 QProkaryotes & unicellular Structure

 Div. via binary. fission.  Cell memb: (select perm) inside cell wall.
 Lack nuc. memb.  Slime layer/capsule (external) = +al protect.
 Doesn’t req. living host to rep.  Flagella: Motility
 Exotoxins (prod. by G. +ve)  diffuse via  Pilli/fimbrae: Hairlike; Attach to transfer
fluids  neurotoxins, vomit etc. DNA.
 Endotoxins (prod by G. -ve)  @ cell wall  Cytoplasm contains:
 release @ death  vasoactive (incr. Cap  Chromosome: 1 long DNA strand.
perm  loss vasc. fluid)  septic shock.  Ribo’s & RNA
 Enzymes  destruct tissue  promo infec.  Plasmid
& assist invade
 Spores  resistant dormant latent form.
Shape Prefix form
 Bacilli (rod-shape)  Diplo (pairs)
 vibrio (curved)  Strepto (chains)
& pleomorphic  Staphylo (irreg,
(variable). grape clusters)
 Spirals (“wavy  Tetrads (packet or
line”)  spirochete square  4 four
(has axial filament) cells)
& spirilla (has  Palisade (lying
flagella) long sides parallel)
 Coccci (spherical)

Bacteria

Fungi: Protozoa:
 Eukaryote  has nucleus.  Eukaryote
 Fungal or mycotic infec.  via unicell yeast or  Unicell, lack cell wall.
multicell molds.  Independently or obligate parasites
 Cause  1ary infec. @ skin/mucous memb.  may  Ex: Trichomoniasis, Malaria,
spread systemically (immunosuppressed). Amebic dysentery
 Ex: Athletes foot, pneumonia.
Virus
 DNA or RNA in prot. coat.
 Obligate parasite (req. living host)
 Active rep:
1. Virus attach to host cell memb.
2. Uncoating  Viral DNA/RNA enters
cell.
3. Uses host’s  synth viral prot &
nucleic acids
4. Virus assembled @ cytoplasm.
5. Virus release by lysis of host cell or
via cell membrane.
 Latent:  same as active, but reproduce
& release when immune depressed.
Chlamydia, Rickettsiae, Mycoplasmas:
 Don’t grow @ artificial media
 Classified as bacteria
 Obligate parasites: rep. by binary fiss. in host
cell.

Infec. Princip: Nosocomial Infections:

 Sporadic:  1 individual  Hospitals etc.
 Endemic  Cont. trans in population  Surgery  weak immune system
 Epidemic  Higher than norm trans/  Health care workers  reservoirs
spread to new geo area
 Pandemic  Trans. @ most continents.
Chain of infec: Mode of trans:
1. Agent: Microbe  Dirrect/indirect contact.
2. Reservoir:  Droplet trans  respir/salivary secr.
 Enviro. Source, ex: contaminated soil.  Aerosol trans  small particles from respir.
 Infected carrier  can be Tract  Suspended in air  farther than
asymptomatic. droplet
3. Portal of exit  Vector-borne  Insect/ animal intermediate
4. Mode of trans: Air; Water; Direct contact; host
Food
Infec. Physio (Periods): Host resist:
 Incub: time between entry & symptoms.  Skin, muc. Memb.
 Prodromal: Fatigue, pain, loss appetite.  Secr. (ex: gastric, tears).
Non-spec kicking in.  Non-spec. Phagocytosis.
 Acute: Infec full develop.  Inflamm.
 Interferon prot: Prod. by host cell  stim
immune syst, stim nearby cells for resistance.
 Pathogenicity: Virulence:
 Microbe’s capacity to Degree of pathogenicity 
invade/cause infec.  Endo/exo toxins.
 Opportunistic: Resident flora  Destruc. Enz.
can become patho if in  Spore form.
wrong loc.  Attach via pili, fimbriae, capsules, spec. memb. recep. sites.
 Avoid host defenses  capsule, mutation (altered antigen.).

Infec patterns Infec S & S Dx

 Local Local inflammation:  Leukocytosis—bact. Infec. (elevated
 Focal: Spread to other  Pain, Tender, Swelling, WBC)
loc. Redness, Warm.  Leukopenia—viral infec. (decr. in
 Systemic (in blood):  Bacterial  purulent WBC)
spread via CVS exudate/pus,  Differential count  monocytosis or
 Septicemia  Viral  serous, clear neutropenia  Neutrophils ( incr. @
(pathogen). exudates. acute); lymphocytes and monocytes
 Bacteremia  Lymphadenopathy  incr @ chronic
 Toxemia swollen/tender lymph  C-react. prot. & ESR (Erythrocyte
 Viremia node sedimentation rate)  incr @
 Mixed inflamm
 1ary: Initial infec. Systemic:
 2ary: Follows 1ary. (Ex:  Fever
too much antibacterial  Fatigue & weak
 fungal infec)  Headache
 Subclinical infec:  Nausea
Assymptomatic.

