Host Microbe Interactions

Host Microbe Interactions

daily we
ingest thousands of microorganisms on the food we
eat
inhale hundreds of thousands of microorganisms in
the air we breath
have microorganisms stick to us wherever we go
most of these invaders have no ill effect on us as we
slough, cough, gag, urinate and defecate them away
we are also protected by the friendly resident
microorganisms found throughout our body

Host Microbe Interactions

microorganisms very easily colonize the warm, moist,
nutrient rich environment we call the human body
usually they live as normal flora
in some cases, they are able to overcome the bodies
defenses, and cause disease
organisms that can cause any noticeable damage,
invade tissue, or produce toxins are called pathogens

Digestive System Infections

Sometimes referred to
as the gastrointestinal
tract
Passageway running
from mouth to anus
Major route of microbial
invasion
Divided into upper and
lower tracts

 The intestinal tract is slightly acidic to neutral and supports

a diverse population of microorganisms in a variety of
nutritional and environmental conditions.

Normal Flora
Important in protecting body from invasion
Flora of digestive tract mainly found in the oral cavity
and intestines
Esophagus has very little flora
Normal stomach is devoid of microorganisms
Killed by stomach acid

 The presence of a population of normal

nonpathogenic microorganisms in the

respiratory tract and urogenital tract is essential
for normal organ function and often prevents
the colonization of pathogens.

 In the upper respiratory tract (nasopharynx,

oral cavity, and throat), microorganisms live in

areas bathed with the secretions of the mucous
membranes.
The normal lower respiratory tract (trachea,
bronchi, and lungs) has no resident microflora,
despite the large numbers of organisms
potentially able to reach this region during
breathing.

Normal Flora
Mouth
Relatively few species colonize oral cavity
Streptococcal species most common

Host limits number of bacteria on mucus membranes

Membrane cells constantly shedding

Teeth are nonshedding surface

Large numbers of bacteria can collect and form biofilm
Masses of bacteria termed dental plaque
100 billion bacteria per gram of plaque

Normal Flora
Intestines
Small number of bacteria colonize upper small intestine
Predominant organisms are aerobic and facultative Gram
negative bacilli and some streptococci

Large intestine contains very high numbers of organisms

Approximately 1011 bacteria per gram of feces
That is 100 billion bacteria!!!!!

High population is due to abundance of nutrients in feces

Escherichia coli and other enterobacteria predominate bacterial
population
Important source of opportunistic infections
Especially of the urinary tract

Normal intestinal flora prevent pathogenic colonization of

large intestine

Anatomical Barriers
in addition to providing barriers to the microbial world,
skin and mucous membranes also create an
environment for interacting microorganisms and the
human body
these interactions are referred to as symbiosis, which
means living together
the players in symbiosis are referred to as symbionts

Anatomical Barriers
symbiotic relationships between microorganisms and a
host include
mutualism
commensalism
parasitism

Mutualism
in this type of relationship, both partners benefit
E. coli synthesizes vitamin K in the intestine
in exchange the large intestine provides nutrients
necessary for survival of the microorganisms

E. coli

Commensalism
one organism is benefited and the other is unaffected by
this type of relationship
many of the microorganisms that make up our normal
flora inhabit places like the eyes, ears, and external
genitalia
these bacteria live on secretions and sloughed off
cells
they bring no benefit to the host and yet the
microorganisms benefit greatly from the
environment they inhabit

Parasitism
one organism benefits at the expense of the other
all pathogens are parasites

parasitic microorganisms

Normal Flora
the presence of normal flora
cover potential adherence sites for invading
microorganisms
consume the available nutrients
produce compounds toxic to other microorganisms

bacteria found on skin

Normal Flora
when the balance between normal flora and
pathogens is upset, disease can result
the normal bacterial microorganisms of the adult
human vagina maintain the pH at about 3.4 4.5
the presence of this normal flora inhibits the
overgrowth of Candida albicans, yeast

Normal Flora
if the presence of the normal flora is eliminated by
antibiotics, or excessive douching, the pH of the
vagina becomes nearly neutral, creating an
environment very conducive to the growth of C.
albicans

