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159 Cards in this Set
- Front
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_________ _______ - any microbial attribute that enhances the ability of the microbe to cause disease
p6 |
virulence factors
simply contribute to the pathogenic abilities |
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examples of major virulence factors include (6 listed), name 3
p7 |
transmissibility (acid resistant)
adherence (biofilm, pili) invasiveness (ie collagenases, invastions ie bites) evade immunity (capsules, Ag variation) Damage Mechanisms (enzymes, endotoxins, induce hyperreactions) Ab resistance (ie staphoriuses new) |
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what are some examples of the mechanisms of endotoxins?
p7 |
endotoxins (LPS) include
A-B, Cytolytic and Superantigen |
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difference between Gram + and - relative to endotoxins/exotoxins
p7 |
gm "-" - all have LPS aka endotoxins that are potent inflammatory agents. often have 1+ exotoxins too
gm "+" - no endotoxins. often 1+ exotoxins. Exotoxins are secreted, endotoxins are Not |
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Normal gut flora has mostly gram "-" rods, with their LPS continually leaking through our gut tissue, effects?
p7-8 |
= normal immune system development. keeps alert. Recognized by TLR 4 to LPS. binding gets inflammation going, especially macrophages
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LPS in gut, body binds and responds by macrophage and ...?
p8 |
LPS bound by TLR-4 = inflammation (macrophages & Monocytes = cytokines. Lot of pro inflammatory mediators like IL1 and TNF alpha (make NO --> precapillary sphincters relax) and inflammation.
active macrophages --> also lipid porstaglandin mediators and protein enzymes |
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LPS activates by itself a response of
p8 |
complement cascade (alternative ptwy = inflammation)
hageman factor (coagulation) platelets (coagulation) macrophages/monocytes body attacks via innate/inflammation w/o adaptive! |
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Lg amnt gm "-" in blood, which F?
a. hypovolemic shock b. disseminated intravascular coagulation c. multiple organ shutdown d. acute respiratory distress e. gonorrhoeae |
e.
Lg amnt gm "-" in blood can cause: hypovolemic shock, disseminated intravascular coagulation (internal bleeding b/c coagulation proteins used up), multiple organ shutdown and acute respiratory distress (ards) |
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page 9 picture shows LPS pathology. what causes sphincter tightening and blood back-up?
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NO release (from the TNF-alpha (released from MO/, which binds TLR-4 to LPS)) or
Alternative Pathway (no Ab) -> compliment - anaphylatoxins -> mast cells ->histamine -> edema |
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a toxin can be described as all but one
a. exotoxin (protein toxin from bacteria) b. neurotoxins (effects nerves) c. conjugation (via transduction) d. entertoxin (acts on GI tract) e. super Ag f. A-B toxin g. Cytotoxin (descrbing mech of action) |
c. this is how plasmids transport genes (via transduction or conjugation), these are stain dependent
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actions of exotoxins happen in all but one of the follow ways
a. collagenases b. cytolytic toxins c. A-B toxins d. superantigens p10 |
a.
LPS binds TLR-4 on MO/ which triggers protein enzyme collagenase = collagen fibers destruction. |
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what's the difference between the 3 exotoxins?
p10 |
cytolytic - punches holes in cell membrane
AB toxins - B (binding) A (active unit)-> enzymatically acts, intereferes with intracellular mechanisms -> death (powerful poison) Super Ag- MHC II on MO/ bound to Th via S.Ag. enough of these & velcro effect -> cytokines released from MO/ & Th (cytokine storm) |
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AB toxin where muscles are always on:
a. pseudomonas aerguginosa b. clostridium tetani c. clostridium botullinum d. bordetella pertussis e. shigella dysenteriae p 13 |
B.
a - burn victoms, ribose blocked, low ribosomes/ protein c - muscles off. blocks vesicle fusion d - ribose blocks->camp up->ion imbalance, h20 losee e - cuts Rrna -> less protein |
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symbiosis: algae on turtle is an example of
a. mutalism b. commensalism c. parasitism d. saprophytism p14 |
B. doesn't hurt/help turtle
a - most flora, both happy c - 1 benefits at expense of #2 d - benefits from dead orgamism |
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Streptococci - gram + or "-"
staphlococci - gram + or "-"? p14 |
both major gram + cocci that infect and cause disease in humans
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define: pyogenic
p15 |
puss forming - from neutrophils piling up, both streptococcus pyogenes and staphlococcus aureus are pygenic gram + cocci
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what's the difference b/w streptococcus pyogenes and staphlococcus aureus?
