1
Q
Who developed the idea of selective toxicity?
A
The German chemist Paul Ehrlich developed the idea of selective toxicity
2
Q
What is the principle of selective toxicity?
A
Selective toxicity is the idea that certain chemicals can be toxic to some organisms (e.g., infectious bacteria) while being harmless to other organisms (e.g., humans).
3
Q
Who first discovered penicillin and in what year?
A
Penicillin was first discovered in 1896 by Ernest Duchesne, a twenty-one-year-old French medical student.
4
Q
Why is penicillin called the first true antibiotic?
A
it is a natural microbial product
5
Q
Whose earlier work on penicillin was forgotten before rediscovery?
A
The work of Ernest Duchesne
6
Q
Who accidentally rediscovered penicillin in 1928?
A
Alexander Fleming, a Scottish biologist.
7
Q
What did Fleming observe about Penicillium notatum?
A
Penicillium notatum, a common mold, destroyed Staphylococcus bacteria in culture.
8
Q
In what year did Howard Florey and Ernst Chain purify penicillin, and where
A
1939, at Oxford University.
9
Q
From whom did Florey and Chain obtain the Penicillium culture?
A
Alexander Fleming
10
Q
What is the “zone of inhibition”?
A
a clear zone around the fungal colony where no bacteria are growing
11
Q
What caused the zone of inhibition around Penicillium?
A
due to diffusion of a substance with antibiotic properties from the fungus
12
Q
Who discovered Prontosil red and in what year?
A
Gerhard Domagk discovered it in 1927.
13
Q
What was Prontosil red originally used for?
A
It was a new dye for staining leather.
14
Q
Against which pathogens did Prontosil red protect mice?
A
. It protected mice completely against pathogenic streptococci and staphylococci.
15
Q
What was significant about Prontosil red’s toxicity?
A
It protected against pathogens without apparent toxicity
16
Q
Who demonstrated that the body metabolized Prontosil into sulfanilamide?
A
Jacques and Therese Trefouel.
17
Q
Who received the 1939 Nobel Prize in Physiology or Medicine, and for what discovery?
A
Gerhard Domagk, for the discovery of sulfonamides (sulfa drugs).
18
Q
Who isolated streptomycin and when?
A
In 1944, Selman Waksman and Albert Schatz, American microbiologists, isolated streptomycin and other antibiotics.
19
Q
From what organism was streptomycin isolated?
A
Streptomyces griseus
20
Q
What is defined as any chemical used in the treatment, relief, or prophylaxis of a disease?
A
Chemotherapeutic drug
21
Q
What is the use of a drug to prevent imminent infection of a person at risk?
A
Prophylaxis (a way to use describe the use of drug)
22
Q
What is the use of chemotherapeutic drugs to control infection
A
Antimicrobial chemotherapy
23
Q
What is the all-inclusive term for any antimicrobial drug, regardless of origin?
A
Antimicrobials
24
Q
What are substances produced by natural metabolic processes of some microorganisms that can inhibit or destroy other microorganisms?
A
Antibiotics
25
What are drugs chemically modified in the laboratory after being isolated from natural sources?
Semisynthetic drugs.
26
What are antimicrobial compounds synthesized entirely in the laboratory by chemical reactions?
Synthetic drugs.
27
(Enumeration) Differentiate between narrow-spectrum and broad-spectrum antimicrobials.
Narrow spectrum (limited spectrum): Effective against a limited array of microbial types
(e.g., mainly gram-positive bacteria).
• Broad spectrum (extended spectrum): Effective against a wide range of microorganisms
(e.g., both gram-positive and gram-negative bacteria).
28
What does the microbiologist’s definition of a chemotherapeutic agent require?
That the agent must be used for an antimicrobial purpose and excludes synthetic agents used for non-microbial diseases.
29
What term does pharmacology use for microbiologists’ chemotherapeutic agents?
Synthetic antibiotic.
30
According to microbiologists, what are antibiotics?
Antimicrobial agents produced by microorganisms that kill or inhibit other microorganisms.
31
What is the broadened definition of an antibiotic?
Any chemical of natural origin (from any type of cell) that kills or inhibits the growth of
other types of cells
32
According to pharmacologists, what does the term antibiotic refer to?
To any antimicrobial chemical used in the treatment of infectious disease.
33
Substances produced by various species of microorganisms (bacteria, fungi, actinomycetes)
that suppress the growth of other microorganisms and destroy them.
antibiotics
34
35
What additional compounds are included today under the term “antibiotics”?
Synthetic antibacterial agents, such as sulfonamides and quinolones.
36
What are chemotherapeutic agents (synthetic antibiotics)?
Antimicrobial agents of synthetic origin useful in the treatment of microbial or viral disease.
37
Give examples of synthetic antibiotics.
1. Sulfonilamides
2. Isoniazid
3. Ethambutol
4. AZT
5. Nalidixic acid
6. Chloramphenicol
38
What are semisynthetic antibiotics?
Molecules produced by a microbe that are subsequently modified by an organic chemist to
enhance their antimicrobial properties or to render them unique for a pharmaceutical patent.
