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510 Cards in this Set
- Front
- Back
what is sulfamethoxazole used for?
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antibacterial, metabolite that inhibits folic acid synthesis
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what is trimethoprim used for?
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antibacterial, inhbits the enzyme that makes folic acid
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what is ciprofloxacin used for?
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antibacterial, inhibits DNA gyrase
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what is levofloxacin used for?
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antibacterial, inhibits DNA gyrase
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what is maxifloxacin used for?
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antibacterial, inhibits DNA gyrase
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what is rifampin used for?
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antibacterial and antituberculosis, inhibits RNA polymerase
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what is nitrofurantoin used for?
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antibacterial, produces intracellular free radicals
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What is alpha hemolysis, and how does it show up on blood agar?
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incomplete lysis of RBCs. Shows up as green color on blood agar
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What is beta hemolysis, and how does it show up on blood agar?
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complete lysis of RBCs. Shows up as clear area on blood agar
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Which strep bugs are alpha-hemolytic?
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strep pneumoniae, strep viridans, random oral strep bugs
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Which strep bugs are beta-hemolytic?
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Group A, B, C are usually beta-hemolytic
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Group A strep is characterized by what organism?
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strep pyogenes
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What antigens are unique to group A strep?
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M,T, and R surface antigens
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Strep pyogenes has a capsule made of.........?
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hyaluronic acid
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Which antigen imparts virulency to group A strep?
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M protein
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Which antigen in group A strep does not contribute to virulency?
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T and R proteins
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In what ways does M protein contribute to virulency of strep pyrogenes?
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point of attachment for lipoteichoic acids (aid in cell adherence), and prevents the action of complement
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What are the 7 substances strep pyogenes secretes extracellularly?
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streptolysin O, streptolysin S, pyrogenic exotoxin, streptokinase, hyaluronidase, DNase, proteinase
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What does streptokinase do when group A strep bugs secrete it?
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dissolves clots in the blood by activating plasminogen
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What does hyaluronidase do when group A strep bugs secrete it?
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dissolve the ground substance of connective tissue
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Group A strep bugs secrete pyrogenic exotoxin; what does it do?
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cause fever, damage heart tissue, cause rash
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What are the 5 main syndromes caused by group A strep?
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pharyngitis, skin infections, Scarlet fever, ARF, APSGN
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What is ARF, and how can group A strep cause it?
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Acute Rheumatic Fever. autoimmunity against joints, CNS, and heart valves following strep pharyngitis
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What is APSGN and how can group A strep cause it?
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Acute Post-Strep Glomerulo Nephritis. Immune complexes lodge in the glomerulus after skin or throat infection with strep
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What kinds of skin infections can group A strep cause?
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abscesses, cellulitis, impetigo
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What 3 signs point to Scarlet Fever as the diagnosis?
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fever, red rash, strawberry tongue. due to systemic strep pyogenes infection
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Beyond the 5 common diseases, Strep pyogenes can also cause rapid, severe infections in:
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lung, bone, and brain
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Acute Rheumatic Fever never ever follows Strep infection of the......?
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Skin. ARF only follows strep pharyngitis
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How does Group A strep cause autoimmunity in ARF?
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antigenic cross-reaction between the pyogenes antigen and heart-valve antigens
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Strep pyogenes secretes streptolysin O. What does it do, and what inhibits it?
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lyses RBCs, but not neutrophils. Oxygen impedes it and cholesterol inhibits it.
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Strep pyogenes secretes streptolysin S. What does it do, and what inhibits it?
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lyses RBCs and neutrophils. Nothing inhibits it
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To make a vaccine against group A strep, which protein do you need to bind to?
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M protein
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What are the 2 main differences in the structure of group A and group B strep?
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A: hyaluronic acid capsule, M T R antigens
B: variable capsule makeup, no M T R antigens |
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Which factor determines the virulency of group B strep?
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Lipoteichoic Acid (LTA). The more there is, the more dangerous the bug
|
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The different capsules in group B strep are made of what substances?
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glucose, glucosamine, galactose, sialic acid
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What is the characteristic organism of the Group B strep bugs?
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Strep agalactiae
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What 5 things do Group B strep bugs secrete extracellularly?
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neuraminidase, protease, beta-hemolysin, hyaluronidase, CAMP
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Group B strep secretes neuraminidase. What does it do?
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dissovles polysaccharides and glycoproteins
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Group B strep secretes CAMP. What does it do?
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CAMP enhances lyis of staph aureus
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What group is most succeptable to Group B strep infection, and how do they get it?
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newborns get it from the vagine or rectum of their moms during birth
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Can group B strep cause ARF or APSGN?
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NO!!!!! No!!!!! NO!!!!!
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What protects newborns from Group B strep infection?
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Maternal IgG can cross the placenta and immunize the fetus
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What antigen do group D strep and enterococci share?
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lipotecholic acid in their cell membrane
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What are 2 characteristic bugs from the enterococcus group?
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E faecalis and E faecium
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Unlike all other streps, Enterococci are resistant to which class of drugs?
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Penicillins
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What 3 lab tests are used to identify a bug as an enterococcus?
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ability to grow in salt solution, ability to grow in bile, ability to hydrolyze esculin
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What 2 traits do Group D strep bugs share with enterococci?
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ability to grow in bile and ability to hydrolyze esculin
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Group D strep and Enterococci are normal indiginous flora found, where?
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GI tract, upper respiratory tract, urinary tract, skin
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Group G strep bugs are uncommon, but what do they share with group A strep bugs?
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have M protein, secrete streptolycin O and streptokinase, cause pharyngitis and APSGN
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Group G strep can cause ARF. True or false?
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False!!! False!!! False!!! Group G strep does NOT cause ARF, ever!
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Group D strep and enterococci can cause heart valve infection. True or false?
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True!!! True!!! True!!! Not the same as ARF, but still.
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Group C strep are uncommon, but what do they share with Group A strep?
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cause pharyngitis, secrete streptolysin O, cause APSGN
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What antigen characterizes the Strep Viridans group?
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There isn't a group specific antigen
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What characteristic is common to all strep viridans bugs?
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they are all alpha-hemolytic, producing green biliverdin on blood agar plates
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Which two conditions are due to strep viridans infection?
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dental caries and endocarditis
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How do strep viridans bugs produce their ill effects?
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ability to stick to things (like tooth enamel or heart valves)
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What percentage of endocarditis cases are due to strep viridans?
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50%
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Hemophilus Influenzae is gram (positive/negative), (cocci/rod).
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H Influenzae is gram negative, and a rod
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Strep Pneumoniae is gram (positive/negative), (cocci/rod).
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Strep pneumoniae is gram positive, and a cocci
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Neisseria Meningitidis is gram (negative/postive), (rod/cocci).
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Neisseria meningitidis is a gram negative cocci
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What does strep pneumoniae look like under the microscope?
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lancet-shaped diplococci
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what does neisseria meningitidis look like under a microscope?
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bean-shaped diplococci
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What factors found in blood does hemophilus influenza require to live?
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NAD and heme
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Both strep viridans and strep pneumoniae are alpha hemolytic. How do you distinguish them in the lab?
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Optochin will kill s. pneumoniae, but not s. viridans
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How do you detect neisseria meningitidis in the lab?
