Title: Infectious disease

Q: Which food-borne illness is from pre-formed toxin?
A: S. aures
Bacillus cereus
Clostridium botulinum

Q: Which agents cause toxin production after ingestion?
A: Vibrio cholerae
Shigella
Shiga-toxin E. coli

Q: Incubation period of salmonella
A: 24-48 hours

Q: Incubation period of Campylobacter and Shigella
A: 2-6 days

Q: Which foodborne illnesses cause predominant vomiting?
A: S. aureus, B. cereus, Astrovirus, Rotavirus, Norovirus

Q: Which microbial agents cause persistent diarrhoea?
A: Giardia, Cyclospora, Entamoeba, Cryptosporidium

Q: Foodborne neurological illnesses
A: C. botulinum
Scrombroid
Ciguatoxin
Tetrodotoxin
GBS

Q: When is stool testing indicated?
A: Watery diarrhoea with hypovolaemia
Bloody diarrhoea
Febrile
>1 week illness
Severe abdominal pain
Hospitalised
Recent antibiotic use (C. diff)
Recent travel
>70yo
Immunosuppressed
Pregnant
Infants
IBD

Q: Utility of stool culture?
A: Will identify non-typhoidal Salmonella, Campylobacter and Shigella

Q: Which patients need stool OCP sent?
A: Immunocompromised
Illness >2 weeks
Community outbreaks of waterborne illness
Recent travel
MSM

Q: When are antibiotics indicated for diarrhoeal illness?
A: Systemically unwell
Significant leukocytosis
Abdominal tenderness
High-volume watery diarrhoea
Bloody diarrhoea
Immunocompromised
>1 week of symptoms
Returned traveller

Q: When are antibiotics indicated for non-typhoidal salmonella?
A: Severe illness
Immunosuppressed
Elderly
Infants
Prosthetic valves
Haemoglobinopathies

Q: Which patients with Shigella need antibiotics?
A: Unwell
Immunocompromised
Children <6yo
Institutionalised
MSM
Food handlers
Healthcare workers

Q: How does Yersinia present?
A: Acute enterocolitis, pharyngitis and mesenteric adenitis (pseudoappendicitis)
Post-infectious arthralgia
Erythema nodosum

Q: What is the most common cause of gastro in adults and children?
A: Norovirus

Q: Criteria for gastroenteritis in NH residents?
A: 3 or more loose bowel motions above baseline over 24 hours
2 or more episodes of vomiting over 24 hours
Symptoms with identified pathogen on stool testing

Q: Most common cause of travellers diarrhoea?
A: ETEC

Q: DDx of persistent diarrhoea in returned traveller
A: Post-infectious IBS
Post-infectious lactose intolerance
Coeliac disease
Ongoing infection

Q: How does ciguatera poisoning present?
A: GI symptoms within 1 hour of consumption followed by neurological sequelae

Q: Neurological symptoms in ciguatera poisoning?
A: Peripheral paresthesias
Reversal of hot/cold sensation

Q: What causes ciguatera poisoning?
A: Reef fish contaminated by dinoflagellate Gambierdiscus toxicus, which produces ciguatoxin

Q: What is scrombroid?
A: Improper temperature control of fish leads to bacterial conversion of histidine to histamine then consumed
Symptoms like anaphylaxis within 30 minutes to 24 hours and lasting 3-6 hours

Q: Which fish cause scrombroid?
A: Tuna, mackerel, bonito
Mahi-mahi, bluefish, herring, sardines

Q: Which proportion of dysentery patients suffer reactive arthritis?
A: 2%

Q: Complications of foodborne illnesses
A: GBS
Reactive arthritis
HUS
TTP

Q: Risk of GBS after Campylobacter?
A: 1/1000

Q: Which cells are primarily killed by the HIV virus?
A: CD4+ T cells

Q: How common is acute retroviral syndrome?
A: 50-90% of HIV positive

Q: When does acute retroviral syndrome occur?
A: 2-4 weeks after acquiring HIV

Q: How long does acute retroviral syndrome last?
A: 2-10 weeks

Q: Symptoms of acute retroviral syndrome?
A: Fever, fatigue, pharyngitis, rash, lymphadenopathy, malaise, diarrhoea

Q: Mean time to AIDS if untreated?
A: 8 years (2 years for children <5yo)

Q: Where does HIV preside while in early phase?
A: Lymphoid follicular dendritic cells

Q: What cells are infected with HIV later in course?
A: CD4+ T cells, microglial cells of CNS and macrophages

Q: How is HIV progression categorised?
A: Acute retroviral syndrome
Early (CD4>500)
Intermediate (CD4 200-500)
Advanced (CD4 <200)

Q: What syndromes are associated with early HIV infection?
A: GBS
Idiopathic thrombocytopaenia
Reiter's
Polymyositis
Sjogren's
Bell's palsy

Q: What syndromes are associated with intermediate HIV?
A: Tinea
Onychomycosis
Gingivitis
Seborrhoeic dermatitis
Molluscum contagiosum
Herpes zoster
TB
Sinusitis

Q: What syndromes are associated with advanced HIV?
A: Kaposi's sarcoma
Non-Hodgkin's lymphoma
Cervical intraepithelial neoplasia
Primary CNS lymphoma
Oral candidiasis
Oral hairy leukoplakia
Herpes simplex
Cryptococcosis
MAC
CMV-related illness

Q: What are the best predictors of HIV progression?
A: HIV viral load and CD4+ count

