Medical Bacteriology
MBIO 460
Lecture 5
Dr. Turki Dawoud
2nd Semester
1436/1437 H
Chapter Two
Microbial Interactions with Humans
 Beneficial Microbial Interactions with Humans.
 Harmful Microbial Interactions with Humans.
 Virulence Factors and Toxins.
 Host Factors in Infection.
BENEFICIAL MICROBIAL INTERACTIONS
Overview of Human–Microbial Interactions
• Through normal everyday activities, the human body is exposed to
numerous microorganisms in the environment.
• In addition, hundreds of species and manyindividual microbial cells,
collectively referred to as the normal microbial flora, grow on or in the
human body.
• Most, but not all, microorganisms are not harmful in effect; as only some
contribute directly to our health, and even fewer cause direct threats to
health.
Colonization by Microorganisms
 Mammals in utero develop in a sterile environment and have no
exposure to microorganisms.
 Starting with the birth process, colonization, growth of a
microorganism after it has gained access to host tissues, begins as
animals are exposed to microorganisms
 The skin surfaces are readily colonized by many species.
 Likewise, the oral cavity and gastrointestinal tract acquire
microorganisms through feeding and exposure to the mother's body,
which, along with other environmental sources, initiates colonization of
the skin, oral cavity, upper respiratory tract, and gastrointestinal tract.
 Different populations of microorganisms colonize individuals in different
region and at different times.
 For example, Escherichia coli, a normal inhabitant of the human and animal
gut, colonizes the guts of infants in developing countries within several days
after birth.
 Infants in developed countries, however, typically do not acquire E. coli for
several months; the first microorganisms to colonize the gut of these infants
would more typically be Staphylococcus aureus and other microorganisms
associated with the skin.
 Genetic factors also play a role. Thus, the normal microbial flora is highly
dependent on the conditions to which an individual is exposed.
 The normal flora is highly diverse in each individual and may differ
significantly between individuals, even in a given population.
Pathogens
 A host is an organism that harbors a parasite, another organism that lives
on or in the host and causes damage.
 Microbial parasites are called pathogens.
 The outcome of a host–parasite relationship depends on pathogenicity, the
ability of a parasite to inflict damage on the host.
 Pathogenicity differs considerably among potential pathogens, as does the
resistance or susceptibility of the host to the pathogen.
 An opportunistic pathogen causes disease only in the absence of normal
host resistance.
 “Pathogenicity” is basically the ability to cause disease; and the degree of
pathogenicity is termed “Virulence”.
 Virulence can be expressed quantitatively as the cell number that
elicits disease in a host within a given time period.
 Neither the virulence of the pathogen nor the relative resistance of the
host is a constant factor.
 The host–parasite interaction is a dynamic relationship between the
two organisms, influenced by changing conditions in the pathogen, the
host, and the environment.
Infection and Disease
 Infection refers to any situation in which a microorganism is
established and growing in a host, whether or not the host is harmed.
 Disease is damage or injury to the host that impairs host function.
 Infection is not the same with disease because growth of a
microorganism on a host does not always cause host damage.
 Thus, species of the normal microbial flora have infected the host, but
seldom cause disease.
 However, the normal flora sometimes cause disease if host resistance is
compromised, as happens in diseases such as cancer and acquired
immune deficiency syndrome (AIDS).
Host–Parasite Interactions
• Animal hosts provide favorable environments for the growth of many
microorganisms.
• They are rich in the organic nutrients and growth factors required by chemo-
organotrophs, and provide conditions of controlled pH, osmotic pressure, and
temperature.
• However, the animal body is not a consistent environment.
• Each region or organ differs chemically and physically from others and thus
provides a selective environment where the growth of certain microorganisms is
favored.
• For example, the skin, respiratory tract, and gastrointestinal tract provide
selective chemical and physical environments that support the growth of a highly
diverse micro-flora.
• The relatively dry environment of the skin favors the growth of
organisms that resist dehydration, such as the gram-positive bacterium
Staphylococcus aureus.
