Microbiology is the study of microorganisms. The overall theme of the Microbiology course is to study the relationship between microbes and our lives. Microorganisms (microbes) are organisms that are too small to be seen with the unaided eye, and usually require a microscope to be seen. This relationship involves harmful effects such as diseases and food spoilage as well as many beneficial effects.

1. Chemotherapy of Bacterial Infections
~~~~~~~~
Antimicrobials
Making sense of them

2. Antimicrobial Drugs
I. Terminology of chemotherapy
II. Where antimicrobial drugs come from
III. How antimicrobials work
IV. Drug resistance
V. Interactions between drugs and hosts
VI. Selecting the right antimicrobial drug

3. Definitions
Chemotherapy is the drug treatment for the diseases caused by bacteria and the other
pathologic microorganisms, parasites, and tumor 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.
In most instances, the selective toxicity is relative, rather than absolute.

5. Where do antimicrobials come from?
• Fleming’s discovery of _______________
• Main sources of useful antibiotics: Streptomyces and Bacillus
(________BACTERIA____), Penicillium and Cephalosporium
(____MOLdS_____)
• Thousands have been discovered; relatively few of these are
___________.

6. How do they work?
• The main trick if one were to “design” an antibiotic: find something the
target pathogen has or does (e.g. a structure or pathway) which the host cell
doesn’t. For example, most bacteria have peptidoglycan while eukaryotes
don’t so a compound which destroys it or inhibits its production (like
penicillin) shouldn’t affect eukaryotes.
• Toxicity to the host is a major concern

7.  Inhibition of cell wall synthesis
 Inhibition of nucleic acid structure and function
 Inhibition of protein synthesis
 Interference with cell membrane structure or function
 Inhibition of folic acid synthesis
•Penicillins
•Cephalosporins
•Vancomycin
•Bacitracin
•Novobiocin
•Nalidixic
acid
•Rifampin
•Tetracyclines
•Aminoglycosides
(Streptomycin,
Kanamycin,
Gentamicin)
•Erythromycin
•Chloramphenicol

8. Beta-lactam antibiotics:
 Penicillins
 Inhibitors of beta-lactamases and combined drugs,
 Cephalosporins
 Monobactams
 Tienamycin (carbapenems).
Sulfonamides
Quinolones
Macrolides, azalides, streptogramins, prystinamycines.
Linkozamides.
Tetracyclines.
Aminoglycosides.
Chloramphenicols.
Glycopeptides.
Cyclic polipeptides (polimixins).
Other antibiotics
ANTIBIOTICS

9. Dose-dependent Time-dependent
Antibacterial effect directly
depends on their
concentrations in the locus of
inflammation
(high doses 1-2 times/24h)
Aminoglycosides
Fluoroqinolones
Metronidazol
Amphotericin B
Effectiveness depends on a
period of time, during which
concentration in blood
overwhelms MIC for a
particular causative agent
(constant i.v. infusion or 3-6
times/24h)
Beta-lactames
Glycopeptides
Macrolides
Linkozamides
ANTIBIOTICS

10. Inhibition of Cell Wall Synthesis: b-Lactam Drugs
Irreversibly inhibit enzymes involved in the final steps of cell wall synthesis
These enzymes mediate formation of peptide bridges between adjacent stands
of peptidoglycan
β-lactam ring similar in structure to normal substrate of enzyme
Drug binds to enzyme, competitively inhibit enzymatic activity
Some bacteria produce β-lactamase- enzyme that breaks the critical β-lactam ring.
β-lactam drugs include: penicillins and cephalosporins
Acid-labile.
Gram+ bacteria.
So, take phenoxymethylpenicillin.
Large Vd, but penetration into brain: poor, except when the meninges
are inflammed.
Broad spectrum penicillins: amoxicillin and ampicillin are more
hydrophillic and therefore, are active against gram- bacteria.

11. b-lactam
Inhibition of Cell Wall Synthesis

13. Penicillinase-resistant penicillins – Flucloxacillin
Indicated in infections caused by penicillinase-producing pen-resistant
staphlococci.
