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285 Cards in this Set
- Front
- Back
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antibacterials
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treatment of disease producers by chemical agents
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Ignaz Semmelweiss
time period and contribution |
1800s: hand washing w/ chlorine solution to stop Step
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Joseph Lister
time period and contribution |
1865: first antiseptic surgery
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Morton
time period and purpose |
1800s: first to use ether in ether dome at MGH
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Paul Erlich
time period and contribution |
1908: selective toxicity is mandatory
ex. salvarsan vs. syphilis |
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Alexander Fleming
time period and contribution |
1929: identified that mold killed his bacteria colonies
work followed by Ernst Chain and Howard Florey (penicillin) |
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means of prevention of infectious disease
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public health programs, sanitation, hygiene, nutrition, vaccines, quarantine
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What do you need for good prevention (2 things)
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vaccines, asepsis
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What do you need for good care (3 things)
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asepsis, anesthesia, antibiotics
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Issues in Drug manufacture
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1.) metabolize drug too quickly (useless)
2.) metabolize drug too slowly (toxic) 3.) find genes in person to get correct dosage |
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Main goals of drug manufacturing
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selective toxicity
narrow spectrum drug high chemotherapeutic index |
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high chemoterapeutic index
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max. tolerated dose per body weight/min. curative dose per kg body wt
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Alexander Fleming
time and contribution |
mold infected some of his plates
led to penicillin by Ernst Chain and Howard Florey 1929 |
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What do you need for good prevention
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vaccines, asepsis
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What do you need for good care
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asepsis, anesthesia, antibiotics
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Issues with drug manufacture and metabolism
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too quickly=drug useless
too slowly=toxic |
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Main goal of creating antibiotic
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selective toxicity
narrow spectrum drug |
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chemotherapeutic index
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max. tolerated dose per body weight/ min. curative dose per kg of body wt
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Do you want a high chemotherapeutic index or a low chemotherapeutic index?
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high
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Problem with oral administration of antibiotics
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stomach acid could destroy it, but you want the drug to be absorbed in stomach rather than intestines
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Advantage of IV-IM drug administration
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faster and can give higher concentration
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Disadvantage of IV-IM drug administration
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fatal allergies and infection from needle
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Indifferent drug combination
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neither drug affects action of the other (good)
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Synergism: drug combination
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together drugs have effect that neither one could accomplish alone
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antagonism: drug combination
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if you give a bacteriostatic drug and then give a bacteriocidal agent it wipes out effect of bacteriostatic drug
(bad) |
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Why use a bacteriostatic drug
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prevents bacteria from multiplying but allows your own immune system to take care of bacteria left
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Why do they want to make some bacteriostatic drugs bacteriocidal?
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bacteriostatic drugs don't work on immunocompromised person
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prophylaxis
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to prevent certain diseases (like tetanus) especially if you've had an implant
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suprainfection
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from treating one infection you get another
common w/ broad spectrum antibiotics |
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main way antibiotics work
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produce hydroxyl radicals (o2-) to oxidize bacterial cell contents and kill them
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what happens to bacteria cell wall w/ antibiotics
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prevent formation of cell walls or break NAM-NAG links
causes bacterial cells that are hypertonic to human fluids to swell and pop |
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what happens to bacteria metabolism w/ antibiotics
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bacteria convert PABA to folix acid using catalyst
antibiotics produce sulfa-containing drugs that look similar to PABA catalyst enzyme binds to sulf-thing instead of PABA so bacteria can't produce folic acid (vitamin B) |
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Another way that antibiotics hurt bacteria metabolism
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ciprofloxacin interferes w/ DNA metabolism in bacteria
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how can antibiotics interfere w/ protein synthesis
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ex. tRNA can't bind w/ subunit (bacteriostatic), causes misreading of bacterial mRNA, freezes ribosome, inhibits RNA polymerase, competes w/ mRNA for sites on bacterial ribosome
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how does antibiotics destroy plasma membrane
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ex. antifungals
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what is nucleoside analogues in antibiotics
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some part of antibiotic mimics something involved in DNA or mRNA such as guanin
safe in noninfected cells |
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5 ways antibiotics kill microbes
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inhibit cell wall synthesis
interfere with metabolism interfere with protein synthesis destroy plasma membrane function nucleoside analogues |
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4 side effects of antibiotic use
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allergies: anaphylaxis, skin rashes, smooth muscle contration, etc.
