WK 3 - microbial control Flashcards
(148 cards)
1
Q
The first requirement needed by the bacteria is the
A
correct temperature.
2
Q
On the basis of preferred range of temperature,
bacteria can be classified as:
A
Psychrophiles, mesophile, thermophile, hyperthermophile
3
Q
grows in
temperature within 0 ̊C to 15 ̊C
(Alaska)
A
Psychotrophs-
4
Q
able to
grow between 20 ̊C to 30 ̊C
(Canada)
A
Moderate psychophiles-
5
Q
live between 50 ̊C to 60 ̊C
A
thermophile
6
Q
▪ need 80 ̊C or higher temperature
requirement
▪ some can tolerate as much as 121 ̊C
(same in autoclave)
A
hyperthermophile
7
Q
▪ involved in infectious disease
process
▪ live in moderate temperature
(between 25 ̊C to 40 ̊C)
▪ the optimum temperature is between
35 ̊C to 37 ̊C (body temperature)
▪ When culturing bacteria, set the
incubator at ±35 ̊C to cater the
optimum temperature that the
mesophiles would need.
A
mesophile
8
Q
Most bacteria grow best in a narrow pH range neutrality
A
between 6.5-7.5
9
Q
Lowest pH (acidic) recorded bacteria where it is able to
grow is pH 1 is
A
Chemoautotrophic bacteria
(cyanobacteria).
10
Q
Molds and yeasts grow at
A
pH 5 to 6,
11
Q
If the bacterial cellular water passes out
to the plasma membrane the bacterial
cell will shrink and will die
A
Hypertonic environment
12
Q
Bursting means lysing of the cell, the
bacterial cell will die.
A
hypotonic environmenr
13
Q
- salt loving bacteria that can tolerate 30% salt
A
Halophiles
14
Q
strictly needed for a hypertonic
environment for them to be able to live
A
Obligate halophiles
15
Q
2-5% salt concentration is what
they need in order to grow
A
Facultative halophiles
16
Q
what compsoes the dry weight of the bacteria
A
Nitrogen makes up the 14% of the dry weight of the bacterial
cell. Sulfur and Phosphorous are about 4%
17
Q
nitrogen sulfur and phosphorus
A
- These chemicals are needed by the bacteria for synthesis
of protein - For protein synthesis (Nitrogen and Sulfur)
- For DNA and RNA synthesis
- K, Mg, and Ca are also needed as co-factors for bacterial
enzymes
18
Q
trace elements in bacteria
A
- (Fe) Iron
- (Cu) Copper
- (Mo) Molybdenum
- (Zn) Zinc
- They are naturally present in tap water
19
Q
part time anaerobes, basically
aerobes their energy will decrease in the absence of
oxygen, they can use oxygen to their advantage
A
facultative anaerobe
20
Q
strict anaerobes, they can live
without the presence of oxygen
A
obligate anaerobe
21
Q
anaerobes that can tolerate
oxygen, they cannot use oxygen to their advantage
A
aerotolerant anaerobe
22
Q
– strict aerobes, oxygen is a requirement
A
obligate aerobe
23
Q
type of bacteria that can only tolerate
small amount of oxygen, around 5-10% of oxygen. Oxygen
in the air is around 21%.
A
microaerophiles
24
Q
needs carbon dioxide when
they metabolize and live
A
capnophile
25
is normal O2 boosted into a higher energy
state and is extremely active
singlet oxygen
26
formed in small amounts during the normal
respiration of organisms. SOD neutralizes
this.
superoxide free radicals
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Toxic from which is neutralize by catalase
converts it to water and oxygen;
Peroxide anion (O2
2-
)
28
Intermediate form of oxygen and probably the
most reactive. It is formed in the cellular
cytoplasm by ionizing radiation.
