Term
|
Definition
| Streptococcus and staphylococcus. Streptococcus is catalase negative (aerotolerant), while staphylococcus is catalase positive (facultative anaerobe) |
|
|
Term
|
Definition
| 1. Bacillus (catalase +; spore +) 2. Clostridium (catalase +; spore +) 3. Corynebacterium (catalase +; spore -) 4. Listeria (catalase +; spore -) 5. Lactobacillus (catalase -) 6. Mycobacterium (kind of- acid-fast) |
|
|
Term
| How do you differentiate between streptococcus and staphylococcus? |
|
Definition
| Streptococcus is catalase negative (aerotolerant) while staphylococcus is catalase positive (facultative anaerobe). Also, streptococci forms chains while staphylococci form clusters |
|
|
Term
| Gram positive cocci that is catalase negative |
|
Definition
|
|
Term
| Gram positive cocci that is catalase positive |
|
Definition
|
|
Term
| How do you differentiate btw the different types of streptococcus? |
|
Definition
| All are catalase negative. Beta hemolysis= S.pyrogenes and s. agalactiae Alpha= S. pneumoniae and viridens Gamma=enterococci |
|
|
Term
| Gram positive cocci that is catalase negative with beta hemolysis (2) |
|
Definition
| 1. Strep pyrogenes/Grp A 2. Strep agalactiae/Grp B |
|
|
Term
| Gram positive cocci that is catalase negative with alpha hemolysis (2) |
|
Definition
| 1. S. pneumoniae 2. Strep viridens |
|
|
Term
| Gram positive cocci that is catalase negative and gamma hemolysis |
|
Definition
|
|
Term
| How do you differentiate btw the different types of staphylococcus? |
|
Definition
| All are gram positive cocci that are catalase positive (facultative anaerobes). Staph aureus is coagulase positive, which the others are coagulase negative (staph saprophyticus and staph epidermidis) |
|
|
Term
| Gram positive cocci, positive catalase test and positive coagulase |
|
Definition
|
|
Term
| Gram positive cocci, catalase positive, coagulase negative (2) |
|
Definition
| 1. Staphylococcus saprophyticus 2. Staphylococcus epidermidis |
|
|
Term
| Gram positive rod with positive catalase (4) |
|
Definition
| Bacillis, corynebacterium, listeria, mycobacterium. All except for mycobacterium (obligate aerobe) are facultative anaerobes. Bacillus and mycobacterium make spores |
|
|
Term
| Gram positive with negative catalase (2) |
|
Definition
| Clostridium and lactobacillus **Both also make spores |
|
|
Term
| Gram positive rod with positive catalase and positive spores (2) |
|
Definition
| Bacillis and mycobacterium |
|
|
Term
| Gram positive rods with negative catalase that makes spores (2) |
|
Definition
| Clostridium and Lactobacillus |
|
|
Term
| Gram positive rod with positive catalase that does not make spores (2) |
|
Definition
| 1. Corynebacterium 2. Listeria |
|
|
Term
|
Definition
| Streptococcus pyogenes. B-hemolysis (like Brp B/agalactiae). |
|
|
Term
|
Definition
| Streptococcus agalactiae. B-hemolysis (like Grp A/pyogens) |
|
|
Term
|
Definition
| Superficial infections: Strep throat and impetigo. Invasive disease: Scarlet fever, pneumonia, necrotizing fascitis Sequela Diseases: rheumatic rever and acute glomerulonephritis |
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|
Term
| Strep Pyogenes Virulence Factors |
|
Definition
| 1. Spreading enzymes (streptokinase and hyaluronidase) 2. M protein (acts as a superantigen and is anti-phagocytic; interfering w/the complement componenet C3b) 3. Hyaluronic acid capsule (anti-phagocytic) 4. Toxins (Streptolysin S/O, Erythrogenic toxin, Exotoxin A, Exotoxin B) |
|
|
Term
|
Definition
| One of it's virulence factors. Pili-like structure that adheres to the host cell. Acts as a superantigen (elicits a strong immune reaction in host->disease). Anti-phagocytic (interferes w/complement componenet C3b |
|
|
Term
|
Definition
| In strep pyogenes; hemolysins that are responsible for strep throat. S is oxygen-stable, and is responsible for the degradation of RBCs and leukocytes in the presence of oxygen (blood agar plates and strep). Streptolysin O is oxygen-labile hemolysin, which binds to cholesterol and is toxic to the heart and other tissues |
|
|
Term
|
Definition
| In S. pyogenes, one of the toxins it produces. Oxygen-stable hemolysin; responsible for blood agar rxn and strep throat. Toxic to tissue, leukocytes, and RBCs |
|
|
Term
|
Definition
| In Strep Pyogenes. Oxygen sensitive/labile hemolysin that binds cholesterol and is toxic to the heart and other tissues |
|
|
Term
|
Definition
| In s. pyogenes. Encoded on lysogenic bacteriophage. A superantigen. Responsible for scarlet fever rash |
|
|
Term
|
Definition
| In strep pyogenes. Causes streptococcal TSS. Superantigen. Works by the same mechanism as staphylococcal TSS. |
|
|
Term
|
Definition
| In strep pyogenes. Causes necrotizing fascitis. 30% mortality |
|
|
Term
| Virulence factors responsible for strep throat |
|
Definition
| Streptolysin S and O (hemolysins that destroy cells) in s. pyogenes |
|
|
Term
| Virulence factors responsible for scarlet fever rash |
|
Definition
| Erythrogenic toxin in s. pyogenes. This is encoded on a lysogenic bacteriophage (mobile genetic toxin; moves cell to cell). Is a superantigen |
|
|
Term
| Virulence factor responsible for Streptococcal TSS |
|
Definition
| Exotoxin A in strep pyogenes. This is a superantigen and works by the same mechanism as staphylococcal TSST |
|
|
Term
| Toxin responsible for necrotizing fascitis |
|
Definition
| Exotoxin B in strep pyogenes. |
|
|
Term
| Poststreptococcal sequela diseases |
|
Definition
| After an acute reaction, there can be an immunological reaction against an M-protein on s. pyrogenes. Occurs after initial infection, usually as a result of untreated infections. Host cells make Abs against M-antigen left over after insufficient treatment. Abs recognize host cells, too, like heart muscle (rheumatic fever) or glomeruli (acute glomerulonephritis). |
|
|
Term
|
Definition
| Poststreptococcal sequela disease (following strep pyogenes infection). Antibodies against certain M proteins on strep pyogenes cross-react w/myosin protein in the heart, causing heart valve damage |
|
|
Term
|
Definition
| Poststreptococcal sequela disease following strep pyogenesinfection. M protein-49 antigen-antibody complexes lodge in glomeruli of kidney |
|
|
Term
| Leading cause of meningitis in adults |
|
Definition
| Streptococcus pneumoniae (pneumococci) |
|
|
Term
| How do you distinguish between strep pneumoniae and strep viridans? |
|
Definition
| Both are gram positive "cocci," negative catalase and alpha hemolytic. Neither has an antigen on it's surface. But S. pneumoniae forms diplococci (pairs or short chains of cells), while strep viridans forms cocci in chains |
|
|
Term
| Drug of choice for strep pyogenes? |
|
Definition
| Penicillin. Little antibiotic resistance |
|
|
Term
| Is strep pyogenes a normal inhabitant of the body? |
|
Definition
|
|
Term
| Is streptococcus pneumonia/pneumococci a normal inhabitant of the body? |
|
Definition
| Yes; normal inhabitant of the upper respiratory tract. |
|
|
Term
| Virulence for strep pneumoniae (3) |
|
Definition
| 1. Capsule (only encapsulated strains are virulent) 2. Secretory IgA protease (destroys IgA antibodies) 3. Pneumolysin (cytolytic toxic that suppresses phagocytosis by interfering w/lysosomes, activates complement) |
|
|
Term
|
Definition
| Destroys IgA antibodies. Virulence factor in Streptococcus pneumoniae |
|
|
Term
|
Definition
| Virulence factor produced by streptococcus pneumoniae. Suppresses phagocytosis by interfering w/lysosomes. Cytolytic toxin- makes pores in the cell membrane. Activates complement |
|
|
Term
|
Definition
| Group B strep. Beta hemolysis, like strep pyogenes. Frequently colonizes the colon and female GU tract. Uncommon cause of invasive disease in adults, but the most common cause of invasive bacterial disease in newborns (neonatal sepsis and meningitis). Normal gut flora |
|
|
Term
| Is strep agalactiae normal gut flora? |
|
Definition
| Yes. Frequently colonizes the colon and female UG tract |
|
|
Term
| Most common cause of invasive disease in infants |
|
Definition
| Streptococcus agalactiae/Group B strep. Causes neonatal sepsis and meningitis |
|
|
Term
|
Definition
| Penicillin or ampicillin is drug of choice |
|
|
Term
|
Definition
| Same thing as strep viridans. Alpha-hemolytic (like strep pneumoniae), but unlike strep pneumoniae, it forms long chains of cocci. Neither have an antigen on its surface |
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|
Term
|
Definition
| Gram positive cocci without a surface antigen that grows in long chains. Alpha hemolysis. Another name for it is S. mutans. Normal inhabitant on the skin. Rarely causes invasive disease- oral flora and dental plaque. Can cause endocarditis. Live in mouth, and is a problem if they enter the blood stream. Tx: Penicillin |
|
|
Term
|
Definition
|
|
Term
| Is strep viridans part of normal flora? |
|
Definition
| Yes. Oral flora, dental plaque. Rarely causes invasive disease, but will if they enter blood stream->endocarditis. Tx with penicillin |
|
|
Term
|
Definition
