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Dr.

Gabriella Rizzo
Learning Objectives

0 Brief review of bacteria and their structure


0 Interaction with bacteria and the host
0 Infection
0 How to choose an antibiotics
0 Clinical cases
Which antibiotic?
0 Spectrum (Gram +/- ; anaerobes) and in vitro susceptibility
0 Mechanism of action
0 Route of administration
0 Penetration
0 Side effects
0 Dosing regimen and compliance
0 Special populations
0 Resistance
0 Clinical uses
0 Cost
Bacteria
 Cell membrane
 Unicellular organism (prokaryotes)-diameter  Protein and phospholipids: osmotic barrier
between cell and environment, electron
0.4-1.5μm transport, solute and cell product transport
 Cell wall
 Free circular DNA, ribosomes, no mitochondria
 Direct pathogenic action
and a complex peptidoglycan cell wall  Endotoxin (Gram -) activate directly the
inflammation process
 External structure
 Cell wall components
 Capsule, pili, flagella  important surface antigens
 activation of immune system and
 Spores (cell metabolically inert in a
virulence factor (Streptococcus pyogenes)
protective coat, surviving heat, drying,  Antibiotic sensitivity
 Capsule (mucoid polysaccharide layer, lost in
chemicals cultures)
 Virulence factor
 Resists phagocytosis
 Nomenclature: the first name is its genus and
 Adhesivity (tissue, prostheses, catheters)
the second its species  Flagella/Pili

 Staphylococcus aureus, Staphylococcus


epidermidis
Bacteria-Gram negative structure
Bacteria-Classification
 Shape
 Cocci/Bacilli
 Stain
 Gram positive
 Gram negative
 Acid-fast stain (Ziel-neelsen)
 Ability to grow with or without oxygen
 Aerobes/anaerobes
 Size, growth characteristics
 Special features
 spores, enzymes, antibiotic resistance, antigens
 DNA content (G+C content)
Gram +ve vs Gram -ve bacteria
 able to retain a Crystal violet dye when 0 do not retain crystal violet dye in the Gram stain
washed in a decolorizing solution during 0 a counterstain (commonly Safranin) is added
the Gram stain process (more after the crystal violet, coloring all Gram-
peptidoglycan layers) negative bacteria a red or pink color
 Phospholipid bilayer surrounded by
peptidoglycan  Second outer lipid bilayer, containing
protein and lipopolisaccharide
0 Gram-positive bacteria appear blue or violet
(endotoxin
under a microscope

0 Pseudomonas aeruginosa (pink-red rods)


Bacteria
Filamentous bacteria

True bacteria
• Mycobacterium, Actinomyces, Nocardia,
Streptomyces

Spirochete
• Gram+ bacilli
• Aerobes (Listeria, Corynebacterium)
• Anaerobes (Clostridium) • Borrelia, Treponema, Leptospira
• Gram+ cocci
• Staphylococcus, Streptococcus, Enterococcus
• Gram- cocci Mycoplasmas
• Aerobes (Neisseria)
• Gram-bacilli
• Aerobes (Escherichia, Klebsiella, Salmonella, • Mycoplasma, Ureaplasma
Proteus, Shigella, Yersinia, Pseudomonas,
Haemophilus, Brucella, Bordetella)
• Anaerobes (Fusobacterium, Bacteroides) Rickettsia and Chlamydiae
• Gram-vibrios
• Vibrio, Campylobacter, Helicobacter
• Rickettsia, Chlamydia, Coxiella
Infectious Diseases
Infective agents Host
Bacteria

Microbes which can cause disease in humans

• Normal flora (mouth , nose, vagina, GI, skin)


• Protection from invading microbes (physical presence, production of bacteriocins/antibiotics)
• Immune stimulation (IgA)
• No disease in normal hosts
Opportunistic pathogens
(if host defences are impaired)
• Primary pathogens
• Disease in host with normal defences

• Latent pathogens
• Lie dormant in a normal host but cause disease when host defences are compromised
Antibiotics
Mechanism of action

0 Bactericidal death

0 Bacteriostatic growth cessation

0 Note: high concentrations of some bacteriostatic agents are also bactericidal, whereas low
concentrations of some bactericidal agents are bacteriostatic
Mechanism of action