C. albicans

Foodborne pathogens
Food-Borne Diseases
It can be classified
into three forms:

foodborne intoxication
foodborne infection
foodborne toxicoinfection

Food Pathogens

www.textbookofbacteriology.net
Todar's Online Textbook of Bacteriology

Microrganisms that cause food borne infection or

intoxication:

E.coli
Salmonella

Listeria

Campylobacter

Botulinum

Staphylococci

Foodborne Intoxication
illness from microbial exotoxin
microorganism does not cause the illness, the toxin
released by the microorganism does
common exotoxin producing microorganisms

Staphylococcus aureus

Clostridium botulinum

INTOXICATION
Ingestion of FOOD CONTAINING
TOXIN causes illness
Microbes produce toxin while growing
in food
Ingestion of the microbes
themselves may be harmless

Toxic bacterial food poisoning

some bacteria grow in food and produce a
toxin within the food which is then consumed
e.g. Bacillus cereus and Staphylococcus
aureus. When the food is consumed viable
cells of the bacteria do not need to be
present.

Following ingestion, Toxins are absorbed through

the gastrointestinal epithelial lining and cause
local tissue damage and may induce inflammation
resulting in diarrhea or vomiting.
In some cases, toxins are translocated to distant
organs or tissues such as liver, kidney, peripheral,
or central nervous system where they can cause
damage.

Toxins
Some bacteria release poisons known as
toxins which cause food poisoning.
Some toxins, known as exotoxins multiply in
food. These toxins are not easily destroyed
by cooking and may remain in food once
they have developed.
Other bacteria produce toxins inside the
human body only after the food has been
eaten. These are called endotoxins

Toxins
Substances that contribute to pathogenicity
Exotoxins are secreted out of the cell during cell life.
Endotoxins from inside the cell. Released upon
cell lysis.
Toxemia

Presence of toxin the host's blood

Exotoxins
soluble protein, thus readily carried through
body by lymphatics or blood
exotoxins are soluble in body fluids which makes them
easily diffused into blood and then are rapidly
transported throughout the body
exotoxins work by destroying particular parts of the host
cells or by inhibiting certain metabolic functions

Exotoxins
exotoxins are highly specific
exotoxins are among the most lethal substances known
to man
1 gram of the exotoxin produced from Clostridium
botulinum is capable of killing the entire population of
the United States, close to 300 million people
the danger with exotoxins is not the ingestion of the
bacterium, but the ingestion of the toxin

Clostricium botulinum

Exotoxins
most exotoxins are grouped according to the tissues
they adversely impact
neurotoxins damage the nervous system
entereotoxins upset the intestinal system
cytotoxins afflict their damage on many different types
of cells by disrupting cellular function of by lysing the
cell

Exotoxins
Mostly seen in Gram (+)
Bacteria
Most gene that code for
exotoxins are located on
plasmids or phages

Figure 15.4a

Exotoxin
Exotoxin
Source
Metabolic product
Chemistry

Mostly Gram +
By-products of growing cell
Protein
Water soluble

Fever?

No

Neutralized by antitoxin

Yes

LD50

Small - Very potent

1 mg of Clostridium botulinum
toxin can kill 1 million guinea
pigs

Exotoxins - three types

1. Cytotoxins
kill cells
2. Neurotoxins
interfere with normal nerve
impulses
3. Enterotoxins
effect cells lining the G.I. Tract
Many toxins have A-B subunit toxins or
type III toxins
A - active
Causes change in
host
B - binding

Figure 15.5

Exotoxins
Exotoxins - soluble, heat-labile, proteins and usually
released into the surroundings as bacterial pathogen
grows
humans exposed to exotoxins in three main ways
ingestion of preformed exotoxin
bacterial colonization of a mucosal surface followed by exotoxin

production
colonization of a wound or abscess followed by local exotoxin
production

most exotoxin producers are gram-positive

often travel from site of infection to other tissues or cells
where they exert their effects

Exotoxins
Membrane-disrupting toxins or type II toxins
Lyse hosts cells by:
Making protein channels in the plasma membrane
(e.g., leukocidins, hemolysins)
Disrupting phospholipid bilayer

Cholera
enterotoxin
Vibrio cholerae
Gram (-) comma shaped rods

 Botulinum toxin consists of seven

related toxins that are the most potent
biological toxins known (Figure 21.20).

