Antibacterial, antitubercular, anti leprosy, drugs for peptic ulcer diseases & their mechanism

Southeast University
Pharmacology
Prepare by: Md. Mehedi Hasan Shawon
Department of Pharmacy

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Contents
Pharmacology ....................................................................................................................................3
Antibacterial Drugs.............................................................................................................................3
Classification of anti-bacterial drug......................................................................................................3
Bacterial Resistance............................................................................................................................4
Cell wall synthesis inhibitor ................................................................................................................4
Penicillin........................................................................................................................................4
Classification of penicillin ...........................................................................................................5
Mechanism of action ...................................................................................................................6
Cephalosporin ................................................................................................................................6
Classification of Cephalosporin....................................................................................................7
Carbapenems..................................................................................................................................7
Carbapenem group of Drag..........................................................................................................8
NON β-lactam cell wall synthesis inhibitors .....................................................................................9
Protein synthesis inhibitor ...................................................................................................................9
Aminoglycosides ..........................................................................................................................10
Classification of Aminoglycosides..............................................................................................10
Mechanism of action .................................................................................................................10
Tetracyclines ................................................................................................................................11
Classification of Tetracylines .....................................................................................................11
Chloramphenicol ..........................................................................................................................12
Macrolides ...................................................................................................................................13
Name of macrolide ....................................................................................................................13
Erythromycin............................................................................................................................13
Clarithromycin..........................................................................................................................14
Azithromycin............................................................................................................................14
Mechanism of Action ................................................................................................................15

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Nucleic acid synthesis inhibitor .........................................................................................................15
Anti-folate drugs ..............................................................................................................................16
Sulfonamide .................................................................................................................................16
Fluoroquinolones ..........................................................................................................................17
Classification of Fluoroquinolones .............................................................................................17
Anti-tubercular drugs ........................................................................................................................18
Anti-tubercular drugs ....................................................................................................................19
Isoniazid ......................................................................................................................................19
Rifampicin ...................................................................................................................................20
Anti-leprosy drugs ............................................................................................................................21
Type of leprosy.............................................................................................................................21
Dapsone.......................................................................................................................................21
Drugs for peptic ulcer diseases ..........................................................................................................21
Antacids.......................................................................................................................................21
H2-receptor blocker.......................................................................................................................22
H2-receptor blocker antagonist ...................................................................................................22
Proton pump inhibitor ...................................................................................................................23
Sucralfate.....................................................................................................................................24
Bibliography ....................................................................................................................................24

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Pharmacology
Pharmacology is the study of drug action. It involves looking at the interaction of chemical
substances with the systems in our bodies, as well as identifying ways in which our biological
systems affect drugs. (Anonymus, 2020)
Antibacterial Drugs
Antibacterial drug an antibiotic is a type of antimicrobial substance active against bacteria. It is
the most important type of antibacterial agent for fighting bacterial infections, and antibiotic
medications are widely used in the treatment and prevention of such infections.
Classification of anti-bacterial drug
1) Inhibition of cell wall synthesis
i. Antibacterial activity: Penicillin, Cephalosporin
ii. Antifungal activity: Caspofungin
2) Inhibition of protein synthesis
i. Action of 50S ribosomal submit: Chloramphenicol, Erythromycin
ii. Action of 30S ribosomal submit: Tetracycline, Aminoglycosides
3) Inhibition of nucleic acid synthesis
i. Inhibition of nucleotide synthesis: Sulfonamide
ii. Inhibition of DNA synthesis: Quinolones
iii. Inhibition of mRNA synthesis: Rifampicin

