Infectious Diseases Mbchb4


1. Surgical site infections (SSI)
a. Mortality – 5.8% if SSI, 1.3% if Ø SSI
b. SP infection (skin/subcut tis) 4.2% / Deep (fascia/muscle) infection 5.7% / Organ space infection 13.2%
c. Mean extra hospital stay – 8.5 days
2. Determinants of wound infection
a. Bacterial load, virulence, resistance
b. Extent of tis injury
c. Foreign material
d. Vs.
e. General and local host defences
f. Appropriate peri-operative A/Bs
3. Antimicrobial prophylaxis of wound infections
a. Aseptic techniques minimise but do not eliminate bacterial contamination of operative field
b. Optimal prophylaxis provides adequate A/B levels from time of incision to wound closure
c. Too soon selects for inf with resistant organisms
d. Too late means inf is established and a course of tx is needed
4. Classification of wounds by degree of contamination
a. Clean – respiratory, GI, GU tracts not entered, w/o inflammation or break in technique, non-traumatic
b. Clean-contaminated – tracts entered but w/o spillage, or minor break in technique, non-traumatic
c. Contaminated – trauma, spillage, inflammation etc
5. A/Bs and Infection Rates with prophylaxis w/o prophylaxis
a. Clean 0.8% 5.1%
b. Clean-contamin 1.3% 10.1%
c. Contaminated 10.2% 21.9%
6. Benefits and risks of A/B prophylaxis
a. Risk of SSI
b. Potential consequences of SSI
c. Effectiveness of prophylaxis
d. Consequences of adverse effects – in individual pt and on the resistance of bacteria in the hospital
e. Cost-benefits
7. Rule of thumb
a. Prophylaxis is useful in clean-contaminated and contaminated procedures and in clean procedures where a prosthesis is inserted (bec the consequences of inf are then much greater)
8. Bacteria commonly causing wound infections
a. S.aureus 20%
b. Coag negative Staph 14%
c. Enterococcus 12%
d. Others <10% → Streptococcus spp., E.coli, Pseudomonas, B.fragilis
9. Sources of bacteria
a. Skin flora – esp Staph
b. Mucosal flora – esp G-ves
c. Exogenous – attendants, airborne, equipment
d. Later – drains, IV lines etc
10. Principles of prophylaxis
a. Antibiotic covers the most common pathogens causing SSI
b. A single dose, provided there is a reasonable ½ life, given IV 30 mins prior to incision
c. Additional dose(s) may be needed if procedure lasts >2 hrs or if blood replacement exceeds 1500 mls
11. Pathogens according to site of surgery and procedure
a. Skin wound or incision anywhere – S.aureus, S.pyogenes
b. Above waist – Oral anaerobes
c. Abdominal – Enterobacteriaceae, Anaerobes (B.fragilis), Enterococcus spp.
d. Prosthesis, graft or shunt – coagulase negative staphylococci
12. Examples
a. Elective orthopaedic surgery w/o prosthesis – none
b. Total joint replacement, open reduction or internal rotation fixation of a fracture – cephalosporin
c. Gastroduodenal or biliary – Cephalosporin
d. Appendix or Colorectal – cefoxitin or cefotetan, amoxy-clav, gent + metronidazole
13. B-lactam allergy
a. Consider – vancomycin, erythromycin, clindamycin where G+ve bacteria are of a concern
b. Consider – gent or Cotrimoxazole or a quinolone where G-ve aerobic bacilli are a concern
c. Consider – Metronidazole or clindamycin where anaerobes are a concern


1. Overview
a. Most cases of fever → harmless self-limiting infection
b. Diagnostic challenge → identify the cause and differentiate serious life-threatening bacterial causes
c. Serious sepsis can occur w/o a fever!
d. Normal distribution of core temp → 36.1-37.8 (slightly higher than adults, diurnal variation)
e. >38 = fever
f. Core temperature → rectal (small risk of bowel perforation/anal infections etc), never if child <5 yrs
g. Site → under tongue, axillary, tympanic (digital) – generally good but can be less reliable
h. If a parent reports a fever, always assume it is valid
2. Pathophysiology
a. Fever is the end result of activated endogenous pyrogen
b. Vasoconstriction
c. ↑ metabolic rate
d. ↑ heat production
e. Hyper-pyrexia can be life threatening
f. Is a useful adaptive mechanism
3. Differential Dx
a. Infections 95%
b. Drugs and toxins
c. CT dis
d. Neoplasms
e. Metabolic
f. CNS
g. Miscellaneous eg immunisation
4. Causes of febrile illness 3-36 monhts
a. Viral illness - (75%) – esp URTI, LRTI, gastroenteritis, then otitis media and bacterial pn, UTI
b. URTI, bronchiolitis, pn, exanthema, gastroenteritis
c. Otitis media
d. Bacterial pn
e. Soft tissue infections (cellulitis, abscess)
f. Bone and joint infections
g. Meningitis
h. Septicaemia
5. Clinical Approach
a. Find infective focus
b. Does hx and severity of illness match eg coryza can co-exist with meningitis
c. FWF (fever without focus)
i. Not fever of unkwown origin
ii. 5-10% will have Ø localising signs
d. 3% of children <2 yrs with core body temp >39 potentially have a serious bacterial inf
6. Assessment of the febrile child
a. Most Common Sxs
i. Fever
ii. Coryza, cough
iii. Diarrhea +/- vomiting
iv. Lethargy, poor feeding, irritability
v. Rashes
b. Hx
i. Age (>2 yrs signs of a specific illness)
ii. Recent immunisation, exposure to infection
iii. Past Hx
iv. Immunodeficiency or recurrent inf
v. Chr dis
vi. Meds? On A/Bs?
vii. Immunisation status
viii. Ethnicity
c. Exmn
i. Well or unwell?
ii. Hydration
iii. Skin rash
iv. Specific sgins
v. Vital signs, LOC
vi. Otitis media, tonsillitis/pharyngitis
vii. ↑ RR, retraction, crackles, wheeze
viii. Meningism
ix. Joint or bony tenderness
x. Abdo tenderness
7. Red Flags
a. Height of fever alone does not identify serious illness
b. Higher risk of bacterial infection
i. <3 months, T>38
ii. 3-6 months, T>39
c. T>41 – usu not infective cause, eg malignant HTN
8. Recognising sick and febrile child
a. S/S
i. Fever + seizure
ii. Devt of non-blanching rash
iii. Fever >5 days
iv. Parent increasingly worried and believes child is unwell
b. ABCDE + don’t ever forget glucose
9. Febrile seizures
a. 3% of children 0-5yrs have underlying susceptibility for febrile seizures
b. Ø ↑ risk of serious infection
c. Purpose – to cool body rapidly
d. Assoc w rapid change in temperature, Ø height of fever
10. Management
a. <1 month
i. High risk of bacterial inf → 10%
ii. Full septic screen always → blood, CSF, urine cultures, CXR
iii. Directed tests if site identified → eg wound swab, limb x-ray, joint aspirate
iv. Admit and tx with A/Bs
b. 1-3 months
i. High risk bacterial infection → esp if Temp >40
ii. Full septic screen
iii. Directed tests if site identified
iv. Admit almost always
v. Tx w A/Bs usually
c. 3-36 months
i. Specific tx if site of inf obvious → eg UTI, otitis media (in well child), pn, meningitis etc
ii. No focus, T>39
iii. Often septic screen +/- CSF
iv. Tx depends on focus found, infant well or unwell and other risk factors
11. Anti-pyretics
a. Tepid sponging + fans → neither use nor recommended
b. Ø over or underdress
c. Use anti-pyretics when child has fever and is distressed
i. Paracetamol Q4H or Ibuprofen Q6H
ii. Ø prevent febrile seizure
d. Ø Asprin → Reyes syndr in <12 yrs (acute LF assoc w varicella or influenza)
e. Ibuprofen → side effects incl bronchospasm in asthmatics and assoc w necrotising fasciitis (chickenpox)

Case 1
1. 21 day old girl
a. PC – feeding problems, unsettled 12/24
b. O/E – 38.2 febrile, mottled peripheries, CRT 4 secs, full fontanelle, Ø neuro signs, Ø other abnormalities
c. Ixs – full septic screen reqd (<1 month)
i. WCC 14, Neut 11.2
ii. CSF wcc 8,800, rcc 140, protein 2.4, glucose 1, organisms seen
iii. Blood/CSF cultures +ve for Grp B Strep
d. Tx – empiric amoxy + gent
e. In first pregnancy with earlier child, mother had pos swab test for Grp B Strep
f. Neonatals
i. ↓ chance of specific signs
ii. ↑ chance of bacterial focus
iii. wider range of susceptible organisms
iv. ↓ ability to contain inf to one region – eg ↑ permeability of bbb
v. Immature immune func - ↓ IgA, IgG, complement et

Case 2
1. 9 month F
2. PC – Fever T=39, ØE+D well, awake and irritable 48/24
3. O/E – Corzyal, Ø focus, Normal exmn
4. Ixs - Urine dipstick neg
5. Mgt – return home and review next day
6. 1 day later → exanthema subitum (rash) + fever → “rubella rash”

Case 3
7. 9 month M
8. PC – Fever >24/24, awake, drowsy, limp
9. O/E – T=39, corzyal, RR 45, HR 190, Chest clear, Øfocus, looks unwell, evolving purpuric rash
10. Dx – Meningococcal septicaemia
11. Mgt – IV penicillin + 1x dose ceftriaxone (to clear nasal passages), contact public heatlh, family offered prophylactic rifampicin (↑ risk by 500x)
12. Ø LP performed
13. Blood cultures +ve for N.meningitidis
14. Transferred to ICU


“broad spectrum, bactericidal, oral”
“too good to be true? too good to last?”

