Transcript Introduction to Biotechnology

© Professor P. M. Motta et al / Science Photo Library
Microbiology: A Clinical Approach © Garland Science
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Entry – getting in
Establishment – staying in
Defeat the host defenses
Damage the host
Exit the host and be transmitted to another host
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Pathogens use virulence factors as part of the
infection process.
› They allow pathogens to survive and thrive in the
host.
› They make harmless organisms dangerous and make
dangerous organisms deadly.
Any point at which pathogens can enter is called
a portal of entry.
 There are three categories of portals of entry:
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› Mucous membranes
› Skin
› Parenteral routes
Mucous membranes are in direct contact with the
external environment.
 They allow pathogens to gain access into the
body.
 They are found in the:
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› Respiratory tract
› Gastrointestinal tract
› Genitourinary tract
This is the most favorable portal of entry to
pathogens because we have to breathe
continuously.
 Pathogens can be found on droplets of moisture
as well as on dust particles.
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This is the second most favorable portal of entry
for pathogens since we have to eat and drink
regularly.
 It has many barriers to infection but is still the
entry point for many pathogens.
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This is the second most favorable portal of entry
for pathogens since we have to eat and drink
regularly.
 It has many barriers to infection but is still the
entry point for many pathogens.
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Pathogens using the GI tract include:
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Salmonella
Shigella
Escherichia
Hepatitis virus
Giardia
Entamoeba
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The GI tract is also an important portal of exit.
› Pathogens can be found in fecal material after leaving
the body.
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The fecal-oral route of contamination is very
important in the infection process.
This portal of entry is more complicated than the
ones previously discussed.
 Urinary tract infections (UTIs) are more common
in women than in men.
 These types of infections cause major problems
in hospitals and clinical settings.
 Diseases of the reproductive tract are usually
sexually transmitted and are also part of this
portal of entry.
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Pathogens using the genitourinary tract include:
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Mycobacterium
Chlamydia
Herpesviruses
HIV
The skin is the largest organ in the body.
The large surface area of the skin provides a vast
area through which microorganisms may enter
the body.
 Many microorganisms reside on the skin.
 Skin provides an impermeable barrier to most
microbes and must be broken to allow entry.
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The term parenteral route refers to breaks in the
skin which permit entry of microorganisms.
 The parenteral route depends on injections, cuts,
or wounds, and surgical procedures to provide an
entry point.
 Insect bites can also allow entry of microbial
organisms.
 Insect transfer is referred to as vector
transmission.
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© Professors P. Motta & F. Carpino / Univer- Sity "La Sapienza", Rome / Science Photo Library
Microbiology: A Clinical Approach © Garland Science
© Professor P.M. Motta Et Al / Science Photo Library
Microbiology: A Clinical Approach © Garland Science
© Professor P.M. Motta Et Al / Science Photo Library
Microbiology: A Clinical Approach © Garland Science
Pathogens can use adhesins (glycolipids or
glycoproteins) to adhere to tissue.
 An example of this is the plaque found on teeth.
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› Plaque forms when a pellicle coats the tooth and
bacteria subsequently adhere to it.
› As many as 300 to 400 different types of bacteria will
adhere to each other building a biofilm on the tooth.
This is the plaque.
Spirochetes like
Treponema pallidum
(the causative agent
of syphilis) corkscrew
into tissues.
© CDC/ Dr. David Cox
Increasing the number of pathogens can establish
the infection in the host.
 Rapid growth and increased numbers of
pathogens can happen very quickly.
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› Some pathogens can double their numbers in as short
a period as twenty minutes.
› An organism that doubles every twenty minutes will
become 1 x 1021organisms in just 24 hours.
The body possesses powerful defense
mechanisms.
 Pathogens must avoid, evade, or compromise
these defenses in order to survive and thrive.
 Pathogens can defeat host defenses in 2 ways:
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› Passive defense – using built-in structures found on
the pathogen cell.
› Active defense – attacking the host defenses
The main passive defense mechanism is the bacterial
capsule which inhibits phagocytosis by host cells.
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Another method of passive defense is through
components of the bacterial cell wall.
› Mycolic acid is a waxy material found in the cell
walls of Mycobacterium species.
 It can inhibit phagocytosis and the entry of antibiotics.
