Transcript Immunty to inf 2 MT

DIAGNOSTIC IMMUNOLOGY
IMMUNITY TO INFECTION
Major classes of pathogens
Definitions
Two organisms live in close association.
Mutualism:
Both members benefit from the association.
e.g., Protozoa live in the gut of termites.
Communalism:
When an organism benefits from the host
but the host neither benefits nor is harmed.
e.g. Entomoeba gingivalis in human mouth.
*Parasitism:
When an organism actually harms its host
or lives at the expense of the host.
e.g., Infections with viruses, bacteria, fungi,
protozoa, or helminthes.
The course of a typical infection and immune responses
can be divided into phases
If no innate
immunity
The establishment of an infection depends on several factors:
• Characteristics of the microorganism
• Number of organisms
• Mode of transmission (how and where they contact the host)
• Stability of the organism (in and outside of the host)
TYPES OF DEFENSE SYSTEMS
1- Immediate immune response
Complement
Phagocytosis
Natural Antibodies
2- Early immune response
3- Late immune response
The Early IR
4-96 hours past infection
1- Macrophages >>>> Cytokines

Increase vascular permeability
Recruits polymorphs and macrophages
Triggers platelets activation
2- Natural killer cells ( Viral infection)
3- Interferon's
The Late IR
 After
about 4 days
 Degradation and Ag presentation
 MHC molecules involvement
 Activation of T and B lymphocytes
 Cellular and humoral response
 Specific antibodies
Immunity to Bacterial Infection
 The
first line of defense is NOT dependent
on antigen recognition
Innate immunity
 Complement activation
 Phagocytosis
 NK cells

Most bacteria are killed by phagocytosis:
Oxygen independent killing
- Cationic proteins killing
- Acidic pH and lactoferrin
-
Complement is an effective mechanism but
bacteria may be able to avoid complement
mediated damage.
The second line of defense is characterized
by the secretion of specific antibodies;
Neutralize toxins by preventing its binding to
the target
- Interfere with motility by binding to flagellae
- Secretory IgA stops binding to epithelial
cells
- Aid in targeting complement
-
Immunity To Fungal Infection
 Is
a growing problem in immunologically
compromised hosts
 Seen in HIV infection
 Seen in cancer patients undergoing
chemotherapy
 Patients on immunosuppressive drugs
 In patients taking long term corticosteroids

Little is known about the precise mechanisms
involved
 Thought to be similar to those against bacteria
Fungi infection in human
Specific mycoses.
Subcutaneous mycoses.
Respiratory mycoses.
Proposed mechanisms
Based on cell immunity:
T Helper cells
Cytokines
Activation of macrophages
Elimination of fungi
Immunity to Viruses

Viruses are obligate intracellular microorganisms
 They
require the host cells to drive protein
synthesis and metabolize sugar
 Viroids are infectious agents that consist of
nucleic acids alone
 Prions are infectious proteins associated with
degenerative neurological diseases of human
Innate IR to viral infection
 The
early stage of the infection is a race
between the virus and the host IS
 The initial defense is the integrity of the
body surfaces
 Innate defense system involves;
Interferon
Nk cells
Macrophages
Mechanisms involving T cells
CD8+ cells ; These are MHC class 1 restricted
cells that focus on the site of virus
replication and destroy virus infected cells
CD4+ cells ;
Key factor in defense against viral infection
INF gamma is important for the activation of
TNF alpha which induce apoptosis
Evading IR by Viruses
a)
Mutation
b)
Producing of short stretches of RNA that
work against interferon
c)
Production of proteins that inhibit
transporting to cell surface such as in
infection with CMV
Immunopathology of Viral Infection
1- Response to viral infection may cause
tissue damage
Ag-Ab complex deposition in kidney and
blood >>> inflammatory response >>> T
cell mediated damage >> killing of host
cells
2- Virus may infect immune cells
3- Viral infection may induce
autoimmunity due to antigenic mimicry
Immunity to Parasites
 Stimulate
a number of immunological
defense mechanisms
 Both humoral and cellular responses
 Immune response depends on the stage and
the type of infection
 Most parasites pass through a complicated
life cycle
Features of Parasitic infection:
1- Infect large number of people
2- Parasitic infection have common features
Varity and large quantity of Ag
Ability to change their surface Ag
Complicate life cycle
Different mode of entry
3- Most parasites are host specific
4- Host resistance to parasite may be
genetic
5- Many parasitic infections are chronic
Effector mechanisms by Immune cells
MACROPHAGES
 Provide strong defense against small parasites
 Secrete factors that kill parasites without
ingestion
 Secrete cytokines that activate other immune
cells
 Synthesize nitric oxide that act as parasite toxin
 Activation of macrophages is a general feature
of early stage of infection
NEUTROPHILS
 Can kill large and small parasites
 Phagocytic activation
 Have granules that contain cytotoxic proteins
 Have Fc and complement receptors >> ADCC
PLATELETS
 Cytotoxic activities against larval stages
 Activation are enhanced by cytokines
EOSINOPHILS
 Characterize parasitic infection
 Thought to be specific against tissue
parasites
 Limit migration of parasites through the host
 Less phagocytic than neutrophils
 Act in accordance with mast cells
Role of T cells
 The
type of T cells involved is determined by
the type and the stage of the infection
 Cytokines
enhance protective immunity
against intracellular parasites
T
helper 2 cells are essential for the
elimination of intestinal worms
Role of Antibodies
 Parasites
induce production of specific
and non specific Abs
 Antibodies have several functions on
parasites
-Act directly on protozoa
-Block attachment to host cells
-Important for Phagocytosis