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antisera against the polysaccharide capsule, usually on latex beads
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How do you detect hemophilus influenzae in the lab?
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antisera against the polysaccharide capsule, usually on latex beads
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What is the most critical virulence factor in h. influenzae, s. pneumoniae, and n. meningitidis?
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whether it has a capsule or not
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What is unique about h. influenza's capsule, compared to the other encapsulaed bacterias?
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shares antigen with other gram-positive bugs, leading to increased incidence of immunity
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Which encapsulated bacteria has the most capsular serotypes?
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s. pneumoniae has 90 different serotypes in its capsule
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What is unique about n. meningitidis's capsule, compared to the other encapsulated bugs?
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One serotype is non-immunogenic in humans, which has prevented vaccine development
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Which unique enzyme do all encapsulated bacteria secrete?
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IgA protease, which chews up IgA. This enables them to infect mucus membranes so easily
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What is unique about pneumolysin, secreted by s. pneumoniae?
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S. pneumoniae releases pneumolysin when it autolyses itself
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do gram positive bacteria have endotoxin?
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NO!!!!! only gram negative bacteria have endotoxin
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What is the most common cause of meningitis in children and teenagers?
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Neisseria meningitidis
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What is the most common cause of meningitis in adults?
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strep pneumoniae
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What is the leading cause of otitis media in children?
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s. pneumoniae (50% of cases)
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Which drugs are used for prophylactic treatment for people exposed to the encapsulated bacterias?
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rifampin and ciprofloxacin
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How is polysaccharide vaccine currently used to treat h.influenzae?
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It's not, because it is not effective
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Why do polysaccharide vaccines not work against h. influenzae?
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pure polysaccharides do not induce a T-cell response in infants, to whom this vaccine was given to
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How do conjugate vaccines work against h. influenzae?
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capsule polysaccharide is joined to inactive diptheria protein, and this produces a T-cell response in infants
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Which bugs does the Tetramune vaccine protect against?
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h. influenzae, and diptheria, pertussis, tetanus (DPT)
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What bug does Menactra vaccine protect against?
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N. meningitidis
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What bug does Menomune protect against?
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N. meningitidis
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Menactra vaccine is targeted to what age range?
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11-55 years old
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Menomune vaccine is targeted to what age range?
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2-10 years old
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What DISEASE does the Pneumovax vaccine protect against?
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S. pneomoniae bacteremia
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What DISEASE does the Pneumovax vaccine give no protection against?
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S. pneumoniae pneumonia
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Which bug does the Prevnar vaccine protect against?
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strep pneumoniae
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Which is the most expensive routine childhood vaccine, and how much does it cost?
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Prevnar, which protects against s. pneumoniae, costs 58$ a pop
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Staphylococcus are gram (negative/positive), and catalse (negative/positive)
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staph are gram positive, catalase positive
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In general, what is the biggest difference between infectious staph and strep?
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strep is catalase negative, staph is catalse positive
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What are 2 imporant virulence factors staph uses to infect organisms?
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Clumping factor and protein A
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What does clumping factor do in staph bacteria?
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attaches the cell wall to fibrinogen, clumps all the staph cells together to resist phagocytosis
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What does protein A do in staph bacteria?
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binds the Fc region of antibody, thwarting it and protecting itself from phagocytosis
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Lipoteichoic acid in staph bacteria has a special name, and that name is.....?
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Ribitol
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Some staph strains secrete exfoliatin. What does it do?
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dissolves desmosomes at the GM4 glycolipid, causing separation of skin layers in humans
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Some staph strains secrete leukolysin. What does it do?
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kills WBCs. Common in MRSA
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What purpose does coagulase serve in Staph bacteria?
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serves to clump bacteria together, where they have a better chance at survival
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Some Staph secrete enterotoxin. What does it do?
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cause cytokine release from mast cells, leads to food poisoning
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Some staph strains secrete TSST-1. What does it do?
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causes TNF and interleukin release from WBCs, leads to toxic shock syndrome. Very dangerous
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How do staph bacteria genetically recombine?
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usually by transduction through a bacteriophage
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What is the D-test?
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tests to see if staph bugs are resistant to clindamycin when erythromycin is present
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What general pattern of distribution does staph tend to follow when it infects you?
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Tend to localise. As opposed to strep infections, which tend to spread
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Coagulase negative staph is usually less infectious, except when.....?
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It can form biofilms on catheters etc. and cause infection through that route
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Where do many people carry colonies of Staph Aureus?
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In their nostrils
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where do many people carry colonies of coagulase-negative staph?
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On their skin
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which gene does MRSA carry that normal staph aureus does not have? What does it code for?
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mecA, which codes for an alternate penicillin binding protein
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What are some drugs that will work against MRSA and VRSA?
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sulfa/trimethoprim, daptomycin, linezolid, synercid
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What is the most common cause of osteomyelitis? What is osteomyelitis?
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staph aureus. osteomyelitis is a purulent abcess in the bone
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What factors describe Job's Disease?
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cold abscesses, poor neutrophil chemotaxis, elevated IgE levels
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What 5 signs make up Toxic Shock syndrome?
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acute fever, erythroderma, hypotension, involvement of at least 3 major organ systems, exclusion of other disease
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What are the main advantages for a bacteria to live inside a eukaryotic cell?
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easy access to nutrients, protection from extracellular defense
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What distinguishes facultative from obligate intracellular bacteria?
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obligate have lost the genes for certain metabolic functions, and so must use the host cell's instead
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Name 5 obligate intracellular bacteria species
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chlamydia, coxiella, ehrlichia, ricksettia, mycobacterium leprae
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Explain the zipper model of cellular entry by bacteria
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tight interactions between proteins on the two cell surfaces wrap the cell's membrane around the bacteria, bringing it inside itself
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Explain the trigger model of cellular entry by bacteria
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bacteria secrete proteins that cause the host cell's membrane to splash and ripple, the bacteria enters during the confusion
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Which intracellular bacteria use the zipper method to gain entry into cells?
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listeria monocytogenes, mycobacterum tuberculosis, legionella
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Which intracellular bacteria use the trigger method to gain entry into cells?
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salmonella, shigella
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What are some dangers intracellular bacteria face inside of host cells?
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phagosomes become lysosomes and try to kill the bug with NADPH oxidase system, nitrous oxide, and other lysozymes
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How does listeria escape intracellular defenses?
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lyses the phagosome it is in, thus avoiding digestion
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How does legionella escape intracellular defenses?
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inhibits the phagosome from aquiring lysosomal proteins and enzymes
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How does salmonella escape the intracellular defenses of its host cell?
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produces superoxide dismutase and catalse to neutralize reactive compounds sent to kill it
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What does it mean if a bacteria species is non-fusogenic?
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intracellular bacteria that stays in the phagosome, but prevents it from becoming a lysosome
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What does it mean if a bacteria species is fusogenic?
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intracelluar bacteria that stays in the phagosome even after becoming a lysosome
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what is the one fusogenic bacteria?
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coxiella burnetti
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Which intracellular bacteria lives in RBCs?
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bartonella
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Name 2 non-fusogenic bacteria
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chlamydia, mycobacteria
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How do aminoglycosides enter cells?
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by pinocytosis
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How does tetracycline enter cells?
