1
Q
First line of defense
A
- skin mucous membrane and their secretions
- skin- closely packed cells
- mucous membrane- mucus -> traps bacteria
- gastric juice- hydrochloric acid -> kills microbes
- cysts of protozoa and helminth -> resistant to acids -> hide through food particles
- tears, saliva, mucus -> lysozyme
- lysozyme- damages peptidoglycan cell wall -> kills bacteria
2
Q
secondary line of defense
A
- phagocytosis, inflammation, antimicrobial substances
- phagocytosis- deals with WBCs -> granulocytes
- 3 types of granulocytes:
- neutrophils
- eosinophils
- basophils
3
Q
neutrophils
A
- active during the initial stage of the infection
- phagocytic
- WBCs
- granules
- majority
4
Q
eosinophils
A
-phagocytic- not as good as neutrophils
‘-there are less eosinophils then neutrophils
-number of cells increase during protozoan and helminthic infestations
5
Q
basophils
A
-release histamine
6
Q
monocytes
A
- WBCs
- transform into macrophages in the tissue
- non phagocytic until it becomes a macrophage
7
Q
macrophages
A
- phagocytic
- active during the later stages of the infection
- derived from monocytes
- large
8
Q
lymphocytes
A
-immunity
9
Q
phagocytosis
A
- chemotaxis- response to chemicals that are released by the damaged cells -> phagocyte ends up in the area where the damage cells are
- attachment to microbes
- if the bacteria is not capsulated -> no trouble attaching
- if there is a capsule -> the microbe can escape (more pathogenic)
- bacteria is ingested by phagocyte
- microbe is in a vesicle -> phagosome (in the cytoplasm of phagocyte)
- lysosome fuses with the phagosome -> digestive enzymes in the lysosome are released on the bacteria
- bacterial cell is bathing in digestive enzymes -> breakdown phospholipids, DNA, RNA, proteins, peptidoglycans
- phagocyte directly kills microbes
10
Q
inflammation
A
- second line of defense
- response to tissue injury
- redness, pain, swelling
- caused by chemicals (acids), sharp objects, bacteria
- histamine- chemical that is released by mast cells in the connective tissue and basophils in the blood stream -> vasodilation
- leukotrienes are also released by mast cells and basophils -> increase vascular permeability
11
Q
leukotrienes
A
- released by mast cells and basophils (in addition to histamine)
- increase vascular permeability
- plasma in the blood leaks out of the blood vessels and ends up in the damaged area -> swelling
- plasma has anti-microbial proteins -> help destroy the microbes
12
Q
histamine
A
- chemical
- released by mast cells in the connective tissue
- also released by basophils in the blood stream
- released when basophils or mast cells are damaged
- causes vasodilation -> increase in diameter of blood vessel
- increase blood blow to damaged area
- mast cells and basophils also release leukotrienes
13
Q
inflammation mechanism
A
- sharp object cuts tissue
- object has microbes
- damaged mast cells and basophils release chemicals -> histamine and leukotrienes
- histamine causes vasodilation
- leukotrienes causes increase in vascular permeability -> plasma leaks out and causes swelling
- neutrophils circulate in the blood and come out of the blood vessels (squeeze through capillary walls) -> go to damaged area to destroy microbes (phagocytosis)
- monocytes come out of the blood vessel to the damage area -> becomes a macrophage in the tissue -> kills microbe and dead neutrophils and cells by phagocytosis
14
Q
neutrophils come out of the blood vessels before monocytes during inflammation
A
-true
15
Q
complement system
A
- second line of defense
- serum proteins (20 different)
- system can be activated by classical pathway and alternative pathway
- once activated it directly kills microbes
- the system kills bacteria
- also causes inflammation
- enhances phagocytosis
16
Q
classical pathway
A
- activates the compliment system
- antigen-antibody complex activates complement system
- bacterial cell (antigen)
- antibody attached to antigen -> antigen-antibody complex is formed -> complement proteins interact
- 20 different complement proteins -> numbered
- when the complement proteins interact the complement protein is converted to an enzyme -> breaks down another complement protein -> C3
- C3 is broken into 2 fragments -> C3a and C3b
- this activates complement system
- C3a and C3b have their own functions
17
Q
C3a
A
- fragment of C3
- attaches to mast cells and basophils -> stimulates release of histamine -> inflammation
18
Q
C3b
A
- fragment of C3
- opsonization- enhancement of phagocytosis by coating with C3b
- C3b fragments attach to the surface of the bacterial cell until its covered
- phagocyte can easily attach to the capsulated bacteria that underwent opsonization (cant escape anymore)
- also interacts with C5 and fragments it into -> C5b and C5a
19
Q
C5a
A
- fragment of C5 (cleaved by C3b)
- chemotaxis
- attracts phagocytes to the are of damage
- attaches itself to mast cells and basophils -> stimulate them to release histamine -> inflammation
20
Q
C5b
A
- fragment of C5 (cleaved by C3b)
- interacts with other complement proteins -> they all come together to form a complex on the cell wall/membrane of the bacteria
- complex makes a hole in the cell well/membrane
- cytoplasm leaks out -> death of bacterial cell
- complement proteins get together and directly kill microbes