1. Inhibition of cell wall synthesis

Cell wall rigidity


(peptidoglycan)
Cell hyperosmolarity

protection from osmotic rupture


Mechanism of action
β-lactam glycopeptides
(functional group)

inhibit addition
of subunit to the backbone
DD transpeptidase

Inhibition of peptidoglycan cross-links



↑↑ precursors CYTOLYSIS
(due to osmotic pressure)

cell wall hydrolases/autolysin
Penicillin
0 Spectrum 0 Side effects
0 Streptococci, Gonococci, Meningococci, 0 allergy ( 1-10% rash, <0.05% anaphylaxis),
Leptospira, Antrax, Dyphteria, Lyme disease, 0 diarrhoea (broad spectrum)
Tetanus 0 If major reaction (anaphylaxis or urticaria)
0 Mechanism of action immediately after dose → no penicillin lifelong
(unless desensitization)
0 Interfere with bacterial cell wall synthesis
0 If minor rash or >72 hrs after dose →caution but
0 Mechanism of resistance can be given if necessary
0 inactivated by β-lactamases and penicillinase
(staph.) 0 NOTE
0 Pharmacokinetic 0 If allergic to one allergic to all !!
0 Absorption 0 Cross allergy with other β-lactam
0 inactivated by gastric acids; GI absorption is
low→ best given IV/IM
0 Distribution
0 good in all body fluids and tissues; poor in
the CSF unless meninges are inflamed
0 Excretion-urine
Other β-Lactams
1. Penicillinase-resistant penicillins
 Flucoxacillin
0 Not inactivated by penicillinases
0 Active on Staphilococcus
0 Pharmacokinetic:
0 Acid stable→ oral administration
0 Side effects : cholestatic : jaundice

2. Broad-sprectrum penicillin
0 Active on Gram –ve rods (E. coli, Salmonella, Shigella, H. influenzae
 Ampicillin
0 Well excreted in the bile and urine
0 Low GI absorption , ↓ by food
0 Side effects: rash
 Amoxicillin
0 Better GI absorption
 Amoxicillin-clavulanic acid
o Clavulanic acid inactivates β-lactamases
o Staph. Aureus, E. coli, Haemophilus influenzae, Streptococcus pneumoniae
Other β-Lactams
0 Antipseudomonal penicillins
0 Pseudomonas, Proteus, bacterioides
0 Piperacillin/ureidopenicillin (TAZOCIN)
0 Carbapenem
0 Gram –ve and +ve, aerobes and anaerobes
0 Imipenem
0 Meropenem
0 Aztreonam
0 Pseudomonas aeruginosa, Neisseria meningitidis,
Haemophylus influenzae
Cephalosporines
0 Spectrum: Broad-spectrum (Penicillinase-producing, methicillin-susceptible Staphilococci, Streptococci)
0 Pharmacology similar to penicillin
0 Side effects
0 hypersensitivity and 0.5-6.5% of penicillin-sensitive patients will also be allergic to cephalosporine
0 Antibiotic-associated colitis (Cl. difficile)

Gram - Gram +

1st 2nd 3rd 4th


Klebsiella Haemophylus Broader spectrum Pseudomona
E. coli Neisseria gonorrhae s

Cefradine Cefaclor Ceftazidime Cefepime


Cefazolin Cefuroxime Ceftriazone
Cefamandole Cefixime
Glycopeptides
0 Spectrum: Narrow-spectrum, Gram +ve and Methycillin-resistant staphylococcus aureus (MRSA)
0 Mechanism of action
0 Bactericidal but bacteriostatic with Enterococci
0 Pharmacokinetic:
0 Do not cross the BBB
0 IV administration

 Vancomycin
0 Per os in antibiotic associated-colitis
0 Side effects
0 Rash if given faster then 60 min (red man syndrome)
0 nephrotoxicity

 Teicoplanin
Mechanism of action
2. Inhibition of protein synthesis

Aminoglycosides Macrolides
(30S Subunit-irreversibly) (50S subunit)
Initiation of synthesis protein chain elongation

Ribosome

Tetracyclines Chloramphenicol
(30S-reversibly) (50S-reversibly)
Death
Macrolides
 Erythromycin
0 Absorption reduced by food
0 Spectrum: Gram +ve and Mycoplasma,
0 Accumulates in macrophages
Campylobacter, Legionella, Mycobacteria ( 0 Side effects:
0 ++ nausea and vomiting, hepatotoxic, ototoxic
Chlarytromycin
0 Clarithromycin
0 Mechanism of action 0 Second line treatment for TB, atypical pneumonias
0 Inhibition of protein synthesis 0 Elimination: urine

