Rickettsial Diseases, including Typhus and Rocky Mountain Spotted Fever (page 6)
(This chapter has 6 pages)
© Kenneth Todar, PhD
Boutonneuse Fever and African Tick-bite
Boutonneuse fever and its
agent were first described in North Africa
in 1910, and variants of R. conorii have been identified in
Africa, Kenya, Somalia, Israel, Morocco, Ethiopia, Russia, India and
In parts of Africa, tick-transmitted diseases caused by R. conorii
and R. africae overlap geographically. Although their clinical
also overlap, there are differences sufficient to distinguish two
disease agents. Generally milder than boutonneuse fever, African tick
fever has a lower incidence of rash, which is more often vesicular and
sparse, a higher incidence of eschars that are frequently multiple, and
more prominent regional lymphadenopathy. Each of these diseases has
diagnosed in the United States after patients return from vacation
particularly from African safaris.
R. akari has been recognized mainly in the urban United
as an agent of rickettsialpox
The organism maintained in a mite-mouse cycle with humans as an
host. The organism may, however, have a broader host range and
A papule appears at the site of mite feeding in the skin during the
incubation period, and over 2-7 days, evolves into an eschar. Later
chills, malaise, headache, and myalgia develop, followed after 2-6 days
by a macular rash that becomes maculopapular and then vesicular before
crusting and healing. Fatalities have not been reported.
Cat Flea Typhus
Despite the widespread geographic distribution and prevalence of R.
felis in cat fleas, there have been only a handful of clinical
of undertaken to diagnose cat flea
Among eight reported cases of human infection with R. felis (five
diagnosed by polymerase chain reaction [PCR] and three by differential
antibody titers), all had fever and constitutional symptoms. The
majority manifested rash, headache, and central nervous system (CNS)
and variable proportions suffered nausea, vomiting, diarrhea, abdominal
pain, myalgia and conjunctivitis. The actual spectrum of illness of
infection requires further clinical studies.
Rickettsia prowazekii infections occur in three situations:
epidemics, reactivation of a long-standing latent infection, and
infection transmitted from flying squirrels by their ectoparasites.
of disease is characterized by fever, chills, headache, and myalgia.
of 2-6 mm usually appear first on the trunk on day 5 and later spread
the extremities. Rales, conjunctival injection, and delirium are
manifestations. Reactivated typhus is a milder version with the same
and symptoms. Flying squirrel-associated typhus has also been described
as less severe; whether this is due to antimicrobial treatment or less
virulent strains of rickettsiae is unclear.
Flea-borne R. typhi infections cause extreme discomfort but
seldom fatal healthy young individuals. The difficulty in detecting a
in darkly pigmented skin was evident in a study finding only 20% of
infected African-American volunteers had rashes, compared to 80% of
volunteers. The infection can follow a mild course in children with as
many as half suffering only fever at night, but necessitates intensive
care unit support in 10% of hospitalized adult patients. Pneumonitis or
meningoencephalitis can be the major manifestation in some patients.
Treatment of Rickettsioses
Doxycycline is the drug of choice for the treatment of infections
by Rickettsia except in cases of pregnancy and tetracycline
some studies have shown that doxycycline is superior to chloramphenicol
for the treatment of Rocky Mountain spotted fever as it is associated
a lower case fatality rate and a lower hospitalization rate. Several
azithromycin, and clarithromycin, have been used successfully to treat
boutonneuse fever but are not recommended for more pathogenic
It should be emphasized that rickettsiae are highly resistant to most
Most fatal cases of Rocky Mountain spotted fever have received
courses of antimicrobial treatment, including beta lactams,
and erythromycin. Sulfonamide antimicrobials actually appear to
the severity of rickettsial infections.
Rickettsial infection stimulates an early innate immune response
activation of natural killer cells and production of gamma interferon
which act in concert to dampen rickettsial growth. Acquired immunity
with clonal expansion of CD4 and CD8 T lymphocytes as well as
B cells. Clearance of intraendothelial rickettsiae is achieved by
effects due to cytokine activation of the infected endothelial cells
Cell mediated immunity (CMI) plays an important role as expected in
by an intracellular parasite, but antibodies (including those directed
at epitopes of OmpA and OmpB) also play a role in protective immunity.
END OF CHAPTER
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