| Gamma hemolysis. Gram positive cocci, but not a streptococci. Normal inhabitant of the gut, and a rare cause of invasive disease in healthy ppl (sometimes a UTI). Usually a nosocomial pathogen, causing an UTI that may lead to endocarditis. Virulence: few classical virulence factors. Highly resistant to antibiotics. Ampicillin use to be drug of choice, but there is more resistance for this now. Also, ampicillin is just static for enterococcus, and this bacteria is hard to clear from the body. If you add aminoglycoside/gentomycin, this will do the trick! (if the strain is not resistant- highly resistant!!). May also use vancomycin and linezolid |
|
|
Term
|
Definition
| Usually a nosocomial pathogen, causing an UTI that may lead to endocarditis. Highly resistant to antibiotics. Ampicillin use to be drug of choice, but there is more resistance for this now. Also, ampicillin is just static for enterococcus, and this bacteria is hard to clear from the body. If you add aminoglycoside/gentomycin, this will do the trick! (if the strain is not resistant- highly resistant!!). May also use vancomycin and linezolid |
|
|
Term
| Is enterococcus a normal flora? |
|
Definition
| Yes. Normal inhabitant of the gut. Rarely causes invasive diseases in healthy ppl, but it is a common nosocomial infection (ppl are given a ton of antibiotics, which allows enterococcus, a highly resistant bacteria, to overgrow). Nosocomial UTIs can develop and may lead to endocarditis |
|
|
Term
| Tx for MRSA in chromosomal mediated resistance in nosocomial pts |
|
Definition
|
|
Term
| Tx for MRSA in community acquired, chromosomally mediated resistance |
|
Definition
| TMP-SMX, Clindamycin, Vancomycin, Linezolid, Doxycycline |
|
|
Term
| Tx for plasmid-mediated resistance in MRSA |
|
Definition
1. Plasmid mediated resistance (acquires a gene that produces B-lactamase)
a. Inactivate the B-lactamase by adding a B-lactamase inhibitor to penicillin (Ampicillin/Clavulanate=Augmenten)
b. Use a penicillin drug that protects the B-lactam ring (Nafcillin has a chain that physically protects the B-lactam ring)
c. Use a drug not cleaved by B-lactamase (Cephalosporin like Cefazolin or a macrolide like erythromycin, which doesn’t have a B-lactam ring) |
|
|
Term
| Staph aureus is the most common cause of what? (6) |
|
Definition
| **Think skin/bone/joint diseases and food poisoning. Impetigo, Cellulitis, Osteomyelitis, septic arthritis, acute endocarditis. |
|
|
Term
| Is staph aureus a normal flora? |
|
Definition
|
|
Term
| Is staph epidermidis a normal flora? |
|
Definition
|
|
Term
| Virulence factors in S. aureus (11) |
|
Definition
| Hyaluronidase and collagenase, coagulase, leukocidins, staphylokinase, lipase, B-lactamase, polysaccharide slime layer, protein A, cytolytic toxins (food poisoning), exfoliative toxin (skin peels off), TSST |
|
|
Term
| Skin/bone/joint infections |
|
Definition
| Staphylococcus aureus or B-hemolytic streptococci (Grp A/Strep pyogenes). To cover both, tx with a penicillinase resistant drug- cefazolin or nafcillin |
|
|
Term
|
Definition
| Coagulase negative and novobiocin sensitive. Associated with infections of catheters and implants. Much less likely to cause disease than S. aureus. Endocarditis, infections of catheters and implants when normal flora of the skin moves into the body. Not a great pathogen bc not many virulence factors and no toxins. No B-lactamase |
|
|
Term
| Virulence factors of staph epidermidis (3) |
|
Definition
| Not many- not a great pathogen. 1. Hyaluronidase and collagenase 2. Lipase 3. Polysaccharide slime layer |
|
|
Term
| Staphylococcus saprophyticus |
|
Definition
| Second leading cause of UTIs. Coagulase negative. Much less likely to cause disease than S. Aureus (only virulence factor is hyaluronidase and collagenase). Novobiocin resistant. |
|
|
Term
| Who does listeria effect? |
|
Definition
| Immunocompromised patients: HIV, newborns, transplant patients |
|
|
Term
| How does listeria enter the body? |
|
Definition
| Contaminated food or water. Intracellular facultative anaerobe (catalase positive; no endospores) |
|
|
Term
| What does listeria cause? |
|
Definition
| Sepsis, meningitis, and GI issues in newborns and immunocompromised individuals (with HIV or transplant pts). This is bc cell-mediated immunity in immune-competent adults detect the presence of listeria in neutrophils and macrophages and destroys them. |
|
|
Term
|
Definition
| Virulence factor in listeria. Class of hemolysin. Breaks down phagosome before lysosome can fuse with it. allows listeria to live inside cells where the immune system can't see it (in immunocompromised and neonates; healthy immune systems can detect it and these ppl won't get sick). |
|
|
Term
|
Definition
| Listeriolysin O breaks down phagosome before fusion with lysosome, so that it can live inside cells where the immune system of immunocompromised/neonates cannot see it. It also uses host's actin network to move from cell to cell, evading the host immune system (takes actin from phagocytes, and the actin tail propels listeria from cell to cell) |
|
|
Term
|
Definition
|
|
Term
| Virulence factors of the clostridium spp (5) |
|
Definition
| Endospores, multiple exotoxins, collagenase, protease, hyaluronidase |
|
|
Term
|
Definition
| Clostridium tetani spores are commonly found in soil and animal feces, and when deposited into a wound, they germinate when there is an anaerobic environment (necrotic tissue). From there, Clostridium tetani releases its exotoxin, tetanospasmin. This prevents the release of inhibitory neurotransmitters, causing spastic paralysis. (inhibits exocytosis of inhibitory neurotransmitters) |
|
|
Term
|
Definition
| Spores float in the air and can land on food. If the food is not cooked sufficiently, and then is placed in an anaerobic environment (like cans), the clostridium botulinum spores germinate and synthesize the neurotoxin. The toxin blocks release of activating NT acetylcholine, and inhibits components of exocytosis of Ach (VASP, SNAPS). Muscles can't contract->flaccid paralysis. Most potent natural toxin |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Severe diarrhea. Pseudomembranous colitis. Results from long-term antibiotic tx, which depletes natural flora. Can tx with oral vancomycin (doesn't get absorbed, just takes out the C. defficile in the gut) |
|
|
Term
|
Definition
| Caused by cutaneous entry of bacillus anthracis (most common) |
|
|
Term
| Bacillus anthracic portals of entry (3) |
|
Definition
| Inhalation (most lethal; inhale endospores), GI (rare), cutaneous (most common, eschar lesion) |
|
|
Term
| How do bacillus and clostridium cause disease? |
|
Definition
| By releasing exotoxins. Both are spore formers, but bacillus is a facultative anaerobe while clostridium is an obligate anaerobe |
|
|
Term
| What is the only bacteria to have a capsule composed of protein (poly-D glutamic acid?) |
|
Definition
|
|
Term
| Virulence factors for bacilus anthracis (3) |
|
Definition
| Endospores, glutamic acid capsule (only bacteria w/protein capsule), anthrax toxin (three parts; cytotoxic- PA, EF, LF) |
|
|
Term
|
Definition
| Three parts to it. Cytotoxic and multifunctional (three proteins). 1. PA/Protective antigen; B subunit of the AB toxin that is not enzymatically active but carries the other two through the plasma membrane into the cytosol where they catalyze rxns that disrupt normal cellular physiology; enter into phagocytic cells 2. EF: Edema factor; acts as an adenylate cyclace, increasing cAMP and leading to cell water loss and edema c. LF/lethal factor; destroys signaling proteins w/in the cell by protease activity and causes cell death |
|
|
Term
|
Definition
| Part of anthrax toxin that acts as an adenylate cyclase, increasing cAMP and leading to cell water loss and edema |
|
|
Term
|
Definition
| Part of anthrax toxin that destroys signaling proteins w/in the cell by protease activity and causes cell death |
|
|
Term
|
Definition
| Mycobacterium tuberculosis and leprae (intracellular pathogens) |
|
|
Term
|
Definition
| Acid-fast bacilli; obligate aerobes that make spores. Intracellular pathogens. Either mycobacterium tuberculosis or mycobacterium leprae. |
|
|
Term
| Mycobacterium tuberculosis |
|
Definition
| Acid-fast bacilli; obligate aerobe; grows within alveolar macrophages in lungs to cause tuberculosis |
|
|
Term
|
Definition
| Leprosy. Acid-fast bacilli; obligate aerobe; intracellular pathogen that grows w/in neuroglia of peripheral nerve endings; skin cells of fingers, toes, lips |
|
|
Term
| Virulence factors of mycobacterium (2) |
|
Definition
| Mycolic acid in cell wall allows cell wall to remain viable for long periods in aerosol drops. Cord factor is a cell wall protein that causes daughter cells to remain attached in parallel alignment (toxic to mammalian cells) |
|
|
Term
|
Definition
| Virulence factor in mycobacterium. Allows cells to remain viable for long periods in aerosol drops. |
|
|
Term
|
Definition
| Virulence factor in mycobacterium diseases. Cell wall protein that causes daughter cells to remain attached in parallel alignment. Toxic to mammalian cells |
|
|
Term
| Is neisseria meningitidis part of normal flora? |
|
Definition
| Yes, in upper airway. Uncommon but devastating invasive diseases: meningitis and sepsis |
|
|
Term
| Is neisseria gonorrhoeae part of normal flora? |
|
Definition
|
|
Term
|
Definition
| Gram-negative diplococci that is found intracellularly. Oxidase + |
|
|
Term
| Pathogenic gram negative cocci |
|
Definition
|
|
Term
| Virulence factors in neisseria meningitides (one that was mentioned in review of the week) |
|
Definition
|
|
Term
| Tx for neisseria meningitidis |
|