0 Mechanism of resistance 0 Azithromycin


0 High concentration in phagocytes; high tissue
0 Resistance: plasmid-mediated or mutation concentration
0 Pharmacokinetic 0 Elimination: bile
0 Side effects
0 Do not cross the brain-blood barrier
0 QT prolongation
0 Substitute penicillin if allergy
Aminoglycosides
0 Spectrum: Gram –ve bacteria, pseudomonas, staphylococci, mycobacteria
0 Mechanism of action
0 Inhibit protein synthesis-bactericidal

0 Pharmacokinetic
0 No GI absorption, IV administration
0 Elimination: renal (accumulation in renal failure)

0 Side effects
0 Ototoxicity (reversible) and nephrotoxicity are dose related

0 Gentamicin
0 Streptomycin
0 Amikacin
0 Tobramycin
Tetracyclines
0 Spectrum: Intracellular bacteria
0 Chlamydia, Rickettsia, Brucella, Spirochete,
Borrelia
0 Pharmacokinetic
0 Absorption is reduced by antiacids, milk
0 Side effects
0 ↑Hepatic impairment, exacerbate SLE, ↑
muscle weakness in Myastenia gravis
0 Avoid in pregnancy

 Tetracycline
 Doxycycline
 Malaria (treatment and prophylaxis)
Mechanism of action
3. Inhibition of nucleic acid synthesis or activity

Topoisomerases IV
a. Quinolones DNA girase
negative supercoiling of DNA

b. Rifampicin

DNA-dependent-RNA polymerase

Cell death
c. Metronidazole
DNA damage
Quinolones
0 Spectrum: broad and bactericidal antibiotics
0 Quinolones and Fluoroquinolones (fluoro group attached the central ring system at the 6-position)
0 Second line treatment for TB

0 Mode of action:
0 inhibit the bacterial DNA girase (Gram–ve) or the Topoisomarases IV enzymes (Gram+ve), thereby inhibiting DNA replication
and transcription
0 enter cells easily → used also to treat intracellular pathogens such as Legionella and Mycoplasma

0 Resistance
0 efflux pumps (↓intracellular drug concentration)
0 plasmid-mediated resistance (proteins that bind to DNA gyrase)
0 mutations in DNA gyrase or topoisomerase IV genes(↓effectiveness)

0 Side effects
0 spontaneous tendon ruptures or damage, especially with the concurrent use of a systemic steroids
0 Convulsions

0 Nalidixic acid Oxifloxacin


0 Ciprofloxacin Levofloxacin
0 Moxifloxacin
Mechanism of action
4. Inhibition of bacterial metabolism

Folic acid
(SYNTHESIS)
-coenzyme
Sulfonamides

Trimethoprim

synthesis of timidine, purine, AA

CELL GROWTH CESSATION


Others
 Metronidazole
 Fucidic acid o anaerobic bacteria and protozoa; Cl difficile
0 Narrow-spectrum (but quick resistance)
0 penicilln-resistant staphylococci o Side effects: nausea
 Chloramphenicol  Sulphamethoxazol+ trimethoprim
0 Broad spectrum 0 Pneumocystosis treatment and prophylaxis
0 Haemophylus influenzae, typhoid fever 0 Side effects: bone marrow depression
0 Side effect: severe neutropenia

 Linezolid
 Gram +ve, MRSA and VRSA
 PO and IV
 Side effects: thrombocytopenia, anaemia
(reversible)
Pharmakinetics

1. Absorption

2. Distribution

3. Penetration

4. Metabolism

4. Elimination
Pharmakinetics
 Absorption
0 Oral (pills, liquid form)/intramuscolar/intravenous administration
 Aminoglycosides: not absorbed in the GUT so only IV or IM
 Benzylpenicillin is inactivated by gastric acids

0 Distribution
0 The serum concentration of antibiotic must exceed the minimum concentration to inhibit bacterial
growth (MIC)

0 Penetration to site of infection


0 CSF, prostate, eye, cardiac vegetations
0 Lipid-solubility CSF ( not for Macrolides, Tetracycline, Quinolones)
0 pH (↓ Aminoglycosides)
0 Intracellular bacteria (Legionella, Brucella, Chlamydia, Salmonella)→β-lactams have poor cell
penetration