disturbance in normal host parasite relationship: super infection especially in colon human mitochondria like bacterial toxicity |
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Toxicity of
chloramphenicol streptomycin tetracycline neomycin kanamycin amoxicillin rifamycin |
c: aplastic anemia
s: deafness and cranial never t: liver dystfunction, dental pigment in babies, irritat alimentary tr act n: absorption in intestine k: nephrotoxic, deafness a: kidney liver damage r: red man syndrome |
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triclosan
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like antibiotics found in many common objects and might not even help against infection
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what is better to use than triclosan and why
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better: quickly evaporating chemicals like chlorine bleach, alcohol, ammonium etc.
b/c kill immediately |
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why is MRSA linked to societal drugs
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societal drugs affect people around person taking the drug. people taking antibiotic have more anitbiotic R' bacteria on skin which is easily transmitted
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anticancer drugs
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only affect person on therapy
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ESKAPE bacteria
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name for spread of drug R' of some bacteria
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one big concern in drug resistance besides mrsa
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gram -s becoming a drug R' problem
ex. injured soldiers returning from Iraq |
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10-1-2 rule of thumb
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10 years to develop drug
1 year of effective use 2 years = R' |
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10-10-10 rule of thumb
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10 years it's miracle drug
10 years its side effects 10 years law suits |
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Phase I of testing drug
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tests max. tolerated dose and possible side effects
less than 100 patients usually on death beds |
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Phase II of testing drug
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identifies diseases of stages of disease that are affected by experimental therapy
around 100 patients |
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Phase III of testing drug
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compared to another drug already approved by FDA or w/ a placebo
several thousand patients |
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Dilemma with phase testing of drugs
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everyone wants to be in phase III experimental group and not in placebo group
becomes scientists v. pleas of dying patients |
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4 Factors Contributing to bacterial R'
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1. R' evolutionarily favorable mutation
2. R' easily transferred (community acquired R') 3. Increase in Immunocompromised people who need more antibiotics (nosocomial) 4. Livestock feed |
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. why use antibiotics in livestock?
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1. promote growth of livestock
2. prevent illness in herd |
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ex. of problem with livestock antibiotics
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salmonella in beef
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VRE (vancomycin enterococci R' bacteria) biggest 2 problems
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1. lethal in immunosuppressed patients
2. big problem in hospitals |
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vancomycin
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antibiotic of last resort
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where are most R' factors carried and why is this problem
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plasmid, very mobile
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4 bacterial R' mechanisms
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1. inactivate antibiotic as it enters
2. mutate cell membrane pumps to get rid of antibiotic 3. change molecular target of antibiotic 4. transfer R' to nonR' strain by transformation and conjugation |
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Alternative to antibiotics in hospitals
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wash hands, one way traffic through operating rooms, isolate R' patients
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6 ways doctors can help R' bacteria problems
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1. wash hands
2. not overprescribe 3. don't give patient drugs just b/c they want them 4. don't increase dose of drug if it isn't working, instead change drug 5. try targeting narrow range of bacteria 6. shorten course of antibiotics |
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2 ways pharmaceutical companies can help drug R'
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1. develop vaccines for prevention and treatment rather than antibiotics
2. try to design antibiotics to prevent microbes from R' "antibiotics that resist resistance" |
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5 ways patients can prevent drug R'
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1. don't pressure doctor for drugs
2. follow directions exactly and finish presciption, don't use in future if leftovers 3. wash fruits and vegetables thoroughly, avoid raw eggs/meat 4. try not to use soaps shampoos and other everyday things w/ antibacterial chemicals unless necessary 5. don't stockpile leftover drugs |
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How can agriculture help avoid drug R'
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reduce anibiotics in livestock feeds
vaccinate livestock instead |
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What is phage therapy
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using bactriophages to target specific becterial strains and use it to kill bacterial that harm human
possible replacement of antibiotics |
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problems with phage therapy
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1. if you have internal bacterial infection: patient would see phage as foreign and destroy it (phage=useless)
2. if used internally phage could become temperate instead of lytic and recombine with patient's genes |
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bioinformatics and overcoming bacterial R' to antibiotics
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system to organize and analyze all discovered gene sequences
know bacteria gene and know its prtein |
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combinatorial chemistry and overcoming bacterial R' to antibiotics
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pharmaceutical chemists create collections of small organic compouds and vary units in compounds to make many combinations
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high-throughput screening and overcoming bacterial R' to antibiotics
