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Figure 1: Axillary eschar. Figure 2: View of the chest
demonstrating the multiple erythematous macules.
 Tsutsugamushi disease (scrub
typhus) is an acute infectious
disease caused by Rickettsia
tsutsugamushi transmitted
through the bite of larvae of
certain trombiculid mites
(chiggers). This disease has
been recognized for more
than a hundred years on the
northern Honshu island of Japan
as a serious endemic
disease.(1) It is also seen in
Southeast Asia, Indonesia,
India, and Nepal.
All age patients may be involved.
Presumably, anyone bitten by a
Rickettsia-infected mite may
become infected. Key diagnostic
features include the presence of an
eschar, high fever,
lymphadenopathy, and the rash.
Patients may develop
elevated liver function tests
due to hepatic involvement.
Differential diagnosis includes
drug reactions and viral exanthem.
Treatment is usually initiated with
tetracycline 1 gm/day or doxycycline
200 mg/day for seven days.
The response usually occurs
within three to four days.
Incomplete treatment is usually
followed by a reappearance of
the disease. Fatal cases
appear to be rare and are
probably due to inappropriate
antibiotic treatment. Untreated
patients may die of disseminated
intravascular coagulation.
The classic tsutsugamushi
disease occurs during the
summer, has a high mortality
rate, and is transmitted by
Leptotrombidium akamushi. The
so-called new type of
tsutsugamushi disease has been
increasing in almost
all parts of Japan since 1976,
although this type of disease
is milder than the classic one.
Annual registered cases to the
Ministry of Health and Welfare
have reached 800 recently.(2)
This new tsutsugamushi disease
is seen from autumn to spring
and is transmitted by L.
pallidum or L. scutellare.
One of the reasons that
tsutsugamushi disease has
increased recently in Japan is
that the first choice of
antibiotics has changed.(3)
Tetracycline and
chloramphenicol, which were
highly effective against
tsutsugamushi disease, have
been generally replaced with
penicillins and cephalosporins
in the treatment of infectious
disease. The banning of
pesticides such as DDT and BHC
has allowed an increase in
vector mite colonies and may
have contributed to this
phenomenon.(2)
After the bite
of chigger larva, the primary
lesion enlarges in size and
undergoes central necrosis
which becomes an eschar within
one or two weeks. The illness
begins suddenly with headaches
and fever along with the
maturation of an eschar. This
is followed by a skin rash
resembling roseola or rubella.
If an eschar is found,
tsutsugamushi disease is
diagnosed easily. However, it
resembles also drug reaction
eruption. If the correct
diagnosis and the proper
treatment are not available,
the prognosis is serious.
Twenty fatal cases were
reported from 1977 to 1989 in
Japan.(4)
The clinical
diagnosis of tsutsugamushi
disease can be confirmed by
demonstrating an antibody
elevation to R. tsutsugamushi
antigens, including complement
fixation test, indirect
immunofluorescent antibody
test, indirect
immunoperoxidase test, and
ELISA in which Karp, Gilliam,
and Kato strains are usually
used. Weil-Felix agglutination
test is now thought to be
neither very sensitive nor very
specific.(5) Serodiagnosis
usually takes time and late
treatment may bring serious
clinical outcome. When
tsutsugamushi disease is
suspected, empiric treatment
with tetracycline
or chloramphenicol should be
considered.
 References
1. Tamiya T: Recent advances in studies of tsutsugamushi disease in
japan, Tokyo: Medical Culture Inc, 1962: 42.
2. Kawamura A, Tanaka H:
Rickettsiosis in Japan. Jpn J Exp Med 1988; 58:169-184.
3. Suto T: Recent
tsutsugamushi disease and its rapid detecting method ( In Japanese). Jpn
Med J
1982; 3034:43-49.
4. Takeshita T, Koga T: Tsutsugamushi disease in saga
prefecture (English abstract). Nishinihon J Dermatol 1991; 53:60-64.
5. McDonald JC, MacLean JD, McDade JE: Imported rickettsial disease:
clinical
and epidemiologic features. Am J Med 1988; 85:799-805.
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