Enterotoxins
Enterotoxins are exotoxins that specifically

affect the small intestine, causing changes in

intestinal permeability that lead to diarrhea.

Many enteric pathogens colonize the

small intestine and produce A-B
enterotoxins. Food-poisoning bacteria
often produce cytotoxins or
superantigens.

 The action of cholera enterotoxin is

shown in Figure 21.22.

Foodborne Infection
requires consumption of microorganism
symptomatic about 1 day following ingestion of
contaminated food
common foodborne infecting microorganisms
Salmonella and Campylobacter
poultry product infections
Escherichia coli 0157:H7
undercooked hamburger

Campylobacter

Salmonella

Infective bacterial food poisoning

infections occur when pathogens are ingested
via contaminated food and the bacteria is
established in the body, usually growing inside
the intestinal tract and irritating intestines e.g.
Salmonella spp. and Campylobacter jejuni.
The infection may involve subsequent growth
in other tissues

Principles of Infectious Disease

a parasitic relationship between a microorganism and a
host is called an infection
infections can be subclinical or inapparent: meaning
no symptoms or the symptoms are so mild as to be
noticed
infection that causes impairment of body function is
called disease

Principles of Infectious Disease

pathogenicity is the ability of a microorganism to cause
disease by overcoming the host defenses
Pathogen invasion starts at the site of adherence and
may spread throughout the host via the circulatory
systems.

Factors Impacting Outcome of

Host-Parasite Relationships
Factors:
number of organisms present
the degree of virulence of pathogen
virulence factors
e.g., capsules, pili, toxins

hosts defenses or degree of resistance

Pathogens gain access to host

tissues by adherence to mucosal
surfaces through interactions
between pathogen and host
macromolecules.

Colonization and Growth

A pathogen must gain access to nutrients and

appropriate growth conditions before

colonization and growth in substantial
numbers in host tissue can occur. Organisms
may grow locally at the site of invasion or may
spread through the body.

 If extensive bacterial growth in tissues occurs,

some of the organisms are usually shed into the

bloodstream in large numbers, a condition
called bacteremia.

Shigellosis
Pathogenesis
S. dysenteriae
Rarely encountered
in United States
Produces potent A-B
toxin
Shiga Toxin
Acts much like
cholera toxin
Toxin associated
with fatal hemolytic
uremic syndrome

Helicobacter pylori Gastritis

Pathogenesis
Bacteria survive
extreme acidity of
the stomach
Able to neutralize
environment

Organism uses
flagella to corkscrew
through mucosal
lining
Inflammatory
response begins

Mucus production
decreases
Without mucus stomach lining
not protected from acidic
environment

Infection persists for years

Possibly for a life time

Virulence
Virulence is determined by invasiveness,

toxicity, and other factors produced by a

pathogen. Various pathogens produce proteins
that damage the host cytoplasmic membrane,
causing cell lysis and death.

Major virulence determinants:

toxins - destroy, damage, inactivate
natural defense mechanism of host
exotoxins
endotoxins

enzymes - assist bacteria in establishing

infection and producing disease

 Because the activity of these toxins is most

easily detected with red blood cells

(erythrocytes), they are called hemolysins
(Table 21.4). In most pathogens, a number of
factors contribute to virulence.

 Salmonella displays a wide variety of

traits that enhance virulence (Figure
21.17).

Virulence Factors and

Toxins
Virulence Factors
Pathogens produce a variety of enzymes that

enhance virulence by breaking down or altering

host tissue to provide access and nutrients.

Still other pathogen-produced virulence

factors provide protection to the pathogen
by interfering with normal host defense
mechanisms. These factors enhance
colonization and growth of the pathogen.

Endotoxins
Endotoxins are lipopolysaccharides derived

from the outer membrane of gram-negative

Bacteria. Released upon lysis of the Bacteria,
endotoxins cause fever and other systemic
toxic effects in the host.

 Endotoxins are generally less toxic

than exotoxins (Table 21.5).

 The presence of endotoxin detected by the

Limulus amebocyte lysate assay indicates

contamination of a substance by gram-negative
Bacteria.

