Lecture chapter 05

ISBN: 978-0-8153-6514-3Microbiology: A Clinical Approach, by Tony Srelkauskas © Garland ScienceMicrobiology: A Clinical Approach (2nd
Edition) © Garland Science
CHAPTER 5
REQUIREMENTS FOR INFECTION

WHY IS THIS IMPORTANT?
 This chapter introduces you to the mechanisms
involved in the infectious disease process
 Understanding the requirements necessary for
infection is critical to understanding treatment
 Four of the five requirements for infection will
be discussed in this chapter

OVERVIEW

REQUIREMENTS FOR A
SUCCESSFUL INFECTION
 Entry–getting in
 Establishment–staying in
 Defeat the host defenses
 Damage the host
 Exit the host and be transmitted to another host

VIRULENCE FACTORS
 Pathogens use virulence factors for the
infection process
 They allow pathogens to survive and thrive in the
host
 They make harmless organisms dangerous and
make dangerous organisms more dangerous

PORTALS OF ENTRY
(GETTING IN)
 Any point at which pathogens can enter is
called a portal of entry
 There are three categories of portals of entry:
 Mucous membranes
 Skin
 Parenteral routes

PORTALS OF ENTRY
(GETTING IN)

MUCOUS MEMBRANES
 Mucous membranes are in direct contact with
the external environment
 They allow pathogens to gain access into the
body
 They are found in the:
 Respiratory tract
 Gastrointestinal tract
 Genitourinary tract

THE RESPIRATORY 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

THE RESPIRATORY TRACT
 Pathogens using the respiratory tract include:
 Viruses that cause common cold
 Bacteria and viruses that cause pneumonia
 Mycobacterium tuberculosis
 Influenza virus
 Measles virus
 Smallpox virus

THE GASTROINTESTINAL
TRACT
 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

THE GASTROINTESTINAL TRACT
 Pathogens using the gastrointestinal tract
include:
 Salmonella species
 Shigella species
 Escherichia coli
 Vibrio cholerae
 Hepatitis A virus
 Giardia

 The gastrointestinal tract is also an important
portal of exit
 Pathogens can be found in fecal material after
leaving the body
 The fecal-oral route of contamination is very
important in the infection process

 Helicobacter pylori infects the stomach and
duodenum of the small intestine
 It survives the acidic environment of the
stomach by producing an alkaline halo around
itself
 It takes up residence in the mucus that lines
the stomach and duodenum
 Infection with H. pylori is a known risk factor
for stomach and duodenal ulcers

THE GENITOURINARY TRACT
 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

THE GENITOURINARY TRACT
 Pathogens using the genitourinary tract
include:
 Proteus mirabilis
 Chlamydia trachomatis
 Herpes simplex virus
 HIV

SKIN
 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

THE PARENTERAL ROUTE
 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

ESTABLISHMENT
(STAYING IN)
 After entry into the host, pathogens must find
a way to stay in the body
 Pathogens use structures, such as capsules or
fimbriae to attach to the surface of cells or
tissues

ESTABLISHMENT
(STAYING IN)
© Professors P. Motta & F. Carpino / University "La Sapienza", Rome / Science Photo Library

ESTABLISHMENT
(STAYING IN)
© Professor P.M. Motta / University "La Sapienza", Rome / Science Photo Library

ESTABLISHMENT
(STAYING IN)
© Professor P.M. Motta Et Al / Science Photo Library

ESTABLISHMENT
(STAYING IN)
 Pathogens can use adhesins (surface proteins)
to adhere to tissue
 An example of adherence is the plaque found
on teeth
 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

ESTABLISHMENT
(STAYING IN)
Spirochetes like
Treponema
pallidum (the
causative agent of
syphilis)
corkscrew into
tissues.
© CDC/ Dr. David Cox

INCREASING THE NUMBERS
 Increasing the number of pathogens can
establish the infection in the host
 Rapid growth and increased numbers of
pathogens can happen very quickly
 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 1021
organisms in just 24 hours

 Some pathogens are more virulent than others
– fewer pathogens are needed for a successful
infection
 We use the terms ID50 and LD50 to characterize
these differences between pathogens

 ID50 = infectious dose 50%
 The number of organisms required for 50% of the
host population to show signs of infection
 LD50 = lethal dose 50%
 The number of organisms required to kill 50% of a
host population

 Binary fission is the form of reproduction seen
in most bacteria
 One cell divides to yield two
 Two divide to become four and so on
 The number of bacteria can increase very quickly

 In viral infections, the number of viruses
increases even more dramatically
 Virally infected cells will lyse and this releases
millions of viral particles
 Each particle can infect a new cell
 Each newly infected cell will produce millions of
viral particles

DEFEATING THE HOST’S
DEFENSES
 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 two
ways:
 Passive defense – using built-in structures found
on the pathogen cell
 Active defense – attacking the host defenses

PASSIVE PROTECTION
STRATEGIES: Capsules
The main passive protection strategy is the bacterial
capsule which inhibits phagocytosis by host cells.

