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50 Cards in this Set
- Front
- Back
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Ebola |
5 types negative ssRNA names based where they were discovered 4 of them cause disease in humans |
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how is it transmitted? |
infected animals to humans through close contact human to human right now infectious when they're showing symptoms humans not natural host not airborn as of yet |
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incubation period |
2-21 days |
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symptoms |
sudden fever, fatigue, myalgias, HA, sore throat if you have symptoms you are infectious later symptoms :vomiting, diarrhea, rash, acute renal failure, liver failure, hemorrhaging |
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filovirus and dendritic cell invasion |
filovirus infects dendritic cell prevents production of inflammatory cytokines (IFN alpha, beta; no TNF) decreases costimulatory action--> death by apoptosis increases coinhibition |
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filovirus and monocyte/macrophage |
infection--> release TNF, IL-6, increase tissue factor, NO IFNalpha or IFNbeta --> inflammation--> endothelial leakage--> rash, hemorrhage
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filovirus and neutrohpil |
degranulation--> leads to more inflammation (early signs: increase in immunity, increase signal to adaptive immunity) (late signs: fever, malairse, GI distress, septicemia) |
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filovirus and NK cell |
depletes it. kills the police |
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overall poor immune response has what effect on body? |
high viremia. many cells and tissues affected late in disease--> storm hits. increase viral burden. decrease immune response. increase inflammation |
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cytokine storm |
IL2, IL6, IL10 TNF alpha proinflammatory cytokines except IL10 (inhibits inflammation)
TNF alpha: high fever; hypothalamic effects; increases set point. leads to systemic vasodilation. hyotension. shock
il10: antiinflammatory; contributes to scarring and fibrosis
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once virus goes to the liver.. |
virus continues to replicate. endothelial cells leaky. platelets come in to repair. cells slough off and die. that allows for virus to circulate. once it reaches hepatocytes which make clotting factor, you can't clot anymore . you bleed out.
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z MAT |
take myeloma cells (with virus particles) fuse with spleen cells--> hybridomas culture for positive cells so you can harvest monoclonal antibodies
problems: rejection because of chimeric ingredients |
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consequences of staph infections |
TSS respiratory infection osteomyelitis skin infections endocarditis food poisoning
MRSA is the skin infection one: chews up fatty acid protective measures of skin (acid mantle)
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why is it hard to treat staph infections? |
they have capsules which prevents antibodies from sticking to it. |
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MRSA treatment |
Vancomycin |
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food poisoning wiht staph |
the staph superantigens (toxins secreted by staph) tickles the vagus nerve which goes up to medulla and the vom center which makes you vomit |
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staph bacteria |
gram + organism
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SUPERANTIGENS |
CAN survive boiling, proteases and gastric juices |
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TSS |
caused by staph TNF alpha, iL-1 acute multisystem disease syndrome oxygen bubbles trapped in tampons are growing environment for staph. staph releases enzymes to chew mucosal cells--> release of superantigens into blood. --> superantigens into circulation, activation of T cells--> vasodilation (fever, hypotension)--> decreased perfusion to multiple organs--> failure
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ova and parasites Giardia |
Giardia: G. intestinalis most common pathogenic parasitic infection in humans fecal contamination in water flagellated no golgi body , ER, mitochondria self limiting infection of small intestine causes acute or chronic diarrhea giardia can change surface receptors to evade host
igA (GI antibody) and IL-6 important for clearing |
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salmonella typhoid |
typhoid rare in US: intestinal hemorrhages which can perf bowel.