p15 |
1. strep: chains, cannot use O2, has protective outer protein coat >100 --> scarlet fever
2. staph: grape clusters, O2!, enzymes and secreted Proteins --> toxic shock |
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what are the three hemolytic streptococcuses & associated colors?
p16 |
beta hemolytic - clear
alpha h. - greenish gamma h. - none |
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what's path of infection for following?
beta hemolytic - clear alpha h. - greenish gamma h. - none p16 |
beta hemolytic - (group A -> pyrogenes, group B -> agalactiae) lyse RBC's
alpha h. - pheumonic and viradans, change Hg chemically gamma h. - enterococci (endofail) no RBC effect |
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of the helolytic's, which is most commonly found in oral cavity (most by number)
p16 |
alpha-hemolytic 'viradans' strep
opportunitst |
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all but 1, mj streptococci pathogens
a. s. pneumoniae b. s.agalactiae c. s. pyogenes d. s. nosocomialae e. viridans strep |
d. nosocomial is an infection aquired in a hospital
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S. pyogenes is B-hemolytic, group A, seen with many toxins. effects are?
a. strep throat b. sepsis c. pneumonia d. rheumatic fever e. cellulitis f. endocarditits g. FEB p17 |
S pyogenes
Beta hemolytic, group A many toxins (pyogenic) Strep throat, rheumatic fever, cellulitis, scarlet fever, FEB, endocarditis |
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S. pyogenes evades host by Facilitating colonization what is this?
p19 |
facilitating colonization - using bacterial cell components (M & F Protein) to cross link pili to host fibronectin on host epithelial cells
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s. pyogenes evades host immune system by which of these:
a. facilitating colonization b. camouflaging itself c. strain variatio to escape Ab d. produce cytolytic toxins e. reduce complement fxn f. petechiae p19 |
A-E
f (petechiae) means rash, and is seen in sub-acute infective endocarditis |
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s. pyogenes damages host via
1. ? 2. toxic systemic disease 3. ? |
s. pyogenes damages host via
1. pyogenic infection (toxins kill pmn's) 2. toxic systemic disease 3. immune sequelae diseases (hypersensitivity) |
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pyogenic infections are #1 in streptococcus pyogenes, they are local and do damage with inflammation. examples include? give 3/5
p20 |
1. strep throat
2. puerperal fever (mom/baby die) 3. pneumonia 4. skin infection (impetago, cellulitis, gangrene) 4. vascular disease (lymphangitis, adenopathy) 5. necrotizing fasculitits (FEB) |
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toxic systemic disease are #2 in streptococcus pyogenes, infection is local, pathology distant (toxins). examples include? give 2/3
p20 |
1. scarlet fever (get it only once)
2. toxic shock-like syndrome 3. erythrogenic toxin (super Ag, causes super red color) |
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immune sequelae disease are #3 in streptococcus pyogenes, only 50% of the 10% get it (around 3%) examples include? give 1/2
p20 |
1. rheumatic fever (cross reactive Ag - immune system attacking self Ag, effects heart) TYPE II
2. glomerulonephritis (Ag-Ab-C') TYPE III |
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Rheumatic Fever is on the increase. 1.preventable?
2.cause? 3. inflammed heart valves/tissue, joints, lung & pleura, skin, vessels, CNS seen when? p23 |
1. preventable via penicillin
2.caused by immune response to strep antigens (cross rx Ag, type II damage) 3. after 2-4 weeks of strep throat. bacterial adherence to valve is bad, perminant heart valve damage |
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1. when's post-strep glomerulonephritis occur?
