Symbiosis

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Symbiosis

• Symbioses are intimate, relatively long-term
  interaction between organisms
• Typically at least one of the organisms benefits
  from the relationship
• We can classify Symbioses in terms of the degree
  to which the other organism (e.g., the host)
  benefits or is harmed
• Commensalism
• Mutualism
• Parasitism

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Commensalism
A Lion's Mane Jellyfish and a commensal fish.
The fish lives with the jellyfish and hides in
its tentacles for protection. (http//www.aquaima
ges.net/alaska.html) The fish clearly gains.
Does the jellyfish? Does the relationship cost
the jellyfish anything? If neither, then this is
an example of commensalism!
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Commensalism
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Normal Flora

• Normal flora are the harmless microorganisms
  found on your body
• Normal flora are found on every part of your body
  that normally comes in contact with outside world
  (deep lungs and stomach are exceptions)
• Normal flora can be transient or permanent
  (transient vs. resident microflora)
• Note that not all normal flora is always harmless
  normal flora includes opportunitic pathogens,
  e.g., E. coli ?urinary tract infections

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Normal Flora
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Mutualism (lichen)
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Mutualism (3-way)
A remarkable 3-way mutualism appears to have
evolved between an ant, a butterfly caterpillar,
and an acacia in the American southwest. The
caterpillars have nectar organs which the ants
drink from, and the acacia tolerates the feeding
caterpillars. The ants appear to provide some
protection for both plant and caterpillar.
Research of Diane Wagner, American Museum of
Natural History Southwestern Research Station
(http//www.dimijianimages.com/More-page5-mutualis
ms/3-way-mutualism.htm)
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Normal Flora Doing Good!

• Normal flora can help the host (e.g., you) by
  synthesizing vitamins (I.e., vitamin K)
• Normal flora can help the host by metabolizing
  materials into useful nutrients (e.g., cellulose
  digestion in termites, ungulates, and even
  primates)
• Normal flora can help the host by effecting
  Microbial Competition, a.k.a., Microbial
  Antagonism

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Parasitism

• Basically, all infectious pathogens are parasites
• That is, they harm their hosts in the course of
  stealing space, nutrients, and/or living tissue
• I.e., normal (and not so normal) flora doing bad!

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Disease

• Disease is a disturbance in the state of health
• Microbes cause disease in the course of stealing
  space, nutrients, and/or living tissue from their
  symbiotic hosts (e.g, us)
• To do this, microbes must
• Gain access to the host (contamination)
• Adhere to the host (adherence)
• Replicate on the host (colonization)
• Invade tissues (invasion)
• And produce toxins or other agents that cause
  host harm (damage)

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Disease

• Encounter The agent meets the host
• Entry The agent enters the host
• Spread The agent spreads from the site of entry
• Multiplication The agent multiplies within the
  host
• Damage The agent, the host response, or both
  cause tissue damage
• Outcome The agent or the host is eliminated, or
  persistent infection occurs

From http//www.sh.lsuhsc.edu/new_curric/mod2/Mic
ro_Infectious_Diseases/c1_8.ppt
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Systemic E. coli Infection
1. Access to Mucosa, 2. Competition with other
Bacteria, 3. Adherence to Host Tissue, 4.
Colonization of Intestinal Epithelium, 5.
Host-Cell Damage, 6. Resistance to Host Defenses,
7. Invasion, 8. Proliferation, 9. Systemic Spread
Host defenses
From http//www.md.huji.ac.il/md/courses/cmicrobio
logy/ppt/Ecoli.ppt
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Pathogenicity

• The less pathogenic, the more organism required
  to effect disease
• But note that some authors use the same
  definition for virulence (I dont)
• Opportunisticpathogens (e.g., most E. coli)
  usually have a low pathogenicity

