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318 Cards in this Set

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Bugs with exotoxins
"Some Say Cobra Venom Entering Buttocks Could Cause Complete Blindness So Suck"
[S aureus/pyogenes SuperAgs]
[C. diptheria, V. Cholera, E. coli, B. pertusis----ADP ribosylation/A-B toxin]
[C.perfringens, C. tetani, C. botulinum, B.antrhax, Shigela, S. pyogenes----other toxins]
some toxins encoded by lysogenic phages.
ABCDE

-shigA-like toxin
-Botulinum toxin
-Cholera toxin
-Diphtheria toxin
-Erythrogenic toxin of -Streptococcus pyogenes
examples of Obligate anaerobes
Anearobes know their ABC's

-Actinomyces
-Bacterioides
-Clostridium
Catalase

what it does and why it's bad
Catalase degrades H2O2, an antimicrobial product of PMNs. H2O2 is a substrate for myeloperoxidase.
what makes coagulase
S. aureus makes coagulase,

whereas S. epidermidis
and S. saprophyticus do not.
bacterial cAMP inducers
cAMP

-Choerae
-Anthrax
-E.coli (imagine the heat (heat -labile) has caused the E to faint and as fallen over to make an M
-Pertussis
Zoonotic bacteria
Big Bad Bugs From Yer Pet

-Bartonella henselea
-Borrelia burgdorferi
-Brucella spp.
-Francisella tularensis
-Yersinia pestis
-Pasteurella multocida
Cat scratch fever aka
Bartonella henselae
Bartonella henselae

disease states
cat scratch fever
lymphadenopathy (swelling of the lymph nodes) and fever. and Peliosis Hepatis
Peliosis Hepatis
describe
is an uncommon vascular condition characterised by randomly distributed multiple blood-filled cavities throughout liver.
is an uncommon vascular condition characterised by randomly distributed multiple blood-filled cavities throughout liver.
Peliosis Hepatis
Peliosis Hepatis
causes
HIV
bartonella
malignancy
drugs
treatment of choice for most
rickettsial infections.
Tetracycline is the
Rocky Mountain spotted fever

where in the country
Endemic to East Coast (in spite of name).
Classic cause of atypical “walking” pneumonia
Mycoplasma pneumoniae
Leptospira interrogans

appearance and where found
Question marke shape spirochete bacteria in water contaminated with animal urine
Question marke shape spirochete bacteria in water contaminated with animal urine
Leptospira interrogans
Leptospira interrogans

clinical findings
fluelike with fever, headache, stomach pain and jaundace

also Weil's disease - severe form of jaundice and azotemia from liver and kidney dysfunction; fever, hemorrhage, and anemia
Weil's disease
aka icterohemorrhagic leptospirosis - severe form of jaundice and azotemia from liver and kidney dysfunction; fever, hemorrhage, and anemia
aka icterohemorrhagic leptospirosis - severe form of jaundice and azotemia from liver and kidney dysfunction; fever, hemorrhage, and anemia
Weil's disease
VDRL mech
VDRL detects nonspecific antibody that reacts with
beef cardiolipin. Used for diagnosis of syphilis, VDRL detects nonspecific antibody that reacts with
beef cardiolipin. Used for diagnosis of syphilis, but
many biologic false positives
detects nonspecific antibody that reacts with
beef cardiolipin. Used for diagnosis of syphilis, VDRL detects nonspecific antibody that reacts with
beef cardiolipin. Used for diagnosis of syphilis, but
many biologic false positives
VDRL
Systemic mycoses can mimic
TB
(granuloma formation).
“Tricky T’s”
-Typhoid fever=Salmonella typhi
-C.trachomatis=bacteria, STD.
-Trichomonas vaginalis=protozoan, STD.
-Trichinella spiralis=worm in pork.
-Trypanosoma=Chagas’ disease or African ss.
-Treponema=spirochete; causes syphilis (T. pallidum) or yaws (T. pertenue).
Rubella aka
(German measles)
German measles aka
Rubella
Hepatitis virus families
HEP A-picornavirus
HEP B-Hepaddnavirus
HEP C-flavivirus
HEP D-deltavirus
HEP E-Calicivirus/hepivirus
Rubella findings
fever, lympadenopathy, arthralgias. mild in children, but serious congenital disease)
congenital rubella findings
# malformations of the heart (especially patent ductus arteriosus), eyes or brain
# deafness
# eye defects (especially cataract and microphthalmia
# thrombocytopenic purpura (presents as a characteristic "blueberry muffin" rash)
# malformations of the heart (especially patent ductus arteriosus), eyes or brain
# deafness
# eye defects (especially cataract and microphthalmia
# thrombocytopenic purpura (presents as a characteristic "blueberry muffin" rash)
congenital rubella findings
"lots of spots"
rubella
rubeola
varicella
variola
vaccina
TORCHES infection findings

Toxoplasma
"clasic triad" of chorioretinitis, intracranial calcifications (ring enhanced lesions) and hydrocephalus
TORCHES infection findings

rubella
deafness, cataracts, PDA/pulmonary artery stenosis, retardation
TORCHES infection findings

CMV
petechial rash, intracranial calcifications, mental retardation, hepatosplenomgaly, jaundice. 90% are asymptomatic at birth
TORCHES infection findings

