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About This Presentation

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Slide Content

Microbiology an Introduction
Thirteenth Edition, Global Edition
Chapter 1
The Microbial World and You
Copyright © 2021 Pearson Education Ltd.All Rights Reserved

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The First Observations
•1665: Robert Hooke reported that living things are
composed of “cells”
•The first microbes were observed from 1623 to 1673
by Anton van Leeuwenhoek
–“Animalcules”viewed through magnifying lenses
للاخ نم اهتدهاشم متي ةيناويح تانئاكةربكملا تاسدعلا

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The Golden Age of Microbiology
•1857–1914
•Beginning with Pasteur's work, discoveries included
the relationship between microbes and disease,
immunity, and antimicrobial drugs

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The Golden Age of Microbiology
•Pasteur showed that microbes are responsible for
fermentation
•Fermentationis the microbial conversion of sugar to
alcohol in the absence of air
•Microbial growth is also responsible for spoilage of
food and beverages

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The Germ Theory of Disease
•1876: Robert Koch discovered that a bacterium
causes anthrax and provided the experimental steps,
Koch's postulates,to demonstrate that a specific
microbe causes a specific disease
• فشتكا ببست ايريتكبلا نأ خوك تربور ةثيبخلا ةرمجلا تاوطخلا مدقو
ةيبيرجتلا ، اًضرم ببسي اًنيعم اًبوركيم نأ تابثلإ اًنيعم

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The Birth of Modern Chemotherapy:
Dreams of a “Magic Bullet”
•Treatment of disease with chemicals is called
chemotherapy
•Chemotherapeutic agents used to treat infectious
disease can be synthetic drugs or antibiotics
•Antibioticsare chemicals produced by bacteria and
fungi that inhibit or kill other microbes

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A Fortunate Accident—Antibiotics
•1928: Alexander Fleming discovered the first antibiotic
(by accident)
•Fleming observed that Penicilliumfungus made an
antibiotic, penicillin, that killed S. aureus

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Figure 1.6 The Discovery of Penicillin
Normal
bacterial
colony
Area of
inhibited
bacterial
growth
Penicillium
colony

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Microbes in Our Lives
•Microorganismsare organisms that are too small to
be seen with the unaided eye
•Microbes include bacteria, fungi, protozoa,
microscopic algae, and viruses

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Microbes in Our Lives
•A few are pathogenic(disease-producing) (examples
only 3% of bacteria are pathogenic)
•Decompose organic waste
•Generate oxygen by photosynthesis
•Produce chemical products such as ethanol, acetone,
and vitamins
•Produce fermented foods such as vinegar, cheese,
and bread.

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Nomenclature
•Escherichia coli (E. coli)
–Honors the discoverer, Theodor Escherich
–Describes the bacterium's habitat—the large
intestine, or colon
•Staphylococcus aureus
–Describes the clustered (staphylo-) spherical
(coccus) cells
–Describes the gold-colored (aureus) colonies

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Nomenclature
•After the first use, scientific names may be
abbreviated with the first letter of the genus
(capitalized) and the and full letters of the species
(lower case)
•(Ex: E. coli)
–Escherichia coliand Staphylococcus aureus
are found in the human body
–E. coliis found in the large intestine, and S.
aureusis on skin

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Types of Microorganisms
•Bacteria
•Archaea
•Fungi
•Protozoa
•Algae
•Viruses and other acellularentities (acellularinfectious
agents)
•Multicellular Animal Parasites

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Figure 1.2 Types of Microorganisms
Bacteria
Food
particle
Sporangia
Pseudopod
ZikVNerve cell

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Bacteria
•Prokaryotes
–“Pre nucleus”
•Single-celled
•Peptidoglycan cell walls
•Divide via binary fission
•Derive nutrition from organic or inorganic chemicals or
photosynthesis
•May “swim” by using moving appendages called flagella

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Figure 1.2a Types of Microorganisms
Bacteria