21
Q
alternative pathway
A
- activates complement system
- polysaccharides on the bacterial cell surface itself reacts with C3 -> fragments it into C3a and C3b
- all the other steps from the classical pathway are the same here
- no antigen-antibody complex required
22
Q
interferon
A
- prevents the spread of the virus from the infected host cells to other cells in the area
- anti-microbial
- protein that is produced by virus infected cell
- releases the interferon into external environment
- interferon diffuses to the neighboring host cells (not infected)
- attaches to the plasma membrane of the neighboring cell
- stimulates this cell to make anti-viral protein
- warns the other cells that a virus is in the are
- the original host cell that had the virus will release virus
- virus will penetrate and uncoat in neighboring cells
- biosynthesis of the virus doesnt take place bc the antiviral proteins will prevent
- reproduction of virus is stopped
23
Q
resistance
A
- 2 types:
- innate
- acquired
24
Q
innate resistance
A
- one is born with the resistance
- all humans are resistant to certain animal disease such as canine distemper
- distemper virus infects the nervous system of dogs
- humans cant get the disease because humans do not have the receptor for the virus
- born without receptor for the virus
- no attachment -> no damage
25
acquired resistance
- acquired immunity
- artificially or naturally acquired
- resistance is acquired during one's lifetime
- immunity is a specific defense response
- there is an interaction between an antigen and the immune system
- immune system makes antibodies in response to antigen
- antibodies are specific
- 2 types: natural and artificial (can be active or passive for each)
26
antigen
- anything from outside of body
- not made by our body
- antigen is a foreign substance
- bacteria, pollen, insect venom, transplanted tissue
27
acquired immunity: naturally acquired
- active- antigens enter the body naturally (ingestion, cut, etc.) -> body produces antibodies and specialized lymphocytes
- takes a long time to make these antibodies -> person usually gets the disease
- antibodies are made by the persons own immune system
- passive- antibodies pass from mother to fetus via placenta or to infant in the mothers milk
28
acquired immunity: artificially acquired
- active- antigens are introduced in the vaccines -> body produces antibodies and specialized lymphocytes
- antibodies are made by the persons own immune system
- lasts long time
- passive- preformed antibodies in immune serum introduced into body by injection
- from another person that is immune
- neutralize toxin
- tetanus
- immunity doesnt last long
29
active immunity
- long lasting
- antigens introduced
- antibodies made by the person themselves
- can be artificial or natural
30
passive immunity
- can be artificial or natural
- not long lasting
- antibodies are introduced from someone else who is already immune
31
antigenic determinant (epitope)
- molecules that are found on the surface of the antigen
- stick out
- easily interact with the immune system -> stimulate to make antibodies
- each has own unique shape
- makes antibodies specific to the epitopes unique shape
- if there are 3 different types of epitopes on the antigen -> 3 different specific groups of antibodies will be made
32
antibody
- protein -> made up polypeptide chains
- 2 heavy chains
- 2 light chains- shorter and fewer amino acids
- Y-shaped
- 2 antigen bindings sites
- shape of antigen binding site is complementary to the epitope -> lock in key fit
- Fc region- stem region of antibody -> only heavy chains present
- Fc region attached to WBCs like neutrophils and basophils
33
IgG
- antibody
- IgG (immunoglobulins)- 80% of the antibodies in the serum
- IgG is the only antibody that can cross placenta and give passive immunity to the fetus
- protect against viruses, bacteria, and toxins that are circulating in the body fluids
- activates the compliment system -> directly kills microbes
- enhances phagocytosis
34
IgM
- 5-10% in the blood
- pentamers- 5 units of antibodies are attached
- first antibodies to show up in the response to the initial infection
- activates the complement system
- agglutinates (clump) antigens
35
IgA
- 10-15% in the blood
- found in body secretions -> mucus, saliva, tears
- secretory IgA is a dimer -> 2 units of antibodies are attached
- prevent the attachment of bacteria and viruses to the mucosal surfaces
- when they cant attach -> no destruction
36
IgD
- .2% of the serum antibodies
- no clear function
- found on the surface of the B lymphocytes
- functions as an antigen receptors
37
IgE
- .002% of the serum antibodies
- involved in allergic reactions
- cause allergic reactions
38
immunity
- humoral immunity- B lymphocytes, antibodies
| - cell mediated immunity- T lymphocytes
39
humoral immunity
- branch of immune system
- B lymphocytes- B cells
- B cells respond to extracellular antigens
- antigen attached to b cells -> b cells reproduce itself
- some copies become plasma cells and some memory
- B cells develop from the stem cells in the bone marrow
- clonal selection
- mature in the bone marrow
- they then migrate to the lymph, lymph nodes, blood and spleen
40
clonal selection: humoral immunity
- produce antibodies
- salmonella ex.
