Rickettsiae - Student

Rickettsial (Spotted & Typhus
Fevers) & Related Infections
(Anaplasmosis & Ehrlichiosis)
 General characteristics
 Consists of 3 genera
 Obligate intracellular parasites.
 Small Gram (-) coccobacilli (0.3-0.5 um)
 Cell membrane similar to Gram (-) bacteria with LPS &
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
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
 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
 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
 During the first few days of incubation period
 local reaction caused by hypersensitivity to tick or vector
 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
 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
 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
 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
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

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