2. when S. pyogenes Ag immune complexes combo with S. pyognes specific Ab's what happens? p23 |
1. 1-2 weeks
2. form soluble Ag-Ab complexes that can filter out of circulation onto basement membrane of kidneys. get lodged, complement is activated & phagocytes come. in removal of complex - drooling damage |
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T/F. always give antibiotic prophylaxis for dental patients, who have a heart transplant.
p24 |
current recommendations call for reduced use of antibiotic prophylaxis, but sometimes, not a bad idea
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_____ _______ __________ -
could = 2-3 weeks death. Staph aureus and strep pyrogens get into the normal heart via bloodstream. |
Acute Infective Endocarditis
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__ ___ ____ _____ - opportunist takes advantage of prior heart damage. drug abuse (staph), dental viridans, or Gi surgery -(valve)-> 1. platelets/fibrin 2. bacteremia 3. attach and grow 4. heart damage
p25 |
Sub Acute infective Endocarditis
pre-procedure penicillin/antibiotic prevents this. look for rheumatic fever, prosthetic valves, congenital defects. symptoms: fever, night sweats, weight loss, murmurs, petechiae (6-12 weeks - death) |
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who pretreat with penicillin?
a. heart valve replacement b. previous endocarditis c. furncle/carbuncle patients d. congestive heart failure e. heart transplant (cardiac valvlopathy) |
all but C.
furuncle/carbuncle are cutaneous problems with staph oreus |
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who rocks the Beta Lactam ring? how could this be dangerous?
p26 |
penicillin. R-CCNC=O. 15% make Ab to penicillin, type I (A.shock), II, III or IV hypersensitivity. C=O grabs Lysine on protein on RBC, Macrophages & lymphocytes.
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Define: MRSA
p27 |
Methicillin-resistant Staphylococcus aureus
antibiotic Resistant. nosocomal. kills 19K/yr, more than aids. gm+ pyogenic staphylococci (grapes) |
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T/F staphlococcus: non-motile, non-spore forming, moist yellow/white, 10+ species in flora, non-fastidious, in nose, resists: drying, heating, Ph., is Catalase +, and is facultative (faster in O2)
p28 |
True
catalase + protects them from PMN H2O2 in phagolysosome. resists heat up to 60' for 30 min. dry for weeks/months. 3 cause most diseases |
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what are the 3 most caused diseases of staphylococcus?
p28 |
S. aureus
S. eppidermidis S. saprophyticus |
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which of the Staphlococci pathogens are this: no coagulase, white colony, capsule, frequenly drug resistant, and catheter & prosthetic implant infections
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S. eppidermidis
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which of the Staphlococci pathogens are this: no coagulase, white colony, UTI's in young ladies
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S. saprophyticus
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which of the Staphlococci pathogens are this: Coagulase +, yellow, protein A (many secreted enzymes/toxins), often drug resistant *MRSA, food poisioning, osteomyelitis, Toxic shock, skin infections (absesses)
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S. Aureus
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which of the Staphlococci pathogens are this: moist skin surfaces, GI tract (1/3), high carrier rate, produces coagulase, Ab resistant, multiple virulence factors
p29 |
Staphlococcus Aureus
or S. Aureus |
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what are S. Aureus's multiple virulence factors?
a. fibrin bindng proteins on cell wall b. protein A binds Fc of IgG, blocking opsonization c. enzymes destroy ECM d. cytolytic toxins kill nearby host e. superAg toxins secreted p29 |
all true.
a. helps bacteria colonize cells and tissues b. protein A is part of cell wall c. "spreading factors" d. kill nearby host cells (including PMN defenders) e. activate Th cell and macrophage cytokine production, resulting in local and systemic pathologies, (ie. food poisoning) |
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S. Aureus virulence factors. how many are there?
T/F factors include micro-capsules, survive PMNs(via catalase), Fibronectin-binding proteins (bind host), spreading factors, using toxins, protein A, and Secreted coagulase. p30 |
over 32 factors are recognized
True |
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how does Protein A work as a major virulence factor?
p30 |
it blocks Ab-mediated opsonization by binding to Fc portion of IgG - saves bacteria from destruction from PMN's and macrophages
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S. aureus secrete Coagulase causing two major effects. what are these two Major Effects?
p31 |
1. binds fibrin to bacterial cell for camouflage from immune system
2. Lg amounts of fibrin deposits around local infection ==> walled off from body restricting immune system access |
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Mj classifications of Staph disease:
____ _____ _______ include 1. local skin infections (leads to?) 2. deep localized infections (ie?) 3. acute endocarditis 4. pneumonia (often get it when?) p31 |
local pyogenic infections
1. skin infection --> cellulitis, bacteremia, abscesses, impetigo 2. abscesses of spleen liver, kidney, osteomyelitis, septic arthritis 3 - 4. following influenza |
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how does staph build a "larger fort?"