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Archaea
•Are prokaryotes
•Lack peptidoglycan cell walls
–May lack cell wall entirely
•Often live in extreme environments
•Include:
–Extreme halophiles
–Extreme thermophiles
•Generally not known to cause disease in humans

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Fungi
•Eukaryotes
–Distinct nucleus surrounding DNA genetic material
•Chitin cell walls
•Absorb organic chemicals for energy
•Yeasts are unicellular
•Molds and mushrooms are multicellular
–Molds consist of masses of mycelia, which are
composed of filaments called hyphae

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Figure 1.2b Types of Microorganisms
Sporangia

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Protozoa
•Eukaryotes
•Absorb or ingest organic chemicals
•May be motile via pseudopods, cilia, or flagella
•Free-living or parasitic (derive nutrients from a living
host)
–Some are photosynthetic
•Reproduce sexually or asexually

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Figure 1.2c Types of Microorganisms
Pseudopod
Food
particle

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Algae
•Eukaryotes
•Cellulose cell walls
•Found in freshwater, saltwater, and soil
•Use photosynthesis for energy
–Produces oxygen and carbohydrates
•Sexual and asexual reproduction possible

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Figure 1.2d Types of Microorganisms

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Viruses
•Acellular
•Consist of DNA or RNA core
•Core is surrounded by a protein coat (capsid)
•Capsid has same cell wall function
1-isolation, 2-protection, 3-Diffusion, 4-Shaping
–Coat may be enclosed in a lipid envelope
•Are replicated only when they are in a living host cell
–Inert outside living hosts
other a cellular entities (acellularinfectious agents)viroids,
virusoids(satalleties) and prions

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A cellular agents (viruses)

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Figure 1.2e Types of Microorganisms
Nerve cell ZikV

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Multicellular Animal Parasites
•Eukaryotes
•Multicellular animals
•Not strictly microorganisms
•Parasitic flatworms and roundworms are called
helminths
–Some microscopic stages in their life cycles (ex:
ova)

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Which groups of microbes are prokaryotes? Which
are eukaryotes?

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Bacteriology, Mycology, and
Parasitology and virology
•Bacteriologyis the study of bacteria
•Mycologyis the study of fungi
•Parasitologyis the study of protozoa and parasitic
worms

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Microbes and Human Welfare
Learning Objectives
1-15List at least four beneficial activities of
microorganisms.
1-insect pest control by microorganism
2-Sewage treatment
3-Biotechnology and DNA technology
4-Recycling vital elements
5-Commercial Application (synthesis of vitamins ,
enzymes and drugs)

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•Microbes and Human disease
•Infection: is the entry of microbe into the host
•Disease: infection followed by the appearance of signs and
symptoms
•Pathogen:aninfectious or disease agent
•Opportunistic pathogen : is amicrobethat causes disease in
immunocompromised hosts or when the microbiotais altered
like:
•1.AIDS (Aquiredimmune deficiency syndrome)
2.Pneumocytosis pneumonia,themost common
opportunistic infection
3.E.coli. If it moves itself to another site ,it can cause
infection

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Normal Microbiota/Microbiome
•Microbes normally present in and on the human body
are called normal microbiota
–Normal microbiota prevent growth of pathogens
–Normal microbiota produce growth factors such as
vitamins B and K
•Resistanceis the ability of the body to ward off
disease
•Resistance factors include skin, stomach acid, and
antimicrobial chemicals

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Biofilms
•Microbes attach to solid surfaces and grow into
masses
•They will grow on rocks, pipes, teeth, and medical
implants and clog medical devices(catheter)
•Biofilms can cause infections and are often resistant
to antibiotics because the biofilm offer a protective
barrier .

