Prepared by:

REYSAN S. COSAS, RPh

 Module 5: BACTERIOLOGY
I. Definition of bacteria & bacteriology
II. Classification of Bacteria
III. Antibacterial chemotherapy
IV. Medical Bacteriology
Bacteriology is a subdivision of microbiology
which involves the identification, classification, and
characterization of bacterial species.
Etymology
• The word bacteria is the plural of the New Latin bacterium,
which is the latinisation of the Greek βακτήριον (bakterion),
the diminutive of βακτηρία (bakteria), meaning "staff, cane",
because the first ones to be discovered were rod-shaped.
•Bacteria (singular: bacterium) constitute a large domain of
prokaryotic microorganisms.
•Bacteria are microscopic organisms whose single cells have
neither a membrane-enclosed nucleus nor other membrane-
enclosed organelles like mitochondria and chloroplasts.
• Fastidious microorganisms
• do not grow on ordinary culture media, requiring additional growth
factors for successful cultivation.
• Non-fastidious microorganisms
• are easily cultivated because of their ability to grown on ordinary
media such as NA, and NB.
• Many bacterial pathogen can be isolated on solid agar-
containing media:
• Non-selective media (usually enriched medium)
• Differential media
• Selective media
• Also called as structural characteristics
• Bacterial shapes may be:
• Spherical (cocci)
• Rod (bacilli)
• Comma (vibrios)
• Corkscrew (spirochetes)
• Spiral (spirilla)
• This staining technique broadly divides bacteria on the basis of
fundamental differences in the structure of their cell walls.
• Differential gram staining procedure classify bacteria broadly
as:
• Gram-positive (purple color)
• Gram-negative (pink color)
• OXIDASE TEST
• It is used to distinguish organisms on the basis of the presence or
absence of a respiratory enzymes, cytochrome C, the lack of which
differentiates Enterobacteriaceae from other gram-negative rods.
• CATALASE TEST
• The test is particularly useful in differentiation of Gram-positive cocci:
staphylococci (positive) from streptococci (negative)
• COAGULASE TEST
• It is used to differentiate Staphylococcus aureus from other less
pathogenic staphylcocci.
• Serological testing can differentiate not only among microbial
species, but also among strains within species.
• Strains with different antigens are called serotypes, serovars, or
biovars.
• Serologic tests may include:
• ELISA
• Western blotting
CLINICALLY IMPORTANT ANTIBACTERIAL AGENTS
• An ideal antimicrobial agent exhibits selective toxicity, which means
that the drug is harmful to a pathogen without being harmful to the
host.
• There are four major sites in the bacterial cell that are sufficiently
different from the human cell that they serve as the basis for the action
of clinically effective drugs:
ücell wall
üribosomes
ünucleic acids
ücell membrane
• These are agents produced from a microorganisms that can inhibit the
growth of other microorganisms.

• 2 general types:
• Bactericidal drug kills bacteria.
• Bacteriostatic drug inhibits their
growth but does not kill them.
• Bactericidal drug kills bacteria.