1. Quinolones
a. Norfloxacin / Ciprofloxacin
i. Broad spectrum
ii. Ø Streptococci
iii. Intra-abdominal infections
b. Moxifloxacin + others
i. Improved spectrum
ii. Including Streptococci
iii. Intra-abdominal infections + respiratory infections
2. Mechanism of Action
a. Bind to enzymes responsible for DNA replication and coiling
i. DNA gyrase and DNA topoisomerase
b. Generate double strand breaks in DNA
c. Cell death
3. Mechanisms of Resistance
a. Selection of mutants with –
i. Altered DNA gyrase or topoisomerase and/or
ii. Altered efflux pumps (pumps drugs out of cell)
4. Spectrum of Activity
a. Ciprofloxacin
i. Susceptible →
1. G-ve bacilli – E.coli, Proteus, Klebsiella, Enterobacter, Pseudomonas (only oral drug active against pseudomonas)
2. H.influenzae
3. N.gonorrhea
ii. Borderline → Staphylococci, ?Streptococci
iii. Resistant → Enterococci, MRSA, Anaerobes
b. Moxifloxacin and the new respiratory quinolones
i. ↑ activity vs Streptococci and Staphylococci
ii. ↓ activity vs Pseudomonas
5. Quinolone Uses
a. Ciprofloxacin – 500-750 mg BD PO or 200 mg Q12H IV
i. Urinary tract infections
ii. Intra-abdo infections (+/- metronidazole)
iii. Gonorrhea (be weary of resistance)
iv. Pseudomonas infection – eg in CF
b. Moxifloxacin – 400 mg OD PO
i. Pneumonia due to S.pneumoniae or atypical organism eg Chlamydia, mycoplasma, legionella
ii. ?Acute exacerbations of bronchitis
6. Major Adverse effects
a. Ciprofloxacin – problems are rare
b. Moxifloxacin – QT prolongation, warning
7. Minor Adverse effects
a. Ciprofloxacin
i. N/V, abdo pain, diarrhea 3-8%
ii. Headache, drowsiness, other CNS 1-3%
iii. Photosensitivity 0.5%
iv. Achilles tendon rupture Rare
8. Summary
a. Very useful oral drugs
b. In general, safe for 2nd line use
c. Resistance is a major concern
d. Wide range of adverse effects

1. Susceptible organisms
a. G-ve bacilli – except pseudomonas
b. H.influenzae
c. S.aureus
d. S.pneumoniae +/-


“Death to aerobic gram –ve bacilli”

1. Aminoglycosides
a. Gentamicin
b. Others – Streptomycin, Neomycin, Tobramycin, Amikacin
2. Mode of Action
a. Bactericidal
b. Bind to ribosome
i. Inhibit protein synthesis
ii. Misreading of mRNA
c. Bind to cell envelope
i. ?Disruption of cell wall
3. Mechanisms of Resistance
a. Aminoglcyoside modifying enzymes
i. Present in bacterial cytoplasm
ii. Inactivate the drug
b. O2 dependent transfer across cell wall → all anaerobes are resistant
4. Susceptibility to Aminoglycosides
a. E.coli 99%
b. Klebsiella sp 99%
c. Enterobacter sp 96%
d. Proteus sp 96%
e. Pseudomonas aer 78%
f. S.aureus 98%
g. Streptococci 0
h. Anaerobes 0
5. Gentamicin Dosing
a. Concentration dependent bacterial killing
i. Higher conc → Better killing
b. Long post-antibiotic effect
i. Continued bacterial killing after disappearance of drug
c. Intermittent bolus dosing every 24 hours
d. ~ 5-7 mg/kg/24 hrs (eg 70 kg person → 400 mg OD)
e. Gentamicin comes in 80 mg ampoules
f. Ensure undetectable trough concentration levels
6. Indications for Gentamicin therapy
a. Serious infections due to aerobic enteric G –ve bacilli
b. Esp if pseudomonas is a possible pathogen
c. Clinical examples
i. Pyelonephritis
ii. Cholecystitis / cholangitis*
iii. Peritonitis*
iv. Intra-abdominal abscess*
v. Febrile neutropenia*
d. * = may need to be given with another agent
e. Initial empiric therapy of sepsis when MRSA is a possibility and wish to avoid vancomycin use - eg fluclox + gent
f. In combination with penicillin (or ceftriaxone) for synergistic bacterial killing in endocarditis due to viridans streptococci or enterococci – eg penicillin + gent
7. Gentamicin Toxicity
a. Nephrotoxicity = ~15%
i. Reversible (days to weeks)
ii. Non-oliguric ARF
iii. 5-7 days after starting tx
iv. Risk in elderly, liver dis, shock, dose duration
b. Ototoxicity = 2-30%
i. Irreversible destruction of hair cells
ii. Auditory (high tone) and vestibular – often unnoticed as high pitch above human speech is only lost
iii. May occur late (weeks)
iv. Risk in bacteraemia, shock, dose, duration
8. Avoiding Gentamicin Toxicity
a. Avoid using in elderly, those with hearing loss
b. Use for minimal duration – ie >4-5 days
c. Monitor – 2x week RF, 1x week audiometry


1. Adverse consequences of IV cannulae
a. Infection is the most dangerous consequence
b. Extravasation (to pass out of blood etc into tissues)
c. Chemical phlebitis – red angry veins can be due to chemical irritation of IV administered drugs
d. Thrombosis - clotting
e. Bacteraemia → spread to lungs, joints etc
f. Note – organisms from clot may be dislodged everytime a drug injected into bloodstream via cannula, therefore if pt experiences transient fever and rigors after an injection, consider possible infection and remove cannula, perform cultures etc
2. Sources of infection of intravascular cannulae
a. Hands of medical personnel – wash hands, gloves
b. Pts microflora on and in deeper levels of skin
3. Technique
a. Choose insertion site – hand or forearm, not leg
b. Wash + dry your hands
c. Wear clean (not necessarily sterile) gloves
d. Clean insertion site – use alcohol wipe or chlorhexidine solution
e. Use a plastic cannula
f. Fix the cannula with tape +/- gauze or a transparent dressing
g. Initial and date the dressing
h. Do not routinely remove cannulae before day 3 or 4
i. Inspect cannula daily → remove if phlebitis
j. Be alert to possibility of local infection with bacteraemia and distant sepsis
k. Remove cannula from day 5 onwards
4. Suspected infection of cannula
a. Collect blood cultures – through cannula and from another site
b. Swab cannula exit site if purulent
c. Remove cannula and sent tip for culture
d. Look for metastatic sepsis – eg septic pulmonary emboli, endocarditis, bone joints etc
e. Consider empiric tx – flucloxacillin 2g q6h + gent 4-5 mg/kg/day
5. Tx of cannula-associated bacteraemia
a. Tx >10 days
b. Observe for metastatic infection eg lungs, joints
c. Consider echo


1. Macrolides
a. Erythromycin (40s)
b. Roxithromycin (90s)
c. Clarithromycin (90s) – slightly greater activity
2. Azalide
a. Azithromycin
3. Lincosamide (related drug)
a. Clindamycin