Q: Definition of AIDS
A: CD4 <200
CD4 <15% of all lymphocytes
AIDS-defining illness

Q: Name AIDS defining illnesses
A: Recurrent bacterial pneumonia
Candidiasis of bronchi/oesophagus/trachea/lungs
Invasive cervical cancer
Coccidioidomycosis (disseminated or extrapulmonary)
CNS lymphoma
CMV retinitis
Cryptococcus (extrapulmonary)
Cryptosporidiosis (chronic intestinal)
CMV (other than liver, spleen, nodes)
HIV encephalopathy
Herpes simplex: Chronic ulcers/bronchitis/pneumonitis/oesophagitis
Histoplasmosis (disseminated or extrapulmonary)
Isosporiasis (Chronic intestinal)
Kaposi's sarcoma
Burkitt's lymphoma
Immunoblastic lymphoma
MAC
TB
PCP
Progressive multifocal leukoencephalopathy
Recurrent salmonella septicaemia
CNS Toxoplasmosis
HIV wasting syndrome

Q: Sensitivity and specificity of ELISA for HIV?
A: 99% each

Q: Specificity of Western blot for HIV?
A: 100%

Q: How can acute HIV be diagnosed?
A: HIV viral load, p24 antigen or PCR
NOT ELISA or Western blot antibody techniques

Q: Mean time to HIV viral load positive?
A: 17 days

Q: Mean time to HIV p24 antigen positivity?
A: 22 days

Q: Mean time to ELISA positive HIV?
A: 25 days

Q: Mean time to Western blot positive HIV?
A: 31 days

Q: What is immune reconstitution syndrome?
A: Lymphadenitis and fever in weeks after HIV therapy initiated

Q: Most common cause of encephalitis in HIV?
A: Toxoplasmosis

Q: How does CNS toxoplasmosis present in HIV?
A: Encephalitis
Multiple ring-enhancing subcortical lesions on CT

Q: DDx of ring enhancing lesion in HIV?
A: Toxoplasmosis
CNS lymphoma
Cerebral TB
Cryptococcal meningitis

Q: Testing of CSF in AIDS
A: Opening pressure
Cell count
Glucose
Protein
MCS
India ink
Bacterial/Viral/Fungal PCR
Fungal culture
Toxoplasmosis/Cryptococcus antigen assay
Coccidioidomysosis titre

Q: Management of headache in HIV?
A: Low threshold for Ix
If <200, must do CT

Q: How do CNS toxoplasmosis and cryptococcal meningitis differ?
A: Toxoplasmosis is more common and occurs usually if CD4 <100 with multiple ring-enhancing lesions in cortex on contrast CT
Cryptococcal usually if CD4 <50 with normal neuroimaging

Q: Most common pulmonary complications of HIV
A: CAP
PCP
TB
CMV pneumonitis
Cryptococcus
Histoplasmosis
Neoplasms

Q: DDx of diffuse interstitial pattern CXR in HIV
A: PCP, CMV pneumonitis, TB, MAC, Histoplasmosis, Coccidioidomycosis, lymphoid interstitial pneumonitis

Q: DDx of focal consolidation in HIV
A: CAP, Mycoplasma, PCP, TB, MAC

Q: DDx of nodular lesion on CXR in HIV
A: Kaposi's sarcoma
TB
MAC
Fungal infection
Toxoplasmosis

Q: What is the most common opportunistic infection in AIDS?
A: PCP

Q: Causes of oesophagitis in AIDS
A: HSV, candida, CMV

Q: DDx of AIDS-related diarrhoea
A: Enterobacteriaceae
Entamoeba
C. diff
Giardia
Cryptosporidium
Microspora
Isospora
Cryptococcus
Late-stage
MAC
CMV both need biopsy for Dx

Q: What do Kaposi's sarcoma appear like?
A: Painless, raised, brown or purple papules that do not blanch on face, chest, genitals and mouth

Q: 5 classes of antiretrovirals
A: Nucleoside RT inhibitors
Non-nucleoside RT inhibitors
Protease inhibitors
Entry inhibitors
Integrase inhibitors

Q: Indications for ART therapy
A: CD4 <350
AIDS-defining illness
Pregnancy
HIV-associated nephropathy
HepB co-infection requiring therapy

Q: Common adverse effects to antiretrovirals
A: Stevens-Johnson syndrome
Pancreatitis
Peripheral neuropathy
Lactic acidosis
Dyslipidaemia
Hyperglycaemia

Q: Risk of transmission from HIV + source not on ARV with needle stick?
A: 1/440

Q: HIV seroprevalence in MSM in Australia?
A: 8-10%

Q: HIV seroprevalence in IVDU population in Australia?
A: 0.5%

Q: HIV seroprevalence in MSM + IVDU in Australia?
A: 30%

Q: Overall prevalence of HIV in Australia?
A: 0.14%

Q: When is PEP indicated?
A: All except oral intercourse without mucous membrane breach if known HIV positive
If MSM or high-prevalence country if unknown HIV status

Q: If PEP recommended for discarded needlestick injury?
A: No

Q: When is PEP recommended following sexual assault?
A: All male-to-male
Not recommended for heterosexual assault unless assailant from high-prevalence country

Q: Why can anaemia occur rapidly in P. falciparum?
A: Can infect any age RBC/reticulocyte with high percentage of infected erythrocytes

Q: Incubation period of P. falciparum
A: 8-25 days

Q: Signs that point to alternative to malaria
A: Lymphadenopathy
Maculopapular or petechial skin rash

