PowerPoint Lecture
Presentations prepared by
John Zamora
Middle Tennessee State
University
CHAPTER 23
Microbial
Interactions
with Humans
Pearson Education Limited 2015
I. Normal Human-Microbial Interactions
23.1 Beneficial HumanMicrobial Interactions
23.2 Microflora of the Skin
23.3 Microflora of the Oral Cavity
23.4 Microflora of the Gastrointestinal Tract
23.5 Microflora of Mucosal Tissues
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23.1 Beneficial HumanMicrobial Interactions
Most microorganisms are benign
Few contribute to health, and fewer pose direct threats
to health
Normal microbial flora
Microorganisms usually found associated with human
body tissue
Humans are colonized by microorganisms at birth
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23.1 Beneficial HumanMicrobial Interactions
Pathogens
Microbial parasites
Pathogenicity
The ability of a parasite to inflict damage on the host
Virulence
Measure of pathogenicity
Opportunistic pathogen
Causes disease only in the absence of normal host
resistance
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23.1 Beneficial HumanMicrobial Interactions
Infection
Situation in which a microorganism is established and
growing in a host, whether or not the host is harmed
Disease
Damage or injury to the host that impairs host function
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23.1 Beneficial HumanMicrobial Interactions
Animals provide a favorable environment for the
growth of many microorganisms
Infections frequently begin at sites in the animal's
mucous membranes (Figure 23.1)
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Mucus Colonization
Microbial
cells
Epithelial
cell
2015 Pearson Education, Inc. Figure 23.1
23.2 Microflora of the Skin
The skin surface varies greatly in chemical composition
and moisture content
Three microenvironments
Dry skin
Moist skin
Sebaceous skin
Skin microflora examined by molecular ecology methods
19 phyla detected
Each microenvironment shows a unique microbiota
(Figure 23.2)
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Others 1%
Bacteroidetes
6.3%
Gram
negative
Proteobacteria
16.5%
Actinobacteria
51.8%
Other
Firmicutes Flavobacteriales
24.4%
Betaproteobacteria
Gram Corynebacteria
positive Staphylococci
Propionibacteria
2015 Pearson Education, Inc. Figure 23.2
23.2 Microflora of the Skin
The skin microflora
Composition is influenced by:
Environmental factors (e.g., weather)
Host factors (e.g., age, personal hygiene)
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23.3 Microflora of the Oral Cavity
The oral cavity is a complex, heterogeneous
microbial habitat
Saliva contains antimicrobial enzymes
But high concentrations of nutrients near surfaces in the
mouth promote localized microbial growth
The tooth consists of a mineral matrix (enamel)
surrounding living tissue (dentin and pulp;
Figure 23.3)
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Enamel
Dentin
Crown
Gingival crevice
Pulp
Gingiva
Alveolar bone
Periodontal
membrane Root
Bone
marrow
2015 Pearson Education, Inc. Figure 23.3
23.3 Microflora of the Oral Cavity
Bacteria colonize tooth surfaces by first attaching
to acidic glycoproteins deposited there by saliva
(Figure 23.4)
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2015 Pearson Education, Inc. Figure 23.4
23.3 Normal Microflora of the Oral Cavity
Metagenomic analysis of human microflora shows
a complex microbial community
Most microorganisms are facultatively aerobic
Some are obligately anaerobic
Some are obligately aerobic
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23.4 Microflora of the Gastrointestinal Tract
The human gastrointestinal (GI) tract (Figure 23.5)
Consists of stomach, small intestine, and large intestine
Responsible for digestion of food, absorption of
nutrients, and production of nutrients by the indigenous
microbial flora
Contains 1013 to 1014 microbial cells
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Esophagus
Major bacteria present Organ Major physiological processes
Prevotella Esophagus
Streptococcus
Veillonella
Helicobacter Secretion of acid (HCI)
Stomach Digestion of macromolecules
Proteobacteria
Bacteroidetes pH 2
Actinobacteria
Fusobacteria
Duodenum
Enterococci Continued digestion
Lactobacilli Jejunum Small Absorption of monosaccharides,
intestine amino acids, fatty acids, water
Bacteroides pH 45
Bifidobacterium
