ANTIBIOTICS,CHEMOTHERAPY , AMINOGLYCOSIDES, PENICLLINS ,CEPHAROSPORINS,MACROLIDE,SULPHONAMIDES, QUINOLONES

1. (ANTIBIOTICS)
MWEETWA L: Pharmacologist
University of Zambia & Lusaka Apex Medical University
Pharmacy Faculty
CHEMOTHERAPEUTIC DRUGS

2. Learning objectives
• Understand Guiding Principles of antimicrobial therapy
• Understand Bacteria Structure
• Understand Classification and Mechanisms of Action of
Antimicrobial agents and other chemotherapeutic drugs
• Understand Factors influencing Drug Resistance

3. Introduction to principles of chemotherapy
I. DEFINITIONS
II. HISTORY
III. MECHANISMS OF ANTIMICROBIAL AGENTS
IV. MECHANISMS OF ANTIBACTERIAL RESISTANCE
V. GENERAL PRINCIPLES OF ANTI-INFECTIVE
THERAPY
VI. IDEAL ANTIMICROBIAL DRUG

4. Principles of Chemotherapy
• Antimicrobial therapy takes advantage of :-
• 1.Biochemical differences that exist between
microorganisms and human beings.
• 2. Antimicrobial drugs are effective in the treatment of
infections because of their selective toxicity; that is, they
have the ability to injure or kill an invading microorgan-ism
without harming the cells of the host.
• 3. In most instances, the selective toxicity is relative rather
than absolute, requiring that the concentration of the drug
be carefully controlled to attack the microorganism, while
still being tolerated by the host.

5. SELECTION OF ANTIMICROBIAL
AGENTS
• Selection of the most appropriate antimicrobial agent requires knowing
• 1) the organism’s identity - gram -/+
• 2) the organism’s susceptibility to a particular
• agent,
• 3) the site of the infection - blood-brain barrier effects, Protein binding, lipid
solubility and MW of the drug
• 4) patient factors-Renal/Hepatic nature,age,sex,pregnacy,lactation and immune
system
• 5) the safety of the agent, e.g chlorampheniciol and aminoglycosides and
• 6) the cost of therapy. However, some patients require empiric therapy.

6. SELECTION OF ANTIMICROBIAL
AGENTS
• INFLUENCE OF ROUTE OF ADMINISTRATION
• The oral route of administration is chosen for
infections that are mild and is favorable for
treatment on an outpatient basis.
• However, some antibiotics, such as vancomycin,
the aminoglyco-sides, and amphotericin B, are so
poorly absorbed from GIT

7. SELECTION OF ANTIMICROBIAL
AGENTS
• INFLUENCE OF RATIONAL DOSING
• Rational dosing of antimicrobial agents is based on their
pharmacodynamics AND phar-macokinetic properties
• Three important properties that have a significant body influence on the
frequency of dosing are
• 1. concentration-dependent killing,
• 2. time-dependent killing, and
• 3.postantibiotic effect.
• Utilizing these properties to optimize antibiotic dosing regimens can
improve clinical out-comes and possibly decrease the development of
resistance.

8. Understanding Bacteria structure
• Most pathological bacterial species are
referred to by genus name only e.g
klebsilla,Pseudomonas,proteus etc
• Some are referred by species name e.g E.Coli

9. TAXONOMY OF BACTERIA

10. TAXONOMY OF BACTERIA

11. GRAM STAIN

12. Gram-negative bacteria are a class
of bacteria that do not retain the crystal
violet stain used in the Gram staining method
of bacterial differentiation

13. coccobacilli

14. Practical classification of bacteria

15. Bacterial Etiologies

16. Common Normal flora bacteria

17. BACTERIA INFECTION SITES

18. COMMON Etiologic Bacteria

19. introduction
Chemotherapy is the drug treatment for the
diseases caused by pathologic microorganisms,
parasites, and tumour cells.
The objective of chemotherapy is to study and to
apply the drugs that have highly selective toxicity to
the pathogenic microorganisms and have no or less
toxicity to the host.

20. WHAT IS AN ANTIBIOTIC?
 “Antibiotic” is from antibiosis, meaning
• against life.
 Substances produced by various species
• of microorganisms: bacteria, fungi,
• actinomycetes— to kill or suppress the
• growth of other microorganisms.
 Today the term antibiotic extends to include
• synthetic antibacterial agents: sulfonamides and
quinolones.