Q: Severe malaria
A: Coma with/without seizures
Prostration
Severe anaemia
Hypoglycaemia
Acidosis
AKI
ARDS
Jaundice
Intravascular haemolysis
Shock
DIC

Q: CSF results in cerebral malaria?
A: High opening pressure but otherwise normal

Q: Sensitivity of thick film for malaria?
A: 90%
Therefore, if highly suspicious, treat and repeat test (esp. early P. falciparum)

Q: Typical FBC in malaria
A: Normochromic normocytic anaemia
Thrombocytopaenia
Normal or low WCC

Q: Treatment of uncomplicated malaria
A: Artemether + Lumefantrine PO or
+ Primaquine course if P. ovale/vivax to eliminate hypnozoites
+ Primaquine stat if P. falciparum and in northern Australia (where Anopheles exists) to prevent transmission

Q: Treatment of severe malaria
A: IV artesunate 2.4mg/kg BD

Q: Is melioid gram-negative or positie?
A: Gram-negative

Q: Patients at risk of melioid
A: Immunosuppressed
ATSI
Alcoholics
Diabetics
Elderly
CKD
Chronic lung disease

Q: Rate of septic shock in melioidosis?
A: 20%

Q: How is melioid confirmed?
A: Culture of body fluids (Ashdown's medium)

Q: Treatment of melioid
A: Meropenem 1g TDS for 14 days
If CNS - Meropenem 2g TDS for 4 weeks
If CNS/osteomyelitis/septic arthritis/GU/soft tissue
 - Add Bactrim 320/1600mg BD + Folic acid 5mg daily for eradication
All patients get CT pan-scan for abscesses

Q: Vector of leptospirosis
A: Urine of rodents

Q: How does lepto present?
A: Flu-like illness, conjunctivitis, jaundice, hepatosplenomegaly for 5 days
Immune phase follows with renal/hepatic failure, aseptic meningitis and pulmonary haemorrhage (Weil's syndrome)

Q: Treatment of Lepto
A: Mild - Doxycycline 100mg BD for 7 days
Severe - BenPen 1.2g q6h for 7 days

Q: Mechanisms of pseudomonas resistance
A: Protein efflux
Cephalosporinases
AmpC beta-lactamases
Porin for imipenem

Q: Beta-lactam killing profile
A: Bactericidal and time-dependent

Q: Minimum time above MIC for beta-lactams?
A: 60%

Q: Are monobactams beta-lactams?
A: Yes

Q: Carbapenem killing profile?
A: Time-dependent with some post-antibiotic effect

Q: Aminoglycoside killing profile?
A: Concentration dependent with significant post-antibiotic effect

Q: Quinolone killing profile?
A: Combination time and concentration-dependent killing
Some post-antibiotic effect
AUC/MIC ratio is best predictor of efficacy

Q: Glycopeptide killing profile
A: Time-dependent + post-antibiotic effect

Q: Name a second generation cephalosporin
A: Cefuroxime

Q: Name a fourth generation cephalosporin
A: Cefepime

Q: Name a 5th gen cephalosporin
A: Ceftaroline

Q: Name a monobactam?
A: Aztreonam

Q: How do macrolides work?
A: Inhibit protein synthesis

Q: How does clindamycin work?
A: Inhibits protein synthesis

Q: How does linezolid work?
A: Inhibits protein synthesis

Q: How do fluoroquinolones work?
A: Inhibit DNA synthesis

Q: Empirical therapy for ESCAPPM
A: Meropenem

Q: Agents effective against MRSA
A: Vancomycin
Rifampicin
Bactrim
Moxifloxacin

Q: Organisms resistant to imipenem
A: Stenotrophomonas
Pseudomonas maltophila
Pseudomonas cepacia
Enterococcus faecium
MRSA

Q: Aerobic Gram-positive cocci
A: S. epi
S. aureus
Strep pneumoniae
Strep pyogenes

Q: Aerobic gram-pos bacilli
A: Bacillus anthracis
Corynebacterium diphtheria
Nocardia asteroides

Q: Aerobic Gram-negative cocci
A: Moraxella catarrhalis
Neisseria gonorrhoea
Neisseria meningitidis

Q: Aerobic Gram-negative bacilli
A: Pseudomonas aeruginosa
Stenotrophomonas maltophilia
Acinetobacter baumanii
Burkholderia cepacia
Haemophilus influenzae
Serratia
Bordatella pertussis
Legionella pneumophila
Vibrio cholerae

Q: Facultative Anaerobic Gram-pos cocci
A: E. faecalis
E. faecium

Q: Facultative Anaerobic Gram-pos bacilli
A: Listeria monocytogenes

Q: Facultative anaerobic Gram-negative bacilli
A: E. coli
Citrobacter
Enterobacter cloacae
Klebsiella
Morganella morganii
Proteus
Salmonella typhi
Shigella
Yersinia

Q: Obligate anaerobic Gram-pos bacilli
A: C. difficile
C. perfringens
C. botulinum
C. tetani

Q: Obligate anaerobic Gram-negative bacilli
A: Campylobacter
Helicobacter pylori
Bacteroides
Peptostreptococcus

Q: What are ESCAPPM bacteria?
A: Gram-negative with inducible chromosomal AmpC cephalosporinase/beta-lactamase.
Includes:
 - Enterobacter
 - Serratia
 - Citrobacter
 - Acinetobacter
 - Aeromonas
 - Proteus
 - Providencia
 - Morganella
Confers resistance to cephalothin, cefazolin, cefoxitin, most penicillins and beta-lactamase inhibitor/beta-lactam combinations