- lymphocyte clones with different receptor shapes are hanging out in the lymph nodes
- salmonella shows up in the lymph nodes
- bacteria selects a clone to react with based on the selective shape
- interaction stimulates proliferation -> many more B cell clones are made
- some of the copies of the clone become memory cells and some plasma cells
- plasma cells make the antibodies -> antibodies are transported throughout the blood
- these antigens are specific to salmonella
41
agglutination
- antibodies cause agglutination of antigens
- clump antigens
- helpful to phagocytes
- phagocytes can scoop up a bunch of antigens at
- time efficient
- enhances phagocytosis and reduces number of infectious units to be dealt with
42
opsonization
- antibodies attach to surface of antigen until it is covered
- capsulated bacteria is now able to be phagocytized
- coating antigen with antibody enhances phagocytosis
43
neutralization
- antibodies block attachment site that are found on the virus
- prevent virus from attaching to host cells
- block bacteria from attaching to the mucus membrane by attaching themselves to the surface of the bacterial cell
- antibodies can attach themselves to the fimbriae so they cant attach to mucous membranes
- neutralize toxin
- toxins can interact with cells in our body
- blocks active site of toxin
44
action of compliment system
- antigen-antibody complex activate the compliment system
- complement system directly kills microbes by making holes in them
- once the complement system is activated some of the compliment proteins cause inflammation -> 2nd line of defense
45
antibody-dependent cell-mediated cytotoxicity
- antibodies attached to target cell cause destruction by non-specific immune system cells
- used to destroy large pathogens like helminths
46
antibodies
- do not directly kill microbes but they help
- protective mechanism of binding antibodies to antigens
- agglutination
- opsonization
- neutralization
- antibody-dependent cell-mediated cytotoxicity
- inflammation
- activation of compliment system
47
memory cells: primary response
- antigen goes into system for the first time
- a few days after IgM antibodies that are specific to the antigen show up
- IgM are the first antibodies to show up
- IgG show up after
- amount of antibodies in the blood increase slowly and gradually
- pathogen grows and causes damage -> symptoms show up -> person gets the disease
- once the person produces enough antibodies -> pathogen is removed -> antibodies decrease
- antibodies are made but it takes a while -> person gets the disease -> recovery -> memory cells are made
48
memory cells: secondary response
- if the same antigen enters the system
- memory cells differentiate into plasma cells
- IgG antibody production explodes
- IgG help the complement system to remove the pathogen
- pathogen is killed quickly become the pathogen gets a chance to cause sickness
- no symptoms
- immune to pathogen
49
cell mediated immunity
- T cells have receptors for antigen
- T cells respond to intracellular antigens
- clonal selection is involved
- memory cells are made
- when T cells are stimulated by antigen they do not make antibodies (unlike humoral/b cells)
- they make proteins known as cytokines
50
Intracellular antigens
- T cells do not respond to antigens floating around in the body fluids
- only respond to intracellular antigens
- antigen has to be processed and presented to the T cells by an antigen presenting cell -> macrophage
51
T lymphocytes
-develop from bone marrow
-migrate to thymus gland
-maturation in the thymus gland
-T cells migrate to the lymph nodes, spleen, blood, lymph
3 types:
-helper T cells (TH)
-cytotoxic T cells (Tc)
-suppressor T cells (Ts)
52
helper T cells
- protect us from infections
- respond only to the intracellular antigens
- antigen must be presented by antigen presenting cell (APC) -> macrophage
- macrophage picks up the antigen -> phagocytosis -> antigen is broken down -> fragments of the antigen migrate to the surface of the APC -> helper T cells bind with complementary receptor
- stimulates the macrophage to release interleukin-1 (IL-1) -> stimulates helper T cell to release interleukin-2 (IL-2)
- interleukin-2- T cell growth factor -> helper T cells are cloned
- some copies of the helper T cell clones become: cytotoxic T cells, some activated helper T cells, and some memory cells
- memory cells give immunity (secondary response)
- activated helper T cells release cytokines ( B cell growth factor and gamma interferon) and proteins
- cytotoxic T cells- protect us from virus infections
53
activated helper T cells