• Bacteriostatic drug inhibits their growth but does

not kill them.
• Broad-spectrum antibiotics are active against several types of
microorganisms
• e.g., tetracyclines are active against many gram-negative rods,
chlamydiae, mycoplasmas, and rickettsiae
• Narrow-spectrum antibiotics are active against one or very few
types
• e.g., vancomycin is primarily used against certain gram-positive cocci,
namely, staphylococci and enterococci
• Erythromycin (Streptomyces erythraea)
• Thienamycin (Streptomyces cattleya)
• Streptomycin (Streptomyces griseus)
• Chlortetracycline (Streptomyces aureofaciens)
• Vancomycin (Streptomyces orientalis)
• Nystatin (Streptomyces noursei)
• Amphotericin B (Streptomyces nodosus)
• Neomycin (Streptomyces fradiae)
• Oxytetracycline (Streptomyces rimosus)
• Natamycin (Streptomyces natalensis)
• Kanamycin (Streptomyces kanamyceticus)
• Chloramphenicol (Streptomyces venezuelae)
• Rifampicin (Streptomyces mediterranei)
• Cycloserine (Streptomyces orchidaceus)
• Clindamycin (Streptomyces lincolnensis)
• Daptomycin (Streptomyces roseosporus)
• Capreomycin Sulfate (Streptomyces capreolus)
• Tobramycin (Streptomyces tenebrarius)
• Quinupristin (Streptomyces pristinaespiralis)
• Paromomycin (Streptomyces rimosus)
• Clavulanic acid (Streptomyces clavugeris)
• Mitomycin C (Streptomyces caespitosus)
• Dactinomoycin (Streptomyces parvilus)
• Daunorubicin (Streptomyces peucetius)
• Doxorubicin (Streptomyces peucetius var. caesius)
• Bleomycin (Streptomyces verticillus)
• Bacitracin (Bacillus subtilis)
• Gramicidin (Bacillus brevis)
• Polymyxin B (Bacillus polymyxa)
• Griseofulvin (Penicillium griseofulvum)
• Penicillin (Penicillium notatum)
• Gentamicin (Micromonospora purpurea)
• Colistin (Aerobacillus colistinus)
• Teicoplanin (Actinoplanes teichomyceticus)
• Cephalosporins (Cephalosporium spp.)
1. Inhibition of cell wall synthesis
2. Inhibition of cell membrane function
3. Inhibition of protein synthesis (ie, inhibition of translation and
transcription of genetic material)
4. Inhibition of nucleic acid synthesis
1. ADDITION
2. SYNERGISM
3. ANTAGONISM
4. POTENTIATION
INHIBITOR OF CELL WALL SYNTHESIS

β-LACTAM ANTIBIOTICS
INHIBITOR OF CELL WALL SYNTHESIS

β-LACTAM ANTIBIOTICS
• Mechanism Action
• Beta lactam antibiotics binds to a variety of receptors in the bacterial
cell membrane and cell wall, called penicillin-binding proteins (PBPs).
• Beta lactam antibiotics act by inhibiting transpeptidases, the enzymes
that catalyze the final cross-linking step in the synthesis of
peptidoglycan
• Autolytic enzymes called murein hydrolases are activated in penicillin-
treated cells and degrade the peptidoglycan.
INHIBITOR OF CELL WALL SYNTHESIS

β-LACTAM ANTIBIOTICS
• Clinical Uses
• Effective for both gram-negative and gram-positive bacteria
• Ineffective for the following conditions:
• Cell wall-less microorganisms
• Acid fast bacterium
• Intracellular parasites
• Resistant microorganisms
• Adverse Effect
• Causing allergic or anaphylactic reaction
• Cross-sensitivity reaction
• Jarisch-Herxheimer reaction
INHIBITOR OF CELL WALL SYNTHESIS

Penicillins
• Natural Penicillins
• Benzylpenicillin
• Aqueous penicillin G, which is metabolized most rapidly.
• Procaine penicillin G, metabolized more slowly and is less painful when injected
intramuscularly.
• Benzathine penicillin G, metabolized very slowly and is often called a “depot”
preparation.
• Phenoxymethylpenicillin
• Semisynthetic Penicillins
• Penicillinase-Resistant Penicillins
• Isoxazolylpenicillins
• Extended-Spectrum Penicillins
• Aminopenicillins, Carboxypenicillins, Ureidopenicillins
• Penicillins Plus β-Lactamase Inhibitors
INHIBITOR OF CELL WALL SYNTHESIS