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Figure 1.10 Biofilm on a Piece of
Plastic
Serratialiquefaciens
Capsular material
Plastic

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Emerging infectious diseases (EIDs):
new diseases and old diseases increasing in incidence

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Emerging Infectious Diseases (4 of 7)
Middle East respiratory syndrome (MERS) Caused by Middle East
respiratory syndrome coronavirus (MERS-CoV) Common to SARS
•H1N1 influenza
–Also known as swine flu( (ريزانخلا ازنولفنا
–First detected in the United States in 2009
▪Declared a pandemic, or worldwide large-scale outbreak, by WHO in
2009
•Avian influenza A (H5N1) رويطلا ازنولفنا) )
–Influenza A virus
–Primarily in waterfowl and poultry
–Sustained human-to-human transmission has not yet occurred
•Corona virus COVID 19 SARS-2

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Figure 13.3b Morphology of an
Enveloped Helical Virus
Spikes

Microbiology an Introduction
Thirteenth Edition, Global Edition
Chapter 2
Copyright © 2021 Pearson Education Ltd.All Rights Reserved

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CamScanner

CamScanner

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CompoundLightMicroscope

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.
Immersion oilhas the same index of refraction as
glass slide, preventing light loss from refraction

Instruments of Microscopy:
. Compound Light Microscopy
Total magnification: Obtained by multiplying
objectivelens power by ocularlens power.
(Condenser lenses do not magnify image).
Lens Magnification Ocular Mag.Total Mag.
Scanning 4 X 10 X= 40 X
Low power 10 X 10 X = 100 X
High power 40 X 10 X= 400 X
Oil immersion100X 10 X= 1000 X

2008
•Light objects are
visible against a
dark background.
•Light reflected off
the specimen
enters the
objective lens.
DarkfieldMicroscopy
Figure 3.4a, b
Useful to examine live or
unstained specimens.

2008
•Accentuates diffraction of
the light that passes
through a specimenuses
two beams of light .
•Image: Direct rays and
reflected light rays come
together,
•Permits detailed
examination of internal
structures.
Phase-Contrast Microscopy
Figure 3.4c

2008
•Uses UV light.
•Fluorescent
substances absorb
UV light and emit
visible light.
•Cells may be stained
with fluorescent dyes
(fluorochromes).
Fluorescence Microscopy
Figure 3.6b

Preparation of Specimens for Light
Microscopy
A.Basic dyes:
Chromophoris in positiveions.
Most commonly used dyes.
Bacteria are slightly negatively charged at pH
7, therefore they stain with basic dyes.
Examples:
Crystal violet
Methylene blue
Saffranin
Carbolfuchsin

Preparation of Specimens for Light
Microscopy
B.Acidic dyes:
Color is innegativeions.
Stain the background: negative staining.
Bacteria do not stain with acidic dyes.
Used to observe cell shape, size, and capsules.
Minimal distortion because heat fixing is not
necessary an dye is not taken up by cells.
Examples:
Eosin
Nigrosin
India ink.

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Preparation of Specimens for Microscopy
2. Differential Stains
React differently to different types of bacteria.
Can be used to distinguish among different
groups of bacteria.
There are two important differential stains used
in microbiology:
A. Gram stain
B. Acid-Fast stain

Preparation of Specimens for Microscopy
2. Differential Stains
A. Gram Stain
The most useful staining procedure in medical
microbiology andisa diagnosticprocedure .
Distinguishes bacteria of two large and medically
important groups:
Gram-positive bacteria
Gram-negative bacteria
Provides useful information for disease
treatment.

Gram positive bacteria and
Gram negative bacteria
Gram positive bacteria retain the dye and remain
purplebecause they have asinglethick cellwall
(peptidoglycan)that is not easily penetrated by the
solvent.
Gram negative bacteria do not retain the
Dye . They are decolorizedbecause they havecell
walls with much thinner layers that allow removal
of the dye by the solvent. They are colorless until
counterstained with a red dye .