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diffusion
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Where in our cells do the aminoglycosides end up?
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inside lysosomes and phagosomes
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Where in our cells does tetracycline end up?
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in the cytosol
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why are intracellular bacteria resistant to aminoglycosides?
|
aminoglycosides work best at pH 7, but end up inside acidic lysosomes inside our cells, where they don't work
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why are intracellular bacteria susceptable to tetracycline?
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tetracycline works best near pH 7, and end up in the neutral cytosol, so they retain their activity
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What is unique about the way listeria can travel throughout the body?
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listeria can move between cells without ever leaving the intracellular environment
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How do listeria species move around in the cytosol of our cells?
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they acquire actin at one end, which they use to move around in and between our cells
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How does nitrofurantoin work?
|
creates reactive species inside of bacteria, which tear up their DNA
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What is nitrofurantoin used for, and why?
|
UTIs, because it concentrates in the kidney but has a very short half-life in the plasma
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What is metronidazole used for?
|
anaerobe and protozoan infection
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How does metronidazole work?
|
creates reactive species inside the pathogen, which tears up their DNA
|
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Which common antibiotics must you be careful of drug-drug interactions with?
|
Chloramphenicol, Clindamycin, Rifampin, Isoniazid, Metronidazole, Erythromycin, Streptogrammins, Sulfonamides (CRIMES)
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How does polymyxin work?
|
bacteriocidal drug that is like soap, it disrupts the bacterial cell membrane
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What would you use polymyxin for?
|
To kill gram negative bacteria
|
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What kind of bacteria does polymyxin not work against?
|
gram positive bacteria. Peptidoglycan wall is too thick for the drug to get to the membrane
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What would you use daptomycin for?
|
methicillin and vancomycin resistant Gram positive bacteria
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what is naldixic acid's effect on: gram-, gram+, pseudomonas, atypical, and anaerobic bacteria?
|
gram-: ++
gram+: - pseudo: - atypical: +/- anaerobic: - |
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What disease would you treat with naldixic acid?
|
UTI's
|
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what is ciprofloxacin's effect on: gram-, gram+, pseudomonas, atypical, and anaerobic bacteria?
|
gram-: ++
gram+: + pseudo: + atypical: + anaerobic:- |
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what diseases would you treat with ciprofloacin?
|
UTI's, soft tissue infections
|
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what is levofloxacin's effect on: gram-, gram+, pseudomonas, atypical, and anaerobic bacteria?
|
gram-: ++
gram+: ++ pseudo: - atypical: + anaerobe: + |
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What disease would you treat with levofloxacin?
|
bronchitis, pneumonia, MRSA
|
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what is moxifloxacin's effect on: gram-, gram+, pseudomonas, atypical, and anaerobic bacteria?
|
gram-: ++
gram+: ++ pseudo: + atypical:+ anaerobe:+ |
|
What diseases would you treat with moxifloxacin?
|
use as a last resort against bugs that won't be killed by anything else
|
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Who is contraindicated for treatment with fluoroquinolones?
|
pregant women and kids under 12
|
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what are 4 side effects of the fluoroquinolones?
|
GI upset, dizziness, rash, arthralgia
|
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What is the target for fluoroquinolone drugs in gram negative bacteria?
|
DNA gyrase
|
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What is the target for fluoroquinolone drugs in gram positive bacteria?
|
topoisomerase 4
|
|
What are the species of enterobacteria that commonly cause diarrhea?
|
shigella, salmonella, E. coli, and yersinia
|
|
What bacterial species closely related to enterbacteria commonly cause diarrhea?
|
cambylobacter, vibrio
|
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The enterobacteria and related species are all gram (negative/positive) (cocci/rods)
|
all enterobacteria are gram-negative rods
|
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What do campylobacter and vibrio species look like under a microscope?
|
squiggly or curved
|
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Are enterobacteria aerobic or anaerobic?
|
they can do either one (facultative anaerobes)
|
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All enterobacteria are oxidase (+/-), catalase (+/-), and glucose fermenting (+/-)
|
All enterobacteria are oxidase (-), catalase (+), and glucose fermenters
|
|
What are the 3 antigens on enterobacteria, and where are they located?
|
O - On LPS
H - on flagella K - on the capsule |
|
Which antigen on enterobacteria is associated with increased virulence?
|
antigen K, on the capsule
|
|
In enterobacteria, what makes up the variable region of LPS?
|
antigen O repeats
|
|
Metabolically, what is different between the enterobacteria and the vibrio species?
|
vibrio are oxidase positive, enterbacteria are oxidase negative
|
|
What are 3 genetic ways enterobacteria can change their chromosome?
|
plasmids, bacteriophage, pathogenicity islands
|
|
what are some characteristics of watery diarrhea as a symptom?
|
copious, no blood or pus, no tissue invasion, pathology in the small intestine
|
|
what are some characteristics of dysenteric diarrhea as a symptom?
|
scant volume, blood or pus or mucus present, tissue invasion, pathology in large intestine
|
|
what are some characteristics of bloody/watery diarrhea as a symptom?
|
copious, some blood or pus, tissue invasion, pathology in colon or ileum
|
|
what are some characteristics of hemorrhagic colitis as a symptom?
|
copious, like liquid blood, no WBCs, no tissue invasion, pathology in large intestine
|
|
Name 4 diarrhea-causing bacteria that are not normal gut flora
|
salmonella, shigella, vibrio cholerae, and ETEC
|
|
What are the two mechanisms of pathology in the enterobacteria?
|
invasive - bugs invade your cells
toxigenic - bugs stay in the lumen, produce poisons |
|
Is vibrio cholerae invasive or toxigenic?
|
toxigenic
|
|
Is ETEC invasve or toxigenic?
|
toxigenic
|
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Is EHEC invasive or toxigenic?
|
toxigenic
|
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Is salmonella invasive or toxigenic?
|
invasive
|
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Is shigella invasive or toxigenic?
|
both invasive AND toxigenic
|
|
Define exotoxin
|
A substance secreted out of the bacteria that causes symptoms
|
|
Define endotoxin
|
A substance on the surface of the cell (LPS) that causes symptoms
|
|
Define enterotoxin
|
an exotoxin that has specific effects on the intestines
|
|
Which intestine is usually affected in a secretory diarrhea?
|
small intestine
|
|
Which intestine is usually affected in an inflammatory diarrhea?
|
large intestine
|
|
roughly how many shigella bugs do you need to ingest to be infected?
|
10-100
|
|
roughly how many salmonella bugs do you need to ingest to be infected?
|
100-100,000
|
|
roughly how many vibrio bugs do you need to ingest to be infected?
|
10,000-100,000,000
|
|
What bug causes Cholera?
|
vibrio cholerae
|
|
Which serotype of Vibrio is the most infectious?
|
serotype O1
|
|
what kind of diarrhea does vibrio cholerae cause?
|
thin and watery, copious, no blood or pus
|
|
What factor determines if the vibrio cholerae bug can colonize the small intestine?
|
If they have TCP pilus
|
|
How do vibrio cholerae bugs obtain the ability to have TCP pilus on their surface?
|
a bacteriophage
|
|
How do vibrio cholerae bugs obtain the ability to make cholera toxin (CTX)?