21. ANTIMICROBIAL SPECTRUM
• Antimicrobial spectrum : the scope that
• a drug kills or suppresses the growth of
• microorganisms.
• Narrow-spectrum: The drugs that only act
• on one kind or one strain of bacteria.
• (isoniazid )
• Broad-spectrum: The drugs that have a
• wide antimicrobial scope. (tetracycline,
• chloramphenicol )

22. The minimal inhibitory concentration (MIC)
• The minimal inhibitory concentration (MIC)
• the minimum amount of a drug required to inhibit the growth of
bacteria in vitro.
• • The minimal bactericidal concentration (MBC)
• the minimum amount of a drug required to kill bacteria in vitro.
• TYPES
• Natural Antibiotics Antimicrobial drugs produced by
microorganisms.
• Synthetic Antibiotics Antimicrobial drugs
• synthesized in the lab.

23. II.HISTORY
 1929 Penicillin discovered by Alexander Fleming
Messy lab, cool damp weather, luck
 1940 Florey and Chain mass produce penicillin for
war time use, becomes available to the public.
 1935 Sulfa drugs discovered
 1943 Streptomycin discovered
 Western civilization fundamentally changed

25. MECHANISMS OF ANTIMICROBIAL
AGENTS
1. INHIBITION OF CELL WALL SYNTHESIS
2. INHIBITION OF FUNCTIONS OF CELLULAR MEMBRANE
3. INHIBITION OF PROTEIN SYNTHESIS
4. INHIBITION OF NUCLEIC ACID SYNTHESIS
5. INHIBITION OF FOLIC ACID SYNTHESIS

27. CON ...

28. Inhibition of cell wall synthesis
• Penicillins and cephalosporins stop synthesis
• of wall by preventing cross linking of
• peptidoglycan units.
• – Bacitracin and vancomycin also interfere
• here.
• – Excellent selective toxicity

29. 2. Inhibition of functions of cellular membrane:
• – The bacterial cell membrane is also called
cytoplasmic membrane. Its main compounds
are proteins and lipids.
• – Polymyxins can selectively combine with
phosphatide in the cell membrane and cause
the increase of membranous permeability. As the result, some important
materials will outflow from bacterial cells and result in death of bacteria.

30. 3. Inhibition of protein synthesis
• – Due to differences in ribosomes
Eucaryotic cells have 80S (60S + 40S subunits)
ribosomes.
Procaryotic cells have 70S (50S + 30S subunits)
ribosomes.
• – Examples:
• • Chloramphenicol,Macrolides and Clindamycin
bind to the 50S subunit.
• • Tetracyclines and Aminoglycosides bind to
the 30S subunit.

31. Inhibition of nucleic acid synthesis
• – Stop DNA replication
• • Example: Quinolones-inhibiting DNA
gyrase; Metronidazole???-DNA
Polymerase
Or stop RNA synthesis
• • Example: Rifampin -binds to the bacterial
• DNA-dependent RNA polymerase

32. 5. Inhibition of folic acid synthesis
A drug mimics a normal metabolite and
acts as a competitive inhibitor.
– Enzyme of cell recognizes the drug instead of
the normal metabolite-Pathway stops.
– Example: Sulfonamides and trimethoprim are similar to PABA
(para aminobenzoic acid).
inhibit folic acid synthesis by blocking
dihydrofolic acid synthase and reductase
respectively.

33. IV.RESISTANCE TO ANTIBACTERIAL AGENTS
• Drug resistance is the phenomenon that
susceptibility of pathogenic microorganisms
to drugs becomes lower or even loses after
the microorganisms contact with drugs many
times.
• When the bacteria show resistance to one
drug, they are also resistant to some other
drugs. This phenomenon is called cross
drug resistance.