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Gram -positive and Gram –negative bacteria

Preparation of Specimens for Microscopy
2. Differential Stains
B. Acid-Fast Stain
(Fast here means resistant)
Used to detect tuberculosis and leprosy causing organisms
of the genus Mycobacterium and pathogens of the genus
Nocardia.
These bacteria have waxy cell walls (Mycolic acid),
which makes them difficult to stain. Acid fast stain is an
important differential stain that bind strongly to bacteria
that have a waxy material in their cell walls (Mycolic
acid).
Non acid-fastcells are stained blue.(Methylene blue)
Acid-fastcells remain red. (Carbolfuchsinbasic dye)

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Microbiology an Introduction
Thirteenth Edition, Global Edition
Chapter 3
Prokaryotes structure
Bacteria
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Figure4.1

Procaryotic Cell Structure

Prokaryotic Form and Function

Distinguishing Features of Procaryotic
Cells:
1. DNA is:
Notenclosed within a nuclearmembrane.
A singlecircularchromosome.
2. Lackmembrane-enclosed organelles like mitochondria,
chloroplasts, Golgi, endoplasmic reticulum etc.
3. Cell walls usually contain peptidoglycan,
4. Divide by binaryfission.

The ProcaryoticCell: Size, Shape, and
Arrangement of Bacterial Cells
Cell Size:
Dimensions of mostbacterial cells:
Diameter: 0.2 to 2.0 mm.

The ProcaryoticCell: Size, Shape,
and Arrangement of Bacterial Cells
Bacterial Cell Shapes & Arrangements:
Coccus(plural: cocci): Spherical.
May have the following arrangements:
Diplococci: A pair of attached cocci.
Streptococci: Chainlike arrangement.
Tetrads: Groups of four..
Sarcinae: Groups of eight. Staphylococci:
Grapelike clusters.

Common Arrangements of Cocci

The ProcaryoticCell: Size, Shape,
and Arrangement of Bacterial Cells
Bacterial Cell Shapes & Arrangements:
Bacillusتاّيَصُعلا(plural: bacilli): Rod-shaped.
Most bacilli appear as single rods but may see:
Diplobacilli: ةيصعةجودزمApair of attached
bacilli..
Streptobacilli: Chainlike arrangement.
Coccobacillus: ةَرَّوَكُم ٌتاَّيِوَصَع ؛ Intermediate shape
between coccus and bacillus. Oval rods.

Different Types of Bacilli

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Glycocalyx ةقبطةيملاهةيجراخ
•Coating of molecules external to the cell wall, made of sugars
(polysaccharide )and/or proteins.
-Sticky and gelatinous
•Two types:
1.Slime layer-loosely organized and attached
2.Capsule-highly organized, tightly attached
•Contribute to virulence(degreeof pathogenicity of the pathogen )
–Capsules prevent phagocytosis
–Attachment -formation of biofilms
11

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Glycocalyx
For example:
Only Streptococcus pneumoniaewith capsule cause
pneumonia
UnencapsulatedS. pneumoniae cannot cause
pneumonia and are phagocytized

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Figure 24.11 Streptococcus pneumoniae,
the Cause of Pneumococcal Pneumonia
Capsules

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•Fimbriae
–Fimbriae (singular: fimbria) distributed over the entire surface of the
cell.
–number from a few to several hundred per cell (Figure 4.11).
–Hairlikeappendages that allow for attachment/adherencetoeach
other and to surfaces andas a result involved in forming biofilms
–Therefore the main function of Fimbriae is adherence

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Figure 4.11 Fimbriae

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Fimbriae and Pili (2 of 2)
•Pili(singular: pilus)
–Pili are usually longer than fimbriae and number only
one or two per cell.
–Found mainly in gram negative bacteria
–Involved in motility (common pili )
–Conjugation (sex)piliinvolved in DNA transfer from one
cell to another .