Definition
| Penicillin or ampicillin. Little drug resistance |
|
|
Term
| Neisseria gonorrhoeae infections |
|
Definition
| Urethritis and cervicitis. PID and gonorrhea |
|
|
Term
| Virulence of neisseria gonorrhoeae (2 in ROW) |
|
Definition
| Adhesins and antigenic variation (allows repeated episodes of gonorrhea) |
|
|
Term
| Tx for neisseria gonorrhoeae |
|
Definition
| Penicillin and fluroquinolone resistance is widespread. Use ceftriaxone. |
|
|
Term
| Gram negative cocci-bacilli |
|
Definition
|
|
Term
| Is haemophilus influenzae part of normal flora? |
|
Definition
| Yes; normal inhabitant of the upper respiratory tract |
|
|
Term
| Haemopholus influenzae morphology |
|
Definition
| Gram negative, pleomorphic coccobacillus that is very small and requires heme and NAD+ for growth (must live inside cells!) |
|
|
Term
| 5 things that haemophilus influenzae cause |
|
Definition
| 1. otitis media 2. Sinusitis 3. exacerbation of chronic bronchitis 4. Meningitis (now have a vaccine against it; was leading cause of bacterial meningitis in newborns) 5. Pneumonia |
|
|
Term
| Virulence factors in Haemophoilis influenzae (4) |
|
Definition
| 1. Main one is a polysaccharide capsule, and there are 7 variations on this. Most common pathogenic type is type b (Hib, which is what is vaccinated against). No capsule=less virulent 2. Endotoxin/lipid A 3. Fimbriae 4. IgA protease |
|
|
Term
| Tx for haemophilus influenzae |
|
Definition
| 40% have plasmid-mediated resistance to penicillins. First line tx is certriaxone |
|
|
Term
|
Definition
| Mainly caused by gram negatives (Ecoli). Use ciprofloxacin or trimethoprim/sulfa (Bactrim) |
|
|
Term
| Bacterial gastroenteritis |
|
Definition
| Inflammation of the stomach or intestines due to the presence of gram negative bacteria. Associated w/contaminated foods or water and poor living conditions. General symptoms include nausea, vomiting, diarrhea, abdominal pain. Dysentery, a severe gastroenteritis, produces loose, frequent stool containing mucus and blood. Examples include cholera, E.coli, Shigellosis, Campylobacter diarrhea, salmonellosis, and typhoid fever |
|
|
Term
|
Definition
| Facultative anaerobe and a lactose fermentor. Part of normal fecal flora. Can cause UTIs, sepsis, diarrheal syndroms that are either toxin or adhesion mediated. Antigens and exotoxins determine type of disease (5 different types of exotoxins) |
|
|
Term
|
Definition
1. 50% have plasmid mediated resistance to penicillins
2. Use Cephalosporins, aminoglycosides, trimethaprim/sulfa, flouroquinolines |
|
|
Term
| Major cause of gram - sepsis |
|
Definition
|
|
Term
| Three things that ecoli causes |
|
Definition
| UTI, sepsis, and diarrheal syndromes (toxin mediated or adhesion mediated) |
|
|
Term
|
Definition
| Big virulence factor for UTIs. Binds to epithelial cells in UG tract. No p-pilli, no risk for UTIs |
|
|
Term
| Two major virulence factors in Ecoli |
|
Definition
|
|
Term
| Does shingella ferment lactose? |
|
Definition
| No, just like Salmonella and unlike EColi |
|
|
Term
|
Definition
| Gram negative bacillus that is a non-lactose fermentor. |
|
|
Term
|
Definition
| Gram-negative bacillus that is a non-lactose fermentor. SLeading cause of infant mortality worldwide. Signs and symptoms: abdominal cramps, bloody stools, nausea, vomiting, diarrhea. Shiga toxin is an A-B toxin; N-glycosidase that modifies 28S ribosome, thereby inhibiting translation->cells dies->abscesses between endothelial cells->bloody diarrhea |
|
|
Term
|
Definition
| Childhood diarrheal disease (dysentery) caused by shigella, a gram negative rod that is a non-lactose fermentor. ABdominal cramps, bloody stool, nausea, vomiting, diarrhea |
|
|
Term
| Types of Salmonella enterica (4) |
|
Definition
| Enteritidis and Typhimurium cause gastroenteritis. Typhi and paratyphi cause typhoid fever |
|
|
Term
| Salmonella enterica morphology |
|
Definition
| Gram negative rod, non-lactose fermentor. Intracellular |
|
|
Term
| Virulence factors for salmonella (5) |
|
Definition
| 1. Endotoxin 2. Exotoxin 3. Fimbriae (attachment to mucosal surface) 4. Antigenic variation (change expression of flagellar H antigens) 5. Pathogenicity islands to allow for bacteria-directed endocytosis and to prevent phagosome-lysosome fusion |
|
|
Term
| Salmonella pathogenicity islands |
|
Definition
| Chromosomal DNA has these areas. Salmonella Pathogenicity Island 1 (SPI-1) encodes proteins that allow for mammalian cell uptake (it is an intracellular pathogen). Salmonella Pathogenicity Island 2 (SPI-2) prevents phagosome-lysosome fusion |
|
|
Term
|
Definition
| Salmonella Pathogenicity Island 1. Encodes proteins that allow for mammalian cell uptake/bacterial-directed endocytosis of salmonella. |
|
|
Term
|
Definition
| Salmonella pathogenicity island 2. Prevents phagosome-lysosome fusion (how they are able to live inside cells |
|
|
Term
| Are shigella and salmonella parts of the normal flora? |
|
Definition
|
|
Term
| Is pseudomonas aeruginosa a normal part of the flora? |
|
Definition
|
|
Term
|
Definition
| Gram-negative strict aerobic bacillus. Ubiquitous environmental microorganism that is resistant to a wide variety of antibiotics and disinfectants. Major nosocomial opportunistic pathogen, especially burn patients and CF patients. Although it is ubiquitous, it is opportunistic and you need to disrupt the skin in order to get sick |
|
|
Term
| 2 major classes of ppl to get sick from pseudomonas aeruginosa |
|
Definition
| CF patients (problems w/cilia and pseudomonas forms biofilms in lungs) and burn victims |
|
|
Term
| 5 Virulence factors in pseudomonas aeruginosa |
|
Definition
| 1. Fimbriae and adhesions 2. Capsule 3. Pyocyanin (blue green pigment that impairs ciliary function and triggers superoxide formation, killing cells) 4. Elastase 5. Bacteriocins (similar to antibiotics, but directed at microbes that are similar to Pseudomonas) |
|
|
Term
|
Definition
| Blue-green pigment that is a virulence factor in pseudomonas aeruginosa. Impairs ciliary fxn and triggers superoxide formation, killing cells |
|
|
Term
|
Definition
| Similar to antibiotics, but directed at microbes that are similar to Pseudomonas. A virulence factor in pseudomonas aeruginosa |
|
|
Term
| What is the dominant gram negative organism in the colon? |
|
Definition
| Bacteroides fragilis. Part of the normal flora |
|
|
Term
|
Definition
| Augmentin, meropenem, clindamycin |
|
|
Term
| Oxygen for bacterioides fragilis? |
|
Definition
|
|
Term
|
Definition
| Dominant anaerobic organism of the gut that normally lives there w/o a problem. But if you perforate the bowel, B. frag is an opportunistic pathogen, and it will lead out and cause abscess and septicemia. Part of mixed infections following rupture of hollow organ in gut. |
|
|
Term
| Virulence factors for B. Fragilis (5) |
|
Definition
| Endotoxin (lipid A), Enterotoxin (an cause diarrhea), capsule (induces abscess formation), protease (degrades complement components), most make b-lactamase and are resistant to penicillin |
|
|
Term
|
Definition
| Gram negative bacilli that lives in the stomachs of 50% of the ppl in the world. Causes gastric and duodenal ulcers (destruction of mucous layer and exposure to H+). Elaborates a urease, which converts urea to bicarbonate, neutralizing stomach acid and allowing the bacteria to live in the stomach |
|
|
Term
| 4 virulence factors of Helicobacter pylori |
|
Definition
| Urease (converts urea to bicarbonate, neutralizing stomach acid and allowing bacteria to live in the stomach), flagella (allows bacteria to move through mucus and bind epithelial cells; required for pathogenicity), adhesins, toxins |
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Term
|
Definition
| Microbe benefits; host neither benefits nor is harmed (ex- staphylococcus epidermidis) |
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Term
|
Definition
| Both microbe and host benefit (ex- E.col) |
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Term
| Primary or overt pathogens |
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Definition
| Cause disease in healthy people. ex- Shigella->bacillary dysentery |
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|
Term
| 2 ways that a microbe can cause disease |
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Definition
| 1. Invasion and growth in an inappropriate place->inflammation 2. Production of toxic substances (exotoxins and endotoxins) |
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Term
| Indirect host-to-host transmission (3) |
|
Definition
| Living agent (vector; ex- insect), Inanimate object (fomite; ex- doorknob, tabletop); Vehicle (food, water) |
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Term
|
Definition
| A living agent that is an intermediate in the transmission process. ex- insect |
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Term
|
Definition
| An inanimate object that is an intermediate in the transmission process. Ex- doorknob |
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Term
|
Definition
| Food or water that serves as an intermediate in the transmission process. This is thae way that most IDs are passed |
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Term
|
Definition
