Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
86 Cards in this Set
- Front
- Back
|
Gerhard Domagk
|
discovered that prontosil (red
dye) inhibits G+ bacteria |
|
|
Ernest Fourneau
|
discovered sulfanimide portion
of prontosil had antimicrobial activity – led to development of SULFANIMIDES (sulfa drugs) |
|
|
A. Fleming
|
discovered penicillin
|
|
|
Ernest Chain &
Howard Florey |
isolated penicillin and developed methods of mass production – saved many lives during WWII
|
|
|
Explain how semisynthetic and synthetic antimicrobials differ from antibiotics.
|
Antibiotic– Chemical substance produced by
microorganisms which have capacity to inhibit the growth of or kill microorganisms • Synthetic drug– Chemical agents made in the lab • Semisynthetic drug– Synthetic precursor given to micoorganism which completes synthesis of antibiotic with its metabolism |
|
|
Explain the principle of selective toxicity.
|
The property of an antimicrobial drug to be
toxic to the microbe while being nontoxic to the host. |
|
|
List five mechanisms by which antimicrobial drugs affect the growth of pathogens.
|
– Range of different microbes against which an antimicrobial agent acts
– Broad spectrum – agents effective against a great number of microorganisms from a wide range of taxonomic groups, including both G+ and G- (Erythromycin – works on G+, G-, chlamydias & rickettsias) – Narrow spectrum – agents effective on small number of organisms or a single taxonomic group (Penicillin mostly limited to Grampositive bacteria) –Broad spectrum useful when client seriously ill with infection caused by an unidentified organism –If identify of causative agent known a narrow-spectrum drug should be used • Minimizes destruction of microflora of host • Decreases change of resistance |
|
|
Describe the actions of drugs that affect the cell wall of bacteria.
|
• Many bacterial and fungal cells have external cell wall; animal cells lack cell wall
• Inhibiting cell wall synthesis selectively damages bacterial and fungal cells • G+ particularly susceptible |
|
|
Give examples of drugs that affect the cell wall of bacteria.
|
Penicillin, cephalosporin,
bacitracin, vancomycin – destroy peptidoglycan crosslink and thus kill bacteria (but not fungus or archae)• β-lactams most prominent (penicillins & cephalosporins) |
|
|
Give examples of drugs that inhibit protein synthesis in bacteria.
|
• Prokaryotes have 70 S
ribosome (30S and 50S subunits) • Eukaryotes have 80 S ribosome (40S and 60S subunits) • Aminoglycosides (streptomycin) act on 30S subunit to disrupt translation • Tetracyclines blocks docking site of tRNA to stop translation Chloramphenicol acts on 50S portion to inhibit translation • Macrolides (erythromycin) prevent movement of ribosome by binding onto different portion of 50S subunit of ribosome |
|
|
Give examples of drugs that disrupt the cytoplasmic membranes of bacteria.
|
• Polyenes (amphotericin B) attach to constituent of lipid membranes of fungus
• Polymyxin act as a detergent to distort cell membranes of bacteria; G- bacteria are particularly susceptible to polymyxins (Pseudomonas aeruginosa) |
|
|
Inhibitors of Cell Wall Synthesis
|
– Penicillins (Penicillium notatum)
• Penicillin G – parenteral administration; streptococci, meningococci, pneumococci, clostridia, spirochetes, • Methicillin, nafcillin, oxacillin, ampicillin, amoxicillin, carbenicillin, ticarcillin • Generally nontoxic but large doses toxic to kidneys and nervous system – Cephalosporins (Cephalosporium fungus) • Natural cephalosporins limited in antimicrobial activity • Semisynthetics: cephalexin (Keflex), cephradine, cefadroxil, cephalothin • ¼ - 1/3 of pharmacy expenditures in U.S. hospitals • Adverse effects tend to be localized – irritation at injection site, nausea, vomiting, diarrhea – Carbapenems (primaxin, cilastatin sodium) – broad spectrum – Bacitracin (from Bacillus licheniformis) used only in lesions and wounds of skin; toxic to kidneys – Vancomycin (Streptomyces orientalis) not effective against G-; used for MRSA and pseudomembranous colitis; IV; fairly toxic – kidney damage and hearing loss |
|
|
Give examples of drugs that inhibit nucleic acid synthesis of bacteria.