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screen synthetic molecules in large groups, combine them w/ protein target from a bacterium, pass over detector that chows color change when molecules bind to protein
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nanobiotics and overcoming bacterial R' to antibiotics
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new strain of antibiotics that should be difficult for bacteria to R'
composed of rings of aas that assemble in bacteria and kill them |
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Innate Immunity
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nonspecific response:
eosinophils, monocytes, macrophages, NKCs |
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adaptive immunity
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acquired immunity
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cell mediated immune response
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T cell response in adaptive immunity
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antibody response
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(humoral) B cell response in adaptive immunity
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Type I lymphoid organs and their purpose
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thymus: where t cells mature
bone marrow: where all blood cells made |
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Type II lymphoid organs
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spleen: gets rid of worn-out RBCs
tonsils appendix lymph nodes: especially in armpit and groin |
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SALT, MALT or GALT, BALT
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SALT: skin associated lymphoid tissue
MALT or GALT: mucosal or gastro assoc lymphoid Tissue Peyers patches BALT: bronchial Assoc Lymphoid Tissue |
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cross talk
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cells talk to each other to communicate about antigens
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chemical barriers in nonspecific response
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lysozyme (prevents NAM and NAG)
mucus interferons C"(soluble mediator) |
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Physical barriers in nonspecific response
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skin, duplicate organs, phagocytes
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signs of nonspecific response
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rubor (redness)
et tumor (swelling) cum calore (fever) et dolere (pain) all signs of inflammation |
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phagocytes
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cell that engulfs and destroys antigen
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leukocytes
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all white blood cells
B, T, NKC, macrophage etc. |
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step 1 of inflammation
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blood vessels constrict (vaso constriction) and then dilate
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step 2 of inflammation
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damaged tissue cells cause mast cells to make histamine (cause vaso dilation so WBCs can leak through)
clotting blood slows leukocytes stick to sides of blood vessels near injury |
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how does clotting blood slow in inflammation
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prothrombin ---> thrombin (clot) causes
fibrinogen to become fibrin (mesh network) |
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step 3 in inflammation
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C' proteins + histamine attract phagocytes
causes dilation of capillaries allowing for diapedesis (leukocytes squeeze through capillaries) |
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what cell is the first to respond to histamine in inflammation event
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neutrophils
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side effects of histamine diapedisis
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edema, swelling, redness, sensitized neurons, pain (itch)
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step 4 in inflammation response
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polys die and cause pus
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what is pus
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pus: living microbes = living neutrophils + lving and dead macrophages, dead neutrophils, dead/injured tissue
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where is there a large amount of cross talk
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between nonspecific and acquired immune responses
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major characteristics of adaptive immunity
4 |
specificity
memory tolerance cross talk |
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neutrophils
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phagocytic WBC
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lymphocytes
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B cells, T cells, NKC
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monocytes
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APCs, Macs, Dendritic Cells
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2 parts to immune response
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1. cell to cell killing by T cells
2. antibody production by B cells |
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Immunogen (Antigen)
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anything in the body perceived as foreign
molecules on surface of viruses, bacteria, protista, toxins, toxoids, someone else's cells/tissues |
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cell-mediated immunity
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t cell response
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two parts to cell-mediated immunity
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1. killing infected cell vs. foreign materials on surface of host cells rather than free in fluids
2. chemical secretions to activate other cells in immune response |
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humoral immunity
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b cell responses
recognize foreign material free in the fluids w/ antibody production |
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Abbreviations
MHC APC CD CD8 T Cells CD4 T Cells IFN IL |
MHC: major histocompatibility complex
APC: antigen presenting cell CD: cluster differentiation (proteins on surface of leukocytes CD8 T: cytotoxic T cells CD4 T cells: Helper T cells (TH1) IFN: interferon IL: interleukin |
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What happens to the Ag concentration during feedback
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first it rises, so it comes in contact w/ more receptor cells, then immune Rx wins and Ag concentration falls
stimulation of Interleukin secretion and B cell stimulation declines |
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What happens to antibodies during feedback
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Larger concentration of IgM causes B cells to that target specific antigen to produce IgG.