Cephalosporins
FIRST SECOND THIRD FOURTH FIFTH
GENERATION GENERATION GENERATION GENERATION GENERATION
Ceftizoxime
Cefamandole
Ceftriaxone
Cefuroxime
Cefotaxime
Cefonicid
Cephalothin Ceftazidime
Cefaclor
Cephapirin Cefoperazone
Cefoxitin
Cefazolin Moxalactam Cefepime Ceftaroline
Cefotetan
Cephalexin Cefixime Cefpirome Ceftobiprole
Cefprozil
Cephradine Cefpodoxime
Cefmetazole
Cefadroxil proxetil
Cefuroxime axetil
Ceftibuten
Loracarbef
Cefdinir
Cefditoren
INHIBITOR OF CELL WALL SYNTHESIS

𝝱-LACTAM ANTIBIOTICS
combined with 𝝱-lactamase Inhibitors
• CLASS I 𝝱-lactamase Inhibitors
• Clavam (Clavulanic acid)
• Amoxicillin and Clavulanic acid (Co-amoxiclav)
• Penams (Sulbactam, Tazobactam)
• Ampicillin and Sulbactam (Sultamicillin)
• Piperacillin and Tazobactam (Tazocin®, Piptaz®)
• Ceftolozane and Tazobactam
• Diazobicyclocarbamoyl sulfate (Avibactam)
• Ceftazidime and Avibactam
• CLASS II 𝝱-lactamase Inhibitors
• Carbapenems
INHIBITOR OF CELL WALL SYNTHESIS

Monobactams
• Narrow spectrum antibiotics and resistant to β-lactamases.
• Active against gram-negative rods primarily through binding to
PBP3 but not against gram-positive bacteria or anaerobes.
• The first clinically useful monobactam is Aztreonam.
INHIBITOR OF CELL WALL SYNTHESIS

Carbapenems
• Widest spectrum among the β-lactam antibiotics.
• Used for empiric therapy associated with wide variety of
microorganisms.
• Clinically useful carbapenems include:
• Imipenem
• Meropenem
• Ertapenem
• Doripenem
INHIBITOR OF CELL WALL SYNTHESIS

Vancomycin
• Mechanism of Action
• Directly bind to the d-alanyl-d-alanine portion of the pentapeptide,
which blocks the transpeptidation.
• It also inhibits a second enzyme, transglycosylase.
• Clinical uses
• Effective agent against Pseudomembranous colitis
• Drug of choice for resistant infections such as MRSA and MRSE
• Adverse effect
• Red Man Syndrome
INHIBITOR OF CELL WALL SYNTHESIS

Bacitracin
• Mechanisms of Action
• Prevent the dephosphorylation of the phospholipid that carries the
peptidoglycan subunit across the cell membrane. This blocks the
regeneration of the lipid carrier and inhibits cell wall synthesis.
• Clinical uses
• Its only use is for topical application to skin, wounds, or mucous
membranes.
INHIBITOR OF CELL WALL SYNTHESIS

Cycloserine
• Mechanisms of Action
• Inhibit cell wall synthesis by inhibiting the activity of alanine racemase
and d-alanyl-d-alanine ligase.
• Clinical uses
• It is used as a second-line drug in the treatment of tuberculosis.
INHIBITOR OF CELL WALL SYNTHESIS

Other Glycopeptides and Lipopeptides

• Teicoplanin
• Teicoplanin has a structure similar to that of vancomycin.
• Dalbavancin, Oritavancin, and Televancin
• Some newer glycopeptides with hydrophobic substituents which
inhibit the transglycosylation of cell wall peptidoglycan synthesis by
forming a complex with the d-alanyl-d-alanine residues, and they also
depolarize the bacterial cell membrane.
• Daptomycin
• Daptomycin is a naturally occurring cyclic lipopeptide produced by
Streptomyces roseosporus. It cause depolarization of the bacterial
membrane in a calcium- dependent manner. A major adverse effect is
reversible myopathy.
INHIBITOR OF CELL MEMBRANE FUNCTION

