Lecture 16 Flashcards
Antibiotics (56 cards)
1
Q
What are some virulent factors of bacteria?
A
- fimbriae pilli
- flagella
- secretion of toxins and enzymes
- invasion
2
Q
What are fimbriae and pilli?
A
- hair like projections from the surface of bacterial cells
- allow them to attach to certain sites and not wash away
3
Q
What are flagella?
A
- live in aqueous envir. and need to move to survive
- flagellum allows them to “swim”
4
Q
virulences of toxins and enzymes secreted by bacteria
A
- can have wide array of effects = nausea, vomiting, diarrhea, cramps, pain, fever, paralysis
- toxins produced outside of our body can be toxic if they gain entry (ex. poisoning)
- enzymes can degrade tissues, breakdown antibodies
5
Q
Invasion of bacteria
A
- can invade our cells and “hide”
6
Q
What is gram staining of bacteria?
A
- used to classify bacteria as gram + or gram -
- tells us about the cell wall structure of bacteria (amount of peptidoglycan)
- helps us determine which antibiotic to use
7
Q
Characteristics of gram positive cells?
A
- thick peptidoglycan wall that stains purple
- techoic acids: provide rigidity to cell wall
- do not have LPSs
- no outer membrane or porins
8
Q
Characteristics of gram -ve cells
A
- thin peptidoglycan layer, stains pink
- no techoic acid
- lipopolysaccharides (LPSs)- structural component of the outer membrane
- outer membrane (protects from bile salts and detergents)
- porins (allow certain sugars, ions, an amino acids to enter bacteria)
9
Q
What are some common signs of infection?
A
- fever
- overall malaise
- local redness
- swelling
- increased respiratory rate
- tachycardia
10
Q
What is selective toxicity with bacterial infections?
A
- means therapy is able to destroy bacteria without harming the host
- produced by targeting differences between the cellular chemistry of bacteria and humans
11
Q
How can antibiotic therapy produce selective toxicity?
A
- disrupting the bacterial cell wall
- targeting enzymes that are unique to bacteria
- disrupting bacterial protein synthesis (ribosomes btwn bact. and humans are diff.)
12
Q
What are some questions to consider when selecting an antibiotic?
A
- has the infectious bacteria been identified?
- bacterial sensitivity to the antibiotic?
- can the antibiotic access the site of infection?
- is the patient able to battle the infection?
13
Q
How do we identify the bacteria?
A
- gram test for info on structure
- culturing the bacteria (best option)
- cultures rarely taken so its difficult
- cultures can be used to determine minimum inhibitory concentration (MIC) and the minimum bactericidal concentration (MBC) of antibiotic drugs
14
Q
What are bacteriostatic antibiotics?
A
- stops the growth and replication of bacteria
- stops spread, lets immune system attack and and remove
15
Q
What are bactericidal antibiotics?
A
- drugs that kill the bacteria
16
Q
Examples of infections that require careful selection of antibiotics
A
- meningitis
- urinary tract infections
- osteomyelitis
- abscesses
- otitis media
17
Q
What is meningitis?
A
- infection of meninges (membranes that cover the brain and spinal cord)
- effective treatment requires an antibiotic that penetrates the meninges
18
Q
What is a Urinary Tract Infection (UTI)?
A
- occur when bacteria enter any part of the urinary system
- need antibiotics which enter the urinary system
19
Q
What is Osteomyelitis?
A
- infection of the bone
- few antibiotics able to enter bone
20
Q
What are abscesses?
A
- occurs when pus or other infected material collect under the skin
- difficult to treat bc they are poorly perfused with blood
21
Q
What is otitis media?
A
- infection of the middle ear
- more common in children
- antibiotics cannot reach this area and are ineffective
22
Q
What affects the ability of the patient to battle infection?
A
- immunological state
- only bactericidal antibiotics are effective in patients with compromised immune systems (AIDs; organ transplant; cancer chemotherapy)
23
Q
what are some common complications with antibiotic therapy?
A
- resistance
- allergy
- serum sickness
- superinfection
- destruction of normal bacterial flora
- bone marrow toxicity
24
Q
What is bacterial resistance?
A
- bacteria that did respond to an antibiotic and have lost sensitivity over time
- most bacteria show some resistance
25
What are 3 mechanisms by which antibiotic resistance can be acquired?
1. reduction of the drug at the site of the target (decreased uptake + increased efflux pump activity)
2. increased drug inactivation (have enzymes that inactivate drugs ex. beta lactamase)
3. alteration of the bacterial target (may evolve mutations)
26
What are 4 ways to prevent resistance?
1. prevent infection
2. diagnose and treat infection effectively
3. use antibiotics wisely
4. prevent transmission
27
Allergy to antibiotics
- most common: penicillin
| - treat with diphenhydramine or epipen (epinephrine)
28
Signs of antibiotic allergy?
- hives (urticaria)
- anxiety
- swelling of hands, feet, throat
- difficulty breathing
- hypotension
29
What is serum sickness?
- similar to an allergy but develops 1-3 weeks after antibiotic exposure
-bodys immune system improperly identifies a drug/drug-protein complex as harmful
= immune reaction (inflammation, fever, hives, rash, joint pain, itching, angioedma, enlarged lymph nodes)
30
How do we treat serum sickness?