Q: What are ESBL organisms?
A: Extended-spectrum beta-lactamase producers (plasmid-mediated and NOT inducible)
Usually E. coli or Klebsiella
Meropenem is first-line

Q: Differences between E. faecium and E. faecalis?
A: E. faecalis (faecaLESS) is more common and causes less severe illness
E. faecalis is susceptible to BenPen and Ampicillin and resistant to carbapenems
E. faecium is susceptible to Quinupristin-dalfopristin and resistant to vancomycin and carbapenems

Q: Consequences of VRE
A: Isolation
Potential for VRE invasive infection
Potential for transmission of vancomycin resistance to S. aureus

Q: Empirical treatment for clinically significant VRE infection?
A: Linezolid

Q: Risk of percutaneous transmission of HepB if HBsAg pos and HbeAg negative or HbeAg positive?
A: 5% and 40% respectively

Q: Risk of percutaneous HCV transmission?
A: 3%

Q: Management of percutaneous blood exposure
A: Soap and water
Hx
Exposed - HIV Ab, HIV Ag, HBsAb, HCV Ab, HBsAg, hCG
Source - HBsAg, HCV antibody, HIV antibody
Consider ADT, HepB PEP, HIV PEP
Arrange follow-up

Q: HepB PEP
A: If unvaccinated or non-responder - HepB vaccination course + HBIG unless source HBsAg negative
If vaccinated but unknown response
 - Check exposed for anti-HBs:
       - If adequate: No Rx
       - If inadequate and source HBsAg pos --> HBIG + Vaccine booster
       - If inadequate and source unknown --> Vaccine booster and re-check titre in 1-2 months

Q: What proportion of patients on HIV PEP stop due to side effects?
A: 50%

Q: Which patients with needlestick injury need HIV PEP?
A: All if known HIV +
If unknown status, only if source has HIV risk factors

Q: Organisms that require airborne precautions
A: Measles
Varicella
TB

Q: What do airborne precautions include?
A: Isolation room, negative pressure

Q: Which organisms require droplet precautions?
A: Invasive Hib
Invasive meningococcus
Serious bacterial respiratory infection
Strep throat
Adenovirus
Influenza
Mumps
Parvovirus B19
Rubella

Q: What does droplet precautions require?
A: Isolation room if possible
1m between patient and others
Mask if patient not in private room
N95 mask for healthcare workers if within 1m of patient

Q: Which patients need contact precautions?
A: MDR
C. diff
Shigella
Rotavirus
RSV
Parainfluenza
HSV
Impetigo
Cellulitis
Scabies
Herpes zoster

Q: Management of non-immune HCW exposed to varicella?
A: VZIG within 96 hours of exposure
PEP vaccination
Off work day 10-21 from exposure as potentially infectious irrespective of above

Q: Who needs meningococcal PEP?
A: Mouth-to-mouth
INtubation without mask
Suctioning without mask
Family in household for 24 hours
Anyone spending 4 hours continuously with patient
Only after case confirmed

Q: Meningococcal chemoprophylaxis
A: Cipro 500mg PO stat

Q: What is Group A strep?
A: S. pyogenes

Q: What is Group B strep?
A: S. agalactiae

Q: Where do glycopeptides bind?
A: ALA-ALA dipeptide in cell wall peptidoglycan

Q: How does cefotaxime differ from ceftriaxone?
A: Cefotaxime has greater anti-staphylococcal activity and does not displace bilirubin from albumin in neonates

Q: Which cephalosporins are anti-pseudomonal?
A: Ceftazidime and cefepime

Q: Which cephalosporin is active against MRSA?
A: Ceftaroline (5th gen)

Q: How does dicloxaxicillin differ from flucloxacillin?
A: Diclox causes less hepatotoxicity but more interstitial nephritis

Q: Drug of choice for enterococcal infection?
A: Ampicillin

Q: How does amoxicillin differ to BenPen?
A: More gram-negative cover

Q: Indications for glycopeptides
A: MRSA, MRSE and E. faecium

Q: What are clinda/lincomycin effective against?
A: Gram-positive aerobes (not Enterococcus) and most anaerobes
CA-MRSA (but not HA-MRSA)
Antitoxin effect

Q: Complications of macrolides
A: QT prolongation
CytP450 inhibition

Q: Spectrum of Cipro
A: Gram-negative bacteria, Pseudomonas, some GPC
No activity against anaerobes or streptococcus

Q: Spectrum of moxifloxacin
A: Extended spectrum Gram positive cover
Gram-negative aerobes
Anaerobes
Not Pseudomonas (unlike cipro)

Q: Complications of quinolones
A: Tendinitis
Prolonged QT

Q: Gentamicin dosing
A: Severe sepsis - 7mg/kg
Severe sepsis >80yo or CrCl 40-60 - 5mg/kg
Severe sepsis CrCl <40 - 4mg/kg

Q: Empirical Ab for CA-sepsis of unclear source
A: Gent 4-7mg/kg + Fluclox 2g q4h IV
Replace fluclox with vanc if at risk of MRSA
Use Mero 1g TDS instead if risk of MDR Gram-negative or tropical region
If meningitis suspected, treat as for meningococcal sepsis
Risk factors for MDR Gram-negative:
 - Travel to area of high prevalence in last 6mo
 - Prolonged hospitalisation
 - Long-term care facility
 - Colonisation or infection with MDR Gram-negative