|
from a bacteriophage
|
|
What is the structure of cholera toxin, and what does each part do?
|
A and B subunits. B subunit binds to cell surface, A subunit enters the cell
|
|
What is the mechanism of cholera toxin within the host cell?
|
subunit A permanently turns on Adenylate cyclase, which leads to increased Cl- efflux and fluid secretion
|
|
How does vibrio cholerae kill enterocytes?
|
It doesn't. It poisons them, then they live a normal cell lifespan
|
|
Should you use antibiotics in people with cholera?
|
Sure. They might shorten the course of the disease
|
|
What is the best treatment for cholera?
|
rehydration and electrolyte replacement, either orally or IV
|
|
Which bacteria most likely causes gastroenteritis in people who ate raw or undercooked shellfish?
|
vibrio parahemolyticus
|
|
What does ETEC stand for?
|
EnteroToxigenic E. Coli
|
|
What kind of diarrhea is caused by ETEC?
|
watery, loose, copious, no blood or pus
|
|
What other symptoms accompany diarrhea caused by ETEC?
|
vomiting, cramps
|
|
Which antibiotics should you use in people who have diarrhea caused by ETEC?
|
NONE! Don't use antibiotics in these people!
|
|
What 2 toxins are responsible for the diarrhea caused by ETEC?
|
heat-labile enterotoxin and heat-stable enterotoxin
|
|
Heat-labile enterotoxin produced by ETEC: how does it work?
|
Same mechanism of cholera toxin: high cAMP levels -> Cl- efflux -> fluid secretion
|
|
Heat-stable enterotoxin produced by ETEC: how does it work?
|
peptide toxin that raises cGMP levels, which leads to fluid efflux
|
|
Where does ETEC set up shop, and how does it do so?
|
ETEC express adhesins on their fimbriae, which help them stick in the small intestine
|
|
How should you treat ETEC-caused diarrhea?
|
fluid/electrolyte replacement, rest. Infection is self-limiting
|
|
What does EPEC stand for?
|
EnteroPathogenic E. Coli
|
|
What age group is commonly affected by EPEC-caused diarrhea?
|
infants less than a year old
|
|
What kind of diarrhea does EPEC cause?
|
loose, watery, no blood or pus
|
|
What other symptoms may be seen along with EPEC-caused diarrhea?
|
vomiting, low fever
|
|
What is the treatment for EPEC-caused diarrhea?
|
rehydration, restore electrolytes, ANTIBIOTICS.
|
|
Which diarrhea-causing e. coli subtype is the only one you should treat with antibiotics?
|
EPEC. the one with the P
|
|
How does EPEC cause diarrhea?
|
adhere to enterocytes, leading to microvilli destruction, leading to decreased absorption
|
|
What does EHEC stand for?
|
EnteroHemorrhagic E. Coli
|
|
What kind of diarrhea does EHEC cause?
|
hemorrhagic colitis. Lots of liquid blood, no WBCs
|
|
In addition to diarrhea, what else does EHEC commonly cause?
|
hemolytic uremic syndrome (HUS)
|
|
Which serotype of EHEC is the most virulent?
|
O157:H7
|
|
Where does EHEC set up shop in the GI tract?
|
Large intestine (other E. coli sause problems in the small intestine)
|
|
How does EHEC cause diarrhea?
|
adheres to colon cells, produce shiga-like toxins that cause the hemorrhage
|
|
What are the 2 ways in which shiga-like toxin produced by EHEC cause problems?
|
binds to sphingolipids in the bowels and kidneys, and binds to rRNA and stops protein production
|
|
What is the most common way invasive enterobacteria get into your tissues?
|
M cells in the GI tract
|
|
What is the most common species of Shigella in the USA?
|
shigella sonnei
|
|
What is the most common species of shigella in India?
|
shigella Boydii
|
|
What is the most common species of shigella in the developing world?
|
shigella flexnari
|
|
What is the most common species of shigella found in homosexual men?
|
shigella flexnari
|
|
What is the most virulent species of shigella?
|
shigella dysenteriae
|
|
In general, what is the name of the disease caused by shigella species?
|
bacterial dysentary
|
|
What is the mechanism of shigella infection?
|
entry through M-cells -> uptake by macrophages -> lyse macrophages -> invade basal side of enterocytes -> spread directly into neighboring cells
|
|
What species of shigella causes the most mild symptoms?
|
shigella sonnei
|
|
true or false: humans are the only resevoir for shigella; they can't live anywhere else
|
True! Lucky us!
|
|
How is shigells spread between people?
|
the 4 F's: food, fingers, feces, flies
|
|
What are the symptoms of dysentary?
|
fever, malaise, vomiting, early watery diarrhea followed by frequent small bloody/mucusy stools, cramps
|
|
How do you treat dystentary caused by shigella?
|
rehydration, support, antibiotics for severe cases
|
|
Which bacteria is the second-most common cause of gastroenteritis?
|
salmonella
|
|
Which bacteris is the most common cause of gastroenteritis?
|
campylobacter
|
|
How does salmonella spread between people?
|
fecal-oral, and zoonitic through poultry, eggs, contaminated veggies
|
|
What is unique about salmonella typhi compared to other salmonellas?
|
salmonella typhi is more adapted to humans as its host
|
|
Which cells in the GI tract do salmonella bugs initially invade?
|
M cells AND enterocytes both
|
|
How long after infection with shigella would you experience symptoms?
|
1 to 4 days
|
|
How long after infection with salmonella would you experience symptoms?
|
24-48 hours
|
|
What are the 3 different infections that salmonella can cause?
|
gastroenteritis, septicemia, and Typhoid fever
|
|
What are the symptoms of salmonella-caused gastroenteritis?
|
fever, nausea, headache, cramps, watery diarrhea
|
|
How do you treat gastroenteritis caused by salmonella?
|
It is self-limiting, antibiotics are not needed
|
|
What are the symptoms of salmonella-caused septicemia?
|
fever, no diarrhea, positive blood cultures.
|
|
How do you treat salmonella-caused septicemia?
|
antibiotics
|
|
What are the symptoms of Typhoid Fever?
|
inflammatory diarrhea, fever
|
|
What is the most severe sequela of Typhoid Fever?
|
colonize the gall bladder, intestinal perforation
|
|
How do you treat Typhoid fever?
|
Antibiotics. I'm not sure which ones.
|
|
Why is it that you can have multiple infections of salmonella?
|
There are over 2500 different serotypes of salmonella
|
|
What are the symptoms of Yersinia gastroenteritis?
|
invasive, fever, watery diarrhea with blood and leukocytes
|
|
What is the most common way of ingesting Yersinia?
|
with undercooked pork or contaminated dairy products
|
|
What is one unique sequela of Yersinia enteritis?
|
can lead to reactive arthritis (Reiter's Syndrome)
|
|
In what patients can Yersinia lead to reactive arthritis?
|
Those with HLA-B27 can develop Reiter's Syndrome
|
|
What are some symptoms of Campylobacter enteritis?
|
diarrhea, fever, cramps. Half of patients have bloody stools, some have leukocytes
|
|
What are 2 unique sequela of campylobacter enteritis?
|
Reiter's Syndrome, and Gullian Barre Syndrome (nerve demyelination)
|
|
What three factors determine the virulency of campylobacter?