p32 |
isolate with fibrin fort (coagulase), defend themselves with Protein A to inhibit phagocytosis (secrete cytolytic toxins to kill phagocytic cells) and 'spreading factors' breakdown ECM
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Mj classifications of Staph disease:
____ _____ _______ include 1.scalded skin syndrome 2. food poisoning 3. toxic shock syndrome 4. staph caused entercolitis p33 |
Systemic Toxic Diseases (due to specific toxins (or combo))
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why is staph so dangerous?
p33 |
nosocomial/iatrogenic
b/c many individuals are carriers, many strains are now antibiotic resistant. Staph antibiotic resistance is generally encoded by plamids, shared b/w species & enteric bacteria and staph |
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what's the "foreign body effect"?
p34 |
100 million bacteria without suture = abscess
just one-hundred bacteria + suture = abscess |
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treat abscess?
p34 |
drain abscess, remove foreign debris. hope for effective macrophage mop-up
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Enteric Gm '-' rods are medically important enteric bacilli, transfer via the five F's. FFFFF?
p37 |
Food
Fluids Fingers Flies Feces |
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enteric gm '-' bacteria share virulence via gene transfer. what mechanism of gene transfer?
p37 |
via conjugation, plasmids, transformation or by bacteriophage transduction
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define: zoonotic
p37 |
disease/microbe that normally exists in other animals, but can be transferred to infect humans
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which are normal commensal flora that may become infections?
a. salmonella typhi, shigella b. escherichia coli c. yersinia pestis d. klebsiella pneumonia, proteus mirabilis p37 |
B and D become opportunitts
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enteric gm '- ' rods are all but 1:
a. non-fastidious, normal in GI b. metabollically diverse c. strict anaerobes d. major gi tract, opportunists |
c. they are faculatative anaerobes
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T/F
E.Coli, klebsiella, proteus and Bacteriodes are normal flora p38 |
True
bacteroides is most numberous by #. true anaerobe, in colon |
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letter designations for serotype designations:
H Ag's- K - O - p38 |
H antigens- Flagella
K antigens - capsule O antigens - exotoxins |
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explain the antigen phase variation
p39 |
multiple genes are available for each antigen. certain genes bacteria can turn on/off, or multiple genes make "flagella"
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opportunist to pathogen:
a. adhesive factors, siderophores (fe capture) b. epithelial cell to cell transmission, macrophage taxi c. bacterial-induced endocytosis; capsules(phago resistant) d. antibiotic resistant; toxins (endotoxin all, exo vaires) p39 |
all true. most gain a single virulence factor changing organism from opportunist to Pathogen
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Malabsorption can be caused by Adhesions. explain
p40 |
bacterial fimbrae, gm '-' ie EPEC e coli alter microvilli = malabsorption
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bacterial-directed endocytosis is a major virulence factor (GI). who/how is this seen?
p40 |
actin assembly is initiated and start internalization into cells they attach to. EIEC and Shigella (cytoplasm) Salmonella/ Yersina (macrophage taxis)
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Endotoxins (LPS) are on all gm '-'. activate macrophages, such as...
p41 |
Cytokines - IL-1, TNF alpha (-->NO)
Lipid Mediators - PGE2 (prostaglandin) |
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review: LPS itself activates? name 2/4
p 41 |
macrophages, hageman factor (coagulation), platelets, alternative complement pthwy (inflammation, mast cell degradation)
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T/F
Lg gm '-' in blood = sepsis, quickly fatal. hypovolemic shock and disseminated intravascular coagulation could occur. p 41 |
T
disseminated intravascular coagulation leads to multiple organ shut down and ARDS |
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get figure on p 42 down. PGE 2 (lipid mediator) will have what effect, coming from MO/?
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PGE2 = osteoclasts activated and Bone Absorbed
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'good guy' gm '-' 's via conjugation or bacteriophage transduction get pathogenic strains. what kind of A-B exotons might one see?
p42 |
AB enterotoxin cause ribosylation of regulatory protein.