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Virulence

• An organisms virulence is a measure of the
  extent of disease it has the potential to produce
• For example, a highly virulence pathogen could
  kill you
• On the other hand, there are plenty (though not
  all) of normal flora that simply do not effect
  disease, even under of unusual circumstances
• Organisms typically possess molecules (virulence
  factors) that affect their ability to cause
  disease
• Note that Opportunistic Pathogens can have a high
  virulence even though their ability to actually
  cause disease (pathogenicity) may be relatively
  low

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Virulence Factors

• Virulence factors are microbial products that
  determine an organisms capacity to cause disease
• Three major classes
• Extracellular products (e.g., toxins)
• Surface components (e.g., fimbriae)
• Gene regulation factors
• Virulence factors can affect pathogenicity in
  addition to virulence (e.g., by controlling
  pathogen attachment to host tissue via fimbriae)
• Bacterial pathogenesis is complex and
  multifactorial

Adapted from http//www.sh.lsuhsc.edu/new_curric/
mod2/Micro_Infectious_Diseases/c1_8.ppt
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Virulence Factors
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Virulence Evolution

• On the other hand, virulence can be Attenuated by
  rewarding pathogens that have mutated away from
  higher virulence
• This is how live-attenuated vaccines are
  generated, by growing pathogens in strange
  environments (e.g., different hosts or in tissue
  culture) that select for attributes that conflict
  with those necessary to cause disease in the
  original host
• E.g., measles, mumps, rubella, and live-polio
  vaccines

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Toxins

• Toxins
• Chemical (often protein) agents that damage
  host tissue
• Endotoxins
• Lipid A portion of LPS (not protein) that
  causes host overreaction
• Exotoxins
• Protein toxins, typically produced by
  Gram-positives as exoenzymes or equivalents
• But also many Gram-negatives
• Neurotoxins, Enterotoxins
• Intoxication
• Toxoid

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Toxins
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Exotoxins vs. Endotoxins
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Exotoxins as Exoenzmes
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Kinds of Disease

• Infectious Disease
• Disease caused by microorganism
• Communicable Disease
• Infectious Disease spread from host-to-host
  (same species)
• Noncommunicable Disease
• Infectious Disease not spread from
  host-to-host (same species), e.g., tetanus
• Contagious Disease
• Highly Communicable Disease

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Kochs Postulates
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Kochs Molecular Postulates

• Gene or factor should be associated with
  pathogenic condition or phenotype
• Inactivate or alter this gene should lead to
  measurable decrease in virulence or pathogenicity
  (e.g., via antibody therapy, chemotherapy, or
  genetic engineering)
• Specifically replace gene should restore virulence

Adapted from http//www.med.umich.edu/microbio/pp
t/532_11prevcontrol.ppt
25
Infectious Disease Descriptors

• Infectious (Non-Infectious), Communicable
  (Non-Communicable), Contagious
• Sign, Symptom, Syndrome
• Acute, Chronic, Subacute, Latent, Inapparent
  (Subclinical)
• Local, Focal, Systemic
• Septicemia, Bacteremia, Viremia, Toxemia
• Primary Infection, Secondary Infection,
  Superinfection, Mixed Infection

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Infectious Disease Descriptors
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Systemic Infection
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Rapidity of Disease Onset
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Stages of Infectious Disease
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Incubation Periods
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Prodromal, Invasive, Etc. Periods
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Sequelae (sing. Sequela)

• An inability of the body to fully repair the
  damage due to an infection can result in sequelae
  which are persisting disease aftereffects, e.g.,
• Strep throat ? Rheumatic Fever
• Polio myelitis ? PPS (Post-Polio Sequelae)