39
What is the most important property of a clinically useful antimicrobial agent?
Selective toxicity
40
What does selective toxicity mean?
The antimicrobial agent acts in a way that inhibits or kills bacterial pathogens but has little
or no toxic effect on the animal taking the drug.
41
What effects can antibiotics have on microbes?
They may have either a cidal (killing) effect or a static (inhibitory) effect.
42
Differentiate between broad spectrum, narrow spectrum, and limited
spectrum antibiotics.
Broad spectrum: Effective against prokaryotes, kill or inhibit a wide range of Gram-
positive and Gram-negative bacteria.
• Narrow spectrum: Effective mainly against either Gram-positive or Gram-negative
bacteria.
• Limited spectrum: Effective against a single organism or disease.
43
What is meant by “mode or mechanism of action” of an antimicrobial agent?
refers to the antimicrobial agent’s adverse effects.
44
What are the general categories of cellular targets of physical and chemical agents?
1. Cell wall
2. Cell membrane
3. Proteins
4. Cellular synthetic processes (DNA and RNA)
5. Inhibitors of metabolic pathways (antimetabolites)
45
What are the other antimicrobial drug groups aside from antibiotics?
1. Antiviral agents
2. Antifungal agents
3. Antiprotozoal agents
4. Antihelminthic agents
46
What is the function of the bacterial cell wall?
It maintains the integrity of the cell, allowing it to keep its shape even in a hypotonic
environment.
47
What happens when the bacterial cell wall is weakened or disrupted?
It can no longer prevent the cell from bursting due to osmotic effects (water rushing into
the cell).
48
What is the key chemical feature of beta-lactam antibiotics?
They contain a 4-membered beta-lactam ring.
49
From which fungi are beta-lactam antibiotics produced?
Penicillium and Cephalosporium molds
50
(Enumeration) What two main groups of antibiotics do beta-lactams represent?
1. Penicillins
2. Cephalosporin
51
What structural feature of penicillins inhibits peptidoglycan crosslinking in bacterial cell walls?
beta-lactam ring
52
Penicillins are most effective against which organisms?
Gram-positive organisms
53
Are penicillins bactericidal or bacteriostatic?
Bactericidal, but they act only on dividing cells.
54
Why are penicillins not toxic to animal cells?
Because animal cells have no cell wall.
55
From what are beta-lactams synthesized?
From the amino acids valine and cysteine.
56
Which organisms produce beta-lactams?
Fungi (including some ascomycetes) and several actinomycete bacteria.
57
Why do penicillins not cross the blood-brain barrier in appreciable concentrations?
Because they are poorly lipid soluble.
58
When can penicillins cross the blood-brain barrier effectively?
When the meninges are inflamed (e.g., in meningitis).
59
How are penicillins excreted from the body?
They are actively excreted unchanged by the kidney.
60
What must be done to penicillin dosage in severe renal failure?
The dose should be reduced.
61
What causes bacterial resistance to penicillins?
The production of beta-lactamase, which destroys the beta-lactam ring.
62
Name bacterial species in which beta-lactamase resistance occurs.
• Staphylococcus aureus
• Haemophilus influenzae
• Neisseria gonorrhoeae
63
What properties can vary among penicillins?
They may be acid labile or acid stable, and may have a narrow or broad spectrum.
64
An acid-labile, beta-lactamase sensitive penicillin given only parenterally.
Benzylpenicillin (Penicillin G)
65
What infections is Penicillin G effective against?
A32. Streptococcus pyogenes, S. pneumoniae, Neisseria
66
What infections is Penicillin G effective against?
Streptococcus pyogenes, S. pneumoniae, Neisseria meningitidis, N. gonorrhoeae,
Treponemes, Listeria, Actinomycetes, and Clostridia
67
An acid-stable penicillin given orally for minor infections, otherwise similar to Penicillin G
Phenoxymethylpenicillin (Penicillin V)
68
How does Ampicillin differ from Benzylpenicillin?
Less active against Gram-positive bacteria but with a wider spectrum that includes
Streptococcus faecalis, Haemophilus influenzae, some E. coli, Klebsiella, and Proteus.
69
What are the properties of Ampicillin?
It is acid stable, given orally or parenterally, but is beta-lactamase sensitive
70
How does Amoxicillin compare with Ampicillin?
Similar spectrum, but better absorbed orally.
71
Why is Amoxicillin sometimes combined with Clavulanic acid?
Because clavulanic acid binds strongly to beta-lactamase, blocking its action and
extending amoxicillin’s spectrum.
72
What are the properties of Flucloxacillin?
Acid stable, given orally or parenterally, beta-lactamase resistant, narrow spectrum for
Staphylococcus aureus infections.
73
Acid labile, parenteral use only, beta-lactamase sensitive, broad spectrum including Pseudomonas aeruginosa and Proteus species,
used IV for life-threatening infections (esp. in
immunocompromised patients, together with aminoglycosides).
Azlocillin
74
What are the adverse effects of penicillins?
