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;
69 Cards in this Set
- Front
- Back
|
What are the 4 Main Antibiotic Target Sites?
|
-Cell Wall Synthesis
-Protein Synthesis -Nucleic Acid Synthesis -Cell Membrane |
|
|
Why do antibiotics that target cell wall synthesis have low toxicity for our cells?
|
Because our cells do not have cell walls
|
|
|
What are the two main types of cell wall synthesis drugs and what are some examples of each?
|
B lactams
-Penicillin -Cephalosporins -Carbapenems -Monobactams Glycopeptide antimicrobials -Vancomycin -Teichoplanin |
|
|
How do beta lacatams prevent cell wall synthesis?
|
By binding to transpeptidase (responsible for cross-linking) which prevents cross-linking. No stability!
|
|
|
How do glycopeptide antimicrobials prevent cell wall synthesis?
|
By binding to terminal AA's of PEP side chains to prevent cross-linking. Only good for gram positive bacteria.
|
|
|
What are aminoglycosides? What kind of bacteria do they work on and are they toxic to us?
|
-Bactericidal drugs that bind to either the 30s or 50s ribosome preventing complexing with tRNA.
-Work only on aerobic bacteria and there is some toxicity to us. |
|
|
What are tetracyclines? What kind of bacteria do they work on and are they toxic to us?
|
-Bacteriostatic drug that reversibly binds to 30s ribosomes preventing tRNA attachment.
-Works in both gram positive and negative bacteria -Strong affinity for tooth enamel especially in children |
|
|
What are macrolides? What kind of bacteria do they work on?
|
-Bacteriostatic drugs like erythromycin and azithromycin that bind to 50s unit in gram +/- bacteria preventing translocation (protein synthesis)
|
|
|
What are Chloramphenicols? What kind of bacteria do they work on and are they toxic to us?
|
-Reversibly binds 50s ribosomes blocking peptidyl transferase (protein synthesis)
-Readily absorbed by CNS and human cells but only ribosomes of the intracellular microbes are effected making it a minimally toxic drug |
|
|
What is clindamycin? What kind of bacteria do they work on?
|
-Bacteriostatic drug that affects protein synthesis
-Affects gram negative and positive anaerobes and mitigates toxin production by staph/strep |
|
|
What are oxazolidonones? What kind of bacteria do they work on?
|
-New drug that binds to 50s ribosome and works against gram positives resistant to other agents
|
|
|
What are quinolones?
|
-Drugs like ciprofloxacin that inhibit DNA gyrase, preventing microbial nucleic acid synthesis
-Probably toxic to ourselves since we also need gyrase |
|
|
What is metronidozole and which types of microbes does it affect?
|
-Drug that induces ss breaks in DNA
-Only affects anaerobic bacteria, fungi and parasites because the nitro group on the drug is activated only by anaerobic conditions |
|
|
What is rifampin?
|
-Nucleic acid synthesis drug that binds to the b-subunit of RNA polymerase preventing transcription
|
|
|
What are folate inhibitors?
|
-NA synthesis drugs like sulfamethoxazole that prevent amino acid and thus DNA synthesis
|
|
|
What are polymixins and why are they highly toxic to humans?
|
-Polymixins are cell membrane disruptors that act as a detergent
-Dangerous to us because we have a lot of cell membranes in the body |
|
|
What is the additive effect?
|
When each drug works NO better or NO worse alone or in conjunction with the other drug. (Get the exact effects of both drugs)
|
|
|
What is the synergistic effect?
|
-Two drugs that work better in combination than alone at the same total concentration
(Folate inhibitors sulfanilamide and trimethoprim. If sulfanilamide doesn catch it, trimeth will) |
|
|
What is the antagonistic effect?
|
-Drugs work much more poorly together than they do alone
|
|
|
What is intrinsic drug resistance?
|
-When a drug is not toxic to an organism because of some innate characteristic it possesses
|
|
|
What are the factors that can contribute to acquired drug resistance?
|
-Mutations in the organism
-Resistance from the plasmids of other organisms via conjugation (direct transfer of plasmids) or transposition (movement of pieces of DNA into another cell) |
|
|
What are the three mechanisms of resistance?
|
-enzymatic inactivation
-altered transport -altered target |
|
|
How does enzymatic inactivation cause resistance against beta-lactam antibiotics?
|
By modifying/degrading the beta lactam with beta lactamase
|
|
|
Name two altered targets for beta-lactam and describe how it adds to resistance
|
-Altered ribosomes generate new enzymes that have resistance to macrolides and clindamycin
-Topopisomerase adds resistance because there are only 4 possible hiding subunits. |
|
|
How does altered transport contribute to antibiotic resistance?
|
-Antibiotics are excluded from the cell
-Has efflux which is an important mechanism to tretracylcines, macrolides, etc |
|
|
What is the minimal inhibitory concentration (MIC)?
|
The lowest concentration of antibiotic able to inhibit growth of the microorganism. MUST BE BELOW ACHIEVABLE BLOOD LEVELS
|
|
|
Define the term resistant
|
Organisms that are not inhibited by clinically achievable doses of antimicrobial agent
|
|
|
Define the term sensitive or susceptible
|
When an organism is inhibited by clinically achievable doses of antibiotics
|
|
|
How do dilution tests work?
|
-Have several test tubes with the same concentration of microorganisms in the broth.