|
invasiveness, enterotoxin production, and cytotoxin production
|
|
Where in the GI does campylobacter set up shop?
|
terminal ileum and proximal colon
|
|
How is campylobacter transmitted?
|
contaminated dairy or water, raw poultry, pets with diarrhea
|
|
How common is person-to-person transmission of campylobacter?
|
Rare rare rare. Doesn't happen much.
|
|
What demographics are affected most often by campylobacter?
|
young infants, and young adult males
|
|
How do you treat campylobacter?
|
antibiotics: erythromycin or fluoroquinolones
|
|
what is the most common bacterial human pathogen?
|
helicobacter
|
|
Where does helicobacter set up shop in the GI tract?
|
stomach, and nowhere else
|
|
Is helicobacter invasive or toxigenic?
|
toxigenic. Does not invade tissues.
|
|
What factors increase the virulency of helicobacter?
|
urease activity, pathogenicity islands in the genome
|
|
What factors contribute to helicobacter prevalence in a population?
|
overcrowding, lower income status, individual genetics. Infections are rarer in more industrialized areas
|
|
How do you diagnose helicobacter infection?
|
urease test on biopsy specimens, breath urease test, histological examination, ELISA
|
|
What percentage of peptic ulcers are caused by helicobacter?
|
70%
|
|
What percent of duodenal ulcers are caused by helicobacter?
|
all of them
|
|
What is the treatment for helicobacter?
|
proton-pump-inhibitor plus bismuth plus tetracycline
|
|
What special requirement do Neiserria species require to be grown in culture?
|
5% carbon dioxide
|
|
What are the 5 surface characteristics that Neiserria possess that contribute to their toxicity?
|
1) Pili
2) OPA proteins 3) Porins 4) Lip-oligo-saccharide 5) IgA protease |
|
In the world of bacteria, what is "phase variation"?
|
The ability to switch off gene expression in order to avoid exposing antigen to our immune systems
|
|
How do pili help N. gonorrhoea cause disease?
|
Help it adhere to mucosa
|
|
How do pili NOT help N. gonorrhoea cause disease?
|
They are antigenic, and so are potential targets for antibody
|
|
How do OPA proteins help N. gonnorrhoea bacteria infect people?
|
They can help with adhesion at specific sites in our body
|
|
Are OPA proteins found in N. gonorrhoea bugs antigenic?
|
Yes they are, and there are hundreds of different serotypes
|
|
N. gonorrhoea bugs have LOS on their surface. What is LOS?
|
Lipo-Oligo-Saccharaide. Similar to LPS, but doesn't contain the O antigen repeats.
|
|
Which surface factor in N gonorrhoea is responsible for the inflammatory process seen in the disease?
|
LOS
|
|
How does N gonorrhoea use IgA protease to infect humans?
|
IgA protease cleaves the Fc portion of IgA, allowing the bug to adhere to mucosa without interference
|
|
What percentage of men will be infected with N. gonorrhoea after one exposure?
|
20-30%
|
|
Are men or women more likely to be asymptomatic carriers of N gonorrhoea?
|
Women are more likely to be asymptomatic carriers of N Gonorrhoae
|
|
What is Opthalmia neonatorum?
|
when mothers with N Gonorrhoea infect the eyeballs of their infants as they give birth to them
|
|
What is the most common cause of N-Gonorrhoea infection in pre-adolescent children?
|
sexual abuse
|
|
How many new cases of gonorrhea arise every year?
|
600,000
|
|
What are some symptoms of local gonorrhea seen only in women?
|
cervicitis, abscesses in vaginal glands, endometriosis, PID,
|
|
What are some symptoms of local gonorrhea seen only in men?
|
Epididymitis
|
|
What are some symptoms of local gonorrhea seen in both men and women?
|
urethritis, proctitis, pharyngitis, peritonitis, ophthalmia neonatorum in infants
|
|
What are some symptoms of systemic (disseminated) gonococcal infections?
|
Dermatitis-arthritis-tenosynovitis syndrome, septic arthritis, endocarditis, meningitis
|
|
PID is more likely to occur in women with what form of N. gonorrhoae infection?
|
recent asymptomatic gonorrhea is more likely to lead to PID
|
|
Histologically, how do you diagnose an infection of N. gonorrhoea?
|
gram stain the urethral/vaginal exudate, look for neutrophils with diplococci inside them
|
|
Which type of agar should N. gonorrhoea be cultured on?
|
chocolate agar or Thayer-Martin agar
|
|
How can you distinguish N gonorrhoea from N meningitidis in the lab?
|
gonorrhoae is oxidase +, ferments only glucose.
meningititis is oxidase +, fermants glucose AND maltose |
|
What recently developed N. gonorrhoeae detection method is 25-40% more sensitive than culture?
|
NAAT (nucleic acid amplitude test)
|
|
What are some advantages that NAAT testing has over culture, as far as N. gonorrhoea is concerned?
|
less invasive, can take samples from additional areas, 25-40% more sensitive, can be self-administered
|
|
What other STD is commonly seen alongside gonorrhea?
|
chlamydia tachomatis
|
|
What 2 antibiotics are good agents against gonorrhea infections?
|
doxycycline and azithromycin
|
|
What antibiotics should you not use against gonorrhea, because of resistance?
|
quinolones
|
|
How do you treat opthalmia neonatorum?
|
silver nitrate drops in the eyes soon after birth
|
|
4 ways Spirochetes differ from other bacteria:
|
1) corkscrew shape
2) gram (-), but no LPS 3) thin, hard to see 4) end flagella wind around the body of the cell |
|
What disease does Treponema Pallidum cause?
|
syphilis
|
|
What disease does T. pallidum pertenue cause?
|
Yaws
|
|
What disease does T. pallidum endemicum cause?
|
Bejel
|
|
What disease does T. pallidum carateum cause?
|
Pinta
|
|
How long does it take between initial infection and appearance of primary syphilis?
|
3 weeks
|
|
How long does the primary stage of syphilis last?
|
2-6 weeks
|
|
How long can the asymptomatic phase last between primary and secondary syphilis?
|
2-24 weeks
|
|
How long does the secondary stage of syphilis last?
|
2-6 weeks
|
|
How long can the latent phase of syphilis last between secondary syphilis and tertiary syphilis?
|
3 to 30 years
|
|
What outward sign characterizes primary syphilis?
|
chancre
|
|
How many patients can successfully clear syphilis from their system all on their own?
|
25%
|
|
What outward signs characterizes secondary syphilis?
|
maculopapular rash on palms and soles of feet, lymphadenopathy, and possible hair loss.
|
|
What is the transmissability of syphilis during its various stages of development?
|
1 - very transmissible
2 - very transmissible latent - not transmissible 3 - somewhat transmissible |
|
What are some neurological symptoms of tertiary syphilis?
|
tabes dorsalis, paralysis, insanity
|
|
What are some cardiovascular symptoms of tertiary syphilis?
|
heart failure, aortic aneurysms
|
|
How can syphilis affect pregnant women?
|
It causes the fetus to abort at 20 weeks gestation
|
|
What special microscope technique is used to visualize treponema pallidum?
|
darkfield
|
|
What symptoms make up the Jarish-Herxheimer Reaction?