Pili enable conjugation to occur, which is the transfer of DNA
from onebacterial cell toanother.
Fig. 4.8 Three bacteriain the processof conjugating(“threesome”)

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Flagella (singular: flagellum)
•Filamentous appendages external of the cell
•Propel bacteria
•Made of protein flagellin

ProcaryoticCell Structure
I. Structures Externalto the Cell Wall
2. Flagella (Sing. Flagellum):
About half of all known bacteria are motile, most
use flagella.
Long, thin, helical appendages.
A bacterium may have one or several flagella,
which can be in the following arrangements:
Monotrichous: Single polar flagellum at one end.
Amphitrichous: Two polar flagella, one at each end.
Lophotrichous: a bunch of flagella coming from one
pole
Peritrichous: Many flagella over entire cell surface.

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Gram-Positive Cell Walls (1 of 3)
•In gram-positive bacteria, the cell wall consists of:
-Thick peptidoglycan
-Have no Outer membrane

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Figure 4.13b Gram positive Cell Walls

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Gram-Negative Cell Walls (1 of 4)
•In gram-negative bacteria, the cell wall consists of:
•Thin peptidoglycan
•Outer membrane : made of polysaccharides, lipoproteins,
and phospholipids.

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Figure 4.13c Gram-negative Cell
Walls

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Atypical Cell Walls (1 of 2)
•Acid-fast cell walls
–Like gram-positive cell walls
–Contain waxy lipid (mycolic acid) bound to
peptidoglycan .
–Stain with carbolfuchsin
–InMycobacterium ايريتكبةرطفتملاةيلسلا
–InNocardia

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Atypical Cell Walls (2 of 2)
•Mycoplasmas :
•smallest known bacteria that can grow and reproduce out
side living host cells
–Lack cell walls
-Unique plasma membrane contains lipids called
sterols,whichprotect them from osmotic lysis.
•Archaea (Archaebacteria) :
•May lack cell walls.

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Figure 24.7 Mycobacterium
tuberculosis
Corded
growth

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The Cell Wall (2 of 2)
•The major functions of the cell wall:
-Prevents cell from rupturing from too much water (osmotic lysis)
-Responsible for the shape of a bacterium
-Contributes to pathogenicity
•In bacteria, the cell wall is made of peptidoglycan.
-The chemical composition of cell wall is used to
differentiate major types of bacteria
•Site of action of by some antibiotics like pencillin

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Bacterial Internal Structures
•Inclusions in cytoplasm
–Intracellular storage bodies for certain nutrients
–Bacterial cell can use them when environmental
sources are depleted

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Endospores
•Dormant bodies formed within some gram positive bacteria that allows
for their survival in adverse conditions .
•resistant to disinfectants, heat, chemicals, and
radiation
•Bacillus, Clostridium

Microbiology an Introduction
Thirteenth Edition, Global Edition
Chapter 4
Microbial Mechanisms of
Pathogenicity
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How Microorganisms Enter a Host
•Pathogenicity:the ability to cause disease
•Virulence:the degree of pathogenicity
•To cause disease :
-most pathogens must gain access to the host,
-adhereto host tissues,
-penetrate or evade host defenses,
-and damage the host tissues.

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How Microorganisms Enter a Host
•Portals of entry
Thethreemainportalsofentryare:
–Mucous membranes
–Skin
–Parenteral route

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Numbers of Invading Microbes (1 of 3)
ID
50:infectious dose for 50% of a sample (test)
population
–Measures virulence of a microbe
•LD
50:lethal dose for 50% of a sample (test) population
–Measures potency of a toxin

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Numbers of Invading Microbes (2 of 3)
Bacillus anthraciscan cause infection via threedifferent
portals of entry.
Portal of EntryID
50
Skin 10–50 endospores
Inhalation 10,000–20,000 endospores
Ingestion 250,000–1,000,000 endospores

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Numbers of Invading Microbes (3 of 3)
Toxins
Toxins LD
50
Botulinum 0.03 ng/kg
Shiga toxin 250 ng/kg
Staphylococcal enterotoxin1350 ng/kg