1. Mechanism of action
a. Bind to 50S ribosomal subunit
b. Inhibits RNA dependent protein synthesis
c. Bacteristatic effect (not bactericidial unless v high concentrations)
2. Mechanism of resistance
a. Impermeable outer membrane (all G-ve bacteria)
b. Alteration of bacterial ribosome leading to decr macrolide binding (staphylococci, strep and others)
3. Erythromycin susceptibility
a. Spectrum of activity v similar to penicillin
b. S.aureus – 85%
c. MRSA – 50%
d. S.pyogenes – 97%
e. S.pneumoniae – 87%
4. Azithromycin vs Erythromycin
a. Higher levels in cell and tissues (10-200x higher serum levels)
b. Less activity against G+ve bacteria but more activity against G-ve bacteria
c. Reliably active vs H.influenzae
d. Long ½ life
5. Macrolide uses
a. Strep infections – eg pharyngitis, cellulitis in penicillin allergic pts
b. Atypical respiratory infections – eg mycoplasma, Chlamydia, pertussis
c. STDs
6. Indications
a. Respiratory infections eg whooping cough, legionnaires dis
b. Clamydia infections
c. Camplylobacter enteritis
7. Adverse effects
a. Generally v safe
b. N/V, epigastric discomfort, diarrhea (most common) – due to degradation product which stimulates gastric motility
c. Erythromycin estolate can cause hepatotoxicity
d. Inhibits hepatic cytochrome P450 enzyme – potential interactions eg carbamazepine, ciclosporin


1. Definition
a. Inflammation of meninges and CSF
b. May be assoc w involve of brain parenchyma (= encephalitis)
c. Commonly viral or bacterial cause
d. Acute – onset over hours (common)
e. Chronic – onset days-weeks (rare)
2. Etiology
a. Viral
i. Most commonly due to enteroviruses
1. Enteroviruses – common
2. Mumps virus – unusual
3. Herpes simplex - rare
ii. Usu self limiting + Ø sequelae
b. Bacterial
i. Most commonly due to N.meningitidis and S.pneumoniae
1. N.meningitidis – epidemics, children, winter, rash
2. S.pneumoniae – preceding respiratory inf, CSF leak
3. Infants – Grp B Streptococci, E.coli, Gut flora
4. Head injury – Staphylococci, Enterobacteriaceae
5. Immunocompromised – Listeria, Cryptococcus
ii. High mortality w/o tx
3. Presentation
a. Fever
b. Headache
c. Photophobia
d. Rash – macules, Petechiae, purpora
e. Neck stiffness
f. Focal neurological signs – CN3,4,6,7 (uncommon)
g. Papilloedema (v rare)
4. Laboratory Dx
a. CSF examination via lumbar puncture
i. Can rapidly confirm clinical dx
ii. Carries v small risk of adverse effects
1. Brain herniation – exclude space occupying lesion / ↑ ICP etc
2. Hamorrhage – check platelets >100, INF >1.4
b. CT before LP?
i. CT sometimes required to determine if LP is safe
ii. Delays LP and may lead to delays in starting tx
iii. CT not reqd if –
1. age <60 yrs
2. Ø immunocompromised
3. Ø hx prior CNS dis
4. Ø seizure activity in last week
5. Ø neurological findings – LOC, answer 2 questions, perform 2x commands, gaze, visual fields, facial n palsy, motor arm/leg, ataxia
c. CSF Interpretation
i. CSF bloody → subarachnoid hemorrhage
ii. CSF cloudy → infection
iii. Bacteria seen on microscopy → infection
iv. WBCs, neutrophils, glucose, proteins → pattern of bacterial/viral meningitis
v. Bacterial cultures
d. 50% → bacteria seen on microscopy; if not then bacterial meningitis indicted when;
i. Protein >1.5 g/L
ii. Glucose <2.5 mmol/L
iii. WBC >500 x 10(6)/L
iv. Neutrophils >500 “ “
e. CSF rapidly sterilised
i. <12 hrs N.meningitidis
ii. 12-48 hrs S.pneumoniae
5. Tx of meningitis
a. N.meningitidis (most common bacterial cause) → always susceptible to penicillin
b. S.pneumoniae (less common bacterial cause) → approx 80-90% susceptible to penicillin
c. Early tx improves outcome
i. Before arrival at hospital
ii. Before LP performed or results available
iii. Tx should be started <1 hr after arrival at hospital
d. Penicillin levels should be approx 10x greater than the bacterium’s MIC continuously during tx
i. Requires high dose IV tx – eg Penicillin 2-4 MU (mega units) Q4H
e. Doses
i. N.meningitidis → benzyl penicillin 2MU (1.2g) Q4H 3 days
ii. S.pneumoniae (penicillin susceptible) → Benzyl penicillin 2MU Q4H 7 days
iii. S.pnuemonaie (penicillin resistant) → Vancomycin 500 mg Q6H >7 days
iv. Alternatives - Ceftriaxone 2g 24 hourly, or Cefazidine / Cefotaxime 1-2g Q8H
f. Approach
i. Use penicillin alone for obvious meningococcal dis
ii. Add vancomycin if –
1. hx of CSF leak or assoc sinus or lung dis
2. G+ve cocci seen in CSF
3. S.pneumoniae grown (while awaiting sensitivity results)
6. Other Mgt Issues
a. Dexamethasone started immediately improves outcome in H.influenzae and S.pneumoniae infections
b. SIADH can complicate mgt
c. Convulsions can be a problem
d. Hearing impairment (sensorineural deafness) is the most common morbidity
e. Prophylaxis w rifampicin for close contacts of pts w dis due to N.meningitidis
f. Notify MOH


23 F
• generalised severe headache 18/24
• sleepy + confused 2/24
• fever 38.8
• stiff neck
• Ø rash
• Penicillin 2MU IM Stat given 40 mins ago

1. Differential Dx
a. Meningitis – bacterial, viral
b. Encephalitis
c. Brain abscess
d. Infection at other site eg pneumonia with delirium
2. Prognosis
a. Appropriate tx → 5% mortality in NZ from N.meningitidis, worse outcome for S.pneumoniae
b. W/o appropriate tx → 60+% mortality within days for bacterial meningitis, viral meningitis benign outcome
3. Management Plan over next 4 hours
a. Confirm dx of meningitis → Lumbar puncture – within 30 mins (ideally before starting A/B but may not be possible)
b. Determine likely etiology
c. Cintinue anti-microbial tx if indicated
d. Manage complications eg convulsions etc


Penicillins (Beta-lactam antibacterials)

Important Penicillins
1. Narrow Spectrum → streptococci, a few staphylococci, meningococci, many (not all) anaerobes
a. Penicillin G (benzyl penicillin) – IV IM
b. Penicillin VK (original oral penicillin) - PO
c. Benzathine penicillin (long acting) – IM; used only for prevention in rheumatic fever
2. Flucloxacillin – PO IV → anti-staphylococcal
3. Amoxycillin – PO IV → some G- activity
4. Amoxy-clav – PO IV → ↑ G- activity

Important Uses
1. Penicillin
a. S.pyogenes, S.pneumoniae, N.meningitidis
b. Pharyngitis, pneumonia, menigitis
2. Flucloxacillin
a. S.aureus, (S.pyogenes, S. pneumoniae)
b. Skin infections
3. Amoxycillin
a. Streptococci, H.influenzae (S.pyogenes, S.pneumoniae, E.faecalis, N.meningitidis, Proteus)
b. Respiratory infections
4. Amoxy-clav
a. Broad spectrum
b. Respiratory, Intra-abdominal infections

1. Penicillins inhibit synthesis of the peptidoglcan layer of cell wall surrounding some bacteria by binding to the enzyme transpeptidase
2. Beta lactamase is produced by the bacteria → destroying the structure of penicillin

1. Poor absorption → take on empty stomach (~1 hr prior to meals or ~2 hrs after meal)
a. Good absorption for amoxicillin and clavulanate despite food
2. Good distribution – except to CSF, eye, joints
3. Variable protein binding (95% for fluclox)
4. Renal excretion (reduced by probenecid)

Adverse Effects
1. Non-toxic drugs
2. Rash 5-10%
3. Anaphylaxis 1/10,000 (usu IV tx) → some cross reactivity with cephalosporins
4. Rare → hepatitis, leucopenia, haemolytic anemia