Has an isoxazolyl group at R1  sterically hinders access of the enzyme to
the β-lactam ring.
Less effective than benzylpen.
So, should be used only for pen-resistant infections.
Well-absorbed orally, but in severe infections, should be i.v. and not alone.
Staphlococci aureas-resistant strains to flucloxicillin and MRSA (methicillin-
resistant Staph aureas) – increasing problem.
Penicillins (Benzylpenicillin)

14. Ampicillin and amoxicillin – very active against non-β-lactamase-producing gram+
bacteria.
Because they diffuse readily into Gram- bacteria, also very active against many
strains of E. coli, H. influenzae, and Salmonella typhimurium.
Orally, amoxicillin is better because absorption is better.
Ineffective against penicillinase-producing bacteria (e.g., S. aureus, 50% of E. coli
strains, and up to 15 % of H. influenzae strains.
Many baterial β-lactamases are inhibited by clavulaic acid ± amoxicillin (co-
amoxiclav)  antibiotic is effective against penicillinase-producing organisms.
Co-amoxiclav indicated in resp and UT infections, which are confirmed to be
resistant to amoxicillin.
Broad-Spectrum Penicillins

15. Way of
introduction
Generation of cephalosporin antibiotics
first I second II third III fourth IV
Injection Cefaloridin
Cefadroxil*
Cefazolin*
Cefalexin*
Cephradin*
Cefamandole
* Cefoxytyn*
Cefuroxime*
Cefotaxime*
Ceftriaxone*
Cefoperazone
*
Ceftazidime*
Cefpirome
*
Cefepime*
Oral Cephalexin *
Cefadroxil*
Cefuroxime
axetyl*
Cefaclor *
Cefixime *
Ceftibuten * -
Classification of Cephalosporins

16. Used for treatment of meningitis, pneumonia, and septicemia.
Same mech and p’col as that of penc.
May  allergic rxn and cross-reactivity to pen.
Similar to pens in broad-spectrum antibacterial activity.
Cedadroxil (for UTI) in case of antibact resist.
Cefuroxime (prophylactic in surgery) – Resistant to inactivation by β-lactamases
and used in severe infections (others ineffective).
Ceftazidine – wide range of activity against gram- including Pseudomonas
aeruginosa), but is less active than cefurozime against gram+ bact (S aureus).
Used in meningitis (CNS-accessible) caused by gram- bacteria.
Cephalosporins

17. Not well absorbed orally.
Inhibits peptidoglycan formation.
Active against most gram+ organisms.
I.v. treatment for septicemia or endocarditis caused by
MRSA.
Used for pseudomembranous colitis (superinfection of the
bowel by Clostridium difficile – produces a toxin that
damages the colon mucosa)
Vancomycin

18. Antibacterial Medications that Inhibit Protein Synthesis
Target ribosomes of bacteria
Aminoglycosides: bind to 30S subunit causing it to distort and malfunction;
blocks initiation of translation
Tetracyclines: bind to 30S subunit blocking attachment of tRNA.
Macrolides: bind 50S subunit and prevents protein synthesis from continuing.

20. Mode of action - The amino glycosides irreversibly bind to the 16S ribosomal RNA
and freeze the 30S initiation complex (30S-mRNA-tRNA) so that no further
initiation can occur. They also slow down protein synthesis that has already initiated
and induce misreading of the mRNA. By binding to the 16 S r-RNA the
aminoglycosides increase the affinity of the A site for t-RNA regardless of the
anticodon specificity. May also destabilize bacterial membranes.
Spectrum of Activity -Many gram-negative and some gram-positive bacteria; Not
useful for anaerobic (oxygen required for uptake of antibiotic) or intracellular
bacteria.
Resistance - Common
Synergy - The aminoglycosides synergize with β-lactam antibiotics. The β-lactams
inhibit cell wall synthesis and thereby increase the permeability of the
aminoglycosides.
