BMS2052 Study Guide - Final Guide: Lymphadenopathy, Tsetse Fly, Intracellular Parasite
4 May 2018
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Parasitic infections
Pathogenesis is the origin or development of
disease.
Parasitism is the host-pathogen relationship
that is both of benefit and detriment to the
parasite. An Ectoparasite lives in the host. An
Endoparasite lives within the host.
TOXOPLASMOSIS, toxoplasma are
aplicomplexas. In healthy people causes flu
like symptoms. In immunocompromised can
involve serious gut, heart and brain damage
and fetal abnormalities (blueberry muffin
baby). Can be diagnosed through serology,
PCR, histology and gross pathology. Can be
treated with antibiotics in Immunocom. There
is no vaccine.
Trypansosomes are protozoan paratsites that
live in a symbiotic relationship in the host.
They are from the class Kinetoplastida which
are flagellated and motile and transmitted by
animal vectors. They have no specialised
organised to help invasion. They have a
nucleus, flagellum, mitochondria, nucleolus
and a kinetoplast which contains DNA. This
can be Maxi-circle (direct translation) or mini-
circle (guide RNA). When parasites enter the
blood stream of the host they get thicker
gain a coat.
TRYPANOSOMES – AMERICAN cause Chagas
disease by T.cruzi. this is INTRACELLULAR and
transmitted via the Reduviid bug. It causes a
chronic disease. Is responsible for more
morbidity in America than malaria.
Tranmistted through bug faeces. Use
Romanas sign (swollen eye). These are
intracellular but do not have a specialised
invasion strategy. They get into the cells
through phagocytosis (into macrophages).
There is an acute and chronic stage of
infection. Predominant sites of infection are
the gut and heart. In chronic stages see
swelling of these areas. Use a mosaic coat of
mucins to evaid the immune system. These
are O-glycosylated glycoproteins. Can be
treated with antiparasitics.
TRYPANOSOMES – AFRICAN causes African
sleeping sickness by T.brucei. this is zoonotic
in the east and nt in west. It is transmitted via
the tsetse fly acute lethal disease. There
are two subspecies that infect humans
T.brucei gondii and T.brucei rhodeniense.
Note that human African trypanomiasis can
be caused. The parasite develops in the
midgut of the fly and goes to the salivary
glands to be transmitted. Can infect the blood
and CSF in humans. Can be diagnosed with
winterbottoms sign (swollen lymph node).
Symptoms include fever, weight loss and
meningoencephalitis which causes coma. The
parasite evased the immune system with
different antigenically distinct VSGs (surface
glycoproteins). Do not use PCR in diagnosis.
Treatment is toxic, prevention is best.
LEISHMANIASIS is transmitted via the female
sandflies and zoonitic. It is an obligate
intracellular parasite that gets inside
macrophages via phagocytosis. Causes three
main forms off disease.
Cutaneous is involving the skin at the site of
the bite. These will heal spontaneously.
Visceral from skin to LN these infect the
spleen, liver and bone marrow. Fever, weight
loss, anaemia, hepato- and splenomegaly.
Mucocutaneous can be a consequence of
cutaneous.
treatment is all highly toxic.
Document Summary
Pathogenesis is the origin or development of disease. Parasitism is the host-pathogen relationship that is both of benefit and detriment to the parasite. In immunocompromised can involve serious gut, heart and brain damage and fetal abnormalities (blueberry muffin baby). Trypansosomes are protozoan paratsites that live in a symbiotic relationship in the host. They are from the class kinetoplastida which are flagellated and motile and transmitted by animal vectors. They have no specialised organised to help invasion. They have a nucleus, flagellum, mitochondria, nucleolus and a kinetoplast which contains dna. This can be maxi-circle (direct translation) or mini- circle (guide rna). When parasites enter the blood stream of the host they get thicker gain a coat. Trypanosomes american cause chagas disease by t. cruzi. this is intracellular and transmitted via the reduviid bug. Is responsible for more morbidity in america than malaria. These are intracellular but do not have a specialised invasion strategy. They get into the cells through phagocytosis (into macrophages).
