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;
58 Cards in this Set
- Front
- Back
size range for bacteria
|
0.2 - 2.0 mcm
|
|
variation in form and shape within a single species
|
pleomorphism
|
|
strepto- means
|
long string
|
|
staphylo- means
|
cluster like grapes
|
|
4 steps to gram staining. gram positive is ___ and gram negative is ___
|
crystal violet, gram iodine, decolorizer, sarafin red
g+ is purple, g- is red |
|
3 features of Acid Fast staining Mycobacterium (TB, leprosy)
|
- gram positive
- thick lipid layer blocks other stains and protects against acidic or alkalinic env. - slow growth |
|
pro-typical alkaphilic bacteria
|
Vibrio Cholerae (cholera from flooding)
|
|
__ like the cold
__ moderate temp. __ high temp |
psychrophiles
mesophiles thermophiles |
|
example of a hospital acquired obligate aerobe (some say it has fruity smell)
|
Pseudomonas
|
|
grow best in low oxygen environment
|
microaerophile
|
|
thrive in low oxygen, high carbon dioxide
|
capnophiles
|
|
protein secreted by many species of bacteria to obtain iron from the environment
|
siderophore
|
|
attacks cell walls
|
lysozyme
|
|
Are the following found in gram + or -
PEPTIDOGLYCAN TEICHOIC ACIDS OUTER MEMBRANE LIPOPOLYSACCHARIDE PERIPLASMIC SPACE |
PEPTIDOGLYCAN (gram±)
TEICHOIC ACIDS (gram +) OUTER MEMBRANE (gram -) LIPOPOLYSACCHARIDE (gram -) PERIPLASMIC SPACE (gram -) |
|
penecillin prevents the linking of
|
peptidoglycan
|
|
Key point:
toxin in gram negatives |
LIPOPOLYSACCHARIDE
ENDOTOXIN USED TO IDENTIFY GRAM NEGATIVES PART OF CELL WALL RELEASED WITH DEATH OF BACTERIA POLYSACCHARIDES REPEATING SIDE CHAINS UTILIZED IN IDing GRAM NEGATIVES LIPID A – TOXIC PROPERTIES OF GRAM NEGATIVES |
|
worsening list of effects of endotoxin mediated toxicity
|
fever
leukopenia - leukocytosis thrombocytopenia (marked by peticia) vasodialation - hypotension shock death |
|
with ___ temp spikes with ___ fever then temp usually drops
|
gram+, gram-
|
|
main organisms for sporulation
|
bacillus and clostridia
|
|
impetus for sporulation
|
decreased nitrogen or carbon
|
|
can spores reproduce
|
no
|
|
outer layer of spore is made of
|
keratin
|
|
tennis racket shaped spores
|
claustridia
|
|
one organism benefits and the other neither benefits nor is harmed
|
commenslaism
|
|
both organisms benefit
|
mutualism
|
|
one organism benefits one is harmed
|
parasitism
|
|
microorganisms found in or on the body that do not normally cause disease
|
Normal Microflora
|
|
organisms that are always present on or in the body
|
Resident Microflora
|
|
microflora present temporarily and under certrain conditions
|
Transient Microflora
|
|
resident or transient microflora that can cause disease under certain conditions or in certain locations in the body
|
Opportunists
|
|
___ = Spreading factor
___ – Lyse RBCs ___ – Destroy neutrophils ___ – Accelerates blood clotting ___ – Digests blood clots and helps pathogens spread to body tissues |
HYALURONIDASE = Spreading factor
HEMOLYSINS – Lyse RBCs LEUKOCIDINS – Destroy neutrophils COAGULASE – Accelerates blood clotting STREPTOKINASE – Digests blood clots and helps pathogens spread to body tissues |
|
___ is toxin secreted by gram positive
|
exotoxin
|
|
___ = bacteria killed
___ = bacterial growth inhibited |
Bacteriocidal (penecillin),
Bacteriostatic (tetracycline) |
|
antibiotic levels must be above ___ to be effective
|
minimum inhibitory concentration (MIC)
|
|
Describe antibiotic types:
Type I Type II Type III |
Type I - concentration dependent, persistent effects
Type II - time dependent, minimal persistent effects Type III - concentration and time |
|
describe the factors promoting antibiotic resistance
|
Improper medical use - 100 million courses per year, half are unnecessary, unwarranted prophylaxis, insufficient dose/selection, poor patient compliance
Agricultural use - half of antibiotics in US used for growth promotion and prophylaxis |
|
Methods of bacterial gene transfer
__ = take up DNA __ = bacterial sex __ = via virus |
transformation
conjugation transduction |
|
List the 4 main mechanisms of antibiotic resistance
|
1. Limit access (don’t let it in)