Ag is destroyed excess unbound IgG binds to and inhibits B cell activity |
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What inhibits B cell activiy after an immune response
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unbound IgG binds to B cell
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What cells activate suppression of the immune system
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CD4 T regulator cells
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where are T cells made
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bone marrow
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Where do T cells go once they are made?
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Thymus
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Where are T cells activated
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Thymus
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How is T cell immunity maintained after puberty?
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new areas mimic thymus such as lymphoid organs (spleen, appendix, tonsils, adenoids, etc.)
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How do T cells know where to go?
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adhesion molecules and cytokines (protiens we make to fight bacteria)
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Where are B cells developed?
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bone marrow
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Where to B cells go after the bone amrrow
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II lymphoid organs w/ T cells
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Where do mechanisms to recognize self cells occur and when
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thymus, early development
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clonal selection theory
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during development animal makes wide variety of lymphocytes each having ability to react w/ diff. antigen
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Naive lymphocytes
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lymphocytes that haven't yet encountered Ag
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expression
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different cell surface protein on each lymphocyte allows it to react w/ different antigen
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what causes lymphocyte to multiply
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binding to an Ag
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Clone
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a cell line of B or T cells forever committed to reacting against a given Ag
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What is a clone composed of
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Effector cells: respond to immune Rx
Memory cells: survive months/years inactivated until Ag returns |
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Characteristics of I response of immune system
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long lag phase
Ab response or T cell response is low memory T cells migrate to nonlymphoiod tissues ex. skin |
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Characteristics of II response of immune system
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lag phase is shorter
immune response is higher |
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what happens when naive cells meet antigen
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the divide to become activated cells or memory cells
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what cell makes antibodies
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plasma cells
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what is another name of Ab
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immunoglobulin Ig
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where do B cells keep Igs once they are made
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in the plasma membrane to serve as receptors
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what are the 5 classifications of Abs and what is classification due to?
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IgG, IgM, IgA, IgE, IgI
due to constance region of molecules |
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Describe the formation of the IgG antibody
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monomer
2 heavy chains 2 light chains: held on by S-S bonds hinge region held by S-S bonds |
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What is the importance of the hinge region?
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enable Ab to bind to Ags that are various distances apart
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Variable ends
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Ag binding sites w/ amino acids that vary
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constant end
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arrangement of aa remains same for this class
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when are IgG produced the most
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II Rx
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What/Which Ab can cross placenta to fetus
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IgG
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What Ab is most abundant
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IgG
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The four functions of IgG
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neutralization, precipitation soluble Ags, Agglutination of particulate Ags ,Activation of Complement
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Neutratlization
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antibodies fill surface of receptors on virus or active site on bacterial protein and prevents them from attaching to target cells
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precipitation soluble Ags
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aggregate antifen molecules
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Agglutination of particulate Ags
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makes Ags immobile
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Activation of complement
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tail ends activate complement proteins that break and pop bacterial cells
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IgM structure
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pentamer
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When is IgM most important
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first in Ab response, most prevalent during first 3 days of response
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What is the first Ig in embryonic development and evolution of Igs
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IgM
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IgA structure and where it is found
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dimer found in mucus lining of body, saliva, tears, breast milk, etc.
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when is IgA most prevalent
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after 3 days
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why can humans make 10^9 different Ab molecules
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b/c antibodies are proteins coded for by genes which can change in somatic recombination
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what cell does somatic recombination of Ig genes occur in?