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4) Alteration of cell membrane function
i. Antibacterial activity: Polymyxin
ii. Antifungal activity: Amphotericin
5) Other mechanism of action
i. Antibacterial Activity: Isoniazid
ii. Antifungal activity: Pentamidine (Abdullah, 2019)
Bacterial Resistance
Antibiotic resistance happens when the germs no longer respond to the antibiotics designed to
kill them. That means the germs are not killed and continue to grow. It does not mean our body
is resistant to antibiotics. (Anonymus, Antibiotic Resistance Questions and Answers, 2020)
Cell wall synthesis inhibitor
Penicillin and cephalosporin are the major antibiotics that inhibit bacterial cell wall synthesis.
They are called beta-lactams because of the unusual 4-member ring that is common to all their
members.
Penicillin
Penicillin is a group of antibacterial drugs that attack a wide range of bacteria. They were the
first drugs of this type that doctors used. The discovery and manufacture of penicillin have
changed the face of medicine, as these drugs have saved millions of lives.

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Classification of penicillin
1. According to source
a) Natural penicillin: Penicillin V, Penicillin G
b) Semisynthetic penicillin: e
2. According to spectrum coverage
a) Narrow spectrum: Penicillin V, Penicillin G
b) Broad spectrum: Ampicillin, Amoxicillin
c) Extended spectrum: Azlocillin, Ticarcillin
3. According to β-lactamase sensitivity
a) β – lactamase sensitive: Ampicillin, Amoxicillin
b) β-lactamase resistance: Nafcillin, Oxacillin
4. According to duration of action
a) Long acting: Benzathine Penicillin
b) Short acting: Amlpicillin, Amoxicillin
5. According to gastric acid sensitivity
a) Acid labile: Penicillin G
b) Acid stable: Penicillin V

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Mechanism of action
Penicillin kills bacteria through binding of the β-lactam ring to DD-transpeptidase, inhibiting its
cross-linking activity and preventing new cell wall formation. Without a cell wall, a bacterial cell
is vulnerable to outside water and molecular pressures, and quickly dies. Penicillin binds with
and inactivates some PBPs present on the bacterial cell membrane and thus alters the
morphology of bacteria & also kills them. Many bacteria produce degradative enzyme that
participate in the normal remodeling of the bacterial cell wall. In the presence of penicillins, the
degradative action of the autolysis proceeds in the absence of cell wall synthesis. (Abdullah,
2019)
Cephalosporin
Cephalosporins are a large group of antibiotics derived from the mold Acremonium (previously
called Cephalosporium). Cephalosporins are bactericidal (kill bacteria) and work in a similar
way to penicillins. They bind to and block the activity of enzymes responsible for making
peptidoglycan, an important component of the bacterial cell wall. They are called broad-
spectrum antibiotics because they are effective against a wide range of bacteria. (Fookes, 2018)

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Classification of Cephalosporin
Cephalosporin can be classified into four major groups or generations. They are:
1. 1st generation
a) Oral: Cephardine, cefadroxil
b) Parental: Cephalothin, Cefazolin
2. 2nd generation
a) Oral: Cefaclor, Cefprozil
b) Parental: Cefmetazole, Cefoxitin
3. 3rd generation
a) Oral: Cefixime, Cefdinir
b) Parental: Cefotaxime, Cefoperazone
4. 4th generation
a) Only Parental: Cefepime, Cefpriome (Abdullah, 2019)
Mechanism of action
Same as penicillin
Carbapenems
Carbapenems are a class of beta-lactam antibiotic that are active against many aerobic and
anaerobic gram-positive and gram-negative organisms. Carbapenems are notable for their ability
to inhibit beta-lactamase enzymes (also called penicillinase) - a type of enzyme that greatly
reduces the activity of antibiotics such as penicillins and cephamycins. Carbapenems inhibit
bacterial cell wall synthesis by binding to the penicillin-binding proteins and interfering with cell
wall formation. (Anonymus, carbapenems, 2020)

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Carbapenem group of Drag
1. Doribax: Doribax (doripenem) is an antibiotic that fights bacteria. Doribax is used to
treat severe infections of the stomach, bladder, or kidneys. Doribax may also be used for
purposes not listed in this medication guide.
2. Doripenem: Doripenem is a beta-lactam antibiotic agent belonging to the carbapenem
group, with a broad spectrum of bacterial sensitivity including both gram-positive and
gram-negative bacteria. In vivo, doripenem inhibits the synthesis of cell walls by
attaching itself to penicillin-binding proteins, also known as PBPs.