2. Inactivation (destroy it) - cross-resistance 3. Modification of target (make obsolete) 4. Active efflux (pump it out) = multi drug resistance (MDR) |
|
Consider steps you can take to reduce resistance risks
|
wash hands
do not accede to patients' demands use narrow spectrum isolate patients with MDR familiarize with local data |
|
List the 5 main targets of antibiotics
|
1. Cell wall
2. Cell membrane 3. Protein synthesis 4. Nucleic acid synthesis 5. (Metabolic pathways) |
|
Beta-lactams examples and mech. of action
|
penicillins
cephalosporins carbapenems monobactams Inhibit transpeptidation, blocks peptidoglycan crosslinking |
|
Glycopeptides (vancomycin)
|
Mainly bacteriocidal, G+ (size limits target access)
Bind D-Ala-D-Ala portion of UDP-NAM pentapeptide Prevents transpeptidation (also transglycosylation) Useful against multi-drug resistant bacteria and MRSA |
|
Cycloserine
|
G-
Structural analog of D-Ala that inhibits its synthesis High toxicity, used in some TB cases. |
|
Bacitracin
|
Broad spectrum (G+)
Interferes with recycling of bactoprenol (a phospholipid carrier in the synthesis of peptidoglycan). High toxicity limits use to superficial skin infections. |
|
Polymyxin
|
Broad spectrum (G-)
Disrupts cell membrane Similarity of bacterial and eukaryotic membranes gives poor selective toxicity Combination therapy with bacitracin to kill G+ and G- Antiseptic/disinfectants often target cell membrane, particularly detergents |
|
Rifamycins (rifampin, rifabutin)
|
Bacteriocidal, mainly broad spectrum
Bind β subunit of bacterial RNA polymerase inhibit initiation Main therapeutic use treatment of tuberculosis Rif is bright orange Turns patients orange! (urine, saliva, sweat) |
|
Quinolones (nalidixic acid)
|
Targets DNA - Bacteriocidal, narrow spectrum, Gram-negative UTI
|
|
Fluoroquinolones (ciprofloxacin)
|
Bacteriocidal, broad spectrum G+&G-
Impair DNA gyrase causing destruction of cellular DNA Side affects limit use in children and pregnant women |
|
Metronidazole
|
Targets anaerobes, microaerophiles, and some protozoa
Once activated, metronidazole can bind and break DNA May also disrupt electron transport chains “Mutagenic” potential originally raised concern (You do not want YOUR DNA broken) Useful for ulcers caused by microaerophile Helicobacter pylori and AAD caused by Clostridium difficile |
|
Aminoglycosides (kanamycin, gentamicin)
|
Bacteriocidal, broad spectrum
Prolonged use may cause hearing loss Bind 30S, block elongation Empirical treatment of severe infections Resistance uncommon |
|
Tetracyclines
|
Bacteriostatic, broad spectrum (diarrhea)
Prolonged use may discolor teeth Bind 30S, blocks AA-tRNA binding Excellent properties, given orally, but… overuse (acne, livestock) led to widespread resistance |
|
Chloramphenicol
|
Bacteriocidal or bacteriostatic, broad spectrum
Binds 50S, blocks peptidyl transferase Bone marrow toxicity may include direct effects and indirect effects mediated through mitochondrial ribosomes |
|
Macrolides (large ring) (erythromycin)
|
Bacteriostatic, wide spectrum
Binds 50S, prevents translocation Azithromycin Particularly effective for STD Chlamydia, gonorrhea Only 1 or 2 doses! (patient compliance, DOT), but $$$ |
|
Lincosamides (clindamycin)
|
Target protein synth - Bacteriostatic, wide spectrum (G+, anaerobes)
Similar mechanism and resistance as macrolides Useful against some protozoa and anaerobes, but… wipes out normal intestinal flora leading to antibiotic associated diarrhea or pseudomembranous colitis |
|
Streptogramins (synercid)
|
Bacteriostatic/bacteriocidal (G+)
Bind 50S, cause release of growing peptide Not used to treat humans until recently Effective against MRSA and VRE! |
|
Oxazolidinones (Zyvox)
|
New class
Narrow spectrum (G+), MRSA Bind 70S Inhibit fmet-tRNA binding |
|
Sulfonamides
|
In use since 1930s!
Analogues of PABA, a precursor of tetrahydrofolate (THF) Humans do not make THF de novo, most bacteria do THF is required to synthesize A, G, T nucleotides |
|
Trimethoprim
|
Inhibits dihydrofolate reductase recycling of DHF-THF
Both humans and bacteria do this (FYI the human enzyme is a target of anti-cancer drugs) |