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b cell
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Heavy chain somatic reconmbination involves what gene segments
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V (variable), D (diversity), J (joiner)
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Differences between heavy chain somatic recombination and light chain somatic recombination
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light chain has two forms (kapp on chrom. 2 and lambda on chrom 22), light chain only hs V and J region so only 1500 different combos for each type of chrom. while heavy chaing has 12,000 diff. combos
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allelic exclusion
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process by which heavy and light chain expression is reduced to 1 gene set per cell (clone)
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four steps in class switching
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surface IgM and IgG meet Ag (both have same variable ends)
IgM secreted B cell turns to plasma cell switch to secrete IgG, IgA, IgE |
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T-cell Receptors, Igs, and Major Histocompatability Proteins are all...
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Recognition molecules
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characteristics of natural active immunity
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exposed to Ag, may either R' or get disease
I Immune Rx Don't die long-lived immunity |
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characteristics of natural passive immunity
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receive Abs across placent in colostrum, short-lived immunity
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characteristics of artificial active immunity
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exposed to Ag, vaccine, you make your own Abs
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characteristics of artificial short-lived immunity
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Abs from another source, used in emergencies and travel
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describe when modern immunization practices began
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Edward Jenner, milk-maids w/ cow pox never got small pox
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Two types of bacterial vaccines
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microbe, toxoids
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two types of bacterial microbe vaccines
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killed
attenated |
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two types of viral vaccines
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killed whole virus
live attenuated virus |
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what are the advantages to using a live attenuated virus vaccine
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longer immunity
faster immunity can be taken orally |
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Two types of selected surface proteins for vaccinations
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1. using proteins from the pathogen and just removing the toxic element
2. using antivector protein ex. against saliva in a mosquito bite |
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what is DAM in selected surface protein vaccination
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DNA adenin methylase which is produced in many pathogens, so vaccine could be effective against many different bacteria
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What are the 5 main types of vaccines
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1. bacterial
2. viral 3. combination bacterial and viral vaccines 4. selected surface proteins 5. DNA of any pathogen |
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what is immune sera and when is it used
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it is getting someone else's antibodies
used in emergencies |
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main difficulty with vaccines
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if it's weak enough to not damage host it may be too weak to damage pathogen
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3 other difficulties with vaccination
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1. routes
2. pathogen hides in body and can't be attacked by antibodies 3. pathogen constantly changes its covering |
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why is tuberculosis so hard to vaccinate
4 main reasons |
1. lives in phagosomes of infected macs
2. thick cell wall 3. secretes enzyme to destory host's anti-bacterial chemicals 4. cuases host to destory its own lung tissue |
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main problem with flu vaccinations
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influenze has two surface proteins neuraminidase and hemagglutinin that constantly change since the are RNA
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advantages of nasal/oral routes of vaccination
5 reasons |
1. stimulates IgA and IgG
2. mucosal immune system all connected so just need to give vaccine at one site 3. no infection from needle 4. more pleasant 5. can put in food for children |
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two ways to deliver vaccine nasally
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direct: ex. flumist
via vectors |
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Problem with delivering vaccine orally
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needs to survive stomach and intestines
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advantages to using potatoes for vaccination
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cheap, genes easy to manipulate, easy to administer, good b/c you need Abs in digestive system
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problem w/ using potatoes as vaccination method
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cooking potato denatures protein
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other possible plant vectors for vaccination
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banana/tomato
toothpast soybeabs vs. cancer |
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advantage/disadvantage of injected plant viruses
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good: plant viruses are harmless to us
bad: could cause autoimmune disease which makes vaccination pointless ex. HIV |
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Hypo Rx
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gentically lack component of immune system or microbial infection prevents immune system from functioning properly
ex. SCIDS, HIV |
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Hyper Rx
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ex. allergies and autoimmune disorders
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allergen
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antigenic substance triggering allergic state
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Sensitizing (immunizing) Dose
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first contact w/ allergen may not be perceptible
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Shocking (Provocative) Dose
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meet Ag any time after first time=violent response
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four common routes allergens reach body