- some helper T cells differentiate into activated helper T cells
- release cytokines and proteins
- cytokines: B cell growth factor and gamma interferon
- B cell growth factor- helps B cell to grow and make antibodies
- gamma interferon- helps macrophage to do its job better
54
cytotoxic T cell
- attaches itself to virus infected cell
- releases a protein -> perforin
- perforin makes holes in the virus infected cell
- virus infected cell dies
- virus cannot reproduce
- cytotoxic T cells protect us from virus infections by killing and destroying cells that are infected with virus
55
gamma interferon
- produced by activated helper T cells
- activates macrophages
- activated macrophages look different than normal macrophages
- activated macrophages are larger and ruffled
- activated macrophages are better at phagocytosis
56
T independent antigens
- polysaccharide antigens such as those found in the capsules of bacteria
- B cells can make antibodies for the T independent antigens on their own
- they do not need help from the T cells
57
T dependent antigens
- made of proteins such as those found in the capsids of viruses
- B cells cannot make antibodies against T dependent antigens on their own
- they have to get help from helper T cells to make antibodies against T dependent antigens
58
suppressor T cells
- prevent the antibodies from attacking ones own cells/organs
- stop the immune response once the antigen has been removed from the system
59
natural killer cells
- different class of lymphocytes
- they come in contact with tumor cells
- produce toxins and enzymes
- destruction of the tumor cells
60
lymphocytes
- T lymphocytes
- B lymphocytes
- Natural killer cells
61
antibody dependent cell mediated cytotoxicity
- process by which the immune system gets rid of large parasites (like helminths)
- phagocytosis wont help bc the parasites are larger than the phagocytes
- immune system makes antibodies against the cells that make up the helminth
- attach to the cells on the surface of helminth
- Fc region (stem) of the antibody is sticking out on the surface of the helminth
- phagocytes, neutrophils, eosinophils, macrophages -> attached to the stem region
- these phagocytes release various enzymes like perforin that makes holes in the cells
- enzymes break down
- parasite can be killed
62
HIV
- retrovirus
- has reverse transcriptase
- RNA is the genetic material
- has a capsid that is surrounded by an envelope
- it has spikes made of glycoproteins -> attachment sites
- virus uses glycoprotein to attach itself to host cell
- host cell for this virus the helper T cell (HIV attaches to helper T cell via receptor)
- helper T cell has the receptor the HIV -> CD4 receptor
- CD4 is a type of protein found on the plasma membrane of the cell -> cell function and also receptor function
- HIV doesnt infect other cells bc they dont have the receptor
- once HIV enters the helper T cell the viral DNA is made with reverse transcriptase
- viral DNA migrates to the nucleus of the host cell
- DNA inserts into the chromosome
- biosynthesis of the virus
- viral RNA is made and translated -> viral proteins
- assembly of virus
- virus takes over helper T cell
- helper T cell cant make cytokines anymore
63
how the virus escapes the immune system
- damages the cell that plays a central role in the immune response -> weakens immune system
- virus has RNA as genetic material -> high mutation rate
- many strains of the virus are developed
- antibodies that are produced against one strain are not effective against the other strains
- virus stays as a provirus -> allows to hide from immune system
- stays within the vesicles in the host cell
- stimulates the infected cell to fuse with the uninfected cell in the area
- virus is hopping from one host cell to another without even coming out of the host cell
- immune cannot see the virus
64
treating HIV
- indirect ELISA test diagnoses HIV infection
- transmitted by sexual contact -> blood transfusion
- contaminated needles
- one of the drugs used to treat the disease -> zidovudine (AZT)
65
hypersensitivity, allergy, anaphylaxis
- abnormal immune response
- IgE antibodies are produced against antigens (pollen, insect venom, fungal spores) -> instead of IgG
- first exposure- the person becomes sensitized (weak response)
- IgE antibodies are made
- IgE antibodies use the stem region to attach to mast cells and basophils
- antigen binding sites are exposed
- secondary response- subsequent exposure results in anaphylaxis
- when antigen gets into system ag -> antigen attached to binding site of IgE on surface of mast cells and basophils -> release histamine -> anaphylaxis
