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Introduction to Infectious Diseases

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mariam kavtaria

on 10 September 2018

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Transcript of Introduction to Infectious Diseases

Introduction to Infectious Diseases
Mariam Kavtaria
Infectious Agents
Immune System
Innate/ Natural Immunity
Immediate defense
Protects without prior exposure to inf. agent
Activates adaptive immunity
Is non-specific
No long lasting immunity
= no memory
Adaptive/ acquired Immunity
Develops over time
Capable of distinguishing
Self from non-Self
Highly specific
for particular antigen
Has
Memory cells
– stronger, quicker response to previously encountered antigen:
B cells
– produce antibodies
T cells:
Helper CD4+ T cells:
stimulate B cells - production of immunoglobulins
Cytotoxic CD8+ T cells:
directly attack and lyse cells that express foreign antigens

2nd line:
Phagocytic Cells
- Neutrophils, macrophages, monocytes, NK cells
Complement system
Inflammation
Inflammatory Cytokines

MHC I:
Is expressed on
ALL nucleated cells
Presents
endogenous antigens
to CD8 T cells

T lymphocytes are activated by antigens on major histocompatibility complex (MHC)
Reticuloendothelial system
Phagocytic (Kupffer cells) and Ito cells in the liver
Alveolar macrophages in the lungs,
Macrophages and dendritic cells in the spleen and lymph nodes
Mesangial cells in the kidneys,
Microglia in the brain

clears circulating microorganisms
functions more efficiently when pathogens
are opsonized

Opsonization
- identifying the pathogen
C3b , antibodies
- opsonins
After opsnin binds the pathogen, phagocitic cells are attracted to it
Extracellular pathogens are attacked by the humoral immune system:
Humoral Immune System
Antibodies
The complement cascade
Phagocytic cells
Antibodies are produced by
mature B lymphocytes:

ANTIBODIES:
Directly block the invading organism
neutralize secreted toxins and enzymes
facilitate the recognition and removal of the antigen by phagocytic cells (opsonization)
promote the deposition of complement components on the surface of the invader.

IgG
-

predominates in the circulation
persists for many years
after exposure - "Chronic Antibody"
IgM

-
earliest antibody to appear
in response to infection; "Acute Antibody"
IgA
-
immunity at
mucosal surfaces, Breast-milk, tears, saliva,

IgE
- allergic and parasitic diseases.

Antibodies Circulate in body fluids
Secreted on mucosal surfaces
Specifically
recognize and bind to foreign antigens
COMPLEMENT SYSTEM
Some of these proteins (
C3b
) acts as
opsonins
for destruction of microbes by phagocytes.
The "terminal" components (
C6, C7, C8, and C9
) can directly kill invaders by forming a
membrane attack complex
- damages cell membrane
Other components,
(C5a)
, act as
chemoattractants
for PMNs.
Complement activation occurs by:
the
classic pathway
- activated by immune complexes (
antibody bound to antigen
),

Alternative pathway
- activated directly by microbial components

Consists of proteins functioning as a cascade of enzymes
Disrupts the surface
of invading organisms.
short-lived
white blood cells
- engulf and kill invading microbes
are attracted to inflammatory sites by
chemoattractants
such as C5a.
Adhere to
Selectins -
molecules expressed by endothelial cells
-
Localize the site of infection
Intercellular adhesion molecule 1 (ICAM-1)
on endothelial cells -
binds to integrins on PMNs
- facilitating diapedesis

PMN CELLS
Microbial Entry
The most common sites of entry are:
mucosal surfaces
(respiratory, alimentary, urogenital tracts)
skin
Routes of microbial entry:
Ingestion
Inhalation
Parenteral
Sexual contact
To enter the tissue - Most microbes must
anchor themselves
to a tissue receptor


Adhesins
- located on host surface
anchors the microbe to a tissue
promotes cellular entry


Viral Adhesins
All viral pathogens must
bind to host cells
, enter them, and replicate within them




Epstein-Barr virus:
microbial ligand: Envelope protein
host receptor: CD21 (CR2)
HIV
Microbial ligand: Surface glycoprotein gp 120
Host Receptor: CD4 and chemokine receptors (CCR5 and CXCR4)
Used by gram-negative bacteria for
attachment to host cells

shorter, straighter, thinner than flagella





Escherichia coli:
ligand-  Pili
host receptor: Ceramides/mannose and digalactosyl residues
long appendages attached to:
One or both ends
of the bacterial cell, or
Distributed
over the entire cell
surface
Composed basic protein
Plasmodium vivax
binds to the
Duffy antigen Fy
on erythrocyte and to enter it and cause Malaria
loss of host receptors may confer resistance to a population
70% of individuals in West Africa lack Fy antigens and are resistant to P. vivax infection
Pili / fimbriae
Trichamona vaginallis
Flagella
RBC
P. Vivax
Duffy antigen
Duffy binding protein
The production of cytokines
IL-1, IL-18, TNF- alpha
, leads to
fever, muscle proteolysis.