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1. respiratory tract (most common)
2. digestive tract 3. skin 4. direct injection |
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how are allergies categorized
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by response not by the allergen itself
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what is the main characteristic of type I immediate hypersensitivities
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IgE binds to Fc-receptors on mast cells and basophils
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what happens in the sensitization stage of type I immediate hypersensitivity
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macrophage degrade allergen and present to T cells which secrete IL4 which leads to B cells secreting IgE
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what happens during provocation phase of type I immediate hypersensitivity
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allergen molecules bind to IgE on mast cell receptors, enzymes that release chemical mediators are formed
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severity of Type I immediate hypersensitivity response depends on... (5)
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solubility of Ag
Route of Ag Genetics Length of interval between exposure and shocking dose |
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what are the mediators of anaphylaxis (type I)
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histamine
serotonin bradykinen heparin Cytokines, IL-3, IL-5, CM-CSF, IL-4, IL-13 TNF-alpha Leukotrienes |
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anaphylaxis
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allergic reaction
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source of histamine
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mast cells, basophils, damaged tissues
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what is the activity and symptoms of histamine in type I response 5 main things
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1. contracts smooth muscle bronchoconstrictor (diarrhea, vomiting, wheezing
2. vasodilation (edema: swelling) 3. increases permeability small vessels (diffuse redness erythema) 4. stimulates nerve endings (pain, itching) 5. stimulates mucous secretion (congestion) |
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best treatment of Type I immediate hypersensitivity
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avoid contact w/ allergen
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Epinephrine
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relaxes smooth muscle, dilates bronchioles, blood vessels stop dilating/leaking, blocks release of mediators of allergy
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8 treatments of type I immediate hypersensitivity response
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1. avoid
2. epinephrine 3. maintain airway 4. cardiac massage 5. (following treatment) aspirin/corticosteroids 6. desensitization 7. antihistamines 8. sodium cromoglycate |
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good things about aspirin
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good against pain and inflammation
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problems w/ aspirin
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1. causes bleeding stomach lining/ulcers and damages kidneys
2. not specific 3. disabels COX prostaglandan until more is producted |
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COX prostaglandan
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enzyme needed for prostaglandins to allow functioning of stomach/kidney
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what is desensitization
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you inject small amounts of Ag into patient to make IgG or IgA so if allergen comes IgE doesn't have to be made and it is blocked
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how do antihistamines help
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block receptors for histamines b/c they look similar
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what is sodium cromoglycate used to treat and how does it work
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treats hay fever and allergic asthma
prevents inflow of Ca++ which happens when mast cell contacts Ag and IgE stalls chain of events causing mast cell breakdown |
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what is main event in Type II antibody-dependent cell-mediated cytotoxicity (ADCC)
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IgG and IgM bind to target cells and trigger complement cascade
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what common Ags provoke Type II reaction
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1. MHC molecules on transplants
2. Body's own cells in autoimmunity 3. ABO/Rh Blood group Ags on rbcs |
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describe problem w/ Rh on durin pregnancy
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if baby has Rh+ and mom is Rh- during birth mom can make anti Rh+ abs which during second pregnancy could kill Rh+ fetus
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3 types of Type II disease
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autoimmunity
transplants ABO and Rh reactions |
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treatment of Rh+ problem during pregnancy
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give mother IgG vs. Rh+ antigens w/in 72 hours of delivery
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what happens in a type IV delayed (cell-mediated) hypersensitivity response
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T cells attracted to site of reatcion, no IgE, T cells stimulate infected macs to aggregate
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Granulomas
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mass of inflamed tissue that occurs in type IV reaction
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urticaria
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hives seen in Type I and Type IV reactions
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Treatment of Type IV
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treatments blocking IgE don't work
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Main examples of Type IV reaction
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poison ivy, reaction to gold/silver
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How is normal self-tolerance regulated
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A. clonal abortion: self reactive T cells killed while immature
B. Functional Deletion: stops immune activity C. Clonal Anergy: lack of reaction to foreign bodies |
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4 factors associated w/ autoimmune diseases
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genetic/gender
aging infection stress |
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treatment of autoimmune diseases
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replace destroyed tissue
enhance oral tolerance interrupt process of inflammation |
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Addison's disease
target and problem |
target: adrenal gland
problem: hypoadrenalism so you would have things like low blood pressure |
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Crohn's disease
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gut