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Mechanism of action
Same as penicillin
NON β-lactam cell wall synthesis inhibitors
1. Glycopeptide Antibiotics: Teicoplanin, Telavancin
2. Other cell wall active agent: Daptomycin, Cycloserine (Abdullah, Pharmacology, 2019)
Protein synthesis inhibitor
A protein synthesis inhibitor is a substance that stops or slows the growth or proliferation of cells
by disrupting the processes that lead directly to the generation of new proteins.

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Aminoglycosides
Aminoglycosides are a class of antibiotics used mainly in the treatment of aerobic gram-negative
bacilli infections, although they are also effective against other bacteria including Staphylococci
and Mycobacterium tuberculosis. They are often used in combination with other antibiotics.
Classification of Aminoglycosides
According to source
1. Natural: Kanamycin, Streptomycin.
2. Semisynthetic: Amikacin
Mechanism of action
Aminoglycosides are irreversible inhibitors of protein synthesis, but the precise mechanism for
bactericidal activity is not known. The initial event is passive diffusion via porin channels across
the outer membrane. Drug is then actively transported across the ce Aminoglycosides are a class
of antibiotics used mainly in the treatment of aerobic gram-negative bacilli infections, although
they are also effective against other bacteria including Staphylococci and Mycobacterium
tuberculosis. They are often used in combination with other antibiotics.ll membrane into the
cytoplasm by an oxygen-dependent process. The transmembrane electrochemical gradient
supplies the energy for this process, and transport is coupled to a proton pump. Low extracellular
pH and anaerobic conditions inhibit transport by reducing the gradient. Transport may be
enhanced by cell wall-active drugs such as penicillin or vancomycin; this enhancement may be
the basis of the synergism of these antibiotics with aminoglycosides. Aminoglycosides bind to
specific 30S-subunit ribosomal proteins (S12 in the case of streptomycin). Protein synthesis is
inhibited by aminoglycosides in at least three ways
1. Interference with the initiation complex of peptide formation;
2. Misreading of mRNA, which causes incorporation of incorrect amino acids into the
peptide and results in a nonfunctional or toxic protein

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3. Breakup of polysomes into nonfunctional monosomes. (Daniel H. Deck)
Tetracyclines
Tetracyclines are a class of antibiotics that may be used to treat infections caused by susceptible
microorganisms such as gram positive and gram negative bacteria, chlamydiae, mycoplasmata,
protozoans, or rickettsiae.
Classification of Tetracylines
According to source
1. Natural: Chlortetracycline, Oxytetracycline
2. Semi-synthetic: Doxycycline, Monocycline
Mechanism of action
The tetracyclines are primarily bacteriostatic; inhibit protein synthesis by binding to 30S
ribosomes in susceptible organism. Subsequent to such binding, attachment of aminoacyl-t-RNA
to the acceptor (A) site of mRNA-ribosome complex is interferred with. As a result, the peptide
chain fails to grow. The sensitive organisms have an energy dependent active transport process
which concentrates tetracyclines intracellularly. In gram-negative bacteria tetracyclines diffuse
through porin channels as well. The more lipid-soluble members (doxycycline, minocycline)
enter by passive diffusion also (this is partly responsible for their higher potency). The carrier