| Site where pathogens are maintained as a source of infection. Most cannot live long outside their host (we are major resevoirs). Three types: Animal resevoir, human carriers that are sublinically infected, and non-living resevoir (soil, food, often due to fecal contamination) |
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Term
|
Definition
| Individual in incubation period of disease. a type of human resevoir |
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Term
|
Definition
| A person who carries a disease at a subclinical level for an extended period of time. ex- Typhoid Mary |
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Term
|
Definition
| A disease always present in a population, usually at low incidence. ex- STDS |
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Term
|
Definition
| When an unusual number of ppl in a given area contract a disease w/in a relatively short time |
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Term
|
Definition
| A widely distributed epidemic; two or more continents. ex- HIV, TB, flu |
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|
Term
| What do biofilms provide for microbes? |
|
Definition
| A protective environment. Shields against antibodies, phagocytic cells and enzymes. Limits access to antibiotics |
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|
Term
| Three phases of biofilm formation |
|
Definition
| 1. Attachment (microbes use specialized adhesin proteins and/or glycocalyx to attach to surfaces) 2. Growth (cells multiply and are encased in a polysaccharide material termed the ECM) 3. Detachment (can lead to further colonization w/in the host or microenvironment) |
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|
Term
| Normal microbiota of the skin |
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Definition
| Primarily gram positive bacteria and fungi associated with sweat glands. Type and number can be affected by age, weather, and personal hygiene |
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|
Term
| Normal microbiota of the mouth |
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Definition
| The mouth is great bc it is a moist envirnonment w/plenty of nutrients and physiological pH. Must be able to adhere to surfaces due to salivary flow. Viridans Streptococci (alpha-hemolytic; strep mutans) |
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|
Term
| Normal microbiota of the respiratory tract |
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Definition
| Normally there is staph and strep in the URT. LRT should be axenic (microbes are cleared by antibodies and ciliary action). |
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|
Term
| Normal microbiota of the UG tract |
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Definition
| Upper regions should be axenic. Urethra is primarily colonized w/facultative anaerobic gram-negative bacteraia (Ecoli) |
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|
Term
| Where are the three major locations for nosocomial infections? |
|
Definition
| UTIs, pneumonias, and bloodstream. These areas are normally azenic! |
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Term
|
Definition
| Provides complete killing or removal of microbes |
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Term
|
Definition
| Destroys pathogenic microbes; viable microbes may remain |
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Term
|
Definition
| Made of peptidoglycan. Has repeating disaccharides w/4AAs in a side chain extending from each disaccharide. The AA chains of the peptidoglycan covalently bind to other AAs from neighboring chains. This results in a stable cross-linked structure, and the enzyme that catalyzes the formation of this linkage is transpeptidase |
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Term
|
Definition
| Enzyme in tears, saliva, and skin. A defense of the body to make sure that the cell wall of bacteria won't stay intact. Lysozyme attacks Beta linkages in the sugar chain of peptidoglycan |
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|
Term
| N-acetylglucosamine/N-acetylmuramic acid/pentapeptide precursors |
|
Definition
| What make up peptidoglycan. Have to get the charged sugars through the hydrophobic membrane in order to reach the cell wall. Must use lipid bactoprenol to do this |
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Term
|
Definition
| Disrupts cell wall synthesis by inhibiting Bactoprenol, the lipid that helps transport charged sugars through the cell membrane to the cell wall in order for them to be incorporated into peptidoglycan |
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Term
|
Definition
| Formation of peptide cross-links btw adjacent glycan chains. Catalyzed by PBPs. |
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Term
|
Definition
| Proteins that cleave the B(1-4) linkage btw NAG and NAM (two of the sugars in the peptidoglycan). This is the same as lysozyme, but it is produced by the cell itself, which aids in cell wall enlargement during growth. Cell wall is constantly being turned over! |
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Term
|
Definition
| Teichoic and lipoteichoic acids are virulence factors that provide adhesion and a negative charge to the wall. They can induce septic shock and may regulate autolysin function. |
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|
Term
| Cell walls of mycobacteria |
|
Definition
| (TB and leprosy causing). Similar to gram positive. Has mycolic acid residues linked to the peptidoglycan. Mycolic acids are long chain fatty acids that are extremely hydrophobic and are responsible for the acid fast properties of mycobacteria. Causes cells to grow slowly and not stain well. Need a gram stain derivative to recognize mycobacteria |
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Term
|
Definition
| Has lipopolysaccharides embedded in the outer membrane of the cell wall LPS is made up of O and A components. The O component is an external polysaccharide antigen that is organism-specific. The A part is the endotoxin (lipid portion), and this is the toxic part of the LPS. Lipid A/endotoxin can cause fever and shock in patients |
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Term
|
Definition
| Used to figure out the gram negative bacterial species. O antigens are cell wall sugars (part of LPS) |
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Term
|
Definition
| A way to distinguish btw gram negative bacterial species. H antigens are found in the flagella |
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Term
|
Definition
| In gram-negative bacteria, a way to distinguish btw species. K antigens are found in the capsule |
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Term
|
Definition
| Composed of the protein pilin. Numerous hair-like structures over the surface of the cell. Fxn in attachment to surfaces and other cells. ex- Neisseria gonorrhoeae cells use pili to attach to cells in the GU tract; essential forvirulence. ex- E.coli uses P-pili to attach to cells in urinary tract UTI |
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Term
|
Definition
| Most pathogens are chemoheterotrophs. They need chemical compounds for energy (ATP) and organic compounds for C. Our cells are great carbon resources! |
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Term
|
Definition
| Acts against microbes on surfaces of inanimate objects non-specifically. Dangerous if used on skin or parenterally |
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Term
|
Definition
| Act against microbes non-specifically. Non-toxic to the skin or other tissue. ex-mouthwash |
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|
Term
| How do disinfectants and antiseptics work? (2) |
|
Definition
| Either by disrupting cell membranes (remove or interact w/lipids of the cell membrane; ex- detergents or lipid solvents) 2. Alter proteins irreversibly (act as oxidants, alkylating agents or sulfhydryl-reacting reagents) |
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|
Term
|
Definition
| Ability of an organism to cause disease. Either is or is not a pathogen (unlike virulence, which is a quantitative measure of pathogenicity) |
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Term
|
Definition
| Leathal Dose 50. Measure of virulence. The number of microbes needed to kill half of infected hosts |
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|
Term
|
Definition
| Infectious Dose 50. The number of microbes needed to infect half of the hosts |
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|
Term
|
Definition
| Glycocalyx, adherence proteins, lipoteichoic acid, fimbriae (pilli) |
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|
Term
| Hyaluronidase and collagenase and what two organisms have these enzymes |
|
Definition
| Found in strep and staph. Degrade hyaluronic acid, a component fo the ECM and collagen- spreading factors. Help them get through the first protective layer of the epidermis |
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Term
| Coagulase and what has it |
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Definition
| Coagulase helps the bacteria evade the immune system by forming blood clots that provide hiding places for microbes. Staph aureus has it, while staph epid and saprophyticus do not. |
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|
Term