Aminoglycosides (Bactericidal)
streptomycin, kanamycin, gentamicin, tobramycin, amikacin, netilmicin,
neomycin (topical)

21. Gentamicin – used for acute, life-thretening gram- infections. Has synergism
with pen and van and combo.
Amikacin – used for bact that are gent-resistant.
Netilmicin – less toxic than gentamicin.
Neomycin – too toxic for parenteral use. Used for topically for skin infections
and orally for sterilizing bowel before surgery.
Streptomycin – active against Mycobacterium tuberculosis. But bec of its
ototoxicity, rifampicin replaces.
Rifampicin – resistance develops quickly alone; so, with TB, combine with
isoniazid, ethambutol, and pyrazinamide for the 1st 2 mos of treatment, followed
by another 4 mos with rifampicin and isoniazid.
Aminoglycosides

22. Very safe drugs.
Ususally given orally.
Erythromycin and clarithomycin
Effective against gram- bact and can be used as an alt to pen-sensitive patients, esp in
infections caused by streptococci, staphylococci, pneumococci, and clostridia.
Don’t cross the BBB – ineffective against meningitis.
Resistance- occurs bec of plasmid-controlled Δ of their receptor on the 50S subunit.
Erythromycin – in high doses, may cause nausea and vomiting (less so with
clarithromycin and azithromycin).
Azithromycin – very long t1/2 (~40-60 hr) and a single dose is as effective in treating
chlamydial non-specific urethritis as tretracycline admin over 7 days,
Macrolides

23. Tetracyclines
Broad-spectrum.
Penetrate microorganisms well.
Sensitive organisms accumulate it through partly passive diffusion and partly
through active transport.
Resistant organisms develop an efflux pump and do not accumulate the drug.
Genes for tet-resistance transmitted by plasmids.
Closely assoc with those for other drugs to which the organisms will also be
resistant (e.g., sulphonamides, aminoglycosides, chloramphenicol).
Tets bind to Ca in growing bones and teeth  can discolor teeth. So, should
be avoided in children < 8 yrs old.

24. Chloramphenicol
Broad-spectrum.
Serious side-effects: bone marrow aplasia, suppression of RBCs, WBCs,
encephalopathy, optic neuritis.
So, periodic blood counts required, esp in high doses.
Large Vd, including CNS.
Inhibits the actions of other drugs and may incr the actions of phenytoin,
sulphonlureas, and warfarin.
Neonates cannot met the drug rapidly  accum  ‘grey baby’ syndrome
(pallor, abdominal distension, vomiting, and collapse).

26. Sulfadiazine well-absorbed orally. Used to treat UTIs.
But many strains of E. coli are resistant.
So, use less toxic drugs instead.
Adverse effects: allergic rxns, skin rashes, fever.
Trimethoprin – used for UTIs and Resp TIs
Co-trimoxazole (trimethoprin + sulfamethoxazole) – used mostly for
pneumonia, neocarditis, and toxoplasmosis.
Sulphonamides

28. Inhibit DNA gyrase.
Nalidixic acid – used only for UTIs.
Ciprofloxin (6-fluoro substituent) that greatly enhances its effectiveness
against both gram- and gram+ bacteria.
Well-absorbed both orally and i.v.
Eliminated largely unchanged by the kidneys.
Side-effects (headache, vomiting, nausea) are rare; but convulsions may
occur.
Quinolones (GABA antagonists)

29. 5-Nitroimidazoles
Wide-spectrum
Metronidazole – against anaerobic bacteria and protozoan infections.
Tinidazole – longer duration of action.
Diffuses into the organism where the nitro group is reduced  chemically
reactive intermediates are formed that inhibit DNA synthesis and/or
damage DNA.

30. Antibacterial Drugs that Inhibit Nucleic Acids

31. Drugs that Prevent the Virus from Entering or Leaving the Host Cells
Amantadine – interferes with replication of influenza A by inhibiting the
transmembrane M2 protein that is essential for uncoating the virus.