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involved in active transport of tetracyclines is absent in the host cells. Moreover, protein
synthesizing apparatus of host cells is less susceptible to tetracyclines. These two factors are
responsible for the selective toxicity of tetracyclines for the microbes. (TRIPATHI, Essentials of
Medical Pharmacology, 2013)
Chloramphenicol
Chloramphenicol is a man-made antibiotic. It slows growth of bacteria by preventing them from
producing important proteins that they need to survive. Chloramphenicol is effective against S.
typhi, H. influenzae, E. coli, Neisseria species, Staphylococcus and Streptococcus species,
Rickettsia, and lymphogranuloma-psittacosis group of organisms. (Ogbru, 2020)
Mechanism of action
Chloramphenicol is a potent inhibitor of microbial protein synthesis. It binds reversibly to the
50S subunit of the bacterial ribosome and inhibits peptide bond formation (step 2).
Chloramphenicol is a bacteriostatic broad-spectrum antibiotic that is active against both aerobic
and anaerobic gram-positive and gramnegative organisms. It is active also against Rickettsiae but
not Chlamydiae. Most gram-positive bacteria are inhibited at concentrations of 1–10 mcg/mL,
and many gram-negative bacteria are inhibited by concentrations of 0.2–5 mcg/mL. H
influenzae, Neisseria meningitidis , and some strains of bacteroides are highly susceptible, and
for these organisms, chloramphenicol may be bactericidal. Low-level resistance to
chloramphenicol may emerge from large populations of chloramphenicol-susceptible cells by
selection of mutants that are less permeable to the drug. Clinically significant resistance is due to

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production of chloramphenicol acetyltransferase, a plasmid-encoded enzyme that inactivates the
drug. (Daniel H. Deck L. G.)
Macrolides
The macrolides are a group of closely related compounds characterized by a macrocyclic lactone
ring (usually containing 14 or 16 atoms) to which deoxy sugars are attached. The prototype drug,
erythromycin, which consists of two sugar moieties attached to a 14-atom lactone ring,
Clarithromycin and azithromycin are semisynthetic derivatives of erythromycin.
Name of macrolide
Erythromycin
It was isolated from Streptomyces erythreus in 1952. Since then it has been widely employed,
mainly as alternative to penicillin. Water solubility of erythromycin is limited, and the solution
remains stable only when kept in cold.

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Clarithromycin
The antimicrobial spectrum of clarithromycin is similar to erythromycin; in addition, it includes
Mycobact. avium complex (MAC), other atypical mycobacteria, Mycobact. leprae and some
anaerobes but not Bact. fragilis. It is more active against Helicobacter pylori, Moraxella,
Legionella, Mycoplasma pneumonia and sensitve strains of gram-positive bacteria. However,
bacteria that have developed resistance to erythromycin are resistant to clarithromycin also.
Azithromycin
This azalide congener of erythromycin has an expanded spectrum, improved pharmacokinetics,
better tolerability and drug interaction profiles. It is more active than other macrolides against H.
influenzae, but less active against gram-positive cocci. High activity is exerted on respiratory
pathogens—Mycoplasma, Chlamydia pneumoniae, Legionella.

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Mechanism of Action
Macrolide and ketolide antibiotics are bacteriostatic agents that inhibit protein synthesis by
binding reversibly to 50S ribosomal subunits of sensitive microorganisms at or very near the site
that binds chloramphenicol Erythromycin does not inhibit peptide bond formation per se but
rather inhibits the translocation step wherein a newly synthesized peptidyl tRNA molecule
moves from the acceptor site on the ribosome to the peptidyl donor site. Gram-positive bacteria
accumulate about 100 times more erythromycin than do gram-negative bacteria. (MacDougall, p.
1059)
Nucleic acid synthesis inhibitor
Classification of Nucleic acid synthesis inhibitor
1. Direct:
i. DNA synthesis inhibitor: Quinolones
ii. RNA synthesis inhibitor: Rifamycin
2. Indirect:
i. Anti-folate drugs: Sulfonamide (Abdullah, Pharmacology, 2019)