Hydroxyl radical (OH-
)
29
Organic Growth Factors
amino acids, purines,
pyrimidines, vitamins den ata
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chemically combine with dissolved oxygen and deplete the
oxygen in the medium
Reduced media is used such as sodium thioglycollate
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the step of mechanisms involved in the
development of the disease
Pathogenesis
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– the ability to cause disease
Pathogenicity
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study of the structural and functional
manifestation of the disease
pathology
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Injurious contamination of body or parts of the
body by bacteria, viruses, fungi, protozoa, and
rickettsia or by the toxin that they may
produce.
infection
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First time that the host will encounter a
microbe, virus, or any microbe is the primary
infection
primary infection
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o Subsequent infection by same organism in a
host (after recovery)
o After recovery, the same organism will attack
the host
reinfection
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o Infection by same organism in a host before
recovery
o Infection by the same organism before the
host could hardly recover
superinfection
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o When in a host whose resistance is lowered
by preexisting infectious disease, a new
organism may set up infection
o The host could have a bacterial infection in the
beginning, because of the
immunocompromised situation of the patient,
another infection set up by maybe a virus is
now on its way
secondary infection
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o It is the condition where due to infection at
localized sites like appendix and tonsil, general effects are produced.
o Only in a certain area of the body
focal infection
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o When a patient suffering from a disease and
new infection it set up from another host or
external source
o One patient with the disease, the infection is
transmitted to another host
cross infection
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o Cross infection occurring in hospital
o Hospital acquire infections
nosocomial infection
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disease cause by a microbe
and the microbes that cause infectious disease are
collectively referred to as pathogens.
Infectious disease
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The infection is in the patients but there are
no signs and symptoms that would tell you
that the patient is infected with the certain
microbe
subclinical infection
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, according to many microbiologists, means
colonization by a pathogen.
Infection
45
Acute, Subacute, and Chronic Disease
acute disease
- Has rapid onset usually by a relatively rapid recovery
- these are acute diseases you would recover from 1 to
2 weeks
chronic disease
- Has a slow onset and last a long time.
* Examples: Tuberculosis, leprosy, syphilis
* It will take a long time for a patient to recover from these
set of illness.
subacute
* Diseases that come on more suddenly than chronic
diseases but less suddenly than acute diseases.
* Somewhere in between acute and chronic illness
\
46
A disease that may go from being symptomatic to
asymptomatic and then back to being symptomatic.
latent infection
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The causative agent or pathogen remains inactive for a
period of time and then becomes active again when it
changes its mind and produce symptoms again
Latent Infections
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some evidence of a disease that is experienced or
perceived by the patient only
Symptoms
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some type of objective evidence of a disease
signs
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The time that elapses between the arrival of the
pathogen and the onset of symptoms
Incubation Period
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4 Periods in the Course of an Infectious Disease
1. incubation period
2.prodormal period
3. period of illness
4. convaslescent epriod
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Signs and symptoms are present but not specific
(nonspecific signs and symptoms)
Prodromal Period
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The time when the person experiences the symptoms
of the disease. Communicable diseases are mostly
easily transmitted during this stage
period of illness
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The time when the person recovers. Person may
recover from the illness but there may be permanent
damage of tissues of the affected area
convalescent period
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Steps in the Pathogenesis of Infectious Disease
ENTRY of the pathogen into the body
ATTACHMENT of the pathogen to some tissues
MULTIPLICATION of the pathogen
INVASION/SPREAD of the pathogen
EVASION of host defenses
DAMAGE to host
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It is a measure of the degree of pathogenicity; different
species or different strains of microbe vary in durability to
cause disease.
Virulence
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the phenotypic characteristics of
microorganisms that enable it to cause disease
Virulence factors
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capable of causing disease
Virulent Strains –
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not capable of causing disease
Avirulent strains
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Virulence Factors
attachment, endotoxin, exoenzyme
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Used to describe the molecule on the surface of
the pathogen that is able to recognize and bind to
a particular receptor
Adhesins and Ligand
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Therefore, the receptors and integrins are in the
host. While the adhesins and ligands are on the
pathogens.
Therefore, the receptors and integrins are in the
host. While the adhesins and ligands are on the
pathogens.
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enable the bacteria to
attach to the surfaces and cause infection
fimbriae / pilli
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Long thin, hair-like, flexible projections composed
of primarily of an array of proteins
pilli
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must live
within the host cells in order to survive and
multiply
Obligated Intracellular Pathogens
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When the pathogen is inside cell, antibodies
will not work for them because they are inside
the host cell
Obligated Intracellular Pathogens
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Pathogens that are able to survive
intracellularly and extracellularly. These
microorganisms are able to survive within
phagocytes.