HIV
hepatosplenomgaly, neurologic problems, and frequent infections
TORCHES infection findings

HSV2
encephalitis, conjunctivitis, vesicular skin lesions
TORCHES infection findings

Syphilis
cutaneous lesions, hepatosplenomgaly, jaundice, saddle nose, saber shins, hutchinson teeth, CNVIII deafness,
hutchinson teeth
teeth that are smaller and more widely spaced than normal and which have notches on their biting surfaces. a sign of congenital syphilis
teeth that are smaller and more widely spaced than normal and which have notches on their biting surfaces.
hutchinson teeth-a sign of congenital syphilis
"clasic triad" of chorioretinitis, intracranial calcifications (ring enhanced lesions) and hydrocephalus
TORCHES infection findings

Toxoplasma
TORCHES infection findings

deafness, cataracts, PDA/pulmonary artery stenosis, retardation
rubella
TORCHES infection findings

petechial rash, intracranial calcifications, mental retardation, hepatosplenomgaly, jaundice. 90% are asymptomatic at birth
CMV
TORCHES infection findings

hepatosplenomgaly, neurologic problems, and frequent infections
HIV
TORCHES infection findings

encephalitis, conjunctivitis, vesicular skin lesions
HSV2
TORCHES infection findings

cutaneous lesions, hepatosplenomgaly, jaundice, saddle nose, saber shins, hutchinson teeth, CNVIII deafness,
hutchinson teeth
Top three causes of pneumonia in

Children (6 wks–18 yr)
-Viruses (RSV)
-Mycoplasma
-Chlamydia pneumoniae
Top three causes of pneumonia in

Adults (18–40 yr)
-Mycoplasma
-C. pneumoniae
-S. pneumoniae
Top three causes of pneumonia in

Adults (40–65 yr)
-S. pneumoniae
-H. influenzae
-Anaerobes
Top three causes of pneumonia in

Elderly >65
-S. pneumoniae
-Viruses
-Anaerobes
What age group has this pneumonia pattern

-Viruses (RSV)
-Mycoplasma
-Chlamydia pneumoniae
Children (6 wks–18 yr)
What age group has this pneumonia pattern

-Mycoplasma
-C. pneumoniae
-S. pneumoniae
Adults (18–40 yr)
What age group has this pneumonia pattern

-S. pneumoniae
-H. influenzae
-Anaerobes
Adults (40–65 yr)
What age group has this pneumonia pattern

-S. pneumoniae
-Viruses
-Anaerobes
Elderly >65
Top three causes of meningitis in

Newborn (0–6 mos)
-Group B streptococci
-E. coli
-Listeria
Top three causes of meningitis in

Children (6 mos–6 yrs)
-Streptococcus pneumoniae
-Neisseria meningitidis
-Haemophilus influenzae type B
Top three causes of meningitis in

6–60 yrs
-N. meningitidis
-Enteroviruses
- S. pneumoniae
Top three causes of meningitis in

60 yrs +
-S. pneumoniae
-Gram-negative rods
-Listeria
What age group gets this pattern of meningitis

-Group B streptococci
-E. coli
-Listeria
Newborn (0–6 mos)
What age group gets this pattern of meningitis

-Streptococcus pneumoniae
-Neisseria meningitidis
-Haemophilus influenzae type B
Children (6 mos–6 yrs)
What age group gets this pattern of meningitis

-N. meningitidis
-Enteroviruses
- S. pneumoniae
6–60 yrs
What age group gets this pattern of meningitis

-S. pneumoniae
-Gram-negative rods
-Listeria
60 yrs +
UTI bugs
SSEEK PP.

Serratia marcescens, staphylococcus saprophyticus
E. coli, Enterobacter cloacae
Klebsiella, Proteus mirabilis
Pseudomonas aeruginosa
Name the Gram + Rods
Anaerobes
Anaerobes
p Acne/
Clostridum/
fragilis (is gram but is in the mnemonic)/
a. Israeli /
mobiluncus muleris
Name the Gram + Rods
Aerobes
-Cornybacterium
-Listeria
-Bacillus
-Erysipelothrix
Name the Gram - Rods
Yersinia / Haemophilus / vibrio / Helicobacter / Pseudomonas / Campylobacter / Bordatella / Bacteriodes fragilis (the only anaerobe) / Brucella / Legionella / Pasturella / Klebsiella / Shigella / E. coli / Salmonella / Francesella
Name the Gram + Cocci
Strep
Staph
Enterococcus
Name the Gram - Cocci
Nissera
Name the Gram + Rods
Anaerobes
Anaerobes
p Acne/
Clostridum/
fragilis (is gram but is in the mnemonic)/
a. Israeli /
mobiluncus muleris
Name the Gram + Rods
Aerobes
-Cornybacterium
-Listeria
-Bacillus
-Erysipelothrix
Name the Gram - Rods
Yersinia / Haemophilus / vibrio / Helicobacter / Pseudomonas / Campylobacter / Bordatella / Bacteriodes fragilis (the only anaerobe) / Brucella / Legionella / Pasturella / Klebsiella / Shigella / E. coli / Salmonella / Francesella
Name the Gram + Cocci
Strep
Staph
Enterococcus
Name the Gram - Cocci
Nissera
Penicillin