• Allergy: in 0.7–1.0% of patients (always ask patient history)
• Superinfections: e.g., caused by Candida
• Diarrhea: especially with Ampicillin, less common with Amoxicillin
• Rare effects: hemolysis, nephritis
75
How can Ampicillin or broad-spectrum antibiotics decrease the effectiveness of oral contraceptives?
diminishing enterohepatic circulation.
76
Give examples of anti-staphylococcus penicillins.
Oxacillin and Cloxacillin
77
What makes anti-staphylococcus penicillins special?
They are resistant against staphylococcus penicillinases
78
What group of antibiotics accounts for the majority of all antibiotics administered?
Cephalosporins
79
From what mold were cephalosporins isolated?
Cephalosporium acremonium mold
80
How is the structure of cephalosporins described?
They are synthetically altered beta-lactam structures
81
What are the main properties of cephalosporins?
• Relatively broad-spectrum
• Resistant to most penicillinases
• Cause fewer allergic reactions
82
How are cephalosporins administered?
Some are given orally; many must be administered parenterally.
83
What roots are commonly found in the generic names of cephalosporins?
“cef,” “ceph,” or “kef”
84
What structural feature gives cephalosporins their activity?
The β-lactam ring
85
Are cephalosporins bacteriostatic or bactericidal?
They are bactericidal
86
When are cephalosporins good alternatives to penicillins?
When a broad-spectrum drug is required.
87
Should cephalosporins be used as first choice drugs?
No, they should not be used as first choice unless the organism is known to be sensitive.
88
What is the mechanism of action of cephalosporins?
They are bactericidal drugs that modify cell wall synthesis.
89
How are cephalosporins classified?
• First generation: early compounds
• Second generation: resistant to β-lactamases
• Third generation: resistant to β-lactamases with increased spectrum
• Fourth generation: increased spectrum of activity
• Fifth generation: similar to 4th generation but active against MRSA (binds altered PBP2a)
90
Give examples and properties of first-generation cephalosporins.
Examples: cefadroxil, cefalexin (cephalexin), cefazolin, cefadrine.
• Most active vs Gram-positive cocci
• Alternative to penicillins for staph and strep infections
• Useful in UTIs
91
Give examples and properties of second-generation cephalosporins.
Examples: cefaclor, cefoxitin, cefuroxime.
• Active vs Enterobacteriaceae (E. coli, Klebsiella, Proteus)
• May be active vs H. influenzae and N. meningitidis
92
Give examples and properties of third-generation cephalosporins.
Examples: cefixime, cefotaxime, ceftriaxone, ceftazidime.
• Very broad spectrum
• Effective vs Gram-negative rods
• Less activity vs Gram-positive organisms
93
Give examples and properties of fourth-generation cephalosporins.
Examples: cefepime, cefpirome.
• Better vs Gram-positive than 3rd generation
• Better vs Gram-negative, esp. Enterobacteriaceae & Pseudomonas aeruginosa
• Given intravenously only
94
Give an example and properties of fifth-generation cephalosporins.
Example: ceftaroline
• Still covers Gram-positive and many Gram-negative bacteria (not Pseudomonas)
• Used for MRSA infections, community-acquired pneumonia, and skin infections
95
What are the adverse effects of cephalosporins?
• Allergy (10–20% of patients with penicillin allergy are also allergic)
• Nephritis and acute renal failure
• Superinfections
• Gastrointestinal upsets (when given orally)
96
What is vancomycin used for, and what are its limitations?
• Narrow spectrum, effective for staphylococcal infections resistant to penicillin/methicillin or in penicillin-allergic patients
• Toxic, hard to administer, and restricted in use
97
What is bacitracin, and how is it used?
Narrow-spectrum, produced by Bacillus subtilis strain, used topically in ointments.
98
What is isoniazid (INH), and how does it act?
Interferes with mycolic acid synthesis; used to treat Mycobacterium tuberculosis
infections.
Administered orally with rifampin, ethambutol, etc.
99
What is the function of the plasma membrane?
Contains cytoplasm and internal cell contents, controls passage of chemicals into/out of
the cell.
100
What happens when the plasma membrane is damaged?
Cellular contents leak out; bacteria die due to metabolic disruption or lysis.
101
What is the mode of action of antimicrobial drugs that disrupt membranes?
They disorganize bacterial membrane structure or inhibit function.
102
What drug group interacts with phospholipids causing leakage, particularly in Gram-negative bacteria?
Polymyxins (produced by Bacillus polymyxa)
103
What are the clinical uses of polymyxins?
Mainly topical; sometimes for UTIs caused by Pseudomonas resistant to gentamicin, carbenicillin, tobramycin.
104
Which antifungal drugs disrupt fungal membranes by binding to sterols?
Amphotericin B and nystatin
105
Why is protein shape important for bacterial survival?
Protein function depends on 3D structure; denaturation prevents function.
106
How do many antibiotics interfere with proteins?
They inhibit translation steps by targeting 70S ribosomes (not 80S), ensuring selective toxicity.
107
Which major antibiotic groups inhibit protein synthesis?