Host Factors in Infection

Host Risk Factors for
Infection

 Conditions of age, stress, diet, general health,

lifestyle, prior or concurrent disease, and

genetic makeup may compromise the host's
ability to resist infection.

Innate Resistance to
Infection
Nonspecific physical, anatomical, and

chemical barriers prevent colonization of the

host by most pathogens (Figure 21.24). Lack
of these defenses results in susceptibility to
infection and colonization by a pathogen.

 Table 21.6 shows tissue specificity in

infectious disease.

Toxins
endotoxins
produced only by gram negative bacteria
part of the outer cell wall (lipopolysaccharide
coat)
lipid A component is toxic
side chains (O, H antigen) are immunogenic

released in large amounts at cell death

heat stable, not destroyed by autoclaving
less potent and less specific than exotoxins

Toxins
endotoxins
pyrogenic
toxic to most animals, producing similar range
of biological effects regardless of source
fever
increased WBC
DIC (disseminate intravascular coagulopathy)
hypotension
shock
death

degraded by oxidizing agents

examples: E. coli, Salmonella, Shigella

Enzymes
spreading factors
hyaluronidase (gram +) - attacks interstitial
cement of connective tissue
collagenase (Clostridium) - break down
collagen, facilitating invasion of muscle and
gas gangrene formation
neuraminidase (Vibrio and Shigella) - break
down intercellular cement of intestinal
epithelial cells
kinase (Strep and Staph) - digests fibrin,
preventing clotting and allowing rapid
diffusion

Enzymes
cell lysis

hemolysins (Staph, Strep, and Clostridia)

lecithinases (C. perfringens)
phospholipases (C. perfringens) - toxin

coagulase (Staph) - causes clotting

adenylate cyclase activity - bacterial
toxins having immediate (short-range)
effects that promote invasion
Ex: anthrax toxin - edema factor

Principles of Infectious Disease

the more virulent a pathogen is the more disease
promoting attributes it possesses
virulence factors are substances or features of a
microorganism that help it infect and cause disease
they may include
ability to adhere
ability to overcome host defense
ability to evade host defense

Colonization and Growth

A pathogen must gain access to nutrients and

appropriate growth conditions before colonization and

growth in substantial numbers in host tissue can occur.
Organisms may grow locally at the site of invasion or
may spread through the body.

 If extensive bacterial growth in tissues occurs, some

of the organisms are usually shed into the bloodstream

in large numbers, a condition called bacteremia.

Flagellar Function
Guide bacteria in a direction in response to external

stimulus:
1) chemical stimuli chemotaxis; positive and negative
2) light stimuli phototaxis
Signal sets flagella into rotary motion clockwise or
counterclockwise

Axial Filaments

Periplasmic, internal flagella, enclosed between cell

wall and cell membrane of spirochetes
Produce cellular motility by contracting and imparting
twisting or flexing motion

Fimbriae
Fine, proteinaceous, hairlike bristles from the cell
surface
Function in adhesion to other cells and surfaces

Pili
Rigid tubular structure made of pilin protein
Found only in Gram negative cells
Function to join bacterial cells for partial DNA transfer called
conjugation

Glycocalyx

Coating of molecules external to the cell wall,

made of sugars and/or proteins
Two types:
1. slime layer - loosely organized and attached
2. capsule - highly organized, tightly attached

Functions:

protect cells from dehydration and nutrient loss

inhibit killing by white blood cells by phagocytosis
contributing to pathogenicity

Bacterial Pili

Capsules

Attachment

 Pathogen growth on the surface of a host,

often on the mucous membranes, may result
in infection and disease

Mechanisms of Pathogenesis
pathogenesis is the manner in which a disease develops
patterns that disease-causing microorganisms may
follow include
production of ingested toxins
foodborne intoxication
the causative agent must produce toxins
few organisms are capable of causing disease
this way, the few that can include Clostridium
botulinum or Staphylococcus aureus

Mechanisms of Pathogenesis
colonization of host surface, then toxin production
invading pathogen is able to grow to high
numbers on host surfaces such as the
respiratory and intestinal tract
they then produce a toxin that is damaging to
the cells
organisms that use this mechanism include
Vibrio cholerae, which causes cholera or
Corynebacterium diphtheriae, which causes
diphtheria

