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Hemoflagellates
Family Trypanosomidae
3 species known to be pathogenic
in human are:
1. Trypanosoma gambiense
2. Trypanosoma rhodesiense
3. Trypanosoma cruzi
Trypanosoma gambiense
General
Trypanosoma gambiense
Morphology
The
Vector
Glossina
(Tsetse fly)
African
Trypanosomiasis
Trypanosoma
gambiense
Life Cycle
Gambian Trypanosomiasis
General
Gambian Trypanosomiasis
Clinical manifestations
Subcutaneous
stage: local
inflammation in
the biting site
(raises after
about 3 wks),
leads to primary
chancre
Gambian Trypanosomiasis
Clinical manifestations
Hematogeneous
stage: fever,
malaise, anorexia,
headache, and
postcervical
lymphadenopathy
(Winterbottoms
sign)
Gambian Trypanosomiasis
Clinical manifestations
Chronic stage: expresses 612 months after the first
onset: increased fatigue,
mental dullness to
somnolence.
Sleepiness progresses to
coma and eventually death.
Gambian Trypanosomiasis
Treatment
Successful treatment depends on
early patient management
Drugs commonly used:
pentamidine, suramin, melarsoprol
Pentamidine is used for early stage,
admministerde by im injection
Suramin is for early stage by iv
Melarsoprol is for chronic stage by
iv administration
Trypanosoma rhodesiense
General
Rhodesian Trypanosomiasis
Clinical manifestations
East African sleeping sickness
Vectored by Glossina pallidipes, G.
morsitans, and G. swynnertoni
The stages of diseases and symptomatology
parallel those of prior trypanosomiasis; only
the disease progresses rapidly and has
shorter clinical course
The entire course may take only 9-12
months
Rhodesian Trypanosomiasis
Diagnosis and Treatment
The diagnosis is made in the
same manner as the prior one
The drugs used in rhodesian
trypanosomiasis are also the
same
Prognosis is poor since the
clinical course is shorter
Immunoregulation:
Trypanosome Elimination
Antibody mediated
Destruction by Kupffer cells
Splenic macrophages minor role (cf malaria)
Uptake - C3b - C3bi - direct?
C mediated lysis not important
Trypanosome destroyed within minutes
Immunoregulation
No secondary response to VSGs unless cured by
chemotherapy
Failure of 1ry or 2ndry response prior to death
Non specific polyclonal activation
Suppresser Macrophages
Failure of Ag presentation
Anti idiotype responses
Immunoregulation:
Variable Surface Glycoprotein
60kd (450aa) glycoprotein (CHO 7-17%)
C-terminal anchored in membrane
Often as a dimer (alpha helix)
Densely clustered 107molecules/parasite
Only epitopes in end third of N-terminal exposed
Presented as topographical array
T-independent antigen
Immunoregulation:
VSG
Constant & Variable regions
Random rearrangement of N terminal end (2/3)
Almost no homology between V VSGs
Except cystein residues S-S bonds
Switching not initiated by IR
But selected
VSG Specific IR
3-4 days post infection strong IgM response
Trypanosome disappear within hours
VSG specific IgG appears - not relevant
IgM response often >IgG
After several cycles VSG abs vanish
But abs to invariant ags remain elevated
Trypanosoma cruzi
General
Trypanosoma cruzi
Life Cycle
Chagas Disease
Clinical manisfestations
Chagas Disease
Clinical manisfestations
It develops to
conjunctivitis
and unilateral
edema o/t
face and
eyelids called
Romanas sign
Chagas Disease
Clinical manisfestations
Acute stage appears 4-14 dys
later, characterized by fever
and chill, malaise, myalgia,
and fatigue
Abdominal rash may also occur
The most severe symptoms are
seen if CNS is involved
Chagas Disease
Clinical manisfestations
The symptoms of chronic stage
are dependent on the organ
system affected and the extend
of cellular damage
Cardiomegaly, dyspnea, and
aphasia may occur due to the
involvement of heart, lung, and
CNS
Chagas Disease
Treatment and Prevention
Drugs of choice:
Nifurtimox
Nifrofurazone
Preventive action is the
combination of disease and
vector control
Trypanosoma
Laboratory diagnosis :
Microscopic examination : blood,
lymphnode fluid, CNS fluid, biopsy of
chancre
Concentration techniques and serial
examinations are frequently needed.
Serologic testing , normally is used for
screening purposes only
Leishmania spp.
General
Class Zoomastigophorea
Order Kinetoplastida
Family Trypanosomidae
3 species known to be pathogenic
in humans are:
1.
2.
3.
Leishmania donovani
Leishmania tropica
Leishmania braziliensis
Leishmania donovani
General
The Vector
Sand fly
Leishmania donovani
Morphology
Leishmania donovani
Morphology
Promastigotes
Leishmania donovani
Life Cycle
Leishmaniasis
Cutaneous Leishmaniasis
Mucocutaneous Leishmaniasis
Visceral Leishmaniasis
Leishmaniasis
Etiologic agents
Cutaneous leishmaniasis:
Oriental sore :
is caused by Leishmania tropica complex
Distributed in India and Middle East countries
Vectored by Phlebotomus sandfly
Bay sore
is caused by Leishmania mexicana complex
Extends from southern Texas, Mexico, Central and South America
Vectored by Lutzomyia sandfly
Mucocutaneous leishmaniasis
Caused by Leishmania braziliensis complex
Visceral leishmaniasis
Caused by Leishmania donovani complex
Cutaneous Leishmaniasis
Clinical manifestations
Cutaneous Leishmaniasis
Clinical manifestations
Cutaneous Leishmaniasis
Diagnosis
Cutaneous Leishmaniasis
Treatment and Prevention
Mucoutaneous Leishmaniasis
General
Mucoutaneous Leishmaniasis
Clinical manifestations
Mucoutaneous Leishmaniasis
Clinical manifestations
Clinical
progression may
take years, results
in ulcers that erode
soft tissue o/t face
and palate
Mucoutaneous Leishmaniasis
Clinical manifestations
Leishmanioma
Mucoutaneous Leishmaniasis
Diagnosis and Treatment
Visceral Leishmaniasis
General
Visceral Leishmaniasis
Clinical manifestations
Visceral Leishmaniasis
Clinical manifestations
Physical examination:
hepatosplenomegaly
and lymphadenopathy
Hyperpigmentation o/t
forehead and hands
(kala azar) may be
observed
Prognosis of untreated
cases is poor
Visceral Leishmaniasis
Diagnosis
Visceral Leishmaniasis
Treatment and Prevention
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