Polymyxins
• Mechanism of Action
• Bind to cell membranes rich in phosphatidylethanolamine and
destroying membrane functions of active transport and permeability
barrier.
• Clinical Uses
• Because of their toxicity and poor distribution to tissues, the
polymyxins were used primarily topically and rarely for systemic
infections.
• Clinically useful member is Polymyxin E (colistin) and Polymyxin B.
INHIBITOR OF PROTEIN SYNTHESIS
INHIBITOR OF PROTEIN SYNTHESIS

GENERAL MECHANISMS OF ACTION

PROTEIN SYNTHESIS INHIBITORS
INHIBITOR OF PROTEIN SYNTHESIS

Aminoglycosides
• Mechanism of Action
• Inhibit protein synthesis of bacteria by attaching to and inhibiting the
function of the 30S subunit of the bacterial ribosome.
• Clinical uses
• Used most widely against gram-negative enteric bacteria or when there
is suspicion of sepsis. Poor bioavailability, hence, IM administration.
• The group includes streptomycin, neomycin, kanamycin, amikacin,
gentamicin, tobramycin, sisomicin, netilmicin, arbekacin, and
dibekacin. Spectinomycin is an aminocyclitol antibiotic (related to
aminoglycosides)
• Adverse effects
• All are potentially ototoxic, vestibulotoxic and nephrotoxic, although to
different degrees.
INHIBITOR OF PROTEIN SYNTHESIS

Aminoglycosides
• Characteristics
• All are poorly absorbed from the gastrointestinal tract. Therefore, most
aminoglycosides are administered intramuscularly.
• All aminoglycosides are more active at alkaline pH than at acid pH.
• All are potentially ototoxic and nephrotoxic, although to different
degrees.
• All can accumulate in renal failure; therefore, marked dosage
adjustments must be made when nitrogen retention occurs.
INHIBITOR OF PROTEIN SYNTHESIS

Tetracyclines
• Mechanism of Action
• Inhibit the binding of amino-acyl-tRNA to the 30S unit of bacterial
ribosomes
• Clinical uses
• Widest or broadest spectrum among the antibiotics and susceptible
against gram-positive and gram-negative bacteria & are drugs of choice
in infections caused by rickettsiae, Anaplasma, Bartonella, chlamydiae,
and Mycoplasma pneumoniae.
• Include tetracycline, doxycycline, minocycline, demeclocycline.
• Adverse effects
• Avid chelators of metals, contraindicated in children, Fanconi-like
syndrome, renal failure, ototoxicity, and phototoxicity.
INHIBITOR OF PROTEIN SYNTHESIS

Glycylcyclines
• Synthetic analogs of the tetracyclines.
• Clinical Uses
• Tigecycline, the only agent, is the 9-tert-butyl-glycylamido derivative
of minocycline.
• Tigecycline is active against a broad spectrum of gram-positive and
gram- negative pathogens.
• Compared with the tetracyclines, it is more active against MRSA and S
epidermidis, drug-susceptible and drug-resistant S pneumoniae, and
enterococci.
INHIBITOR OF PROTEIN SYNTHESIS

Macrolides
• Mechanism of Action
• Macrolides attach to a receptor (a 23S rRNA) on the 50S subunit of the
bacterial ribosome. They inhibit protein synthesis by interfering with
translocation reactions and the formation of initiation complexes.
• Clinical Uses
• Substitutes for penicillins in persons with hypersensitivity.
• Clinically useful agents include erythromycin, azalides (clarithromycin
and azithromycin). The ketolide, Telithromycin, is semisynthetic
derivative of erythromycin.
• Adverse effects
• Drug fever, mild GI upsets. Cholestatic hepatitis in erythromycin
estolate. Cardiac arrhythmias in azithromycin.
INHIBITOR OF PROTEIN SYNTHESIS