inflammation of gut |
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Goodpasture's syndrome
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kidney and lungs
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graves' disease
target and problem |
thyroid
make antibodies against receptors that get rid of extra thyroxin, so you see things like bulging eyeballs |
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Hashimoto's thyroiditis
target and problem |
thyroid
antibodies made against thyroid, too little thyroxin, most comon in older women |
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Insulin-dependent diabetes mellitus
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makes antibodies against pancreatic beta cells
type I is most severe, lack insulin |
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multiple schlerosis
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make antibodies against brain and spinal cord
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myasthenia gravis
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nerve/muscle synapses
can't move skeletal muscles, starts in eye, muscle cells can't pick up stimuli from acetylcholine receptors |
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rheumatoid arthritis
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make antibodies against connective tissue
more systemic not organ specific |
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systematic lupus erythematosus
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DNA, platelet, other tissues, dead cells don't get cleared fast enough
more systemic not organ specific |
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3 ways that genetic/gender impact autoimmune diseases
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1. certain MHC (HLA) patterns
2. deletion of supressor T cell Clone 3. Gender: more common in woman than men |
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how can aging increase possibility of autoimmune diseases
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somatic mutation: new clones of self-reactive TH or B cells
clones escape normal surveillance for deleting mutant cells |
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Give an example of how infection can lead to autoimmunity
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ex. mycobacterium tuberculosis: contains protein similar to cartilage
ex. streptococcus contains cell-wall M protein which leads to rheumatic fever |
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how can stress cause autoimmune disease
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trauma affects endocrine system
hypothalamus and pituitary become inflammed |
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how can you interrupt process of inflammation in autoimmune diseases
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block antibodies and block T cells
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characteristics of Staph
1. gram stain result 2. shape 3. formation 4. main problem it causes |
1. gram +
2. cocci 3. grape-like clusters 4. pyogenic |
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pyogenic
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producing or generating pus
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what form of staph is the most severe
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staph aureus
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what is the dangerous triangle
and what disease is it associated w/ |
area of face where no mechanical barriers are between here and the brain which can cause impetigo
concern in staph infection |
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what are the four types of infection of staph
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1. skin abscesses
2. nosocomial 3. gastoenteritis (change in normal floral of GI tract) 4. toxic shock syndrome 5. pneumonias |
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main ways to prevent and control staph
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aseptic technique, proper use of antibiotics, one way traffic flow, developing a vaccine, painting surgical area w/ lactobacillus fermentum to prevent S. aureus from binding to host cell
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streptococci
1. gram stain 2. shape 3. formation |
1. gram +
2. cocci 3. chains |
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what is the group of bacteria that produces the greatest variety of diseases
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streptococci
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what drug is most affective against streptococci
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penicillin derivatives
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what does ScpC do in Strep M14
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destroys Il-8 which summons so neutrophils aren't started
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main problem w/ Strep M14
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doesn't have SiLCR so ScpC is on full force
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treatment for Strep M14
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try to make drugs to reduce ScpC or enhance SiLCR
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What is the goal of a vaccine against strept
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get humans to make antibodies against M protein on Strep surface
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Disease of Step (8)
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1. Toxic Shock like Syndrome
2. M14 Flech-Eating bacteria 3. Puerperal Sepsis: Child-birth fever 4. Strep throat 5. Scarlet Fever 6. Rheumatic Fever (damaged heart valves) 7. erysipelas: allergic reaction to Strep 8. pneumonias |
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Neisseriae meningitides
1. gram stain 2. shape 3. formation |
1. gram -
2. cocci 3. often in 2s |
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what are symptoms of a healthy person who is infected w/ neisseriae meningitides
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fever
malaise headache neck rigidity aversion to bright lights |
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what can happen if neisseriae meningtides goes untreated
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coma, deafness, paralysis, mental retardation, fatal shock, blindness, endocarditis, arthritis, retinitis
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where is meningtides common
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colleges b/c binge drinking
subsaharan Africa |
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if you are a carrier of meningitides where do you carry the disease
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colonizes lining throat and spreads through nasal secretion (nasopharynx)
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when does meningitides become pathogenic
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when it goes into blood (septicemia) it can then cross meninges into cerebrospinal fluid
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what type of toxin does meningitides produce and what does it do
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endotoxin
increases permeability blood vessels |
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how do you prevent or treat neisseriae meningitides
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prevent: vaccination v. 4 strains
treat: early w/ antibiotics |