-Has a narrow spectrum; so, flu vaccine is usually preferable.
Zanamivir – inhibits both influenza A and B neuraminadase. Decr duration
of symptoms if given within 48 hr of the onset of symptoms. Prophylactic in
healthy adults.
Immunoglobulins – Human Ig contains specific Abs against superficial Ags
of viruses  can interfere with their entry into host cells. Protection against
hepA, measles, and rubellla (German measles).

32. Drugs that Inhibit Nucleic Acid Synthesis
Nucleoside and Nucleotide Analogs
Acyclovir- used to treat genital herpes
Cidofovir- used for treatment of cytomegaloviral infections of the eye
Lamivudine- used to treat Hepatitis B
HSV and VZV contain a thymidine kinase (TK) that  acyclovir to a monophosphate
phosphorylated by host cell enzymes to acycloguanosine triphosphate, which
inhibits viral DNA pol and viral DNA synthesis.
Selectively toxic (TK of uninfected host cells activates only a little of the drug).
Viral enzymes have a much higher affinity than the host enzymes for the drug.
Effective against HSV, but does not eradicate them.
Need high doses to treat shingles.
Acyclovir

34. Mechanisms Responsible for Resistance to Antimicrobial Drugs Include the
Following:
1. Inactivating enzymes that destroy the drug (e.g., β-lactamases).
2. Decreased drug accumulation (e.g., tet).
3. Altering the binding sites (e.g., aminoglycosides and erythromycin).
4. Development of alternative metabolic pathways (sulphonamides (
dihydropteroate synthease) and trimethoprim (dihydrofolate reductase).

35. Antifungal drugs

36. Human fungal infections have increased dramatically
in recent years, owing mainly to advances in surgery,
cancer treatment, and critical care accompanied by
increases in the use of broad-spectrum antimicrobials
and the HIV epidemic.
Fungal infections are usually more difficult to treat
than bacterial infections, because fungal organisms grow
slowly and because fungal infections often occur in
tissues that are poorly penetrated by antimicrobial agents
(e.g., devitalized or avascular tissues). Therapy of fungal
infections usually requires prolonged treatment.

37. Superficial fungal infections involve cutaneous
surfaces (skin, nails, and hair), and mucous membrane
surfaces (oropharynx and vagina).
Deepseated or disseminated fungal infections caused
by dimorphic fungi, the yeasts Cryptococcus neoformans,
and various Candida spp. respond to a limited number
of systemic agents: amphotericin B (a polyene),
flucytosine (a pyrimidine antimetabolite), the newer
azoles (ketoconazole, fluconazole, itraconazole, and
voriconazole), and caspofungin (an echinocandin).

38. I. Antifungals damaging permeability
of the cell membrane
•Imidazoles: Bifonazole, Clotrimazole, Econazole,
Ketoconazole, Miconazole
•Triazoles: Fluconazole, Itraconazole, Voriconazole
•Allylamines: Terbinafine, Naftifine
•Morpholines: Amorolfine
•Thiocarbamates: Tolciclate, Tolnaftate
•Substituted pyridones: Ciclopirox
•Polyene antibiotics: Amphotericin B, Nystatin
II. Antifungals inhibiting chitin synthesis in the cell wall
•Caspofungin, Griseofulvin
III. Antifungals inhibiting synthesis of nucleic acids
•Flucytosine

39. 1. Polyene antibiotics
Amphotericin B and Nystatin bind to the fungal cell
Membrane component ergosterol, leading to
increased fungal cell membrane permeability and
the loss of intracellular constituents. Amphotericin has
a lesser affinity for the mammalian cell membrane
component cholesterol, but this interaction does
account for most adverse toxic effects.
Amphotericin B has activity against Candida spp.,
Cryptococcus neoformans, Blastomyces dermatitidis,
Histoplasma capsulatum, Sporothrix schenckii,
Coccidioides immitis, Paracoccidioides braziliensis,
Aspergillus spp., Penicillium marneffei, etc.

