Terms related to

bacterial
infection.
Adherence (adhesion, attachment): The process by
which bacteria stick to the surfaces of host cells.
adherence is a major initial step in the infection process.
The terms adherence, adhesion, and attachment are
often used interchangeably.
Carrier: A person or animal with asymptomatic infection
that can be transmitted to another susceptible person or
animal.
Infection: Multiplication of an infectious agent within the
body.
Invasion: The process whereby bacteria, animal
parasites, fungi, and viruses enter host cells or tissues
and spread in the body.
Microbiota: Microbial flora harbored by normal, healthy
individuals.
Nonpathogen: A microorganism that does not cause
disease; may be part of the normal microbiota.
Opportunistic pathogen: An agent capable of causing
disease only when the host’s resistance is impaired
Infection: Multiplication of an infectious agent within the
body.
Pathogen: A microorganism capable of causing disease.
Pathogenicity: The ability of an infectious agent to
cause disease.
Superantigens: Protein toxins that activate the immune
system by binding to major histocompatibility complex
(MHC) molecules and T-cell receptors (TCR) and
stimulate large numbers of T cells to produce massive
quantities of cytokines.
Toxigenicity: The ability of a microorganism to produce a toxin that contributes to the development of disease

Virulence: The quantitative ability of an agent to cause disease. Virulent agents cause disease when introduced into
the host in small numbers. Virulence involves adherence, persistence, invasion, and toxigenicity
Guidelines for
establishing the causes of
infectious diseases
IDENTIFYING BACTERIA THAT
CAUSE DISEASE

It can be difficult to show that a specific Koch’s postulates have remained a mainstay of microbiology;
bacterial species
however, since the late 19th century, many microorganisms

is the cause of a particular disease. In 1884, that do not meet the criteria of the postulates have been
Robert Koch proposed shown to cause disease.

a series of postulates that have been applied For example, Treponema pallidum
broadly to
(syphilis) and Mycobacterium leprae (leprosy) cannot

link many specific bacterial species with be grown in vitro; however, there are animal models of
particular diseases. infection

Koch’s postulates are summarized in Table 9-1. with these agents.

IDENTIFYING BACTERIA THAT
CAUSE DISEASE

In other instances, Koch’s postulates have been at least The host’s immune responses also should
be considered
partially satisfied by showing bacterial pathogenicity in
an when an organism is being investigated as
the possible cause
in vitro model of infection rather than in an animal
model.
of a disease. Thus, development of a rise in
For example, some forms of Escherichia coli (E
specific antibody
coli)–induced
during recovery from disease is an
diarrhea have been defined by the interaction important adjunct to

of the E coli with host cells in tissue culture. Koch’s postulates.

IDENTIFYING BACTERIA THAT
CAUSE DISEASE

Modern-day microbial genetics has opened Molecular cloning has allowed investigators
new frontiers to isolate and modify specific virulence genes and

to study pathogenic bacteria and study them with models of infection. The ability to
differentiate them study

genes associated with virulence has led to a

from nonpathogens.
proposed form

of molecular Koch’s postulates. These postulates

are summarized

in Table 9-1
IDENTIFYING BACTERIA THAT
CAUSE DISEASE
Analysis of infection and disease through
the application
of principles such as Koch’s postulates
leads to classification
of bacteria as pathogens, opportunistic
pathogens, or
nonpathogens.
Some bacterial species are always
considered
to be pathogens, and their presence is
abnormal; examples
include Mycobacterium tuberculosis
(tuberculosis) and
Yersinia pestis (plague). Such bacteria
readily meet the criteria
of Koch’s postulates.
IDENTIFYING BACTERIA THAT
CAUSE DISEASE

Other species are commonly part of Strains of E coli that cause disease are differentiated

the normal microbiota of humans (and animals) but
also can
frequently cause disease. For example, E coli is part
of the gastrointestinal
microbiota of normal humans but is also a common
from those that do not by determining (1) whether they
are virulent in animals or in vitro models of infection and (2)
whether they have a genetic makeup that is significantly
associated
with production of disease. Other bacteria (eg, Pseudomonas

