Haemoflagellates Leishmania - PowerPoint Presentation

Slide1

Haemoflagellates

Leishmania

spp.

Trypanosoma

spp.

Slide2

EpimastigoteHaemoflagellates of medical importance

There are 4 parasitic stages (or forms):

Amastigote & Trypomastigote occur in vertebrate hosts Promastigote & Epimastigote occur in invertebrate hosts

Amastigote

Trypomastigote

Promastigote

Leishmania

spp.

and

Trypanosoma

spp.

have digenetic life cycles,

involving vertebrate hosts (man and reservoir animals)

and

invertebrate hosts (arthropods: vectors).

Slide3

Amastigotes (donovan bodies): Non-motile intracellular stage. In vertebrates hosts.

Morphology)

Promasitogtes

(flagellated form): Motile (with anterior flagellum)

Slide4

Morphology)Trypomasitogtes (flagellated form):

Motile (with anterior flagellum & undulating membrane).

Slide5

Trypanosomes are flagellated protozoa,

trypomastigote in shape, with elongated body,

central nucleus

,

posterior kinetoplast

,

long undulating membrane

and anterior free flagellum

.

Trypanosomes

Slide6

TrypanosomiasisParasitic diseases caused by Haemoflagellates belonging to the genus Trypanosoma. There are 2 main forms:

[1] African Trypanosomiasis [Sleeping sickness]:

A] West African Sleeping sickness

caused by Trypanosoma brucei gambiense B] East African Sleeping sickness caused by Trypanosoma brucei rhodesiense

[2] American trypanosomiasis [Chagas’ disease]:

caused by

Trypanosoma

cruzi

Slide7

Trypanosomiasis African Trypanosomiasis (Sleeping sickness): caused by species of T. brucei

complex and transmitted by

Glossina spp. (t

setse fly):T. b. gambiense  West African Trypanosomiasis

T.

b.

rhodesiense



East African

Trypanosomiasis

American

Trypanosomiasis

(

Chagas’ disease): caused by

T. cruzi and transmitted by Triatoma

spp. (winged bug).

Occurs in Central & South America

Slide8

Classification1- Polymorphic trypanosomes

The parasite has different size &

shape in blood e.g.

T. brucei complex: a] T. brucei gambiense & b]

T. brucei rhodesiense

2- Monomorphic trypanosomes

The parasite has the same size

&

shape in blood

e.g.

T. cruzi

Polymorphic trypanosome

s

Monomorphic trypanosomes

Slide9

Slide10

Trypanosomiasis[1] African Trypanosomiasis [Sleeping sickness]:

Slide11

Tributary of Lopori River near Bongan danga in Gambiantrypanosomiasis-endemic area of northwestern DemocraticRepublic of the Congo. Note forested Tsetse flies

Slide12

[1] African Trypanosomiasis[Sleeping Sickness Disease]Geographical distribution: corresponds to that of the vector which is approximately 20° N

& 20° S of the equator

G

. palpalis

In

West & Central

Africa

G

. morsitans

In East

Africa

Annual cases estimated in 50.000–70.000:

Slide13

HabitatDuring the early stages of the disease; Trypanosomes are found extracellular in the peripheral blood / lymph

/ tissue spaces of various organs of R.E.S. [

Liver, Lymph

nodes, Bone marrow, Spleen]. In the terminal stages; in CNS

a-

D.H. ( man)

b-

R.H. (animals) as, antelopes, pigs, goats, dogs

;

in which the parasites exist as

Trypomastigotes

only in their blood stream.

Slide14

5 mmTsetse Fly

Glossina sp. (tsetse fly), the

vector of African trypanosomiasis

both males and females can serve as vectors

Slide15

Vector: Glossina spp. [tse tse fly],

Transmission:

Cyclopropagative transmission.

Infective stage: Metacyclic trypomastigotes. Mode of transmission

Bite of the fly :

infective stages are

introduced with

the

Saliva

of infected vector; (Anterior station transmission,) &

may be

transmitted by

- mechanical transmission (e.g.

stomoxys

)

- blood transfusion,

- organ transplantation - congenital

Slide16

T. brucei: only as trypomastigotes in vertebrate hosts, presenting with different size and shape in blood [Polymorphic].

Morphology

Slide17

Morphology [Cont.]a- Epimastigote

in the midgut.

b- Metacyclic or short stumpy trypanosomes (infective stage)

in salivary gland.

2. in the vector

Slide18

Life cycle of African trypanosomiasis

Slide19

Life cycle of T. gambiense & T. rhodesiense

During a

bite,

infected tsetse-flies (♀ & ♂)

inject

metacyclic

trypomastigotes

into

skin tissue of

hosts.

These

transform into

bloodstream trypomastigotes and are carried to various body fluids (blood, lymph,

spinal,

etc..) where they multiply by binary fission (T. rhodesiense

much more actively than T.

gambiense).