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Sequelae Foodborne Disease
A number of chronic sequelae may result from
foodborne infections, including ankylosing
spondylitis, arthropathies, renal disease,
cardiac and neurologic disorders, and nutritional
and other malabsorptive disorders (incapacitating
diarrhea). The evidence that microorganisms or
their products are either directly or indirectly
associated with these long-term sequelae ranges
from convincing to circumstantial (1-4). The
reason for this disparity is that, except in rare
circumstances, chronic complications are unlikely
to be identified or epidemiologically linked to a
foodborne cause because these data are not
systematically collected. Moreover, host symptoms
induced by a specific pathogen or product of a
pathogen are often wide-ranging and overlapping
and therefore difficult to link temporally to a
specific incident. These impediments manifest
themselves because the problems associated with
chronic disease can result from an infection
without overt illness. Alternatively, the chronic
sequelae may be unrelated to the acute illness
and may occur even if the immune system
successfully eliminates the primary infection
therefore, activation of the immune system may
initiate the chronic condition as a result of an
autoimmune response (2-4). Lindsay, J.A.
(1997). Chronic Sequelae of Foodborne Disease.
Emerging Infectious Diseases 3(4)
(http//www.cdc.gov/ncidod/eid/vol3no4/lindsay.htm
)
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Sequelae Streptococcus
Rheumatic fever causes chronic progressive damage
to the heart and its valves. Until 1960, it was a
leading cause of death in children and a common
cause of structural heart disease. The disease
has been known for many centuries. Baillou
(1538-1616) first distinguished acute arthritis
from gout. Sydenham (1624-1668) described chorea
but did not associate it with acute rheumatic
fever (ARF). In 1812, Charles Wells associated
rheumatism with carditis and provided the first
description of the subcutaneous nodules. In 1836,
Jean-Baptiste Bouillaud and, in 1889, Walter
Cheadle published classic works on the
subject. The association between sore throat and
rheumatic fever was not made until 1880. The
connection with scarlet fever was made in the
early 1900s. In 1944, the Jones criteria were
formulated to assist disease identification. These
criteria, with some modification, remain in use
today. The introduction of antibiotics in the
late 1940s allowed for the development of
treatment and preventive strategies. The dramatic
decline in the incidence of rheumatic fever is
thought to be largely owing to antibiotic
treatment of streptococcal infection. ARF is a
sequela of a previous group A streptococcal
infection, usually of the upper respiratory tract
I.e., strep throat. One beta- streptococcal
serotype (eg, M types 3, 5, 18, 19, 24) is linked
directly to ARF. The disease involves the heart,
joints, central nervous system (CNS), skin, and
subcutaneous tissues. It is characterized by an
exudative and proliferative inflammatory lesion
of the connective tissue, especially that of the
heart, joints, blood vessels, and subcutaneous
tissue. Parrillo, S., Parrillo, C.V. (2001).
Rheumatic Fever. e-Medicine (http//www.emedicine.
com/EMERG/topic509.htm)
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Sequelae Mycobacterium ulcerans
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Sequelae Adult Circumcision
Five men underwent circumcision in adulthood for
reasons of infection, inflammation, or phimosis.
Several years later, they reported on the
erotosexual sequalae. All reported a prolongation
of the period prior to ejaculation, though none
had been genuine premature ejaculators. Other
variable sequalae were diminished penile
sensitivity, less penile gratification, more
penile pain, and cosmetic deformity. Orgasm
frequency was the same or less, and there was not
postsurgical impotence. Loss of stretch receptors
and reflexes might explain the major erotosexual
changes. In most instances, a dorsal cut and/or
antibiotic treatment achieves the same effect as
circumcision, and is less risky in terms of
possible pathological sequelae. Money, J.,
Davison, J. (1983). Adult Penile Circumcision
Erotosexual and Cosmetic Sequelae. The Journal of
Sex Research, Volume 19(3)289-292.
(http//www.cirp.org/library/complications/money/)
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Link to Next Presentation
38
Acknowledgements
http//www.sh.lsuhsc.edu/new_curric/mod2/Micro_Inf
ectious_Diseases/c1_8.ppt http//www.med.umich.edu
/microbio/ppt/532_11prevcontrol.ppt