cause of urinary tract infections, traveler’s diarrhea, species, Stenotrophomonas maltophilia, and many
and
yeasts and molds) only cause disease in immunosuppressed
other diseases.
and debilitated persons and are opportunistic pathogens.
the process of bacterial transmission
of infection
 Transmission of Infection
● Bacteria acana adapt to a variety of environment
(soil, internal milieu)
● Bacteria don’t usually kill the host, instead they
produce asymptomatic infection or mild disease
to increase their survival
● Some bacteria that commonly cause disease in
humans exist from animals and accidentally
transmitted to humans which organisms have not
adapted to humans: (therefore diseases may be
severe)
● Yersina pestis (plague) -from rodents to fleas
to humans
● Bacillus anthracis - environment to animal
hairs, to humans
● Clostridium species - environment then
ingested by humans
● Clostridium tetani - soil to open wounds
● S aureus - from one person to another then
enters the body to sites where mucus
membrane meet the skin (respiratory, gi,
genitals, urinary tract, open wound)
 Infectious Process
1. Attaching to host cells
2. Multiply and spread directly through the tissues or via lymphatic
system to bloodstream
3. Continuous to spread to the tissues until suitable place to multiply
Genomics and
Bacterial
Pathogenicity
Genomics and Bacterial Pathogenicity

The availability of hundreds of bacterial genome sequences has altered the study of
bacterial pathogenesis, affecting both design of experiments and analysis of results.

Comparative genomics and genomic tools have been used to identify virulence factors and
genes involved in environmental persistence of pathogens.
Genomics and Bacterial Pathogenicity

Bacteria are haploid and have limited genetic interaction

- Change their chromosome

- Disrupt their adaptations and survival

Important result of the conservation of chromosomal genes in bacteria is CLONAL

Few clonal types spread in the world during the period of time

- meningococcal meningitis
- Neisseria meningitidis
- Two clonal types of Bordetella pertussis
Mobile Genetic Elements
Primary mechanisms exchange of genetic information between bacteria and transmissible
mobile genetic elements

Transformation of occurs when DNA from

- Organisms is released into the environment
- Taken up by different organisms

Genes encode many bacterial virulence factors

- Plasmids: extrachromosomal pieces of DNA and are capable of replicating
- Transposons: highly mobile segments of DNA that can move from one part of the DNA
to another
- This can result in recombination between extrachromosomal DNA and the
chromosome and if this occurs the genes coding for virulence factors may become
chromosomal

Bacterial viruses or phages are another mechanism by which DNA can be moved from one
organism to another.
Mobile Genetic Elements
Pathogenicity Islands
Large groups of genes associated with pathogenicity and located on the bacterial
chromosome

- Large organized groups of genes

- 10- 200kb in size
- One or more virulence genes
- Present in the genome of pathogenic virulence members of a species but absent in the
nonpathogenic member
- different guanine plus cytosine
- associated with tRNA genes
- parts of the genome associated with mobile genetic elements
- often represent mosaic structures with components acquired at different time
Pathogenicity Islands
Regulation of
bacterial
virulence factors
Pathogenic bacteria (and other pathogens) have adapted both to saprophytic or
free-living states, possibly environments outside the body, and to the human
host.

Common signals include temperature, iron availability, osmolality, growth

phase, pH, and specific ions (eg, Ca2+) or nutrient factors.
Corynebacterium
diphtheriae

● the leading causing agent of diphtheria

● carried on temperate bacteriophages.
● bacteriophages. Toxin is
● produced only by strains lysogenized by the phages.
● Toxin is produced only by strains lysogenized by the phages.
● greatly enhanced when C diphtheriae is grown in a medium
with low iron.
B pertussis
(Bordetella pertussis )
is enhanced when the
bacteria are grown at 37°C
and suppressed when they
are grown at lower
temperatures or in the
presence of high
concentrations of
magnesium sulfate or
nicotinic acid.
V cholerae ( Vibrio cholerae )

are regulated on multiple levels and by

many environmental factors. Expression
of the cholera toxin is higher at a pH of
6.0 than at a pH of 8.5 and higher also at
30°C than at 37°C.

Osmolality and amino acid composition

also are important. As many as 20
other genes of V cholerae are similarly
regulated.
Y pestis ( Yersinia pestis )
a series of virulence plasmid-encoded
proteins. One of these is an
antiphagocytic fraction 1 capsular
protein that results in antiphagocytic
function.
expressed maximally at 35–37°C, the
host temperature, and minimally at
20–28°C, the flea temperature at which
antiphagocytic activity is not needed.
Motility of bacteria enables them to spread and multiply in their
environmental niches or in patients. Yersinia enterocolitica and
Listeria monocytogenes are common in the environment where
motility is important to them.
Bacterial
Virulence Factors
Bacterial Virulence Factors:

● Adherence Factors
● Invasion of Host Cells and Tissues
● Toxins
● Enzymes
● Antiphagocytic Factors
● Intracellular Pathogenicity
● Antigenic Heterogeneity
● Bacterial Secretion systems