The doctor announced that the second exam will be on 30th of April and it

will be to the end of this lecture,

The second part of this lecture is not included in the

second exam.
Today we will talk about inflammation and phagocytosis, which is the
second half of the last time’s lecture, and afterword we will talk about an
introduction about infectious diseases.

Let’s continue with the last lecture: 

Another example of the second line of defense is the process of

inflammation. Inflammation refers to series of events that the body makes
in response to local injury, irritation, microbial invasion or bacterial toxins.
This process basically has 6 steps; the three most important steps are the
following:

Step 1: An increase in the diameter of the capillaries which increase the

blood flow to the inflamed area this is called Vasodilatation.

Step 2: Increase permeability of capillaries allowing escape of plasma and

plasma proteins.

Step 3: Exiting of the leukocytes from the capillaries and the accumulation
at the site of injury.

The series of inflammation are summarized in this figure << look at slide 13
>>.

So here in this example we have tissue injury by a sphincter, so the sphincter

basically damaged some cells and introduced some bacteria into the tissue of
the skin, so the damaged tissue will produce various chemical substances
that will act on the capillaries of the skin to induce vasodilatation which will
result in increase the blood flow and increase permeability of blood
vessels , so there will be plasma and plasma proteins exiting the blood vessel
to the tissue , this will lead to swelling of the tissue which is called edema.

Next we will have white blood cells that will exit the capillaries and enter the
damaged tissue.

The fifth step is chemotaxic, so any white blood cell that will leave the
capillary will start to move toward the site of injury, and the site of injury will
have large concentration of chemicals called chemokines and the white
blood cells will start migrating in the direction of increasing concentration of
chemokines.
Finally some of the white blood cells, which are called phagocytes which are
the macrophages and the neutrophils and they will basically engulf and
digest any bacteria or foreign body.

So this whole process in known as inflammation, and these are the six steps
again

• Tissue injury

• Vasodilatation of blood vessels

• The emigration of the leukocyte from the blood vessels to the tissue

• Chemotaxis: the movement of the WBCs to the site of injury

• And finally the phagocytosis of any foreign material.

So what are the purposes of inflammation?!

We have four goals:

1. To localize the infection.

2. Prevent the spread of the microbial invaders.

3. To neutralize any toxins produced at the site of injury.

4. Help in the reaper and heeling of damaged tissue.

Inflammation usually characterized by four signs and

symptoms:
1. Redness: due to increase in the blood flow at the site of injury.

2. Heat: basically the site of inflammation will feel worm due to increase
in the blood flow and increase in the metabolic rate of tissue at that
site of inflammation.

3. Swelling: due to the efflux of the plasma proteins to that site.

4. Pain: because the local nerves might be damaged or there might be

pressure or irritation on the nerve endings.

Basically at the site of inflammation there will be accumulation of plasma or

tissue fluids , an accumulation of bacteria and cellular debris and also
WBCs, so all these components together well be referred to as
inflammatory exudates.
 Sometimes the inflammatory exudates will become thick and greenish and
yellow in color, and in this case the inflammatory exudates will be referred as
purulent exudates or pus.

We have certain organisms are more likely to produce large amount of pus
and these are called payogenic microorganisms or pus producing
microorganisms including the Staphylococcus aurous and
Streptococcsy , and these microorganisms will produce many enzymes that
well destroy WBCs and host cells leading to increase the amount of pus .

It is important to know that not only inflammatory reaction are associated

with inflammatory exudates, some inflammatory reaction happens without
the presence of this exudates an example of this is arthritis, which is
basically an autoimmune reaction .In this case we don’t have any bacteria
and the immune cells are directly targeting the joint tissue.

As we said one of the steps of the inflammation is the phagocytosis of foreign

material and cell debris and the cells that will form this, are the phagocytes
which are the macrophagese and the neutrophils .