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Active bacterial defenses involve the production
of extracellular enzymes which can:
› Increase protection against host defenses.
› Enable the spread of infection by attacking and killing
host defensive cells.
Pathogens can also hide in order to defend
themselves.
 Getting inside a host cell can protect the
pathogen from the host immune defense
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› Viruses are obligate intracellular parasites and can
easily enter host cells.
› Bacteria have to use the host cell cytoskeleton
(microtubules and microfilaments) to get into and
move around a host cell.
› Bacteria can also use the molecule cadherin to move
into adjacent cells.
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Damage to the host committed by the pathogen
can be direct or indirect
› Direct damage
 Is obvious and includes the destruction of host cells or
tissues
 Is usually controlled by the host immune response.
› Indirect damage
 Involves systemic infection as a result of toxin
production by the pathogen.
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Bacterial toxins are:
› Very poisonous
› Soluble in aqueous solutions
› Easily diffusible into blood and lymph which causes
distal pathology.
Bacterial toxins can produce fatal outcomes in
patients.
 They produce common symptoms such as fever,
shock, diarrhea, cardiac and neurological trauma,
and the destruction of blood vessels.
 There are 2 types of toxins:
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› Exotoxins
› Endotoxins
Exotoxins are produced by and exported from
certain pathogens and then enter host cells.
 They are among the most lethal substances
known.
 They are usually an enzymatic protein soluble in
the blood and lymphatic system.
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There are 3 types of exotoxins:
› Cytotoxins – kill cells
› Neurotoxins – interfere with neurological signaling
› Enterotoxins – affect the lining of the digestive
system.
Anthrax toxin is a cytotoxin.
It is produced by Bacillus anthracis (a grampositive rod commonly found in pastures).
 It is made up of three parts which are:
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› Produced separately within the pathogen
› Assembled outside the anthrax organism cell wall.
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It increases vascular permeability in host cells.
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Diphtheria toxin is a cytotoxin.
It is produced by Corynebacterium diphtheriae.
It is first produced in an inactive form.
It inhibits protein synthesis in the host.
A single molecule can kill a host cell.
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Botulinum toxin is a neurotoxin.
It is produced by Clostridium botulinum.
There are seven forms of this toxin, all of which
inhibit the release of the neurotransmitter
acetylcholine.
› This disrupts neurological signaling of the skeletal
muscle.
› This disruption causes paralysis.
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Tetanus toxin is a neurotoxin.
It is produced by Clostridium tetani.
It causes loss of skeletal muscle control.
› Prevents muscle relaxation
› Causes uncontrollable convulsive muscle contractions
› Lock jaw is an early symptom
Vibrio toxin (also known as cholera toxin) is an
enterotoxin.
 It is produced by Vibrio cholerae.
 It has a 2 chain polypeptide structure
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› The β chain binds to the target cell
› The α chain causes cells to release large amounts of
electrolytes.
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The release of large amounts of electrolytes
causes potentially lethal diarrhea and vomiting.
Toxic shock syndrome is caused by the
enterotoxin from Staphylococcus aureus.
 This condition causes excessive loss of
electrolyte fluids.
 The loss of the fluids leads to hypotensive shock.
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Endotoxins cause the following symptoms:
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Chills
Fever
Aches
Muscle weakness
Large amounts of endotoxins can cause disseminated
intravascular clotting (DIC).
Viral host cell damage is referred to as a
cytopathogenic effect (CPE).
 The cytopathogenic effect of viruses occurs in
three ways:
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› From viral overload
› From cytocidal effects (killing of host cells)
› From noncytocidal effects (damage caused by host
defense)
Viral host cell damage is referred to as a
cytopathogenic effect (CPE).
 The cytopathogenic effect of viruses occurs in
three ways:
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› From viral overload
› From cytocidal effects (killing of host cells)
› From noncytocidal effects (damage caused by host
defense)
© CDC/ Dr. Edwin P. Ewing, Jr.
Microbiology: A Clinical Approach © Garland Science
Microbiology, A clinical Approach -Danielle
Moszyk-Strelkauskas-Garland Science
2010
 Lecture PowerPoints Prescott’s Principles of
Microbiology-Mc Graw Hill Co.
 http://en.wikipedia.org/wiki/Scientific_me
thod
 https://files.kennesaw.edu/faculty/jhendri
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