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Hello again. My name
is Catarina Gadelha.
I'm a reader in
molecular cell biology
at the University of Nottingham.
My research topic is
host-parasite interactions, with
a particular focus on the
cell surface receptors
and ligands that enable
these interactions.
In this part of the lecture,
we will look at leishmaniasis
and schistosomiasis.
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Leishmaniasis is caused by
several species of
the genus Leishmania,
all transmitted between
mammalian hosts
by female sandflies.
Following a period of
incubation, different species
cause different clinical
manifestations ranging
in severity from self-curing
cutaneous lesions to
life-threatening visceral disease.
The outcome, as usual,
is determined by parasite
and host genetics.
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Cutaneous leishmaniasis,
caused by Leishmania major
or L. tropica is usually
limited to an ulcer
that self heals over
several months,
but can also lead to
scarring and disfigurement.
Mucocutaneous
leishmaniasis is caused
by species of the Viannia group:
Leishmania braziliensis
or L. guyanensis.
It is characterized by
destructive lesions
of the nasal septum,
lips, and palate, and it's
caused by a strong
immunopathological response.
Visceral leishmaniasis,
caused by
Leishmania donovani in Asia
and Africa, or Leishmania
infantum in the Mediterranean,
the Middle East, Central Asia,
and Latin America is the most
severe form of the disease.
Usually fatal unless treated.
Post-kala-azar
dermal leishmaniasis
is a skin manifestation that
occurs in otherwise
healthy people
after treatment of
visceral leishmaniasis.
Table one in this publication
of the journal Lancet,