Q: Empirical Ab for hospital-acquired sepsis, source not apparent
A: PipTaz 4.5g q6h or Meropenem 1g TDS if risk factors for MDR Gram-neg
Add vanc if risk of MRSA or line sepsis likely
Consider voriconazole if risk factors for candidaemia

Q: Empirical Ab for CA-sepsis, source not apparent in child <2mo
A: Meningitis not excluded - Cefotaxime 50mg/kg IV q6h + Ampicillin 50mg/kg IV q6h +- Aciclovir
Meningitis excluded - Gent 7.5mg/kg + Ampicillin 50mg/kg IV q6h

Q: Empirical Ab for CA-sepsis in child >2mo
A: Cefotaxime 50mg/kg IV q6h + Gentamicin 7.5mg/kg + Vancomycin 30mg/kg IV
Remember dex 0.15mg/kg if meningitis +- Acyclovir

Q: Empirical Ab for line sepsis
A: Gent 7mg/kg + Vancomycin 30mg/kg IV then 15mg/kg BD
Consider removal of line
Consider antifungals if failure to improve, previous fungaemia

Q: Patient selection for HITH
A: Appropriate antibiotic available as HITH dosing
Medically stable
Willing and able to return to hospital if required
Compliant
Good social/home situation

Q: Suitable infections for HITH
A: Cellulitis
Infective exacerbations CF/bronchiectasis
Endocarditis
Osteomyelitis
Septic arthritis
Bacteraemia
Tertiary syphilis

Q: Relative CI to aminoglycosides
A: Auditory/vestibular impairment
FHx of aminoglycoside-induced vestibular/auditory impairment
CrCl <40
Rapidly deteriorating renal function
Age >80

Q: Treatment of bat scratch/bite
A: Soap and water 5 minutes
Virucidal antiseptic (povidone-iodine or alcohol)
HRIG 20IU/kg around wound +- IM on ipsilateral deltoid or thigh if cannot fit it all
Rabies vaccine IM on contralateral limb on days 0, 3, 7 and 14
Follow-up serology 2 weeks after last dose

Q: How does clinical rabies present?
A: Acute encephalitis
Incubation period 20 days to 5 years
Encephalitic (80%)
 - Excitability, disorientation, hallucination, bizarre behaviour, hypersalivation, hyperthermia, tachycardia, piloerection, arrhythmias and priapism
Paralytic (20%)
 - Paresis of bitten limb spreading to all
50% have classic hydrophobia

Q: What is aerophobia?
A: Aversion to wind on face

Q: Mortality of patients presenting to ED with temp >38?
A: 3%

Q: What proportion of patients in ED with lactate 2-3.9 deteriorate?
A: 25% need ICU (12.5% mortality)

Q: What proportion of patients with sepsis have temp <38.3?
A: 50%

Q: Define sepsis?
A: Life-threatening organ dysfunction caused by a dysregulated host response to infection (Sepsis-3)

Q: Clinical criteria for sepsis
A: Increase of 2 or more points in SOFA score

Q: qSOFA score
A: 2 or more of below = likely to have prolonged ICU stay or die in hospital
 - Hypotension <100
 - ALOC
 - Tachypnoea >22

Q: Define septic shock
A: Sepsis with circulatory and cellular/metabolic dysfunction

Q: Clinical criteria for septic shock?
A: Both of:
 - Persistent hypotension requiring vasopressors to achieve MAP 65
 - lactate >= 2

Q: Hospital mortality of severe sepiss?
A: >40%

Q: Overall mortality rate of sepsis?
A: 10%

Q: Initial fluid resus in sepsis
A: 30mL/kg within first 3 hours (surviving sepsis)

Q: Maximal delay to antibiotics in order to get cultures in sepsis?
A: 45 minutes

Q: Target for time to antibiotic delivery in sepsis?
A: Within 1 hour

Q: Increase in mortality for every hour delay in antibiotic delivery in sepsis?
A: 4%

Q: Risk factors for invasive candida
A: Immunocompromise
Prolonged invasive devices
TPN
Necrotising pancreatitis
Recent abdominal surgery
Prolonged admission
prolonged broad-spectrum antibiotic use
Recent fungal infection

Q: Empirical antifungals for candida
A: Anidulafungin

Q: Tests for invasive Aspergillus
A: Galactomannan and beta-D-glucan

Q: How soon should source control be achieved in sepsis?
A: Target within 6-12hours (surviving sepsis)

Q: What to do about tunnelled catheters with sepsis?
A: Leave in and treat for line infection
Remove only if septic shock or suffering fungaemia in liaison with treating team after achieved alternative access

Q: Target ScvO2?
A: >70%

Q: What did the VASST trial show?
A: Potential improved outcomes if NA kept to <15mcg/min through vasopressin addition

Q: How long does metaraminol bolus last?
A: 20-60 minutes

Q: When are corticosteroids indicated in sepsis?
A: Shock refractory to vasopressors
Hydrocort 50mg QID

Q: When should insulin be initiated in sepsis?
A: 2 consecutive BSL >10 and target <10

Q: Mortality of lactate >4 in sepsis?
A: 28%

Q: How sensitive is procalcitonin for bacteraemia?
A: 80-100% in ED population

Q: Incubation period of influenza?
A: 1-4 days

Q: Sensitivity of GeneXpert for influenza?
A: Up to 80% (therefore if high risk group/resp HDU - wait for PCR)

Q: High risk groups for influenza
A: <5yo
>65yo
ATSI
Cardiopulmonary comorbidities
Severe neurological conditions
Immunosuppressed
Pregnant
Patients <19 on aspirin
Morbid obesity
Nursing home residents
Down syndrome
Homeless

Q: Which patients benefit from neuraminidase inhibitors?
A: Within 48 hours or longer if severe/hospitalised

Q: Benefits of neuraminidase inhibitors
A: Reduce complications, hospitalisation and death in observational studies
RCT's on young healthy individuals have not shown benefit

Q: Dose of oseltamivir in adults
A: 75mg BD (150mg BD if intubated)

Q: Which contacts of influenza cases need oseltamivir course?
A: Household contacts with risk factors/comorbidities
NH or long-term care facility residents

Q: Mortality of HSV-1 encephalitis?
A: 70% if untreated

Q: Is topical aciclovir effective for primary HSV-1 or HSV-2 disease?
A: No.