Facultative Intracellular Pathogens
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Once ingested, they could opt to leave the cell and go
outside the host cell.
facultative intracellular pathogens
69
They can evade phagocytosis because they
are sticky or slimy
capsule
70
They enable to invade aqueous area of the
body that non-flagellated bacteria will not be
able to do. It is hard to be targeted by host
defense mechanism because moves around.
flagella
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enzymes that are liberated by the bacteria outside.
exoenzyme
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o Bacteria produce proteases and lipases which
cause destruction of tissues
necrotizing enzyme
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clot plasma and thereby form a sticky coat of
fibrin around themselves for protection
against phagocytes, antibodies, etc. so that
they may not be engulfed or not be
recognized by the phagocytes
coagulase
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Substance that will dissolve the fibrin clot that
the host will attempt to form (escape from
clots)
kinases or fibrinolysins
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Substance that will dissolve the fibrin clot that
the host will attempt to form (escape from
clots)
Hyaluronidase
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polysaccharide
cement that holds the tissues together
hyaluronic acid
77
Once the bacteria have this enzyme the tissue
will fall apart. When the tissue is destroyed,
the pathogen can spread throughout the
connective tissue.
Hyaluronidase
78
Breaks down collagen which is the supportive
protein found in tendons, cartilage and bones
enabling the pathogen to invade tissues
Collagenase
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o Enzymes that cause destruction of RBCs.
o Provides iron to the pathogen
o The pathogen lyses the RBCs so that it can
capture the iron
o The Hemolysins could be alpha-beta or
gamma hemolysis
hemolysins
80
breaks down phospholipids collectively
referred to as lecithin. This enzyme is
destructive to cell membrane of RBC and
other tissues
Lecithinase
81
Integral part of the cell walls of gram-negative
bacteria producing septic shock, chills, fever,
prostration, and septicaemia during gram negative
infection.
endotoxins
82
endotoxin aka
cell wall contains lipopolysaccharide
(LPS) called LIPID A, which is actually the endotoxin.
83
Characteristics of Endotoxins
* Proteins polysaccharide lipid complex heat stable
* Forms part of cell wall (don’t diffuse into medium)
* Obtained only by cell lysis
* They have no enzymatic action
* Effect is non-specific action
* No specific tissue affinity
* Active only in large doses 5 to 25 mg
* Weakly antigenic
* Neutralization by antibody infective
* Cannot be toxoided
* Produce in gram negative bacteria
84
They are also poisonous substances but they are
producing within the bacterial cells and it is released
from them. They are usually named from the target
organs that they affect.
exotoxins
85
Produced by strains of S. aureus and S.
pyogenes which primarily affect the integrity
of capillary walls.
Toxic shock syndrome toxin (TSST)
86
Also called epidermolytic toxin, causing sloughing
of the epidermal layers of the skin leading to SSSS
(staphylococcal scalded skin syndrome) cause by
Staphylococcus aureus or by some Streptococcus
pyogenes
exfoliative skin
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It is usually seen in newborn babies (skin reddish
and sloughing). The epidermal layer is removed in
the process.
wxfoliative toxin
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Toxin produced by Corynebacterium which
inhibits protein synthesis killing mucosal epithelial
cells and PMN’s (polymorphonucleus)
diptheria toxins
89
characteristic of exotoxin
* Heat labile protein
* Diffuse readily into the surrounding medium
* Highly potent, e.g. 3kg botulinum can kill all the inhabitants
of the world
* They are generally formed by Gr+ bacteria and also by some
Gr- organisms like Shigella, V. cholorae, and E. coli
- Usually produced primarily by gram positive
* Exotoxin is specifically neutralized antitoxin
* Can be separated from culture by filtration
* Action is enzymatic and it has specific tissue affinity
* Cannot cause pyrexia (high fever) in a host
* Can be toxoided
90
Pathogens are able to periodically change their
surface antigens
antigenic variation
91
They can mimic or coat and hide themselves.