Clinical use
-gram-positive cocci,
-gram-positive rods, -gram-negative cocci,
and
-spirochetes.
Penicillin

Toxicity
Hypersensitivity reactions, hemolytic anemia.
penicillinase-resistant penicillins

names
Methicillin, nafcillin, dicloxacillin
Methicillin, nafcillin, dicloxacillin (penicillinase-resistant penicillins)

Mechanism
Same as penicillin
Methicillin, nafcillin, dicloxacillin (penicillinase-resistant penicillins)

Clinical use
S. aureus (except MRSA; resistant because of altered penicillin-binding protein target site).
Methicillin, nafcillin, dicloxacillin (penicillinase-resistant penicillins)

Toxicity
Hypersensitivity reactions; methicillin––interstitial nephritis.
aminopenicillins
names
Ampicillin, amoxicillin
Ampicillin, amoxicillin (aminopenicillins)

Mechanism
Same as penicillin. Wider spectrum; penicillinase
sensitive. Also combine with clavulanic acid
Ampicillin, amoxicillin (aminopenicillins)

Clinical use
Extended-spectrum penicillin––certain gram-positive bacteria and gram-negative rods "HELPS" (Haemophilus influenzae, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, enterococci).
Ampicillin, amoxicillin (aminopenicillins)

Toxicity
Hypersensitivity reactions; ampicillin rash;
pseudomembranous colitis.
combine with clavulanic acid
(penicillinase inhibitor) to enhance spectrum.
Ampicillin, amoxicillin (aminopenicillins)
Ampicillin, amoxicillin (aminopenicillins)

wrt combinations
combine with clavulanic acid
(penicillinase inhibitor) to enhance spectrum.
penicillin forms
Penicillin G (IV form), penicillin V (oral)
aminopenicillins

aka
Ampicillin, amoxicillin
Ampicillin, amoxicillin

aka
aminopenicillins
anti-pseudomonals

aka
TCP: Takes Care of
Pseudomonas.

Ticarcillin, carbenicillin, piperacillin
Ticarcillin, carbenicillin, piperacillin

aka
TCP: Takes Care of
Pseudomonas.

anti-pseudomonals
use with clavulanic acid.
Ticarcillin, carbenicillin, piperacillin (anti-pseudomonals)

Ampicillin, amoxicillin (aminopenicillins)
Ticarcillin, carbenicillin, piperacillin (anti-pseudomonals)

use wit
clavulanic acid (penicillinase inhibitor) to enhance spectrum.
Ticarcillin, carbenicillin, piperacillin

Mechanism
Same as penicillin. Extended spectrum.
Ticarcillin, carbenicillin, piperacillin

Clinical use
Pseudomonas spp. and gram-negative rods;
Ticarcillin, carbenicillin, piperacillin

Toxicity
Hypersensitivity reactions.
β-lactam drugs that inhibit cell wall synthesis but are
less susceptible to penicillinases. Bactericidal.
Cephalosporins
Cephalosporins

Mechanism
β-lactam drugs that inhibit cell wall synthesis but are
less susceptible to penicillinases. Bactericidal.
1st generation Cephalosporins

Clinical use
PEcK.

gram-positive cocci, Proteus mirabilis, E. coli, Klebsiella
pneumoniae.
2nd generation Cephalosporins

Clinical use
HEN PEcKS.

gram-positive cocci, Haemophilus influenzae,
Enterobacter aerogenes, Neisseria spp., Proteus, E. coli, Klebsiella , Serratia.
3rd generation Cephalosporins

Clinical use
serious gram-negative infections resistant to other
β-lactams; meningitis (most penetrate the blood-brain
barrier). Examples: ceftazidime for Pseudomonas;
ceftriaxone for gonorrhea.
4th generation Cephalosporins

Clinical use
↑ activity against Pseudomonas and gram-positive organisms.
Cephalosporins

Toxicity
Hypersensitivity reactions. Cross-hypersensitivity with
penicillins occurs in 5–10% of patients. nephrotoxicity of aminoglycosides; Disulfiram type reaction with ethanol
which Cephalosporins

Disulfiram type reaction with ethanol
with a methylthiotetrazole group, e.g., cefamandole
1st generation Cephalosporins

Names
1st generation...All cephalosporin sounds like CEF except 1st generation in 1st generation there is PH rather CEF like..->CePHalothin ,CePHaprin, CePHradine, CePHalexin

dont be FAZed, this exception is out O' LINe ..CeFAZOLIN
2nd generation Cephalosporins

Names
FOXes have FACe FUR

ceFOXitin, ceFAClor, ceFURoxime)–
3rd generation Cephalosporins

names
TRI to TAX TAZ
cefTRIaxone, cefoTAXime, cefTAZidime
4th generation Cephalosporins

names
Cefepime is the only one
what generation Cephalosporin is

cephalexin
1st generation
what generation Cephalosporin is

cefazolin
1st generation
what generation Cephalosporin is

cefuroxime
2nd generation
what generation Cephalosporin is

cefaclor
2nd generation
what generation Cephalosporin is

cefoxitin
2nd generation
what generation Cephalosporin is

ceftriaxone
3rd generation
what generation Cephalosporin is

cefotaxime
3rd generation
what generation Cephalosporin is

ceftazidime
3rd generation
what generation Cephalosporin is

cefepime
4th generation
Aztreonam

Mechanism
A monobactam resistant to β-lactamases. Inhibits cell wall synthesis (binds to PBP3). Synergistic with aminoglycosides. No cross-allergenicity with penicillins.
Aztreonam