The Doctor here reviewed with us the elements of the blood:

The elements of blood: the RBCs, platelets and lymphocytes, and the
lymphocytes can be T cells or B cells or can be natural killer cells, we
have also the monocytes which later develop to macrophages, and then
we have the granulocytes which contain the (neutrophils , besophils and
eosinophils). The eosinophils basically involved in the allergic reaction and
in fighting various parasitic diseases .The neutrophils are phagocytotic cells.

So the neutrophils and the macrophages which are derived from the
monocytes are the basic phagocytes in the body.

So phagocytosis involves four major steps:

1. Chemotaxic : which is the migration of the phagocytes
( macrophages and neutrophils) to the site of injury.

2. Recognizing the foreign body and attaching to it:

In the normal situation the bacteria will not be phagocytosed unless

the phagocytic cell recognized this bacteria, and one way of
recognizing the bacteria is by recognizing various opsomenzs which
are fragments of complement proteins and the phagocyte has a
receptors which are here appearing in red that can recognize the
complement protein and once the recognition happen the cell can
engulf the pathogen.
 So the phagocytes will not recognize the bacteria directly they will
recognize the complement fragment which are deposed on the surface
of the pathogen.

Another example of opsomenzs or material that allows the

macrophages and the neutrophils to recognize the pathogens are the
antibodies, in this case the body produce antibodies against the
pathogen, these antibodies will bind to the pathogen and the
phagocytotic cells have special receptors to the tail reign <<>> of the
anti body to bend to it and able it to phagocytes it.

So the key point here that u need specific molecule that allow the
phagocyte to recognize the pathogen and these are called opcenecs ,
and an example on the opcenecs is complement components and
anti bodies.

At the end in this step the macrophages are adjacent to the bacteria.

3. Formation of the Pseudopodia around the object and

engulf it completely:

Once the recognition happens the phagocytic cell will start to express
pseudopodia around the pathogen and eventually engulf it completely.

4. Destroying the engulfed body by using lysosomal

enzymes.

The pathogen will end up in a vacuole inside the cell called phagosome,
so the pathogen inside the phagosome is safe because the phagosome
does not contain any enzymes or anything that will destroy the pathogen.

The factors and enzymes that will destroy the pathogen are in found
inside another vesicle called lysosome, so the lysosome will come next
to the phagosome and fuse with it releasing all the components of
lysosome inside the phagosomal space.

So ones the fusion happens the phagosome is now called

phagolysosome and the entire hydrolytic enzymes will be released is
this space. So this is how phagocyte will get rid of the pathogens.
 Here is an example of amacrophage engulfing protozoa parasite called
Giardia Trophozoites( look at slide 24) , so this is the parasite it is a pear
shaped and it is basically inside the phagosome and hare is a picture of
the same process using scan electron microscope .

A: so here early in the phagocytotic process , you

have pseudo odes starting to extend .

B: this is late in the process, after the complete

engulf of the pathogen.

There are certain microbe can evade the process of phagocytosis either
temporarly or for a while of time, and we will mention some of the factors
that will allow the microbes to escape from the phagocyte.
 One of the most famous examples is the bacterial capsule which is o
large polysaccharide stricture that is very slippery that will allow the
escaping from the pseudopodia.

One exception to this that if your body produces antibodies against the
capsule components and the antibodies attached to the capsule the
phagocyte can engulf the bacteria with the antibodies.

Another way to evade the phagocytosis is producing enzymes that will kill
the phagocytotic cells and these enzymes are called leukosidels.

Other bacteria such as mycobacterium tuberculosis has a very waxy cell

wall, which is very resistant to many enzymes and chemicals, so if the
mycobacterium was phagocytosed , the enzymes in the lysosome will not
be able to easily digest and destroy the mycobacterium .

And we have other mechanisms that the microorganism can evade

phagocytosis or evade being killed by the lysosome, and most of them are
unknown and the ones are known vary between pathogen to pathogen.

>>> Some people have various disorders that affect their ability to produce
an inflammatory response and to produce a successful phagocytic event
example of these:

• Leucopenia: which as name implies a lack in the number of WBCs and

the immune response will be weak.