- antihistamine for itching
- analgesics for pain
- corticosteroids for inflammation
31
What is a superinfection?
- special type of resistance
- new infection that develops during the course of antibiotic therapy (due to broad spectrum antibiotics killing normal bacterial flora = new bacteria can flourish)
- difficult to treat
32
What are some of the consequences (other than superinfection) of the destruction of normal bacterial flora?
- patients taking warfarin at increased risk of bleeding bc vitamin K low when intestinal bacteria killed
- increase blood drug levels and toxicity due to decreased metabolism of drugs in intestine
- decrease of enterohepatic recycling = decreased drug therapy
33
What is bone marrow toxicity?
- rare but serious side effect of antibiotic therapy
| - causes aplastic anemia, thrombocytopenia, agranulocytosis, leukopenia
34
What do penicillin antibiotics target?
- transpeptidases form cross bridges between peptidoglycan strands of poptidoglycan layer of cell wall making it strong
- autolysins= bacterial enzymes that degrade peptidoglycan cell wall
- T + A = penicillin binding proteins and are primary target
35
What is the mechanism of action of penicillin?
- inhibit transpeptidases and activate autolysins = disrupts cell wall synthesis and promotes cell wall destruction
- bacterial cells take up excess water and die (lyse)
- is bactericidal, effective against bacteria that is actively growing and dividing
- more effective against gram + bc no outer mem.
36
What is penicillin resistance caused by?
1. inability to reach its target
2. inactivation
3. mutations in PBPs that = low affinity for penicillins
37
What is the predominant mechanism of resistance?
inactivation by enzymes called beta lactamases which target beta lactam ring of penicillins
- now have beta lactamase inhibitors which block this enzyme
38
What are the 4 different classes of penicillins?
1. narrow spectrum
2. narrow spectrum penicillinase resistant
3. broad spectrum
4. extended spectrum
39
Characteristics of narrow spectrum penicillins
- good for gram +
- IV or IM admin (destroyed by gastric acid)
- treat pneumonia and meningitis
- drug allergy is primary adverse effect
40
Characteristics of narrow spectrum penicillinase resistant penicillins?
- have altered side chain = not susceptible to inactivation by beta lactamase enzymes
- can treat penicillinase producing staphylococci
- less effective vs non-penicilliase producing bacteria
- no good for abscesses or bone
- only some resistant bacteria
41
Characteristics of broad spectrum penicillins?
- good for both gram +/-
- able to penetrate the outer mem of gram -
- readily inactivated by beta lactamases
42
Characteristics of extended spectrum penicillins
- good for gram +/-
- effective for treating pseudomonas aeruginosa (resistant to all other pen's)
- susceptible to degradation by beta lactamases
43
What are cephalosporins?
- same mechanism of action as penicillin (so good replacement for those with pen allergy)
- are bactericidal and have 4 generations
- from 1 -4th = increase in activity against gram -, increase destruction by beta lactamases, increase ability to penetrate the cerebrospinal fluid
- adverse effect: allergy
44
What is vancomycin?
- potentially toxic, only used to treat serious infections
- inhibits cell wall synth. by binding to precursors of cell wall synth to block the transglycosylation step
- may cause otoxicity and "red person syndrome"
45
What are tetracyclines?
- protein synthesis inhibitors
- bring to the 30S ribosomal subunit of bacteria = prevent the addition of amino acids to the peptide chain
- broad spectrum, bacteriostatic
46
What are the adverse effects of tetracyclines?
- GI irritation
- photosensitivity
- susceptible to superinfection
47
What are macrolide antibiotics?
- protein synthesis inhibitors
- block the 50S ribosomal subunit of bacteria = block addition of amino acids to the peptide chain
- broad spectrum and bacteriostatic
48
What are the adverse effects of macrolide antibiotics?
- GI upset
| - QT interval prolongation
49
What are oxazolidinones?
- bacteriostatic protein synthesis inhibitors
- bind to specific region of the 50S ribosomal subunit to inhibit protein synthesis
- narrow spectrum, gram +
- reserved for treating MRSA and vancomycin resistance enterococci (VRE)
50
What are the adverse effects of oxazolidinones?
- reversible myelosuppression
51
What are aminoglycosides?
- bactericidal, narrow spectrum, gram -, protein synthesis inhibitors
- act by binding to the 30S ribosomal subunit to prevent protein synthesis
- rapidly lethal to bacteria (mechanism unknown)
52
what are the adverse effects of aminoglycosides?
- irreversible otoxicity
| - reversible nephrotoxicity
53
What are sulfonamides and trimethoprim?
- survival of bacteria dependent of synthesis of folic acid to incorporate into DNA
- act at different stages to block the synthesis of folic acid
- often given in combo and are bactericidal
54
What are the adverse effects of sulfonamides and trimethoprim?
- hypersensitivity rxns such as fever and photosensitivity
| - small risk of severe hypersensitivity rxn called Stevens-Johnson Syndrome
55
What are fluoroquinolones?
- inhibit DNA replication by inhibiting DNA gyrase and topoisomerase IV
- bactericidal and broad spectrum
- adverse effects: GI symptoms
56
What is isoniazid?
- primary treatment for tuberculosis
- inhibits the synthesis of mycolic acid (unique to tuberculosis bacteria cell wall)
- adverse effect: peripheral neuropathy and hepatotoxicity