PASSIVE PROTECTION
STRATEGIES: Cell Walls
 Another passive protection strategy is through
components of the bacterial cell wall
 M proteins are found in the cell wall of
streptococcal organisms

They increase virulence by increasing adherence to host
cells

They can also inhibit phagocytosis

PASSIVE PROTECTION
STRATEGIES: Cell Walls
 Another passive protection strategy 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

ACTIVE PROTECTION
STRATEGIES: Enzymes
 Active bacterial protection strategies 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

EXAMPLES OF BACTERIAL
PROTECTIVE ENZYMES
 Leukocidins – destroy white blood cells
 Hemolysins – attack red and white blood cells
 Coagulase – causes the formation of fibrin clots
 Kinases – break down fibrin and destroy clots
 Hyaluronidase and collagenase – break down
connective tissue and collagen

EXAMPLES OF BACTERIAL
PROTECTIVE ENZYMES

HIDING FROM THE HOST
DEFENSE
 Pathogens can also hide in order to defend
themselves
 Getting inside a host cell can protect the pathogen
from the host immune defense:
 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

DAMAGING THE HOST
 Most of the damage to a host can be divided
into two causes:
 Damage that occurs because pathogens are present
and active
 Damage that occurs because of host defense
mechanisms

DAMAGING THE HOST
 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

BACTERIAL TOXINS
 Bacterial toxins are:
 Very poisonous
 Soluble in aqueous solutions
 Easily diffusible into blood and lymph which
causes distal pathology

BACTERIAL TOXINS
 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 two types of toxins:
 Exotoxins
 Endotoxins

EXOTOXINS
 Exotoxins are are specific to a certain
pathogen and secreted by the pathogen and can
then even enter host cells
 They are among the most lethal substances
known
 They are usually an enzymatic protein soluble
in the blood and lymphatic system

EXOTOXINS
 Exotoxins rapidly diffuse into tissues where
they inhibit metabolic function
 They are usually produced as pro-enzymes
 Many genes that code for toxins are carried on
prophages or plasmids

EXOTOXINS

EXOTOXINS
 There are three types of exotoxins:
 Cytotoxins – kill cells
 Neurotoxins – interfere with neurological signaling
 Enterotoxins – affect the lining of the digestive
system

EXOTOXINS:
Anthrax Toxin
 Anthrax toxin is a cytotoxin
 It is produced by Bacillus anthracis (a Gram-
positive rod commonly found in soil of pastures)
 It is made up of three parts which are:
 Produced separately within the pathogen
 Assembled outside the anthrax organism cell wall
 It interrupts signaling capability of host
macrophages and dendritic cells

EXOTOXINS:
Diphtheria Toxin
 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

EXOTOXINS:
Diphtheria Toxin
 The structure of diphtheria toxin is well
studied and composed of two chains called
A and B
 The B chain binds to the target cell and
facilitates the entry of the A chain
 The A chain causes inhibition of protein
synthesis

EXOTOXINS:
Botulinum Toxin
 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

EXOTOXINS:
Tetanus Toxin
 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
 Lockjaw is an early symptom

EXOTOXINS:
Cholera Toxin
 Cholera toxin is an enterotoxin
 It is produced by Vibrio cholerae
 It has a two chain polypeptide structure
 The B chain binds to the target cell
 The A chain causes cells to release large amounts
of electrolytes
 The release of large amounts of electrolytes
causes potentially lethal diarrhea and vomiting

EXOTOXINS:
S. aureus Toxin
 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

ENDOTOXINS
 The damage to the host caused by endotoxins
is very different from the damage caused by
exotoxins
 Endotoxins are part of Gram-negative cell
walls and are released on the death of the
bacterium
 Lipopolysaccharides contain a particular lipid
called lipid A, which has endotoxin properties

ENDOTOXINS

EXOTOXINS AND ENDOTOXINS

ENDOTOXINS
 Endotoxins cause the following symptoms:
 Chills
 Fever
 Aches
 Muscle weakness
 Large amounts of endotoxins can cause
disseminated intravascular coagulation (DIC)

ENDOTOXINS
 Exotoxins can elicit an immune response
 Endotoxins do not elicit an immune response
 Endotoxins can contaminate materials and
equipment
 There are tests for endotoxin contamination

VIRAL PATHOGENIC EFFECTS
 Viral host cell damage is referred to as a
cytopathogenic effect (CPE)
 The cytopathogenic effect of viruses occurs in
three ways:
 From viral overload
 From cytocidal effects (killing of host cells)
 From non-cytocidal effects (damage caused by
host defense)

 Viral cytopathology can be seen
microscopically
 Viral inclusions such as Negri bodies can be seen
in rabies infections
 Syncytia (giant cells) can be present

Lecture chapter 05

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Lecture chapter 05

Similar to Lecture chapter 05 (20)

More from kevperrino

More from kevperrino (20)

Recently uploaded

Recently uploaded (20)

Lecture chapter 05