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Adherence (adhesion)
Attachment between of microbeto host tissue
requires:
•Adhesins(ligands) on the pathogenbind to
receptorson the host cells
•Adhesinsmay be located on a microbe’s glycocalyx,
pili, fimbriae, and flagella .
•Microbes form biofilms(communities that share
nutrients)

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Figure 15.1 Adherence
Adhesin (ligand)
Pathogen
Host
cell
surface
Surface molecules on a pathogen, called
adhesins or ligands, bind specifically to
complementary surface receptors on cells
of certain host tissues.
E. coli bacteria (yellow) on human
urinary bladder cells
Bacteria (purple) adhering to
human skin
Receptor

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How Bacterial Pathogens Penetrate
Host Defenses
Capsules
•Glycocalyxaround the cell wall
•Impair phagocytosis, e.g. of capsule producing bacteria:
–Streptococcus pneumoniae—pneumonia (يوئر باهتلا)
–Haemophilus influenzae—pneumonia and meningitis (باهتلااياحسلا)
–Bacillus anthracis—anthrax : ةرمجلاةثيبخلا
–Yersinia pestis—plague نوعاط
•The capsule resists the host’s defenses by impairing phagocytosis by WBCs.
تاعافد ةلوسبكلا مواقتفيضملا(لئاعلا )ءاضيبلا مدلا تارك ةطساوب ةمعلبلا ةقاعإ قيرط نع.
•Host can produce antibodies against capsule, which attach to microbe and
allow phagocytosis حمستو بوركيملاب طبترت يتلاو ، ةلوسبكلا دض ةداضم ماسجأ جاتنإ فيضملل نكمي
ةمعلبلاب

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Microbial Mechanisms of Pathogenicity:
How Microorganisms Cause Disease

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Cell Wall Components
•The cell walls of certain bacteria contain chemical
substancesthat contribute to virulence. For
example:
•M proteinresists phagocytosis
–Streptococcus pyogenes
•Opaprotein allows attachment to host cells
–Neisseria gonorrhoeae
•Waxy lipid(mycolic acid) resists digestion
–Mycobacterium tuberculosis

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Enzymes
•Virulence of some bacteria is aided by the production of
extracellular enzymes (exoenzymes) and related
substances.
•These chemicals can digest materials between cells
and form or digest blood clots, among other functions:
Coagulases:coagulate fibrinogen (Blood)
•Kinases:digest fibrin clots
•Hyaluronidase:digests polysaccharides(hyaluronic acid)
that hold cells together
•Collagenase:breaks down collagen
•IgA proteases:destroy IgA antibodies

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Antigenic Variation
•Some pathogens can alter their surface antigens, by a
process called antigenic variation. (e.gN. gonorrhoeae)
•For example, N. gonorrhoeaehas several copies of the
Opaencoding gene, resulting in cells with different
antigens and in cells that express different antigens over
time.

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Biofilms
•Play a role in evading phagocytes
•Biofilm bacteria more resistant to phagocytosis,
shielded by extracellular polymeric substance (EPS)
of biofilm

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How Bacterial Pathogens Damage
Host Cells (1 of 2)
Learning Objectives
15-9Describe the function of siderophores.
15-10Provide an example of direct damage, and
compare this to toxin production.
15-11Contrast the nature and effects of exotoxins and
endotoxins.

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Using the Host’s Nutrients:
Siderophores
•Iron is required for most pathogenic bacteria
Siderophoresare proteins secreted by pathogens that
bind & take iron from host iron-binding proteins

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Figure 15.3 Structure of Enterobactin,
One Type of Bacterial Siderophore

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Direct Damage
•Disrupts host cell function
•Useshost cell nutrients
•Produces waste products
•Multiplies in host cells and causes ruptures

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Production of Toxins
•Toxins:poisonous substances produced by
microorganisms that contribute to pathogenicity
–Produce fever, cardiovascular problems, diarrhea,
and shock
•Toxigenicity:ability of a microorganism to produce a
toxin
•Toxemia:presence of toxin in the host’s blood