Clinical use
Gram-negative rods––Klebsiella spp., Pseudomonas spp., Serratia spp. No activity against
gram-positives or anaerobes. For penicillin-allergic patients and those with renal
insufficiency who cannot tolerate aminoglycosides.
Aztreonam

Toxicity
Usually nontoxic; occasional GI upset.
Synergistic with aminoglycosides. No cross-allergenicity with penicillins.
Aztreonam
Gram-negative rods––Klebsiella spp., Pseudomonas spp., Serratia spp. No activity against
gram-positives or anaerobes. For penicillin-allergic patients and those with renal
insufficiency who cannot tolerate aminoglycosides.
Aztreonam
Imipenem/cilastatin, meropenem

Mechanism
Imipenem is a broad-spectrum, β-lactamase-resistant
carbapenem.
Imipenem/cilastatin, meropenem

Clinical use
Gram-positive cocci, gram-negative rods, and
anaerobes. Drug of choice for Enterobacter (esp UTI)
Imipenem/cilastatin, meropenem

Toxicity
GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels.
Always administered with cilastatin
Imipenem
Imipenem Always administered with what and why
Always administered with cilastatin (inhibitor of renal dihydropeptidase I) to ↓
inactivation in renal tubules.

With imipenem, “the kill is
LASTIN’ with ciLASTATIN.”
Drug of choice for Enterobacter.
Imipenem/cilastatin, meropenem
Vancomycin

Mechanism and resistance
Inhibits cell wall mucopeptide formation by binding D-ala D-ala portion of cell wall precursors. Bactericidal. Resistance occurs with amino acid change of D-ala D-ala to
D-ala D-lac.
Vancomycin

Clinical use
Used for serious, gram-positive multidrug-resistant organisms, including S. aureus and Clostridium difficile (pseudomembranous colitis).
Vancomycin

Toxicity
Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing––“red man syndrome”
(can largely prevent by pretreatment with antihistamines and slow infusion rate). Well tolerated in general––does NOT have many problems.
Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing
“red man syndrome” Vancomycin
Inhibits cell wall mucopeptide formation by binding D-ala D-ala portion of cell wall precursors. Bactericidal. Resistance occurs with amino acid change of D-ala D-ala to
D-ala D-lac.
Vancomycin
30S inhibitors:
A = Aminoglycosides [bactericidal]
T = Tetracyclines [bacteriostatic]
50S inhibitors:
C = Chloramphenicol, Clindamycin
E = Erythromycin [bacteriostatic]
L = Lincomycin [bacteriostatic]
L = Linezolid [bacteriostatic]
Aminoglycosides

names
Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin.

“Mean” GNATS canNOT
kill anaerobes.
Aminoglycosides

Mechanism and resistance
Bactericidal; inhibit formation of initiation complex and cause misreading of mRNA. Require O2 for
uptake; therefore ineffective against anaerobes.
Aminoglycosides

Clinical use
Severe gram-negative rod infections. Synergistic with
β-lactam antibiotics. Neomycin for bowel surgery.
Aminoglycosides

Toxicity
Nephrotoxicity (especially when used with cephalosporins ,Ototoxicity (especially when
used with loop diuretics). Teratogen.
-“Mean” GNATS canNOT kill anaerobes.
Severe gram-negative rod infections. Synergistic with
β-lactam antibiotics.
Aminoglycosides
Bactericidal; inhibit formation of initiation complex
and cause misreading of mRNA. Require O2 for
uptake; therefore ineffective against anaerobes.
Aminoglycosides
Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin.
Aminoglycosides
Tetracyclines

names
-CYCLINE

TetracCYCLINE, doxyCYCLINE, demecloCYCLINE, minoCYCLINE.
Tetracyclines

Mechanism
bind to 30S and prevent attachment of aminoacyl-tRNA; limited CNS penetration.
Tetracyclines

Clinical use
VACUUM THe BedRoom.
Vibrio cholerae, Acne, Chlamydia, Ureaplasma
Urealyticum, Mycoplasma pneumoniae, Tularemia,
H. pylori, Borrelia burgdorferi (Lyme disease), Rickettsia.
Tetracyclines

Toxicity
GI distress, discoloration of teeth and inhibition of
bone growth in children, photosensitivity.
bind to 30S and prevent attachment of aminoacyl-tRNA; limited CNS penetration.
Tetracyclines
Tetracyclines

contraindications
-Doxycycline is fecally eliminated and can be used
in patients with renal failure.
-Contraindicated in pregnancy.
Must NOT take with milk, antacids, or iron-containing
preparations because divalent cations inhibit its
absorption in the gut.
Tetracyclines
GI distress, discoloration of teeth and inhibition of
bone growth in children, photosensitivity.
Tetracyclines
Macrolides

names
Erythromycin, azithromycin, clarithromycin.
Macrolides

Mechanism
Inhibit protein synthesis by blocking translocation; bind to the 23S rRNA of the 50S
Macrolides