40. Amphotericin uses i.v. for treatment of Candida esopha-
gitis, rapidly progressive mucormycosis or invasive
aspergillosis. Intrathecal infusion of amphotericin B is
useful in patients with meningitis caused by Coccidioides.
Intravenous administration of amphotericin B is the
treatment of choice for mucormycosis and is used for the
initial treatment of cryptococcal meningitis, severe or
rapidly progressing histoplasmosis, blastomycosis,
and coccidioidomycosis.
Intraocular injection has
been used successfully
for fungal endophthalmitis.

41. The major acute reaction to i.v. amphotericin B is
fever and chills. Tachypnea and respiratory stridor
or modest hypotension also may occur. Patients with
preexisting cardiac or pulmonary disease may
tolerate the metabolic demands of the reaction
poorly and develop hypoxia or hypotension.
Although the reaction ends spontaneously in 30 to
45 minutes, pethidine may shorten it.
Pretreatment with oral paracetamol or use of i.v.
hydrocortisone hemisuccinate, at the start of the
infusion decreases reactions. Azotemia occurs in
80% of patients who receive amphotericin
in deep mycoses.

42. Several lipid formulations of amphotericin B – colloidal
dispersion and liposomal amphotericin B, have been
developed in an attempt to reduce the toxicity profile
of this drug and to increase its efficacy. Formulating
amphotericin with lipids alters drug distribution, with
lower levels of drug in the kidneys, reducing the
incidence of nephrotoxicity. While less toxic, the
lipid formulations are significantly more expensive
than conventional amphotericin B.
Polyene binds

43. Nystatin is a polyene antifungal drug with
a ring structure and a mechanism of action
similar to that of amphotericin B. Too toxic
for systemic use, nystatin is limited to the
topical treatment of superficial infections
caused by C. albicans. Infections commonly
treated by this drug include oral candidiasis
(thrush), mild esophageal candidiasis,
and vaginitis.

44. 2. Antifungal Azoles are synthetic drugs
with broad-spectrum fungistatic activity. Azoles can be
divided into two groups: the older imidazole agents
(clotrimazole, ketoconazole, miconazole) in which
the five-member azole nucleus contains two nitrogens
and the newer triazole compounds
(fluconazole, itraconazole, and voriconazole),
in which the azole nucleus contains three nitrogens.

45. All azoles exert antifungal activity by inhibiting
cytochrome P450 enzymes responsible for the
demethylation of lanosterol to ergosterol.
Reduced fungal membrane ergosterol concen-
trations result in damaged, leaky cell membranes.
The toxicity of these drugs depends on
their relative affinities for mammalian and fungal
cytochrome P450 enzymes.
The triazoles tend to have fewer side effects,
better absorption, better drug distribution in
body tissues, and fewer drug interactions.

47. Fluconazole does not require an acidic
environment, as does ketoconazole, for GI absorption.
About 80 to 90% of an orally administered
dose is absorbed, yielding high serum drug levels. The
t1/2 of the drug is 27 to 37 h, permitting once-daily
dosing in patients with normal renal function. Only 11%
of the circulating drug is bound to plasma proteins.
The drug penetrates widely into most body tissues.
Cerebrospinal fluid levels are 60 to 80% of serum levels,
permitting effective treatment for fungal meningitis.
About 80% of the drug is excreted unchanged in the
urine. Dosage reductions are required in the presence
of renal insufficiency.

48. Fluconazole is very effective in the treatment of infec-
tions with most Candida spp. Thrush in the end-stage
AIDS patient, often refractory to nystatin, clotrimazole,
and ketoconazole, can usually be suppressed with oral
fluconazole. AIDS patients with esophageal candidiasis
also usually respond to fluconazole. A single 150 mg
dose has been shown to be an effective treatment for
vaginal candidiasis. A 3-day course of oral fluconazole is
an effective treatment for Candida urinary tract infection.
Stable non-neutropenic patients with candidemia
can be adequately treated with fluconazole.

49. Fluconazole may be an alternative to amphotericin B
in the initial treatment of mild cryptococcal
meningitis and coccidioidal meningitis.