AB toxin cleaves rRNA, blocking protein synthesis (kidney/cns) |
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what is this equation for?
virulence x dose/ host resistance p43 |
disease potential =
virulence x dose/ host resistance |
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what time of year does the gm "-' rods
p43 |
summer b/c warm wather, picnics, swimming, jimmy & the sheep
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who gets Sigellosis Dysentery, what kind of bacteria - what are characteristics of sigellosis?
p45 |
kids (seen in daycares, nurseries, schools). gm -, shigella is very acid resistant (live through stomach)
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how does shigella cause shigellosis in the colon?
p 45 |
by infecting mucosal epithelium via bacterial-directed endocytosis of M-Cells. out of endocytic phagosome and divide in cytoplasm, can exit to Lamina Propria and spread more
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shigella can induce formation of actin-directe pseudopodia, that thrust what where?
p45 |
thrust bacteria directly into adjacent mucosal epithelial cells w/o exposure to plasma proteins or phagocytic cells. stays local. causes dysentary
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what's dysentary?
p45 |
blood and pus in the stool
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S. dysenteria produces exotoxin called what?
p45 |
Shiga toxin - it's an AB toxin that cleaves ribosomal RNA. causes damage to intestinal epithelial cells
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what if S. dysenteria gets from intestine into the blood?
p45 |
starts to damage glomerular endothelial cells, resulting in renal failure - HUS (hemolytic uremic syndrome)
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EHEC?
like s. dysenteria, EHEC has a toxin called what? p45 |
enterohaemorrhagic E. coli have plasmid encoding 'shiga-like' toxin. even have HUS response
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M cells. IgA story. Ag presenting cells, sample outside and presnt to t cells below.
what is 0157:H7? p46 |
it's EHEC (non-invasive)
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How does Salmonella infect the GI? what's the difference b/w this and salmonella typhi?
p47 |
can cause mild to severe diarrhea. s.Typhi more serious b/c it breaks through gut epithelium and rides the macrophage taxis = typhoid fever (typhoid mary)
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salmonella is most infectious, insult?
amount necessary for infection? p 48 |
most infectious from eating contaminated foods. sensitive to stomach acid, need high doses - often food stored wrong = replication
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pathogenic path into body for salmonella?
p48 |
once in Small Intestine, Salmonella invades epithelial cells (endocytosis). kill cells. phagocytes in & intestinal integrigy down = diarrhea. macrophage taxi
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salmonella and macrophage taxi?
p48 |
s. typhi evade destruction in macrophage and hitcha ride. prelicate and cause Bacteriemia (in blood).
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what's
ETEC EHEC EPEC EIEC? which is 0157:H7? p52 |
ETEC - enterotoxic e.coli
EHEC - enterohemorrhagic 0157:H7 EPEC - enteropathogenic e.coli EIEC - enteroinvasive e.coli |
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ecoli ... usually part of normal flora, how come bad rep?
p52 |
b/c genes for virulence factors (effecting adhesions/ exotoxins) transferred. get genes from Shigella (1'), V.cholera and salmonella, and become pathogens.
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ETEC
p 52 |
enterotoxic e.coli
- V. cholera exotoxin gene - watery diarrhea |
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EHEC
p 52 |
aka 0157:H7
- shiga-like exotoxin -verotoiin - blody dysentery HUS |
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EPEC
p52 |
enteropathogenic e.coli
- shigella exotoxin gene - adherence gene - diarrhea |
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EIEC
p52 |
enteroinvasive e.coli
- invasive genes - dysentery |
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which one is "travelers diarrhea" for e.coli?
p53 |
ETEC
entertoxic e.coli - v.cholera exotoxin gene - watery diarrhea |
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What do you know about UTI's? include
gm +/- bacteria from where? specialized how? p55 |
start in colon, ascend into bladder, gm -, have specialized adhesions, most a uropathogenic strain of e. coli
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all but one are gm - rods
a. vibrio cholera, campylobacter jejuni b. heliobacter pylori, bacteriodes c. pseudomonas aeruginosa d. staphylococcus aureus e. brucella abortus, bortetella pertusis |
d. staph aureus is gm + pyogenic cocci, grape clusters & ultimately toxic shock p15
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potenital biogenic agents, 1 F
a. anthrax b. chicken pox c. botulism, plague d. sm. pox, tularemia e. viral hemorrhagic fever p56.5 |
b. chicken pox
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what do you know about yersinia pestis? gm -/+, alternate name, carriers, mortality rates?
p57 |
enteric gm '-' rod. causes plague. is zoonotic (rats, squirrels, fleas) bacteria replicate in lymph node (bubo - bubonic plague) 75% mortality
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what do you know about neisseriae species? gm+/-, 2 mj pathogenic ones, diseases caused?
p59 |
gm '-' diplococci. N. meningitides & N. gonorrhoeae. cause purulent (pus) infections, ie. gonorrhea 650K & pelvic inflammatory diease 300K cases/yr. (200K deaths for both/yr)
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you have bacterial meningitis, what's that mean?
p59 |
the N. meningitides (or meningococcus) leaves nasopharynx & gets into the fluid lining brain/spinal cord.