Clinical use
URIs, pneumonias, STDs––gram-positive cocci (streptococcal infections in patients
allergic to penicillin), Mycoplasma, Legionella, Chlamydia, Neisseria.
Macrolides

Toxicity
GI discomfort (most common cause of noncompliance), acute cholestatic hepatitis,
eosinophilia, skin rashes. Increases serum concentration of theophyllines, oral
anticoagulants.
eosinophilia, skin rashes. Increases serum concentration of theophyllines, oral
anticoagulants.
Macrolides
Inhibit protein synthesis by blocking translocation; bind to the 23S rRNA of the 50S
Macrolides
Clindamycin

Mechanism
Blocks peptide bond formation at 50S ribosomal subunit.
Clindamycin

Clinical use
Treats anaerobes above the
diaphragm.
(e.g., Bacteroides fragilis,
Clostridium perfringens).
Clindamycin

Toxicity
Pseudomembranous colitis (C. difficile overgrowth),
fever, diarrhea.
Sulfonamides

names
Sulfamethoxazole (SMX), sulfisoxazole, triple sulfas, sulfadiazine.
Sulfonamides

Mechanism
PABA antimetabolites inhibit dihydropteroate synthase.
Sulfonamides

Clinical use
Gram-positive, gram-negative, Nocardia, Chlamydia. Triple sulfas or SMX for simple UTI.
Sulfonamides

Toxicity
Hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (TIN), kernicterus in infants, displace other drugs from albumin (e.g., warfarin).
Hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (TIN), kernicterus in infants, displace other drugs from albumin (e.g., warfarin).
Sulfonamides
Trimethoprim

Mechanism
Inhibits bacterial dihydrofolate reductase.
Trimethoprim

Clinical use
Combination TMP-SMX used for recurrent UTIs, Shigella,Salmonella, Pneumocystis carinii pneumonia.
Trimethoprim

Toxicity
Trimethoprim = TMP:
“Treats Marrow Poorly.”

Megaloblastic anemia, leukopenia, granulocytopenia.
(May alleviate with supplemental folinic acid.)
Why TMP with SMX
synergy
Trimethoprim

Toxicity Tx
Megaloblastic anemia, leukopenia, granulocytopenia.
(May alleviate with supplemental folinic acid.)
Fluoroquinolones

names
-Floxacin (fluoroquinolones)

and

nalidixic acid (a quinolone).
Fluoroquinolones

Mechanism
Inhibit DNA gyrase (topoisomerase II)
Fluoroquinolones

Clinical use
Gram-negative rods of urinary and GI tracts (including Pseudomonas), Neisseria,
Fluoroquinolones

Toxicity
GI upset, superinfections, skin rashes, headache,
dizziness.
Contraindicated in pregnant women and in children damage to cartilage. Tendonitis and tendon rupture in adults;
leg cramps and myalgias in kids.
FluoroquinoLONES hurt
attachments to your
BONES.
GI upset, superinfections, skin rashes, headache,
dizziness.
Contraindicated in pregnant women and in children damage to cartilage. Tendonitis and tendon rupture in adults;
leg cramps and myalgias in kids.
Fluoroquinolones
Inhibit DNA gyrase (topoisomerase II)
Fluoroquinolones
Metronidazole

Mechanism
Forms toxic metabolites in the bacterial cell.
Metronidazole

Clinical use
GET GAP on the Metro!
Anaerobic infection below
the diaphragm.

Antiprotozoal. Giardia, Entamoeba, Trichomonas,
Gardnerella vaginalis, anaerobes (Bacteroides,
Clostridium). Used with bismuth and amoxicillin (or tetracycline) for “triple therapy” against H. Pylori.
Metronidazole

Toxicity
Disulfiram-like reaction with alcohol; headache, metallic taste.
Disulfiram-like reaction with alcohol; headache, metallic taste.
Metronidazole
Polymyxins

names
Polymyxin B, polymyxin E.
Polymyxins

Mechanism
’MYXins MIX up membranes.

Bind to cell membranes of bacteria and disrupt
their osmotic properties. Polymyxins are cationic, basic proteins that act like detergents.
Polymyxins

Clinical use
Resistant gram-negative infections.
Polymyxins

Toxicity
Neurotoxicity, acute renal tubular necrosis.
Anti-TB drugs

names and complications
INH-SPiRE (inspire). 2C

-Isoniazid (INH),
-Streptomycin,
-Pyrazinamide,
-Rifampin,
-Ethambutol.
-Cycloserine (2nd-line therapy).