Clostridium IIeum
Enterobacteria
Enterococcus
Escherichia
Eubacterium Absorption of bile acids,
Colon Large
Klebsiella vitamin B12
intestine
Lactobacillus pH 7
Methanobrevibacter
(Archaea)
Peptococcus
Peptostreptococcus
Proteus
Ruminococcus Anus
Staphylococcus
Streptococcus
2015 Pearson Education, Inc. Figure 23.5
23.4 Microflora of the Gastrointestinal Tract
Microbial populations in different areas of the GI
tract are influenced by diet and the physical
conditions in the area
The acidity of the stomach and the duodenum of
the small intestine (~pH 2) prevents many
organisms from colonizing the GI tract
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23.4 Microflora of the Gastrointestinal Tract
Functions and products of intestinal flora
Intestinal microorganisms carry out a variety of essential
metabolic reactions that produce various compounds
The type and amount produced are influenced by the
composition of the intestinal flora and the diet
Compounds produced include:
Vitamins
Gas, organic acids, and odor
Enzymes
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23.5 Microflora of Mucosal Tissues
A restricted group of organisms colonizes the
upper respiratory tract (Figure 23.7)
Examples: staphylococci, streptococci, diphtheroid
bacilli, and gram-negative cocci
The lower respiratory tract lacks microflora in
healthy individuals
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Sinuses
Nasopharynx
Upper
respiratory Pharynx
tract
Oral cavity
Larynx
Trachea
Lower
respiratory Bronchi
tract
Lungs
2015 Pearson Education, Inc. Figure 23.7
23.5 Microflora of Mucosal Tissues
Urogenital tract (Figure 23.8a)
The bladder is typically sterile in both males and
females
Altered conditions (such as change in pH) can cause
potential pathogens in the urethra (such as Escherichia
coli and Proteus mirabilis) to multiply and become
pathogenic
E. coli and P. mirabilis frequently cause urinary tract
infections in women
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Female Male
Bladder
Ovary
Uterus
Cervix Prostate
Bladder
Pubis Rectum
Urethra
Pubis
Rectum
Urethra
Penis
Vagina Testis
2015 Pearson Education, Inc. Figure 23.8a
23.5 Microflora of Mucosal Tissues
The vagina of the adult female is weakly acidic
and contains significant amounts of glycogen
Lactobacillus acidophilus, a resident organism in the
vagina, ferments the glycogen, producing lactic acid
(Figure 23.8b)
Lactic acid maintains a local acidic environment
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2015 Pearson Education, Inc. Figure 23.8b
II. Pathogenesis
23.6 Pathogenicity and Virulence
23.7 Adherence
23.8 Invasion, Infection, and Virulence Factors
23.9 Exotoxins
23.10 Endotoxins
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23.6 Pathogenicity and Virulence
Pathogens use various strategies to establish
virulence (Figure 23.9)
Virulence is the relative ability of a pathogen to
cause disease
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2015 Pearson Education, Inc. Figure 23.9
23.6 Pathogenicity and Virulence
Measuring virulence
Virulence can be estimated from experimental studies of
the LD50 (lethal dose50)
The amount of an agent that kills 50% of the animals in a
test group (Figure 23.10)
Highly virulent pathogens show little difference in the
number of cells required to kill 100% of the population
as compared to 50% of the population
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2015 Pearson Education, Inc. Figure 23.10
23.6 Pathogenicity and Virulence
Attenuation
The decrease or loss of virulence
Toxicity
Organism causes disease by means of a toxin that
inhibits host cell function or kills host cells
Toxins can travel to sites within host not inhabited by
pathogen
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23.6 Pathogenicity and Virulence
Invasiveness
Ability of a pathogen to grow in host tissue at densities
that inhibit host function
Can cause damage without producing a toxin
Many pathogens use a combination of toxins,
invasiveness, and other virulence factors to
enhance pathogenicity
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23.7 Adherence
Bacteria and viruses that initiate infection often
adhere specifically to epithelial cells through
interactions between molecules on the surfaces of
the pathogen and the host cell (Figure 23.12)
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2015 Pearson Education, Inc. Figure 23.12
