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Unformatted text preview: Important Point: Basically every
surface (except deep
lungs and, perhaps,
the stomach). Note that much of those
locations not mentioned
are sterile in healthy
individuals. Normal flora are helpful to us for a number of reasons
including supplying nutrients, priming our adaptive
immunity, and protecting us from pathogens. Normal Flora “Relatively few microbes are able to inflict any
noticeable damage, invading tissues or producing
toxic substances,” which is fortunate considering that
microbial cells living on the human body, our Normal
Flora, outnumber our own cells.
“Those minority of microorganisms that can cause us
harm we call Pathogens.”
To immunocompromised individuals the subset of
microbes that are potentially pathogenic is larger than
for those whose defenses are fully intact.
Host compromised or not, pathogens “have distinct
patterns of interaction with the host that enable them
to have the upper hand in the relationship and elude
at least some of the body’s defenses.”
“This chapter will explore some of the ways in which
microbes colonize the human host, living either as
members of the normal flora in harmony with the host
or subverting the host defences and causing
disease.” Normal flora may be differentiated in terms of the
duration of their residence in/on our bodies.
Resident Flora persists with us for relatively long
times, often colonizing us early in life and
persisting until death (plus passing on from
parent to offspring).
Transient Flora, on the other hand, persists for
only relatively short periods.
Among transient flora are those organisms that come
into contact with us but never successfully colonize.
One reason for this transience is that resident flora
already occupy niches (space, food) that
consequently are denied to transients. Antibiotic-Associated Superinfection Normal Flora Locations & Species Host-Microbe Interactions Chapter 19:
Interactions Among those flora denied residence by normal
flora are potential pathogens.
Thus normal flora can play a protective role by
preventing pathogen colonization.
Circumstances where normal flora are disrupted,
such as following antibiotic treatment, therefore
can result in disease (a superinfection).
One common superinfection is the overgrowth of the
yeast Candida albicans following the antibioticmediate destruction of vaginal Lactobacilli.
Another common superinfection is antibioticassociated colitis caused by Clostridium difficile.
In both cases the pathogens are considered
Opportunistic since normally these organisms
can come into contact with us without causing
disease. 1 More Terms Infectious Disease Terms
Symptom = indications of disease that cannot be
objectively measured, e.g., “It hurts!”
Sign = indications of disease that can be
objectively measured, e.g., body temperature.
Syndrome = a collection of signs and symptoms
that typically are associated with a given cause.
Subclinical or Inapparent Infection = symptoms
are sufficiently mild that they go unnoticed.
Opportunistic Pathogen or Opportunist = flora
that do not normally cause disease except under
unusual circumstances or in unusual locations.
Virulence = relative level of symptoms
associated with a given pathogen. Course of Infectious Disease Pathogen Communicability Infectious Disease Terms
Infection = colonization by a pathogenic
organism. Bacteremia dose not
disease. Contrast with “Localized.” An infectious disease is caused by a microorganism,
but is not necessarily communicable.
A Communicable Disease can be passed from
person to person.
A Contagious Disease (contrary to what your text
says) is a communicable disease that is easily
passed from person to person (i.e., highly
We can measure the potential for infection associated
with a pathogen in terms of its Infectious Dose.
Infectious dose typically is expressed as ID50
which is the number of organisms that must be
applied to establish infection in 50% of
An individual who is asymptomatic but still contagious
is described as a carrier. Course of Infectious Disease
a time of
illness. Incubation period is
and illness onset. Depending on various
factors an individual may
still be infectious during
either incubation or
convalescence. 2 Inactivation or alteration of this gene leads to
measurable decrease in virulence or
pathogenicity (e.g., inactivation via antibody therapy,
chemotherapy, or genetic engineering).
Restoration of gene or factor restore virulence.
In other words, the gene or factor must be shown
to be associated with a given pathogenic
condition in a causative manner.
Caveat: Just because causation cannot be
shown using Koch’s or these molecular
postulations does not prove lack of causation
(i.e., these postulates are how one proves
causation, not lack of causation). For most pathogens, cells must adhere to tissues
(and then colonize) before infection can take place,
even if ultimately damage results from invasion or
Bacteria typically employ proteins known as
Adhesins to attach to host tissues, which usually
are located on ends of fimbriae.