The
lipid A portion
of gram-negative LPS - gram-negative bacterial sepsis

An inability to kill or contain the microbe usually results in damage that can degrade the host tissues
The staphylococcal enterotoxins, toxic shock syndrome toxin 1, and the streptococcal pyogenic exotoxins behave as
Superantigens -
Toxin directly stimulates T cells
leading to
massive release of cytokines
-
damage host tissues
Laboratory Diagnosis
To grow bacterial, fungal, or viral pathogens,
an
appropriate sample must be placed into the proper medium for growth
Culture - The most accurate test
Gram's stain :
differentiates organisms with
thick peptidoglycan cell walls
(gram-positive)
thin peptidoglycan cell walls
(gram - negative)
Staining:
The acid-fast stain identifies organisms
that retain dye
after acid/organic solvent disruption
Direct Immunofluorescent Antibody
technique
fluorescent antibody is directed at a specific antigen to visualize organisms or subcellular structures

Indirect technique
- two-antibody system is used: Each unlabeled antibody is attached to the second antibody and the visual signal is amplified.
Nucleic Acid Tests -

detection of specific DNA and RNA

sequences
used for organisms that are difficult to identify or culture
determines whether two separate isolates are related
used to predict the sensitivity of organisms to chemotherapeutic agent

Target nucleic acid sequence can be amplified to detectable levels
PCR
, most common NAAT, requires
repeated heating of the DNA

separates two complementary strands of the double helix
Extends complimentary strand using PCR amplification
Detects signal via a labeled probes
Treatment
Life-threatening
infections (bacterial meningitis, sepsis) must be treated
immediately -
even

before a specific causative organism is identified

Treatment
should cover
the causing organism
Treatment should be as
specific

and narrow spectum as possible

1. Careful History taking
-
the most important part - gives clues about the possible causes
Identifies Risk factors
- Exposure to pathogens, occupational history, travel history, Family history, Ill contacts;
2. The physical examination
must be thorough
3. Diagnostic tests and Laboratory studies
must be directed toward establishing an etiologic diagnosis in the:

Approach to Patient
PREVENTION
Active

Vaccines
-
Live or inactivated

Toxoids
-
Bacterial toxin modified to be non-toxic

Passive
Antibodies –
immune globulins
antitoxins

Immunization
https://thinkprogress.org/vaccines-have-almost-totally-eliminated-these-13-infectious-diseases-in-the-u-s-653d4a8f930e#.2q39czn0z
1st line:
Skin/ Mucous membranes/ secretions
Normal flora
MHC II:
Expressed
only on antigen presenting cells (APC)
:
Dendritic cells,
Macrophages
B lymphocytes
Presents antigen to CD 4 T cells
Vaccine Types
Live attenuated Vaccine
Measles
Mumps
Rubella
Cholera
Hepatitis A
Influenza (injectable)
Rabies
safer than live vaccines
induces weaker immune response
booster shots usually required
Induces strong/lifelong immunity
may cause disease in immunocompromised host
Killed Vaccine
Wash your Hands!!!!
THANK YOU FOR YOUR ATTENTION!
references:
1.Harrison's Principles of internal medicine - 19TH edition
2. the merck manual of diagnosis and therapy - 19Th edition
3. Kaplan Lecture Notes for USMLE step 1- year 2016 Edition
IL-7
GM-CSF, IL-3
CD4 TH cell
CD8 TC Cell
IL-5
Myeloid Cells
Most Abundant
circulating cell
Granulocyte with segmented nuclei (3-5 lobes)
Small pink cytoplasmic granules
Function: Phagocytosis; Kills
extracellular pathogens
Lymphoid Cell - Lymphocytes
Location:
Bloodstream, Secondary lymphoid Tissues
(lymph nodes, spleen)
Large, Dark staining nucleus/ Small cytoplasm
B cell surface markers:
CD19, 20, 21
T Cell Surface markers:
CD3
T helper: CD4
/
T cytotoxic: CD8
Requires activation

Plasma Cell
- Terminally differentiated B cell
Secretes Antibodies
Natural Killer Cell
Surface markers: CD16, 56
Kills virally infected and cancer cells
Neutrophil, Polymorphonuclear (PMN) cell

Monocyte - circulating cell;
Precursor of tissue macophages
Kidney-shaped nucleus
Macrophages
- Residents in all tissues
Phagocyte
Antigen presenting cell
T-cell activator
Dendritic Cell
Phagocyte
Antigen presenting cell
T cell activator
Eosinophils, Basophills, Mast cells
Elimination of
large extracellular parasites
Hypersensitivity type 1
B cell
Bacterial toxins
Tissue Tropism
- certain microbes cause disease by infecting
only specific tissues
1. Bacteria
2. Viruses
T cells
Giardia Lamblia
CD8 cytotoxic cell - directly damages the infected cell
CD4 T helper T cell - Regulates various immune responses
Bacterial toxins can be classified as
exotoxins or endotoxins
.
Exotoxins are actively secreted;
Endotoxins are part of gram negative
bacterial outer membrane
(Lipopolysaccharides (LPS))
not released until the bacterium is killed
The body's response to an endotoxin can involve severe inflammation.
3. Fungi
4. Parasites
Examples:
shortest possible
time
at the lowest possible
cost
with the least possible
discomfort
to the patient

Varicella
Ifluenza (intranasal)
Yellow Fever
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