- symptoms show up within a few minutes after the exposure to the antigen
66
systemic anaphylaxis
- caused by injected antigens such as insect venom
- some people are allergic to bee sting
- venom binds to IgE present on the surface of mast cells and basophils -> stimulate them to release chemical mediators (histamine)
- histamine causes vasodilation -> drop in blood pressure
- cause damage to the blood vessels -> drop in blood pressure known as shock
- treated with epinephrine
67
localized anaphylaxis
- caused by inhaled antigens such as pollen and fungal spores
- attach to IgE antibodies on the mast cells lining the respiratory tract release histamine
- watery eyes, runny nose, coughing and sneezing
- antihistamine
68
allergic contact dermatitis
- T cells are involved (IgE isnt involved for this one)
- reaction to poison ivy is an example
- first exposure- might not be any symptoms
- secondary exposure- response is stronger -> larger amount of cytokines are produced
- cause damage to the cells which result in rash
- poison ivy has chemical named catechol -> attach to proteins in the skin cells
- T cells react to the catechol attached to skin cells -> memory cells produced in primary response
- secondary response- memory cells become activated helper T cells that release cytokines -> cause damage to skin -> rash
69
autoimmune disorders: myasthenia gravis
- antibodies are produced against ones own muscles
- death due to respiratory failure
- suppressor cells are not working right
- antibodies are made against ones own cells
70
normal flora (normal microbiota)
- normal flora is found in respiratory tract, GI tract, genitourinary tract and skin
- fetus growing in the uterus has no normal flora
- baby picks up the bacteria when the baby comes through the birth canal
- usually lactobacillus -> first to colonize the baby
- as the baby starts breathing and drinking more and more bacteria colonizes the baby
71
symbiosis
-relationship between the normal flora and the host
72
commensalism
- one of the organism is benefited while the other is unaffected
- type of symbiotic relationship
- ex. corynebacterium live son the surface of the eye -> get nutrients from sloughed of tissue
- bacteria benefits from the host but doesnt benefit/harm the host
73
mutualism
- both organisms benefit from each other
- type of symbiotic relationship
- E. coli in the large intestine makes vitamin K
- vitamin K is absorbed into the blood and used for blood clotting
- E. coli gets shelter and nutrients from the host
74
parasitism
- one organism is benefited at the expense of the other
- pathogens such as mycobacterium tuberculosis are parasites
- benefit from the host and cause infections to host
75
opportunists
- part of the normal flora
- do not cause problems when ones immune system is healthy
- they can cause infection such as UTI when ones immune system is weak
76
sporadic disease
- the disease shows up once in a while in a population
| - typhoid fever in the USA
77
endemic disease
- the disease is constantly present in a population
| - common cold, malaria in africa
78
epidemic disease
- many people in a given area get the disease within a short time
- 50% of the population here get flu within a week
- flu is an epidemic disease
79
pandemic disease
- epidemic disease that is worldwide
- AIDS is a pandemic disease
- COVID-19
80
acute disease
- develops rapidly and lasts only for a short time
| - influenza
81
chronic disease
- develops slowly and lasts for a long time
- can lay dormant
- tuberculosis
82
latent disease
- microbe stays inactive for a long time and then becomes active to produce symptoms
- herpes simplex virus 1
83
local infection
- infection is limited to a small area of the body
| - blisters, vesicles
84
systemic infection
- microbes or their products spread throughout the body
| - diptheria- diptheria toxin is in the blood throughout the body
85
septicemia
-growth of bacteria in the blood
86
primary infection
- infection causing the initial illness
- viruses
- influenza virus- causes damage to cells lining respiratory tract
87
secondary infections
- caused by an opportunist after the primary infection
- hemophilus influenzae- part of normal flora of throat
- once primary infection causes damage to the respiratory tract it takes advantage of it
- causes pneumonia
88
source of reservoir of the disease: humans
- some people are carriers of pathogens
- transmit the microbe directly or indirectly to others
- typhoid fever (only in humans)
89
source of reservoir of the disease: animals
- some diseases are transmitted from animals to humans