• Some conditions affect the ability of WBCs to move towards the

pathogen or the site of infection.

• Other conditions disable the ability of the phagocytes to destroy the

pathogen inside the phagosome.

• Other factors that reduce the immune response including :

 The nutritional status so people with malnutrition usually have

weaker immune system.
  Increase iron level in the body will make it easier for the
bacteria to divide and multiply.

 Stress: is associated with decrease immune system function.

 Cancer and chemotherapy: also reduces the immune status.

 Age: Extreme ages, old people (above 50 years old) have weaker
immune system and infants also have weak immune system.

 AIDS: HIV infection leads to destruction of the CD4 T cells of the

immune system which leads to decrease immunity.

 Drugs (steroids): can suppress the immune system.

So this is the end of the second exam material now we will talk about
infectious diseases …..

This is for the final material

Introduction to infectious diseases

>>Generally speaking the pathogen can cause diseases by 2 ways or

diseases can be classified into 2 types:
 1) Microbial intoxication: in which the clinical manifestations of the
disease are due to a toxin that is produced by the pathogen such
as:

*Food poising by staph.

*Aureus in which you ingest a premade toxin.

In other forms the toxin is produced while the pathogen is inside

the body example is tetanus where it enters a deep wound and
produces toxin there.

2) Other diseases can result from pathogen replication and destruction

of tissues and these are called infectious diseases.

So infectious diseases happen when; a pathogen infects a certain

location of your body or if it colonizes or infects multiple
locations in your body and in some infectious diseases the
infection starts at one site and then disseminate to other
locations.

>>>Opportunistic pathogens: are organisms that normally don’t cause

disease in normal immune competent individuals but with certain conditions
such as removal of normal flora or if they were introduced into foreign sites
then they might be able to produce a disease , also if we have weakened
immune system they might cause disease.

Examples:

• aspergillosis which is a fungal infection, infects the immune

compromised.

• Candidiasis infection with Candida albicans which infects

certain sites in the body.

• CMV (cytomegalovirus).

• Tuberculosis and toxoplasmosis happens in immune

compromised patients such as Aids patients.

• Pneumocystis infection sort of pneumonia usually happens

in AIDS patients.
>>>How does the bacteria cause disease??

Basically the bacteria have various virulence factors that enable the
bacteria to cause disease example of the virulence factors are:

The adhesion factors that allow them to attach to specific tissues so

adherence and colonization factors allow the bacteria to cause disease.

bacteria also has various ways to evade the immune system they have
certain ways to prevent the activation of complement so they prevent
the cells from killing the bacteria by direct effect of complement or by
directing the phagocytes towards them, they can evade phagocytosis by
the phagocytes, they might produce factors that prevent destruction
within the phagocytes,

They can also produce factors that suppresses the immune system, also
gram negative bacteria has within the structure if the cell wall the
lipopolysaccharide which has an endotoxin activity that will lead to fever.

Many bacteria can produce exotoxins such as:

• >>cytotoxin which destroys the host cells, enterotoxin which can

lead to gastroenteritis

• neurotoxins which causes central nervous system disease.

Many bacteria can produce tissue destructive enzymes such as lipases

and proteases which can damage tissues.

>>>how do viruses cause disease??

Viruses are obligate intracellular pathogens that requires host cells in

order to replicate so these viruses get inside the host cells and usually after
virus replication ends the cell will be destroyed either by lyses of the cell or
by the immune system targeting the cell for destruction so the clinical
manifestations are either by direct destruction of cells or as an effect of the
immune system towards the virus infected cells.

>>>how do fungi causes disease??

Fungi can cause a disease by a variety of mechanisms, as the fungus
replicate inside the tissue it invades and destroys vital structures within these
tissues, also the immune system could be fighting the infected tissue and
causes the destruction, also fungi can form large masses inside any empty
space so they can cause obstruction in the bronchi of the respiratory system
and the ureter of the urinary system and the veins and arteries of the
circulatory system thus leading to hypoxia and necrosis of the tissues.