Affected CNS  sleeping sickness.

New vectors ingest trypomastigotes

from infected hosts. These transform into dividing

procyclic

trypomastigotes

that migrate to salivary gland, convert into multiplying

epimastigotes

, then transform to infective

metacyclic

trypomastigotes

.

Slide20

2- Haemolymphatic stage [Blood & Lymph nodes]

Trypomastigotes invade blood & lymphatic system and multiply

producing >>>

Toxic manifestations & Lymphocytic hyperplasia.Enlarged liver & spleen, lymphadenopathy especially

in posterior triangle of neck

>>>

“Winter bottom sign

”

Slide21

2- Haemolymphatic stage [Blood & Lymph nodes]

Trypomastigotes invade blood & lymphatic system and multiply

producing >>>

Toxic manifestations: Patient gets irregular fever, headache, joint & muscle pain and rash. Bone Marrow affection: Anaemia

[

Hypoplastic anaemia

]

,

Leucopenia

&

Thrombocytopenia

.

Slide22

3- Meningoencephalitis stage [CNS] (Sleeping sickness stage)

By end of 1st year;

Trypomastigotes invade CNS

>> perivascular infiltration of cerebral vessel with chronic inflammatory cells >> ischaemia & haemorrhage >> Meningoencephalitis

&

Meningomyelitis

.

Patient suffers of:

Severe headache, mental apathy, slow speech, tremors, involuntary movements

&

convulsions.

Sleeping stage develops

>> Coma & death [

from

the disease

or

from intercurrent infections as

pneumonia].

Coma before death

Slide23

Section of cerebral cortex ofZambian patient with Rhodesiantrypanosomiasis, showing markedcongestion and scattered petechialhemorrhaging in white matter.

Slide24

Gambian Sleeping sickness [T. gambiense ]Parasite: Less virulent

Disease Progresses slowly; Chronic

Parasite in blood

: Scanty [Low parasitaemia.Typical sleeping sickness symptoms.

Animal inoculation: Refractory

Rhodesian Sleeping Sickness

[

T. rhodesiense

]

Extreme virulence

Progresses rapidly.

Acute

Plenty [

High parasitaemia].

Usually fatal before

sleeping sickness symptoms

appear.

Susceptible with posterior-nuclear shift.

Clinical features

of Gambian and Rhodesian disease are similar,

but

they

vary in

severity

and

duration

:

Slide25

Diagnosis of African trypanosomiasis I- Clinical diagnosis History Fever especially if associated with enlarged lymph nodes

Residence or traveling to

endemic area.

Clinical picture. II- Laboratory Diagnosis Direct. Indirect.

Slide26

Direct Laboratory Diagnosis To demonstrate the parasite Early: in chancre aspirate, blood, lymph node, bone marrow & Late: in CSF BY

Microscopic

examination of fresh unstained or Giemsa stained films: >>>

polymorphic trypomastigote.

b) Culture

(NNN or

Weinmann’s

media:

>>>

epimastigote

.

c) Animal inoculation

d) CSF examination:

Trypomastigotes

, and Morula cells;

vaculoted

plasma cell.

==

.

==

Morula cell of Mott

Slide27

Polymorphic Trypanosomes in blood film

Slide28

Polymorphic Trypanosomes in blood film

Slide29

DiagnosisAspiration of swollen gland

Lumber puncture for CSF

Slide30

==

Laboratory diagnosis

Card Agglutination Trypanosomiasis Test [CATT]: It is a simple & rapid test for detection of circulating antigens in the blood of the patient. It is useful in surveys specially for T. b. gambiense.

Other methods:

Molecular techniques

(e.g.

PCR

)

.

Slide31

==

Indirect Laboratory diagnosis

Detecting

anti-Trypanosoma Abs by serological methods (ELISA, IFA, IHA etc..), But can't distinguish between current and previous infections.

Slide32

How can African trypanosomes evade the host immune system?Parasite’s surface is coated with a layer of glycoprotein called Variable Surface Glycoprotein “VSG” - coat protein -.Antigenic Variation

After infection,

the host

evokes an immune mechanism against Parasite’s surface coat protein [VSG].

The parasite

changes this surface glycoprotein to protect the underlying surface membrane from the host’s defence mechanisms.

New populations

of parasites with different coat proteins appear >>>

can not

be recognized >>> and

can not

be attacked by the immune factors specific to the previous generation

.

Slide33

TreatmentEarly

1-

Suramin (Antrypol):

Late

(

Drugs that pass CNS barrier

)

1-

Tryparsamide

2-

Melarsoprol

(Mel B)

Early

&

late stages

1-

Eflornithine

Prevention

& control

1-

Protection by skin repellents.

2-

Treatment of patients.

3-

Control of

Glossina

(vector).

4-

Chemoprophylaxis in endemic areas

[

Pentamidine

at

4-6 months intervals

].

No

vaccine