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Exotoxins (1 of 6)
•Proteins produced and secreted by bacteria
–Soluble in body fluids; destroy host cells and inhibit
metabolic functions
•Antitoxins:antibodies against specific exotoxins
•Toxoids:inactivated exotoxins used in vaccines

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FOUNDATION Figure 15.4 Mechanisms of Exotoxins and
Endotoxins(1 of 2)
Proteinsproducedinsidepathogenicbacteria,most
commonlygram-positivebacteria,aspartoftheirgrowth
andmetabolism.Theexotoxinsarethensecretedintothe
surroundingmediumduringlogphase.
Cell wall
Exotoxins: toxic substances
released outside the cell
Clostridium botulinum, an
example of a gram-positive
bacteriumthat produces
exotoxins (A-B).

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Exotoxins(2 of 6)
•Exotoxins are divided into three principal typeson the
basis of their structure and function:
(1) A-B toxins,
(2) membrane-disrupting toxins
(3) superantigens.
•A-B toxinscontain an enzyme component (A part)
and a binding component (B part), e.g. Diphtheria
toxin. A-B toxin is Genotoxins, which damage DNA
(causing mutations, disrupting cell division, and
leading to cancer)

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The Action of an A-B Exotoxin

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Exotoxins (3 of 6)
•Membrane-disrupting toxinslyse host cells by
disrupting plasma membranes
–Leukocidins—kill phagocytic leukocytes
–Hemolysins—kill erythrocytesby forming protein
channels
–Streptolysins—hemolysinsproduced by
streptococci

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Exotoxins (4 of 6)
•Superantigenscause an intense immune response
due to release of cytokines from host cells (T cells)
–Cause symptoms of fever, nausea, vomiting,
diarrhea, shock, and death
–E.g.Food poisoning caused by staphylococcus
aureus causes diarrhea .

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Endotoxins(5 of 6)
•Lipid Aportion of lipopolysaccharides (LPS) of
gram-negative bacteria
•Released during bacterial multiplication and
when gram-negative bacteria die
–Stimulate macrophages to release cytokines
–All endotoxins produce the same signs and
symptoms: chills, fever, weakness, aches,
and, in some cases,shock and even death.

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FOUNDATION
Figure 15.4
Mechanisms of
Exotoxins and
Endotoxins(2 of 2)
Lipidportionsoflipopolysaccharides(LPS)
thatarepartoftheoutermembraneofthecell
wallofgram-negativebacteria(lipidA).The
endotoxinsareliberatedwhenthebacteriadie
andthecellwalllyses,orbreaksapart.
Salmonella
typhimurium, an
example of a gram-
negative bacterium that
produces endotoxins
Endotoxins: toxins
composed of lipids
that are part of the
cell wall

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Exotoxins versus Endotoxins

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Figure 15.6 Endotoxins and the
Pyrogenic Response
A macrophage ingests a
gram-negative bacterium.
The bacterium is degraded
in a vacuole, releasing
endotoxins that induce the
macrophage to produce
cytokines, interleukin-1
(IL-1), and tumor necrosis
factor alpha (TNF-α(.
The cytokines are
released into the blood-
stream by the macrophages,
through which they travel to the
hypothalamus, the temperature
control center of the brain.
The cytokines induce the
hypothalamus to produce
prostaglandins, which reset
the body's "thermostat" to a
higher temperature, producing
fever.
Nucleus
Macrophage
Endotoxin
Bacterium
Endotoxin
Cytokines
Vacuole
Blood
vessel
Hypothalamus of brain
Prostaglandin
Pituitary
gland
Fever

2008
Exotoxin
Source Mostly Gram +
Metabolic product By-products of growing cell
Chemistry Protein usually with two parts (A-B)
Fever No
Neutralized by antitoxin Yes
LD
50 Small

2008
Endotoxins
Source Gram–bacteria
Metabolic product
Present in LPS of outer membrane of cell
wall
Chemistry
Lipid portion (lipid A) of LPS of outer
membrane
Fever Yes
Neutralized by antitoxin No
Lethal dose (LD
50 Considerably larger

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Pathogenic Properties of Viruses
(1 of 3)
Learning Objective
15-15List seven cytopathic effects of viral infections.