| Streptokinase and staphylokinase and who has it (2) |
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Definition
| Staphylococcus and streptococcus species have these, which help them digest through blood clots and release microbes, spreading throughout the body |
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Term
|
Definition
| Can be used for attachment to the host cell (as an adhesin). Also are good for eluding macrophages/blocking phagocytosis, as they are composed fo polysaccharides found in the body; not recognized as foreign by the immune system. It is also hard for the phagocytes to engulf the bacteria |
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|
Term
| Three examples of anti-phagocytic chemicals |
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Definition
| 1. Some prevent fusion of lysosome and phagocytic vesicles 2. M protein of Strep pyogenes resists phagocytosis by interfering w/complement component C3b 3. Leukocidins of Staph aureus destroys phagocytic WBCs |
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Term
|
Definition
| Act on intracellular targets (neutrotoxins, enterotoxins). Found in Gram positive and gram negative |
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Term
|
Definition
| Act on cell surface forming pores in membrane. This disrupts the osmotic balance and leads to host cell death |
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|
Term
| Typhoid fever, endotoxic shock, UTIs, meningococcal meningitis are all caused by what toxin? |
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Definition
|
|
Term
| Botulinum, tetanus, gas gangrene, diptheria, cholera, staphylococcal food poisoning are all caused by what kind of toxin.. |
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Definition
|
|
Term
| Are exo or endotoxins fever producing? |
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Definition
| Endotoxins are fever producing. Exotoxins almost always are not fever producing, except that superantigens do give you a fever |
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|
Term
| Gram positive cocci that is catalase positive and coagulase positive, presenting with food poisoning |
|
Definition
| Staph aureus. May also give skin diseases |
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|
Term
| Cell wall and membrane in gram + vs - |
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Definition
| Have identical cell walls. Both have periplasm/peptidoglycan layer of cell wall, but this is thick in Gram + and thin in Gram -. The big difference is that gram -s have an outer cell wall, which is where the LPS is located |
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|
Term
| What are exotoxins vs endotoxins made of? |
|
Definition
| Exotoxins are made of protein, and endotoxins are lipopolysaccharide. Therefore, exotoxins are heat labile, unlike endotoxins. Exotoxins sometimes can cause an immune response, but not usually bc they are small and easily overlooked by the immune system. Endotoxins never are attacked by the immune system bc they are not proteins, and that is what the immune system is designed to attacik. |
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|
Term
| Toxicity of exotoxins vs endotoxins |
|
Definition
| Exotoxins are more potent (low LD50) |
|
|
Term
| How widespread is the effect of endotoxin vs exotoxin? |
|
Definition
| Exotoxins: specific (not widespread) Endotoxin: non-specifically activate the immune system |
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|
Term
| Three ways that exotoxins work |
|
Definition
| 1. membrane disruption (cell dies) 2. Interruption/alteration of cellular enzymes 3. Indiscriminate activation of T cells (superantigens get all sorts of T cells revved up->system goes crazy) |
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|
Term
| Membrane disruption in exotoxins |
|
Definition
| Putting a hole in the membrane kills the cell. Cytolytic; disrupt the phospholipid layer, or form a protein channe. May work by the enzymes phospholipase or amphipathic peptides |
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|
Term
| Corynebacterium diphtheriae |
|
Definition
| Causes diptheria. A gram + rod, + catalase and no spores. Works by secreting an A-B toxin that disrupts protein synthesis and causes cell death in pharynx. B subunit stays on the host cell membrane (specific to the pharynx) whle the A subunit moves inside the cell and binds to EF-2, disabling it. Without EF-2, protein translation cannot continue, and the cell dies. There is a highly effective vaccine against diphtheria, so it is a rare disease in the US. Associated with a pseudomembrane in the pharynx->airway obstruction |
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Term
|
Definition
| Cholera toxin in the gut gets translocated inside the cell and binds to a G protein. This keeps adenylate cyclase on, so you keep making cAMP. This causes channels to open, solutes rush out, followed by water. No tissue damage or cell death, just extreme intravascular water depletion |
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|
Term
| What does tetanus toxin bind? |
|
Definition
| Inhibitory neuron. Prevents it from firing |
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|
Term
| What are the first signs of botulism? |
|
Definition
| Bulbar/CN signs- diploplia |
|
|
Term
| Does the clostridium toxins kill the cells? |
|
Definition
|
|
Term
| Clinical utility of botulism toxin (3) |
|
Definition
| Whenever you want flaccid paralysis. Spasticity, blepharospasm (eyelid twitch), wrinkles |
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|
Term
|
Definition
| Antigen-presenting cells present peptide in MHCII. Only one clone of helper T-cells recognize the antigen-MHC complex. Superantigens bind directly and indiscriminately to the MHC and T-cell receptors (bind the sides, not in the antigen-binding groove). Therefore, they activate many clones of T-cells ->excessive cytokines are produced and you get shock |
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|
Term
| Two bacteria that cause TSS |
|
Definition
| S aureus (staphylococcal TSS and food poisoning caused by the exotoxin) and S pyogenes (GABHS. Exotoxin A is the superantigen that leads to streptococcal TSS) |
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Term
|
Definition
| Superantigens! S. aureus releases a TSS exotoxin that causes toxic shock and food poisoning, while S. pyogenes releases exotoxin A that causes streptococcal TSS |
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|
Term
| Symptoms of fever, hypotension, diffuse erythroderma, red eyes |
|
Definition
| TSS. Multi-system organ involvement. Caused by superantigens produced by S. aureus and S. pyogenes (exotoxin A for this) |
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Term
|
Definition
| Fever (cytokines being dumped out); hypotension, diffuse erythroderma, red eyes, multi-system organ involvement, skin and mucous membrane changes, fever, myalgias, abdominal pain, weakness, hypotension and oliguria, confusion, headache and vomiting, diarrhea |
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|
Term
|
Definition
| Released from s. aureus as an exotoxin/superantigen, and causes toxic shock and food poisoning. May be associated w/tampon use. Tx is primarily fluids and pressure support, antibiotics to tx S. aureus. At risk for recurrence; no tampons for a year. |
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|
Term
| B-lactamase producing organisms (plasmid mediated) (5) |
|
Definition
| 1. S. aureus (99%!) 2. B. fragilis (over 90%) 3. E. coli (50%) 4. H. influenzae (40%) 5. N. gonorrhoeae (variable) |
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|
Term
| B-lactamase producing organisms (chromosomally mediated) (2) |
|
Definition
| 1. Enterobacter 2. Pseudomonas |
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|
Term
|
Definition
| These are B-lactamase inhibitors, just like B-clavulanate. Combined with penicillin |
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|
Term
| Suicide B-lactamase inhibitors |
|
Definition
| Very weak cephalosporin antibiotics. Remove the B-lactamase on a 1:1 basis. B-lactamase recognizes the B-lactam ring, but it cannot let it go. Remove each enzyme, and S. Aureus is now susceptible again to penicillin |
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|
Term
| Penicillinase resistant penicillin |
|
Definition
| Nafcillin. Side chain prevents it from B-lactamase destruction. Used to treat susceptible S. Aureus infections. Excreted unchanged in the urine; doesn't cross the BBB unless meninges are inflamed |
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|
Term
| What antibiotic is frequently modified by an enzyme? |
|
Definition
| Aminoglycoside/gentamycin. The antibiotic is modified so that it is no longer functional. This confers a high level of resistance to aminoglycosides. Plasmid or transposon mediated |
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|
Term
| Two examples of organisms w/altered antibiotic target sites |
|
Definition
| S. pneumoniae and S. aureus |
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|
Term
|
Definition
| Mean amount of drug necessary to inhibit the growth of 50% of the organisms. Increases with an increase in number of PBP mutations in s. pneumoniae and s. aureua |