23.7 Adherence
Bacterial adherence can be facilitated by
Extracellular macromolecules that are not covalently
attached to the bacterial cell surface
Examples: slime layer, capsule (Figure 23.13)
Fimbriae and pili (Figure 23.14)
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2015 Pearson Education, Inc. Figure 23.13
2015 Pearson Education, Inc. Figure 23.14
23.8 Invasion, Infection, and Virulence Factors
The initial inoculum of a pathogen is insufficient to
cause host damage
The pathogen must multiply and colonize the
tissue
The availability of nutrients is most important in
affecting pathogen growth
Pathogens may grow locally at the site of invasion
or may spread throughout the body
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23.8 Invasion, Infection, and Virulence Factors
Bacteremia: the presence of bacteria in the
bloodstream
Septicemia: bloodborne systemic infection
May lead to massive inflammation, septic shock, and
death
Infection: any situation in which a microorganism
(not a member of the local flora) is established and
growing in a host
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23.8 Invasion, Infection, and Virulence Factors
Infection requires attachment to surface as well as
growth
Attachment and growth have been well studied in
the formation of biofilms on tooth surfaces
Acidic glycoproteins from saliva form a thin film
Streptococci colonize the film
Streptococcus sobrinus and Streptococcus mutans are
common agents in tooth decay (Figure 23.15)
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Dextran
Cells
2015 Pearson Education, Inc. Figure 23.15
23.8 Invasion, Infection, and Virulence Factors
Extensive growth of oral microorganisms, especially
streptococci, results in a thick bacterial layer (dental
plaque; Figure 23.16)
As plaque continues to develop, anaerobic bacterial
species begin to grow
As dental plaque accumulates, the microorganisms
produce high concentrations of acid, resulting in
decalcification of the tooth enamel (dental caries)
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2015 Pearson Education, Inc. Figure 23.16
23.8 Invasion, Infection, and Virulence Factors
Pathogens produce enzymes that:
Enhance virulence by breaking down or altering host
tissue to provide access to nutrients
Example: hyaluronidase
Protect the pathogen by interfering with normal host
defense mechanisms
Example: coagulase
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23.8 Invasion, Infection, and Virulence Factors
Salmonella species encode a large number of
virulence factors (Figure 23.17)
Several genes that direct invasion are clustered
together on the chromosome as pathogenicity islands
Another Salmonella pathogenicity island contains genes
that promote a more systemic disease
Salmonella also contains resistance plasmids (R
plasmids)
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Enterotoxin
(diarrhea) Siderophores
Injectisome (iron uptake)
(inv and prg
products form Type fimbriae
complex) (adherence)
Endotoxin in
LPS layer Virulence
plasmid
(fever) SP2
SP1
Anti-
phagocytic
proteins
induced Cytotoxin
by oxyR (inhibits host cell protein
synthesis; Ca2+ efflux
O antigen from host cell; adherence)
(inhibits Vi capsule antigen;
phagocyte inhibits complement binding
killing) Pathogenicity
islands on Flagellum (motility)
chromosome H antigen (adherence;
inhibits phagocyte killing)
2015 Pearson Education, Inc. Figure 23.17
23.9 Exotoxins
Exotoxins
Proteins released from the pathogen cell as it grows
Three categories
Cytotoxins
AB toxins
Superantigen toxins
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23.9 Exotoxins
Cytotoxins (cytolytic toxins)
Work by degrading cytoplasmic membrane integrity,
causing cell lysis and death
Toxins that lyse red blood cells are called hemolysins
(Figure 23.18)
Staphylococcal -toxin kills nucleated cells and lyses
erythrocytes (Figure 23.19)
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2015 Pearson Education, Inc. Figure 23.18
RCSB PDB 3ANZ
Efflux of
cytoplasmic
components
Out
Cytoplasmic In
membrane -Toxin pore
Influx of
extracellular
components
2015 Pearson Education, Inc. Figure 23.19
23.9 Exotoxins
AB toxins
Consist of two subunits, A and B
Work by binding to host cell receptor (B subunit) and
transferring damaging agent (A subunit) across the cell
membrane (Figure 23.20)