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what's meningococcemia?
p59 |
N. meningitides (meningococcus) causes this diease which is rapidly progressing bacteremia and sepsis
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virulence factors of N. meningitides? name 2/4
p59 |
1. pili (resist phagocytosis, attach in nasopharynx)
2. capsule (antiphagocytic, Antigenic differences b/w strains) 3. IgA Protease 4. Blebs of LPS (huge amnt) |
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how would one aquire N. meningitides?
p. 60 |
10% asymptomatic carriers. spread by respiratory droplets. have anti-phagocytic capsules, those w/o opsonizing Ab's (ie kids). nose - blood - bacteremia (b/c not opsonized)
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why are kids/ elderly more susceptible to meningitis?
p60 |
babies who have mothers IgG levels drop as their own humoral immunity is developing. other teens/army get crowded, old are just so old
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what's the deal with meningococcal sepsis?
p61 |
serious. bacteria replicate fast in blood. endotoxins bleb causing momocytes cytokines (tnfA, IL6) = disseminated intravascular coagulation. plasma out of vessels, damaged sm. vessels. super low BP
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T/F
meiningococcal sepsis (leading to septic shock) and meningitis are both similar in their pathology p61 |
True.
meningitis bacteria cross from blood to membrane around brain. endotoxin stimulates inflammatory cascade |
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what is disseminated intravascular coagulation?
p 61 |
LPS blebbing off in meningitis will cause capillary blockage/damage
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what's the difference b/w meningitis and meningococcemia?
p59 |
meningitis (infection of fluid lining brain/spinal cord).
meningococcemia - rapidly progressing bacteremia and sepsis |
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T/F
50-75% meningococcal infections are meningococcemia the bulk of the rest are meningitis |
False, other way around
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pitfalls of meningitis vaccine?
p62 |
yes. doesn't cover endemic in NW, works poorly in children (for kids over 10 only). good for traveling to Africa though, quadra-valent
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what's worse, viral meningitis or bacterial meningitis?
p63 |
viral meningitis is usually much milder
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one can aquire a brian infection via Otitis, _______ (bact., virus, fungi, prion) lymphocytic meningitis, chronic ganulomatiis and acute ____ ______
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encephalitis (bacterial, virual, fungi, prion)
acute purulent meningitis - big 3: 1. H. influenza 2. Nmening 3. strep pneu |
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if your kid gets a rash, does he have meningitis?!
p64 |
do the clear glass test. if under the pressure of the glass it blanches - then rash. no blanch = meningitis
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anything to increase chances of meningitis?
p64 |
doesn't help if you're young, live in a smoking environment or crowded environment (daycare, army)
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pheumonic for top 7 STD's
"the 'home channel' has GAS". what are they/how many? p67 |
1. trichomonias (protozoa) 7.5
2. hpv (warts) 6 million 3. chalmydia 4 mil 4. herpes 1 mill 5. gonorrhea 650K (2nd usa) 6. AIDS/HIV 55K 7. syphilis 25K |
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gonorrhea - women or men or animals only?
p65 |
both. n gonorhoeae via sexual contact. women 50% chance, men 20% risk when sexing with infected partner. men show usually, women rarely
no animal carriers |
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"doc, i have buring sensation and a yellowish white discharge from the penis, what is it?"
p66 |
the calp
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PID?
p 66 |
pelvic inflammatory disease - chronic inflammatory resposne to infection which can result in scarring, ectopic pregnancy and sterility = most pelvic surgery in women (from chlamydia and gonorrhea)
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treat gonorrhea, antibiotics? vaccine?
p 66 |
resistant strains now. although still use an antibiotic - but one that covers both gonorrhea and chalmydia together. no vaccine b/c Ag-variation
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why drop silver nitrate into the kids eyes right after birth?
p 66 |
its an antibiotic, helps if the birth canal has bacteria, including clamydia/ gonorrhea. standard practice
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Rickettsia, chlamydia & mycoplasma: gm +/-?