All are hepatotoxic.
Isoniazid aka
INH
INH aka
Isoniazid
Isoniazid (INH)

Mechanism
↓ synthesis of mycolic acids.
Isoniazid (INH)

Clinical use
Mycobacterium tuberculosis. The only agent used as solo prophylaxis against TB.
Isoniazid (INH)

Toxicity
"INH Injures Neurons and
Hepatocytes"

Hemolysis if G6PD deficient, neurotoxicity, hepatotoxicity, SLE-like syndrome.
Pyridoxine (vitamin B6) can prevent neurotoxicity.
Isoniazid (INH)

half-life
Different INH half-lives in fast
vs. slow acetylators.
Rifampin

Mechanism
Inhibits DNA-dependent RNA polymerase.
Rifampin

Clinical use
Mycobacterium tuberculosis; delays resistance to
dapsone when used for leprosy. Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with
Haemophilus influenzae type B.
Rifampin

Toxicity
Minor hepatotoxicity and drug interactions (↑ P-450).

orange body fluids
Inhibits DNA-dependent RNA polymerase.
Rifampin
↓ synthesis of mycolic acids.
Isoniazid (INH)
Minor hepatotoxicity and drug interactions (↑ P-450).

orange body fluids
Rifampin
Rifampin mnemonic
Rifampin’s 4 R’s:
RNA polymerase inhibitor
Revs up microsomal P-450
Red/orange body fluids
Rapid resistance if used
alone
Resistance mechanisms for various antibiotics

Penicillins/
cephalosporins
β-lactamase cleavage of β-lactam ring
Resistance mechanisms for various antibiotics

β-lactamase cleavage of β-lactam ring
Penicillins/
cephalosporins
Resistance mechanisms for various antibiotics

Aminoglycosides
Modification via acetylation, adenylation, or phosphorylation
Resistance mechanisms for various antibiotics

Modification via acetylation, adenylation, or phosphorylation
Aminoglycosides
and
Chloramphenicol (acetylation only)
Resistance mechanisms for various antibiotics

Vancomycin
Terminal D-ala of cell wall component replaced with D-lac; ↓ affinity.
Resistance mechanisms for various antibiotics

Terminal D-ala of cell wall component replaced with D-lac; ↓ affinity.
Vancomycin
Resistance mechanisms for various antibiotics

Chloramphenicol
Modification via acetylation
Resistance mechanisms for various antibiotics

Macrolides
Methylation of rRNA near erythromycin’s ribosome-binding site
Resistance mechanisms for various antibiotics

Methylation of rRNA near erythromycin’s ribosome-binding site
Macrolides
Resistance mechanisms for various antibiotics

↓ uptake or ↑ transport out of cell
Tetracycline
Resistance mechanisms for various antibiotics

Tetracycline
↓ uptake or ↑ transport out of cell
Resistance mechanisms for various antibiotics

Sulfonamides
Altered enzyme (bacterial dihydropteroate synthetase), ↓ uptake, or ↑ PABA synthesis
Resistance mechanisms for various antibiotics

Altered enzyme (bacterial dihydropteroate synthetase), ↓ uptake, or ↑ PABA synthesis
Sulfonamides
Nonsurgical antimicrobial prophylaxis

Meningococcal infection
Rifampin (drug of choice), minocycline.
Nonsurgical antimicrobial prophylaxis

Rifampin (drug of choice), minocycline.
Meningococcal infection
Nonsurgical antimicrobial prophylaxis

Gonorrhea
Ceftriaxone.
Nonsurgical antimicrobial prophylaxis

Ceftriaxone.
Gonorrhea
Nonsurgical antimicrobial prophylaxis

penicillin.
Syphilis (Benzathine penicillin G)

Endocarditis with surgical or dental procedures (penicillin)
Nonsurgical antimicrobial prophylaxis

Syphilis
Benzathine penicillin G.
Nonsurgical antimicrobial prophylaxis

TMP-SMX.
-History of recurrent UTIs

Pneumocystis jiroveci
pneumonia
Nonsurgical antimicrobial prophylaxis

-History of recurrent UTIs
TMP-SMX.
Nonsurgical antimicrobial prophylaxis
TMP-SMX (DOC) , aerosolized pentamidine.
Nonsurgical antimicrobial prophylaxis

Endocarditis with surgical or dental procedures
Penicillins.
Amphotericin B

Mechanism
Amphotericin “tears” holes in
the fungal membrane by forming pores.

Binds ergosterol (unique to fungi); forms membrane
pores that allow leakage of electrolytes and
disrupt homeostasis.
Amphotericin B

Clinical use
Used for wide spectrum of systemic mycoses.
Cryptococcus, Blastomyces, Coccidioides,
Aspergillus, Histoplasma, Candida, Mucor (systemic mycoses). Intrathecally for fungal meningitis; does not cross blood-brain barrier.
Amphotericin B

Toxicity
Fever/chills (“shake and bake”), hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis
(“amphoterrible”). Hydration reduces nephrotoxicity.
Nystatin

mechanism
Binds to ergosterol, disrupting fungal membranes
Nystatin

Clinical use
Too toxic for systemic use.

“Swish and swallow” for oral candidiasis (thrush); topical for diaper rash or vaginal
candidiasis.
Binds to ergosterol, disrupting fungal membranes. Too toxic for systemic use.
Nystatin
-AZOLES

Mechanism
Inhibit fungal steroid (ergosterol) synthesis. by blocking the final step from Lanosterol to ergosterol
-AZOLES

Clinical use and which ones
Systemic mycoses. Fluconazole for cryptococcal meningitis in AIDS patients and candidal
infections of all types (i.e., yeast infections). Ketoconazole for Blastomyces, Coccidioides,
Histoplasma, Candida albicans; hypercortisolism.
-AZOLES

Toxicity
Hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome
P-450), fever, chills.
Inhibit fungal steroid (ergosterol) synthesis. by blocking the final step from Lanosterol to ergosterol
-AZOLES
Flucytosine