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Pathogenic Properties of Viruses
(2 of 3)
•Cytopathic effects (CPE)are visible effects of viral
infection on a cell
–Stopping cell synthesis
–Causing cell lysosomes to release enzymes
–Changing host cell function or inducing chromosomal
changes
–Inducing antigenic changes on the cell surface
–Loss of contact inhibitionin the cell, leading to cancer

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Pathogenic Properties of Viruses
•Alpha and beta interferons
–Produced by virally-infected cells
–Protect neighboring cells from viral infection
Inhibit synthesis of viral proteins and host cell
proteins
Kill virus-infected host cells.

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Figure 15.8 Human Fibroblasts are Transformed by Rous Sarcoma
Virus
Rounded up
fibroblast

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Pathogenic Properties of Fungi,
Protozoa, Helminths, and Algae
Learning Objective
15-16Discuss the causes of symptoms in fungal,
protozoan, helminthic, and algal diseases.

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Pathogenic Properties of Fungi
virulence factors
•Somefungiproduce
-Toxic metabolic products
-Provoke an allergic response
-Trichothecenetoxins, which inhibit protein synthesis
-Capsulesthat prevent phagocytosis

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Fungi (2 of 2)
-Ergot, which are alkaloid toxins that cause hallucinations
•Aflatoxin, which is a carcinogenic toxin produced by
Aspergillus
•Mycotoxins, whcihare produced by mushrooms and are
neurotoxic, e.g. Phalloidinand amanitin

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Protozoa
•Presence of protozoa and their waste products
causes symptoms
•Protozoa avoid host defenses by:
–Digesting cells and tissue fluids
–Growing in phagocytes
–Antigenic variation

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Helminths
•The presence of helminthsalso often produces
disease symptoms in a host:
-Use host tissue for growth
-Produce large masses; cause cellular damage
-Produce waste products that cause symptoms

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Algae
•A few species of algae produce neurotoxins, e.g. the
toxin saxitoxin

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Portals of Exit (2 of 2)
•Respiratory tract
–Coughing and sneezing
•Gastrointestinal tract
–Feces and saliva
•Genitourinary tract
–Urine; secretions from the penis and vagina
•Skin
•Blood
–Arthropods that bite; needles or syringes

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When the balance between host and microbe tips in favor of the microbe, an
infection or disease results. Learning these mechanisms of microbial
pathogenicity is fundamental to understanding how pathogens are able to
overcome the host's defenses.
H1N1 flu virus
Mucous membranes
• Respiratory tract
• Gastrointestinal tract
• Genitourinary tract
• Conjunctiva
Skin
Parenteral route
Capsules
Cell wall components
Enzymes
Antigenic variation
Invasins
Intracellular growth
Siderophores
Direct damage
Toxins
• Exotoxins
• Endotoxins
Lysogenic conversion
Cytopathiceffects
Generally the same as
the portals of entry for a
given microbe:
• Mucous membranes
• Skin
• Parenteral route
Number of
invading microbes
Adherence
Clostridium
tetani
Mycobacterium
intracellulare
•Several factors are required for a microbe to cause disease.
•After entering the host, most pathogens adhere to host tissue,
penetrate or evade host defenses, and damage host tissues.
•Pathogens usually leave the body via specific portals of exit, which
are generally the same sites where they entered initially.
KEYCONCEPTS
portals of entry
penetration
or evasion of
host defenses portals of exit
damage to host
cells
FOUNDATION Figure 15.9 Microbial
Mechanisms of Pathogenicity