camouflage and mimicry
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– pathogen surface would
resemble the host antigens. It will not be
recognized by the immune capabilities
molecular mimicry
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Some bacteria can produce molecules or enzymes
that could destroy our antibodies produced.
desctruction of antibodies
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ability to ward off disease
resistance
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Defenses that protect
against all pathogens like virus, bacteria and fungi
nonspecific
96
– vulnerability or lack of resistance. If you are
susceptible, you are prone to contract disease and different
infections brought by different microbes or pathogen.
susceptibility
97
Serve to protect the body from a variety of foreign
substances or pathogens (first and second line of
defense)
Non-specific Host Defense Mechanism
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Would cater to all types of pathogens. It will not
recognize if it is a virus, microbe, or bacteria.
* Will serve for all substances (toxins or pathogens)
Non-specific Host Defense Mechanism
99
Are directed against a particular foreign substance or
pathogen that has entered the body (third line of
defense)
specific host defense mechanism
100
If the first line of defense did not work, the second line
of defense will be activated. And when the second
defense did not work, the third line defense will be
activated.
specific host defense mechanism
101
Are non-specific natural barriers which restrict entry of
pathogens. It is naturally found in human.
first line of defense is (SHDM)
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second line fo defense (SHDM)
* Macrophages and neutrophil (phagocytic leukocytes)
* Proteins that are anti-microbial against different
pathogen
* Innate that provide rapid response against invading
pathogens once it breaches the first line of defense
(entering the skin or mucus membrane), the second
line of defense will be activated.
103
3rd line of defense (SHDM)
* It has antigen specific immune responses. The invaders
that will pass in two levels of non-specific defenses will
be attack specifically.
* B and T lymphocytes
* Y shape antibodies
* It develops in the process.
104
NSHDM FIRST LINE OF DEFENSE
PHYSICAL AND CHEMICAL BARRIERS
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Oily substance produced by sebaceous
glands that forms a protective layer over skin.
Contains unsaturated fatty acids which inhibit
growth of certain pathogenic bacteria and fungi.
SEBUM
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low, skin pH usually between 3 and 5. Caused
by lactic acid and fatty acids.
PH
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produced by sweat glands. Contain
Lysozyme and acids
EPRSPIRATION
107
Enzyme that breaks down gram-
positive cell walls. Found in nasal secretions, saliva
and tears.
LYSOZYME
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Parietal cells secrete mixture of
hydrochloric acid enzymes, and mucus. Ph
between 1.2 to 3 kills many microbes and destroys
most toxins. Many enteric bacteria are protected
by food particles.
GASTRIC JUICE
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By indigenous microflora; and over
all nutritional status and state of health
Microbial Antagonism AKA MICROBIOTA
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It is bacteria that inherently present in our body
that provides protection against invading
pathogens (no need to activate).
MICROBIOTA
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SECOND LINE OF DEFENSE IN NSHDM
TRNASFWERRIN, LACTOFERRIN
FEVER
INTERFERONS
INFLAMMATION
PHAGOCYTOSIS
COMPLEMENT SYSTEM
112
Are tie up iron (iron binding
protein), thereby preventing pathogens access to this
essential mineral.
TRANSFERRIN AND LACTOFERRIN
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That augments host defense by stimulating
leukocytes to deploy and destroy invaders, reducing
available free plasma iron, inducing of 1L - 1, which causes
proliferation, maturation, and activation of lymphocytes in
the immunologic response.
FEVER
114
Are small, antiviral proteins that prevent viral
multiplications in virus infected cells and serve to limit viral
infections.
INTERFERONS
115
Localizes an infection and prevent the
spread of microbial invaders, neutralizes toxins and aid in
the repair of damaged tissues.
INFLAMMATION
116
Involves approximately 30 different
blood proteins that interact in a step-wise manner known as
the complement cascade.
COMPLEMENT SYSTEM
117
CONSEQUENCE OF ACTIVATION OF THE COMPLEMENT
SYSTEM:
* Initiation and amplification of inflammation.
* Approximately 30 activated directly by pathogen.
* Indirectly by antigen antibody reaction.