p 72 |
very small gm '-' bacteria that cause considerable human disease
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arthropod-spread ______ cause variety of related 'fevers'. these cause enormous morbidity and mortality each year. historically have been deciding factors in wars
p72 |
Rickettsia
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_____ is responsible for blindness in millions, also an STD, 500K/yr usa of PID, and NGU, eye infections and pneumonia. spread by bird poo - pneumonia
p72 |
Chlamydia
NGU is non-gonococcal urethritis. C. psittaci is what's spread via poo |
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____ are among smallest known free-living cells. cause pneumonia, Urogenital disease and possibly vascular disease.
p72 |
mycoplasma
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similarities/differences with rickettsia and chlamydia?
p 73 |
both are 'small' and obligate intracellular parasites, steal AAs and ATP. Rick is systemic & causes rash and fever (b/c LPS). chlam - local in mucosal epithelium w/ LPS inflammation = epithelial damage & scarring
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Myoplasma steals what from who?
p 73 |
steals lipids and scholesterol to strengthen its membrane. cause local infection on epithelium and release super Ag - main cause for epithelial damage
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Rick's Rickettsia was aquired:
a. while fooling around with kim b. tick bite while on a walk in india c. while fooling around wtih tim d. eating raw meat p74 |
b. disease is maintained in animal and arthropod reservoirs (ticks, mites, lice, fleas). rick is an "accidental host"
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how would rick know he has ricketssia? symptoms?
p 74 |
fever(chills) rash, headache,endothelial cells infected. replicate slow and kill endothelial cells = block blood flow (rash). LPS = inflammation (local and systemic)
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worldwide, the most common rickettsial disease is _____. different flavers b/c different arthropod vectors.
p 74 |
typhus
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how is R. prowazekii transmitted?
p74 |
via human body louse. someone with typhus fever. lice excrete rickettsiae on 2nd host. rub fecal matter/crushed lice into bite wound
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T/F
Rocky Mountain Spotted fever is the most sever and most frequently reported rickettsial illness in the USA p75 |
True
but is more often in the SE usa |
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Ticks - ____ ____ ____ ____
mites - scrub typhus lice - epidemic typhus flea - endemic (murine) typhus p 75 |
rocky mountian spotted fever
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what can rickettsia lead to? (when pathology wins)
p 76 |
LPS into blood and headache/ fever/ chills/ rash, multi-organ vascular damage in Skin, CNS, liver, lung speen ==> shock and Death
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difference b/w thyphus and typhoid
p77 |
typhus is Rickettsia.
typhoid mary (p47) is salmonella. both show fever and rash. |
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____ are all obligate intracellular parasites, small, no cell wall, 2 bilipidlayers & LPS, gm '-', ATP theifs
p78 |
chlamydia
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which is not a human pathogen (bird)? which is STD?
a. C. trachomatis b. C. pneumoniae c. C. psittaci p78 |
a. trach - human, STD, Trachoma (most common cause of infectious blindness)
b. human, bronchitis, pneumonia, CHD c. psittachi - bird, pneumonia (psittacosis) |
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C. trachomatis leads to 2 diseases, what are they?
p78 |
Trachoma (blindness)
STD (most common in USA) |
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how does trachoma (blindness via chlamydia) occur?
p78 |
endemic in middle east, N. africa and india. kids resevoir. eye to ey via hands, flies. eyelid scars and turns inward. abrade cornea - scarring and blind 6-7 mill people
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T/F
chalmydia trachomatis is uncommon in USA. p78 |
False.
4 mill/yr usa. like gonorroeheae symtomatic in men, not women. PID inwomen often occurs from STD |
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what makes chlamydia a unique structure?
p79 |
gm '-', LPS out outer memB (all normal) But, no PGcan cell wall b/w the 2 membranes.
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T/F
C. psittaci (bird poo) = respiratory disease C. pneumonia (community) = bronchitis & pneumonia p80 |
true. psittaci especially in immunocompromised.
pneumonia - 2-300K/yr. 50% people have had it |
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C. pneumonia is related to
a. strep throat b. diarrhea c. atherosclerosis p80 |
c. atherosclerosis. Chlamydia directs cells it infects to produce lipids at 5X the normal rate, casuing cardovascular problems
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_____ & the related ureaplasma are the smallest self-replicating orgamisms with smallest genomes (~500genes)
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mycoplasma
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why are myoplasma cell walls unique?
p83 |
trick question.