Mechanisms of Pathogenesis
invasion of host tissue
breaching bodys barriers then multiplies in the
bodys tissues
these organisms have mechanisms that allow
them to avoid macrophage destruction
some are also capable of avoiding detection by
antibodies
organisms that use this mechanism include
Mycobacterium tuberculosis, causative agent
for tuberculosis, and Yersinia pestis, causative
agent for plaque

Mechanisms of Pathogenesis
invasion of tissue, then toxin production
breach the bodys barriers, then make toxins
in addition to invasion, these organisms also
make toxins
organisms that use this mechanism include
Shigella dysenteriae and Streptococcus
pyogenes

Mechanisms of Pathogenesis
in order to cause disease microorganisms need to be
able to
adhere and colonize host tissue
avoid the innate defenses
avoid the adapted defenses
cause damage related to the disease

Adherence
to establish disease the causative agent needs to
adhere
difficult to overcome our first-line defenses so
adherence is imperative
many bacteria have adhesions, generally found on
the pili

Shigellosis

Pathogenesis
S. dysenteriae
Rarely encountered in
United States
Produces potent A-B
toxin

Shiga Toxin
Acts much like cholera
toxin
Toxin associated with
fatal hemolytic uremic
syndrome

Colonization
causative agent needs to
multiply in order to colonize
to multiply, they must compete successfully with
the normal flora for space and nutrients
toxins that may be produced by the normal flora
must be overcome

Avoiding Innate System

while some bacteria are able to cause disease while
remaining on the surface of the skin or mucosa,
many need to penetrate that barrier
once this is done, those pathogens have it on easy
street, exclusive rights to rich nutrition and
multiplying without any competition
penetrating the skin is extremely difficult
bacteria take advantage of trauma to provide a
break in the skin
West Nile Virus is transmitted to the host through
a mosquito bite, a penetration of the skin

Avoiding Innate System

mucous membranes penetration is the most common
entry for most microorganisms
one method that is used is referred to as ruffling
once the microorganism attaches to the
membrane, it can direct the that cell to engulf the
bacterium: this is referred to as ruffling

ruffling on the surface of

mucous membrane

Avoiding Innate and Adaptive System

several mechanisms can be used by microorganisms to
avoid the potentially lethal effects of our immune system
hide inside a host cell
phagocytes, complement and antibodies cant find
them: remember self and non-self!
interfere with the activation of complement (which
attracts phagocytes)

Avoiding Innate and Adaptive System

avoid destruction by phagocytes by simply preventing
encounters with phagocytes
C5a peptides are an enzyme that is made by some
bacteria
C5a peptide destroys the complement component
if the complement is not activated, neither are the
phagocytes
some bacteria produce membrane-damaging toxins
that kill phagocytes

Avoiding Innate and Adaptive System

avoid recognition and attachment to phagocytes by
producing capsules to prevent phagocytosis
Streprococcus pneumoniae procduces capsules
survive in the phagocyte
they dont worry about being engulfed, simply enjoy
the free ride
some microorganisms can escape from the
phagosome before being fused with the enzyme
lysosome

Avoiding Innate and Adaptive System

survive in the phagocyte
some microorganisms can block the fusion of the
phagosome and lysosome
a few organisms can actually survive the lysosome
environment

Avoiding the Adaptive System

avoiding antibodies which integral to the adaptive
system; this can be accomplished several ways including
IgA protease
cleaves IgA class of antibodies found in mucus and
other secretions
antigenic variation
alter structure of antigens
stay ahead of antibody production and destruction
by altering the structure the antibodies are
searching for
mimic host molecules
some microorganisms have the ability to cover
themselves with molecules similar to self

Host Damage
in order for disease to happen damage of some sort
must happen to the host
in most cases damage to the host facilitates dispersal
of the pathogen
damage to the host can occur either
directly
indirectly

Direct Host Damage

toxins produced by the invading pathogen cause direct
damage to the host which results in disease
toxins capable of causing damage include
exotoxins
a protein toxin released from a living cell
mostly found in Gram + cells