1. 1st → 2nd → 3rd Generation
a. Improved activity against G-ve bacilli (at expense of G+ve activity)
b. Increased ability to cross bbb
c. Increased effect against b-lactamase producing organisms
2. Action→ Inhibit bacterial wall synthesis in a manner similar to penicillins
3. All are effective against streptococci and staphylococci
4. None are effective against MRSA
5. None are effective against enterococci
6. Types
a. 1st Generation
i. Cephazolin, Cephalexin
ii. Surgical prophylaxis for clean surgery eg cardiothoracic, orthopaedic
b. 2nd Generation
i. Cefuroxime (Cef), Cefoxitin, Cefaclor
ii. Cefuroxime →
1. PO - 250 mg bd for most infections, double dose for pneumonia
2. OV = 750 mg Q6-8H
iii. Tx for serious medical/surgical infections
c. 3rd Generation
i. Ceftriaxone, Cefotaxime, Ceftazidime
ii. Immunocompromised, meningitis
7. Pharmacology
a. Only 1st gen (eg Cefaclor) are well absorbed PO
b. Good distbn
c. Poor penetration to obstructed biliary tract and CSF – but 3rd gen penetrate CSF well)
d. Adverse effects rare
8. Sensitivities
a. 1st Gen - S.pyogenes, S.pneumoniae, S.aureus, E.coli, Proteus, Klebsiella
b. 2nd Gen – As above + H.influenzae
c. 3rd Gen – As above + better coverage against Enterobacter species and N.meningitidis
9. Side-effects
a. Skin rashes
b. N/V
c. Diarrhea (incl C.difficile)
d. Hypersensitivity reactions


1. Definition
a. 2ndry peritonitis – gut contents spill into empty peritoneal cavity
b. Primary peritonitis – bacteria in blood seed pre-existing ascetic fluid
c. CAPD peritonitis – bacteria contaminate peritoneal diasylate
2. Normal flora in gut
a. Stomach → Prox jejunum
i. Viridans streptococci, micro-aerophilic streptococci, Candida species, Lactobascillus species
b. Distal jejunum → Colon
i. E.coli, Klebsiella species, Proteus species, Enterococcus species, Bacteroides fragilis
ii. 1 aerobe per 1000 anaerobes
3. Sources of peritoneal contamination for 2ndry peritonitis
a. Gut perforations – ulcer, ischemia, infection, injury, cancer etc
b. Local spread – salpingitis
c. Other
4. Peritoneal host defences
a. Lymphatic clearance
b. Phagocytosis
c. Fibrin sequestration
d. Exudation of fluid
5. 2ndry peritonitis
a. Pathophysiology
i. Peritonitis, septicaemia, shock → first few days (due to aerobes)
ii. Localised abscesses → days to weeks (due to anaerobes)
b. Microbiology
i. Aerobes – 2-3 species esp E.coli
ii. Anaerobes – approx 10 species esp Bacteroides fragilis
c. Treatment
i. Surgery
1. control source of peritoneal contamination
2. drain collections → wash out wound
ii. Antimicrobial therapy → vs aerobes AND anaerobes
1. Gent + Metronidazole
2. Cefuroxime + Metronidazole
3. Surgical triple → Gent + Metro + Amoxicillin (Annual General Meeting)
a. Gent → Aerobes - E.coli
b. Metronidazole → Anaerobes – B.fragilis + others
c. Amoxy → Enterococcus faecalis (G+ve cocci)
4. Outcome generally the same with Metro/Gent or Triple surgical therapy
iii. Physiological support
1. Fluids → maintain BP (note if pt goes into ARF, be cautious with Gent ie only use for first day or two)
2. O2 → manage hypoxia
iv. Situations when tx not reqd -
1. Early acute appendicitis
2. Acute suppurative appendicitis – no gangrene, no perforation, no abscess
3. Simple acute cholescystitis – no perforation, no abscess, no cholangitis
4. Simple bowel ischemia – no peritonitis, no abscess
5. Ulcer or other perforations – operated on within 12-24 hrs
6. Primary Peritonitis
a. Pathogenesis
i. Pre-existing ascites
ii. Seeding of ascites by a single organism (via blood or by tport across gut wall)
iii. Nephritic syndrome – eg children with S.pneumoniae (declining incidence)
iv. Liver failure – alcoholics with E.coli – underlying chr illness, high mortality
7. CAPD peritonitis
a. Contamination of dialysate +/- catheter
b. Approx 1x episode per year
c. S.epidermidis > S.aureus > E.coo
d. Local infection
e. Low mortality


56 M
Develops severe abdo pain, cold and sweaty 2/7 post hemi-colectomy
Fever 38.2, HR 110, BP 105/65
Abdo rigid, absent bowel sounds

1. Differential Dx
a. Peritonitis
b. Bowel ischemia
c. Infective process – intra-abdominal, wound, pneumonia, elsewhere
d. Other process eg PE
2. Prognosis
a. 30% mortality over next 2-3 days from septic shock
b. In survivors → collections of infection occur (abscess)
c. E.coli and other aerobes are killed off via abscess formation
d. Anaerobes fester in abscess conditions → pt continues to be febrile and feel unwell (morbidity)
e. Hence combined tx reqd


1. Etiology
a. Exact microbial cause difficult to determine
b. CAP – 30-50% etiology unknown
c. Rapid diagnostic techniques lacking
d. Clinical picture not specific
e. Empiricism rules
2. Severity in CAP
a. Prognosis depends on severity
b. High RFs
i. RR >30
ii. DBP <60
iii. Urea > 7 mmol/L → confusion
iv. New onset AF
v. Major co-morbidity
c. Lower RFs
i. Albumin <35 g/L
ii. WCC <4000 or >25,000
iii. Multi-lobar involve
iv. Pre-existing lung dis
d. Moderate CAP – 1x high RF + 1x lower RF OR 3x lower RFs
e. Severe CAP – 1x high RF + 2+ lower RFs OR 2x high RFs
3. Investigations
a. CXR – PA, Lateral
b. Bloods – FBC, elytes, Urea, Glucose
c. Sputum gram stain/culture
i. Specimen quality impt → <10 epithelial cells, >25 PMN/LPF
ii. Not all pts produce sputum
iii. Antigen and nucleic acid detection evolving
iv. Certain organisms require special techniques – eg Legionella
d. Blood culture – only 1-16% +ve in CAP (can be very useful in the severly sick)
e. Serology for atypical organisms
f. Molecular techniques evolving – eg PCR for legionella
g. Pulse Ox / ABG → guide to O2 therapy
h. Other ixs depend on circumstances – eg pleural aspiration, bronchoscopy, CT, HIV test
4. Tx
a. Depends on likely organism and severity
b. Almost all initial therapy is empiric
c. Many different guidelines
d. Principle of A/B selection → cover the possible causes and modify if able
e. Mild CAP → macrolide only
i. Macrolide eg erythromycin, roxithromycin (rulide) → covers S.pneumoniae and atypicals but not H.influenzae
ii. Doxycycline (alternative)
iii. Home Tx – amoxicillin 500 mg TDS PO or Erythromycin 500 mg qid PO
f. Moderate/Severe CAP → Beta-lactam + Macrolide
i. Beta lactams → cefuroxime, amoxy-clav
ii. Macrolides → erythromycin, roxythromycin, clarythromycin
1. Erythromycin covers atypicals while Cefuroxime covers H.influenze
iii. Emerging drugs → respiratory quinolones eg levofloxacin, moxifloxacin


55 M
PC – fever, sweats, rigor lasting 7 mins, cough productive of brownish phlegm 1/7
20 pack year smoking hx
Temp 36.6, HR 120, BP 135/85
Percussion dullness, inspiratory crackles L base posteriorly

1. Differential Dx
a. Pneumonia*
b. Infective exacerbation of COPD
c. PE
2. Organisms
a. Strep.pneumoniae → 40%
b. Unidentified → 30%
c. H.influenzae → 10%
d. Atypicals 25% (non-typicals 75%)
3. Prognosis
a. CURB score
4. Management Plan
a. Cefuroxime will cover all the common causes of pneumonia incl H.influenzae
b. Erythromycin covers all organisms – except H.influenzae and Klebsiella; useful bec effective for Chlamydia and legionella