34. TYPES OF RESISTANCE
• Intrinsic or natural resistance
• e.g., no target site in the bacteria
• Acquired resistance
–Resistance acquired by mutation is unusual,
–Resistance acquired by R-factors on plasmids is common, very
rapid method of acquiring
resistance that often involves resistance to
many antibiotics. (R factor contains genes
coding for enzymes that make the cell resistant to antibiotics)

35. ANTIBIOTIC Resistance
• 1.Alteration of the target site of the antibiotic?
• One of the most problematic antibiotic resistances worldwide,
• methicillin resistance among Staphylococcus aureus.
• 2.Enzyme inactivation of the antibiotic?
• β-lactam antibiotics (penicillins & cephalosporins) can be
• inactivated by β-lactamases.
• 3. Active transport of the antibiotic out of the bacterial cell
• Active transport of the antibiotic out of the bacterial cell
• (efflux pumps) ?
• Removal of some antibiotics (i.e. tetracyclines, macrolides, &
• quinolones)
• 4.Decreased permeability of the bacterial cell wall to the
• antibiotic?
• Alteration in the porin proteins that form channels in the cell membrane e.g Resistance of
Pseudomonas aeruginosa to a variety of penicillins and cephalosporins

36. ANTIBIOTIC Resistance

37. Antibiotic resistance animation

39. 1. Mechanisms of antibacterial
resistance
• Antibiotic inactivation
– bacteria acquire genes encoding
enzymes that inactivate antibiotics
• Examples include:
– b-lactamases
– aminoglycoside-modifying enzymes
– chloramphenicol acetyl transferase

40. 2. Mechanisms of antibacterial resistance
Altered uptake of antibiotics, resulting in:
– decreased permeability
– increased efflux
– For example, gram-negative bacillus can
induce some special proteins to block porin
channels in cell wall and prevent tetracyclines
into the bacillus.

41. 3. Mechanisms of antibacterial resistance
Structurally modified antibiotic target site
– For example, as the receptor protein on the
30s ribosomal subunit may be deleted or
altered as a result of mutation, some
aminoglycosides cannot combine with the
bacteria.

42. 4.Mechanisms of antibacterial resistance
Develop an altered metabolic pathway
– Bacteria can develop an altered metabolic
pathway that bypasses the reaction inhibited
by drugs.
– For example, sulfonamide resistance my
occur as a result of mutations that cause
over-production of PABA or cause production
of a folic acid-synthesizing enzyme that has
low affinity for sulfonamides.
Mechanisms of antibacterial resistance
PABA, p-aminobenzoic acid

43. GENERAL PRINCIPLES OF ANTI-INFECTIVE THERAPY
• ① Identification of the infecting organism should
• precede antimicrobial therapy when possible.
• ② The pathogenic microorganism susceptibility to
antimicrobial agents should be determined, if a
suitable test exists.
• ③ Factors that influence the choice of an
antiinfective agent or its dosage for a patient
include the age, renal and hepatic function,
pregnancy status, and the site of infection, etc.

44. Selection of Antimicrobial Agent
• Empiric therapy - prior to identification of
organism – critically ill patients
• Organism’s susceptibility to the antibiotic
• Patient factors - immune system,
renal/hepatic function
• Effect of site of infection on therapy –blood
brain barrier
• Safety of the agent
• Cost of therapy

46. IDEAL ANTIMICROBIAL DRUG
 Have highly selective toxicity to the pathogenic
microorganisms in host body
 Have no or less toxicity to the host.
 Low propensity for development of resistance.
 Not induce hypersensitive reactions in the host.
 Have rapid and extensive tissue distribution
 Be free of interactions with other drugs.
 Be relatively inexpensive

47. Properties Influencing Frequency of
Dosing
• Post-antibiotic effect (PAE)– persistent
suppression of microbial growth after levels
of antibiotic have fallen below MIC
Antibiotics with a long PAE – aminoglycosides
and fluroquinolines
Minimum bacterial concentration (MBC) is
the lowest concentration of antibiotic that
kills 99.9% of bacteria

48. MIC

49. Chemotherapeutic Spectra
• Narrow-spectrum Antibiotics:
• Act on a single / limited group of micro-organisms;
• e.g., isoniazid given for mycobacterium
• Extended-spectrum Antibiotics:
• Effective against gram-positive organisms and a
• significant number of gram-negative organisms; e.g.,
• Ampicillin
• Broad-spectrum Antibiotics:
• Effective against a wide variety of microbial species;
• e.g., tetracycline & chloramphenicol.
• Can alter the nature of intestinal flora = super infection

50. Combinations of Antimicrobial Drugs
• Advantages
• Synergism; the combination is more effective
than either drug used separately; β-lactams and
Aminoglycosides
• Used for Infections of unknown origin
Disadvantages
Bacteriostatic (tetracycline) drugs may interfere
with bactericidal ( penicillin and cephalosporin)
drugs