- lyme disease- spirochete (Borrelia burgdorferi)
- found in field mice
90
source of reservoir of the disease: nonliving things
- soil transmits fungal spores
| - endospores of clostridium -> tetanus
91
symptoms
- subjective
- not seen by the observer
- cannot be measured
- discomfort
- pain
92
signs
- can be seen by the observer and measured
- fever
- swelling
93
communicable disease
- disease spreads from one host to another
- most diseases caused by microbes
- tuberculosis
- typhoid fever
94
contagious disease
diseased that easily spreads from one person to another
| -plague
95
non communicable
- disease is not spread from one person to another
- tetanus
- tetanus is caused by the bacterium (endospores) in the soil
96
transmission of the disease
-contact transmission
97
contact transmission
- 2 types: direct contact transmission and indirect contact transmission
- direct contact transmission- by kissing, touching, sexual contact
- ex. syphilis, genital herpes
- indirect contact transmission- by a nonliving object -> fomite
- fomite- transmits disease from one host to another
- ex. towels, facial tissues, contaminated needle (HIV), stuffed animals
98
droplet transmission
- droplets released during coughing and sneezing
| - cold, influenza, diphtheria
99
vehicle transmission
-by water, food and air
100
waterborne transmission
- cholera
| - contaminated water
101
foodborne transmission
- undercooked contaminated meat
- tapeworm infestations
- taenia saginata
- taenia solium
102
airborne transmission
- fungal spores
- can be inhaled
- coccidiodomycosis
- caused by fungus -> Coccidioidea immitis -> produces arthrospores
- arthrospores are found in the soil in places like new mexico, arizona
- spores can end up in air -> inhale
- just by driving through
103
vectors
- can transmit infections
- insects
- insects passively transmit disease
- in the context of genetic engineering -> vector = plasmid
104
passive transmission
- insect picks up bacteria from eye infection and release it on to another persons eyes
- insect=vector
- inoculates another host with the bacteria
105
biological transmission
- insect bite can introduce microbe
- injects plasmodium into the blood
- malaria
- mosquito
- insect=vector
106
development of disease: period of incubation
- period between the initial infection and appearance of signs and symptoms
- depends on virulence of microbe, number of infecting organisms, resistance of the host
107
development of disease: prodormal period
- characterized by early mild symptoms
- nonspecific symptoms
- aches, fatigue
108
development of disease: period of illness
- exhibits signs of symptoms of the disease
- fever, chills, pains
- period of illness for scarlet fever- pinkish red rash appears on the skin and mucous membranes
- immune response overcomes the pathogen
109
development of disease: period of decline
- pathogen is removed from immune system
- signs and symptoms subside
- patient is vulnerable to secondary infection by opportunists
110
development of disease: period of convalescence
-the patient regains strengths and recovery has occurred
111
nosocomial infections
- infection one gets when one stays in the hospital
- caused by opportunists such as E. coli
- pseudomonas
112
epidemiology
- a study of the source, transmission, prevention of disease
- 1848 John Snow- interviewed people
- people who drank from the broad street pump got the disease cholera
- people who did not drink from this pump did not get the disease
- he broke the handle of the broad st pump -> dramatically reduced the number of cholera cases
- source- water coming out of the pump
- transmission- drinking the water
- prevention- breaking the pump
113
portals of entry
- pathogens have to enter the system to cause disease
- regions/areas of the body used by microbes to enter the system are portals of entry
- respiratory tract: the easiest and most frequently used -> pneumonia, tuberculosis, common cold
114
portal of entry: GI tract
- contaminated food or water
- dysentery
- cholera
- typhoid
- fever
115
portal of entry: genitourinary tract
- syphilis
- gonorrhea
- lymphogranuloma venereum
116
portal of entry: skin
- intact skin protects us from microbes
| - larvae of necator americanus can make a hole and get into the system via skin
117
portal of entry: parenteral route
- established by cuts, insect bite
- malaria- transmitted through insect bite
- tetanus- enters through deep puncture wound
118
preferred portal of entry
- salmonella typhi causes typhoid fever when the bacteria is ingested
- when the bacteria is rubbed on the skin it wont cause the disease -> cant penetrate the skin