1. Sepsis
a. = Infection + inflammatory response
b. At least 2 of –
i. T >38 or <36
ii. HR >90
iii. RR >20
2. Septic Shock
a. = Sepsis + Sys BP <90
3. Bacteraemia
a. Bacteria in the bloodstream
b. True bacteraemia = bacteria present in blood and causing illness eg E.coli, S.aureus, S.pneumoniae
c. Contaminant bacteraemia = bacteria not arising from bloodstream or causing illness eg S.epidermidis, P.acnes
4. Pathogenesis of Sepsis 1
a. Infection →
i. Inflammatory cascade → leukocyte invasion + activation
ii. Coagulant cascade → coagulation
5. Pathogenesis of Sepsis 2
a. Components of infecting organism eg LPS (endotoxin), cell wall etc →
b. Mphage activation →
c. TNF release →
d. Lymphocyte activation →
e. IL1, IL6 etc release →
i. Neutrophil activation, chemotaxis, phagocytosis
ii. Endothelial cell effects
f. Vasodilation, capillary leak, microvascular occlusion, hypoperfusion
g. Organ dysfunction eg ARDS
6. Pathogenesis of Sepsis 3
a. TNF, IL1 →
b. Activated protein C
c. Thrombin formation, fibrinolysis
d. Clotting
e. Organ dysfunction
7. Clinical Presentation
a. Pts – elderly, underlying illness, recent surgery
b. Site of infection – blood, lung, urinary tract, intra-abdominal, wounds, skin etc
8. Etiology
a. Bacteria – S.aureus, S.pneumoniae and other streptococci, E.coli and other enteric G-ve bacilli, N.meningitidis
b. Fungi – C.albicans
c. Viruses – eg dengue
d. Protozoae eg malaria
9. Outcome
a. Better prognosis
i. Young
ii. Urinary tract, IV line
iii. Community acqd
iv. Ø underlying illness
v. Staphylococci, Streptococci
vi. T >38
vii. BP normal
viii. WBC >4
b. Worse prognosis
i. Old
ii. Lung, intra-abdo, abscess
iii. Hospital acqd
iv. Cirrhosis, haematological dis, malignancy
v. Enterococci, G-ve bacilli
vi. T < 38 (failure to produce a fever or increased white cell count is a poor prognostic sign)
vii. Hypotension
viii. WBC <4
10. Management
a. Ixs
i. Identify pathogen
1. Blood cultures – x2 (20 mls each arm) – one test only 90% accurate, 2 tests nearly 100%
2. Urine
3. Sputum
4. Pus aspirate or swab
5. Wound swab
6. CSF
7. etc
ii. Imaging, FBC + Coag, E/lytes, LFT etc
iii. Monitor pathophysiology
b. Tx
i. Cure infection – anti-microbial tx
1. Prompt, IV, bactericidal, broad spectrum
2. Examples
a. Gentamicin + Fluclox → broad cover of G+ve and –ve
b. Gent + metronidazole + amoxicillin → broad cover gut assoc organism (surgical triple)
c. Gent + cefpirome → braod cover w two agents active against G-ve bacilli
d. Benzylpenicillin → N.meningitidis (also effective against S.pneumoniae) ie meningitis
ii. Correct pathophysiology
1. Gas exchange, perfusion, nutrition etc
iii. Drain pus

11. Prognosis
a. Appropriate antimicrobial tx → 50% ↓ mortality
b. In most severe G-ve sepsis – combination antimicrobial tx → 50% reduction in mortality
c. Mortality remains high despite optimal antimicrobial tx
12. Immunomodulators
a. Ø benefit – probably because given too late in the process
i. Steroids
ii. Anti-endotoxin
iii. Anti-TNF
iv. PAF Receptor Antagonist
v. IL1 receptor antagonist
vii. Activation protein C – 25 vs 30% mortality but not cost effective


Urethritis and cervicitis → gonorrhea, Chlamydia, NSU
Vaginal infection → bacterial vaginosus
Genital skin infections → warts
Genital ulcer dis → herpes

Gonorrhea (‘clap’)

1. Epidemiology
a. 60/100,000, M>F
b. ↑ resistance to drugs – eg ciprofloxacin
2. Transmission
a. Humans – only natural host
b. Peno-vaginal, peno-anal, oro-genital eg vagina to penis risk = 20% per episode
c. Incubation period – 2-14 days; 2-5 days most common
3. Presentation
a. Male
i. Usu symptomatic, but can be asx
ii. Anterior Urethritis
1. Dysuria and Purulent Discharge
2. 95% become asx after 6 month
iii. Rectal infection (proctitis) – gay men
1. May be sx or asx
2. Painless d/c to proctitis with tenesmus and pain
3. Rectal gonorrhea not a reliable indicator of unsafe anal sex
4. Rectal co-infection common
iv. Pharyngeal infection from oral sex
1. Usu asx
2. Sole site of infection in <5% of cases
v. D/C G stain +ve in >95%
b. Female
i. Usu asx
ii. Endocervix usually the primary site of inf
iii. Urethral inf also common
iv. Incubation period less certain; sxs occur usu <10 days
v. Sxs
1. Vaginal d/c
2. dysuria
3. Intermenstrual bleeding
4. Menorrhagia
5. Lower back pain
vi. G stain +ve 40%
4. Microbiology
a. Neisseria gonorrhea (gonococcus)
b. G-ve diplococcus
c. Infects epithelial tract esp urogenital, rectum, pharynx, conjunctivae
5. Ixs
a. G Stain and culture of urethral/endocervical swab
b. Blood culture – to detect dissemination
c. a
6. Management
a. Ceftriaxone 250 mg IV stat OR
b. Azithromycin 2 g PO stat
7. Complications
a. Male → epididymitis
b. Female → salpingitis or PID (10-20%)


1. Definition
a. Type of NGU (non-gonococcal urethritis)
b. Before Chlamydia isolated as cause
c. Technically, new classification should be non-gonococcal non-chlamydial urethritis!
d. Other causes of NGU → ureaplasma, bacteroides, mycoplasma
2. Transmission
a. Chlamydia trachomatis B, D-K
b. Anogenital dis, conjunctivitis, neonatal pneumonia
c. Infects squamocolumnar cells
d. Obligate intracellular parasite
3. Epidemiology
a. Most common cause of sexually acquired and preventable sub-fertility
b. Most common treatable infectious disease in NZ
c. Prev ~7% last five years (M:F 1:3)
4. Presentation
a. Initial infection mild and self-limited
b. Males
i. Urethral d/c
ii. Dysuria
c. Females
i. Usu asx
ii. Ixs for infertility
d. Recurrent infection → severe inflammation
e. 1x Chlamydia PID → infertility 10%
f. 3x Chlamydia PID → infertility 50-60%
5. Diagnosis
a. DNA based tests, nucleic acid amplification eg PCR
b. Can use first pass urine sample → easy, acceptable, painless
6. Tx
a. Azithromycin 1g Stat OR
b. Doxycycline 100 mg BD 7 days
c. Efficacy 97-100%
d. Contact trace all partners over last 60 days or last partner if >60 days ago → Tx all partners
e. Safe sex during tx
7. Complications
a. Females – mild to severe PID
b. Males – persistent or recurrent urethritis, epididymitis
c. Male>Female → Reiters syndr (arthritis, conjunctivitis/uveitis)
d. Neonatal → conjunctivitis, pneumonia

Bacterial Vaginosus

1. Defintion
a. Common – 20-25% of women
b. Sexually assoc – some features like STI but other features are not
c. Recurrence common
d. ↓ Numbers of lactobacilli → overgrowth of anaerobic bacteria
i. lactobacilli = primary microbial agonist against genital infection
e. Elev pH
f. Maladour
g. Watery d/c
2. Organisms
a. Prevotella spp, Mobiluncus spp, Mycoplasma hominis…
3. Diagnosis 3/4 of –
a. Homogenous white adherent d/c
b. Elevated ph >4.5
c. Fishy malodour
d. Microscopy → clue cells
4. Ø vaginal inflammation, normal cervix
5. Tx
a. Metronidazole (anaerobic tx)
b. Tx – if sxs or if pregnant
6. Complications
a. Premature rupture membranes during preg
b. Pre-term labour
c. Chorioamninonitis

Genital Warts

1. Definition
a. Common – visible warts in about 1% of sexually active popn
b. HPV present in 10-30% of popn
c. ↓ prev with age – even adjusting for sexual hx (resistance builds up over time)
d. Majority sexually transmitted
e. Warts not transmissible site to site (ie they are region specific; eg they cant be passed to the hands)
2. Organisms
a. HPV – human papilloma viruses
b. DNA viruses >70 types
c. ~ 30 genital (mucosotropic) types
d. HPV 6,11 → visible warts, Ø complications
e. HPV 16,18 → assoc w cervical ca
3. Presentation → Exophytic warts (fleshy growths)
a. Men - Penile > anal > mouth (rare)
b. Women – Vulval > cervical > anal (rare)
4. Differential Dx
a. Molluscum contagiosum
b. Normal anatomical features → penile papillosus, vestibular papilloma, fordyce spots
5. Tx
a. Physical ablation eg crytotherapy
b. Cytotoxics eg podophyllin
c. Immune eg imiquimod
d. Can be difficult to tx – spontaneous regression occurs
e. All 3x options equally effective → 70% efficacy, 30% relapse
6. Complications
a. Intraepithelial neoplasia – HPV 16-18 high risk
7. Prevention
a. HPV vaccine
b. Only effective prior to first sexual intercourse
c. Gardasil → against HPV 16,18 and 6,11
d. Cevarix → against HPV 16, 18