Mechanism
Inhibits DNA synthesis by conversion to fluorouracil, which competes with uracil.
Flucytosine

Clinical use
Used in systemic fungal infections (e.g., Candida, Cryptococcus).
Flucytosine

Toxicity
Nausea, vomiting, diarrhea, bone marrow suppression.
Terbinafine
Mechanism
Inhibits the fungal enzyme squalene epoxidase. by blocking the initial step from squaline to Lanosterol (in ergesterol synthesis)
Terbinafine

Clinical use
Used to treat dermatophytoses (especially onychomycosis).
Inhibits the fungal enzyme squalene epoxidase. by blocking the initial step from squaline to Lanosterol (in ergesterol synthesis)
Terbinafine
Caspofungin

Mechanism
Inhibits cell wall synthesis.
Caspofungin

Clinical use
Invasive aspergillosis.
Caspofungin

Toxicity
GI upset, flushing.
Tx for Invasive aspergillosis.
Caspofungin
Griseofulvin

Mechanism
Interferes with microtubule function; disrupts mitosis. Deposits in keratin-containing
tissues (e.g., nails).
Griseofulvin

Clinical use
Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea,
ringworm).
Griseofulvin

Toxicity
Teratogenic, carcinogenic, confusion, headaches, ↑ P-450 and warfarin metabolism.
antifunfal that is Teratogenic, carcinogenic, confusion, headaches, ↑ P-450 and warfarin metabolism.
Griseofulvin
Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea,
ringworm).
Griseofulvin
Interferes with microtubule function; disrupts mitosis. Deposits in keratin-containing tissues
Griseofulvin
Amantadine

Mechanism
“A man to dine” takes off his
coat.

Blocks viral penetration/uncoating (M2 protein); may buffer pH of endosome. Also causes the
release of dopamine from intact nerve terminals.
Amantadine

Clinical use
Prophylaxis and treatment for influenza A and rubellA; Parkinson’s disease.
Amantadine

Toxicity
Ataxia, dizziness, slurred speech.
Amantadine

Mechanism of resistance
Mutated M2 protein. In 2006, 90% of influenza A were resistant to amantadine.
Amantadine

mnemonic
Amantadine blocks influenza
A and rubellA and causes problems with the cerebellA.
Rimantidine
a derivative of Amantadine with fewer CNS side effects. Does not cross the BBB.
a derivative of Amantadine with fewer CNS side effects. Does not cross the BBB.
Rimantidine
Zanamivir, oseltamivir

Mechanism
Inhibit influenza neuraminidase. So release of progeny virus is decreased.
Zanamivir, oseltamivir

Clinical use
Both influenza A and B.
Blocks viral penetration and uncoating (M2 protein);
Amantadine
Inhibit influenza neuraminidase
Zanamivir, oseltamivir
Ribavirin

Mechanism
Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase.
Ribavirin

Clinical use
RSV, chronic hepatitis C.
Ribavirin

Toxicity
Hemolytic anemia. Severe teratogen.
drug for

RSV, chronic hepatitis C.
Ribavirin
Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase.
Ribavirin
Acyclovir

Mechanism
Preferentially inhibits viral DNA polymerase when phosphorylated by viral thymidine
kinase.
Acyclovir

Clinical use
HSV, VZV, EBV. Mucocutaneous and genital herpes lesions. Prophylaxis in
immunocompromised patients.
Acyclovir

Toxicity
Delirium, tremor, nephrotoxicity.
Acyclovir

Mechanism of resistance
Lack of thymidine kinase.
drug for

Prophylaxis and treatment for influenza A;
Parkinson’s disease.
Amantadine
drug for

Both influenza A and B.
Zanamivir, oseltamivir
drug for

CMV, especially in immunocompromised patients.
Ganciclovir
Ganciclovir

Mechanism
Phosphorylation by viral kinase; preferentially inhibits CMV DNA polymerase.
Ganciclovir

Clinical use
CMV, especially in immunocompromised patients.
Ganciclovir

Toxicity
Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes
than acyclovir.
Ganciclovir

Mechanism of resistance
Mutated CMV DNA polymerase or lack of thymidine kinase.
Preferentially inhibits viral DNA polymerase when phosphorylated by viral thymidine kinase.
Acyclovir
Phosphorylation by viral kinase; preferentially inhibits CMV DNA polymerase.
Ganciclovir
Foscarnet

Mechanism
FOScarnet = pyroFOSphate
analog.

Viral DNA polymerase inhibitor that binds to the
pyrophosphate binding site of the enzyme. Does not require activation by viral kinase.
Foscarnet

Clinical use
CMV retinitis in immunocompromised patients
when ganciclovir fails; acyclovir-resistant HSV.
Foscarnet

Toxicity
Nephrotoxicity.
Foscarnet

Mechanism of resistance
Mutated DNA polymerase.
drug for

CMV retinitis in immunocompromised patients
when ganciclovir fails;
Foscarnet
drug for

acyclovir-resistant HSV.
Foscarnet
HIV therapy
Protease inhibitors

names
SaquiNAVIR, ritoNAVIR, indiNAVIR, nelfiNAVIR, ampreNAVIR.