|
|
Term
|
Definition
| The mean amount of drug necessary to inhibit growth of 90% of the organisms. Increase number of mutations in PBP in S. pneumonia or S. aureus->increased MIC90 |
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|
Term
|
Definition
| In MRSA. Chromosomally mediated resistance. Different from S. pneumoniae chromosomally mediated resistance, bc that can be overcome. Here, you get an alteration in a PBP that can make the cell wall alone. Penicillin can stil bind to normal PBPs, but this mutant doesn't need their help! MRSA is resistant to all B-lactam drugs (Penicillins and Cephalosporins). |
|
|
Term
| S. pneumoniae chromosomally mediated resistance |
|
Definition
| Mutations in one or more PBP genes causes increase in MIC. Can be overcome by high doses of either penicillin or cephalosporins (does not make B-lactamase, so it doesn't matter which one you choose). |
|
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Term
|
Definition
| Caused by modification of the antibiotic enzymatically or increased efflux |
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|
Term
|
Definition
| Caused by increased efflux |
|
|
Term
|
Definition
| Hyperproduction of the target |
|
|
Term
| Three clinically relevant mycobacteria |
|
Definition
| M. tuberculosis, M. avium complex, M. leprae |
|
|
Term
| Three encapsulated bacteria |
|
Definition
| Strep pneumonia, h. influenza type B, Neisseria meningitides |
|
|
Term
| 5 obligate intracellular bacteria |
|
Definition
| Salmonella, mycobacterium, listeria, rickettsia, chlamydia |
|
|
Term
| Does mycobacterium tb have a capsule? Is it aerobic or anaerobic? Is it intra or extracellular? |
|
Definition
| Intracellular organism that is aerobic and does not have a capsule |
|
|
Term
| Major virulence factors for TB (3) |
|
Definition
| Cord factor, able to live intracellularly, and low infective dose |
|
|
Term
| Membrane and wall of mycobacteria |
|
Definition
| Cell membrane and peptidoglycan layer like the others, but then they have a thick mycolic acid (60%) and short fatty acid and peptide (40%) layer |
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|
Term
|
Definition
| Outside of mycobacterium's cell wall (makes up 60% of it). Very hydrophobic and responsible for the acid-fast |
|
|
Term
| Transmission of M. tuberculosis |
|
Definition
| Droplets. Aerosols from an infectious person coughing stay suspended in the air w/1-3 organisms (very high infectious dose!) Can hang there and drip down |
|
|
Term
| What 4 things determine the probability that TB will be transmitted? |
|
Definition
| 1. Infectiousness of the person w/TB 2. Environment in which the exposure occurred 3. Duration of exposure 4. Virulence of organism |
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|
Term
|
Definition
| Inhale the mycobacterium, and it will not get filtered in the lungs bc it is too small. It is then brought to the lymph nodes by pulmonary macrophages, where T cells should take action. If they do, you develop an immune response and the bacteria is contained. If you are unable to contain it, you will get the disease. TB keeps multiplying inside of the macrophages (is is an intracellular organism). If the T cells are not activated, you will get progressive, systemic disease followed by death (primary pneumonia in children and disseminated disease in both children and adults) |
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|
Term
| Reactivation/Adult type TB |
|
Definition
| Most common. New replication if you get old or immunocompromised. Bacteria were locked away in caseating granulomas but now can replicate. Get an intense inflammatory response as caseating granulomas burst and you get invasion of local tissue and necrosis. Local distruction of tissue->intense inflammatory response. Caseating granulomas are often in the lungs, so bursting them spews bacteria throughout the lungs. This happens when you're older bc T cells stop working as well |
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|
Term
| Cough, hemoptysis, night sweats, weight loss |
|
Definition
|
|
Term
| Two major risk factors for developing TB |
|
Definition
| HIV and Anti Tumor Necrosis Factor therapy. Also being really young or old (T cells aren't as good then) |
|
|
Term
|
Definition
| measures recruitment of macrophages and T cells after injecting M. TB junk. Intra-epidermal, not a good test at all. Interferon assays are much better (take cells from our body and put them into a bath with the antigen. You'll make lots of gamma interfuron if you've seen it before) |
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|
Term
| Three key components to TB tx |
|
Definition
| Never use a single drug, never add a single drug to a failing regimine, and ensure adherence to therapy |
|
|
Term
|
Definition
| Resistant to most drugs. Use multiple ones. 1. Isoniazid 2. Rifampin 3. Ethambutol |
|
|
Term
|
Definition
| Interferes with mycolic acid synthesis. Associated w/hepatic (get hep A and B) and peripheral nerve toxicity |
|
|
Term
|
Definition
| Inhibits a DNA-dependent RNA polymerase and is a powerful inducer of the CYP enzymes. Used for lots of things; not very specific, lots of drug-drug interactions |
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|
Term
|
Definition
| Interferes w/mycolic acid synthesis, and has ocular toxicity. Used for TB |
|
|
Term
|
Definition
| Environmental pathogen with low virulence. common cause of unilateral adenitis in children. Causes bloodstream infections in patients with AIDS. Lymph node infection in kids, sepsis in adults. Intrinsically resistant to antimicrobial therapy; azithromycin and Rifampin-type drugs |
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|
Term
| Tx for Mycobacterium avium |
|
Definition
| Intrinsically resistant to antimicrobial therapy. Azithromycin and rifampin-like drugs |
|
|
Term
| What does M. leprae effect? |
|
Definition
| Grows on colder areas of the body and effects peripheral nerves, skin, and mucous membranes. The clinical spectrum of the disease reflects bacterial proliferation and accumulation at the site of infection, the immunological response, and destruction of nerves. Looks like TB under the microscope. Takes 20-30days to divide, has only been cultured from armadillos (never the lab!) |
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|
Term
|
Definition
| Diffuse or nodular lesions containing many bacteria. Sensory loss due to nerve damage. Predominant humoral response, little cell mediated immunity!! This is what happens when you don't have a good immune response and you only have humoral mediated immunity. Need T cells |
|
|
Term
|
Definition
| Few, well-defined lesions. Few organisms (paucibacillary). Predominantly cell-mediated immunity. Spontaneous regression of tuberculoid leprosy occurs in 90% of cases in children. Have cell-mediated immunity, so they clear it (unlike lepromatous) |
|
|
Term
|
Definition
| Rifampin-like drugs, dapsone |
|
|
Term
| Actinomycetes morphology and how they deal with oxygen |
|
Definition
| Anaerobic; gram + and forming long branching filaments; weakly acid-fast |
|
|
Term
|
Definition
| Infection w/actinomycetes, anaerobic gram +, filamentous bacteria. See lumps in belly and neck w/no respect for anatomic boundaries. Chronic, indolent infections in healthy people w/poor definition. Find cervico-facial disease, firm nodules, and sinus tracts. Pus has sulfer granules (mass of filaments). Tx: long course of penicillin |
|
|
Term
| Chronic, indolent cervico-facial disease, firm nodules, and sinus tracts in healthy people |
|
Definition
| Actinomycosis. Anaerobic gram + that forms long, branching filaments. Weakly acid-fast. Tx with long courses of penicillin |
|
|
Term
|
Definition
| Aerobic, gram positive, forming long branching filaments (as opposed to actinomycoses which are anaerobic!). N. Asteroides is found in the soil. Cause chronic infections in the immunocompromised. clinical findings: skin nodules, pnemonia, brain abscess. tx: long course of sulfonamides |
|
|
Term
| Clinical presentation of N. asteroides |
|
Definition
| Found in soil and causes Nocardia. This is a mycobacterium. See this in the immunocompromised. See skin nodules, pneumonia, brain abscess. Tx w/a long course of sulfonamides |
|
|
Term
| Tx for N, asteroides/nocardia |
|
Definition
| Long course of sulfonamides |
|
|
Term
| Which three classes of antibiotics have a B-lactam ring? |
|
Definition
| Penicillin, cephalosporin, carbapenems (meropenum) |
|
|
Term
| How do you tx oral infections? |
|
Definition
|
|
Term
| How to you tx strep pyogenes? |
|
Definition
|
|
Term
| How do you tx strep agalactiae? |
|
Definition
|
|
Term
| How do you tx enterococcus? First, second, and third line tx |
|
Definition
| 1. Ampicillin w/aminoglycoside 2. Vancomycin 3. (VRE) Linezolid |
|
|
Term
| How do you tx Strep Viridans? |
|
Definition
|
|
Term
| How do you tx community acquired pneumonia? |
|
Definition
| Assume strep pneumonia, and tx w/azithromycin (assume that it is resistant to ampicillin) |
|
|
Term
| How do you tx hospital acquired pneumonia? |
|
Definition
| Azithromycin w/ceftriaxone to get the strep pneumonia. May add vanco for drug-resistant strep pneumo |
|
|
Term
| How do you tx meningitis? |
|
Definition
| Ceftriaxone w/vancomycin. Could also give ampicillin to cover listeria |