0 Metabolism and Elimination


0 Liver
0 Kidneys
0 Dose adjustment in liver and kidney failure
Clinical information
0 Status of the host
0 Immune function (i.e. neutropenia, immunodeficiency)
0 More microorganisms involved, concomitant fungal and viral infections
0 Pregnancy → safety and toxicity
0 penicillins and erythromycin are safe
0 Concomitant viral infection→ HIV/EBV adverse reaction
0 Patient with EBV infection-rash on amoxicillin
0 Comorbidities (i.e diabetes)
0 More microorganisms involved+ complex treatment
0 Renal and liver impairment (dose adjustment)

0 Site of infection

0 Combination
0 Prevent resistance
0 Synergistic or addictive activity
0 Multiple potential pathogens
History presenting complaint
Night
sweats

Weight
Headache loss

Fever
Lymph-
Diarrhoea
adenopathy

Cough Rash
INFECTION-CLASSIFICATION
 Acute
 Rapid onset
 short term
 relatively severe course
 Chronic
 Slow onset
 long-term or lifelong (HBV, HCV, HIV)
 Milder course

 Localized
 confined to identified site
 Localized symptoms such as redness, swelling & pain
 Systemic
 involves more systems/whole body
 Systemic symptoms include fever, fatigue, headache, etc
Septic screen
0 The septic screen combines clinical assessment with laboratory analysis and imaging to identify
the source of infection.
0 The full screen may not be required if there is an obvious focus of infection

Septic screen

• Blood cultures (ideally three sets during pyrexial episodes)


• Sputum
• Mid-stream urine (MSU) or catheter specimen of urine (CSU)
• Stool for ova, cysts and parasites
• Wound swabs from any suspected sites (including old iv cannula sites)
• Throat swab
• CSF where indicated via lumbar puncture
• High vaginal swab
Diagnostic Pyramid

Other more complex tests


(MRI, Biopsy, PET, Bronchoscopy)

Basic RX tests
(CXR, PFA, Ultrasound, CT brain)
Blood tests
(FBC, Bioprofile, CRP, ESR,
Coagulation, Ig)

Septic screen

Physical examination

History (presentation)
Case 1
 A 25 year old student is brought to Accident and Emergency department with a 1
day history of severe headache, neck pain, fever and drowsiness. Her flatmate is
with her. The headache was of gradual onset and is associated with nausea, vomit
and photophobia. She had a recent sore throat and runny nose. On admission she is
drowsy, with no rash; temperature is 39.6°C, HR 120/min and BP 95/60.

 Diagnosis?
 Acute or chronic?
 Systemic or localized?
 Which bacteria/group of bacteria is most likely to cause this?
 IV or PO?
Acute Meningitis

Presentation
Examination
(in hours or days)

• Headache(↑light, noises, movements) • Glasgow Coma scale


• Vomiting (↑ intracranial pressure), not food • Meningism
related, no nausea • Neck stiffness
• Fever • Kernig sign (pain and resistance on passive
• Photophobia knee extension with hip fully flexed)
• Seizure (children) • Petechial rash (in 50% of meningococcal
• Altered mental status →→coma infection)
• VI nerve palsy (↑ intracranial pressure)
Acute Meningitis
0 Inflammation of meninges

Bacterial

• More serious, potentially life-threatening


• Adult and children→ N. meningitis, S. pneumoniae, H. influenzae type b
• Neonates→ Group B beta-hemolityc streptococci, E.coli, Listeria monocytogenes
• Immunocompromized→ M.tuberculosis

Viral

•More benign and self limiting


•Enteroviruses (ECHO,Coxsackie, HSV, parvovirus (Mumps), VZV, HIV, EBV

Fungal

• Immunocompromized : Cryptococcus, Candida


Meningococcal meningitis
 Neisseria meningitidis (Gram –, capsulated diplococcus)

 Reservoir: 10-25% population carriers in naso-pharinx

 Route of transmission: airborne spread

 Epidemiology: more common in children and young adults

 Immunization: vaccination in 3 doses from 2 months of age

 Presentation: 24-72 hrs; fever, meningism

Growth in Invasion of Petechial rash, Invasion


naso- asymptomatic blood bacteraemia, of meningitis
pharinx shock meninges
Pneumococcal meningitis
 Streptococcus pneumoniae (Gram +, short chains or diplococci )

 Reservoir: otitis media, sinusitis


 Route of transmission: airborne spread (through bacteraemia); direct access: skull
fractures
 Epidemiology: more common in children <2, elderly; patients at risk: alcoholism,
splenectomy, myeloma
 Immunization: Pneumococcal vaccination for children from 2 months of age and adult
at risk (every 5 years)
 Presentation: fever, meningism
Treatment
0 Initial empiric therapy
 Benzylpenicilin or cefotaxime /ceftriaxone

