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FINAL Flashcards

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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
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2
Q

secondary line of defense

A
  • phagocytosis, inflammation, antimicrobial substances
  • phagocytosis- deals with WBCs -> granulocytes
  • 3 types of granulocytes:
  • neutrophils
  • eosinophils
  • basophils
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3
Q

neutrophils

A
  • active during the initial stage of the infection
  • phagocytic
  • WBCs
  • granules
  • majority
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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

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5
Q

basophils

A

-release histamine

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6
Q

monocytes

A
  • WBCs
  • transform into macrophages in the tissue
  • non phagocytic until it becomes a macrophage
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7
Q

macrophages

A
  • phagocytic
  • active during the later stages of the infection
  • derived from monocytes
  • large
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8
Q

lymphocytes

A

-immunity

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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
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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
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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
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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
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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
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14
Q

neutrophils come out of the blood vessels before monocytes during inflammation

A

-true

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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
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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
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17
Q

C3a

A
  • fragment of C3

- attaches to mast cells and basophils -> stimulates release of histamine -> inflammation

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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
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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
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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
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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
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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
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23
Q

resistance

A
  • 2 types:
  • innate
  • acquired
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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
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25
Q

acquired resistance

A
  • 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)
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26
Q

antigen

A
  • anything from outside of body
  • not made by our body
  • antigen is a foreign substance
  • bacteria, pollen, insect venom, transplanted tissue
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27
Q

acquired immunity: naturally acquired

A
  • 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
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28
Q

acquired immunity: artificially acquired

A
  • 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
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29
Q

active immunity

A
  • long lasting
  • antigens introduced
  • antibodies made by the person themselves
  • can be artificial or natural
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30
Q

passive immunity

A
  • can be artificial or natural
  • not long lasting
  • antibodies are introduced from someone else who is already immune
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31
Q

antigenic determinant (epitope)

A
  • 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
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32
Q

antibody

A
  • 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
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33
Q

IgG

A
  • 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
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34
Q

IgM

A
  • 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
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35
Q

IgA

A
  • 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
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36
Q

IgD

A
  • .2% of the serum antibodies
  • no clear function
  • found on the surface of the B lymphocytes
  • functions as an antigen receptors
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37
Q

IgE

A
  • .002% of the serum antibodies
  • involved in allergic reactions
  • cause allergic reactions
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38
Q

immunity

A
  • humoral immunity- B lymphocytes, antibodies

- cell mediated immunity- T lymphocytes

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39
Q

humoral immunity

A
  • 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
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40
Q

clonal selection: humoral immunity

A
  • 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
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41
Q

agglutination

A
  • 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
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42
Q

opsonization

A
  • antibodies attach to surface of antigen until it is covered
  • capsulated bacteria is now able to be phagocytized
  • coating antigen with antibody enhances phagocytosis
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43
Q

neutralization

A
  • 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
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44
Q

action of compliment system

A
  • 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
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45
Q

antibody-dependent cell-mediated cytotoxicity

A
  • antibodies attached to target cell cause destruction by non-specific immune system cells
  • used to destroy large pathogens like helminths
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46
Q

antibodies

A
  • 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
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47
Q

memory cells: primary response

A
  • 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
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48
Q

memory cells: secondary response

A
  • 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
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49
Q

cell mediated immunity

A
  • 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
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50
Q

Intracellular antigens

A
  • 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
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51
Q

T lymphocytes

A

-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)

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52
Q

helper T cells

A
  • 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
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53
Q

activated helper T cells

A
  • 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
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54
Q

cytotoxic T cell

A
  • 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
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55
Q

gamma interferon

A
  • 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
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56
Q

T independent antigens

A
  • 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
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57
Q

T dependent antigens

A
  • 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
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58
Q

suppressor T cells

A
  • prevent the antibodies from attacking ones own cells/organs
  • stop the immune response once the antigen has been removed from the system
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59
Q

natural killer cells

A
  • different class of lymphocytes
  • they come in contact with tumor cells
  • produce toxins and enzymes
  • destruction of the tumor cells
60
Q

lymphocytes

A
  • T lymphocytes
  • B lymphocytes
  • Natural killer cells
61
Q

antibody dependent cell mediated cytotoxicity

A
  • 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
Q

HIV

A
  • 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
Q

how the virus escapes the immune system

A
  • 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
Q

treating HIV

A
  • 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
Q

hypersensitivity, allergy, anaphylaxis

A
  • 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
Q

systemic anaphylaxis

A
  • 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
Q

localized anaphylaxis

A
  • 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
Q

allergic contact dermatitis

A
  • 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
Q

autoimmune disorders: myasthenia gravis

A
  • 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
Q

normal flora (normal microbiota)

A
  • 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
Q

symbiosis

A

-relationship between the normal flora and the host

72
Q

commensalism

A
  • 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
Q

mutualism

A
  • 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
Q

parasitism

A
  • 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
Q

opportunists

A
  • 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
Q

sporadic disease

A
  • the disease shows up once in a while in a population

- typhoid fever in the USA

77
Q

endemic disease

A
  • the disease is constantly present in a population

- common cold, malaria in africa

78
Q

epidemic disease

A
  • 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
Q

pandemic disease

A
  • epidemic disease that is worldwide
  • AIDS is a pandemic disease
  • COVID-19
80
Q

acute disease

A
  • develops rapidly and lasts only for a short time

- influenza

81
Q

chronic disease

A
  • develops slowly and lasts for a long time
  • can lay dormant
  • tuberculosis
82
Q

latent disease

A
  • microbe stays inactive for a long time and then becomes active to produce symptoms
  • herpes simplex virus 1
83
Q

local infection

A
  • infection is limited to a small area of the body

- blisters, vesicles

84
Q

systemic infection

A
  • microbes or their products spread throughout the body

- diptheria- diptheria toxin is in the blood throughout the body

85
Q

septicemia

A

-growth of bacteria in the blood

86
Q

primary infection

A
  • infection causing the initial illness
  • viruses
  • influenza virus- causes damage to cells lining respiratory tract
87
Q

secondary infections

A
  • 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
Q

source of reservoir of the disease: humans

A
  • some people are carriers of pathogens
  • transmit the microbe directly or indirectly to others
  • typhoid fever (only in humans)
89
Q

source of reservoir of the disease: animals

A
  • some diseases are transmitted from animals to humans
  • lyme disease- spirochete (Borrelia burgdorferi)
  • found in field mice
90
Q

source of reservoir of the disease: nonliving things

A
  • soil transmits fungal spores

- endospores of clostridium -> tetanus

91
Q

symptoms

A
  • subjective
  • not seen by the observer
  • cannot be measured
  • discomfort
  • pain
92
Q

signs

A
  • can be seen by the observer and measured
  • fever
  • swelling
93
Q

communicable disease

A
  • disease spreads from one host to another
  • most diseases caused by microbes
  • tuberculosis
  • typhoid fever
94
Q

contagious disease

A

diseased that easily spreads from one person to another

-plague

95
Q

non communicable

A
  • disease is not spread from one person to another
  • tetanus
  • tetanus is caused by the bacterium (endospores) in the soil
96
Q

transmission of the disease

A

-contact transmission

97
Q

contact transmission

A
  • 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
Q

droplet transmission

A
  • droplets released during coughing and sneezing

- cold, influenza, diphtheria

99
Q

vehicle transmission

A

-by water, food and air

100
Q

waterborne transmission

A
  • cholera

- contaminated water

101
Q

foodborne transmission

A
  • undercooked contaminated meat
  • tapeworm infestations
  • taenia saginata
  • taenia solium
102
Q

airborne transmission

A
  • 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
Q

vectors

A
  • can transmit infections
  • insects
  • insects passively transmit disease
  • in the context of genetic engineering -> vector = plasmid
104
Q

passive transmission

A
  • insect picks up bacteria from eye infection and release it on to another persons eyes
  • insect=vector
  • inoculates another host with the bacteria
105
Q

biological transmission

A
  • insect bite can introduce microbe
  • injects plasmodium into the blood
  • malaria
  • mosquito
  • insect=vector
106
Q

development of disease: period of incubation

A
  • 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
Q

development of disease: prodormal period

A
  • characterized by early mild symptoms
  • nonspecific symptoms
  • aches, fatigue
108
Q

development of disease: period of illness

A
  • 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
Q

development of disease: period of decline

A
  • pathogen is removed from immune system
  • signs and symptoms subside
  • patient is vulnerable to secondary infection by opportunists
110
Q

development of disease: period of convalescence

A

-the patient regains strengths and recovery has occurred

111
Q

nosocomial infections

A
  • infection one gets when one stays in the hospital
  • caused by opportunists such as E. coli
  • pseudomonas
112
Q

epidemiology

A
  • 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
Q

portals of entry

A
  • 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
Q

portal of entry: GI tract

A
  • contaminated food or water
  • dysentery
  • cholera
  • typhoid
  • fever
115
Q

portal of entry: genitourinary tract

A
  • syphilis
  • gonorrhea
  • lymphogranuloma venereum
116
Q

portal of entry: skin

A
  • intact skin protects us from microbes

- larvae of necator americanus can make a hole and get into the system via skin

117
Q

portal of entry: parenteral route

A
  • established by cuts, insect bite
  • malaria- transmitted through insect bite
  • tetanus- enters through deep puncture wound
118
Q

preferred portal of entry

A
  • 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
Q

infective dosage

A

-a few bacteria enter the body -> the immune system gets rid of the microbes

120
Q

numerous dosage

A
  • numerous bacteria enter the body -> immune system can handle it
  • some stay alive and cause damage -> symptoms
121
Q

virulence factors

A
  • 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
Q

enzymes

A

-made by bacteria -> make bacteria more pathogenic

123
Q

collagenase: enzyme

A
  • 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
Q

endotoxin

A
  • 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
Q

exotoxin

A
  • 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
Q

plasmids

A
  • more pathogen
  • R plasmids make the bacteria resistant to antibiotics
  • harder to kill
127
Q

hyaluronidase: enzyme

A
  • 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
Q

hemolysin: enzyme

A
  • streptococci make hemoylsin
  • kills RBCs
  • not enough O2
  • cannot make proteins well
  • makes more pathogenic
129
Q

leukocidins: enzyme

A
  • streptococci make the enzyme leukocidins -> kills WBCs

- make more pathogenic

130
Q

lysogeny

A
  • 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
Q

neurotoxin

A
  • 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
Q

protozoa

A
  • cause damage to cells
  • cause infections
  • plasmodium causes damage to RBCs
  • grows in the RBCs -> destroys
  • pathogenic
133
Q

helminths

A
  • necator americanus gets into our system
  • attaches to intestinal wall
  • drinks blood
  • weakens immune system
  • anemia
  • pathogenic
134
Q

viruses

A
  • obligate intracellular parasites
  • get into host cells and reproduce
  • once done with reproduction the host cell is destroyed
  • damage to cells
  • pathogenic
135
Q

boiling

A
  • kills microbes by coagulating the proteins
  • endospores are not destroyed
  • endospores are resistant to hostile environments like boiling water
136
Q

autoclaving

A
  • 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
Q

dry heat

A
  • direct flaming is used to sterilize the inoculating loop
  • bacinerator
  • all microbes are destroyed (including endospores)
138
Q

refrigeration

A
  • slows down the growth of microbes
  • does not kill the microbes
  • preserves food products
139
Q

osmotic environment

A
  • high concentration of salt
  • hypertonic
  • kills most microbes
  • water from cytoplasm comes out -> dehydration -> shrink
  • plasmolysis
  • preserves food products
140
Q

UV light

A
  • mutation
  • control microbial growth of nonliving things
  • inducing the formation of thymine dimers in DNA
141
Q

gas sterilization

A
  • ethylene oxide gas is used to sterilize:
  • mattresses
  • petri plates
142
Q

quaternary ammonium compounds

A
  • damage to the plasma membrane of the microbes

- used in mouthwash

143
Q

sodium nitrite

A
  • preserve meat products
  • prevent the germination of botulism endospores
  • used to preserve hot dogs
144
Q

sterilization

A

-removal or destruction of all forms of microbial life

145
Q

pasteurization

A
  • does not get rid of all microbes
  • reduces spoilage organisms and pathogens
  • equivalent treatments
  • beverages are heated at 63C for 30 mins
  • milk
146
Q

filtration

A
  • 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 (8 decks)

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