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Micro Exam 4

Terms in this set (76)

ecology
relationship between organisms and their environment
microbial ecology
microbes interacting with other microbes and other organisms
mutualism
-both benefit
-termites & protozoans that digest cellulose
commensalism
-one benefits, the other is not affected
-normal flora; clown fish & sea anemone
neutralism
not a true relationship
microbial antagonism
-production of bacteriocides or just competition for resources
-bacteria fight with each other (i.e. our normal flora)
parasitism
-disease, one benefits at the other's expense
-tapeworm or the Plasmodium - malaria
-evolution of a parasite
residential flora
-on or within the body
-organisms vary depending on the site, gut and mouth are main places
-many sites are void of microorganisms naturally (blood, lymph, spinal fluid, urine, internal tissue & organs)
animals free of microbes in utero
-Lactobacilli multiply in mother's vagina (dominant bacteria in newborn's intestine)
-E. coli becomes dominant after birth (food, water, environment)
-remember that we need E. coli
Where does the majority of bacteria we accumulate after birth come from?
our food
resident flora
-permanent residence
-do not produce disease
-microbial antagonism (maintains the balance)
transient flora
-temporary
-unable to compete with indigenous/resident flora so don't stay around long
destruction of indigenous microflora (opportunistic invaders)
-microbial antagonism
-Candida albicans (yeast infections occur when for some reason this species is allowed to grow out of control)
-C. diff (abx txt can cause this disease; normally kept in check by indigenous microflora)
How can someone get an infection?
contamination + portal of entry + adhesion/attachment

CANNOT have infection w/o adhesion/attachment!
manifestation of disease
-symptoms: subjective
-signs: objective
-asymptomatic: no symptoms - a carrier or subclinical - not serious enough to go to the hospital
etiology
what actually causes the disease (the organism)
measurements of pathogenicity/virulence (how dangerous the organism is)
LD₅₀ - the lethal dose that will kill 50% of the test population

ID₅₀ - the infectious dose - changes based on the infectious agent
virulence factors
Extracellular enzymes:
-hyaluronidase (breaks down hyaluronic acid) and collagenase (breaks down collagen)
>>hyaluronic acid & collagen hold our cells together
-coagulase (forms blood clots around bacteria so immune system doesn't recognize it while it grows)
-kinase (breaks blood clots when bacteria is done growing, and then can break the clots the immune system makes to try to trap it

Toxins:
-220 known bacterial toxins
-Exotoxins (when the bacteria is releasing toxins out to the environment)...
>>cytotoxins (kills cells)
>>neurotoxins (affect nervous system - tetanus & botulism)
>>enterotoxins (affect the gut - C. diff produces a toxin in the gut when in large numbers)
-Endotoxins (inside the bacteria or a part of the bacteria)
>>lipid of LPS
>>while it's in the bacteria, nothing is going on - when it is released (death of bacteria), it infects the body
stages of infectious diseases (can be contagious in every stage)
1. incubation
2. prodromal
3. illness
4. decline
5. convalescence (i.e. herpes)
sources of infectious diseases
-animal reservoirs
-human reservoirs (carriers)
-non living reservoirs
>>soil
>>water
>>food
>>fomites
transmission of infectious diseases
-contact (human to human)
-vehicle (airborne, waterborne, foodborne)
-vector (someone non-numan i.e. tick, mosquito)
nosocomial infections
Exogenous
-pathogens acquired from environment
-patients as shedders

Endogenous
-normal microbiota of patient
-now pathogenic

latrogenic
-doctor induced
-catheters, invasive diagnostic procedures, surgery, other fomites
incidence
total amount
prevalence
over time
endemic
-associated with a country
-come during seasons (i.e. flu in U.S., malaria in Africa, etc.)
-expected every year in certain numbers
-worry about more of if traveling
epidemic
-associated within a continent (not country)
-increase in incidence or prevalence (i.e. H1N1, Spanish flu)
pandemic
when it cross CONTINENTS (i.e. H1N1)
nosocomial infections -

1. exogenous
2. endogenous
3. iatrogenic
Exogenous:
-from another patient

Endogenous:
-you gave the disease to yourself
-normal microbiota of patient became infectious

iatrogenic:
-"doctor induced" - equipment or medical workers
-catheters, invasive diagnostic procedures, surgery, other fomites
first line of defense - mechanical factors
skin and flushes (tears, urine)
first line of defense - chemical factors
-lysozyme (saliva, tears) - breaks down peptidoglycan
-gastric juice pH
phagocytosis
ingestion of foreign particles
leukocytes
white blood cells
neutrophils
-recognize general signals
-most numerous of WBCs (70%)
-cause of pus
-1st cells to reach infection
-tell the immune system we have an infection
eosinophils
elevated count = parasites
monocytes/macrophages
-monocytes are in the blood, macrophages are in the tissues
-site in the tissue and wait for an infection to come by
-what the neutrophils recruit - they come in after the body says there's an infection
-main role is to tell the body how to fight the infection
-long lasting
-APC (antigen-presenting cell)
-garbage man
-engulfs/phagocytose bacteria, foreign particles, dead cells
APCs
macrophages and dendritic cells
lymphoctes
B and T cells; specific immunity
mechanism of phagocytosis
-infection initiated
-neutrophils followed by macrophages to site
-chemotaxis (attraction to chemicals released by neutrophils - how macrophages find the infection)
-adherence - must attach to them (capsules can prevent)
-ingestion, digestion, elimination
complement system
-multiple proteins
-when they recognize a pathogen, they break up, attach to it, and create more proteins
-two things they do: directly destroy bacteria (punch holes in them), opsonization (attach to it and find macrophages)
interferons
-proteins
-the innate mechanism against viruses
inflammation
-must have to fight something off/create a response
-simply vasodilation that leads to leakage of blood into tissues
-4 classic s/s:
1. redness
2. pain
3. heat
4. swelling
function and method of inflammation
proinflammatories
fever systemic response
-opposite of inflammation
-pyrogens cause a fever, which makes the blood vessels VASOCONSTRICT and elevate the body's core
-purpose is to increase the efficiency of your own immune cells
3rd line of defense
Bone Marrow (B Cells, blood)
-primary immune system
-makes all blood cells
-B cells mature/are educated here
>>make sure its functional, make sure it's not functional against self

