September 2002
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2.
3.
Diagnosis:
Cutaneous Leishmaniasis
Histology: On H&E, the punch biopsy showed a large zone
of granulomatous dermatitis, portions of which conained necrotic
foci (Fig. 2). In a few areas a "swiss chese" pattern
was made by large vacuolated cells containing small, uniform,
rounded structures with small dot- like zones(fig3). These findings
were characteistic of leishmaniasis and a PAS stain was confirmatory.
An AFB stain was negative.
An aspirate taken from the edge of the lesion and cultured in
medium obtained from the CDC. In about 2 weeks, a definitive diagnosis
of L. Mexicana was made. Given the fact that this species has
minimal risk of progressing to systemic involvement and considering
the potential toxicities of therapy with sodium stibogluconate,
a treatment plan of careful clinical monitoring has been elected.
Leishmaniasis results from infection with intracellular protozoan
parasites belonging to the genus Leishmania. These parasites are
inoculated into the human host by way of a bite from an infected
sandfly. Infection results in a wide spectrum of clinical diseases
that can be divided into four broad categories: cutaneous leishmaniasis
(CL), diffuse cutaneous leishmaniasis (DCL), mucocutaneous leishmaniasis
(MCL), and visceral leishmaniasis (VL). The extent and pattern
of leishmaniasis that develops depends on many factors, including
the specific species of Leishmania involved, the number of parasites
inoculated, the site of inoculum, the nutritionalstatus of the
host, and even the last non-blood meal of the vector.
Incidence:
Vector and Life Cycle:
The Leishmania organisms are found in two morphologic forms during
their life cycle: amastigotes and promastigotes. In humans and
other mammalian hosts, they exist within macrophages as round
or oval nonflagellated arnastigotes (also called LeishmanDonovan
bodies). These amastigotes are taken up during a feeding by female
sandflies. Within the midgut of the sandflies, the parasites undergo
a change to the promastigote form and multiply. Once fully developed,
they migrate from the gut to the pharynx and proboscis, where
they remain until they are injected into a new mammalian host.
The promastigotes are taken up by receptors on dermal macrophages.
Within the macrophage, they transform into arnastigotes and are
incorporated into the cells' phagolysosomes, where they are able
to resist destruction and multiply by binary fission. When a macrophage
becomes filled and disrupted, the amastigotes reenter the extracellular
space and are taken up by neighboring macrophages. The cycle of
infection continues when an infected mammal is again bitten, and
amastigotes are taken up by a female sandfly.
Classification:
Within the past decade, new techniques for identifying Leishmania
species have developed, such as monoclonal antibodies, isoenzyme
characterization, DNA hybridization, and PCR. The older clinical
categories of old world versus new world leishmaniasis have been
subdivided to now include recently identified species. Below is
a simple classification scheme for cutaneous leishmaniasis.
Clinical Form Species Major Localities
New World L. mexicana complex Mexico, Central America
The diagnosis of CL depends on finding parasites in the skin.
The most effective method isperforming a tissue smear obtained
by a shallow slit in the skin with a # 11 blade at the edge of
the lesion. After staining with Giemsa, the amastigotes are seen
within the cytoplasm of macrophages. Parasites can also be cultured
from tissue fluid obtained from the lesion. The culture medium
can be either biphasic (Novy-MacNeal-Nicolle) or liquid (Schneider's
insect culture medium). Promastigote forms should appear after
several days; however, cultures should not be discarded as negative
before 4 weeks.
Treatment:
CL is usually self-limited and does not require specific treatment.
A topically applied aminoglycoside antibiotic, paromomycin, is
sometimes effective. Extensive lesions, especially those involving
the face or invading into deeper tissues, are best treated with
intralesional injections of sodium stibogluconate. Up to I mg/kg
body weight may be injected at weekly intervals into the borders
of the lesions. For very extensive lesions, IV sodium stibogluconate
may be given. Other treatment measures include freezing, local
heat, imidazole compounds, and rifampiein.
1. Klaus SN, Frankenburg S. Leishmaniasis and other protozoan
infections. In: Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith
LA, Katz SI, Fitzpatrick TB, eds. Fitzpatrick's Dermatology in
General Medicine. New York: McGraw-Hill, 1999;2609.
My thanks to Arianne Chavez-Frazier and Dr. Jason Fung for their
assistance in the preparation of this case. We also thank Dr.
Madhavi Kandula for providing medical records and
Discussion:
An increase in tourism to "exotic" areas of the globe
is one of the contributing factors to the rising incidence of
leishmaniasis, which the WHO estimates will soon exceed 400,000
new cases annually.
L. major Near East, Africa
Old World L. tropica Near East, former USSR
L. aethiopica Ethiopia, Kenya
L. infanturn Mediterranean rim
It is also in much of the Middle East, especially Iran, Iraq,
eastern Saudi Arabia, the Jordan Valley and the Sinai Peninsula.
L. braziliensis complex Brazil, Bolivia
L. amazonensis Brazil
New World CL is found in Mexico, Central America, as far north
as Texas, and as far south as Brazil.
Diagnosis:
References:
Dr. Gary Weil of the Division of Infectious Diseases for providing
follow-up information.