• Tetracyclines
• Chloramphenicol
• Macrolides (e.g., erythromycin)
• Aminoglycosides (e.g., streptomycin)
108
Antibiotics Targeting the 30S Ribosomal Subunit?
1. Aminoglycosides
• Examples: Streptomycin, Gentamicin, Amikacin, Tobramycin.
2. Tetracyclines
• Examples: Tetracycline, Doxycycline, Minocycline
109
How do aminoglycosides act?
Bind to 30S ribosomal subunit, causing misreading of mRNA.
110
What is their structure of aminoglycosides
Composed of 2 or more amino sugars + an aminocyclitol (6C) ring
111
What are aminoglycosides active against?
Broad spectrum; aerobic Gram-negative rods + some Gram-positives.
112
Antimicrobial Drugs That Disrupt Cell Membrane Function
Polymyxins, Amphotericin B, nystatin
113
Give examples and uses of aminoglycosides.
Streptomycin: bubonic plague, tularemia, TB
• Gentamicin: less toxic, against Gram-negative rods
• Tobramycin & Amikacin: for resistant Gram-negative bacteria
114
Products of various species of soil actinomycetes in genera Streptomyces and Micromonospora
Aminoglycosides
115
bind to membrane phospholipids and thereby interfere with membrane function
Polymyxin
116
disorganize the structure or inhibit the function ofbacterial membranes.
The integrity of the cytoplasmic and outermembranes is vital to bacteria, and compounds that disorganize the membranes rapidly kill the cells
Alteration of Plasma Membrane/Cell membrane inhibitors
117
produced by Bacillus polymyxa
Polymyxin
118
Antibiotics Targeting the 50S Ribosomal Subunit
**Antibiotics Targeting the 50S Ribosomal Subunit**
1. MacrolidesExamples: Erythromycin, Azithromycin, Clarithromycin
2. Lincosamides• Examples: Clindamycin, Lincomycin.
3. Chloramphenicol
4. Oxazolidinones• Examples: Linezolid.
119
Aminoglycosides like ____ _____ insert on sites on the 30S subunit and cause misreading of mRNA.
streptomycin, gentamicin
120
Products of various species of soil actinomycetes in genera
Streptomyces and Micromonospora
121
The balance between effectiveness and damage to the kidney andother organs is dangerously close, and the drug should only be given under close supervision in the hospital.
Polymyxin
122
These actions can denature, or change the shape of a protein. A denatured protein can no longer carry out its function within the cell.
Extreme heat, or certain chemicals
123
The most important antibiotics with this mode of action are the ?
**(most have an affinity or specificity for 70S, as opposed to 80S ribosomes, and they achieve theirselective toxicity in this manner)**
**tetracyclines, chloramphenicol, the macrolides (e.g., erythromycin) aminoglycosides (e.g., streptomycin)**
124
What is the mode of action of tetracyclines?
Reversibly bind to 30S ribosome;
block aminoacyl-tRNA binding to 70S ribosome.
125
What is their spectrum of activity? (Tetracyclines)
Broad spectrum; effective against intracellular bacteria.
126
What are their adverse effects?
**Tetracyclines, Minocycline and Doxycycline**
Destruction of normal intestinalflora resulting in increased secondary infections;
staining and impairment of the structure of bone and teeth.
127
What are clinical features of tetracyclines?
Tetracycline, half-lives
oxytetracycline have short
Doxycycline has a longer half-life and canbe given once per day.
These drugs are only partly absorbed
**They bind avidly to heavy metal ions** and so **absorption is greatly reduced** if taken with food, milk, antacids or iron tablets.
128
Examples and clinical pharmacokinetics of Tetracyclines
They should be taken at least half an hour before food.
§ Tetracyclines concentrate in bones and teeth.
§ They are excreted mostly in urine, partly in bile.
§ They are broad spectrum antibiotics, active against most bacteria **except Proteus or Pseudomonas.**
Resistance is frequent.
They are especially Mycoplasma, Rickettsia, Brucella infections.
indicated Chlamydia for and Their most common use today
129
130
131
Give the adverse effects of cephalosporins.
Allergy (10–20% of penicillin-allergic patients)
Nephritis and acute renal failure
Superinfections
Gastrointestinal upsets when given orally
132
What drug is **narrow-spectrum**, most effective in treatment of staphylococcal infections **in cases of penicillin and methicillin resistance,** or if the patient is allergic to penicillin?
Vancomycin
133
Which drug is toxic, hard to administer, and restricted in use
That is Non Beta-lactam Cell Wall Inhibitors
Vancomycin
134
Which narrow-spectrum antibiotic is produced by a strain of
*Bacillus subtilis* and used topically in ointment?
**Non Beta-lactam Cell Wall Inhibitors**
Bacitracin
135
What drug works by interfering with mycolic acid synthesis?
Isoniazid
136
Give the antimicrobials commonly used in combination with isoniazid to treat Mycobacterium tuberculosis
Ethambutol and rifampin
137
What is the route of administration of isoniazid in tuberculosis treatment?
Oral
138
What does the outer membrane of a cell contain?