NB: 2ary & Superinfec, resident flora

 Adverse effect of anti-infect therapy.

 Destruc of Resident flora.
 Resident flora:
 Inhabit the skin, respir, genitourinary,
GI tracts.
 Useful  prod antibacterial subst &
compete with pathogens for space &
nutrients.
 Removal host flora via antibiotic 
overgrowth of pathogenic microbes.
 Host flora  cause infec if allowed to
proliferate w/o control, or colonies in
wrong locations.
Drugs – Pharm

Class & terms Antiviral

 Antibiotic: derived from organisms (penicillin).  Decr. reproduc. of viruses @ host cell,
 Antimicrobials: class by type: but not destroy.
 Antibacterials  Usually against active rather than
 Antivirals latent stage.
 Antifungals.  Interfere with: attachment to host cell;
 Bactericidal  destroy organisms prot. coat shedding; enzyme act
 Bacteriostatic  decrease rate of reproduction (reverse trans.for DNA/RNA/prot).
 Broad spectrum  antibacterials effective for
both G-ive & G+ive
 Narrow spectrum:  preferred d/t less likely to
upset resident flora  prevent overgrowth of
one organism & 2ary or superinfection.

Antibacterial (antibiotic)
mech act.

 Interfe with bact. cell wall synth

(B-Lactam ring):
 Penicillin.
 Cefazolin (Ancef, Kefzol)

 Inhibiting DNA gyrase &

topoisomerase IV
 Fluoroquinolones: Ciprofloxacin
(Cipro®)

 Increase permeability of bact.

cell memb
 Leakage (polymyxin).

 Interfere with prot. synth. (from

Streptomyces soil
microorganisms)
 Aminoglycosides
(Gentamycin)
 Tetracycline (Sumycin)
 Macrolides (Erythromycin)

 inhibit folic acid/folate synth

 Sulfonamides 
trimethoprim-
sulfamethoxazole (Septra ).

Penecillin G - Drug Card

  Therapy class: Pharmokin: Adverse effect
Antibacterial.  Onset: IM  15-  Diarrhea, nausea, and vomiting.
 Pharm. class: Cell wall 30min; IV  0 min  Pain @ injection site.
inhibitor; natural  Peak: 30 min  Superinfections.
penicilli.  Duration: 4–6 h.  Anaphylaxis.
Action & Uses Interactions
 Against:  Decr. effect of oral contracept.
 Org. that do not prod. penicillinase &  Colestipol  decr. absorp. of penicillin.
 Org. shown susceptible via C&S test.  K-sparing diuretics + Penicillin G
 Susceptible strains of streptococci, potassium  hyperkalemia
pneumococci, staphylococci. Also gonorrhea,  Penicillin antagonize aminoglycoside
syphilis antibiotics.
 Only 15–30% of oral penicillin G absorbed.  Penicillin G  false +ive urinary or
 Better against G+ve. serum prot.
 IV or IM  better absorb. routes.
Mech. Act
 Disrupting cell walls  @ bact. cell wall’s penicillin
binding prot recept.
 @ binding  penicillin weakens cell wall  H2O enter.
 Human cell safe (d/t don’t have cell walls)  penicillins
spec. to bact cells.
 Penecillin’s Beta-lactam ring  antibacterial activity.
 Some bacteria secr an enzyme (beta-lactamase or
penicillinase)  inactivates penicillin.

Cefazolin (Ancef, Kefzol) - Drug Card

 Therapy class: Pharmokine Adverse Effect
Antibacterial  Onset: 1–2 h IM;  Rash, diarrhea.
 Pharm class: Cell wall 5 min IV  Superinfections
inhibitor: 1st gen  Peak: 30 min  Pain & phlebitis @ IM inject sites.
cephalosporin  Duration: 90–  Seizures  rare
135 min  Cefazolin is extensively excreted via kidneys.
Action & Use Interactions
 1ary use: treat G-ive.  With nephrotoxic drugs
 Treat & prophylaxis of bact. infec. by susceptible (aminoglycosides or vancomycin) 
G+ive. incr. nephrotoxicity.
 Treat: RTI’s, UTI’s, skin, biliary tract, bones &  Synergistic antimicrob. act. with other
joints. antibiotics (aztreonam, carbapenems,
 Also genital infec, septicemia, endocarditis. penicillins).
 Not effective against MRSA.  With warfarin  incr. anticoagulant
st
 Longer 1/2t than other 1 gen cephalosporins  effect
less freq dosing.  False +ve urine glucose.
Mech. Act.
 Beta-lactam antibiotic  (bacteriocidal)  attach. to penicillin-bind. prot.  inhibit bact. cell-
wall synt.
 1st-Gen  G+ive (staphylococci & streptococci); Bacteria that prod. beta-lactamase  resistant
to 1st-Gen
 2nd-Gen  resistant to beta-lactamase & incr. spectrum against G -ive
 3rd-Gen  even more incr. spectrum against G -ive; Longer 1/2t; Resist. to betalactamase; Treat
 Pseudomonas, Klebsiella, Neisseria, Salmonella, Proteus, H. influenza
 4th & 5th-Gen  Enter CSF/CNS & treat MRSA infec.