Lincosamides
• Mechanism of Action
• Resemble erythromycin in mode of action, antibacterial spectrum, and
ribosomal receptor site but are chemically distinct.
• Clinical Uses
• Clindamycin and lincomycin are clinically useful agents.
• Active against Bacteroides species and other anaerobes infection.
• Effective for skin and soft tissue infections.
• Adverse effects
• Prominent as a cause of antibiotic-associated colitis caused by C.
difficile.
INHIBITOR OF PROTEIN SYNTHESIS

Chloramphenicol
• Mechanism of Action
• Block the attachment of amino acids to the nascent peptide chain on
the 50S unit of ribosomes by interfering with the action of peptidyl
transferase.
• Clinical Uses
• Its spectrum is similar to those of the tetracyclines.
• Extensively useful for treatment of typhoid fever.
• It is bacteriostatic against Salmonella typhi, but has bactericidal activity
against the three important encapsulated organisms that cause
meningitis: Haemophilus influenzae, Streptococcus pneumoniae, and
Neisseria meningitidis.
• Adverse effects
• Gray baby syndrome, bone marrow suppression (aplastic anemia)
INHIBITOR OF PROTEIN SYNTHESIS

Oxazolidinones
• Mechanism of Action
• Bind to the 23S ribosomal RNA in the 50S subunit and inhibits protein
synthesis.
• Clinical Uses
• Linezolid and tedizolid are useful agents.
• Most frequently used to treat pneumonia, bacteremia, and skin and
soft tissue infections caused by vancomycin-resistant staphylococci and
enterococci.
• Adverse effects
• Reversible thrombocytopenia
INHIBITOR OF PROTEIN SYNTHESIS

Streptogramins
• Mechanism of Action
• Cause premature release of the growing peptide chain from the 50S
ribosomal subunit.
• Clinical Uses
• Quinupristin–dalfopristin (Synercid) is an injectable streptogramin
antibiotic consisting of a 30:70 mixture of two semisynthetic derivatives
of pristinamycin (a group B streptogramin) and dalfopristin (a group A
streptogramin).
• The two components act synergistically to inhibit a wide spectrum of
gram-positive bacteria, including methicillin-resistant staphylococci,
VRE, and penicillin-resistant pneumococci.
INHIBITOR OF PROTEIN SYNTHESIS

Pleuromutilins
• Mechanism of Action
• Inhibit bacterial protein synthesis by binding to the 23S RNA of the 50S
subunit and blocking attachment of the donor tRNA.
• Clinical Uses
• Two of the best-known examples of this group are mutilin and
retapamulin.
• They are effective against gram-positive bacteria.
• Retapamulin is a topical antibiotic used in the treatment of skin
infections, such as impetigo, caused by S. pyogenes and methicillin-
sensitive S. aures.
INHIBITOR OF NUCLEIC ACID SYNTHESIS

Quinolones and Fluoroquinolones

• Mechanism of Action
• Inhibition of bacterial DNA synthesis by blocking of DNA gyrase and
topoisomerase IV.
• Clinical Uses
• Effective in urinary tract infections. Treatment of sexually transmitted
diseases (N. gonorrhoeae and C. trachomatis). Control lower respiratory
infections caused by infection with H. influenzae. Enteritis caused by
salmonellae, shigellae, or campylobacters.
• Adverse effects
• Occurrence of tendinitis in adults resulting in tendon rupture, and
phototoxicity.
INHIBITOR OF NUCLEIC ACID SYNTHESIS

Quinolones and Fluoroquinolones

FIRST SECOND THIRD FOURTH
GENERATION GENERATION GENERATION GENERATION

Norfloxacin Levofloxacin
Nalidixic acid Ciprofloxacin Sparfloxacin Trovafloxacin
Cinoxacin Enoxacin Moxifloxacin Gatifloxacin
Ofloxacin Gemifloxacin

The fluorinated derivatives have greater antibacterial activity and

low toxicity and achieve clinically useful levels in blood and tissues.
INHIBITOR OF NUCLEIC ACID SYNTHESIS