 Meningococcal meningitis
 Benzylpenicillin

 Pneumococcal meningitis or H influenzae meningitis


 Cefotaxime or ceftriaxone

 Listeria meningitis
 amoxicillin/ampicillin+ gentamicin
Case 1
 A 25 year old student is brought to Accident and Emergency department with a 1
day history of severe headache, neck pain, fever and drowsiness. Her flatmate is
with her. The headache was of gradual onset and is associated with nausea, vomit
and photophobia. She had a recent sore throat and runny nose. On admission she is
drowsy, with no rash; temperature is 39.6°C, HR 120/min and BP 95/60.

 Diagnosis? Meninigitis
 Acute or chronic? Acute, high risk, high mortality
 Systemic or localized? Localized→→systemic
 Which bacteria/group of bacteria is most likely to cause this? Str. pneumoniae
 IV or PO? Severe infection, pt drowsy→→IV ceftriaxone
 Adjust treatment after microbiology results of blood culture and CSF analysis
Case 2
 A 37 year old teacher presents to the Accident and Emergency department with a 3 day
history of fever, rigors and right sided chest pain. He has being previously healthy but 3 days
ago he started to feel unwell with cough, green sputum and progressive chest pain, worse in
inspiration. On examination his temperature is 38.5°C, HR 115/min and BP 125/80 mmHg, RR is
24/min. On percussion there is dullness over the right lower lobe and on auscultation there is
reduction of air entry and coarse crackles.

 Diagnosis?
 Acute or chronic?
 Systemic or localized?
 Which bacteria/group of bacteria is most likely to cause this?
 IV or PO?
Pneumonia
0 Inflammation of the lungs with exudation into the alveoli
0 The signs of pneumonia are referred to clinically as a “consolidation”

Symptoms Signs

• Fever/chills /sweats • Tachypnoea


• Productive cough • Reduced expansion on the affected side
• Sputum: mucopurulent→haemoptysis • Trachea deviated towards the affected side in
• Dyspnoea case of collapse
• Pleuritic chest pain • Dullness to percussion over one or more
lobes
• Bronchial breathing
• Coarse crackles
• Vocal resonance is increased over the affected
lobe(s)
• Pleural friction rub in case of a
parapneumonic effusion
Pneumonia-CAP

1. Streptococcus pneumoniae (pneumococcus)

• Reservoir: upper respiratory tract (URT)


• Route of transmission: airborne
• Epidemiology: more common in winter, in patients with chronic respiratory diseases (Asthma,
COPD), splenectomy patients, HIV
• Presentation
• abrupt onset with fever and rigors
• Lobar consolidation
• Herpetic cold sores maybe associated
• Immunization: Pneumovax (every 5 years)

2. Haemophilus influenzae, type B (Gram-, cocco-bacillus,


capsulated)

• Reservoir: URT
• Route of transmission: airborne
• Epidemiology: children <5years old, splenectomy, alcoholism
• Presentation: similar to S. pneumoniae , but less severe
• Immunization: Hib vaccine routinely done in pre-school years
Atypical pneumonias

3. Mycoplasma Pneumoniae

• Route of transmission: airborne


• Epidemiology: young adults
• Presentation: 5-10 days, flu-like syndrome followed by fever and dry cough. Extrapulmonary
features (arthralgia, myalgia, anaemia, rash, hepatitis, diarrhoea, vomiting,
• Investigations: Bilateral infiltrate on CXR, ↓ Na, ↑AST/ALT, Cold agglutinins→ hemolitic
anaemia. Serology
• Treatment: macrolide (Clarithromycin, erythromicin), tetracycline

4. Legionella pneumophila (Gram – bacilli)

• Route of transmission: airborne, outbreaks, air conditioning


• Epidemiology: male adults, smokers, immunocompromized
• Presentation: 5-10 days, flu-like syndrome followed by high fever and dry cough.
Extrapulmonary features: diarrhoea, vomiting,
• Investigations: Bilateral infiltrate on CXR, ↓ Na, ↑AST/ALT, lymphopenia, Urinary legionella
Antigen, Direct immunofluorescence, Serology
• Treatment: macrolide (Clarithromycin, erythromicin), Ciprofloxacin
Pneumonia-Severity index (CURB-65)

