Transcript 10a - Penn State York

Microbial Interactions with Humans
Basic Definitions
Ecological Interactions
Normal Microbiota
Infectious Diseases
Disease = any change in state of health resulting in an inability to carry out
normal function.
Pathogen = an organism, virus or other agent capable of causing disease.
Infectious Disease = a disease caused by a pathogen’s infection.
Infection = invasion and growth of a microorganism in the host’s body.
Pathogenicity = the ability to cause disease by overcoming host defenses.
Virulence = a degree or intensity of pathogenicity; invasiveness and
evasiveness of pathogen.
Resistance = the hosts ability to prevent disease; defensiveness
(antonym = susceptibility).
Ecological Interactions
Between Populations
Gnotobiotic Animals as Models
“Germ” free animals
provide controlled
conditions for studies
of microbe-host
interactions.
gnoto = Greek known
Comparisons between
animals with normal
microbiota and
gnotobiotic animals
leads to insight on the
role of specific
microbes, or known
consortia of microbes
in animal health (good
and bad).
Gnotobiotic chicks used to demonstrate the nutritional
importance of digestive microorganisms (1912).
Normal Microbiota*:
*Transient
Microbiota:
Microbes that are
present for a
short time and
don’t cause
disease.
* Knowledge of where and which
microbiota normally reside
assists medical professionals in
predicting and interpreting clinical
conditions of infection; they may
stimulate host immune response.
Microbial Antagonism
Bacteria of normal microbiota has a negative effect on
opportunistic and/or pathogenic bacteria.
• Non-pathogen = mutualism, neutral interactions with host.
• Opportunist Pathogens = commensalism with host shifts to
parasitism when environmental conditions change that favor growth.
• Primary Pathogens = parasitic upon first interaction with host.
• Examples of Microbial Antagonism as a host defense
in resisting infections disease:
– Non-pathogens or commensal microbes interfer with growth of other microbes.
– Escherichia coli bacteriocins (lethal protein to related bacteria) prevents growth
of Shigella spp.
– Large intestine community prevents growth of Clostridium difficile (cause of
psuedomembranous enterocolitis; necrosis of epithelial cells; bloody stools)
– Vaginal community prevents growth of Candida albicans (“yeast infections”)
– Propionibacterium acnes prevents growth of some Gram- pathogens.
“The Zit Story”: Shift to an Opportunistic Pathogen
Skin can be a dry,
acidic and saline
environment, where
inhibitory agents are
excreted directly or
indirectly and cell layers
are constantly shed.
P. acnes grows normally
on normal supplies of
sebum lipids; releasing
unsaturated fatty acids
toxic to Gram bacteria
(microbial antagonism).
Hormones stimulate
sebum production,
inflammation, comedo
formation resulting in
acne vulgaris.
Propionibacterium. acnes is most sensitive to tetracycline!
Opportunistic and Pathogenic
Microorganisms
Community shifts away from mutualism and commensalism and toward
parasitism; favors the disease.
Conversely, shifts away from parasitism to commensalism and mutualism;
favors an improved state of health.
What influences either such shifts in microbial-host interactions?
Infections disease versus good health in the host depends on the balance
between microbial virulence level and abundance versus the status of host
defense mechanisms (resistance).
Infectious Disease ≈ (Virulence * Abundance)/Resistance
Overview of Host Defenses
• Effectiveness of host resistance depends on three lines of defense.
• If the first line of defense is breeched, elements of the second line of
defense are engaged.
• The second line of defense may establish conditions to speed up its
defense processes by initiating the third line of defense.
•Third line of defense is both cellular and humeral (antibody) mediate.
(neutrophiles)