9ch28 Lecture

Brock Biology of Microorganisms
Twelfth Edition
Madigan / Martinko Dunlap / Clark
Chapter 28
Microbial Interactions with Humans
Lectures by Buchan & LeCleir
Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings
I. Beneficial Microbial Interactions with Humans

28.1 Overview of Human-Microbial Interactions 28.2 Normal Microbial Flora of the Skin 28.3 Normal Microbial Flora of the Oral Cavity 28.4 Normal Microbial Flora of the Gastrointestinal
Tract
28.5 Normal Microbial Flora of Other Body Regions
Normal Flora???
Microbes
Preferred terminology is normal colonizing microbes
28.1 Overview of Human-Microbial Interactions
Most microbes are benign

A few contribute directly to human health and even fewer pose direct threats to health
Normal Colonizing Microbes

Microbes usually found associated with human body tissue
Humans are colonized by microbes at birth
Where are we normally colonized?

Skin Oropharnyx/Upper respiratory tract
Gastrointestinal tract
Urogenital tract
Representative Genera in the Normal Human Flora
Representative Genera in the Normal Human Flora

Pathogens
Microbial parasites
Pathogenicity
The ability of a parasite to inflict damage on the host
Virulence
The quantitative measure of pathogenicity
Opportunistic Pathogen
Causes disease only in the absence of normal host
resistance
Infection
Situation in which a microbe is established and growing in a host, whether or not the host is harmed The connotation of infection is synonymous w/ disease
Disease
Damage or injury to the host that impairs host function
Animals provide a favorable environment for the growth of many microbes Infections frequently begin at sites in the animals mucous membranes
Bacterial Interactions with Mucous Membranes
Figure 28.1
28.2 Normal Microbial Flora of the Skin

The skin is generally a dry, acid environment that does
not support the growth of most microbes

Most areas (e.g., sweat glands) are readily colonized by gram-positive bacteria and other normal flora of the skin
The Human Skin
Figure 28.2
28.2 Normal Microbial Flora of the Skin
The Skin Microflora

Composition is influenced by
Environmental factors (e.g., weather/moisture) Host factors (e.g., age, personal hygiene)
28.3 Normal Microbial Flora 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)
Section Through a Tooth
Figure 28.3
Bacteria colonize tooth surfaces by first attaching to acidic glycoproteins deposited there by saliva
Microcolonies of Bacteria Growing on Model Tooth Surface
Figure 28.4a
Microcolonies of Bacteria
Figure 28.4b

Extensive growth of oral microbes, especially streptococci, results in a thick bacterial layer (dental
plaque)
As plaque continues to develop, anaerobic bacterial
species begin to grow
Distribution of Dental Plaque
Figure 28.5
As dental plaque accumulates, the microbes produce high concentrations of acid that results in decalcification of the tooth enamel (dental caries) The lactic acid bacteria Streptococcus sobrinus and S. mutans are common agents in dental caries
Scanning Electron Micrograph of Streptococcus mutans
Figure 28.7
28.4 Normal Microbial Flora of the Gastrointestinal Tract
The human gastrointestinal (GI) tract

Consists of stomach, small intestine, and large intestine Responsible for digestion of food, absorpsion of nutrients, and production of nutrients by the indigenous
microbial flora
Contains 1013 to 1014 microbial cells/gm of fecal material Obligate anaerobes outnumber facultative GNRs 1000:1 or 1000x time more obligate anaerobes.
The Human Gastrointestinal Tract
Figure 28.8

The microbial populations in the distinct anatomical
areas of the GI tract are influenced by diet and the

physical conditions in each section The acidity of the stomach and the duodenum of the small intestine (~pH 2) prevents many organisms from colonizing it
Gastrointestinal Tract
Stomach pH presents barrier to organisms introduced via food/water
Dr. Barry Marshall identified Helicobacter pylori as infectious cause

of gastric ulcers, production of urease creates favorable
microenvironment

Functions and Products of Intestinal Flora
Intestinal microbes carry out a variety of essential metabolic reactions that produce various compounds
The type and amount produced is influenced by the composition of the intestinal flora and the diet Compounds produced include
vitamins B12 and K gas
Biochemical/Metabolic Contributions of Intestinal Microbes
Gastrointestinal Tract
Small bowel has limited variety of microbes due to pH 3-5
Large bowel has great variety, >1012 microbes/gram of fecal matter
anaerobes outnumber facultative microbes by 1000:1
A restricted group of organisms colonizes the upper
respiratory tract
E.g., staphylococci, streptococci, diphtheroid bacilli, and gram-negative cocci
The lower respiratory tract lacks microflora in healthy individuals
The Respiratory Tract
Figure 28.10

Urogenital Tract
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 E. coli and

P. mirabilis) to multiply and become pathogenic
E. coli and P. mirabilis frequently cause urinary tract infections in women
Microbial Growth in Genitourinary Tract of Male and Female
Figure 28.11a
Gram Stain of Lactobacillus acidophilus
Figure 28.11b
II. Harmful Microbial Interactions with Humans

28.6 Entry of the Pathogen into the Host 28.7 Colonization and Growth
28.8 Virulence
28.6 Entry of the Pathogen into the Host

Pathogens use various strategies to establish virulence Virulence is the relative ability of a pathogen to cause disease
Microorganisms and Mechanisms of Pathogenesis
Figure 28.12
Specific Adherence
A pathogen must usually gain access to host tissues and multiply before damage can be done Bacteria and viruses that initiate infection often adhere
specifically to epithelial cells through macromolecular

interactions on the surfaces of the pathogen and the host cell
Bacterial adherence can be facilitated by