Cytoplasm and all the cell’s internal contents
139
What happens to a cell with a damaged membrane?
Dies from disruption in metabolism or lysis
140
What gives specificity to drugs that disrupt membranes?
Differences in types of lipids in cell membranes
141
Which drug interacts with **phospholipids** and causes leakage, particularly in **Gram-negative bacteria?**
Polymyxins
142
Which drugs form complexes with sterols on fungal membranes causing leakage?
Amphotericin B and Nystatin
143
What is the only antibacterial antibiotic of clinical importance that acts by disrupting membranes?
Polymyxin
144
Which organism produces polymyxin?
Bacillus polymyxa
145
Polymyxin is effective mainly against which bacterial group?
Gram-negative bacteria
146
What is the usual route of administration of polymyxin?
Topical usage
147
They bind to membrane phospholipids and interfere with membrane function
polymyxins
148
For what infection is polymyxin occasionally given when resistant to gentamicin, carbenicillin, and tobramycin?
Urinary tract infections caused by Pseudomonas
149
What is the danger associated with systemic use of polymyxin?
Balance between effectiveness and kidney/organ damage is **dangerously close**
150
Under what conditions should polymyxin be given systemically?
Only under close supervision in the hospital
151
Give examples of macrolides.
Erythromycin, Clarithromycin, Azithromycin, Spiramycin
152
They inhibit translocation by binding to the 50S ribosomal subunit.
Macrolides
153
Spectrum of activity of macrolides.
Gram-positive bacteria, Mycoplasma, Legionella (intracellular bacteria)
154
Which macrolide is **acid labile** but given as an **enterically coated tablet?**
Erythromycin
155
How is erythromycin absorption described?
Erratic and poor
156
How is erythromycin excreted?
Unchanged in bile.
157
What process allows erythromycin to be reabsorbed lower down the GIT?
Enterohepatic circulation
158
Routes of administration of erythromycin.
Oral, parenteral
159
Where are macrolides widely distributed?
Throughout the body, **except the brain and cerebrospinal fluid.**
160
Bacteria genera covered in the spectrum of macrolides.
Staphylococcus aureus
Streptococcus pyogenes
Streptococcus pneumoniae
Mycoplasma pneumoniae
Chlamydia infections
161
Which newer macrolides may have fewer adverse effects?
Clarithromycin, Azithromycin
162
Side effects of macrolides
Nausea, vomiting
Allergy
Hepatitis
Ototoxicity
Interaction with cytochrome P450 3A4 (inhibition)
163
What is the mode of action of **chloramphenicol, lincomycin, and clindamycin?**
Bind to the 50S ribosome and inhibit peptidyl transferase activity.
164
Spectrum of activity of chloramphenicol.
Broad
165
Spectrum of activity of lincomycin and clindamycin.
Restricted range
166
What is the resistance status of these drugs?
**Chloramphenicol, Lincomycin, Clindamycin (Bacteriostatic)**
Resistance common
167
Adverse effects of chloramphenicol.
Toxic (bone marrow suppression)
Used in treatment of **bacterial meningitis** despite toxicity
168
169
From which organism was chloramphenicol originally isolated?
*Streptomyces venezuelae*
170
Is chloramphenicol still derived from natural sources?
No, no longer derived naturally.
171
What unique chemical structure does chloramphenicol have
Nitrobenzene structure
172
What does chloramphenicol block?
Peptide bond formation.
173
Why is **chloramphenicol** restricted in use?
Very toxic; can cause **irreversible damage to bone marrow.**
174
Diseases treated by chloramphenicol.
Typhoid fever
Brain abscesses
Rickettsial infections
Chlamydial infections
175
How is chloramphenicol absorbed?
Well absorbed
176
How is chloramphenicol distributed in the body?
Widely distributed, including the CNS.
177
How is chloramphenicol metabolized?
By glucuronidation in the liver
178
Major indications for chloramphenicol use
Bacterial meningitis caused by *Haemophilus influenzae*
Bacterial meningitis caused by *Neisseria meningitidis*
Bacterial meningitis when organism is unknown
Rickettsia (e.g., typhus)
179
Chloramphenicol – Adverse Effects
rare anemia
Reversible bone marrow depression
Liver enzyme inhibition
180
Clindamycin is chemically distinct but similar to which class of antibiotics?
Macrolides (e.g., erythromycin)
It is Similar to erythromycin in mode of action and spectrum.
181
How well is clindamycin absorbed?
How well does clindamycin penetrate tissues?
Rapidly absorbed.
Penetrates most tissues well, **except CNS.**
182
183
For what infection is **clindamycin** particularly useful systemically due to good bone penetration?
Staphylococcus aureus osteomyelitis.
184
Aside from osteomyelitis, what other type of infections is clindamycin useful for?
Anaerobic infections
185
Clindamycin – Adverse Effects
Diarrhea
Clostridium (Clostridioides) difficile infection
Pseudomembranous colitis (serious inflammation of the large bowel)
186
What cellular components can be damaged or destroyed by chemicals, radiation, and heat?