Q: Which herpes virus causes encephalitis?
A: HSV-1
(HSV-2 only in neonates from birth canal)

Q: Which herpes virus causes meningitis?
A: HSV-2. Benign course. Seen in 25% of primary HSV-2 in women

Q: What is Mollaret syndrome?
A: Recurrent lymphocytic meningitis from HSV-2

Q: How sensitive is CSF PCR for HSV encephalitis?
A: 94-98%

Q: Treatment of HSV encephalitis/disseminated disease/immunocompromised
A: Acyclovir IV 10mg/kg TDS

Q: Treatment of primary HSV-1 or HSV-2 disease?
A: Acyclovir PO 400mg 5 times daily

Q: Treatment of recurrent herpes labialis
A: Topical aciclovir 5% cream 5 times a day

Q: Treatment of HSV genital ulcers
A: First episode - Aciclovir 400mg TDS for 5 days
Recurrent episodes - Aciclovir 800mg TDS for 2 days

Q: How do varicella vesicles arise?
A: Crops with papules/vesicles/crusted lesions simultaneously

Q: Complications of varicella
A: bacterial superinfection
Progressive severe skin rash, lung, liver, brain involvement
Cerebellar ataxia
Meningoencephalitis
Pneumonitis can be particularly severe (esp. pregnant females)

Q: Which patients need treatment for chicken pox?
A: Severe disease
Complications
Chronic skin or pulmonary disease
Long-term salicylate therapy
Immunosuppressed
Pregnant women

Q: Antiviral treatment for chicken pox (if indicated)?
A: Acyclovir 800mg PO 5 times a day for 7 days
Acyclovir 10mg/kg IV TDS for 7 days if immunosuppressed or visceral involvement

Q: When is antiviral therapy indicated in zoster?
A: Within 72 hours or longer if new vesicles arising
Immunosuppressed
ACyclovir 800mg PO 5 times daily
ACyclovir 12.5mg/kg IV TDS if disseminated

Q: Treatment of neuropathic pain in zoster
A: Paracetamol
Prednisone 50mg daily for 7 days then wean over 14
Amitryptiline 10mg nocte
Opioids

Q: Treatment of post-herpetic neuralgia
A: paracetamol
Ice massage
Amitryptiline 10mg nocte
TENS
Opioids
Topical lignocaine/capsaicin

Q: Complications of EBV
A: Splenomegaly and rupture
B-cell lymphoma
Hodgkins lymphoma
Burkitt lymphoma
Nasopharyngeal carcinoma
Meningoencephalitis
GBS
Hepatitis
Myocarditis

Q: What proportion of teenagers with EBV have splenomegaly?
A: 50%

Q: How long should patients with EBV mononucleosis avoid contact sports?
A: 4 weeks to prevent splenic rupture

Q: How do CMV and EBV differ in presentation in adolescents?
A: CMV causes similar mono-type illness but without exudative pharyngitis
CMV is monospot negative
CMV can be treated with ganciclovir if severe or immunocompromised

Q: Name 4 flaviviruses
A: Yellow fever
Dengue
Japanese encephalitis
Murray valley encephalitis

Q: Name 3 alphaviruses
A: ross river fever
Barmah forest virus
Chikungunya

Q: How does yellow fever present?
A: Flu-like syndrome after 5 day incubation
15% have later toxic phase with high fever, hepatitis, jaundice, haemorrhage and AKI
Mortality of toxic phase is 50%

Q: Stages of dengue infection
A: Febrile phase (2-7 days)
 - High fever, chills, breakbone myalgia, arthralgia, retro-orbital pain and headache
 - Blanching maculopapular rash
Critical (1-2 days)
 - Rise in Hct with thrombocytopaenia and leukopaenia
Recovery phase (2-3 days)
 - Gradual resorption of leaked fluid

Q: Testing for dengue
A: NS1 antigen + PCR + serology

Q: Treatment of dengue
A: Supportive care
Avoid nSAID's and antiplatelets
If no warning signs, passing urine and tolerating fluids - outpatient care
 - Abdo pain/tenderness
 - Persistent vomiting
 - Clinical fluid overload
 - Mucosal bleed
 - lethargy
 - Liver enlargement >2cm
 - Increase in Hct with rapid decrease in platelet count

Q: What is erysipelas?
A: Superficial infection of upper dermis with clear demarcation and prominent lymphatic involvement

Q: What is a carbuncle?
A: Multiple interconnecting furuncles

Q: Risk factors for cellulitis
A: Immunosuppression
Lymphoedema
Age
Diabetes
Skin breakdown
venous insufficiency
Peripheral oedema
Obesity
Chronic renal disease
Cirrhosis