Alternatively, adhesins can consist of glycocalyx. 3. Pure
causation. 2. Organism
grown in pure
culture. 4. Same
recovered. Mechanisms of Pathogenicity Gene or factor is expressed and/or present
during pathogenic condition. 1. Same
each case. Individual pathogens display Virulence Determinants
that give rise to characteristic Mechanisms of
“The innate and adaptive immune systems do not
need to be overcome indefinitely, simply long enough
for the pathogen to multiply and then successfully exit
“A pathogen that is too adept at overcoming the host
defenses and causing damage is actually at a
disadvantage because its opportunity to be
transmitted may be limited and it loses an exclusive
source of nutrients if the host dies.”
We can describe four mechanisms of pathogenicity:
Toxin ingestion following production.
Toxin production following colonization.
Invasion of host tissues without toxin production.
Tissue invasion followed by toxin production. Food Poisoning Adhesion to Host Tissues Molecular Postulates Koch’s Postulates Variation in Incubation Periods With food poisoning the pathogen doesn’t need to
be ingested to cause disease, only the toxins it
produces need to be injested.
Another name for food poisoning consequently is
Common causes of food poisoning are
Staphylococcus aureus and Clostridium botulinum.
These cause Staphylococcal Food Poisoning and
Botulism is associated with non-acidic canned food
and the toxin can be inactivated with 10 min of
boiling (at sea level).
The toxin associated with staphylococcal food
poisoning, on the other hand, cannot be inactivated
with boiling (nor would you want to boil your potato
salad that’s been sitting out in the sun all day). 3 Invasion, no Toxin Colonization then Toxin
Invasion Then Toxin Certain diseases are associated with pathogens
that are non-invasive but which produce toxins that
damage body tissues.
In this case, disease does not occur unless
sufficient pathogen numbers are present to
produce sufficient quantities of toxin.
Since they are non-invasive, growth occurs on
tissue surfaces, i.e., on mucous membranes, and
therefore is considered to be colonization.
Vibrio cholerae and Escherichia coli O157 are
examples of gastrointestinal pathogens with this
mechanism of pathogenicity.
Corynebacterium diphtheriae causes respiratory
infections via a similar mechanism.
It is perhaps of interest that the primary toxins produced
by all three of these pathogens (Shiga, vibrio, and
diptheria toxins, respectively) are phage encoded. The virulence factors associated with a number
of pathogens are not so much exotoxins that
directly damage body tissues as factors that
allow tissue invasion and immune-system
In many cases, these organisms avoid immunesystem control by surviving and replicating within
body cells, e.g., as following phagocytosis.
In the process of invasion, however, tissue
damage does occur, and sufficient organism
numbers therefore can result in significant
Mycobacterium tuberculosis, Yersinia pestis, and
various Salmonella species are examples tissueinvading bacterial pathogens. Avoidance of Phagocytosis Organisms such as Shigella dysenteriae and
Streptococcus pyogenes are both invasive and
are producers of exotoxins.
Another good example is certain strains of
Staphylococcus aureus: Endotoxin is LPS (a heat-stable molecule) and the
toxin portion of LPS is the Lipid A portion. Avoidance of Phagocytosis Capsules are Involved
in avoidance of
attachment. Endotoxin As such, Endotoxin is a characteristic of Gramnegative bacteria rather than Gram-positive.
Endotoxin is released mostly upon bacterial death
(e.g., following antibiotic treatment).
Endotoxin serves as a signal to the body, especially
during localized infections, that the body has been
invaded by a Gram-negative organism.
Problems arise when the body is exposed to larger
quantities of endotoxin systemically as during Gramnegative septicemias.
In such cases the body displays what essentially is a
systemic inflammatory response that results, among
other things, in a dramatic drop in blood pressure as
vessels dilate and otherwise leak fluids.
This consequence, known as Septic Shock, is deadly
and is the great concern given Gram-neg septicemia. 4 Exotoxins vs. Endotoxins Exotoxins Exotoxins are proteins that are exported out of cells
and which can damage body tissues. Endotoxin is LPS Link to Next Presentation Exotoxins (along with exoenzymes) are more
associated with Gram-positive bacteria than Gramnegative, though pathogens of both Gram types
Vaccination against exotoxins can be accomplished
via toxoid vaccines, though infection typically is not
sufficient to induce immunity against exotoxins owing
to the relatively small quantities of toxin produced.
Passive immunization against certain exotoxins is
We can describe some toxins in terms of their sites of
Neurotoxins affect neurons.
Enterotoxins affect the gastrointestine.
Cytotoxins damage cells. 5 Infectious Disease Terms 19 Exotoxins vs. Endotoxins 19 ...
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This note was uploaded on 06/03/2011 for the course MCB 205 taught by Professor Abedon during the Spring '11 term at Ohio State.
- Spring '11