Bacillus anthraxis
produces an exotoxin

Immune Response Damage

inflammatory response can destroy tissue
antibody-antigen complexes formed during the
immune response settle in kidneys and joints
activates complement, which produces damaging
inflammation

Key traits to a pathogen

The ability to:
1. Adherence
To host surfaces and not be washed off
2. Avoid phagocytosis
Prevent host defenses from destroying
3. Penetrate
Get into host and spread
4. Produce Enzymes
Spread, prevent host defenses and cause
damage at or near site of infection
5. Produce Toxins
Cause damage at distant site

Adherence
Adhesions/ligands bind to receptors on host cells so
wont get flushed off.
Mechanisms to adhere and avoid host defenses:
Glycocalyx
Streptococcus mutans
Dextran (plaque)

Waxes
Mycobacteria
Fimbriae
Escherichia coli
M protein
Streptococcus pyogenes
Tapered end w/ hooks Treponema pallidum

QuickTime and a
TIFF (LZW) decompressor
are needed to see this picture.

QuickTime and a
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are needed to see this picture.

Capsules

Prevent phagocytosis
and help with attachment
(adherence)
Streptococcus pneumoniae
Klebsiella pneumoniae
Haemophilus influenzae
Bacillus anthracis
Streptococcus mutans
Yersinia pestis

Enzymes to help penetration

Many pathogens secrete enzymes that contribute to their pathogenicity:

Increase virulence by use of enzymes
And avoid phagocytosis
Coagulase
Kinases

Coagulate blood - wall off from host

make boil
Digest fibrin clot - allow
spreading
streptokinase and staphylolinase

Hyaluronidase
Collagenase
IgA proteases
Hemolysins

Hydrolyses hyaluronic
acid connective tissue
Hydrolyzes collagen
Destroy IgA antibodies
lyse RBCs

Hemolysins
Alpha Hemolytic Streptococci
-

secrete hemolysins that cause the incomplete lysis

or RBCs

Beta Hemolytic Streptococci

- secrete hemolysins that cause the complete lysis of RBCs

Leukocidins
Enzymes that attack certain types of WBCs
1. Kills WBCs which prevents phagocytosis
2. Releases & ruptures lysosomes
lysosomes - contain powerful hydrolytic enzymes which
then cause more tissue damage

Enzymes: Necrotizing Factor

Flesh Eating Bacteria
Necrotizing fasciitis
causes death (necrosis) to tissue cells

Summary of How Bacterial Pathogens

Penetrate
Host
Defenses
1. Adherence
2. Capsule
3. Enzymes
leukocidins
Hemolysins
Coagulase
Kinases
Hyaluronidase
Collagenase
Necrotizing Factor

Penetration into the Host Cell

Figure 15.2

Endotoxins
Endotoxins are lipopolysaccharides derived from

the outer membrane of gram-negative Bacteria.

Released upon lysis of the Bacteria, endotoxins cause
fever and other systemic toxic effects in the host.

Endotoxins
endotoxins are lioopolysaccharides (LPS) found in
the lipid portion of the outer wall of Gram bacteria
endotoxins are released when Gram bacteria die
and the cell wall undergoes lysis
antibiotics that are used to treat Gram
diseases can lyse the bacterial cells, releasing
the endotoxin
this can lead to an immediate worsening of
the symptoms
these symptoms usually improve as the
endotoxins break down

Endotoxins - part of the Gram (-)

LPS (Lipopolysaccharides)
O Antigen
Lipid A
Heat Stable (exotoxins are typically heat liable)
Lipid A - Toxin portion of the LPS
responsible for Fever that is associated with
many Gram (-) Bacterial infections
Gram (-) cells are digested endotoxins are
released - fever
Antibiotics
E. coli (0157:H7)
enterotoxin causes a hemolytic inflammation of the
intestines
results in bloody diarrhea

Bacterial cell wall

 Endotoxins are generally less toxic than

exotoxins (Table 21.5).

Endotoxin

Figure 15.4b

Endotoxins

Source

Gram

Metabolic product

Present in LPS of outer membrane

Chemistry

Lipid

Fever?