|
• Rifamycin family inhibits transcription of bacterial RNA by binding to RNA polymerase
• Rifampin more toxic to prokaryotes than to eukaryotic host; used against Mycobacteruim tuberculosis • Clofazimine binds to DNA of Mycobacterium leprae and prevents normal replication and transcription |
|
|
Disrupters of Cell Membranes
|
– Polymyxins A, B, C, D, E (Bacillus polymyxa)
– B and E most common clinically – Applied topically (often with bacitracin) to treat G- skin infections (esp. Pseudomonas) – IV administration to hospitalized clients so kidney function can be monitored – Can cause numbness in extremities, serious kidney damage, respiratory arrest |
|
|
Explain what harmful side effects can occur when taking tetracycline and what things should be avoided while taking tetracycline?
|
• Widest spectrum of activity
• Destroy normal intestinal microflora • Produce GI disorders including liver damage • Interfere with oral contraceptives • Stain of teeth occurs when children <5 receive tetracycline or when pregnant women take it during last half of pregnancy |
|
|
Describe what characteristics an ideal chemotherapeutic agent would have.
|
• Solubility in body fluids
• Selective toxicity • Toxicity not easily altered • Nonallergenic • Stability: maintenance of a constant therapeutic concentration in blood and tissue fluids • Resistance by microorganisms not easily acquired • Long shelf-life • Reasonable cost |
|
|
Describe what is unique about Clostridium difficile and the clinical condition it causes.
|
• Only organism recognized as a common cause of antibiotic-associated colitis
Causes intestinal disease only in patients to whom antibiotics have been administered Once established difficult to remove • May persist in hospitals and nursing homes for months or years – Floor, bedpans, linens, even walls • Endospores germinate once drug is discontinued |
|
|
• Inhibitors of Protein Synthesis
|
– Aminoglycosides (Streptomyces & Micromonospora)
• Streptomycin, neomycin, kanamycin, amikacin, gentamicin, tobramycin, netilmicin • Can act synergistically with other drugs • IM or IV; can damage kidneys – Tetracyclines (Streptomyces) • Tetracyclin, chlortetracycline (Aureomycin), oxytetracycline (Teramycin), doxycycline (Vibramycin) • WIDEST SPECTRUM OF ACTIVITY • Easily absorbed • Mild to severe toxic effects – Chloroamphenicol (Streptomyces venezuelae) • Treat typhoid fever, infections due to penicillin-resistant strains of meningococci, brain abscesses, severe rickettsial infections – Macrolides (Streptomyces erythreus) • Erythromycin, azithromycin (Zithromax), clarithromycin (Biaxin) – Lincosamides • Lincomycin, clindamycin |
|
|
Inhibitors of Nucleic Acid Synthesis
|
– Rifampin (Streptomyces mediterranei)
• Blocks RNA transcription • Used to treat tuberculosis • Can cause liver damage – Quinolones • Nalidixic acid - blocks DNA replication • Norfloxacin, ciprofloxacin (Cipro), enoxacin • Used to treat traveler’s diarrhea and UTIs |
|
|
Red Man Syndrome
|
• Rifampin causes ‘red man syndrome’
• With high doses of rifampin, colored metabolic products of the drug accumulate and are eliminated through sweat glands – Bright orange or red urine, tears, saliva – Skin looks like boiled lobster – Skin secretions can be washed way – Liver damage is slowly repaired |
|
|
List six clinical considerations when prescribing antimicrobial drugs.
|
?
|
|
|
Give examples of drugs that inhibit metabolic pathways of bacteria.
|
?
|
|
|
Distinguish between narrow-spectrum and broad-spectrum drugs.
|
?
|
|
|
Describe when you would choose a narrow spectrum, rather than a broad-spectrum antibiotic, and explain why.
|
?
|
|
|
Describe what is meant by the term resistant as it relates to antimicrobial drugs.
|
– microorganisms once susceptible to action of antibiotic is no longer affected by the drug
|
|
|
Discuss the factors which contribute to antibacterial drug resistance.
|
Globalization
• Widespread misuse of antimicrobial drugs • Antibiotics/antibacterial drugs in animal feed • Unnecessary prescriptions • Unfinished prescriptions |
|
|
Describe the role that spontaneous mutations play in the development of antibacterial drug resistance.
|
?
|
|
|
Describe R plasmids and their role in antibacterial drug resistance.
|
?
|
|
|
Describe the four mechanisms by which microorganisms can become resistant to antimicrobial drugs.
|
Nongenetic
– Microorganisms persist in tissues out of react the antimicrobial agents; evasion (tuberculosis) – L-forms • Genetic – Spontaneous mutations – Acqusition of extrachromosomal DNA • R plasmids (6 – 7 genes; each of which confers resistance to different antibiotic) • R plasmids transferred by transduction and conjugation |
|
|
Define the term superbug.