Genital Herpes

1. Definition
a. Herpes Simplex virus HSV – types 1 (mouth) and 2 (genital)
b. DNA viruses
c. Recurrent HSV2 infection – virus lies dormant in ganglion cells; reactivation by trauma, febrile illness, UV irradiation
2. Presentation
a. Most infections are asx or unrecognised – 70%
b. First episode – asx to severe mucocutaneous/systemic dis
c. Onset <1 wk of inf, vascular lesions, regional adenitis, neuralgia etc
d. Sxs worse in women
e. Painful genital ulceration, fever, L/A
3. Recurrence
a. HSV2 - 95%
b. HSV1 – 50%
c. Men average 5/year
d. Women average 4/year
e. Asx shedding on 10% of days, most common just before and after symptomatic recurrences, more freq in first yr of inf
4. Transmission
a. 19% per year in suscep women
b. 5% per year in suscep men
c. HSV 1 partiall protective
5. Management
a. Acyclovir for severe initial episode or for freq disabling recurrences


1. Definition
a. Acute and chr infectious dis, transmitted by direct contact (usu sexual)
b. First sx → chancre, followed by slight fever and other constitutional sxs (primary syphyilis)
c. Followed by skin eruption of various appearances with mucus patches and generalised L/A (2ndry syphilis)
d. Subsequent formation of gummas, cellular infiltration and functional abnormalities usu resulging from CV or CNS lesions
2. Epidemiology
a. Uncommon prior to 2000
b. Rising incidence
c. Most cases MSM
3. Organism
a. Treponema pallidum
b. Incubation period 10-90 days
4. Primary infection
a. Papule at site of infection → ulcerates to painless firm chancre
b. Heals spontaneously within 2-3 wks
5. 2ndry infection
a. 4-10 wks after primary lesion
b. May be 1 or more of –
i. Fever
ii. Sore throat
iii. Arthralgia
iv. Generalised L/A
v. Widespread skin rash, Øface
c. Sxs subside <1 yr
6. Tertiary infection
a. Latent period followed by granulomatous lesion → skin, bone, liver, testis
b. Cardiovascular syphilis
c. Neurosyphilis
7. Diagnosis
a. Microscopy of lesion fluid
b. Serological tests +/- in primary state
c. T.pallidum enzyme immunoassay (EIA) = screening test of choice
d. +ve test confirmed w T.pallidum haemoglutin assay (TPHA) + VDRL test (veneral dis research lab)
8. Management
a. Procaine benzyl penicillin 1m 10 days for primary or 2ndry syphilis (4 wks tx reqd for tertitiary syphilis)



1. Sepsis = infection + inflammatory response (2 of T >38/<36, HR >90, RR >20)
2. Septic shock = Sepsis + Systolic BP <90
3. Bacteraemia = bacteria in the bloodstream
4. Pathogenesis - Infection → 1. inflammatory cascade, 2. coagulation cascade
5. Presentation
a. Pts – elderly, underlying illness, recent surgery
b. Site – blood, lung, urinary tract, intra-abdominal, skin, wound etc
6. Etiology
a. Bacterial – esp:
i. S.aureus
ii. S.pneumoniae + other strep
iii. E.coli and other G- bacilli
iv. N.meningitidis
b. Other – Fungi (C.albicans), Viruses (dengue), Protozoa (malaria)
7. Ixs
a. Identify pathogen → bld cultures (x2, 20 mls each arm), urine, sputum, pus aspirate, wound swab, CSF etc
b. Bloods – FBC, coagulation, elytes, LFTs etc
c. Imaging
d. Monitor pathophysiology
8. Tx
a. Anti-mircobial tx → prompt, bactericidal, broad spectrum, IV
i. Gent + Fluclox – G+/-
ii. Gent + Metro + Amoxy (AGM) – Gut organisms
iii. Gent + Cefpirome – 2x G- cover
iv. Benzylpenicllin – N.meningitidis
b. Correct pathophysiology – gas x∆, perfusion, nutrition etc
c. Drain pus
9. Prognosis
a. 50% ↓ risk of mortality w appropr anti-microbial tx
b. Mortality remains high despite optimal tx
10. Poor prognostic features
a. Old
b. Lung, intra-abdo, abscess
c. Hospital acqd
d. Cirrhosis, haematological dis, malignancy
e. Enterococci, G-ve bacilli
f. T <38 or wcc <4 – failure to produce a fever or ↑ wcc
g. Hypotension

Penicillins and Cephalosporins (beta lactams)

1. Mechanism – inhibit synth of peptidoglycan layer of cell wall, act by binding transpeptidase
2. Resistance – b-lactamase (produced by the bacteria) destroys the structure of penicillin
a. Beta lactam is part of the ring of several antibiotics including penicillin and cephalosporin
3. Types
a. Penicillin
i. Types
1. Penicillin G (benzyl penicillin) – IV, IM
2. Penicillin VK (generic) – PO
3. Benzathine penicillin – IM (LA – only RF prevention)
ii. Organisms – S.pyogenes, S.pneumoniae, N.meningitidis
iii. Indications – pharyngitis, pneumonia, meningitis
b. Flucloxacillin PO IV
i. Organisms – S.aureus and S.pyogenes/pneumoniae
ii. Indications – skin infections
c. Amoxycillin PO IV
i. Organisms – S.pyogenes/pneumoniae, H.influenzae, N.meningitidis, G-ve activity against E.faecalis and proteus
ii. Indications – respiratory infections
d. Amoxy-clavulanic acid PO IV
i. Clavulanic acid = beta lactamase inhibitor
ii. Indications – Respiratory and intra-abdominal infections (↑ G- activity)
4. Dosing – take on empty stomach (except amoxicillin) due to poor absorption
5. Adverse effects – rash 5-10%, anaphylaxis 1/10000, cross reactivity with cephalosporins

1. Mechanism – inhibit bacterial cell wall synthesis
2. Organisms – active against strep and staph and E.coli
3. Generations - ↑ activity against G-ve bacilli, ↓ activity against G+ve, ↑ crossing bbb, ↑ activity against b-lactamase producing orgs
a. 1st Gen – Cephazolin, Cephalexin → surgical prophylaxis (clean surgery – eg cardiothoracic, orthopaedic)
b. 2nd Gen – Cefuroxime (Cef), Cefoxitin, Cefaclor → serious medical/surgical infections (+ activity against H.influenzae)
c. 3rd Gen – Ceftriaxone, Cefotaxime → immunocompromised, meningitis (↑ cover against enterobacter + N.meningitidis)
4. Adv effects – rash, n/v, diarrhea incl C.difficile


1. Types
a. Macrolides
i. Erythromycin
ii. Roxithromycin
iii. Clarithromycin
b. Azalide – azithromycin (↑ G-ve activity, ↓ G+ve activity, active vs H.influenzae, long ½ life)
c. Lincosamide - clindamycin
2. Mechanism – bind 50s ribosomal subunit → inhibition of protein synthesis (bacteriostatic)
3. Organisms – S.aureus, S.pyogenes/pneumoniae, MRSA 50%
4. Uses
a. Strep infections in penicillin allergic pts – pharyngitis, cellulitis
b. Atypical respiratory infections – mycoplasma, pertussis, legionella, Chlamydia
c. STDs
5. Indications
a. Respiratory infections – whooping cough, legionnaires dis
b. Chlamydia
c. Campylobacter enteritis
6. Adverse effects
a. N/V
b. Epigastric discomfort and diarrhea (stimulation of gastric motility)

Gentamicin (the aminoglycoside)

1. “Death to the G-ve”
2. Mechanism – bind to ribosome → inhibits protein synthesis → bactericidal (unlike macrolides)
3. Organisms – E.coli, klebsiella, enterobacter, proteus, pseudomonas, S.aureus
a. Ø Strep or anaerobes
4. Dose - 5-7 mg/kg Q24H (eg 70 kg person receives a 400 mg od dose)
a. Long post anti-biotic effect
b. Ensure undetectable trough levels prior to next dose
5. Uses
a. Serious G-ve bacilli infections (esp if pseudomonas possible)
b. Synergistic killing in endocarditis (with penicillin or ceftriaxone) → against viridans streptococci and enterococci
6. Indications
a. Pyelonephritis
b. Cholecystitis/cholangitis
c. Peritonitis
d. Intra-abdominal abscess
7. Toxicity
a. Nephrotoxicity (ARF) – 15%, reversible, after 5-7 days
b. Ototoxicity – 2-30%, irreversible, can occur late
8. Contraindications
a. Ø elderly, esp if hearing impaired
b. Use for minimal duration, preferably <4-5 days
c. Monitor – renal function (2x weekly), audiometry (1x weekly)