Tetracycline (Sumycin, others) - Drug Card

 Therapy: Pharmokin Adverse Effect
Antibact  Onset: 1–2h  Affect vaginal, oral, and intestinal flora  superinfections.
 Pharm class:  Peak: 2–4h  Irritat GI mucosa  nausea, vomit, GI burning, & diarrhea.
Tetracycline;  Duration:  Discoloration of teeth.
prot. synth. 12h  Photosensitivity.
inhibit  Contraindication  severe renal/hepatic impair.
Action & Use Interactions
 Broad range G -ive & G+ive:  Milk, Fe+, Mg+, laxatives, antacids  decr. absorp. &
Chlamydia, Rickettsiae, and serum levels.
Mycoplasma.  Tetracycline binds to lipid-lowering drugs (colestipol &
 H. pylori in peptic ulcer. cholestyramine)  decr. the antibiotic absorp.
 PO  short 1/2t  qid.  Decreases effect contraceptives.
 Topical  treat acne.  Lab Tests  incr. blood urea nitrogen (bUN); aspartate
 IM  local irritation & extrem aminotransferase (AST), alanine aminotransferase (ALT),
pain. amylase, bilirubin, & alkaline phosphatase.
Mech. Act.
 Inhibiting bact. prot. synth.  via binding to bact. ribosome.  slow microbial growth
(bacteriostatic effect).
 Extracted from Streptomyces soil microorganisms.

Macrolides: Erythromycin
Therapy class: Antibacterial Pharmokin Adverse Effect
Pharm class: Macrolides;  Onset 1 h  Nausea, abdominal cramping, and vomiting,
protein synthesis inhibito  Peak 1–4 h  Hearing loss, vertigo, and dizziness (especially
 Duration 1.5–2 h with impaired hepatic or renal).
 High dose IV cardiotoxic a dysrythmia.
Action & Use Interactions
 Inactivated by stomach acid  coated in  Anesthetics, azole antifungals, anticonvulsants
acid-resistant tab/capsules  incr. erythromycin serum  toxicity.
 Against: Bordetella pertussis (whooping  With cyclosporine  nephrotoxicity.
cough), Legionella pneumophila  Incr. effects of warfarin.
(Legionnaire’s disease), M. pneumoniae,  With lovastatin/simvastatin  muscle toxicity.
Corynebacterium diphtheriae.  Alcohol  decr. absorp. of erythromycin.
 @ low dose  bacteriostatic.  Lab Tests: interfere with AST & false +ve urinary
 @ higher dose @ susceptible species  catecholamine values.
bacteriocidal.  Herbal/Food: St. John’s wort decr. absorp.
 Against most G +ive, against many G -ive.
Mech. Act.
 Inhibit prot. synth.  binding to bact. ribosome.
 Extracted from Streptomyces soil microorganisms.

Aminoglycosides: Gentamycin
 Therapy class: Pharmoki Interactions
 Antibacterial n  Ototox with amphotericin b, furosemide, aspirin,
 Pharm class:  Onset bumetanide, ethacrynic acid, cisplatin, or paromomycin.
Aminoglycoside; Rapid  With amphotericin b, capreomycin, cisplatin, polymyxin b, or
protein  Peak 1– vancomycin  nephrotox.
synthesis 2h  Lab Tests: Incr. serum bilirubin, serum creatinine, serum
inhibito  duration lactate dehydrogenase (LDH), bUN, AST, or ALT;
8–12 h  Decrease serum calcium, sodium, or potassium

Action & Use Adverse Effect

 Gentamicin  broad-spectrum, bacteriocidal  Rash, nausea, vomiting, and fatigue
antibiotic  serious urinary, respiratory, nervous, or  Neurotox as ototox  loss of
GI infec.  if less toxic antibiotics contraindicated. hearing or balance  permanent
 Infections by aerobic G -ive (E. coli, Serratia, Proteus, with continued use.
Klebsiella, & Pseudomonas.  Tinnitus, vertigo, and persistent
 Effective against few G +ive bact. (MRSA). headaches  early signs of
 For systemic bact. infec.  parenterally d/t Not ototoxicity.
absorbed orally. A topical formulation (Genoptic)  Neurotox signs  paresthesias,
available (infections of external eye) muscle twitching, and seizures.
 Admin concurrently with penicillin, cephalosporin, or Neuromusc block & respir paralysis
vancomycin (enterococcal infec).  Renal  oliguria, proteinuria, incr.
 Orally  local effect @ GI tract  sterilize bowel bUN and creatinine levels.
prior GI surgery.
Mech. Act.
 Inhibit bact. prot. synth.
 Extracted from Streptomyces soil microorganisms.