can infect LN, hepatosplenomegaly, bone marrow
gram negative contaminated foods
with typhoid, il8 is down regulated (you need il8 to call in macros and dc's and neutrophils) because of down regulation, neutrophils don't come to the site and fight infection: systemic consequences
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salmonella non typhoid |
gram negative contaminated foods most often in teh summer and fall fecal oral route spread common in US |
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M cells |
no microvilli sample antigen constantly in gut bring antigens in so that immune cells can be stimulated constant monitoring of foreign antigens |
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where is the initial site of antigen presentation in the gut |
M cells |
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bacterial invasion of gut |
invasion via zipper mechanism or trigger mechanism |
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zipper mechanism |
adheres to gut surface, rearranges cytoskeleton, membrane unzips to bring in bacterium in endosome but bacteria can escape endosomes/phagosomes |
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trigger mechanism |
inserts needle into host membrane and shoots bacterial proteins into cell. ex: shigella type III, IV secretion system. they don't want cells to die they just want to hijack host cell. shoot their proteins into eukaryotic cells to use host cell to replicate allows bacteria to escape phagosome/endosome |
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why does salmonella prefer the ilium? |
it can sense pH differences, temperature differences, oxygen concentration levels. it knows where to land. |
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Shigella |
unencapsulated non motile facultative anerobe most common cause of bloody diarrhea daycare gram negative bacilli can survive gastric juices. likes to infect the left side of the colon. can survive in gastric juices because you only need a few to cause disease |
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shigella and EIEC mechanis |
EIEC: enteroinvasive e. coli shigella has same mechanism as EIEC
EIEC lands on M cell. internalized through endosome. macrophages eats the shigella. shigella induces apoptosis in macrophages now its in the vasolatearl side of the epithelial lining of gut and enters through phagosome hijacks microtubules and then leaves via phagosomes when it wants to to go infect neighboring cells
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EIEC/shigellossi |
acute colitis bloody diarrhea, abominal pain duration: 10 days self limiting |
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campylobacter jejuni |
most common in developed countries comma shaped, flagellated, G- patho poorly understood traveler's diarrhea |
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4 virulence factors of c. jejuni |
motility, adherence, toxin production, invasion |
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contamination of the water. how does this occur |
chicken with the c. jejuni colonization has a bowel movement and contaminates water.
c. jejuni and amoebas can associate and form biofilm in water |
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c. jejuni MOA 1 |
attaches to mucous layer of GI secretes enzyme to chew through epithelial layer zipper mechanism: comes in through phagosome. infected cells secrete IL-8 secretion of il-8 calls neutrophils, DC, macrophages to come to site chew up or eat organisms and become activated NfKB activated which induces expression of proinflammatory cytokines (T1H signal in body)
symptoms: diarrhea, inflammation, you clear infection on your own |
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how can c jejuni cause respiratory paralysis |
c jejuni has LPS which looks alot like gangliosides in peripheral and central nervous system. CNS starts attacking gangliosides thinking it's an LPS
get reactive arthritis. ascending nerve diseas. starts with tingling in feet and ascends up. respiratory paralysis end result.
HLA B27 gene with reactive arthritis |
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different playas with e coli |
enterotoxigenic enterohemorrhagic enteroinvasive |
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Morgan wants to know how are you gettgin watery diarrhea from e coli? heat labile |
sodium water and chloride are leaving e coli binds to receptor on epithelial surface and internalized in a vesicle adenylyl cyclase--> increases amount of CAMP--> increase production of protein kinase A--> sodium chrlodie comes out as well as sodium and water--> diarrhea |
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ecoli's heat stable toxins |
tickles GTP--> cuases activation of CFTR--> sodium chloride water come out |
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big complication of EHEC |
hemolytic uremia syndrome (red blood cells stuck in your kidneys) you can die from this dehydration |
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EHEC |
cattle and ruminants are carriers infection from uncooked meat and raw milk, fruits and vegetables that aren't clean fast food. apple juice story
3-8 day incubation
symptoms: stomach muscle spasm diarrhea fever vomiting |
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when food is exposed to temperature levels, EHEC dies... |
70C or higher |
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how does hemolytic uremic syndrome |
we don't know how EHEC cells enter the cell. it produces a shiga like toxin, but when it does it accesses the endothelial cells of the blood vessel through a vesicle --> stops protein synthesis--> cell death. because there's tissue injury, fibrin come to repair--> microthrombi formation--> ischemia. RBCs traveling through get cut up--> fragments stuck--> clog up kidneys--> hemolytic uremic syndrome--> acute renal failure |
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EIEC toxin production? transmission |
similar to shigella does not produce toxins transmitted via food, water, person to person
build up of waste in kidney. can't filter through. toxic levels of waste. acute renal failure. no filter, no life. |
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pseudomembrane spotted during colonoscopy tells you what |
fibrin, neutrophils, cellular debris, exudates as well as dying cells. inflammatory signal
c. diff can also form pseudomembranes. staph can. candida can. CMV, shigella. |
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how does c diff get out of control if it's normal flora? |
you wipe out normal bacterial gut flora and cdiff comes in smells like liquid gold |
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c diff mechanism to produce pseudomembrane |
c diff produces toxin and colonizes on cell surface. toxins are released. necrosis of epithelial cells. infalmmation with influx of monocyte macrophages and neutrophils. psudomembrane production. toxins kill cells by necrotic mechanisms |
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c diff gram stain motility associated with
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gram + motile associated with advanced age, hospitalization and abx treatment 30% of hospitalized patients colonized with c. diff |
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symptoms of c diff |
fever leukocytosis abdominal pain cramps hypoalbuminemia 10-20 episodes of diarrhea a day low levels of albumin seen can lose alot of proteins this way |
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vanco iv? |
always PO never IV!
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