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neisseriae gonorrhoeae
1. gram stain 2. shape 3. formation |
1. gram -
2. cocci 3. diplococcus |
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where is gonorrhoeae easy to destroy and hard to destroy
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easy: outside host by sun or drying
hard: in mucous membranes of host |
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what is the biggest difference b/w males w/ gonorrhoeae and females w/ gonorrhoeae
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males experience bruning and now they are infected, 80% females don't know they are infected
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where does gonorrhoeae enter in men and women
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men: urethra
women: vagina |
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what happens if gonorhoeae is untreated in males and females
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males: epididymis closes causes sterility
females: ectopic pregnancy (egg can't get down fallopian tube) can be deadly |
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what is the number 1 cause of sterility in both sexes
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gonorrhea
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reasons for gonorrhea spreading
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1. drug resistant strains
2, symptoms may not appear so they don't know they have it 3. 80% women infected not treated 4. change from condom to pill |
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prevention of gonorrhea
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use condom
informing partner: tells who they got it from so it can be stopped medical care erythromycin in newborn (can also use silver nitrate) |
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what cells are an early line of defense and will attack nonspecifically any viral infected cell w/ perforin process
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NKC
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What are the three ways APCs can response once they ingest a virus
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1. process viral antigen
2. present antigen on surgace in MHC Class I 3. Secrete IL-12 |
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what does IL-12 do in a viral infection
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1. keeps NKC dividing and killing viral infected cells
2. activates the TH1 (CD4 T cells) |
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which cell binds to MHC class I presented by APC in viral antigen
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T CD8 (T cytotoxic cell)
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what does an activated T CD8 do
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kill viral-infected cell b/c infected cell displays viral antigen on its surface in MHC Class I
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apoptosis
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reulated cellular destruction
occurs in viral-infected cells and releases virus in to open fluids |
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IL-12 does what
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1. activates NK cells
2. allows TH cells to... a.) become TH1 (CD4 T cells) b.) multiply c. secrete IL-2 and IFN-y |
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Who secretes IL-2
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T CD8, TH1, NKC
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what main thing does IL-2 do and what 5 cells does it affect
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multiplication and activity of
1. Th2 (CD4 T cells) 2. NKC 3. CD8 T cytotoxic cell 4. TH1 (CD4 T Cell) 5. macrophages to clear body fluid of Ag-Ab complexes |
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how is B cell stimulated
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immunoglobulin receptor (that will become and antibody) on B cell recognizes antigen
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what is purpose of TH2 cells
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secrete combination of IL4, 5, 6, and 13
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what does IL4, 5, 6, and 13 do
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convert B cells to plasma cells
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what do plasma cells do
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release antibodies
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what activates macrophages
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IL2, IFN-y, complement
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what does macrophage do in immune response
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phagocytize antigen
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who produces IFN
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CD8 T cells, TH1 (CD4 T cells), infected cells
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what is one main purpose of IFN
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prevent viruses from replicating w/in normal cells
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How does APC cell process bacteria
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presents it in MHC Class II
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how are B cells stimulated
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by IL 4, 5, 6, 13 produced by TH2 cell (CD4) that bound to MHCII on APC
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what purpose does TH1 (CD4 T) cell have in bacter/toxins/toxoids immune response
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produces IL-2 which stimulated TH2, TH1, and macrophages
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overview purpose of each in bacteria and virus immune response
1. NKC 2. APCs 3. T cells 4. plasma cells |
1. early cells to attack viral-infected cells
2. phagocytize and present antigen, produce interleukins 3. T Cells perform cel-cell killing, produce interleukins, interferons 4. make/secrete antibodies |
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what MHC class does CD8 T cell recognize
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MHC I
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what MHC Class does CD4 T cells recognize
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MHC II
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what cells present antigents processed in MHC I for CD8 T cells to recognize
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APCs, viral-infected cells
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Where is MHC Class I present
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every nucleated cell
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where is MHC Class II present
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surface of certain lymphoid cells
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what is held in MHC Class II cells
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proteins of bacteria, toxins, toxoids
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What is the main component of plasma
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H2O
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What are the two main proteins in plasma and their purposes
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albumin: stabilizes blood so it doesn't thin so much
Globulins: antibodies |
