Rickettsiae - Student
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Transcript Rickettsiae - Student
Rickettsial (Spotted & Typhus
Fevers) & Related Infections
(Anaplasmosis & Ehrlichiosis)
RICKETTSIACEAE FAMILY
General characteristics
Consists of 3 genera
Rickettsia
Ehrlichia
Coxiella
Obligate intracellular parasites.
Small Gram (-) coccobacilli (0.3-0.5 um)
Cell membrane similar to Gram (-) bacteria with LPS &
peptidoglycan
General characteristics
The organisms will not show up on Gram stain, but can be seen with
Giemsa stains
Require growth co-factors
Will not grow on artificial media
Grown in embryonated eggs or tissue culture
Cultivation is costly and hazardous because aerosol transmission can
easily occur
All, except Coxiella, are transmitted by arthropod vectors as fleas,
ticks, mites and lice
Louse
Scanning electron microscope
(SEM) depiction of a flea
Electron micrograph of Rickettsia prowazekii in experimentally infected tick tissue
Gimenez stain of tissue culture cells infected
with Rickettsia rickettsii
Rickettsia
Transmission
Rickettsia are usually introduced into human skin by the bite
of an insect (flea or louse) or an arachnid (tick or mite)
R. rickettsii invades the endothelial cells that line the blood
vessels
Incubation period: ~1 week
Virulence factors of Rickettsial species
changes in the host cell phagocytosis
bacterial surface protein
Engorged tick attached to back
of toddler's head. Adult thumb
shown for scale.
Castor bean tick, Ixodes ricinus
Arthropod Vector
Rickettsia rickettsii
Pathogenesis
During the first few days of incubation period
local reaction caused by hypersensitivity to tick or vector
products
Bacteria multiply at the site & later disseminate via
lymphatic system
Bacteria is phagocytosed by macrophages (1st barrier to
rickettsial multiplication)
After 7-10 days
organisms disseminate
replicate in the nucleus or cytoplasm of endothelial cells
causing vasculitis
Infected cells show intracytoplasmic inclusions &
intranuclear inclusions
Endothelial damage & vasculitis progress causing
development of maculopapular skin rashes
perivascular tissue necrosis
thrombosis & ischemia
Disseminated endothelial lesion lead to increased capillary
permeability, edema, hemorrhage & hypotensive shock
Endothelial damage can lead to activation of clotting
system ---> Disseminated intravascular coagulation (DIC)
Pathogenesis: Rickettsia cell-to-cell spread
Rocky Mountain Spotted Fever
Etiologic agent: Rickettsia rickettsiae
Most common rickettsial disease
Individuals younger than 19 years old are usually at risk
Males affected twice as often as females
It is common during summer months
Serious disease with 35% mortality rate
Transmitted by ticks that must remain attached for
hours in order to transmit the disease
Incubation of 2-6 days
Followed by a severe headache, chills, fever, aching,
and nausea
After 2-6 days, a maculopapular rash develops, first on
the extremities, including palms, foot soles, and
spreading to the chest and abdomen
If left untreated, the rash will become petechial with
hemorrhages in the skin and mucous membranes due
to vascular damage as the organism invades the blood
vessels
Death may occur during the end of the second week
due to kidney or heart failure
Rocky Mountain Spotted Fever
Endemic Typhus
Etiologic agent: Rickettsia typhi
Incubation period: 5-18 days
Transmitted to man by rat fleas
cat fleas and mouse fleas are less common modes of
transmission
The disease occurs sporadically
Symptoms: severe headache, chills, fever, and after a
fourth day, a maculopapular rash caused by
subcutaneous hemorrhaging as Rickettsia invade the
blood vessels
The rash begins on the upper trunk and spread to
involve the whole body except the face, palms of the
hands, and the soles of the feet
The disease lasts about 2 weeks and the patient may
have a prolonged convalescence
Ehrlichia
Disease: Ehrlichiosis
Transmitted via tick vectors
Etiologic agent: E. chaffeensis
Invade leukocytes and grow in cytoplasmic vacuoles
making characteristic inclusions known as morulae
Symptoms resemble Rocky Mountain spotted fever
Clinically manifests as acute fever with
leucopenia
thrombocytopenia
elevations of aminotransferase levels
Rash is infrequent
Vasculitis is rare
Coxiella burnetii
The only species of Coxiella genus
Causal agent of Q-fever
Found in infected animals, arthropods or humans and
highly infectious
Transmission
Inhalation of airborne organisms
infected dusts in farm and slaughterhouses
Contact with the milk, urine, feces, of infected animals
It has spore-like form that resists heat and dryness allowing
it to survive in extracellular environment
Q fever
Q for “query” or mysterious febrile illness
Occurs in veterinarians, ranchers, and animal researchers who
are in contact with infected placenta from sheep, cattle, or goats
(no arthropod vector for C. burnetii)
Incubation period: 10-28 days
Disease characterized by fever, influenza-like syndromes; but no
skin rash
Some patients present with bronchopneumonia with patchy
interstitial infiltrates
Rare complications: hepatitis, endocarditis, and
meningoencephalitis
Q fever
Doughnut shaped non-caseating granuloma of Q fever
Laboratory Diagnosis of Rickettsiae
1. Culture & isolation
Difficult & dangerous because of the highly infectious nature
of rickettsiae
2. Serologic test
A. Weil-Felix test: based on cross-reactivity between some
strains of Proteus & Rickettsia
B. Complement fixation: not very sensitive & time consuming
C. Indirect fluorescence (EIA): more sensitive & specific;
allows discrimination between IgM & IgG antibodies which
helps in early diagnosis
D. Direct immunofluorescence: the only serologic test that is
useful for clinical diagnosis, 100% specific & 70% sensitive
allowing diagnosis in 3-4 days into the illness