Nucleic acids (DNA and RNA)
187
What are two results of nucleic acid damage?
Production of **fatal mutations to the DNA**
**Interference with protein synthesis** through action on RNA
188
**Two classes of nucleic acid synthesis inhibitors** with selective activity against prokaryotes and medical utility.
Quinolones
Rifamycins
189
What is the general spectrum of quinolones?
How do quinolones kill bacteria?
Broad-spectrum agents
rapidly kill bacteria
190
191
How are quinolones absorbed?
Well absorbed after oral administration.
192
Give examples of quinolones.
Nalidixic acid, Ciprofloxacin, Ofloxacin, Norfloxacin, Levofloxacin, Lomefloxacin, Sparfloxacin.
193
From what organism are **rifamycins** derived?
Streptomyces
194
Rifampicin is a derivative of what compound?
Semisynthetic derivative of rifamycin
195
Rifampicin is active against which organisms?
Gram-positive bacteria (including Mycobacterium tuberculosis)
Some Gram-negative bacteria
196
**Bind to the A subunit of DNA gyrase(* (topoisomerase) and prevent supercoiling of DNA, thereby **inhibiting DNA synthesis.**
quinolones
197
Spectrum of activity of quinolones.
Gram-positive cocci
Urinary tract infections
198
What was the first quinolone?
Nalidixic acid
199
What is nalidixic acid used for?
urinary antiseptic and for lower urinary tract infections
200
What is Ciprofloxacin classified as?
fluoroquinolone
201
Against what organisms does **ciprofloxacin** have broad spectrum activity?
Gram-negative **bacilli** and Pseudomonas.
202
Infections ciprofloxacin can treat?
Respiratory infections
Urinary tract infections
Serious infections (**peritonitis, Salmonella)**
203
How effective is ciprofloxacin against anaerobic organisms?
Poor activity
204
Should ciprofloxacin be first choice for respiratory tract infections?
No
205
Adverse effects of quinolones.
Gastrointestinal upsets
Fluoroquinolones **may block inhibitory neurotransmitter GABA** → confusion in elderly, lower fitting threshold
Contraindicated in **epileptics**
Allergy and **anaphylaxis**
Possible damage to growing cartilage → not recommended for pregnant women and children
206
Ciprofloxacin may cause life-threatening interaction with which drug?
Theophylline
207
Rifamycins are bacteristatic or bactericidal?
(bactericidal)
208
Examples of Rifamycins.
Rifampin, Rifabutin, Rifapentine.
**Rifa tas (-ampin, -butin,-pentine)**
209
Rifamycins are active against what spectrum of organisms?
range of Gram-positive and some Gram-negative bacteria.
210
Clinical uses of Rifamycins.
Treatment of tuberculosis
Infections caused by *Staphylococcus aureus*
Infections caused by *Neisseria meningitidis*
211
What is the mode of action of Metronidazole?
Binds to DNA and blocks replication.
212
Routes of administration for Metronidazole.
Metronidazole
213
How is Metronidazole distributed in the body?
Widely distributed, including abscess cavities.
214
Metronidazole is effective against which organisms?
Anaerobic bacteria and protozoa
215
Anaerobic bacteria treated by Metronidazole.
Bacteroides, Clostridium
216
In what surgical setting is Metronidazole particularly useful?
Abdominal surgery
217
Protozoa treated by Metronidazole
Trichomonas, Giardia, Entamoeba.
218
What serious colon condition can Metronidazole treat?
Pseudomembranous colitis
219
What gastrointestinal infection has Metronidazole **been increasingly used for** (often in combination therapy)?
**Helicobacter pylori infection** of the stomach/duodenum associated with peptic ulcer disease.
220
Adverse effects of Metronidazole (N,A,M,A)
Nausea
Anorexia
Metallic taste
Ataxia
221
What reaction occurs if Metronidazole is taken with alcohol?
Unpleasant reaction **(disulfiram-like reaction)**; patients should be advised not to drink alcohol during treatment.
222
In which pregnancy period is Metronidazole possibly teratogenic?
First trimester.
223
Are metabolic pathway inhibitors mostly natural or synthetic?
Mostly synthetic chemotherapeutic agents.
224
What are most metabolic pathway inhibitors structurally similar to
Growth factor analogs
225
Two major drug classes that **block enzymes required for tetrahydrofolate synthesis.**
Sulfonamides, Trimethoprim
226
Why is tetrahydrofolate important for bacteria?
Needed for DNA and RNA synthesis.
227
What type of inhibition do **sulfonamides and trimethoprim** cause?
**Competitive inhibition** – drugs compete with the normal substrate for enzyme’s active site.
228
What did Domagk show sulfonamides could treat in mice?
Infections caused by **beta-hemolytic streptococci**
229
Most useful sulfonamides.
Sulfanilamide, Gantrisin
230
What is the most useful combination with sulfonamides?
Trimethoprim
231
**Analogues of para-aminobenzoic acid**; competitively **inhibit formation of dihydropteroic acid.**
Sulfonamides, Sulfones
(bacteriostatic)
232
Spectrum of activity of sulfonamides/sulfones.