|
fever, headache, joint pain
|
|
What disease context is the Jarish-Herxheimer Reaction seen in, and what causes it?
|
Penicillin lyses syphilis bugs, which releases irritating chemicals into circulation
|
|
What is the difference between the 2 types of serological tests used to find syphilis infections?
|
One detects actual antigen against treponema, the other uses cross-reacting antigen than actually reacts with reagin
|
|
True or false: trepomena pallidum can survive for a long time outside the human body.
|
False! They usually can't live for more than 24 hours outside your body
|
|
What antibiotic is useful against syphilis?
|
penicillin
|
|
Yaws is related to syphilis; how is it different?
|
non-venereal, ulcers on arms and legs, affects children in tropical regions
|
|
Bejel is related to syphilis; how is it different?
|
non-venereal, ulcers on arms and legs, affects children in desert regions
|
|
Pinta is related to syphilis; how is it different?
|
non-venereal, papules that progress to dark, hyperkeratotic lesions. Found in latin america
|
|
What activities commonly cause syphilis outbreaks?
|
IV drug use and prostitution
|
|
Leptospira is a gram (-,+) bacteria, shaped like a (rod/cocci/spirochete)
|
leptospira is a gram negative spirochete
|
|
Leptospirosis symptoms include:
|
fever; liver and kidney necrosis leading to jaundice, hemorrhage, and nitrogen retention; aseptic meningitis
|
|
How long can leptospira remain infectious outside the body of an animal?
|
several weeks
|
|
how long does it take a person to develop symptoms after being infected with leptospira?
|
1-2 weeks
|
|
How do humans catch leptospirosis?
|
from water or food contaminated with the urine of infected animals
|
|
What antibiotics treat the symptoms of leptospirosis, but do not eradicate the infection?
|
penicillin and tetracycline
|
|
What antibiotics are used prophylactically against leptospirosis?
|
doxycycline
|
|
What's wierd about the cell wall of chlamydia?
|
the peptidoglycan does not contain N-acetylmuramic acid
|
|
How do lab techs culture chlamydia samples?
|
In egg yolks or in tissue cultures
|
|
What can be added to tissue culture to allow chlamydia more nutrients?
|
radiation or cyclohexamide, to slow down eukaryotic metabolism
|
|
Chlamydia are dependant on host cells _________ and _______ for energy because they can't re-synthesize their own.
|
ATP and NADPH
|
|
What stain is used to visualize chlamydia inclusions in cells?
|
giemsa stain
|
|
What do chlamydia look like in a giemsa stain?
|
You can see inclusions near the nucleus
|
|
Chlamydia have a biphasic lifestyle. The two phases are called......?
|
elementary bodies (EB) and
reticulate bodies (RB) |
|
Which phase of chlamydia's life cycle is the transmissable, infectious phase?
|
The EB phase is what host cells pick up, and also what is released from the lysed host cell
|
|
Which phase of chlamyida's life cycle is metabolically active?
|
The RB phase is when chlamydia multiplies within host cell vacuoles
|
|
Which is bigger, elementary bodies or reticulate bodies?
|
reticular bodies are 1 micron, elementary bodies are 0.3 microns
|
|
How long do RBs multiply within a cell before lysing the cell, releasing many EB's?
|
24-72 hours
|
|
What are the 3 common disease-causing species of chlamydia?
|
c. trachomatis
c. psittaci c. pneumoniae |
|
How is chlamydia trachomatis transmitted?
|
direct person-to-person contact
|
|
How is chlamydia psittacis transmitted?
|
bird-to-person transmission, through inhaled dust or water droplets
|
|
How is chlamydia pneumoniae transmitted?
|
person to person through aerosol particles
|
|
What sequelae does chlamydia infection cause through antigenic mimicry?
|
arthritis and atherosclerosis
|
|
What is trachoma, and what bug causes it?
|
chlamydia trachomatis causes inflammed corneas and conjunctiva, leading to scarring and blindness
|
|
What is the incubation period for trachoma?
|
3-10 days
|
|
What is the main cause of blindness worldwide?
|
trachoma
|
|
how does one usually aquire trachoma?
|
you get it in infancy from your mom
|
|
How do you treat trachoma?
|
surgery, antibiotics, facial cleanliness
|
|
What are the symptoms of urogenital infections with chlamydia?
|
urethritis, dysuria, cervicitis, PID, pus discharge from urethra
|
|
Both gonorrhea and chlamydia produce urethral pus. On that basis, how do you distinguish between the two?
|
gonorrhea=bacteria in neutrophils
chalmydia=nothing in neutrophils |
|
What percentage of STD chlamydia infections are asymptomatic?
|
in men = 50%
in women = 75% |
|
Women with chlamydia have an increased risk for contracting HIV, by how much?
|
women with chlamydia are 3-5 times more likely to contract HIV, if exposed
|
|
What are some sequelae of PID?
|
scarred fallopian tubes, infertility, ectopic pregnancy, chronic pelvic pain
|
|
If a bunch of adolescent girls get tested for chlamydia, how many will be infected?
|
10%
|
|
How many cases of chlamydia are reported every year in the united states?
|
3 million
|
|
NAAT tests for chlamydia have what sensitivity and specificity?
|
sensitivity = 90%
specificity = 99% |
|
What antibiotics do you use to treat chlamydia infections?
|
azithromycin or doxycyclin
|
|
If a person has HIV and chlamydia, how should you alter your treatment of the chlamydia?
|
Don't alter it, treat it just like any other chlamydia: azithromycin or doxycyclin
|
|
What bug causes Lymphogranulomatous Venereum?
|
chlamydia trachomatis
|
|
What are the symptoms of Lymphogranulomatous Venereum?
|
small genital ulcer, followed by swollen, purulent inguinal lymph nodes that leak pus
|
|
What are some sequelae of Lymphogranulomatous Venereum?
|
disseminated bacteremia, peritonitis, colitis
|
|
What antibiotics would you use to treat Lymphogranulomatous Venereum?
|
sulfonamides and tetracycline
|
|
What bug causes psittacosis?
|
Uh, chlamydia psittaci, duh
|
|
what are some symptoms of psittacosis?
|
acute pulmonary infection, with fever, headache, malause, myalgia, unproductive cough
|
|
Psittacosis resembles what other diseases?
|
flu or typhoid fever
|
|
What is the incubation period for psittacosis?
|
10 days
|
|
What antibiotics work to kill of chlamydia psittaci?
|
tetracycline and erythromycin
|
|
Most cases of chlamydia pneumoniae have what kind of symptoms?
|
mild upper respiratory illness
|
|
chronic respiratory disease can result from chlamydia pneumoniae infection in people with what pre-existing conditions?
|
asthma, COPD, cystic fibrosis, lung cancer
|
|
What is the treatment for chlamydia pneumoniae infections?
|
tetracycline or erythromycin
|
|
Human Papilloma virus are how big? DNA or RNA? Enveloped or not?
|
50 nanometers wide, DNA, not enveloped.
|
|
What is the makeup of the protein capsule of HPV?
|
two proteins: L1 makes a pentamer, L2 links the pentamers together into an icosohedron
|
|
What percent of all cervical cancers are caused by HPV?