51. Complications of Antibiotic Therapy
• Resistance – inappropriate use of antibiotics
• Hypersensitivity – penicillin
• Direct toxicity – aminoglycosides = ototoxicity
• Super infections – broad spectrum
antimicrobials cause alteration of the normal
flora; often difficult to treat

52. MECHANISMS OF ANTIBIOTICS

53. MECHANISMS OF ANTIBIOTICS

54. β-LACTAM ANTIOBIOTICS

55. CELL WALL INHIBITORS
• Interfere with the synthesis of the bacterial
cell wall
• Little or no effect on bacteria that are not
growing and dividing

56. Cell wall inhibitors

57. PENICILLINS (bactericidal)
• Most widely effective and least toxic
• Limited use - increased resistance
Mechanism of action
• Inactivates various proteins on bacterial
cell wall

58. Administration and Fate of
PENICILLIN
• Does not penetrate CNS unless meninges are inflamed
• Routes of Administration
• • Oral only –Pen V, Amoxicillin &
• amoxicillin combined with clavulanic
• acid
• IV / IM- Tiracillin, piperacillin, ampicillin with sulbactam, tiracillin with clavulanic acid
and piperacillin with tozobactam
• Absorption
• • Decreases by food in the stomach –
administer before meals 30-60min
Distribution to bone and CSF
• insufficient
Excretion - Kidneys

59. Adverse Effects of Penicillin

60. CEPHALOSPORINS (bactericidal)
• Semi-synthetic antibiotics
β-lactam antibiotics are closely related functionally
and structurally to penicillins
• Mode of action - inhibit the synthesis of the cell
wall
• More resistant than penicillins to certain β –
lactamases
• Classified as 1st, 2nd, 3rd, 4 and 5th generation –
based on spectrum of antimicrobial activity

61. CEPHALOSPORINS classification

62. Most Common Side Effects –
• • Diarrhoea
• • Nausea
• • Abdominal pain
• • Vomiting
• • Headache
Individuals hypersensitive
to penicillins may also be
hypersensitive to
Cephalosporins
• • Dizziness
• • Skin rash
• • Fever
• • Abnormal liver tests
• • Vaginitis
• • Like almost all
antibiotics, may cause mild
or severe cases of
seudomembranous
colitis

63. OTHER β-LACTAM ANTIOBIOTICS

64. OTHER β-LACTAM ANTIOBIOTICS
• Carbapenems:
Imipenem – broad spectrum of activity
against Gram +ve and Gram –ve aerobic
and anaerobic bacteria
• Meropenem – Important for empirical
mono therapy of serious infections

65. OTHER β-LACTAM ANTIOBIOTICS
• Monobactams
• Activity is restricted to Gram –ve aerobic
bacteria
e.g Aztreonam
β-lactamase inhibitors
clavulanic acid –sulbactam and
tazobactam
Do not have significant antibacterial activity
Bind to and inactivate the β-lactamases –protect the
Antibiotics hence
Formulated in combination with
β-lactamase sensitive antibiotics
Clavulanic acid and amoxicillin

66. VANCOMYCIN
• Tricyclicglycopeptide
• • Effective against multiple drug resistant
organisms
• (MRSA) & enterococci
• • Resistance is becoming a Problem
• Enterococcus faecium
• Enterococcusfaecalis
• Side Effects: chills,Fever,Flushing,Phlebitis

67. DAPTOMYCIN
• Cyclic lipopeptide – linezolid and quinupristin /
• dalfopristin
• Treatment of infections caused by resistant
gram +ve
• MRSA – methicillin S. Aureus
• MSSA - methillin susceptible S. Aureus
• VRE - vancomycin- resistant enterococci
• Daptomycin is bactericidal and Concentration dependent
• Inactivated by surfactant – never used in
• treatment of pneumonia

68. TELAVANCIN
• Semi-synthetic lipoglycopeptide antibiotic
• Synthetic derivative of Vancomycin
• Used in Treatment of complicated skin and
skin structure infections caused by resistant
gram +ve organisms including MRSA

69. Mechanism of Action
• • Inhibits bacterial cell wall synthesis
• • Also involves disruption of bacterial cell
membrane
• • Bactericidal against MRSA
• Side effects
• Metallic Taste, foamy urine
• Not recommended in pregnancy
• QT Prolongation, insomnia
• Headache