Quinolones and Fluoroquinolones

CLINICALLY USEFUL AGENTS
• Ciprofloxacin
• Used as treatment and prophylaxis of anthrax
• Ciprofloxacin & Levofloxacin
• Used as treatment for uncomplicated UTI
• Respiratory Fluoroquinolones
• Levofloxacin, Gatifloxacin, Gemifloxacin, Moxifloxacin
• Used as treatment of upper respiratory tract infection (URTI) and lower
respiratory tract infection (LRTI).
INHIBITOR OF NUCLEIC ACID SYNTHESIS

Rifamycins
• Mechanism of Action
• Bind strongly to DNA-dependent RNA polymerase and thus inhibit
RNA synthesis in bacteria.
• Clinical Uses
• Active in vitro against some gram-positive and gram-negative cocci,
some enteric bacteria, mycobacteria, chlamydiae, and poxviruses.
• Some clinically useful agents include rifampin, rifabutin, rifaximin, and
rifapentine.
• Adverse effects
• Rifampin imparts a harmless orange color to urine, sweat, and contact
lenses.
INHIBITOR OF METABOLIC PRECURSORS (ANTIMETABOLITES)

Sulfonamides
• Mechanism of Action
• Competitive inhibition of PABA utilization by blocking
dihydropteroate synthetase.
• Clinical Uses
• Active against gram-negative and gram-positive bacteria, chlamydiae,
nocardiae, and protozoa.
• Prontosil red, silver sulfadiazine, The “soluble” sulfonamides
(trisulfapyrimidines, sulfisoxazole), sulfamethoxypyridazine,
sulfamethoxazole (SMZ)
• Adverse effects
• Erythema multiforme. Stevens-Johnson syndrome. Toxic epidermal
necrolysis. Contraindicated in G6PD Deficiency, hemolysis, and
jaundice.
INHIBITOR OF METABOLIC PRECURSORS (ANTIMETABOLITES)

Trimethoprim, Pyrimethamine, Trimetrexate

• Mechanism of Action
• Inhibition of dihydrofolate reductase
• Clinical Uses
• Clinically combined with sulfonamides to treat urinary tract infections,
shigellosis, and salmonellosis and infections with other gram-negative
bacterial infections and in pneumocystis pneumonia.
• Adverse effects
• Megaloblastic anemia
INHIBITOR OF METABOLIC PRECURSORS (ANTIMETABOLITES)

Antimetabolite Combinations
• Sulfamethoxazole +
Trimethoprim (Co- Trimoxazole)
• The drug of choice for Pneumocystis
carnii pneumonia
• Sulfadiazine + Pyrimethamine
(Daraprim)
• The drug of choice for Toxoplasmosis
• Sulfadoxime + Pyrimethamine
(Fansidar)
• Used for the treatment of malaria
ANTIMYCOBACTERIAL AGENTS
ANTIMYCOBACTERIAL AGENTS

Isoniazid (INH)
• Mechanism of Action
• Act on mycobacteria by inhibiting the synthesis of mycolic acids and
also by inhibiting the catalase-peroxidase enzyme.
• Clinical Uses
• Used in combination with other antimycobacterial agents (especially
ethambutol or rifampin) to reduce the emergence of resistant tubercle
bacilli.
• Adverse effects
• Patients receiving INH excrete pyridoxine in excessive amounts, which
results in peripheral neuritis.
ANTIMYCOBACTERIAL AGENTS

Ethambutol
• Mechanism of Action
• Act by blocking arabinosyl transferase thereby inhibiting the synthesis
of arabinogalactan.
• Clinical Uses
• Used in combination with other antimycobacterial agents to reduce the
emergence of resistant tubercle bacilli.
• Adverse effects
• The most common side effects are visual disturbances (red-green visual
disturbance): reduction in visual acuity, optic neuritis, and perhaps
retinal damage.
ANTIMYCOBACTERIAL AGENTS