• The highly oxygenated environment of the lungs favors the growth of
the obligatory aerobic Mycobacterium tuberculosis.
• The anoxic environment of the large intestine supports growth of
obligatory anaerobic bacteria such as Clostridium and Bacteroides.
• Animals also possess defense mechanisms that collectively prevent or
inhibit microbial invasion and growth.
• The microorganisms that successfully colonize the host have avoid
these defense mechanisms.
The Infection Process
 Infections frequently begin at sites in the animal's mucous membranes. Mucous
membranes consist of single or multiple layers of epithelial cells, tightly packed cells that
interface with the external environment.
 They are found throughout the body, lining the urogenital, respiratory, and gastrointestinal
tracts.
 Mucous membranes are frequently coated with a protective layer of viscous soluble glycoproteins called mucus.
 Microorganisms that contact host tissues at mucous membranes may associate loosely with
the mucosal surface and are usually swept away by physical processes.
 Microorganisms may also adhere more strongly to the epithelial surface as a result of
specific cell–cell recognition between pathogen and host. Tissue infection may follow,
breaching the mucosal barrier and allowing the microorganism to invade deeper into sub-
mucosal tissues (Figure 28.1).
Bacterial interactions with mucous membranes. (a)
Loose association. (b) Adhesion. (c) Invasion into
submucosal epithelial cells.
 Microorganisms are almost always
found on surfaces of the body exposed
to the environment, such as the skin, and
even on the mucosal surfaces of the oral
cavity, respiratory tract, intestinal tract,
and urogenital tract.
 They are not normally found on or in the
internal organs or in the blood, lymph,
or nervous systems of the body.
 The growth of microorganisms in these
normally sterile environments indicates
serious infectious disease.
2.2 Normal Microbial Flora of the Skin
 An average adult human has about 2 m2 of skin surface that varies greatly in
chemical composition and moisture content.
 The skin surface (epidermis) is not a favorable place for abundant microbial growth,
as it is subject to periodic drying.
 Most skin microorganisms are associated
directly or indirectly with the apocrine
(sweat) glands.
 These are secretory glands found mainly
in the underarms, genital regions, the
nipples, and the umbilicus.
 Inactive in childhood, they become fully
functional at teens.
Figure 28.2 The human skin. Microorganisms are
associated primarily with the sweat ducts and the
hair follicles.
 Microbial populations thrive on the surface of the skin in these warm,
humid places in contrast to the poor growth observed on smooth, dry skin
surfaces.
 Similarly, each hair follicle is associated with a sebaceous gland, a gland
that secretes a lubricant fluid.
 Hair follicles provide an attractive habitat for microorganisms in the area
just below the surface of the skin.
 The secretions of the skin glands are rich in microbial nutrients such as
urea, amino acids, salts, lactic acid, and lipids.
 The pH of human secretions is almost always acidic, the usual range
being between pH 4 and 6.
The Skin Microflora
 The normal flora of the skin consist of either resident or transient populations of
bacteria and fungi, mainly yeasts.
 Certain genera are highly conserved in healthy individuals, while others change
over time.
 In all, over 180 species of Bacteria and several species of fungi are found on the
skin when samples from many individuals are gathered.
 Samplings of individuals done several months apart indicate that certain
members of the normal flora are extremely stable.
 The most common and stable resident microorganisms are gram-positive
Bacteria, generally restricted to a few genera, including species of Streptococcus
and Staphylococcus; various species of Corynebacterium; and Propionibacterium,
including Propionibacterium acnes, which contributes to a skin condition called
acne.
 These four genera account for over one-half of all
species found.
 The remaining groups of bacteria found on skin are
much more transient, with over 70% changing with
time and conditions on the individuals sampled.
 Gram-negative Bacteria are occasional constituents
of the normal skin flora because such intestinal
organisms as Escherichia coli are continually being
inoculated onto the surface of the skin by fecal
contamination.
 These gram-negative Bacteria seldom grow on skin
due to their inability to compete with gram-positive
organisms that are better adapted to the dry conditions.
The gram-negative rod Acinetobacter, however, is an
exception and commonly colonizes skin.