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Anti-folate drugs
Sulfonamide
Sulfonamides were the first antimicrobial agents (AMAs) effective against pyogenic bacterial
infections. Sulfonamido-chrysoidine (Prontosil Red) was one of the dyes included by Domagk to
treat experimental streptococcal infection in mice and found it to be highly effective.
Subsequently an infant was cured of staphylococcal septicaemia (which was 100% fatal at that
time) by prontosil. By 1937, it became clear that prontosil was broken down in the body to
release sulfanilamide which was the active antibacterial agent. A large number of sulfonamides
were produced and used extensively in the subsequent years, but because of rapid emergence of
bacterial resistance and the availability of many safer and more effective antibiotics, their current
utility is limited, except in combination with trimethoprim (as cotrimoxazole) or pyrimethamine.
Mechanism of action
Sulfonamide-susceptible organisms, unlike mammals, cannot use exogenous folate but must
synthesize it from PABA. This pathway is thus essential for production of purines and nucleic
acid synthesis. As structural analogs of PABA, sulfonamides inhibit dihydropteroate synthase
and folate production. Sulfonamides inhibit both gram-positive and gram-negative bacteria,
Nocardia sp, Chlamydia trachomatis, and some protozoa. Some enteric bacteria, such as
Escherichia coli, Klebsiella pneumoniae, Salmonella , Shigella , and Enterobacter sp are also
inhibited. It is interesting that rickettsiae are not inhibited by sulfonamides but are instead
stimulated in their growth. Activity is poor against anaerobes. Pseudomonas aeruginosa is
intrinsically resistant to sulfonamide antibiotics. Combination of a sulfonamide with an inhibitor
of dihydrofolate reductase (trimethoprim or pyrimethamine) provides synergistic activity
because of sequential inhibition of folate synthesis. (Daniel H. Deck P. &., p. 831)

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Fluoroquinolones
These are quinolone antimicrobials having one or more fluorine substitutions. The ‘first
generation’ fluoroquinolones (FQs) introduced in 1980s have one fluoro substitution. In the
1990s, compounds with additional fluoro and other substitutions have been developed—further
extending antimicrobial activity to gram-positive cocci and anaerobes, and/or confering
metabolic stability (longer t½). These are referred to as ‘second generation’ FQs.
Classification of Fluoroquinolones
1. 1st generation: Nalidixic acid
2. 2nd generation: Ciprofloxin, Lomefloxacin
3. 3rd generation: Levofloxacin, Gatifloxacin

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4. 4th generation: Moxifloxacin
Mechanism of action
The FQs inhibit the enzyme bacterial DNA gyrase (primarily active in gram negative bacteria),
which nicks doublestranded DNA, introduces negative supercoils and then reseals the nicked
ends. This is necessary to prevent excessive positive supercoiling of the strands when they
separate to permit replication or transcription. The DNA gyrase consists of two A and two B
subunits: The A subunit carries out nicking of DNA, B subunit introduces negative supercoils
and then A subunit reseals the strands. FQs bind to A subunit with high affinity and interfere
with its strand cutting and resealing function. In gram-positive bacteria the major target of FQ
action is a similar enzyme topoisomerase IV which nicks and separates daughter DNA strands
after DNA replication. Greater affinity for topoisomerase IV may confer higher potency against
gram-positive bacteria. The bactericidal action probably results from digestion of DNA by
exonucleases whose production is signalled by the damaged DNA. In place of DNA gyrase or
topoisomerase IV, the mammalian cells possess an enzyme topoisomerase II (that also removes
positive supercoils) which has very low affinity for FQs— hence the low toxicity to host cells.
(TRIPATHI, 2013, p. 709)
Anti-tubercular drugs
Mycobacteria are intrinsically resistant to most antibiotics. Because they grow more slowly than
other bacteria, antibiotics that are mostbactive against rapidly growing cells are relatively
ineffective. Mycobacterial cells can also be dormant and thus completely resistant to many drugs
or killed only very slowly. The lipid-rich mycobacterial cell wall is impermeable to many agents.
Mycobacterial species are intracellular pathogens, and organisms residing within macrophages