|
100%
|
|
What percent of all head and neck cancers are caused by HPV?
|
25%
|
|
HPV codes for E6 protein, which does what to the host cell?
|
inhibits p53
|
|
HPV codes for E7 protein, which does what in the host cell?
|
binds to Rb protein
|
|
What are the three well-known oncogenes within HPV?
|
E5, E6 and E7
|
|
Which cells does HPV infect?
|
basal epithelial cells, the ones that are most undifferentiated
|
|
Which cells release the manufactured HPV?
|
the outermost squamous epitheilial cells release HPV
|
|
What is the lifetime risk among sexually active men and women for contracting HPV?
|
50-70%
|
|
What is the prevalence of HPV infection in the Unites States?
|
20 million
|
|
What is the incidence of HPV infection in the United States?
|
6.2 million per year
|
|
How is HPV most commonly transmitted?
|
genital-genital, oral-genital, manual-genital sexual contact
|
|
What are two ways HPV can be transmitted, but not that often?
|
mother to infant during birth, and through fomites
|
|
What HPV serotypes commonly cause cutaneous warts on hands and feet?
|
HPV 1,2,4, and 7
|
|
What serotype of HPV commonly causes genital warts?
|
HPV 6 and 11
|
|
What serotype of HPV commonly causes warts on the larynx or pharynx?
|
HPV 6 and 11
|
|
What serotype of HPV commonly causes squamous cell carcinoma?
|
HPV 16, 18, 21, 33, and 45
|
|
50% of all squamous cell carcinomas are caused by which serotype of HPV?
|
HPV 16
|
|
20% of all squamous cell carcinomas are caused by which serotype of HPV?
|
HPV 18
|
|
What zone of the cervix gives rise to squamous cell carcinoma?
|
The transitional zone between the columnar epithelium of the uterus and the squamous epithelium of the vagina
|
|
What is the survival rate for head and neck cancers?
|
50%
|
|
What cancers besides cervical and head/neck are commonly caused by HPV?
|
vulva, penis, anus
|
|
WHO divides cervical cancer into 5 stages. From most normal to most malignant, they are:
|
condyloma -> CIN1 (mild dysplasia) -> CIN2 (moderate dysplasia) -> CIN3 (severe dysplasia) -> invasive cancer
|
|
The Bethesda system divides cervical cancer into 4 stages. From mild to malignant, they are:
|
ASC -> LSIL -> HSIL -> Invasive cancer
|
|
LSIL in the bethesda system corresponds to what in the WHO system, regarding cervical cancer?
|
LSIL = CIN1
|
|
HSIL in the bethesday system corresponds to what in the WHO system, regarding cervical cancer?
|
HSIL = CIN2 and CIN3
|
|
What diagnostic test detects cervical cancer changes?
|
the pap smear
|
|
What is the next step if the pap smear shows abnormal cells?
|
colposcopy
|
|
What is the current treatment for cervical cancer?
|
cryosurgery or loop electrosurgical excision, or creams like imiquimod or podofilox
|
|
Gardasil vaccine works against which serotypes of HPV?
|
HPV 6,11,16,18
|
|
Cervarix vaccine works against which serotypes of HPV?
|
HPV 16,18
|
|
What protein are HPV vaccines made out of?
|
L1 capsule protein
|
|
What are some limitations of the HPV vaccine?
|
high cost, doesn't treat existing infections, does not protect against genotypes causing 30% of cancers
|
|
What year was AIDS first described by the CDC?
|
1981
|
|
What year was HIV isolated by the CDC?
|
1984
|
|
When did HIV first jump into humans, and where did it jump from?
|
HIV jumped from chimpanzees around 1900
|
|
Where did HIV first appear in humans?
|
Central West Africa, Cameroon-ish
|
|
About how many people live with AIDS worldwide?
|
33.2 million
|
|
In colorado, which ethnic group has the most HIV infections?
|
white people
|
|
How does primary HIV infection present itself?
|
fever, aseptic meningitis, mononucleosis-like symptoms
|
|
How long after infection with HIV do symptoms first appear?
|
2-3 weeks
|
|
What does an HIV-caused rash look like?
|
maculopapular rash on the trunk
|
|
What receptor does HIV use to enter host cells, and what kind of cells does HIV infect?
|
CD4 on helper T cells
|
|
How long does it take for a new generation of HIV particles to be built inside infected cells?
|
2.6 days
|
|
How long does a helper T cell live after being infected with HIV?
|
2.2 days
|
|
What are the two markers of HIV disease measured during treatment?
|
CD4+ cell count
plasma HIV RNA level |
|
How many HIV particles are made each day in an infected person?
|
10 to the 10th power. What would that be? 10,000,000,000, or ten billion
|
|
What factors contribute to the rapid pace of HIV evolution?
|
no proofreading during DNA duplication,
fast replication rate, selective pressure |
|
what does the word "quasispecies" mean in relation to HIV?
|
HIV in one person evolves into its own subspecies, which will be slightly different from someone else's HIV viruses
|
|
What are the 5 classes of drugs that we use to treat HIV infection?
|
Protease inhibitors, nucleoside RT inhibitors,
non-nucleotide RT inhibitors, entry inhibitors, integrase inhibitors |
|
What co-receptors does HIV use (along with CD4) to gain entry into cells?
|
CCR5 and CXCR4
|
|
How do entry-inhibitors work to supress HIV infection?
|
bind to CCR5 or CXCR4, so HIV can't use CD4 to get into T cells
|
|
People with mutated CCR5 receptors have what response to HIV?
|
They are HIV resistant, but still susceptable to HIV that uses CXCR4
|
|
heterozygotes for the CCR5 mutation have what response to HIV infection?
|
Their disease is longer, milder, and drawn out
|
|
What percent of people are homozygous for the CCR5 mutation?
|
about 1%
|
|
How do nucleoside RT inhibitors supress HIV infection?
|
nucleoside analogs get incorporated into viral genome by RT, gumming it up and causing termination
|
|
How do non-nucleoside RT inhibitors supress HIV infection?
|
non-competitively bind to RT and cause it to stop working
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What are some side effects of non-nucleoside RT inhibitors used to treat HIV infections?
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liver toxicity, rash, CNS effects
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How do Integrase Inhibitors supress HIV infection?
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They block HIV from becoming a provirus inside our own chromosome
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How do the protease inhibitors supress HIV infection?
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They prevent cleavage (and activation) of precursor proteins inside HIV; virus is still produced, but is ineffective
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Why is it so hard to cure HIV infections?
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Virus exists dormant as a provirus
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Do Herpesviruses have envelopes?
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Yes
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In what form do Herpesviruses keep their genome?
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in the form of double-stranded DNA
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In a Herpesvirus, what lies between the capsule and the envelope?
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The tegument
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In a herpesvirus, what does the tegument layer contain?
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viral and cellular proteins, RNA
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What 3 broad classes of genes are expressed by herpesviruses?
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Immediate Early (IE), Early (E), and Late (L)
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In a herpesvirus, what sorts of things do the IE genes usually code for?
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DNA binding proteins, proteins for immune evasion
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In a herpesvirus, what sorts of things do the E genes usually code for?
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nucleotide metabolism, genomic DNA replication
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In a herpesvirus, what sorts of things do the L genes usually code for?
