue or blood
 Gram Stain

 Stain
poorly with Gram’s stain Although the
organisms are gram-negative, they only weakly take
the counter stain, safranin.

Special Stains
 Giemsa,
Castaneda, Macchiavello stains
 Fluorescent labelled antibody used to stain biopsy
tissue.
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Special Stains
Infected tissue may be stained with:
 Macchiavello stain--organisms are bright
red against the blue background of the
tissue.
 Castaneda stain--blue organisms against a
red background.
 Giemsa stain--bluish purple organisms.

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Confirmation
serological reaction (Weil-Felix reaction) in
which the titer of the agglutinins in the patient's
serum against the Proteus strains OX-19, OX-2
and OX-K are determined.
 These Proteus strains have no etiological role in
rickettsial infections, but appear to share
antigens in common with certain rickettsia.

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Proteus Antigens

These antigens are alkali stable polysaccharide
haptens
 distinct
from the group-specific and type-specific
antigens.
Proteus infections are fairly common (especially
in the urinary tract) and that they, too, may
evoke antibodies to the Proteus-OX strains.
 This test is usually positive seven days after the
initial infection.

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Complement Fixation

A more specific complement fixation test is
available but does not show positive results
until 14 days into the infection.
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FIA
The indirect fluorescent antibody test is also
useful for the detection of IgM and IgG
antibodies against rickettsia.
 Diagnostic test of choice for ehrlichiosis.

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SerologyIndirect fluorescent antibody of patient’s
serum and latex agglutination.
 In these tests, the antigen is known and the
unknown is the antibodies to Rickettsia in
the patient’s serum.
 Antibodies are detected 2-3 weeks after
onset of disease with FA.
 Latex agg. can be positve earlier but will
not be sustained as long.

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Rickettsia rickettsii

Disease/Bacterial Factors




Rocky Mountain Spotted
Fever
intracelluar parasite that
multiples in host cytoplasm
Transmission

ticks are primay reservoir
and vector
Risk?


Requires 24-48 hour
exposure to feeding tick
Geography/Season



Western Hemisphere,
southeast Atlantic and south
central USA
April-Sept
Control




tetracyclines &
chloramphenicol
Avoid tick infested areas
insect repellent
remove ticks
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Rickettsia prowazekii

Disease/Bacterial Factors




Louse-borne typhus, BrillZinsser Disease
Transmission

human body louse,
squirrel fleas
Geography/ Season



humans are primary
reservoir
inoculation through break
in skin via body louse
Vector


Risk?



central & south America
no season
Persons in crowded unsanitary
conditions
close contact with infected
persons
Control


tetracyclines, chloramphenicol
louse control
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Rickettsia typhi

Disease/Bacterial Factors




rodents, cats, opossum,
racoons & skunks
Vectors

rat & cat fleas


Global, Southeast & gulf
states of USA
Control

Reservoir


break in skin via infected flea
Geography Season

strict intracellular pathogen
Transmission


tetracyclines,
chloramphenicol
Control of rodent vectors
Risk?

People in crowded areas
infested with rodents
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Coxiella burnetii

Disease/Bacterial Factors




sheep goats, ticks, mammals
birds
Transmission


inhaled airborne particle
contaminated unpasteurized
milk
Geography /Season



Reservoirs


strict intracellular pathogen
multiplies in cytoplasmic
vacuole
stable in harsh envirnments

Control


Global rare in Canada
and USA
not seasonal
tetracyclines
chloramphenicol
Risk?


Livestaock handlers
patients with prosthetic
or damaged heart
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valves
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Ehrlichia chaffeensis


Disease/Bacterial Factors
 Ehrlichiosis
 Strict intracellular
parasite
 vector lone star tick?
Transmission
 break in skin via
infected tick


Geography/Season
 Common in Southeast,
Mid atlantic and South
Central USA
 Most common May
June July
Control
 Tetracycline,
chloramphenicol
 Control of tick vector
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DONE!!!
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