1. “broad spectrum, PO, bactericidal – too good to be true, too good to last”
2. Classification
a. Norfloxacin/Ciprofloxacin
i. B/spec, Ø strep
ii. Intra-abdo infections
b. Moxifloxacin
i. ↑ spectrum incl strep
ii. Intra-abdo and respiratory infections
3. Mechanism – bind to enzymes responsible for DNA replication + coiling → DNA strand breaks → cell death
4. Uses
a. Ciprofloxacin
i. Organisms
1. G-ve bacilli, proteus, klebsiella, enterobacter, pseudomonas (only active po drug)
2. H.influenzae
3. N.gonorrhea
4. Borderline against staph and strep
ii. Indications
1. UTI
2. Intra-abdo infection (+/- metro as Ø action vs anaerobes)
3. Gonorrhea
b. Moxifloxacin (newer)
i. Organisms - ↑ activity vs staph and strep, ↓ activity vs pseudomonas
ii. Indications - Pneumonia due to S.pneumoniae or atypicals (mycoplasma, Chlamydia, legionella)
5. Adv effects
a. QT prolongation (moxifloxacin)
b. N/V, abdo pain, diarrhea, headaches, drowsiness (ciprofloxacin)
6. Resistance is becoming a problem, use only as a 2nd line agent


1. Definition – inflammation of meninges and CSF
2. Etiology
a. Viral – esp enterovirus (most common), self limiting, Ø sequelae
b. Bacterial
i. N.meningitidis → epidemics, children, winter, rash
ii. S.pneumoniae → preceding resp infection, CSF leak
iii. Infants → grp B strep
3. Presentation – acute onset:
a. Fever
b. Headache
c. Photophobia
d. Neck stiffiness
e. Rash
f. Focal neuro signs – CN 3,4,6,7 (uncommon)
g. Papilloedema (v rare)
4. Differential Dx
a. Viral meningitis
b. Encephalitis
c. Brain abscess
d. Infection at another site – eg pneumonia with delirium
5. Ixs
a. Lumbar puncture
i. CSF examination
1. Appearance cloudy (bloody = subarach hem)
2. Microscopy – 50% of bacterial cases will be visible under m/scope
3. Bacterial pattern
a. Protein ↑ >1.5 g/L
b. Glucose ↓ <2.5 mmol/L
c. WCC ↑ >1000 cells per uL
d. Neutrophils ↑
Bacterial meningitis – low glucose, high protein, high white cell count (typically neutrophils)
Viral meningitis – normal glucose, normal-high protein, lower white cell count (typically mononuclear ie lymphocytes)
4. Cultures
ii. Risks (small)
1. brain herniation – exclude ↑ ICP and space occupying lesion
2. hemorrhage – check platelets >100
b. CT sometimes reqd to determine if LP safe – not reqd provided:
i. Age <60 yrs
ii. Ø immunocompromised
iii. Ø hx prior CNS dis
iv. Ø seizure activity in preceding week
v. Ø neuro findings –↓ LOC, answer 2x questions and commands, gaze, VF, facial n palsy, motor arm/leg, ataxia
6. Tx
a. N.meningitidis – Benzyl Penicillin 2-4 mU Q4H IV – 3 day tx
b. S.pneumoniae – as per N.meningitidis (penicillin effective in 80-90% of cases) – 7 day tx
c. Start tx early, prior to hosp arrival, before LP performed or results available
d. Penicillin resistant S.pneumoniae → add vancomycin
i. Consider if likely cause S.pneumoniae while cultures are pending –
1. Hx of sinus or lung disease or CSF leak
2. G+ cocci in CSF (Neisseria is G-ve coccus)
3. S.pneumoniae is grown while awaiting sensitivity results
e. Alternatives → ceftriaxone
f. Dexamethasone → improves outcome in H.influenzae and S.pneumoniae infections
g. Rifampicin → for close contacts
7. Complications
a. Convulsions
b. Sensorineural deafness
8. Prognosis
a. N.meningitidis – 5% mortality w appropriate tx (worse outcome for S.pneumoniae)
b. Ø appropriate tx – 60% mortality for bacterial meningitis


1. Definitions
a. Peritonitis = inflammation of the peritoneum
b. Primary peritonitis – bacteria in blood seed pre-existing ascetic fluid
c. 2ndry peritonitis – gut contents spill into empty peritoneal cavity
2. Sources for peritoneal contamination in 2ndry peritonitis
a. Gut perforations (rupture of a hollow viscus)
i. Ulcer
ii. Ischemia
iii. Appendicitis rupture
iv. Diverticulitis rupture
v. Cholecystitis rupture
vi. Gastric or colorectal carcinoma
b. Disruption of the peritoneum
i. Surgical wound
ii. Trauma
c. Local spread – salpingitis
d. Spontaneous bacterial peritonitis (SBP) – occurs in children or those with ascites
3. Pathophysiology
a. Peritonitis, septicaemia, shock (first few days) – aerobes → 30% mortality
b. Localised abscesses (days to weeks) – anaerobes
i. abscess kills E.coli + other aerobes while anaerobes fester and the pt continues to feel febrile and unwell
4. Organisms
a. Aerobes – mixed esp E.coli
b. Anaerobes – mixed esp bacteroides fragilis
5. Presentation
a. Hx
i. Abdo pain
ii. Cold, sweaty
iii. Recent abdo surgery
b. Signs
i. Fever
ii. Tenderness – exacerbating by coughing
iii. Rebound tenderness (pain as peritoneum snaps back into place)
iv. Rigid abdomen (washboard abdo)
v. Guarding
vi. Absent b/s – ileus paralyticus (also causes n/v)
6. Differentials
a. Bowel ischemia
b. Infection – abdo wound, pneumonia, other
c. PE
7. Management
a. Surgery
i. Control source of peritoneal contamination
ii. Drain collections, wash out wounds
b. Anti-microbial therapy → targeting aerobes and anaerobes
i. Gent + Metro
ii. Cef + Metro
iii. Gent + Metro + Amoxy (added cover against enterococcus faecalis)
c. Phsyiological support – IVF, O2


1. Etiology
a. CAP → ~50% no organism identified → empiricism
2. Ixs
a. CXR – PA, lat
b. Bloods
c. Sputum G stain + culture
d. Blood culture if severely sick
3. Organisms
a. S.pneumoniae 40%
b. Atypicals 25% (mycoplasma, legionella, chlaymydia)
c. H.influenzae 10%
d. Unidentified 30%
4. Presentation
a. Hx
i. Systemic feats – fevers, rigors, vomiting, appetite loss
ii. Cough – initially painful and dry, later expectoration and mucopurulent sputum
iii. CP – pleuritic
iv. Rusty sputum (S.pneumonaie)
b. Exmn
i. Percussion dullness
ii. Inspiratory crackles
5. Classification of CAP severity (similar to CURB criteria but extended)
a. High RFs
i. RR >30
ii. DBP <60
iii. Urea >7
iv. New onset AF
v. Major co-morbidity
b. Low RFs
i. Albumin <35
ii. Wcc <4000 or >25000
iii. Multi-lobar
iv. Pre-existing lung dis
c. Moderate CAP = 1x high + 1x lower or 3x lower
d. Severe CAP = 1x high + 2 x lower or 2x high
6. Tx
a. Mild CAP
i. Macrolide only (erythromycin 500 mg qid or roxithromycin-rulide) - covers S.pneumoniae + atypicals, but Ø H.influenzae
ii. Amoxycillin and Doxycycline are acceptable alternatives
b. Moderate/Severe CAP
i. B-lactam + Macrolide (amoxy-clav or cef) – cef covers H.influenzae

Anti-bacterial Prophylaxis in surgery

1. SSI (Surgical site infection)
2. Classification of wounds by degree of contamination
a. Clean – respiratory/GI/GU tracts not entered, Ø inflammation, no break in technique, non-traumatic
b. Clean-contaminated – tracts entered, but Ø spillage, minor break in technique
c. Contaminated – trauma, spillage, inflammation etc
3. Rule of thumb
a. Prophylaxis useful in clean-contaminated and contaminated procedures and in clean procedures where a prosthesis is inserted
4. Bacterial commonly causing wound infections
a. S.aureus
b. Coagulase negative staph (eg S.epidermidis)
c. Enterococcus
5. Dosage
a. Single dose given IV 30 mins prior to incision
6. Examples
a. Total joint replacement, open reduction, internal fixation of # → cephalosporin
b. Gastroduodenal or Biliary → cephalosporin
c. Appendix or colorectal → cefoxitin, amoxy-clav, gent, metro