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structural proteins for the capsule
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Where in the infected cell do newly-made herpesviruses mature?
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In the golgi
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Where in the infected cell is the herpesvirus's DNA replicated?
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In the nucleus
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How durable are herpesviruses when they are outside of the body?
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Herpesviruses are very fragile when they are not inside their host's body
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How are herpesviruses transmitted between hosts?
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close contact of mucous membranes, usually
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Herpesviruses like to exist in the latent form. What does this mean?
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Existing as a provirus in the genome of the host, expressing few or no proteins
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Herpesviruses can exist in either the lytic or latent phase. What does it mean if the virus is lytic?
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Lytic phase is when the virus immediately takes over the cell and kills it by making it make new copies of virus
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What binds the herpesvirus envelope to the host cell's membrane?
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glycoproteins
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When the herpesvirus envelope is merged with the host cell membrane, what is released into the cell?
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the capsule and the tegument
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Where does the herpesvirus capsule go once the virus enters the host cell?
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the capsule travels along microtubules to a nuclear pore
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Unlike E and L proteins, the IE proteins in the herpesvirus do not need......what?
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to be synthesized by the infected cell; the virus carries them with it in the tegument
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Name the 3 alpha herpesviruses.
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herpes simplex 1 and 2, and varicella-zoster
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What are some characteristics of alpha herpesviruses that set them apart from other herpesviruses?
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they are lytic in mucosa/skin cells, and are latent in nerve ganglia
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What are some characteristics of beta herpesviruses that set them apart from other herpesviruses?
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grow slowly, latent in myeloid and endothelial cells, can be transmitted through saliva, urine, and breastmilk
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Name the 3 beta herpesviruses
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Human cytomegalovirus (HCMV), HHV-6 and 7
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What are some characteristics of gamma herpesviruses that set them apart from other herpesviruses?
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lytic phase in epithelial cells, fibroblasts, lymphocytes. Latent phase in B-lymphocytes
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Name the 2 gamma herpesviruses.
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Epstein Barr virus (EBV) and Kaposi's Sarcoma Herpesvirus (KSHV)
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What is the host range of alpha herpesviruses, in general?
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broad
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What is the host range of gamma herpesviruses, in general?
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narrow
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What are the clinical manifestations of an HSV infection, in order?
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papule, vesicle, pustule
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HSV-1 and HSV-2 are responsible for infections, where?
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HSV-1 = the mouth
HSV-2 = the genitals |
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What is the name for the symptom of severe, painful oral and gum sores due to HSV-1 infection?
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herpetic gingivostomatitis
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Severe pharyngitis in an adolescent or adult is usually caused by one of these three things:
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HSV-1 infection
mononucleosis adenovirus |
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People with latent HSV-1 shed virus approximately how often?
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1 day out of 30, or 3-4% of the time
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What two demographic groups are most likely to be victims of HPV infection, and why?
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kids older than 6 months (maternal IgG protects until then)
adolescents (sexual contact) |
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How does the initial herpesvirus infection compare to recurrent infections?
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recurrent infections are much less serious and clear up faster, due to established immunity
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What are two complications of HSV-1 infection?
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herpetic keratitis, and herpes encephalitis
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What leads to herpetic keratitis, and what can it cause?
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HSV spreads to eyes via saliva on fingers. Normal lesions. Can lead to scarring and blindness
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What leads to herpes encephalitis, and what can it cause?
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HSV reactivation in the trigeminal ganglion can travel to the brain, causing brain necrosis and CNS injury
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How do you diagnose herpes encephalitis, and how do you treat it?
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test CSF for HSV DNA. Treat with IV acyclovir
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HSV-2 infections are more prevalent in these groups:
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the poor, African Americans, women
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What are some symptoms of the initial HSV-2 infection?
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urethritis, adenopathy, severe genital lesions, headache, fever, malaise
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What percent of initial HPV-2 infections are asymptomatic?
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70-80%
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What are some sequelae of HSV-2 infection?
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viral meningitis, severe local lesions
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How do you treat a patient with HPV-2 infection?
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give acyclovir during the prodrome before the actual outbreak
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A person with a prior HSV-1 infection will have (more/less) severe symptoms when they contract HSV-2?
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Their symptoms will be less severe, because they already have partial immunity to herpes simplex
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HSV infection in neonates is best described as?
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fatal. or if not fatal, than severely crippling.
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What is the cheapest test used to detect HSV?
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Immunoassay using fluorescent antibodies
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What is the most expensive test used to detect HSV?
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PCR to detect the DNA
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first time nfection with CMV is likely to be most severe at what age?
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adulthood. In babies, children, and adolescents, it is usually asymptomatic
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CMV infection in adults manifests these symptoms:
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sore throat, adenopathy, fever, malaise, liver involvement
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How can you distinguish mononucleosis caused by CMV from that caused by EBV?
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CMV mono will have no heterophil antibodies in the blood, but EBV mono will.
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What is the most common way to diagnose CMV infection?
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virus culture with spin amplification
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CMV infections are most often seen in what type of patients?
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Those who are immune compromised (AIDS, transplant, on steroids, etc)
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What is the most common manifestation of CMV infection in immune compromised patients?
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interstitial pneumonia, 50% fatal
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What drug is used to treat CMV?
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ganciclovir or foscarnet
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What drug does not work at all in treating CMV?
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acyclovir
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Most babies with CMV infections are asymptomatic, except for those who.....?
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Are a fetus while the mother gets her first exposure to CMV
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Babies born to 1st-time infected mothers suffer from:
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hepatitis, bone marrow suppression, seizures, underdeveloped head/ears/eyes
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Babies born to mothers who have a recurrent CMV infection during the pregancy will suffer from.....?
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nothing, at first. But they might become deaf later in childhood.
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How does a person catch VZV?
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Through water droplets in the air carrying the virus
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How long does it take to develop symptoms after being infected with VZV?
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14-17 days
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What are the symptoms of first-time VZV infection?
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"dewdrops on a rosebud" lesions (papule, vesicle, pustule, scab on a reddish base), fever
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Immunocompromised patients with VZV can expect to experience:
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pneumonitis, hepatits, encephalitis
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How do you treat VZV infection in immune compromized patients?
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acyclovir
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VZV vaccine is____% effective, and only ___% of kids develop a very mild form of the disease after vaccination
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95% effective, 15% of kids have a mini-disease reaction
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Initial VZV infection is called _______. Re-activated VZV infection is called ________.
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chickenpox = initial disease. Shingles = reactivated disease
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How do you diagnose chickenpox?
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clinical diagnosis, but you can do culture and spin amplification if you want to, or PCR older crusty lesions.
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How do you diagnose Shingles?
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vesicles/pustules in a single dermatome that does not cross the midline
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What is the most long-lasting sequala of shingles?
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post-herpetic neuralgia, which is persisting pain in the affected area long after the lesions are gone
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What 2 things can spur a reactivation of VZV?
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being immunocompromised, and growing older
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Which of your body's natural processes is protective in keeping herpesvirus infections latent?
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antibody production, T-cell activity
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HHV-6 causes an infection called.....?
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Roseola
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Roseola presents in what population, with what symptoms?
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children. presents with high fever and rash, and can cause seizures.
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