* It generates active components in order to fight of the
invading pathogens.
118
predominate early in infection
NEUROPHILS
119
Originate from monocytes that
leave blood and enter infected tissue and develop into
phagocytic cells.
WANDERING MACROPHAGE
120
When injury happens, the cells nearby will send off chemical
signals in form of _________ to call out phagocytes to the
site of injury
CHEMOTAXIS
121
triggered by tissue damage due to infection, heat,
wound, etc.
INFLAMMATION
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4 CFARDINAL SYMPTOM OF INFLAMMATION
wound, etc.
* Four Cardinal Major Symptoms of Inflammation
1. Redness- Rubor
2. Pain- Dolor
3. Heat- Calor
4. Swelling- Tumor
but may also observe:
5. Loss of function
123
PURPOSE OF INFLAMMATION
1. Destroy and remove pathogens
2. If destruction is not possible, to limit effects by
confining the pathogen and its products.
3. Repair and replace tissue damaged by pathogen and
its products.
124
Consequences of Complement Activation:
CYTOLYSIS, INFLAMMATION, OPSONIZATION
125
- Due to the formation of a membrane
attack complex (MAC) which produces lesions in
microbial membranes.
\
- The bacterial cell will lies because of the
lesions that be created by the MAC.
CYTOLYSIS
126
Complement components (C3a)
trigger the release of histamine, which increases
vascular permeability.
INFLAMMATION
127
Complement components (C3b)
bind to microbial surface and promote
phagocytosis.
OPSONIZATION
128
Antiviral proteins that interfere with viral multiplication.
INTERFERON
129
TYPES OF INTERFERON
ALPHA, BETA GAMMA
130
INTERFERON produced by B-
lymphocytes, monocytes, and macrophages
ALPHA
131
Interferon : fibroblasts and other virus
infected cells.
beta
132
Interferon : activated by T-
lymphocytes and NK cells.
gamma
133
third line of defense against
pathogens; it is a specific host defense mechanism.
IMMUNE SYSTEM
134
Two types of acquired immunity
ACQUIRED AND PASSIVE
135
that is
acquired in response to the entry of a live
pathogen into the body (i.e., in response to an
actual infection). It has long duration.
Natural active acquired immunity:
136
acquired in response to vaccines. Its duration
for many years; but must be reinforced by
boosters.
Artificial active acquired immunity:
137
acquired by a fetus when it receives maternal
antibodies in utero or by an infant when it
receives maternal contained in colostrum. Its
duration from 6 months- 1 year.
Natural passive acquired immunity:
138
acquired when a person receives antibodies
contained in anti-sera or gamma globulin. Its
duration from 2-3 weeks.
Artificial passive acquired immunity:
139
2 TYPE OF IMMUNITY`
HUMORAL AND CELL-MEDIATED
140
: This is the greatest percentage of antibody molecules
in the blood, these globulins combine to small antigen and
combine and neutralize toxins (antitoxins). Long lived and
crosses the placenta.
IgG
141
is a pentamer, has 10 antigen binding sites, first
antibodies formed in the primary response to antigens.
Does not cross the placenta.
IGM
142
Known as secretory antibodies because they are found
in breastmilk, respiratory and intestinal mucin, saliva, tears,
and vaginal secretions protect these parts of the body from
infectious agents. It exists in three for monomer, dimere,
trimere. 10-20% of the total serum immunoglobulin is
compose of IgA
IGA
143
activities involved in both the resistance to parasites
infections and hypersensitivity. It is found on the surfaces of
basophils and muscles.
IGE
144
antibodies are made up of proteins, globular glycoproteins. It
can be found in the .
blood, saliva, colostrum, lymph
145
10-15% of lymphocytes in Peripheral
blood. B cells migrate to lymphoid tissues where they
produce antibodies that circulate through lymph and
blood. They live about 1-2 weeks.
B LYMPHOCYTES
146
weeks.
* T-lymphocytes: T-cells are phagocytic cells, it engulfs
the antigen or the pathogen that carries that antigen, it
destroys the infected body cells, and it rejects the
foreign tissue. About 70%-80% of the lymphocytes in
T CELL
147