 Malassezia spp. are the most common fungi found on skin.
 At least five species of this yeast are typically found in healthy
individuals.
 The lipophilic yeast Pityrosporum ovalis is occasionally found on the
scalp.
 In the absence of host resistance, as in patients with AIDS or in the
absence of normal bacterial flora, other yeasts such as Candida and other
fungi sometimes grow and cause serious skin infections
Although the resident microflora remains more or less constant,
various environmental and host factors may influence its composition.
(1)The weather may cause an increase in skin temperature and
moisture, which increases the density of the skin microflora.
(2)The age of the host has an effect; young children have a more
varied microflora and carry more potentially pathogenic gramnegative Bacteria than do adults.
(3)Personal hygiene influences the resident microflora; individuals
with poor hygiene usually have higher microbial population
densities on their skin. Organisms that cannot survive on the skin
generally succumb from either the skin's low moisture content or
low pH (due to organic acid content).
QUESTIONS??
Medical Bacteriology
MBIO 460
Lecture 6
Dr. Turki Dawoud
2nd Semester
1436/1437 H
Normal Microbial Flora of the Oral Cavity
 The oral cavity is a complex, heterogeneous microbial habitat.
 Saliva contains microbial nutrients, but it is not an especially good growth
medium because the nutrients are present in low concentration and saliva contains
antibacterial substances.
 For example, saliva contains lysozyme, an enzyme that cleaves glycosidic
linkages in peptidoglycan present in the bacterial cell wall, weakening the wall and
causing cell lysis .
 Lacto-peroxidase, an enzyme in both milk and saliva, kills bacteria by a reaction
in which singlet oxygen is generated
 Despite the activity of these antibacterial substances, food particles and cell debris
provide high concentrations of nutrients near surfaces such as teeth and gums,
creating favorable conditions for extensive local microbial growth, tissue damage,
and disease.
The Tooth and Dental Plaque
 The tooth consists of a mineral matrix of calcium
phosphate crystals (enamel) surrounding living tooth
tissue (dentin and pulp) (Figure 28.3).
 Bacteria found in the mouth during the first year of
life (when teeth are absent) are predominantly
aerotolerant anaerobes such as streptococci and
lactobacilli.
 However, other bacteria, including some aerobes,
occur in small numbers.
 When the teeth appear, the balance of the microflora
shift toward anaerobes that are specifically adapted to
growth on surfaces of the teeth and in the gingival
crevices.
Figure 28.3 Section through a
tooth. The diagram shows the
tooth architecture and the
surrounding tissues that anchor
the tooth in the gum.
 Bacterial colonization of tooth surfaces begins with the
attachment of single bacterial cells.
 Even on a freshly cleaned tooth surface, acidic glycoproteins from
the saliva form a thin organic film several micrometers thick. This
film provides an attachment site for bacterial micro-colonies
(Figure 28.4).
 Streptococci (primarily Streptococcus sanguis, S. sobrinus, S.
mutans, and S. mitis) can then colonize the glycoprotein film.
Extensive growth of these organisms results in a thick bacterial
layer called dental plaque.
Figure 28.5 Distribution of dental plaque
Figure 28.6 Electron micrographs of
thin sections of dental plaque
Figure 28.4 Microcolonies of
bacteria. (a) The colonies are
growing on a model tooth
surface inserted into the mouth
for 6 h. (b) Higher
magnification of the
preparation in (a). Note the
diverse morphology of the
organisms present and the
slime layer (arrows) holding
the organisms together.
 If plaque continues to form, filamentous anaerobes such
as Fusobacterium species begin to grow.
 The filamentous bacteria embed in the matrix formed by the streptococci
and extend perpendicular to the tooth surface, making an ever-thicker
bacterial layer.
 Associated with the filamentous bacteria are spirochetes such
as Borrelia species, gram-positive rods, and gram-negative cocci.
 In heavy plaque, filamentous obligatory anaerobic organisms such
as Actinomyces may predominate.
 Thus, dental plaque can be considered a mixed-culture biofilm, consisting
of a relatively thick layer of bacteria from several different genera as well
as accumulated bacterial products.