Clinical Factor Point


Confusion 1
Blood urea nitrogen >19 mg/dl 1
RR >30/min 1
Systolic BP<90 mmHg or 1
Diastolic BP≤60mmHg
Age ≥65 1

CURB-65 score Recommendation


0-1 Low risk; consider home treatment

2 Short hospitalization or closely supervised OPD

3-4 or 5 Severe Pneumonia; hospitalise


Treatment
0 Low-severity CAP
 Amoxicillin/ampicillin or Amoxicillin + clavulanic acid (Co-amoxiclav) for 7 days
 Alternative (allergic to penicillin or high resistance rate (USA):
o doxycycline
o clarithromycin
o azithromycin
o quinolone (ciprofloxacin)

0 Moderate severity CAP


 Amoxicillin/ampicillin + clarythromicin for 7 days

0 High severity CAP


 Benzylpenicillin+clarithromycin for 7-10 days
Case 2
 A 37 year old teacher presents to the Accident and Emergency department with a 3 day
history of fever, rigors and right sided chest pain. He has being previously healthy but 3 days
ago he started to feel unwell with cough, green sputum and progressive chest pain, worse in
inspiration. On examination his temperature is 38.5°C, HR 115/min and BP 125/80 mmHg, RR is
24/min. On percussion there is dullness over the right lower lobe and on auscultation there is
reduction of air entry and coarse crackles.

 Diagnosis? Community acquired pneumonia


 Acute or chronic? acute
 Systemic or localized? localized
 Which bacteria/group of bacteria is most likely to cause this? Str. Pneumoniae or H. influenzae
 IV or PO? PO according to CURB-65→→Co-amoxiclav for 7 days
 Adjust treatment after microbiology results of sputum culture and sensitivity
Other Classic examples

 Urinary tract infections (95% due to E. coli)


0 Lower UTI: trimethoprim for 3 to 7 Days
0 Pyelonephritis: quinolone (ciprofloxacin)

0 Endocarditis (Staphylococcus, streptococci and enterococci; Candida albicans, Chlamydia trachomatis, Brucella,
Coxiella, HACEK (oral Gram-)
 flucloxacillin ( or benzylpenicillin )+ gentamicin for 4 to weeks
0 If penicillin allergy or MRSA: vancomycin + rifampicin + gentamicin

 Skin (cellulitis) (beta-hemolytic streptococci and MSSA)


 Flucoxacillin +/_ benzylpenicillin
0 If penicillin allergy or MRSA : vancomycin, linezolid, clindamycin

 Sepsis (Gram negatives and anaerobes)


 Broad spectrum antipseudomonal penicillin (Piperacillin-tazobactam, imipenem/meropenem )or
broadsbpectrum cephalosporin (ceftazidime, ceftriaxone)
Treatment of complex infections: TB
0 Isoniazid
0 6 months for pulmonary TB
0 inhibits the synthesis of mycolic acid, required
0 9-12 months for extrapulmonary for the mycobacterial cell wall:
0 bactericidal (but bacteriostatic if bacteria slow-
growing)
0 Rifampicin
2 months 0 inhibits DNA-dependent RNA poymerase
Isoniazid
4 months
0 bactericidal
Rifampicin Isoniazid 0 Pyrazinamide
Pyrazinamide Rifampicin 0 bacteriostatic
Ethambutol 0 Ethambutol
0 bacteriostatic
Last but not least…
0 Drug-drug interaction and side effects:

0 Rifampicin: hepatitis, orange discolouration of body fluids, inactivation of OCP


0 Isoniazid: hepatitis, neuropathy, pyridoxine deficiency
0 Ethambutol: optic neuritis (colour vision is the first to reduce)
0 Pyrazinamide: hepatitis, gout
0 Ciprofloxacin: rupture of tendons; Cl. difficile diarrhoea
0 Penicillin: allergic reaction
0 Metronidazole and erythromycin: nausea and vomiting
0 Vancomycin: if infused too quickly→ red man syndrome
0 Azithromycin: QT prolongation
0 Aminoglycosides: nephrotoxicity and ototoxicity
0 Etc….
References

0 The Washington Manual of Medical Therapeutics


(Lippincott Williams &Wilkins)

0 Johns Hopkins ABX Guide


0 http://www.hopkinsguides.com/hopkins/ub
0 Book or IPhone/IPad and Android app

0 BNF ( British National Formulary)


0 IPhone app

0 Sanford Guide Antimicrobial Therapy


0 http://www.sanfordguide.com/
0 Iphone/IPad

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