they do not have a cell wall adn their cell membrane contains sterols (stolen from the epithelial cells they colonize). |
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mycoplasma has a major pathogen called
a. m. pneumonia b. m. genitalium c. m. hominis |
M. pneumonia
adheres to respiratory epithelium (ciliated). ciliostasis occurs. no cilia = microbes in lower respiratory tract. has super Ag too. |
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what's the bacteria found in dirt? gm +/-?
p85 |
gm + rods, spores
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what's the most hardy, stable form of life known?
p85 |
the bacterial spores, they also make the most powerful exotoxins.
these spore-forming exotin producing bacteria is also used in 'bioterrorism' |
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Koch's postulates (there's four), list them (for gm + spore forming anthrax)
p86 |
1. microorgamism abundant with disease, not in healthy (mary)
2. microorganism must be grown in culture 3. it should cause dsease when introduced into healthy organism 4. it must be reisolated from the inoculated, diseased experimental host and id'd as being same as original |
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what do you know about Corynebacterium diptheriae? gm +/-?
p86 |
gm +, non spore forming rods (baccilli) in plants/ animals. colonize in our skin, respirator and GI tract. opportunist - diptheria
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how does diptheria cause disease?
p 86 |
get local infection. exotoxins get into blood. toxin made when a bacteriophage carrying genetic ifno for toxin. AB toxin (B - heart/nerve, A - inactivates EF2, no ribosome activity) 1 molecule shuts down cell
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besides playing in dirt, how's diptheria spread? what's it look like when infected?
p87 |
some have asymptomatic carriage in throat, spread by drolets. multiply in pharynx - gray-white thick, adherent exudate (pseudomembrane)
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how would one fight back against diptheria?
p87 |
get immunized with toxoid.
if already infected, hard to dislodge pseudomembrane w/o bleeding. spread = cardiac & nerve pathologies. 40% untreated dead. 10% when treated |
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what do you know about spores? gm +/-?
p89 |
some + some '-'. ie genera Colostridium and bacillus (from soil). vegetative state to dormant state (spore) b/c conditions.
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what are layers/contents of a spore?
p90 |
complete chromosomes, minimum proteins, inner membrane (pgcan), thick outer keratin-coat.
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what do you know about clostridium?
p91 |
soil bacteria/water/sewage/ normal flora, gm '-' bacilli (rod) makes spores. obligate anaerobe.
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few clostridium's are pathogens. what do these cause?
c. tetani --> tetanus c. botulism --> ______ c. perfringes --->______ c. difficile --->_______ p91 |
c. tetani --> tetanus (AB nerves)
c. botulinum --> botulism (AB) c. perfringes ---> gas gangrene, "food posioning" c. difficile ---> antibiotic colitis |
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step on a rusty nail, outch. what is the danger?
p 91 |
tetanus b/c deep wound. anaerobic spot where AB toxin gets into blood stream. inhibitory neurotransmitter unreleasable. prolonged spasms = spastic paralysis
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true food poisioning occurs from eatin that bad shrimp, what's happening?
p91 |
botulism. honey to babies zb. blocks release of acetylcholine, prevents muscle contraction, causing flaccid paralysis. diaphragm down - dead. canned foods (obligate anaerobe)
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food poisioning caused how? 'gas gangrene' is caused how?
p 94 |
by clostridum perfringens. infects any dirty deep wound. exotozins & spreading factors problematic. spread fast, gas in wake. Meat out too long spores in S.i. = diarrhea
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C. dificile, Pseudomembranous colitits, what do you know about this?
p94 |
antibiotic associated colitis. antibiotics alter normal GI flora, overgrowth of Clostridium difficile, 2 exotoxins - inflammation/diarrhea
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what do you know about bacillus antracis?
p95 |
spore forming gm + bacillus = antrax. in dirt, grazers eat & spores open, we get rarely, but do from working with infected animals
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3 types of antrhax in humans.
1. 2. 3. G.I tract - contracted from eating food, meat from animal that died of antrax p95 |
1. cutaneous - aquired when a spore enters skin trhough cut/ abrasion
2. pulmonary anthrax - breathing in airborne antrax spores |
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2 antrax toxins relasesd from Antrax?
hint, E.L. p95 |
edema toxin and lethal toxin - together cause edema and shock
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T/F
anthrax is gm '-' anaerobe p95 |
False.
gram + rod, facultative (don't need deep wound) good for bioterrorism. hardy spore |