Peripheral IV Cannulae

1. Complications
a. Infection
b. Extravastion (pass out of bloodstream into tissues)
c. Chemical phlebitis
d. Thrombosis
e. Bacteraemia → spread
2. Remove on day 5
3. Inspect cannula daily
4. If suspected infection →
a. 2x blood cultures (one through cannula)
b. Swab cannula exit site if purulent
c. Remove cannula and send time for culture
d. Look for metastatic sepsis – eg echo for endocarditis
e. Empiric tx – fluclox 2g Q6H + Gent 4-5 mg/kg per day (tx >10 days)


1. Organism – N.gonorrhea (gonococcus) – G-ve diplococcus
2. Transmission – peno-vaginal, peno-anal, oro-genital (20% risk per episode)
3. Incubation period – 2-14 days (usu 2-5 days)
4. Presentation
a. Male (see pic)
i. Usu symptomatic (but can be asx)
ii. Urethrititis → dysuria and purulent d/c (95% become asx after 6 months)
iii. Proctitis (gay men)
iv. Pharyngeal infection (oral sex)
v. G stain of d/c +ve in 95%
b. Female
i. Usu asx
ii. Endocervix and urethra most common sites
iii. Sxs
1. vaginal d/c
2. dysuria
3. intermenstrual bleeing
4. menorrhagia
5. lower back pain
iv. G stain of d/c +ve in 40%
5. Ixs → Urethral / Endocervical swab - G stain + culture
6. Mgt → Azithromycin 2 g PO stat OR Ceftriaxone 250 mg IV stat
7. Complications
a. Male - epididymitis
b. Female – salpingitis, PID (10-20%)

1. Definition – a type of NGU (non-gonococcal urethritis); termed prior to chlamydia being identified as a cause
a. Other NGU – ureaplasma, bacteroides, mycoplasma
2. Epidemiology – 7% prevalence, M:F 1:3
3. Organism – Chlamydia trachomatis (G-ve intracellular parasitic bacteria)
4. Diseases – anogenital dis, conjunctivitis, neonateal pneumonia
5. Presentation
a. Initial infection mild and self-limiting
b. Males → dysuria, urethral d/c (see pic)
c. Females → usu asx, ixs for infertility (see pic)
6. Dx
a. DNA based tests, nucleic acid amplification, PCR
b. Urine sample
7. Tx
a. Antimicrobial - Efficacy 97-100%
i. Azithromycin 1g Stat (can be used for both Chlamydia and gonorrhea) OR
ii. Doxycycline 100 mg bd 7 days
b. Contact trace all partners <60 days or last partner → tx for partners
8. Complications
a. Females – 1x Chlamydia PID = 10% infertility / 3x Chlamydia PID = 50% infertility
b. Males – persistent or recurrent urethritis / epididymitis
c. Reiters syndrome (triad = urethretits, conjunctivitis, arthritis)
d. Neonatal – conjunctivitis, pneumonia

Bacterial Vaginosus
1. Epidem – common, 20% of women, recur often
2. Etiology
a. Sexually associated – some feats like STD, others not
b. ↓ numbers of lactobacilli → overgrowth of anaerobic bacteria (lactobacilli = primary microbial agonist against genital inf)
3. Organisms – anaerobic bacteria
4. Dx reqs 3/4 of –
a. Homogenous white adherent d/c
b. Elevated pH >4.5
c. Fishy malodour
d. Microscopy – clue cells
5. Ø vaginal inflammation, cervix N
6. Tx → Metronidazole – consider when sxs or pregnant
7. Complications
a. Premature rupture of membranes during preg
b. Pre-term labour
c. Chorioamnionitis

Genital Warts
1. Epidem – common, 1% of sexually active popn
a. ↓ prev w age (resistance builds over time)
2. Organisms – human papilloma virus (present in 10-30% of popn)
a. >70 types of DNA viruses
b. HPV 6, 11 → visible warts, Ø complications
c. HPV 16, 18 → assoc w cervical ca (intraepithelial neoplasia)
3. Transmission – sexually transmitted, region specific (ie not transmissible site to site eg cant be passed to hands)
4. Presentation → exophytic warts (fleshy growths)
a. Male – Penile > Anal
b. Female – Vulval > Cervical
5. Tx → 3 equally efficacious options – 70% efficacy, 30% relapse
a. Physical ablation – eg cryotherapy
b. Cytotoxics – eg podophyllin
c. Immune – eg imiquimod
6. Prevention → HPV vaccine (only effective prior to first sexual intercourses)
a. Gardasil → HPV 16,18 and 6.11
b. Cevarix → HPV 16,18

Genital Herpes
1. Organisms - Herpes simplex virus (DNA virus) – type 1 (mouth) and type 2 (genital)
2. Presentation
a. Most infections are asx or unrecognised (70%)
b. First episode – asx to severe mucocutaneous/systemic dis (highly variable)
i. Sxs
1. Local pain and itching
2. Dysuria
3. Tender inguinal L/A
4. Systemic sxs – fever, headache, malaise, myalgias
ii. Onset <1 wk of infection
iii. Sxs typically worse in women
3. Recurrence
a. Virus lies dormant in ganglion cells – reactivation by trauma, stress, febrile illness etc
b. HSV2 90%
c. HSV1 50%
d. Men average 5/year, Women 4/year
e. Asx shedding on 10% of days (most common just before and after symptomatic recurrences), more freq in 1st yr infection
4. Management
a. Acyclovir – for severe initial episode or for freq disabling recurrences

1. Epidemiology – uncommon prior to 2000, ↑ incidence, esp MSM
2. Organism – Treponema pallidum
3. Stages
a. Primary syphilis
i. Papule at infection site → ulcerates to painless firm chancre
ii. Followed by slight fever and other constitutional sxs
iii. Chancre heals spontaneously within 2-3 wks
b. Secondary syphilis
i. 4-10 wks after primary lesion
ii. 1 or more of –
1. fever
2. sore throat
3. arthralgia
4. generalised L/A
5. widespread skin rash (Ø face)
iii. Sxs subside <1 yr
c. Tertiary syphilis
i. Latent period followed by granulomatous lesion → skin, bone, liver, testis
ii. Cardiovascular syphilis
iii. Neurosyphilis
4. Dx
a. T.pallidum enzyme immunoassay (EIA) → screening
b. Confirm a +ve test with T.pallidium haemoglutin assay (TPHA) + VDRL (veneral dis r/srch lab) test
5. Mgt → procaine benzyl penicillin 1M for 10 days (primary or secondary syphilis); 4 wks reqd for tertiary sphilis

Febrile Child

1. Overview
a. Most cases of fever → harmless self-limiting infection
b. Dx challenge → identify the cause and differentiate life-threatening bacterial causes
c. Fever = >38
d. Core temperature – measure rectally, never in child <5 yrs
e. Sites – under tongue, axilla, tympanic (digital)
2. Causes of febrile illness 3-36 months age
a. Viral 75% - URTI, LRTI, gastroenteritis
c. Gastroenteritis
d. Otitis media
e. Bacterial pneumonia
f. Soft tissue infections – cellulitis, abscess
g. Meningitis
h. Septicaemia
3. Clinical Approach
a. Find infective focus
b. Ensure hx matches severity of illness (ie ensure no co-existing infections)
c. FWR (fever without focus) → 5-10% of children will have no localising signs
d. 3% of children <2 yrs age w temp >39 potentially have a serious bacterial infection
4. Red Flags
a. Height of fever alone does not identify serious illness
b. High risk of bacterial infection
i. <3 months, T=>38
ii. 3-6 months, T+>39
c. Temp >41 not typically infective (eg malignant HTN)
5. Recognising sick and febrile child
a. Fever + seizure
b. Devt of non-blanching rash
c. Fever >5 days
d. Parent increasingly worried and believes child is unwell
6. Febrile seizures
a. 3% of children 0-5 yrs have underlying suscep
b. Ø ↑ risk of serious infection
c. Assoc w rapid change in temp, Ø height of fever
7. Management*
a. < 1 month
i. High risk bact infection - 10%
ii. Full septic screen always → blood, CSF, urine cultures, CXR
iii. Directed tests if site identified → eg wound swab, limb xray, joint aspirate
iv. Admit + A/B tx
b. 1-3 months
i. High risk bact infection – esp if T > 40
ii. Full septic screen then directed tests if site identified
iii. Admission and A/B tx usu reqd
c. 3-36 months
i. Specific tx if infection site obvious → eg UTI, otitis media, pn, meningitis etc
ii. Septic screen +/- CSF may be reqd if no focus and T>39
8. Anti-pyretics
a. Use anti-pyretics when child has fever and is distressed → Paracetamol Q4H or Ibuprofen Q6H
i. Ø Aspirin (reyes syndrome in childr <12 yrs)
ii. Weary of bronchospasm using ibuprofen
b. Tepid sponging + fans → Ø recommended
c. Ø over or underdress

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