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Host Parasite Interaction

By:
Dr. drh. Darmawi, M.Si.

Microbiology Laboratory Faculty of


Veterinary Medicine
Syiah Kuala University
2013

Virulence factors:

According to research, the cytokines of the innate immune response play a very important
role in both the prevention and the exacerbation of the severe disease. The ability to invade red
blood cells, adhere onto cells and evade immune response is some of the virulence factors
associated with the protozoa. (8) Based on the hypothesis, certain forms of severe malaria are
the result of excess T-cell-mediated inflammatory response. By being exposed to the malaria
parasite, native T-cells are 'primed' to recognize it in future and secondary infection which
activates those primed cells to release pro-inflammatory cytokines, causing excessive and
potentially damaging inflammation. (8) Studies shows that severe malaria occurs in a window
of incompletely acquired immunity, where the host immune system responds overzealously to a
pathogen it recognizes, without the means to effectively control the inflammation. (8) This
explains why the most people at risk for the malaria disease in the malaria endemic areas
appear to be young children. (8) For travelers visiting a malarious region, the risk of severe
disease increase with age. (8)

Malaria, an infectious disease caused by a parasite called Plasmodium, which infects red blood
cells and is normally spread through four Plasmodium parasites, are known to infect humans.
The four parasites are; Plasmodium falciparium, Plasmodium vivax, Plasmodium ovale, and
Plasmodium malariae

Brugia malayi

Filariasis
Life cycle of Brugia malayi
The typical vector for Brugia malayi filariasis are mosquito species from the genera
Mansonia and Aedes. During a blood meal, an infected mosquito introduces thirdstage filarial larvae onto the skin of the human host, where they penetrate into the
bite wound. They develop into adults that commonly reside in the lymphatics. The
adult worms resemble those of Wuchereria bancrofti but are smaller. Female worms
measure 43 to 55 mm in length by 130 to 170 m in width, and males measure 13
to 23 mm in length by 70 to 80 m in width. Adults produce microfilariae, measuring
177 to 230 m in length and 5 to 7 m in width, which are sheathed and have
nocturnal periodicity. The microfilariae migrate into lymph and enter the blood
stream reaching the peripheral blood. A mosquito ingests the microfilariae during a
blood meal. After ingestion, the microfilariae lose their sheaths and work their way
through the wall of the proventriculus and cardiac portion of the midgut to reach the
thoracic muscles. There the microfilariae develop into first-stage larvae and
subsequently into third-stage larvae. The third-stage larvae migrate through the
hemocoel to the mosquito's prosbocis and can infect another human when the
mosquito takes a blood meal.

Myeloid dan Lymphocyte

Migration of Fagosit

Formation of an antigen-antibody complex.


Image from Purves et al., Life: The Science of Biology, 4th Edition, by Sinauer Associates
(http://www.sinauer.com/) and WH Freeman (http://www.whfreeman.com/), used with permission.

Paparan alergen
Pertama kali
Aktivasi Th2
Switching sel B
Produksi IgE
Ikatan IgE pada FceRI
Pada sel Mast

Paparan alergen berulang

Aktivasi sel Mast


Mediator
Reaksi hipersensitivitas
Tipe I Fase cepat

Vasoaktif amin
Mediator lipid

Sitokin
Fase lambat
(6-24 jam)

Anafilaksis
Abbas, 2003

Hipersensitivitas segera
Antibodi IgE

Alergen menjembatani
antibodi IgE yang fixed

Sel Mast

Histamin dan mediator


lainnya dilepaskan

Activation of helper T
cells

After it engulfs and processes an antigen, the


macrophage displays the antigen fragments combined
with a Class II MHC protein on the macrophage cell
surface. The antigen-protein combination attracts a
helper T cell, and promotes its activation

Activation of cytotoxic T
cells

After a
macrophag
e engulfs
and
processes
an antigen,
the
macrophag
e displays
the antigen
fragments
combined
with a Class
I MHC
protein on
the
macrophag
e cell
surface.

A receptor on a circulating, resting cytotoxic T cell recognizes the


antigen-protein complex and binds to it. The binding process and a
helper T cell activate the cytotoxic T cell so that it can attack and
destroy the diseased cell

Activation of B cells to make antibody

A B cell uses one of


its receptors to bind
to its matching
antigen, which the B
cell engulfs and
processes. The B cell
then displays a piece
of the antigen,
bound to a Class II
MHC protein, on the
cell surface. This
whole complex then
binds to an activated
helper T cell. This
binding process
stimulates the
transformation of the
B cell into an
antibody-secreting
plasma cell

In the following
diagram you can see
the helper T cells
(marked TH) at the
centre of the
immune response

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