 The anaerobic nature of the oral flora may seem surprising
considering the intake of oxygen through the mouth.
 However, anoxia develops due to the metabolic activities of
facultative bacteria growing on organic materials at the tooth surface.
 The plaque buildup produces a dense matrix that decreases oxygen
diffusion to the tooth surface, forming an anoxic microenvironment.
 The microbial populations within dental plaque exist in a
microenvironment of their own making and maintain themselves in
the face of wide variations in the conditions in the macroenvironment of the oral cavity.
Dental Caries
 As dental plaque accumulates, the resident microflora
produce locally high concentrations of organic acids that
cause decalcification of the tooth enamel (Figure 28.3),
resulting in dental caries (tooth decay).
 Thus, dental caries is an infectious disease. The smooth
surfaces of the teeth are relatively easy to clean and resist
decay.
 The tooth surfaces in and near the gingival crevice,
Figure 28.3 Section through a
tooth. The diagram shows the
tooth architecture and the
surrounding tissues that anchor
the tooth in the gum.
however, can retain food particles and are the sites where
dental caries typically begins.
 Diets high in sucrose (table sugar) promote dental caries.
 Lactic acid bacteria ferment sugars to lactic acid. The lactic acid dissolves some
of the calcium phosphate in localized areas, and proteolysis of the supporting
matrix occurs through the action of bacterial proteolytic enzymes.
 Bacterial cells slowly penetrate further into the decomposing matrix.
 The structure of the calcified tooth tissue also plays a role in the extent of dental caries.
For example, incorporation of fluoride into the calcium phosphate crystal tooth matrix
increases resistance to acid decalcification.
 Consequently, fluorides in drinking water and dentifrices inhibit tooth decay.
 Two bacteria implicated in dental caries are Streptococcus
sobrinus and Streptococcus mutans, both lactic acid bacteria. S.
sobrinus is probably the primary organism causing decay of smooth
surfaces because of its specific affinity for salivary glycoproteins
found on smooth tooth surfaces (Figure 28.6).
 S. mutans, found predominantly in crevices and small fissures,
produces dextran, a strongly adhesive polysaccharide that it uses
Figure 28.7 Scanning electron
micrograph of the cariogenic
bacterium Streptococcus
mutans. The sticky dextran material
holds the cells together as filaments.
Individual cells are about 1 µm in
to diameter.
attach to tooth surfaces (Figure 28.7). S. mutans produces dextran
only when sucrose is present by activity of the enzyme
dextransucrase:
Dextransucrase
N -Sucrose
dextran (glucose)+ n Fructose
 Susceptibility to tooth decay varies and is affected by genetic traits in the
individual as well as by diet and other extraneous factors.
 For example, sucrose, highly cariogenic because it is a substrate for
dextransucrase, is part of the diet of most individuals in developed countries.
 Studies of the distribution of the cariogenic oral streptococci show a direct
correlation between the presence of S. mutans and S. sobrinus and the extent of
dental caries.
 In the United States and Western Europe, 80–90% of all individuals are infected
by S. mutans, and dental caries is nearly universal.
 By contrast, S. mutans is absent from the plaque of Tanzanian children, and
dental caries does not occur, presumably because sucrose is almost completely
absent from their diets.
 Microorganisms in the mouth can also cause other
infections.
 The areas along the periodontal membrane at or below
the gingival crevice (periodontal pockets) (Figure 28.3)
can be infected with microorganisms, causing
inflammation of the gum tissues (gingivitis) leading to
tissue and bone-destroying periodontal disease.
 Some of the genera involved include fusi-form bacteria
(long, thin, gram-negative rods with tapering ends) such as
the facultative aerobe Capnocytophaga.
 The aerobe Rothia, and even strictly anaerobic
methanogens, such as Methanobrevibacter (Archaea), may
also be present.
Figure 28.3 Section through a
tooth. The diagram shows the
tooth architecture and the
surrounding tissues that anchor
the tooth in the gum.
QUESTIONS??