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are inaccessible to drugs that penetrate these cells poorly. Finally, mycobacteria are notorious for
their ability to develop resistance. Combinations of two or more drugs are required to overcome
these obstacles and to prevent emergence of resistance during the course of therapy. The
response of mycobacterial infections to chemotherapy is slow, and treatment must be
administered for months to years, depending on which drugs are used.
Anti-tubercular drugs
1. First line drug: Isoniazid, Rifampicin, Ethambutol
2. Second line drug: Clofazimine, Rifabutin
Isoniazid
Isoniazid (isonicotinic acid hydrazide), also called INH is an important drug for the
chemotherapy of drug-susceptible TB. All patients infected with isoniazid-sensitive strains of the
tubercle bacillus receive the drug if they can tolerate it. The use of combination therapy
(isoniazid + pyrazinamide + rifampin) provides the basis for short-course therapy and improved
cure rates.
Mechanism of action
Isoniazid inhibits synthesis of mycolic acids, which are essential components of mycobacterial
cell walls. Isoniazid is a prodrug that is activated by KatG, the mycobacterial catalase-
peroxidase. The activated form of isoniazid forms a covalent complex with an acyl carrier
protein (AcpM) and KasA, a beta-ketoacyl carrier protein synthetase, which blocks mycolic acid
synthesis and kills the cell. Resistance to isoniazid is associated with mutations resulting in
overexpression of inhA , which encodes an NADH-dependent acyl carrier protein reductase;
mutation or deletion of the katG gene; promoter mutations resulting in overexpression of ahpC ,
a putative virulence gene involved in protection of the cell from oxidative stress; and mutations
in kasA . Overproducers of inhA express low-level isoniazid resistance and cross-resistance to
ethionamide. KatG mutants express high-level isoniazid resistance and often are not cross-
resistant to ethionamide. (Daniel H. Deck L. G., p. 839)

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Rifampicin
Mechanism of action
Rifampin binds to the β subunit of bacterial DNA-dependent RNA polymerase and thereby
inhibits RNA synthesis. Resistance results from any one of several possible point mutations in
rpoB , the gene for the β subunit of RNA polymerase. These mutations result in reduced binding
of rifampin to RNA polymerase. Human RNA polymerase does not bind rifampin and is not
inhibited by it. (Daniel H. Deck L. G., p. 841)

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Anti-leprosy drugs
Type of leprosy
1. Paucibacillary
2. Multibacillary
3. Paucibacillary single-leison
Dapsone
Mechanism of action
Same as sulfonamide
Drugs for peptic ulcer diseases
1. Acid neutralized
a) Antacids: Sodium bicarbonate, Calcium carbonate
2. Antisecretory
a) H2-receptor blocker: Ranitidine, Nizatidine
b) Proton pump inhibitors: Omeprazole, Lansoprazole
c) Anti-muscarinc drugs: Dicylomine, Telenzepine
3. Ulcer healing drug: Sucralfate (Abdullah, 2019, p. 664)
Antacids
An antacid is a substance which neutralizes stomach acidity and is used to relieve heartburn,
indigestion or an upset stomach.
Mechanism of action
Antacids are a combination of various compounds with various salts of calcium, magnesium, and
aluminum as the active ingredients. The antacids act by neutralizing the acid in the stomach and
by inhibiting pepsin, which is a proteolytic enzyme.

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H2-receptor blocker
H2-receptor blocker antagonist
1. cimetidine
2. ranitidine
3. famotidine
4. nizatidine
5. roxatidine
6. lafutidine
7. lavoltidine
8. niperotidine
Mechanism of action
H2RAs decrease gastric acid secretion by reversibly binding to histamine H2 receptors located
on gastric parietal cells, thereby inhibiting the binding and action of the endogenous ligand
histamine. H2 blockers thus function as competitive antagonists. By blocking the histamine
receptor and thus histamine stimulation of parietal cell acid secretion, H2RAs suppress both
stimulated and basal gastric acid secretion that is induced by histamine. The onset of gastric
relief provided by H2RAs is approximately 60 minutes with duration of action that ranges from 4
to 10 hours, making them useful for the on-demand treatment of occasional symptoms. All
H2RAs have similar efficacy in decreasing gastric acid secretion. (Nugent, Falkson, & Terrell.,
2020)