|
Multi-drug resistant organisms (MDRO’s)
• 2.5 million cases worldwide • 100,000 deaths – MRSA • VRSA – VRE – NDM-1 (Klebsiella pneumoniae) – Resistant Acentobacter baumanii – Resistant E. coli – XDR - tuberculosis |
|
|
Describe some of the ways by which antibacterial drug resistance can be limited.
|
– Maintaining high levels of antibiotics in a client long
enough to kill all pathogens, including resistant mutant, or to inhibit them so the body’s defenses can kill them – Administering two-antibiotics so they can exert an additive effect (synergism) – Antibiotics should be restricted to essential uses only |
|
|
Define the terms synergism and antagonism as they relate to antibacterial drug resistance.
|
• Synergism – the additive effect when two antibiotics
are administered at the same time – Streptomycin + penicillin – damage to cell wall by penicillin lets streptomycin into the bacterial cell better – Augmentin (clavulanic acid + amoxicillan) – clavulanic acid binds tightly to β-lactamases and prevents them from inactivating the amoxicillin) • Antagonism - when some drugs are less effective when used in combination than when used alone – Tetracycline (inhibit growth) + penicillins (require growth to be effective) |
|
|
MDROs
|
VRE
– UTI – Meningitis – Mortality rate if in bloodstream = 40% • NDM-1 – Klebsiella pneumoniae – Bloodstream – Meningitis – Mortality rate = 50% • Resistant E. coli • Resistant A. baumanii – Immunosuppressed patients – Invasive treatments – CNS infections, meningitis, ventriculitis – Blood, UTIs, pneumonia – Mortality rate ~80% |
|
|
Drugs in Animal Feed
|
• Antibiotics have been used in animal feed for ~55 years
– 2 – 50 grams/ton for improved growth – 50 – 200 grams/ton for disease control • Animals shed antibiotic resistant bacteria in feces • Antibiotic resistant bacteria spread to humans in contact with feces • FDA – fluoroquinolones are a “significant cause” of Campylobacter bacterial infections of the digestive tract – Most acquired by eating antibiotic-fed chicken – 1999 – 9,000 cases – 2000 – 11,000 cases |
|
|
Cross Resistance
|
• When resistance to one drug may lead to
resistance to similar drugs |
|
|
List and discuss the five fundamental requirements for a pathogen to successfully infect a host.
|
1. Enter the host (portal of entry)
2. Establishment 3. Avoid, evade, or compromise the host’s defenses 4. Damage the host (virulence factors) 5. Exit the host (portal of exit) |
|
|
Identify and describe the portals through which pathogens invade the body.
|
– Contamination
• Microbes present in or on body – Infection • Successful invasion of body by a pathogenic microorganism – Disease • Any adverse internal condition severe enough to interfere with normal function |
|
|
Identify and describe the portals of exit that pathogens take from the host’s body.
|
• Secretions
– Eyes (tears) – Ears (wax) – Nose – Mouth (saliva, sputum) • Skin – flakes or blood • Blood – Needles, bites, wounds • Vaginal secretions/semen • Excreted body wastes – Urine, feces, sweat |
|
|
Explain how microbes adhere to host cells and why this is important to pathogenicity.
|
• Adhesion
• Fimbriae, flagella, glycocalyx • Spirochetes • Adhesins • Adhesion factors – Attachment proteins • Viruses & bacteria • Ligands that bind to receptor on host cell |
|
|
List the types of adhesion factors and the roles they play in infection.
|
?
|
|
|
Define ID50 and LD50 and describe their role in the virulence of pathogens.
|
• Lethal dose 50 (LD50)
• Infectious dose 50 (ID50) • Degree of virulence |
|
|
Describe the different strategies pathogens employ to avoid, evade or compromise host defense systems.
|
• Capsules
• Cell Walls – M protein |
|
|
Explain how capsules and cell wall components contribute to pathogenicity.
|
?
|
|
|
Describe the role of enzymes (leukocidins, hemolysis, coagulase, kinases, hysaluronidase and collagenase) in a pathogen’s virulence.
|
?
|
|
|
Endotoxins
|
– Lipid A (Gram -)
– Chills, fever, muscle weakness, aches – Disseminated intravascular clotting |
|
|
The first antibiotic discovered was
|
Penicillin
|
|
|
Most of the available antimicrobial agents are effective against
|
bacteria
|
|
|
Which of these doesn't belong:
Monobactam Cephalosporin Bacitracin Steptomycin Penicillin |
Steptomycin
|
|
|
Which has fewest side effects:
Penicllin Chloramphenicol Tetracycline Erythromycin Streptomycin |
Penicillin
|
|
|
Which of these antimicrobial agents is recommended for use against fungal infections?