Examples: diphtheria toxin, tetanus toxin, botulinum toxin
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Cytoplasmic membrane Diphtheria toxin Out
A B A B
A Receptor protein In
A
EF-2 EF-2*
Amino
acid
A T
A T G
Ribosome
Normal protein synthesis Protein synthesis stops
2015 Pearson Education, Inc. Figure 23.20
Diphtheria and Cholera Toxins
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23.9 Exotoxins
Clostridium tetani and Clostridium botulinum
produce potent AB exotoxins that affect nervous
tissue
Botulinum toxin consists of several related AB
toxins that are the most potent biological toxins
known (Figure 23.21); tetanus toxin is also an AB
protein neurotoxin (Figure 23.22)
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Excitation signals
from the central
nervous system
A A AA AA AA A
AA AA A A AA A A A AA
A A A A
A A
A A A A A A A
A
A A A
A A
Muscle
Normal Botulism
Acetylcholine (A) induces contraction Botulinum toxin, , blocks release of A,
of muscle fibers inhibiting contraction
2015 Pearson Education, Inc. Figure 23.21
Inhibitory
GG
interneuron G
GG G G
GG
G GG G
Inhibition GG
G GG
GG
GG Excitation signals
G from the central Tetanus
nervous system toxin
A AA
AA AA AA A AA
A A AA AA AA
A A A A A
A A A
A
A A A A
A A A A
A A A
Muscle
Normal Tetanus
Glycine (G) release from inhibitory interneurons Tetanus toxin binds to inhibitory interneurons,
stops acetylcholine (A) release and allows preventing release of glycine (G) and relaxation
relaxation of muscle of muscle
2015 Pearson Education, Inc. Figure 23.22
23.9 Exotoxins
Enterotoxins
Exotoxins whose activity affects the small intestine
Generally cause massive secretion of fluid into the
intestinal lumen, resulting in vomiting and diarrhea
Example: cholera toxin (Figure 23.23)
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1. Normal ion movement, Na+ from lumen to blood, 4. Na+ movement blocked, net Cl movement to lumen
no net Cl movement
Blood Intestinal Lumen of
epithelial small intestine
cells
GM1
5. Massive water movement to the lumen; cholera symptoms
2. Infection and toxin production by V. cholerae
Cholera
toxin
AB form
GM1
Vibrio
cholerae
B A cell
3. Activation of epithelial adenylate cyclase by cholera toxin
A subunits
Cholera
toxin B
Adenylate cyclase subunit
ATP Cyclic
AMP
2015 Pearson Education, Inc. Figure 23.23
23.10 Endotoxins
Endotoxin
The lipopolysaccharide portion of the cell envelope of
certain gram-negative Bacteria, which is a toxin when
solubilized
Generally less toxic than exotoxins
Presence of endotoxin can be detected by the Limulus
amoebocyte lysate (LAL) assay (Figure 23.24)
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2015 Pearson Education, Inc. Figure 23.24
III. Host Factors in Infection and Disease
23.11 Innate Resistance to Infection
23.12 Risk Factors for Infection
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23.11 Innate Resistance to Infection
Hosts have innate resistance to most pathogens
(Figure 23.25)
Natural host resistance
Tissue specificity
Physical and chemical barriers
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Lysozyme in
tears and other
secretions
dissolves cell
Removal of particles
walls
including microorganisms Mucus and cilia
by cilia in nasopharynx lining trachea
suspend and
move micro-
Skin is a physical organisms out of
barrier and produces the body
antimicrobial fatty Mucus,
acids and anti- antibacterial
bacterial peptides. peptides, and
Normal flora phagocytes in
inhibit infection lungs prevent
infection
Stomach acidity
Blood and
(pH 2) inhibits lymph
microbial growth proteins inhibit
microbial
growth
Normal flora Rapid pH
compete with change
pathogens in inhibits
the gut and microbial
on the skin growth
Epithelial
cells
throughout
the body
have tight
junctions
that
Flushing of urinary inhibit
tract prevents pathogen
infection invasion and
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infection
Figure 23.25
23.12 Risk Factors for Infection
Compromised host
One or more resistance mechanisms are inactive
The probability of infection is increased
Age is an important factor
Very young and very old individuals are more susceptible
Stress can predispose a healthy individual to disease
Diet plays a role in host susceptibility to infection
Certain genetic conditions can compromise a host
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