Q: Which groups suffer erysipelas more commonly?
A: Very young and old

Q: Organisms responsible for purulent cellulitis vs. non-purulent?
A: S. aureus vs. strep

Q: What is the most common cause of erysipelas?
A: Beta-haemolytic strep (pyogenes)

Q: What causes bullous erysipelas?
A: Synergistic staph (MRSA usually) and beta-haemolytic strep (pyogenes) infection

Q: What is elephantiasis nostra?
A: chronic changes secondary to cellulitis

Q: Indications for BC in cellulitis
A: Surgical or traumatic wound infection
Septic
Need for surgical intervention
Infected ulcers/burns
Deep ulcers over bone >2 weeks

Q: Indications for XR in cellulitis
A: Deep ulcer over bone >2 weeks
Suspected foreign body
Recent trauma

Q: Risk factors for MRSA in cellulitis
A: Purulent infection
Antibiotic use in past month
Failed MSSA therapy
Previous MRSA
Spider bite
High-prevalence in community
Prisoner
High-care NH resident
Soldiers
Daycare
Boarding school
Contact sports
Haemodialysis
IVDU
MSM

Q: Which patients are at risk of Gram-negative cellulitis
A: Elderly, diabetic foot, fish bone injuries

Q: Fresh water bacteria
A: AEromonas

Q: Salt water bacteria
A: Vibrio

Q: Risk factors for pseudomonas cellulitis
A: Hot tub
IVDU
Neutropaenic

Q: Risk factors for Clostridial cellulitis
A: Bite wounds
Diabetic
Necrotising
Gaseous

Q: Organisms in dog and cat bites?
A: Pasteurella
Capnocytophaga

Q: Treatment of mild cellulitis
A: Dicloxacillin 500mg QID for 7 days
Clindamycin 450mg TDS for 7 days if MRSA risk

Q: Treatment of severe cellulitis
A: Flucloxacillin 2g IV QID (q4h if septic)
or
Lincomycin 600mg TDS IV if CA-MRSA
Vancomycin 30mg/kg IV load then 15mg/kg BD if HA-MRSA

Q: Freshwater-related cellulitis Rx
A: Ciprofloxacin 400mg IV BD or 500mg BD PO for 14 days

Q: Saltwater cellulitis Rx
A: Doxycycline 200mg PO stat then 100mg BD for at least 14 days
Add Ceftriaxone 1g BD if severe infection

Q: Is needle aspiration suitable for cutaneous abscess drainage?
A: No

Q: Steps of cutaneous abscess drainage
A: Consent
Infiltrate skin over abscess then abscess itself
No. 11 scalpel blade over area of greatest fluctuance
Cross-shaped incision
Break up loculations with haemostat
Gauze wick
Warm compresses tDS and f/u in 2 days
Antibiotics if indicated

Q: Indications for cutaneous abscess antibiotic therapy
A: Surrounding cellulitis, systemically unwell, immunosuppression or multiple lesions

Q: How effective is staph carriage eradication?
A: 50%

Q: When should staph eradication therapy be performed?
A: After all acute lesions have healed

Q: Protocol for staph eradication
A: Mupirocin 2% nasal ointment BD for 5 days
Chlorhex 2% or Triclosan 1% daily for 5 days
Hot water bed linen wash
Wash towels after each use in hot water

Q: Indications for staph eradication
A: All index cases if confirmed staph
Household contacts if personal hx of staph or ongoing recurrent staph infections in household despite eradication in index case

Q: What proportion of necrotising soft tissue infections are bacteraemic?
A: 30%

Q: Poor prognostic factors for necrotising soft tissue infections?
A: <1yo
>60yo
Immunosuppressed
Diabetic
Obesity
Comorbid CKD/CCF/cirrhosis/cancer
Positive BC
Truncal/perineal involvement
Delayed diagnosis

Q: Types of necrotising soft tissue infection
A: Type I - Polymicrobial
Type II - Monomicrobial
Type III - Vibrio vulnificus
Type IV - Fungal in immunocompromised

Q: What proportion of necrotising soft tissue infections are Type I (polymicrobial)?
A: 70%

Q: Specific sign of necrotising soft tissue infection
A: Tenderness beyond margin of erythema
Pain out of proportion
Brawny oedema
Crepitus
Brown discolouration
Bullae
Serosanguinous discharge
Tachycardia out of proportion to fever

Q: What proportion of cases of necrotising soft tissue infections have hard signs?
A: <50% (crepitus, gas in tissues on XR, bullae, necrosis, hypotension)

Q: Treatment of necrotising fasciitis
A: FLuid resus
Avoid vasoconstrictors if possible
Meropenem 1g TDS + Vancomycin 30mg/kg IV then 15mg/kg BD + LIncomycin 600mg TDS
Urgent surgical consult for debridement
ADT
IVIG +- hyperbaric O2

Q: Most common organism in pilonidal sinus?
A: Staph aureus

Q: Empirical treatment of STI
A: Ceftriaxone 500mg IM
Azithromycin 1g PO stat and in 7 days
Metronidazole 400mg BD for 14 days

Q: DDx of urethritis/cervicitis
A: N. gonorrhoea
Chlamydia trachomatis
Ureaplasma urealyticum
Ureaplasma genitalium
Trichomoniasis
HSV
ADenovirus

Q: partners from how long back need contact tracing for STI?
A: 60 days

Q: How long should sexual abstinence be maintained following STI diagnosis
A: 7 days from treatment completion and all symptoms resolved