Pyrazinamide
• Mechanism of Action
• Act by inhibiting a fatty acid synthetase that prevents the synthesis of
mycolic acid.
• Clinical Uses
• Used in combination with other antimycobacterial agents to reduce the
emergence of resistant tubercle bacilli.
• Adverse effects
• The major adverse effects of pyrazinamide are hepatotoxicity (most
hepatotoxic among anti-TB drugs), nausea, vomiting, hypersensitivity,
and hyperuricemia.
ANTIMYCOBACTERIAL AGENTS

ANTIMYCOBACTERIAL COMMON SIDE EFECTS and

AGENTS RESCUE DRUGS
Harmless orange color to urine, sweat, and contact
Rifampicin (Rifampin)
lenses.
Peripheral neuropathy. Pyridoxine (Vitamin B6) is a
Isoniazid
rescue drug to avoid neuropathy.
Most hepatotoxic. Silymarin (Silibinin) is a rescue drug
Pyrazinamide
to avoid liver toxicity.
Optic neuritis. Blue-green visual disturbance. Lutein is a
Ethambutol
rescue drug to avoid blindness.
ANTIMYCOBACTERIAL AGENTS

Other Antimycobacterial agents

• Treatment of MDR-TB
• Streptomycin (The only aminoglycosides with antimycobacterial activity)

• Second-line treatment during XDR-TB

• Fluoroquinolones (Levofloxacin or Moxifloxacin)
• Ethionamides
• Cycloserine
• P-aminosalicylic Acid
MISCELLANEOUS ANTIBACTERIAL AGENTS

Urinary Antiseptics
• Nitrofurantoin
• Active against many bacteria but may cause gastrointestinal distress.
• Fosfomycin
• A derivative of phosphonic acid and is used primarily in the United
States as single-dose therapy for urinary tract infections caused by E
coli and other Enterobacteriaceae and enterococci.
• Nalidixic acid
• A quinolone effective only in urine, but resistant bacteria may rapidly
emerge in the urine.
• Methenamine mandelate and methenamine hippurate
• Acidify the urine and liberate formaldehyde.
MISCELLANEOUS ANTIBACTERIAL AGENTS

Other Drugs With Specialized Uses

• Dapsone
• Combined therapy with dapsone and rifampin is often given in the
initial therapy of leprosy and treat pneumocystis pneumonia in AIDS
patients.
• Nitroimidazoles (Metronidazole, Tinidazole)
• An antiprotozoal drug used in treating trichomonas, Giardia, and
amoebic infections. Effective for the preoperative preparation of the
colon and in antibiotic-associated diarrhea caused by toxigenic C.
difficile.
• Mupirocin (pseudomonic acid)
• Inhibit the staphylococcal isoleucyl tRNA synthetase. Topically used in
treatment of skin infections caused by Staphylococcus.
1. Microorganisms produce enzymes that destroy the active drug.
2. Microorganisms change their permeability to the drug.
3. Microorganisms develop an altered structural target for the drug.
4. Microorganisms develop an altered metabolic pathway that bypasses
the reaction inhibited by the drug.
5. Microorganisms develop an altered enzyme that can still perform its
metabolic function but is much less affected by the drug.
MEDICALLY IMPORTANT BACTERIA
MEDICALLY IMPORTANT
GRAM-POSITIVE COCCI
Staphylococcus
(catalase-positive)
• Staphylococcus aureus
• Staphylococcus epidermidis
• Staphylococcus saprophyticus
Enterococcus
• Enterococcus faecalis
Streptococcus
(catalase-negative)
• Streptococcus pyogenes
• Streptococcus agalactiae
• Streptococcus pneumoniae
• Viridans Group
Streptococci (e.g., S. sanguis,
S. mutans)
MEDICALLY IMPORTANT