70. PROTEIN SYNTHESIS INHIBITORS

71. TETRACYCLINES
• Broad-spectrum bacteriostatic antibiotic
• Effective against:
• Gram+ve and Gram-ve bacteria and
• Organisms other than bacteria

72. TETRACYCLINES

73. TETRACYCLINES

74. TETRACYCLINES

75. TETRACYCLINE SIDE EFFECTS

76. GLYCYLCYCLINES
• (Pronunciation: gli-sil-sī-klēns)
• Tigecycline – a derivative of minocycline
• Similar to tetracycline
• Broad-spectrum activity against Multidrug-
resistant Gram +ve pathogens Some Gram –ve
organisms Aerobic organisms
• Treatment of complicated skin and soft tissue
infections and complicated intra-abdominal
• infections
Mechanism of action – Binds to 30s Ribosome sub
unit with bacteriostatic action

77. GLYCYLCYCLINES Adverse Effects
• Associated with nausea and vomiting and
• other adverse effects similar to tetracyclines
• Drug interactions
• Inhibits the clearance of warfarin
• Oral contraception with Glycylcyclines –
• less effective

80. AMINOGLYCOSIDES
• Similar antimicrobial spectrum to Macrolides
• Relatively toxic but still useful in treatment of
infections caused by anaerobic Gram –ve bacteria
• Ototoxicity = main limitation
• Inhibit bacterial protein synthesis by acting on
the 30S ribosome subunit
• Good to know: Only available IV
• Not absorbed by gut

81. AMINOGLYCOSIDES spectrum
• Antibacterial spectrum – effective in
combination for empirical treatment of
aerobic Gram –ve bacilli infections –
• Pseudomonas
• Combines with a β-lactam i.e.
• Vancomycin Aminoglycosides and
• bactericidal amikacin,gentamycin,
• tobramycin and streptomycin

82. AMINOGLYCOSIDES mechanism of
action
• Interferes with bacterial protein synthesis by binding to the 30S
ribosomal subunit. An oxygen-dependent transport system is necessary
for aminoglycosides to reach their target site; the transport system is
inhibited by divalent cations (Ca++, Mg++), low pH, anaerobiasis, and
hyperosmolarity.
• Rapidly bactericidal.
• Concentration-dependent bactericidal activity, which means that the rate
and extent of bacterial killing increases as drug concentrations increase.
• Post-antibiotic effect (ie): continued killing of bacteria despite antibiotic
levels below the MIC of the organism.
• These pharmacodynamic properties (concentration-dependent killing and
post-antibiotic effect is the rationale for once daily dosing of
aminoglycosides.

83. aminoglycoside modifying enzymes
• aminoglycoside modifying enzymes that inactivate
the aminoglycoside via
• adenyltransferase --> adenylation of a hydroxyl
group
• acetyltramsferase --> acetylation of an amino group
• phosphotransferase --> phosphorylation of a
hydroxyl group
• Amikacin is less susceptible to aminoglycoside-
modifying enzymes because of protective side
chains, and therefore may still be useful when
resistance to gentamicin or tobramycin develops.

84. AMINOGLYCOSIDES SIDE EFFECTS

85. MACROLIDES

86. MACROLIDES Mode of action
• Macrolides are protein synthesis inhibitors.
• They inhibit bacterial protein biosynthesis, and
are thought to do this by
preventing peptidyltransferase from adding the
growing peptide attached to tRNA to the next
amino acid
• Leading to premature dissociation of the
peptidyl-tRNA from the ribosome.
• Macrolide antibiotics do so by binding reversibly
to the P site on the subunit 50S of the
bacterial ribosome

87. MACROLIDES indications

88. MACROLIDES PHARMACOCKINETICS

89. MACROLIDES SIDE EFFECTS

90. Chloramphenicol
• Active against a wide range of
• Gram +ve and Gram –ve organisms
• High toxicity – bone marrow toxicity
• Restricted for life-threatening infections
where no alternative exists

91. CHLORAMPHENICOL SIDE EFFECTS

92. CLINDAMYCIN
• Mechanism of action same as
• Erythromycin
• Treatment of infections caused by
• anaerobic bacteria – Bacteriodes
• fragilis (infections associated with
• trauma) & MRSA
• Resistance same as erythromycin