-Administer increasing amounts of the antibiotic to see how much is required to kill the bacteria |
|
|
How do diffusion tests work?
|
-Grow a plate with the bacteria and place either an antibiotic disk or antibiotic gradient strip onto the plate
-The MIC can be determined from the strip based upon what concentration the zone of inhibition starts at |
|
|
What is a bacteriophage?
|
-Pathogen that replicates inside bacterial cells and is made out of ss/ds RNA/DNA that is encapsulated by a protein coat
-Can be a virulent phage or temperate phage |
|
|
What is a virulent phage?
|
-A phage whose successful infection will end in cell death via lysis and the release of phage progeny
|
|
|
What is a temperate phage?
|
-A phage whose successful infection can end either in cell death via lysis or formation of a prophage
|
|
|
What is a prophage?
|
-A bacteriophage that has infected a cell and replicates within it but is not being expressed
|
|
|
What is lysogenic bacteria?
|
Bacteria that contain a prophage lying in wait
|
|
|
What is prophage induction?
|
The activation of a prophage from its latent state
|
|
|
What is a transition?
|
Purine for a purine or pyrimidine for a pyrimidine
|
|
|
What is a transversion?
|
Purine for a pyrimidine or vice versa
|
|
|
What is an inversion mutation?
|
When a segment of DNA is removed and re-inserted in the opposite orientation (flipped backwards and upside-down)
|
|
|
What are missense mutations?
|
When base substitutions in DNA result in one AA residue being switched out for another
|
|
|
What are nonsense mutations?
|
When a base substitution creates a pre-mature stop codon or changes an existing one
|
|
|
What are silent mutations
|
When a base substitution does not alter AA composition of the protein because of degeneration of genetic code
|
|
|
What are frame shift mutations?
|
When an insertion or deletion of a base or bases results in altering the reading frame of the protein
|
|
|
What are conditional lethal mutants?
|
Genes that are lethal only under certain restrictive conditions. Normally healthy under passive conditions.
|
|
|
What are temperature sensitive mutants?
|
A class of conditional lethal mutants that die in high temperatures but are fine otherwise
|
|
|
What is true reversion?
|
When a mutant strain is back mutated to form the exact restoration of the wild-type DNA sequence
|
|
|
What are mutant suppressors?
|
Secondary mutations that nullify the first. Can have intragenic (within the same gene) or extragenic (in a different gene) mutations
|
|
|
What are the three main mechanisms of antibiotic resistance?
|
-Decreased uptake or increased efflux of antibiotic
-Alteration of target site -Ability to destroy or modify antibiotic (beta lactamase) |
|
|
Describe the herpes simplex virus
|
-Has a fried egg appearance with dsDNA in an icosahedral capsid surrounded by a viral envelope
-Targets mucoepithelial cell and has is latent in neurons |
|
|
Where is HSV1 predominantly found?
|
In the oral cavity
|
|
|
Where is HSV2 predominantly found?
|
In the genitals
|
|
|
What is HSV3 commonly called and what are the usual symptoms.
|
-It is normally called Varicella-Zoster virus
-Usual symptoms are chickenpox at first and the re-occurring shingles later in life |
|
|
What are the two main diseases associated with the Varicella Zoster Virus?
|
Chickenpox and Shingles
|
|
|
What is the name of the Chickenpox vaccine?
|
Varivax
|
|
|
What is Reye's Syndrome and what is it a result of?
|
-Reye's syndrome is when the patient has acute encephalopathy (brain disease) and a fatty liver
-It is the result of infection by the varicella virus |
|
|
Describe the symptoms of HHV6 and 7 infection and explain what population is predominantly effected. Also mention what specific part of the immune system is attacked.
|
-HHV6 and 7 result in roseola infantum, encepahlitis and acute febrile illness (high fever sometimes accompanied by seizures).
-Occurs mostly in children between the ages of 1 and 3 and targets T-cells, NK cells, and salivary epithelial cells (wide tropism) |
|
|
The progression of what other disease is accelerated by infection with HHV6?
|
The HIV virus because HHV6 induces expression of CD4 which HIV attacks. Causes accelerated cell death.
|
|
|
Which HHV results in Karposi's sarcoma and which group of people is it the most problematic for?
|
Karposi's sarcoma is caused by HHV8 and is a problem for AIDS patients
|
|
|
What is Variola?
|
The poxvirus known as smallpox. Eradicated b/c of vaccine and the fact that there is no other reservoir other than in humans.
|
|
|
Describe the development of an HPV skin wart
|
-HPV infects the basal layer and begins to replicate horizontally and vertically into spinosum layer
-Replication continues pushing up into the stratum corneum (horny layer) where the titer is really high |
|
|
Describe the HPV virus
|
dsDNA w/no envelope that infects the mucosal linings in the body
|
|
|
Describe the structure of parvovirus and the common symptoms.
|
-Non-enveloped ssDNA virus. Lytic and requires a mitotically active host cell
-suppresses blood cell production -Causes "slapped cheek" facial feature |
|
|
What are the three noted complications of measels?
|
-PIE = autoimmune response vs. myelin
-MIBE = fatal encephalitis in immunocompromised individuals -SSPE = progressive mental deterioration, involuntary movements, coma, death |
|
|
What are the three symptoms a fetus may exhibit if the rubella virus crosses the placenta?
|
-Deafness
-Cataracts -Cardiac abnormalities |
|
|
How does the structure of trichophyton differ from epidermophyton and microsporum?
|
-Trichophyton have microconidia and cigar shaped macroconidia
-Epidermophyton do not have microconidia -Microsporum have few microconidia and spindle-shaped macroconidia |
|
|
What is necessary for a subcutaneous fungal infection?
|
Skin trauma
|
|
|
What are the two forms that leishmaniasis can take and which one is the infective state and which is the diagnostic state?
|
Leishmaniasis is infective in the promastigote state and is in the diagnostic state in the amastigote form.
|
|
|
What are the two virulence factors for leishmaniasis and what kind of immune response do they cause?
|
Lipophosphoglycans and acid phsophatases which stimulated Th1 cell mediated response
|
|
|
What is onychomycosis?
|
Systemic infection of the nail bed with thickening and discoloration of the nail
|