Thymus (T Cells)
-primary immune system
-mature/are educated here

Spleen
-secondary immune system
-filters blood for infection

Lymphatic vessels
-secondary immune system

Lymph nodes
-secondary immune system
What is the secondary immune system all about?
recognizing the pathogen
What takes the place of non-specific immunity when it fails?
specific - B and T cells
Antigens
-pieces of usually pathogens that the immune system will see; usually proteins

Exogenous antigens:
-outside cells of body (most infections)
-bacteria

Endogenous antigens
-produced within cells of body
-proteins from replicating viruses
-cancer
B cells
make antibodies
antibodies
proteins with antigen binding sites

Complement:
-trigger it

Neutralization:
-doesn't kill, just blocks

Opsonization:
-attach to it and targets it for phagocytosis

Agglutination:
-clumps the bacteria together so the macrophage can eat them all at once
Immunoglobulins
-constant region (variable doesn't change - your genetics) -only have 5 (IgM, IgG, IgD, IgA, IgE)
-variable region is the part that attaches to the pathogen
IgM
-first antibody produced (only works via Complement)
-doesn't get in tissue well b/c large
-doesn't cross placenta
-only well to make a different antibody is if a T-cell tells it to (w/o a T cell, B cell only makes IgM)
IgG
-Most abundant and soluble (can cross placenta - All functions)
-antibody you want when you're sick - can perform ANY function to stop the infection
-small and can penetrate the tissues
-crosses the placenta
IgA
-Mucosal membranes, resists degradation (Neutralization)
-when excreted find another one and bind with it so they can go into harsh environments i.e. stomach, mucous membranes; neutralizes infection
-given to baby via breast milk
IgE
-Mast cells (parasites (main role), allergies)
-works by attaching to mast cells
-explodes when it meets it's antigen (i.e. cat fur)
MHC Class I
-found on all nucleated cells
-present endogenous antigens (viruses & cancer) to cytotoxic T cells
MHC Class II
-found on dendritic cells & macrophages (only APCs)
-presents exogenous antigens to helper T cells
What is the role of MHCs?
MHC role is to present antigens to T cells (B cells can recognize antigens, T cells can't unless they're attached to an MHC).
T cells can start violent reactions so it's an extra step to check.
Helper T cells
-activate B cells and tell it which class of antibody to make
-create memory
cytotoxic T cells
kill infected cells
memory plasma cell
-Swollen lymph nodes = B cells replicating
-Some B cells become plasma cells
-Plasma cell = B cell that ONLY secretes antibodies (100/sec)
-Helper T cell takes a few plasma cells and makes them memory plasma cells
-Memory plasma cell = constantly secrete the antibody in your blood (what a titer checks for)
initial response
-first time you ever get infected with something
-7-14 days
memory response
-second+ time around, usually before incubation phase ends
-2-6 days
naturally acquired active immunity
actually got the disease
naturally acquired passive immunity
breastfeeding
artificially acquired active
lifelong vaccine
artificially acquired passive immunity
-giving antibodies IV
-antitoxins, antivenoms
attenuated live vaccines (modified live)
-not for pregnant nor immunosuppressed
-weakened form of the pathogen
-can get the pathogen from this, but you shouldn't
inactivated vaccines
-pieces of the actual or whole organism that are killed
-can NOT make you sick
Toxoid immunization
-no organisms in it: just a piece of toxin
-chemically or thermally modified
-diphtheria, tetanus
What is whooping cough/pertussis caused by?
bacteria
Do adults get whooping cough, and is it different?
yes - most adults that get it don't even know they have it (subclinical)
What is believed to be the other reason (besides low vaccination rate) for the rise in whooping cough?
b/c adults don't know they have it; vaccine has been changed - DTwP to DTaP (DTwP had whole cell and worked better but caused worse reactions; DTaP only uses partial cell and doesn't last as long and isn't as effective)
Can whooping cough be eradicated?
In order to be eradicated, it must be HUMAN-ONLY; pertussis is human only, so yes
What is the etiology of TB
bacteria in the lungs
How is TB treated (DOTs included), how contagious is it?
Direct observed treatment - in other countries they won't take TB medicine all themselves and split it among each other, so they must be kept there & observed
What are the reasons why we don't get the vaccine?
-makes skin test positive
-not effective if not exposed to the disease
-cost
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