Broad range (Gram-positive and Gram-negative bacteria)
Primarily **urinary tract infections**
**Nocardia infections**
233
Combination blocks two distinct steps in folic acid metabolism and prevents emergence of resistant strains.
sulfonamides with trimethoprim
234
Mode of action of trimethoprim / methotrexate?
Bind to **dihydrofolate reductase** and **inhibit formation of tetrahydrofolic acid**
235
Spectrum of activity of trimethoprim/methotrexate.
Broad range activity against Gram-positive and Gram-negative bacteria
Used primarily in urinary tract infections
Used in Nocardia infections
(Same sa sulfonamides and sulfones)
236
What enzyme converts folate into tetrahydrofolic acid?
Dihydrofolate reductase.
237
What drug inhibits dihydrofolate reductase in bacteria?
Trimethoprim
238
Pharmacokinetic features of most sulfonamides?
Well absorbed orally
Widely distributed, **including to the CNS**
Excreted by the kidney **unchanged**
For Gram-positive and many Gram-negative organisms.
239
Pharmacokinetic features of trimethoprim.
Well absorbed
Excreted by kidneys
Similar spectrum to sulfonamides
240
What is **cotrimoxazole?**
A combination of **trimethoprim + sulfonamides**
241
Common uses of cotrimoxazole.
Urinary tract infections, upper respiratory tract infections.
242
What is the drug of choice for treating and preventing **pneumonia** caused by *Pneumocystis carinii* (jirovecii) in immunosuppressed patients?
Cotrimoxazole
243
adverse effect of sulfonamides and trimethoprim
Both = Gastrointestinal upsets
For sulfonamides=
Allergy, rash, fever, agranulocytosis, renal toxicity.
trimethoprim = Macrocytic anemia, thrombocytopenia.
244
Serious adverse effect of cotrimoxazole.
Aplastic anemia
245
Widely used for urinary and upper respiratory tract infections, but not first choice due to
adverse effects; it is the drug of choice for treatment and prevention of pneumonia caused by
Pneumocystis carinii in immunosuppressed patients.
cotrimoxazole
246
Why is trimethoprim increasingly used alone?
Because it is less toxic than the combination and equally effective for urinary tract and
upper respiratory tract infections.
247
How do sulfonamides interact with other drugs?
Sulfonamides can decrease metabolism of phenytoin, warfarin, and some oral hypoglycemics, increasing their effects
248
Enumerate common adverse effects of sulfonamides, trimethoprim, and cotrimoxazole.
• Sulfonamides: allergy, rash, fever, agranulocytosis, renal toxicity
• Trimethoprim: macrocytic anemia, thrombocytopenia
• Cotrimoxazole: aplastic anemia
• Gastrointestinal upsets (common to all)
249
Why is selective toxicity difficult for antifungal drugs?
Fungal cells are eukaryotic; a drug toxic to fungal cells is also potentially toxic to human cell
250
Enumerate the five antifungal drug groups.
1. **Macrolide polyene** – amphotericin B (mimics lipids, versatile, topical & systemic), nystatin (topical)
2. **Griseofulvin** – used for stubborn dermatophyte infections, nephrotoxic
3. **Synthetic azoles** – broad-spectrum, e.g., ketoconazole, clotrimazole, miconazole
4. **Flucytosine** – cytosine analog; used in cutaneous mycoses or with amphotericin B for systemic mycoses
5. **Echinocandins** – damage fungal cell walls; e.g., caspofungin
251
Enumerate antimalarial drugs.
Quinine, chloroquine, primaquine, mefloquine.
252
Enumerate anti-protozoan drugs.
Metronidazole (Flagyl®), quinacrine (Atabrine®), sulfonamides, tetracyclines.
253
Enumerate anti-helminthic drugs and their mode of action.
• **Mebendazole, Thiabendazole** – broad-spectrum; inhibit microtubules, interfere with glucose utilization, disable worms
• **Pyrantel, Piperazine** – paralyze muscles
• **Niclosamide** – destroys scolex
254
Why is selective toxicity difficult for antiviral drugs?
Viruses are obligate intracellular parasites; drugs toxic to viruses may harm host cells.
255
How can antivirals block viral infection?
1. Block penetration into host cells
2. Block transcription or translation of viral genetic material using nucleotide analogs
256
Give examples of nucleotide analog antivirals.
• Acyclovir – herpesviruses
• Ribavirin – guanine analog, RSV and hemorrhagic fevers
• Azidothymidine (AZT) – thymine analog, HIV
257
How can antivirals prevent maturation of viral particles?
using protease inhibitors, e.g., for HIV.
258
Enumerate drugs for treating influenza A
Amantidine, rimantidine –
prevent fusion of virus with cell membrane; restricted to influenza A.
259
Enumerate drugs with broader influenza A and B activity.
Relenza and Tamiflu – block neuraminidase.
260
How do antiherpes drugs act?
Many are nucleotide analogs incorporated into growing viral DNA chain, terminating replication.