GRAM-NEGATIVE COCCI

Neisseria Moraxella catarrhalis

• Neisseria meningitidis
• Neisseria gonorrhoeae
Veillonella parvula
(anaerobic)
MEDICALLY IMPORTANT

GRAM-POSITIVE BACILLI
(SPORE FORMERS)

Bacillus (aerobic) Clostridium (anaerobic)

• Bacillus anthracis • Clostridium tetani
• Bacillus cereus • Clostridium botulinum
• Clostridium perfringens
• Clostridium difficile
MEDICALLY IMPORTANT

GRAM-POSITIVE BACILLI
(NON-SPORE FORMERS)

Corynebacterium diphtheriae
Listeria monocytogenes
Erysipelothrix rhusopathiae
Actinomycetes israelii (anaerobic)
Nocardia asteroides
Lactobacillus spp. (anaerobic)
Propionibacterium acnes (anaerobic)
MEDICALLY IMPORTANT

GRAM-NEGATIVE BACILLI
(FACULTATIVE ANAEROBES)

RESPIRATORY PATHOGENS ZOONOTIC PATHOGENS

• Haemophilus • Brucella spp.

• Haemophilus influenzae • Yersinia pestis
• Haemophilus ducreyi
• Francisella tularensis
• Bordetella pertusis
• Pasteurella multicoda
• Legionella pneumophila (fermentative)
MEDICALLY IMPORTANT

GRAM-NEGATIVE BACILLI
(FACULTATIVE ANAEROBES)

• Vibrio (fermentative) • Campylobacter jejuni

• Vibrio cholerae
• Vibrio parahaemolyticus • Helicobacter pylori
MEDICALLY IMPORTANT

GRAM-NEGATIVE BACILLI
Enterobacteriaceae (FACULTATIVE)
LACTOSE FERMENTER (RAPID) LACTOSE FERMENTER (SLOW)

• Klebsiella pneumoniae • Serratia marcescens

• Escherichia coli • Providencia spp.
• Enterobacter aerogenes • Edwardsiella spp.
• Citrobacter spp.
• Arizona spp.
• Erwinia spp.
MEDICALLY IMPORTANT

GRAM-NEGATIVE BACILLI
Enterobacteriaceae (FACULTATIVE)
NON-LACTOSE FERMENTER (RAPID)

• Shigella • Salmonella
• Shigella dysenteriae • Salmonella typhi
• Shigella flexneri • Salmonella choleraesius
• Shigella boydii • Salmonella enteriditis
• Shigella sonnei
• Proteus
• Proteus mirabilis
• Proteus vulgaris
MEDICALLY IMPORTANT

GRAM-NEGATIVE BACILLI

Pseudomonas aeruginosa
(aerobic, non-fermentative)

Bacteroides fragilis
(anaerobic)
MEDICALLY IMPORTANT

ACID-FAST BACILLI

Mycobacterium
TYPICAL
• Mycobacterium tuberculosis
• Mycobacterium leprae

ATYPICAL
• Mycobacterium avium
• Mycobacterium kansasii
• Mycobacterium marinum
MEDICALLY IMPORTANT

SPIROCHETES

Treponema pallidum Borrelia

• Borrelia recurrentis
• Borrelia burgdorferi
Leptospira interrogans
MEDICALLY IMPORTANT

CELL WALL-LACKING BACTERIA

Mycoplasma Ureaplasma urealyticum

• Mycoplasma pneumoniae
• Mycoplasma hominis
• Mycoplasma genitalium
MEDICALLY IMPORTANT

OBLIGATE INTRACELLUAR BACTERIA

(NON-FREE LIVING BACTERIA)

Coxiella burnetii Chlamydia

Anaplasma spp. • Chlamydia trachomatis
• Chlamydia pneumoniae
Ehrlichia spp.
• Chlamydia pssitaci
Rickettsia
• Rickettsia prowazekii
• Rickettsia typhi
• Rickettsia tsutsugamushi
• Rickettsia ricketsii