Fluoroquinolones: Ciprofloxacin (Cipro®)

 Therapy class: class: Pharmokin Adverse Effect
Antibacterial  Onset:  Nausea, vomiting, and diarrhea
 Pharmacologic class: Rapid  Phototoxicity, headache, and dizziness. black box
Fluoroquinolone;  Peak: 1–2 h  Tendinitis & tendon rupture  incr. risk @
bacterial DNA  Duration: kidney, heart, and lung transplant &
synthesis inhibitor 12 h corticosteroid therapy.
 Extreme musc. weak. in myasthenia gravis.
Action & Use Interactions
 More effect against G -ive than G +ive  With Warfarin  incr. anticoagulant
(staphylococci, streptococci, and enterococci). effects  bleeding.
 Infec. of respir, GI, and genitourinary tracts, some  Incr. theophylline levels.
skin & soft-tissue infections.  Antacids, ferrous sulfate, and
 Preferred for the treatment uncomplicated UTIs sucralfate decr. absorp. of
 Second-generation fluoroquinolone. ciprofloxacin.
 UTI, sinusitis, pneumonia, skin, bone and joint infec,  Lab test: Incr. of ALT, AST, serum
diarrhea, eye infections. creatinine, and bUN.
 Rpidly absorb @ oral administration.  Increase serum levels of caffeine;
caffeine.
Mech. Act.
 Bacteriocidal  affect DNA synthesis  inhibiting DNA gyrase & topoisomerase IV.  affects
bacterial replication and DNA repair
Sulfonamides: trimethoprim-sulfamethoxazole (Septra®)
 Therapy Pharmokin Adverse Effect
class:  Onset  Nausea, vomiting, skin rash, itching, fever.
Antibacterial 30–60  Pre-existing renal  crystalluria, oliguria, renal fail.
 Pharm class: min  Agranulocytosis or thrombocytopenia.
Sulfonamide  Peak 1–4  Photosensitivity  avoid direct sunlight
; folic acid h  Pt’s with megaloblastic anemia d/t folate deficiency
inhibitor  Duration  Sulfonamides cross placenta & excreted in milk  kernicterus.
8–13 h  Decr. K+ excretion  hyperkalemia.
Action & Use Interactions
 Wide spectrum  both G -ive than  Enhance anticoagulants.
G +ive.  Ethotrexate toxicity  via decr. hepatic metabolism of
 Also Pneumocystis carinii phenytoin
pneumonia, shigella @ small bowel,  Phenytoin toxicity.
acute chronic bronchitis.  K-sparing effect @ nephron  caution with diuretics
 Resistance is lower than is observed spironolactone (Aldactone). Overdose: Treat via incr.
when either of the agents is used acidification of urine. If bone marrow suppression  5
alone. to 15 mg of leucovorin/day.
Mech. Act.
 Bacteriostatic.
 SMZ and TMP (Synergise)  Suppress bact. growth  inhibit folic acid/folate synth.  folic
acid is a B-complex vitamin essential @ rapid growth, especially @ childhood. Bact also use folic
@ rapid cell div. & growth.

Misc. Antibacterial
Clindamycin Quinupristin-dalfopristin:
 G -ve & -ive.  Combo drug  new class of antibiotics
 Oral infect. by bacteroides  (streptogramins)
Pnseudomembranous colitis  Treat antibiotic resistant G +ive.
 Treatment VRE (vancomycin-resistant
enterococcus faecium)
Linezolid Vancomycin
 Oxazolidinones  Severe infec. from G +ive S.aureus and
 Against MRSA (methicillin-resistant S. aureus streptococcus pneumoniae
infections)  Bactericidal – inhibit bact. cell wall synth.
 IV or PO  Used after others become ressistant.
 May cause thrombocytopenia  MRSA
 Don’t give if ototox.
 IV/PO not IM
 Allergic reaction:
 Red-man syndrome d/t fast infusion:
hypotension, flushing of face, red rash on
face/upper body
 Risk super infections

Fungal Disease (Mycoses)

 Superficial  favour warm, moist @ skin & muc. memb. (scalp, skin, nails etc. under breasts,
 diapered areas)  treat topically
 Sytemic  internal organs  lungs, brain, digestive organs.