Extracellular macromolecules that are not covalently attached to the bacterial cell surface
E.g., slime layer, capsule
Fimbriae and pili
Bacillus anthracis Capsules on Bicarbonate Agar Media
Figure 18.14a
Fimbriae
Figure 28.15
Major Adherence Factors Used to Facilitate Attachment
Pathogen Invasion
Starts at the site of adherence May spread throughout the host via the circulatory or lymphatic systems
28.7 Colonization and Growth
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
28.8 Virulence
Attenuation
The decrease or loss of virulence
Toxicity
Ability of an organism to cause disease by means of a preformed toxin that inhibits host cell function or kills host cells
Toxins can travel to sites within host not inhabited by pathogen
Invasiveness
Ability of a pathogen to grow in host tissue at densities that inhibit host function
Can cause damage without producing a toxin
28.8 Virulence
Many pathogens use a combination of toxins,
invasiveness, and other virulence factors to enhance

pathogenicity
Virulence Factors in Salmonella pathogenesis
Figure 28.17
Exotoxins and Extracellular Virulence Factors
Exotoxins and Extracellular Virulence Factors
III. Virulence Factors and Toxins
28.9
Virulence Factors
28.10 Exotoxins 28.11 Enterotoxins 28.12 Endotoxins
28.9 Virulence Factors
Pathogens produce enzymes that

Enhance virulence by breaking down or altering host tissue to provide access to nutrients
E.g., hyaluronidase
Protect the pathogen by interfering with normal host

defense mechanisms
E.g., coagulase
28.10 Exotoxins
Exotoxins
Proteins released from the pathogen cell as it grows
Three categories
Cytolytic toxins AB toxins Superantigen toxins
28.10 Exotoxins
Cytolytic toxins
Work by degrading cytoplasmic membrane integrity,
causing cell lysis and death

These toxins are called hemolysins
28.10 Exotoxins
AB toxins
Consist of two subunits, A and B
Work by binding to host cell receptor (B subunit) and

transfer ring damaging agent (A subunit) across the cell membrane
E.g., diphtheria toxin, tetanus toxin, botulinum toxin
28.10 Exotoxins
Superantigen toxins
Work by stimulating large numbers of immune cells Result in extensive inflammation and tissue damage Staph. aureus may produce an superAg rx.
28.11 Enterotoxins
Enterotoxins
Exotoxins whose activity affects the small intestine Generally cause massive secretion of fluid into the intestinal lumen, resulting in vomiting and diarrhea
E.g., cholera toxin
28.12 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
Properties of Exotoxins and Endotoxins
IV. Host Factors in Infection
28.13 Host Risk Factors for Infection
28.14 Innate Resistance to Infection
Compromised Host
One in whom one or more resistance mechanisms are inactive and in whom the probability of infection is increased
Age is an important factor for determining susceptibility to infectious diseases

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
28.14 Innate Resistance to Infection

Hosts have innate resistance to most pathogens
Natural host resistance
Tissue specificity
Physical and chemical barriers
Physical, Chemical, and Anatomical Barriers to Infection
Figure 28.25
Tissue Specificity in Infectious Disease
Bloodstream infections
May produce bacteremia (bacteria in bld) Transient, commonly introduced from mucous membranes
Persistent, such as endocarditis

Septicemia host inflammatory response to bacteria.
Bloodstream infection sources

Infections of vascular organs Kidney, pylonephritis from UTI
Lung, from pneumonia
Skin/soft tissue infections

Wounds, abscesses, cellulitis

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Brock Biology of Microorganisms

Madigan / Martinko Dunlap / Clark

I. Beneficial Microbial Interactions with Humans

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Preferred terminology is normal colonizing microbes

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

28.1 Overview of Human-Microbial Interactions

Most microbes are benign

Normal Colonizing Microbes

Humans are colonized by microbes at birth

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Where are we normally colonized?

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Representative Genera in the Normal Human Flora

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Representative Genera in the Normal Human Flora

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

28.1 Overview of Human-Microbial Interactions

28.1 Overview of Human-Microbial Interactions

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

28.1 Overview of Human-Microbial Interactions

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Bacterial Interactions with Mucous Membranes

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

28.2 Normal Microbial Flora of the Skin

not support the growth of most microbes

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

The Human Skin

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

28.2 Normal Microbial Flora of the Skin

The Skin Microflora

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

28.3 Normal Microbial Flora of the Oral Cavity

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Section Through a Tooth

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

28.3 Normal Microbial Flora of the Oral Cavity

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Microcolonies of Bacteria Growing on Model Tooth Surface

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

28.3 Normal Microbial Flora of the Oral Cavity

species begin to grow

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Distribution of Dental Plaque

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

28.3 Normal Microbial Flora of the Oral Cavity

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Scanning Electron Micrograph of Streptococcus mutans

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

28.4 Normal Microbial Flora of the Gastrointestinal Tract

The human gastrointestinal (GI) tract

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

The Human Gastrointestinal Tract

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

28.4 Normal Microbial Flora of the Gastrointestinal Tract

areas of the GI tract are influenced by diet and the

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Dr. Barry Marshall identified Helicobacter pylori as infectious cause

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

28.4 Normal Microbial Flora of the Gastrointestinal Tract

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Biochemical/Metabolic Contributions of Intestinal Microbes

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings