FINAL Flashcards

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
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
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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
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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
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leukocidins: enzyme
- streptococci make the enzyme leukocidins -> kills WBCs | - make more pathogenic
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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
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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
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protozoa
- cause damage to cells - cause infections - plasmodium causes damage to RBCs - grows in the RBCs -> destroys - pathogenic
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helminths
- necator americanus gets into our system - attaches to intestinal wall - drinks blood - weakens immune system - anemia - pathogenic
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viruses
- obligate intracellular parasites - get into host cells and reproduce - once done with reproduction the host cell is destroyed - damage to cells - pathogenic
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boiling
- kills microbes by coagulating the proteins - endospores are not destroyed - endospores are resistant to hostile environments like boiling water
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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
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dry heat
- direct flaming is used to sterilize the inoculating loop - bacinerator - all microbes are destroyed (including endospores)
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refrigeration
- slows down the growth of microbes - does not kill the microbes - preserves food products
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osmotic environment
- high concentration of salt - hypertonic - kills most microbes - water from cytoplasm comes out -> dehydration -> shrink - plasmolysis - preserves food products
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UV light
- mutation - control microbial growth of nonliving things - inducing the formation of thymine dimers in DNA
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gas sterilization
- ethylene oxide gas is used to sterilize: - mattresses - petri plates
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quaternary ammonium compounds
- damage to the plasma membrane of the microbes | - used in mouthwash
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sodium nitrite
- preserve meat products - prevent the germination of botulism endospores - used to preserve hot dogs
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sterilization
-removal or destruction of all forms of microbial life
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pasteurization
- does not get rid of all microbes - reduces spoilage organisms and pathogens - equivalent treatments - beverages are heated at 63C for 30 mins - milk
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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