NAVIR (navir) tease a pro—
pro-tease inhibitors.
HIV therapy
Protease inhibitors

Mechanism
Inhibit assembly of new virus by blocking protease
in progeny virions.
HIV therapy
Protease inhibitors

Toxicity
GI intolerance (nausea, diarrhea), hyperglycemia,
lipodystrophy, thrombocytopenia (indinavir).
HIV therapy
Reverse transcriptase inhibitors
Nucleosides

names
DINE , SINE, and BINE

Zidovudine (AZT), didanosine (ddI), zalcitabine (ddC),
stavudine (d4T), lamivudine (3TC),
Zidovudine (AZT), didanosine (ddI), zalcitabine (ddC),
stavudine (d4T), lamivudine (3TC),
HIV therapy
Reverse transcriptase inhibitors
Nucleosides
SaquiNAVIR, ritoNAVIR, indiNAVIR, nelfiNAVIR, ampreNAVIR.
HIV therapy
Protease inhibitors

NAVIR (navir) tease a pro—
pro-tease inhibitors.
HIV therapy
Reverse transcriptase inhibitors
Non-nucleosides

names
Nevirapine, efavirenz, delavirdine.

Never Ever Deliver nucleosides.
Nevirapine, efavirenz, delavirdine.
HIV therapy
Reverse transcriptase inhibitors
Non-nucleosides

Never Ever Deliver nucleosides.
HIV therapy
Reverse transcriptase inhibitors

Mechanism
Preferentially inhibit reverse transcriptase of HIV;
prevent incorporation of viral genome into host DNA.
HIV therapy
Reverse transcriptase inhibitors

Toxicity
Bone marrow suppression (neutropenia, anemia),
peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (AZT).
HIV therapy
Reverse transcriptase inhibitors

Clinical use
Highly active antiretroviral therapy (HAART) generally entails combination therapy with protease inhibitors and reverse transcriptase.
AZT is used during pregnancy to reduce risk of fetal
transmission.
HAART

when initiated
protease inhibitors and reverse transcriptase
inhibitors. Initiated when patients have low CD4
counts (< 500 cells/mm3) or high viral load.
HIV therapy

what is used during pregnancy to reduce risk of fetal
transmission.
AZT
Interferons

Mechanism
Glycoproteins from human leukocytes that block various stages of viral RNA and DNA
synthesis. Induce ribonuclease that degrades viral mRNA.
Interferons

Clinical use
IFN-α––chronic hepatitis B and C, Kaposi’s sarcoma.
IFN-β––MS.
IFN-γ––NADPH
oxidase deficiency.
Interferons

Toxicity
Neutropenia.
Antibiotics to avoid in pregnancy

just names
SAFE Moms Take Really Good Care.

Sulfonamides, Aminoglycosides,
Fluoroquinolones, Erythromycin, Metronidazole, Tetracyclines, Ribavirin,
Griseofulvin, Chloramphenicol
Antibiotics to avoid in pregnancy problem/cause

Sulfonamides
kernicterus
Antibiotics to avoid in pregnancy problem/cause

kernicterus
Sulfonamides
Antibiotics to avoid in pregnancy problem/cause

Aminoglycosides
ototoxicity
Antibiotics to avoid in pregnancy problem/cause

ototoxicity
Aminoglycosides
Antibiotics to avoid in pregnancy problem/cause

Fluoroquinolones
cartilage damage.
Antibiotics to avoid in pregnancy problem/cause

cartilage damage.
Fluoroquinolones
Antibiotics to avoid in pregnancy problem/cause

Erythromycin
acute cholestatic hepatitis in mom
Antibiotics to avoid in pregnancy problem/cause

acute cholestatic hepatitis in mom
Erythromycin
Antibiotics to avoid in pregnancy problem/cause

Metronidazole
mutagenesis.
Antibiotics to avoid in pregnancy problem/cause

mutagenesis.
Metronidazole
Antibiotics to avoid in pregnancy problem/cause

teratogenic.
Ribavirin
Griseofulvin
Antibiotics to avoid in pregnancy problem/cause

Tetracyclines
discolored teeth, inhibition of bone growth.
Antibiotics to avoid in pregnancy problem/cause

discolored teeth, inhibition of bone growth.
Tetracyclines
Antibiotics to avoid in pregnancy problem/cause

Ribavirin
teratogenic.
Antibiotics to avoid in pregnancy problem/cause

Griseofulvin
teratogenic.
Antibiotics to avoid in pregnancy problem/cause

“gray baby.”
Chloramphenicol
Antibiotics to avoid in pregnancy problem/cause

Chloramphenicol
“gray baby.”
uses of Antiparasitic drugs

Ivermectin
Onchocerciasis (rIVER blindness treated with IVERmectin).
uses of Antiparasitic drugs

Praziquantel
Trematode/fluke (e.g., schistosomes, Paragonimus, Clonorchis)

cysticercosis (tania solium)
Diphilobotorum latum
uses of Antiparasitic drugs

Primaquine
Latent hypnozoite (liver) forms of malaria (Plasmodium vivax, P. ovale).
uses of Antiparasitic drugs

Nifurtimox
Chagas’ disease, American trypanosomiasis (Trypanosoma cruzi ).
uses of Antiparasitic drugs

Suramin
African trypanosomiasis (sleeping sickness).