|
|
Term
| How do you tx HENT infections? |
|
Definition
| Augmentin. Two major causes are S. pneumo and H. influenza. H flu is a gram negative, but amoxicillin (and therefore augmentin) will work against it. |
|
|
Term
| How do you tx nosocomial MRSA? |
|
Definition
| Vancomycin (IV) and linezolid (oral) |
|
|
Term
| How do you tx community acquired MRSA? (3) |
|
Definition
| Bactrim, clindamycin, doxycycline |
|
|
Term
| How do you tx neisseria meningitides? |
|
Definition
| Protocol for meningitis is vanc and ceftriaxone, but if you know that its neisseria, use just ceftriaxone |
|
|
Term
| How do you tx neisseria gonorrhoeae? |
|
Definition
| Ceftriaxone (one shot). Usually give this w/doxycycline for chlamydia |
|
|
Term
| How do you tx a UTI caused by ecoli? First and second line |
|
Definition
| Bactrim is first line, ciprofloxacin is second (don't want to use this bc it is the only oral anti-pseudomonal) |
|
|
Term
| How do you tx typhoid fever? |
|
Definition
|
|
Term
| How do you tx non-typhoid salmonella? |
|
Definition
| Ceftriaxone or ciprofloxacin |
|
|
Term
| Six things that can tx pseudomonas |
|
Definition
| Piperacillin, meropenem, gentamicin, ciprofloxacin, ceftazideme (3.5), cefepime (4th) |
|
|
Term
| How do you tx H flu? (2 depending on location) |
|
Definition
| 1. Amoxacillin/Augmentin for the ear infection 2. Ceftriaxone (and usually vanc, although this won't help for h flu or neisseria) for meningitis |
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Term
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Definition
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Term
| How do you tx lyme disease/borrelia burgdorferi? |
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Definition
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Term
| How do you tx mycoplasma pneumonia? |
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Definition
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Term
| How do you tx rickettsia? |
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Definition
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Term
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Definition
| Doxycycline (oral only) or azithromycin). Can also give a big shot of ceftriaxone to make sure gonorrheea is gone |
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Term
| What are two drugs you can give for complicated intra-abdominal infections? |
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Definition
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Term
| What do you use to tx skin and bone infections and for surgical prophylaxis? |
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Definition
| Cefazolin/first generation cephalosporin |
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Term
| What is used to tx pseudomonas aeruginosa, nosocomial infections, and febrile neutropenia? |
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Definition
| Ceftazidime (3.5 generation) |
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Term
| What is the niche of cefepime? |
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Definition
| Serious nosocomial infections, especially in ppl w/o WBNCs. Great gram neg and pos activity, including pseudomonas (like 3.5 ceftazidime). Crosses BBB like ceftazidime and ceftriaxone |
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Term
| Does meropenum cross the BBB? |
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Definition
| Yes. It also has a B-lactam ring, so it is resistant to MRSA and bacteria w/o a peptidoglycan wall |
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Term
| Vancomycin mech of action |
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Definition
| Binds to the substrate in the transpeptidase rxn (D-Ala-D-Ala terminal of the peptidoglycan). Non B-lactam. |
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Term
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Definition
| All gram positives but only gram positives. Used for resistant gram positive rxns (MRSA included) and gram positive infections in pts allergic to B-lactams. Also combined w/ceftriaxone in txing meningitis caused by strep pneumonia and neisseria meninigtis in order to cover strep pneumo |
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Term
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Definition
| Red man syndrome, dose-dependent ototoxicity and nephrotoxicity, especially in the setting of other nephrotoxic drugs (like gentamicin) |
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Term
| Gentamicin mech of action and niche |
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Definition
| Inhibits the 30S ribosomal subunit and works on aerobic gram-negative rods and is synergistic w/cellwall active agents (B-lactamase and vancomycin and carbapens) for gram positive cocci |
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Term
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Definition
| Potentially sesvere. Nephrotoxic (especially w/vanc), toxic to auditory and vestibular components of the eighth cranial nerve. Must monitor serum levels and renal fxn. |
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Term
| Is gentamicin IV, oral, or both? |
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Definition
| IV oral. Limited tissue perfusion |
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Term
| Is vancomycin oral or IV or both? |
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Definition
| IV only, good tissue distribution |
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Term
| Tetracycline/doxycycline mech of action and niche |
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Definition
| Inhibits the 30S ribosomal subunit. Works against many gram + and negative bacteria, mycoplasms, chlamydiae, and rickettsiae. Outpt for cutaneous MRSA. Used for rickettsiae, borrelia burgdorferi, chlamydia, mycoplasma |
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Term
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Definition
| Diarrhea, vaginal yeast infections, photosensitivity, stains teeth of fetuses and children brown as it binds to calcium. Contraindicated in pregnant women and children under eight |
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Term
| Is doxycycline IV or oral or both? |
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Definition
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Term
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Definition
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Term
| Azithromycin mech of action and niche |
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Definition
| Inhibits the 50S ribosomal subunit. Single dose chlamydia infections, pneumonia, URI (bronchitis), mycoplasma, legionella, s aureus, H flu |
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Term
| What is the toxicity of azithromycin? |
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Definition
| Drug-drug interactions, expecially w/antiarrhythmic drugs. GI upset |
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Term
| Is azithromycin IV or oral or both? |
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Definition
| Both. Excellent oral absorption |
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Term
| What is the mechanism of action of lincosamide/clindamycin? |
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Definition
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Term
| How do you tx penetrating wound infections? |
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Definition
| Aminoglycoside (gentamicin) for the aerobic gram-negatives, and clindamycin for the anaerobes |
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Term
| Is clindamycin IV or oral or both? |
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Definition
| Both! Excellent bioavailability. |
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Term
| Linezolid mech of action and niche |
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Definition
| Inhibits the 50S subunit. Only active against gram positives. Designed for the tx of resistant gram + cocci (MRSA and VRE) |
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Term
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Definition
| Dose-dependent thrombocytopenis, serotonin syndrome when combined w/SSRIs |
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Term
| Is Linezolid oral or IV or both? |
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Definition
| Both! Claim to fame is that bioavailability is the same in both, so it can be used to orally tx more severe MRSAs than doxycycline can |
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Term
| Trimethoprim/Sulfamethoxazole niche |
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Definition
| UTIs and community acquired MRSA, non-bacterial pathogens such as pneumocystic jiroveci, prophylaxis for immunocompromised pts. |
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Term
| Sulfamethoxazole mech of action |
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Definition
| Structural analogues of para-aminobenzoic acid (PABA) which condenses w/pteridine in the first step of bacterial synthesis of dihydrofolate. We don't synthesize DHT in the process of DNA synthesis |