A significant decrease in mortality from deep-seated
mycoses was noted among bone marrow transplant
recipients treated prophylactically with fluconazole.
Fluconazole taken prophylactically by end-stage AIDS
patients can reduce the incidence of cryptococcal
meningitis, esophageal candidiasis, and
superficial fungal infections.

50. Fluconazole is well tolerated. Asymptomatic liver enzyme
elevation has been described, and several cases of
drug associated hepatic necrosis have been reported.
Alopecia has been reported as a common adverse event
in patients receiving prolonged high-dose therapy.
Coadministration of enzyme inhibitor fluconazole with
phenytoin results in increased serum phenytoin levels.

51. Itraconazole is lipophilic and water insoluble
and requires a low gastric pH for absorption.
Oral bioavailability is variable (20 to 60%). It is
highly protein bound (99%) and is metabolized
in the liver and excreted into the bile.
Itraconazole is most useful in the long-term suppressive
treatment of disseminated histoplasmosis in AIDS and
in the oral treatment of nonmeningeal blastomycosis.
It is the drug of choice for all forms of sporotrichosis
except meningitis. Itraconazole has replaced
ketoconazole as the drug of choice in the treatment
of paracoccidioidomycosis and chromomycosis.

52. Sporo-
trichosis
Sporothrix schenkii

53. Ketoconazole (Nizoral®) can be absorbed orally,
but it requires an acidic gastric environment.
It remains useful in the treatment of cutaneous and
mucous membrane dermatophyte and yeast infections,
but it has been replaced by the newer triazoles in the
treatment of most serious Candida infections and
disseminated mycoses. Ketoconazole is usually
effective in the treatment of thrush, but fluconazole
is superior to ketoconazole for refractory thrush.
Widespread dermatophyte
infections on skin surfaces
can be treated easily
with oral
ketoconazole.
Thrush

54. Nausea, vomiting, and anorexia occur commonly with
ketoconazole when high doses are prescribed.
Epigastric distress can be reduced by taking ketoconazole
with food. Pruritis and/or allergic dermatitis occurs in
10% of patients. Liver enzyme elevations during therapy
are usually reversible. Severe ketoconazole-
associated hepatitis is rare. At high doses,
ketoconazole causes a clinically significant
reduction in testosterone synthesis and blocks
the adrenal response to corticotrophin. Gynecomastia,
impotence, reduced sperm counts, and diminished libido
can occur in men, and prolonged drug use can result
in irregular menses in women. These hormonal effects
have led to the use of ketoconazole as a potential
adjunctive treatment for prostatic carcinoma.

55. Clotrimazole is a broad-spectrum fungistatic
imidazole drug used in the topical treatment of oral,
skin, and vaginal infections with C. albicans. It is
also employed in the treatment of infections with
cutaneous dermatophytes. Topical use results in
therapeutic drug concentrations in the epidermis
and mucous membranes; less than 10% of the
drug is systemically absorbed.

56. 3. Fluorinated pyrimidines
Flucytosine (5-flucytosine, 5-FC)
is an analogue of cytosine that was originally
synthesized for possible use as an antineoplastic
agent. 5-FC is converted to 5-fluorouracil inside the cell
by the fungal enzyme cytosine deaminase. The active
metabolite 5-fluorouracil interferes with fungal DNA
synthesis by inhibiting thymidylate synthetase.
Incorporation of these metabolites into fungal RNA
inhibits protein synthesis.
Flucytosine has a significant antifungal activity against
Candida spp. and the fungal organisms responsible
for chromomycosis.

57. 4. Allylamines – reversible noncompetitive
inhibitors of the fungal enzyme squalene
monooxygenase, which converts squalene to lanosterol.
With a decrease in lanosterol production, ergosterol
production is also diminished, affecting fungal cell
membrane synthesis and function. These agents
exhibit fungicidal activity against dermatophytes
and fungistatic activity against yeasts.