>>We can classify fungal infections according to the site of infection into:

1) Superficial mycosis which means fungal infection of the outermost layer

of the body (the epidermis) examples skin, hair, and nail infections which we
call tinea or ring worm infection.

2) Subcutaneous mycosis: infection of the skin and the underlying

connective tissue.

3) Systemic mycosis: systemic infection, usually but not always these

infections begin as a pulmonary infections but can potentially spread to other
tissues and organs in the body.

Parasites:
The word ‘parasite’ usually refers to the microscopic protozoa and the
microscopic worms.

The method by which this group of pathogens cause disease varies greatly
and depends on the pathogen itself, some parasites produce toxin, others
produce destructive enzymes, or it can directly invade the tissue and
lead to destruction of the tissue, sometimes the microsome of the
microscopic protozoa such as leishmania or toxoplasma can replicate inside
the cell and destroy this individual cells, some worms can be present inside
the circulation and lead to occlusion of the blood vessels and other
tubular structures, also the immune system itself can produce damage
and lead to the clinical manifestations of the disease.

Protozoa
The protozoa are mostly unicellular organisms and not all protozoa are
pathogenic we have examples of protozoa that are freely living in the
environment such as paramecium which usually lives in lake water.
Protozoa are classified into 4 groups depending on their method of motion:

1) Amoeba moves by pseudopod.

2) Flagellates by movement of flagella.

3) Ciliates have hair like cilia.

4) Sporozoa unable to move.

The way to diagnose protozoal infections involves the examination of tissue

or feces containing the various forms of protozoa and usually protozoa have 2
forms:

>> The trophozoite which is actively metabolizing and replicating motile

form of the parasite.

>> The cyst: This is the dormant, metabolically inactive, environmentally

resistant form.

So you can look at the tissues or feces and try to find the trophozoite or the
cyst of the protozoa.

Certain protozoa such as trypanosoma and leishmania don’t have the

trophozoite or cyst stage, they have other stages called: amastigote,
promastigote, epimastigote, and trypomastigote.

Helminthes (parasitic worms):

They are divided into 2 major divisions depending on the shape of the
cross section of the worm itself:

1) Nematodes (roundworms): have a round cross section.

2) Flatworms (Platyhelminthes): have flattened shape.

These are further divided into 2 types depending on their length so we have:

1- Cestoda or tapeworms which are very long.

2- The flukes or the Trematoda which are short and leave like in shape.

The helminthes or worms have 3 forms for their lifecycle (egg-larva-adult

worm); the adult worm is usually present inside the host, some of the
worms have separate sexes (male and female) other worms are
hermaphrodite which has both male and female sex organs, so the
hermaphrodite will produce the ova, if the eggs become fertile they will hatch
and produce larva and larva eventually will grow into adult worm.

So the infective stage of the worm is the fertilized eggs which contain the
larva or the free larva itself, most people get the infection by ingesting the
ova containing the larva or by directly ingesting the larva this is the way of
infection for most worms.

But in some worms the larva directly penetrates the skin such as
bilharzia or Schistosoma if you swim in water contaminated with it the
larva will directly penetrate the skin and cause infection.

O heeeeeeeeeeeeeeeeeeeekk 5lsnaaaaaaaaaaa 

Big thaaaaaaaanx to my frinds who helped me (shatha,waleed,rawand,mays)

And special thanx to my friends in B8 and my family for supporting me

B7EBKOOOM MY FRIENDS
(shatha,mays,rawand,mimi,samreen,safa2,ala2,reem,tasneem,
,manar,sma7,suzan,omniah,do3a2,birjees,ala2,mo3a4,7amoda,bashar,walee
d)

O kman bnaat dof3te b7ebkom 

(noor,ala2,arwa,sara,yasmeen,dalia,ruba,lama)

O mwafa2een bel emt7aaaan nshallah kolkm trf3o ras ahaleko o te6l3o a7sn
dentists bel3aalm