Yes

Neutralized by antitoxin

No

LD50

Relatively large

Endotoxins

Figure 15.6

Mechanisms of Pathogenicity

Figure 15.9

Endotoxins
endotoxins can also activate blood-clotting proteins,
causing the formation of small blood clots
blood clots obstruct capillaries, resulting in decreased
blood supply, which can lead to tissue death
this is referred to as disseminated intravascular
coagultaion
endotoxins also cause fever (pyrogenic response) and
rapid blood pressure decrease

Viral Pathogenesis Mechanisms

viral pathogenesis is very dependent on
gaining access to the host
evading the hosts defenses
causing damage to or death of the host cell while
continuing to reproduce themselves
viral access to the host was discussed in the virus
lecture; remember viral attraction is specific to the host
viruses bind more successfully to organisms found in
mucous membranes

Viral Evasion of Host

interferons play a role in limiting the ability of viruses
moving from neighbor cell to neighbor cell
once infected cells are capable of producing a protein
that can regulate and limit viral replication
some viruses are able to encode proteins to shut
down this cellular protective device

Viral Evasion of Host

though limited in the ability to control viruses, those few
antibodies that are used can be circumvented by viruses
that have developed methods to transfer directly from
one cell to its immediate neighbor
since antibodies control viruses by neutralizing
extracellular viral particles, the above renders this
useless

Virus and Host Damage

some viruses take-over and destroy the cell
virus causes inflammatory response more damage
more activation of inflammatory response
often times, in particular with the case of the common
cold, the inflammatory response initiated by the virus
causes much less effect than the domino effect of the
inflammatory response that follows

Mechanisms of Eukaryotic
Pathogenesis
these mechanisms are not clearly understood, though
the mechanisms include colonization of the host, evasion
of the host defenses and damage to the host
fungi
these organisms are generally opportunistic, taking
advantage of a weakening or change in our immune
system
excessive growth of Candida albicans is often a
result in immunocompormised hosts
C. albicans is the causative agent of thrush, a
common occurrence in AIDS patients

Mechanisms of Eukaryotic
Pathogenesis
eukaroytic parasites
are generally found in the intestinal tract or have
gained access through an insect bite
attach with specific receptors
are capable of hiding within the host cell
the damage they can inflict varies
some cause malnutrition by competing for
nutrients
some can cause direct damage by the enzymes
they produce

Terminology of Infectious Diseases

infectious dose
# of microbes needed to establish infection
some microorganisms are less contagious than
others and as a result require a larger number of
pathogens present to establish disease

Terminology of Infectious Diseases

sign
objective changes that are observable and
measurable
examples of signs include swelling, fever, paralysis
symptoms
subjective effects experienced by patient
examples of symptoms include pain or nausea

Terminology of Infectious Diseases

disease stages
incubation
the time between the initial infection and the first
appearance of any signs or symptoms
this time can vary depending on the pathogen and
the condition of the host
illness
signs and symptoms of the disease are experienced
if the disease is not successfully overcome or
treated, the patient dies during this period
convalescence
person regains strength and the body returns to its
pre-diseased state

Terminology of Infectious Diseases

types of infectious diseases
acute disease
rapid onset, short duration
influenza is an acute disease
chronic disease
develop slowly, last longer
the bodys reaction may be less severe
hepatitis B is a chronic disuse
latent disease
causative agent is never completely eliminated
remains inactive, but can become reactivated and
symptomatic if immune response is diminished
shingles is a latent disease

Terminology of Infectious Diseases

localized infections
invading microorganisms are limited to a small area
boils and abscesses are local infections
systemic infections
infectious agent spread throughout body by blood or
lymph
measles is a systemic infection

Control of Microbial Growth

History: Lister and Semmelwiess
Terminology
Physical Methods
Heat: Dry, moist, with pressure
Radiation: Ionizing and non-ionizing

Chemical Methods
Phenols, Halogens, Alcohols, Aldehydes, Metals,
Biguanides, Detergents, Oxides & Peroxides

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The Autoclave

Metabolism
Introductory Concepts
Nutritional patterns, Metabolism, ATP, Enzymes,
Re-Dox reactions, Phosphorylation reactions
Catabolism
Glycolysis, TCA cycle, Electron transport chain

Fermentations
Ethanol, Lactic acid

Anabolism
Biosynthesis

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