261
Give examples of antiherpes drugs.
Acyclovir (Zovirax), Valacyclovir (Valtrex), Famciclovir (Famvir), Penciclovir (Denavir).
262
Oral and topical treatments for oral/genital herpes, chickenpox, and shingles.
Antiherpes Drugs
263
What are the **two chemotherapy targets in retroviruses?**
1. Interference with viral DNA synthesis from RNA using nucleoside/nucleotide reverse transcriptase inhibitors
2. Interference with DNA synthesis using non-nucleoside reverse transcriptase inhibitors
264
Human-based glycoproteins produced primarily by fibroblasts and leukocytes.
Interferons
265
Enumerate the therapeutic benefits of interferons.
1. Reduces healing time and some complications of infections
2. Prevents or reduces symptoms of cold and papillomavirus
3. Slows progress of certain cancers, leukemias, and lymphomas
4. Used in treatment of hepatitis C, genital warts, and Kaposi’s
sarcoma
266
It is an adaptive response in which microorganisms begin to tolerate an amount of drug that
would ordinarily be inhibitory; this is due to genetic versatility or variation and can be intrinsic
or acquired.
acquisition of drug resistance
267
1. Spontaneous mutations in critical chromosomal genes
2. Acquisition of new genes or sets of genes via transfer from another species
acquired resistance
268
What are examples of antibiotic misuse?
1. Using outdated or weakened antibiotics
2. Using antibiotics for the common cold and other inappropriate conditions
3. Using antibiotics in animal feed
4. Failing to complete the prescribed regimen
5. Using someone else's leftover prescription
269
Enumerate the mechanisms of antibiotic resistance.
1. Enzymatic destruction of the drug
2. Prevention of penetration of the drug
3. Alteration of the drug's target site
4. Rapid ejection of the drug
270
Where are resistance genes often located?
Resistance genes are often on plasmids or transposons and can be transferred between bacteria.
271
What are the methods for testing drug susceptibility?
1. Kirby-Bauer disk diffusion test
2. E-test diffusion test
3. Dilution tests – minimum inhibitory concentration (MIC), which is the smallest
concentration of a drug that visibly inhibits growth
272
is a profile of drug sensitivity that guides the choice of a suitable drug.
antibiogram
273
What percentage of people taking antimicrobials experience serious adverse reactions?
Approximately 5% of all persons taking antimicrobials experience a serious adverse reaction.
274
What are the major side effects of antimicrobials?
1. Direct damage to tissue due to drug toxicity
2. Allergic reactions
3. Disruption in the balance of normal flora, which may cause superinfections
275
When should identification of the infectious agent be attempted?
Identification should be attempted as soon as possible, and specimens should be taken
before antimicrobials are initiated.
276
What factors should be considered in selecting an antimicrobial drug?
1. Identification of the microorganism causing the infection
2. Testing the microorganism’s susceptibility (sensitivity) to various drugs in vitro when
indicated
3. The overall medical condition of the patient
277
How does natural selection contribute to drug resistance?
Large populations of microbes likely include drug-resistant cells due to prior mutations or plasmid transfer; these cells have no growth advantage until exposed to the drug.
278
What happens when the microbial population is exposed to the drug?
Sensitive cells are inhibited or destroyed, while resistant cells survive and proliferate.
279
What are the mechanisms of drug resistance?
1. Drug inactivation by acquired enzymatic activity, e.g., penicillinases
2. Decreased permeability to the drug or increased elimination of drug from the cell – acquired or by mutation
3. Change in drug receptors – by mutation or acquisition
4. Change in metabolic patterns – mutation of the original enzyme
280
How is the Kirby-Bauer disk diffusion method performed?
1. A disk of filter paper is soaked in a disinfectant or antibiotic
2. The disk is placed on agar previously inoculated with the test organism
3. After incubation, the inhibition zone is measured
281
Does in vitro activity always correlate with in vivo effect?
No, in vitro activity of a drug is not always correlated with its in vivo effect.
282
How is the therapeutic index defined?
The therapeutic index is the ratio of the dose of a drug that is toxic to humans compared to its minimum effective dose.
283
Where do acquired resistance genes originate from?
They originate from resistance factors such as plasmids encoded with drug resistance and
transposons.
Microbiology
flashcards
Decks in class (22)
# Cards
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Module 6106
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Module 7181
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Module 8. 1132
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Module 8.2115
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Module 8.3283
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Module 9188
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9191
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11.1191
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11.2170
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Module 11.2160
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Module 12 (Slide 1 To 39)94
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Module 12 (Slide 40 To 65)76
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Module 12 (66-101)156
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Module 12 (-110 Last)25
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LAB EXAM 1 EXERCISES31
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LAB EXAM 1 PPT CULTURE MEDIA107
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Module 13 (VIRUSES)64
-
Module Virology Pt.1 (RNA VIRUSES)85
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Module Virology Part 2 (DNA)57
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Module VIROLOGY Part 3 (Introduction)98
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RNA (Picorna-Coronaviridae)83
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RNA VIRUS (REO - RHABDOVIRIDAE)49