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Term
| Mech of action of trimethoprim? |
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Definition
| Structurally resembles folic acid and inhibits the enzyme dihydrofolate reductase. Its specificity for bacteria is due to its much greater affinity for bacterial dihydrofolate reductase than for the human enzyme. |
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Term
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Definition
| Rashes due to the sulfa component and can precipitate in the urine |
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Term
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Definition
| Causes bone marrow suppression or megaloblastic anemia |
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Term
| Example of a fluoroquinolones |
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Definition
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Term
| Ciprofloxacin mech of action and niche |
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Definition
| Inhibits topoisomerase II (DNA gyrase), inhibiting DNA replication. Only oral tx of pseudomonas (like linezolid, oral bioavailability=IV), UTIs, NOT respiratory infections. |
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Term
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Definition
| GI, tendonitis, cartilage problems in developing animals (don't give it to kids!), QT prolongation. |
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Term
| Is ciprofloxin oral, IV, or both? |
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Definition
| Both! Oral bioavailability is equal to IV. Good tissue levels |
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Term
| What causes endocarditis? (4) |
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Definition
| Staph aureus (acute onset; most common), s viridans, enterococcus, s epidermidis are slower onset and less commen |
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Term
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Definition
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Term
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Definition
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Term
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Definition
| Contains supplemental nutrients to help support the growth of fastidious organisms (meaning several growth requirements), most classically neisseria species |
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Term
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Definition
| Beta! Just like s pyogenes and grp B strep |
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Term
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Definition
| Culture medium designed to support the growth of gram -. Contains bile salts and dies that inhibit the growth of gram +. pH indication: organisms that ferment lactose produce acid which lowers the pH->pink. If it turns this color, it's E.coli for our case |
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Term
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Definition
| Means that cytochrome oxidase is present. Used to identify Gram negative microbes (those that carry out aerobic respiration use cytochrome oxidase to transfer electrons). If it turns dark purple, it is positive |
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Term
| Four bugs that use A-B toxins |
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Definition
| Diptheria, cholera, botulism, and clostridium |
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Term
| Cassette of nosocomial MRSA |
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Definition
| Huge, but not very mobile, and this confers a selection advantage when not under antimicrobial pressure. Resistant to many antibiotics |
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Term
| Cassette of community associated MRSA |
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Definition
| Small, very mobile, and little cost to the bacteriuim (can survive without antimicrobial pressure, but is resistant to few antibiotics) |
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Term
| Suicide vs competitive B-lactamase inhibitors |
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Definition
| Suicide- weak cephalosporins Competitive: clavulanate |
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Term
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Definition
| Only if you use a B-lactam with it (wall is too thick for the lg aminoglycoside to get into the cell w/o help) |
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Term
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Definition
| High probability of progression to sepsis. SIRS+infection=sepsis. Tachycardia, tachypnia, hyper/hypothermia, leukocytosis/leukopenia |
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Term
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Definition
| SIRS+infection. Bacterial infection of the blood stream and hypotension, in addition to tachycardia, tachypnea, hyper/hypothermia, and leukocytosis/leukopenia. Lactate up, evidence of necrosis. SIRS secondary to infection |
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Term
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Definition
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Term
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Definition
| Good bc it increases fibrinolysis and inhibits coagulation. Also decreases inflammatory response somehow |
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Term
| What do you give for sepsis due to strep pneumonia? |
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Definition
| APC, ceftriaxone/ciprofloxacin/Vanco, hydrocortisone, pressors, renal failure, |
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Term
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Definition
| Excess inflammatory response due to infection, inappropriate coagulation, impaired fibrionlysis. This leads to endothelial damage, microvascular dysfunction, impaired tissue oxygenation and organ injury |
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Term
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Definition
| Gram - rod associated w/dog bites that can be a cause of sepsis in post-splenectomy patients |
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Term
| Does chlamydia have a cell wall? |
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Definition
| Yes, but not with peptidoglycan. Use macrolides (azithromycin), doxycycline, or fluoroquinolones (ciprofloxacin). Causes urethritis and pneumonia |
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Term
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Definition
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Term
| N. meningitides sepsis tx |
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Definition
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Term
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Definition
| No cell wall!Smallest free living bacteria. Tx w/macrolides (Z), doxycycline, fluroquinolones (ciprofloxacin) |
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Term
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Definition
| Arthropod vector. Survives in endothelial cells. Rocky mountain spotted fever. Tx w/doxycycline |
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Term
| Tx for treponema pallidum? |
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Definition
| This is syphillis. Use penicillin |
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Term
| Tx for borrelia burdorferi |
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Definition
| This is lyme disease. Use doxycycline |
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Term
| Does diptheria cause direct cell death? |
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Definition
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Term
| Normal flora of the skin (3) |
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Definition
| S. epidermidis, S. aureus, S. viridans |
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Term
| Normal flora of the mouth (2) |
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Definition
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Term
| Delayed hypersensitivity response in TB |
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Definition
| T cell success at 2-6 weeks. Kill TB laden macrophages, recruit macrophages and activate them (which kill TB). Need the T cells to help direct and coordinate the immune response. 90% of infection controlled and healed by fibrosis (asymptomatic infection or M. tuberculosis infection w/o disease). Will still have a couple little white spots, but these are just walled off infected macrophages |
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Term
| Anti-tumor necrosis factor therapy and TB |
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Definition
| increases your risk for new replication (adult tb) a ton! |
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Term
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Definition
| Enterococcus, B frag, ecoli, S. agalactiae |
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