93. Quinupristin / Dalfopristin
• They belong to streptogramins antibiotics
• Quinupristin and dalfopristin are protein synthesis
inhibitors in a synergistic manner. While each of the two is
only a bacteriostatic agent, the combination shows
bactericidal activity.
• Dalfopristin binds to the 23S portion of the 50s ribosomal
subunit, and changes the conformation of it, enhancing
the binding of quinupristinby a factor of about 100. In
addition, it inhibits peptidyl transfer
• Quinupristin binds to a nearby site on the 50S ribosomal
subunit and prevents elongation of the polypeptide as well
as causing incomplete chains to be released.

95. LINEZOLID
• It selectively inhibits bacterial protein synthesis
• Binds to bacterial ribosome and prevents the
formation of a functional 70S-initiation complex.
• Specifically, linezolid binds to a site on the
bacterial 23S ribosomal RNA of the 50S subunit
and prevents the formation of a functional 70S
initiation complex, which is an essential
component of the bacterial translation process

96. LINEZOLID

97. NUCLEIC ACID INHIBITORS -
FluroqUINOLONES

98. QUINOLONES MODE OF ACTION
• They inhibit the enzymes topoisomerase II
(DNA gyrase) and topoisomerase IV, which
are required for bacterial DNA replication,
transcription, repair, strand supercoiling
repair, and recombination.
• Indications
 urinary tract infections, acute uncomplicated cystitis,
 chronic bacterial prostatitis, lower respiratory tract infections,
 acute sinusitis, skin and skin structure infections,
 bone and joint infections, complicated intra-abdominal infections (used in
combination with metronidazole),
 infectious diarrhea, typhoid fever (enteric fever), and
 inhalational anthrax (post-exposure).

99. Therapeutic Applications of
Fluroquinolones

101. Adverse Reactions to FlUroquinolones

102. Sulphonamides
• Short-acting
•
• Sulfacetamide
• Sulfadiazine
• Sulfadimidine
• Sulfafurazole
• Sulfisomidine (also known as sulfaisodimidine)
•
• Intermediate-acting
• Sulfadoxine
• Sulfamethoxazole
• Sulfamoxole
• Long-acting
• Sulfadimethoxine
• Sulfamethoxypyridazine
• Sulfametoxydiazine
• Ultra long-acting
• Sulfadoxine
• Sulfametopyrazine

103. SULFONAMIDE MODE OF ACTION
• Sulfonamides inhibit the enzymatic conversion of pteridine
and p-aminobenzoic acid (PABA) to dihydropteroic acid by
competing with PABA for binding to dihydrofolate synthetase,
an intermediate of tetrahydrofolic acid (THF) synthesis. THF is
required for the synthesis of purines and dTMP and inhibition
of its synthesis inhibits bacterial growth. Pyrimethamine and
trimethoprim inhibit dihydrofolate reductase, another step in
THF synthesis, and therefore act synergistically with the
sulfonamides.

106. COTRIMOXAZOLE SIDE EFFECTS

107. CLINICAL CONSIDERATIONS IN
CHEMOTHERAPY
• 1.All cell wall inhibitors are Beta-lactams (penicllins, cephalosporins etc) except
• vancomycin.
• 2. All penicllins are water soluble except nafcillin.
• 3. All protein synthesis inhibitors are bacteriostatic, except for the aminoglycosides
• 4. All cocci are gram positive, except Neisseria spp.
• 5. All bacilli are gram negative, except anthrax, tetanus, botulism and diphtheria bugs
• 6. All spirochaetes are gram negative
• 7.Tetracylcines and macrolides are used for intracellular bacteria
• 8.Beware pregnant women and tetracylcines, aminoglycosides, fluoroquinolones and
• sulfonamides.
• 9.Antibitoics beginning with 'C' are particularly associated with pseudomembranous colitis i.e. Cephalosporins,
Clindamycin and Ciprofloxacin.
• 10. While the penicillins are the most famous for causing allergies, a significant proportion of people with
penicillin allergies may also react to cephalosporins. These should therefore also be
• avoided.

108. CLINICAL CONSIDERATIONS IN
CHEMOTHERAPY

125. END THANKS
Created by Pharmacologist L. Mweetwa for:
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