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Protonpump inhibitor
Proton pump inhibitors (PPIs) reduce the production of acid by blocking the enzyme in the wall
of the stomach that produces acid. Acid is necessary for the formation of most ulcers in the
esophagus, stomach, and duodenum, and the reduction of acid with PPIs prevents ulcers and
allows any ulcers that exist in the esophagus, stomach, and duodenum to heal.
The currently available PPIs include:
1. omeprazole
2. lansoprazole
3. pantoprazole
4. rabeprazole
5. esomeprazole
6. dexlansoprazole
Mechanism of action
Proton pump inhibitors (PPIs) block the gastric H, K-ATPase, inhibiting gastric acid secretion.
This effect enables healing of peptic ulcers, gastroesophageal reflux disease (GERD), Barrett's
esophagus, and Zollinger-Ellison syndrome, as well as the eradication of Helicobacter pylori as
part of combination regimens.

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Sucralfate
Mechanism of action
Sucralfate is a complex of aluminium hydroxide and sucrose octasulfate. It dissociates in the acid
environment of the stomach to its anionic form, which binds to the ulcer base. This creates a
protective barrier to pepsin and bile and inhibits the diffusion of gastric acid. When given orally,
sucrose octasulfate reacts with hydrochloric acid and is polymerized to a viscous sticky
substance that binds to the proteinaceous exudate usually found at ulcer sites. Because of
electrostatic charges, sucralfate preferentially adheres to ulcerated tissues. It protects the ulcer
against hydrogen ion back-diffusion, pepsin and bile and therefore promotes ulcer healing.
(German, 2008)
Bibliography
Abdullah,D.M. (2019). Pharmacology. Dhaka:Blueprint.
Abdullah,D.M. (2019). Pharmacology. Dhaka:Blueprint.

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Anonymus.(2020, January31). Antibiotic ResistanceQuestionsand Answers.Retrievedfrom cdc.gov:
https://www.cdc.gov/antibiotic-use/community/about/antibiotic-resistance-faqs.html
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Anonymus.(2020). whatis pharmacology.Retrievedfromhealthcare:https://www.healthcare-
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Daniel H.Deck,L. G. (n.d.).Chloramphenicol.InKatzung, Basic& Clinical Pharmacology (p.816).New
York.
Daniel H.Deck,P. &. (n.d.).Aminoglycosides& Spectinomycin.InKatzung, Basic&cilinical pharmacology
(p.821). Newyork:McGraw-Hill Education.
Fookes,C.(2018, July20). Cephalosporins.RetrievedfromDrugs.com:https://www.drugs.com/drug-
class/cephalosporins.html#:~:text=Cephalosporins%20are%20a%20large%20group,a%20similar
%20way%20to%20penicillins.
German,A. J.(2008). Small AnimalClinical Pharmacology (Second Edition).
MacDougall,C. (n.d.).Aminogycosides.InA.G.Gilman, Aminogycosides (p.1044).New York: McGraw-
Hill Education.
Nugent,C. C.,Falkson,S.R., & Terrell.,J.M. (2020). New york:StatPearlsPublishingLLC.
Ogbru,O. (2020). Chloramphenical.Retrievedfrommedicinenet:
https://www.medicinenet.com/chloramphenicol-oral/article.htm
TRIPATHI,K. (2013). In K. TRIPATHI, Essentials of Medical Pharmacology (p.733).New Dilhi:JAYPEE
BROTHERS MEDICAL PUBLISHERS (P) LTD.
TRIPATHI,K. (2013). In K. TRIPATHI, Essentialsof Medical Pharmacology (p.729).New Dilhi:JAYPEE
BROTHERS MEDICAL PUBLISHERS (P) LTD.

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