119
infective dosage
-a few bacteria enter the body -> the immune system gets rid of the microbes
120
numerous dosage
- numerous bacteria enter the body -> immune system can handle it
- some stay alive and cause damage -> symptoms
121
virulence factors
- make microbes more pathogenic
- capsules- capsulated bacteria escape from phagocytes
- proteins- certain proteins on the surface of the bacterial surface helps the bacteria to attach itself to the epithelial cells of the host
- M-protein- found on the surface of streptococcus pyogenes to attach to mucous membrane
122
enzymes
-made by bacteria -> make bacteria more pathogenic
123
collagenase: enzyme
- made by clostridium
- breaks down collagen (protein) in the connective tissue
- helps bacteria to spread from initial site of infection to other parts of body
124
endotoxin
- associated with gram - bacteria
- causes septic shock
- made up of lipid A
- lipid A is found in the outer layer of g- bacteria
- g- is more pathogenic then g+
125
exotoxin
- usually associated with G+ bacteria (some g-)
- exotoxin is a protein
- made in the bacterial cell and then released into the external environment
- ex. diphtheria toxin -> killed eukaryotic cells and damage to organs
- more pathogenic
126
plasmids
- more pathogen
- R plasmids make the bacteria resistant to antibiotics
- harder to kill
127
hyaluronidase: enzyme
- clostridium make hyaluronidase
- breaks down polysaccharide hyaluronic acid in the connective tissue
- enzyme helps spread form the initial site of infection to other parts of the body
- makes more pathogenic
128
hemolysin: enzyme
- streptococci make hemoylsin
- kills RBCs
- not enough O2
- cannot make proteins well
- makes more pathogenic
129
leukocidins: enzyme
- streptococci make the enzyme leukocidins -> kills WBCs
| - make more pathogenic
130
lysogeny
- lysogenized bacteria are more virulent (pathogenic)
- phage DNA is inserted into the chromosomes
- phage DNA codes for a toxin
- lysogenized corynebacterium diphtheriae -> produces diphtheriae toxin
- causes damage to eukaryotic cells -> damage organs
131
neurotoxin
- amanita phalloides produces a neurotoxin
- causes hallucinations and damage to liver
- death within a week
- fungus
- alexandrium (algea) also produces a neurotoxin -> causes paralytic shellfish poisoning
- pathogenic
132
protozoa
- cause damage to cells
- cause infections
- plasmodium causes damage to RBCs
- grows in the RBCs -> destroys
- pathogenic
133
helminths
- necator americanus gets into our system
- attaches to intestinal wall
- drinks blood
- weakens immune system
- anemia
- pathogenic
134
viruses
- obligate intracellular parasites
- get into host cells and reproduce
- once done with reproduction the host cell is destroyed
- damage to cells
- pathogenic
135
boiling
- kills microbes by coagulating the proteins
- endospores are not destroyed
- endospores are resistant to hostile environments like boiling water
136
autoclaving
- temperature 121C, 15 PSI, 15 mins
- even the endospores are destroyed here
- all forms of microbial life is destroyed
- medium that needs to be sterilized is placed in the chamber
137
dry heat
- direct flaming is used to sterilize the inoculating loop
- bacinerator
- all microbes are destroyed (including endospores)
138
refrigeration
- slows down the growth of microbes
- does not kill the microbes
- preserves food products
139
osmotic environment
- high concentration of salt
- hypertonic
- kills most microbes
- water from cytoplasm comes out -> dehydration -> shrink
- plasmolysis
- preserves food products
140
UV light
- mutation
- control microbial growth of nonliving things
- inducing the formation of thymine dimers in DNA
141
gas sterilization
- ethylene oxide gas is used to sterilize:
- mattresses
- petri plates
142
quaternary ammonium compounds
- damage to the plasma membrane of the microbes
| - used in mouthwash
143
sodium nitrite
- preserve meat products
- prevent the germination of botulism endospores
- used to preserve hot dogs
144
sterilization
-removal or destruction of all forms of microbial life
145
pasteurization
- does not get rid of all microbes
- reduces spoilage organisms and pathogens
- equivalent treatments
- beverages are heated at 63C for 30 mins
- milk
146
filtration
- sterilization procedure
- sterilize solutions that are sensitive to heat
- solutions of enzymes
- goes through filter -> microbes stay on surface of filter
- separate the microbes from the solution
- does not kill microbes
- removes microbes >.22um
- makes sterile filtrate
Microbiology
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