Amphotericin B Penicillin Bacitracin Cephalosporin Polymyxin |
Ampothericin B
|
|
|
More than half of our antibiotics are
|
Produced by bacteria
|
|
|
Which of the following drugs is NOT used primarily to treat tuberculosis?
Sulfonamide Rifampin Isoniazid Ethambutol |
Sulfonamide
|
|
|
The antimicrobial drugs with the broadest spectrum of activity are
|
Tetracyclines
|
|
|
Which organism would most probably be sensitive to natural penicillin?
|
Steptococcus pyogenes
|
|
|
Streptomyces bacteria produce which antibiotics?
|
erythromycin, nystatin, kanamycin, rifampin
|
|
|
Broad-spectrum antibiotics
|
react with G+ bacteria, G- bacteria and Pseudomonas
|
|
|
A bacteriostatic antibiotic
|
inhibits bacterial growth but does not kill the organism
|
|
|
The difference between peniillin and ampicillin is
|
the side chains affixed to the core ring structure
|
|
|
B-Lactamase is
|
an enyme that cleaves the ring structure of penicillin
|
|
|
All of these are targets for antibiotics except:
the cell wall bacterial ribosomes the glycocalyx the plasma membrane of the bacteria nucleic acids |
the plasma membrane of the bacteria
|
|
|
Carbapenem antibiotics have
|
a different ring structre from penicillin's
|
|
|
The antibiotic isoniazid is
|
used with ethambutol and rifampin for the treatment of tuberculosis
|
|
|
Protein synthesis is
|
a selective target
|
|
|
All target the ribosome, except:
Streptomycin Tetracycline Penicillin Chloramphenicol Erythromycin |
Penicillin
|
|
|
Sulfa drugs target
|
metabolism
|
|
|
resistance to antibiotics is facilitated by which of the following?
the antibody response host immunity frequency of use the inflammatory response |
Frequency of use
|
|
|
All of the following are mechanisms of resistance except:
activation of the antibiotic efflux pumping modification of the target structure inactivation of the antibiotic |
modification of the target structure
|
|
|
the second most often used mechanism in development of antibiotic resistance is
target modification efflux pumping destruction of the antibiotic enhancement of antibiotic activity |
efflux pumping
|
|
|
MRSA stands for?
|
Microbial-resistant Staphylococcus aureus
|
|
|
Increased use of antibiotics can be attributed to the following:
An increasing number of large cities Emerging infectious diseases Increased levels of immunodeficiency diseases all of the above |
All of the above
|
|
|
The best way to deal with antibiotic resistance is to use
More antibiotics Less antibiotics Combination of Antibiotics None of the above |
Combination of antibiotics
|
|
|
the useful life of antibiotics can be extended by
increasing the doses using more broad spectrum antibiotics using combination of antibiotics none of the above |
using combinations of antibiotics
|
|
|
you nicked yourself while shaving and it has become infect. which of the following portals of entry did the pathogen most probably use?
GI tract Skin Respiratory tract Genitourinary tract Exotoxin tract |
Skin
|
|
|
You overhear that the microbe causing an infection in your patient got into the body via the parental route. Meaning...
|
it entered through a break in the skin
|
|
|
A pathogen has entered the body. All of these will have a role in its establishment except:
using fimbriae to attach to cell receptors Releasing several exotoxins to destroy host cells Using adhesins to attach to tissues Creating a biofilm on a body surface Releasing endotoxin that will cause clotting |
Releasing endotoxin that will cause clotting
|
|
|
The LD 50 of a pathogen is the number of organisms required to
|
kill 50% of the host
|
|
|
Organism A has an ID 50 of 20 cells, whereas organism B has an ID 50 of 100 cells. What do you make of this?
|
Organism A could be considered more virulent than organism B
|
|
|
A bacterial toxin that causes damage to the plasma membrane of host red blood cells which results in lysis is
|
Hemolysin
|
|
|
A bacterial enzyme that breaks down connective tissue is
|
Hyaluronidase
|
|
|
An invasin would be used by a microbe to
|
Change the structure of actin filaments in host cells
|
|
|
Your culture of cells are producing exotoxins. The organisms are probably
|
G+ bacteria
|
|
|
Three types of exotoxins are
|
Neurotoxins
Cytotoxins Enterotoxins |
|
|
Botulism toxin is
|
A neruotoxin
|
|
|
Many people refer to tetanus infection with the pathogen C tetani as lockjaw. Explain why
|
these bacteria produce a toxin that causes jaw muscles to remain contracted
|
|
|
Describe endotoxins
|
they are toxins found on G- cell walls
|
|
|
Your patient has DIC. The disease is caused by
|
Endotoxins
|