Naftifine is available for topical use only in the treat-
ment of cutaneous dermatophyte and Candida infections.
Terbinafine (Lamisil®) is available for
topical and systemic use (oral tablet) in
the treatment of dermatophyte skin and
nail infections.

59. Antibiotic
Generic name/ Oral dose Dosage interval Dosage form
Brand name*
Amoxicillin 500-1 000 mg every 8 hours 250 and 500 mg Cap.
(Amoxil® generic) 1 000 mg (pneumonia) 125 and 250 mg Chew. Tab.
Amoxicillin- 250 mg - 125 mg every 8 hours 250 mg - 125 mg Tab.
clavulanate potassium 500 mg - 125 mg every 8 hours 500 mg - 125 mg Tab.
(Clavulin® or others)
875 mg - 125 mg every 12 hours 875 mg - 125 mg Tab.
Azithromycin 500 mg DIE day 1 every 24 hours 250 mg Tab.
(Zithromax® or others) then 250 mg DIE x 4 days
Cefadroxil 1 000-2 000 mg/jour every 12 or 24 hours 500 mg Cap.
(Duricef® generic) (urinary tract infections)
1 000 mg/day (pharyngitis)
Cefprozil 250-500 mg every 12 hours 250 and 500 mg Tab.
(Cefzil® or others) 500 mg (urinary tract infections) every 24 hours
Cefuroxime axetil 250-500 mg every 12 hours 250 and 500 mg Tab.
(Ceftin® or others)
Cephalexin 500-1 000 mg every 6 or 12 hours 250 and 500 mg Cap. or Tab.
(Keflex® generic)
Ciprofloxacin 250-750 mg every 12 hours 250, 500 and 750 mg Tab.
(Cipro® or others)
Ciprofloxacin XL 500-1 000 mg every 24 hours 500 and 1 000 mg Tab.
(Cipro XL®) (urinary tract infections)
Clarithromycin 250 mg (pharyngitis) every 12 hours 250 mg Tab.
(Biaxin Bid® or others) 500 mg (bronchitis, pneumonia, every 12 hours 500 mg Tab.
sinusitis)
(Biaxin XL®) 1 000 mg (bronchitis, pneumonia, every 24 hours 500 mg Tab.
sinusitis, pharyngitis)
Clindamycin 150-450 mg every 6 hours 150 and 300 mg Cap.
(Dalacin C® or others)
Doxycyclin 100 mg (bronchitis, pneumonia) every 12 hours 100 mg Cap. or Tab.
(Vibra-Tabs® or others)
Levofloxacin 250-750 mg every 24 hours 250, 500 and 750 mg Tab.
(Levaquin® or other)
DOSAGE GUIDELINES COMMONLY USED IN ADULTS

60. Antibiotic
Generic name/ Oral dose Dosage interval Dosage form
Brand name*
Metronidazole 250 mg every 6 hours 250 mg Tab.
(Flagyl® generic)
500 mg every 8 hours
Moxifloxacin 400 mg every 24 hours 400 mg Tab.
(Avelox®)
Nitrofurantoin 100 mg every 12 hours 100 mg Cap.
(MacroBid®)
(Macrodantin® generic) 50-100 mg every 6 hours 50 and 100 mg Cap.
Norfloxacin 400 mg every 12 hours 400 mg Tab.
(Generic)
Ofloxacin 200 mg every 12 hours 200, 300 and 400 mg Tab.
(Generic)
Penicillin V 300 mg every 6 hours 300 mg Tab.
(Pen-Vee® generic) 600 mg
(pharyngitis) every 12 hours
Trimethoprim- 160 mg - 800 mg every 12 hours 160 mg - 800 mg Tab.
sulfamethoxazole
(Septra DS® generic)
Trimethoprim 100-200 mg every 12 or 24 hours 100 and 200 mg Tab.
(Generic)
Vancomycin 125-500 mg every 6 hours 125 and 250 mg Cap.
(Vancocin®)
DOSAGE GUIDELINES COMMONLY USED IN ADULTS