is a Gram-negative, non-spore-forming, obligate intracellular
aerobic bacterium, measuring 0.3 to 0.5 μm (micrometres)
by 0.8 to 2.0 μm in size (Figure
1). R. rickettsii
bacteria parasitize vascular endothelial cells
in humans, causing
Rocky Mountain spotted fever.
The infection is transmitted by the bite of an
infected tick while feeding on warm-blooded
animals, including humans. Humans are accidental
hosts in the R. rickettsii–tick life
cycle and are not required to maintain the
organism in nature.
This micrograph reveals the presence of
intracellular Rocky Mountain spotted fever
bacteria, Rickettsia rickettsii.
Spotted fever group Rickettsiae can grow in the
nucleus or in the cytoplasm of the host cell.
Once inside the host the Rickettsiae multiply,
resulting in damage and death of these cells.
rickettsii do not have
flagella. Rather, the bacterium is propelled
through the cytoplasm and into neighboring cells
by stimulating the polymerization of host cell
rickettsii belongs to a large group of
bacteria known as
α-proteobacteria that multiply in eukaryotic
cells. This suggests
that they can only grow and reproduce within the
living cells of their host.
Moreover, this organism is able to
metabolize glutamate, derived from host cells,
via the citric acid cycle and aerobic
respiration (Brenner et al., 2005).
Figure 2. Rickettsiae are
propelled through the host cell cytoplasm. The
arrow points to the polymerization of actin.
Diagnosis is made
difficult by the germ's small size. R.
rickettsii is not visible in
blood smears, nor is it visible with
conventional staining methods. Diagnosis usually
relies on a combination of laboratory findings,
physician findings and epidemiology. The best
diagnostic test for R.
rickettsii infection is
serologic assays. Indirect immunofluorescence
assay is typically used to detect immunoglobulin
G (IgG) or immunoglobulin M (IgM) antibodies.
After the first week of illness, patients
usually have increased levels of IgM. IgG
antibody levels typically appear between seven
to ten days following the infection. The rising
antibody level between IgG and IgM is a
determinant of infection. Other assays include
enzyme-linked immunosorbent assay and dot
rickettsii bacteria are inoculated into
human skin by ixodid (hard) ticks (Figure
3). There are two major R. rickettsii
vectors in North America are the American dog
tick and the Rocky Mountain wood tick. These
ticks have four stages in their life cycle: egg,
larva, nymph, and adult. After the eggs hatch,
each stage must feed once to develop into the
next stage. Both male and female ticks will
bite. Rickettsiae are transmitted to a
vertebrate host through saliva while a tick is
feeding. It usually takes several hours of
attachment and feeding, before the rickettsiae
are transmitted to the host. The risk of
exposure to a tick carrying R. rickettsii
is low. In general, about 1% to 3% of the tick
population carries R. rickettsii, even in
areas where the majority of human cases are
3. This photograph depicts a dorsal
view of both a female (left), and male (right)
Rocky Mountain wood tick, Dermacentor
andersoni. Note the smaller size of the
female’s scutum compared to the male’s larger
scutum. From the Latin word for “shield”, the
scutum (dorsal shield), covers only a small part
of the female’s dorsal surface, thereby,
enabling her abdomen to expand, becoming
engorged during feeding. The male’s scutum
covers his entire dorsal surface, and is mottled
with brown markings overall, while the female’s
small scutum sports an almost entirely a
cream-colored gray surface. Click to
Once inside the
host, R. rickettsii attaches to
endothelial cells using rickettsial outer
membrane protein A (rOmpA). After
attachment, Rickettsiae are phagocytosed by the
host cell into the cytoplasm. Using
phospholipase A2, the bacteria escapes from the
phagosome before cellular lysosomes fuse with
the phagosome, producing a phagolysosome
(Brenner et al., 2005). Within the
cytoplasm, the bacterium replicates by binary
fission. Rickettsiae spread to other cells by
polymerizing host actin (Figure
2). R. rickettsii cause damage to
the host cell by rupturing vascular endothelial
cells, which causes inflammation
and blood leakage. This induces the
characteristic red spots or rash seen as a
result of infection, and facilitates organ
damage, brain damage and hypotension (Figure
4). R. rickettsii infection also
stimulates phagocytic cells to produce cytokines
thereby initiating an immune response to kill
the bacteria (Brenner et al., 2005).
4. Child's right hand and wrist
displaying the characteristic spotted rash of
Rocky Mountain spotted fever.
Symptoms: Symptoms of Rocky Mountain
spotted fever include fever, nausea, vomiting,
severe headache, muscle pain, loss of appetite,
spotted rash (wrists, forearms, ankles, palms
and soles), abdominal pain, joint pain,
diarrhea, low platelet count, low sodium level
in the blood, elevated liver enzymes. Those who
are immunocompromised (people with AIDS or
cancer) are more likely to develop severe
disease symptoms, and mortality rates are higher
in people who are glucose-6-phosphate
Treatment: Appropriate antibiotic
treatment is initiated immediately when there is
a suspicion of Rocky Mountain spotted fever on
the basis of clinical and epidemiological
findings. Treatment should not be delayed until
laboratory confirmation is obtained. In fact,
failure to respond to a tetracycline antibiotic
argues against a diagnosis of Rocky Mountain
spotted fever. Severely ill patients may require
longer periods before their fever resolves,
especially if they have experienced damage to
multiple organ systems.
adults at 100 mg every 12 hours or for children
under 45 kg at 4 mg/kg body weight per day in
two divided doses) is the drug of choice for
patients with Rocky Mountain spotted fever.
Therapy is continued for at least three days
after fever subsides and until there is
unequivocal evidence of clinical improvement,
generally for a minimum total course of five to
ten days. Severe or complicated disease may
require longer treatment courses.
Chloramphenicol is an alternative drug that can
be used to treat Rocky Mountain spotted fever;
however, this drug may be associated with a wide
range of side effects and may require careful
monitoring of blood levels, since it can cause aplastic anemia.
Krieg, N., Garrity, G., & Staley, J. (2005).
Bergey’s Manual of Systematic Bacteriology
Volume Two: The Proteobacteria (Part C). USA:
Williams & Wilkins.