Q: Rate of symptoms in men with gonorrhoea?
A: 90%

Q: How does disseminated gonococcal infection present?
A: Pustular dorsum of wrist/ankle lesions, tenosynovitis and polyarthralgia OR
Purulent arthritis without rash

Q: What proportion of gonorrhoea cases have disseminated disease?
A: 3%

Q: What proportion of disseminated gonococcal disease have positive BC?
A: Around 50%

Q: Which patients with disseminated gonorrhoea are more likely to be BC positive?
A: Rash, tenosynovitis, polyarthralgia vs. septic arthritis

Q: What proportion of synovial fluid is culture positive in gonococcal septic arthritis?
A: 50%

Q: Treatment of disseminated gonorrhoea
A: Ceftriaxone 1g BD IV then switch to augmentin

Q: How does trichomoniasis present?
A: Malodorous, thin watery discharge, vulvar irritation, pruritis, dyspareunia and lower abdominal pain
Classic 'champagne' yellow-green frothy discharge is rare
Punctate cervical haemorrhages (strawberry cervix)
Urethritis in men

Q: Treatment of trichomoniasis
A: Metronidazole 400mg PO BD for 14 days + treat partners to prevent re-infection

Q: DDx of genital ulcers
A: Syphilis
HSV
Donovanosis
Chancroid
Lymphogranuloma venereum

Q: Which genital ulcers are painful?
A: HSV
Chancroid

Q: What causes chancroid?
A: Haemophilus ducreyi

Q: How does granuloma inguinale present?
A: Beefy red bleeding ulcers without inguinal lymphadenopathy

Q: Features of tertiary syphilis
A: Gumma (granulomas)
Meningitis
Dementia
Tabes dorsalis
Thoracic aortic aneurysm

Q: When do VDRL and rapid reagin tests become positive for syphilis?
A: 1-4 weeks after chancre arises

Q: Treatment of primary or secondary syphilis?
A: Penicillin G 2.4 million units stat

Q: What is the Jarisch-Herxheimer reaction?
A: ACute febrile illness, headache and myalgia within 24 hours of initiating syphilis treatment

Q: Treatment of tertiary syphilis
A: Penicillin G 2.4million IU IM weekly for 3 weeks

Q: Which HSV causes genital ulcers?
A: HSV_2

Q: Do HSV genital ulcers show lymphadenopathy
A: Yes

Q: How long do HSV genital ulcers last?
A: 3 weeks

Q: Treatment of first episode HSV-2 genital ulcers
A: Acyclovir 400mg TDS for 7 days (if proctitis or oral --> 5 times daily)

Q: Treatment of chancroid
A: Azithromycin 1g PO stat

Q: Emergency contraception dosing
A: Levonorgestrel 1.5mg PO stat

Q: Mortality of clinical tetanus
A: 20%

Q: How does tetanus cause symptoms?
A: Tetanospasmin toxin acts at motor end plates of skeletal muscle, spinal cord, brain and sympathetic nervous system to cause sympathetic overdrive, spasm and tetany

Q: Causes of tetanus
A: Wound infection
Surgical procedures
Otitis media
IVDU
Umbilical stump infection

Q: What proportion of tetanus cases are generalised?
A: 80%

Q: How does generalised tetanus present?
A: Pain and stiffness in masseter (lockjaw)
Face affected first (shortest axons)
Trismus (risus sardonicus)
Opisthotonus
extension of lower extremities
Normal mental status
Laryngospasm/respiratory muscle spasm can be fatal
Hypersympathetic state can be fatal

Q: How does neonatal tetanus present?
A: Unsterile treatment of stump leads to weak, irritable, weak suck and deterioratoin in week 2 of life

Q: How does cephalic tetanus present?
A: Head wound/otitis media with CN VII dysfunction and poor prognosis

Q: Treatment of tetanus
A: ABCDE
Minimise environmental stimuli (leads to spasms)
Tetanus IG
 - Does not improve symptoms but mops up circulating toxin
 - 6000IU IM
Wound management
Metronidazole 500mg BD IV
IV midazolam for muscle relaxation

Q: Does tetanus disease provide immunity?
A: No

Q: What proportion of patients receive appropriate tetanus-prophylaxis?
A: 60%

Q: Tetanus-prone wounds
A: Compound fractures
Deep penetrating wounds
Wounds containing foreign bodies
Wounds with pyogenic infection
Wounds with extensive tissue damage
Contaminated wounds
REplantation of avulsed tooth

Q: Which patients need tetanus IG?
A: Clinical tetanus
<3 vaccinations with anything but a clean minor wound

Q: Which patients need tetanus booster?
A: At least 3 vaccinations with
 - 5-10 years from last dose with non-clean minor wound
 - >10 years from last dose with any wound

Q: Causes of toxic shock syndrome?
A: Strep pyogenes and Staph aureus

Q: Toxins in staph toxic shock syndrome?
A: Toxic shock syndrome toxin-1 (TSST-1)
Staphylococcal enterotoxins

Q: Toxins in strep toxic shock syndrome?
A: Streptococcal pyogenic exotoxins A and B

Q: Risk factors for staph toxic shock syndrome/
A: Retained placenta
Nasal packing
Skin and soft tissue infection
Varicella
Surgery
Trauma
Childbirth
Influenza

Q: Risk factors for strep toxic shock syndrome
A: Necrotising infection
Varicella
Surgery
Trauma
Childbirth
Influenza

Q: BC positive in staph toxic shock syndrome?
A: 5%

Q: BC positive in strep toxic shock syndrome?
A: 60%

Q: Which has higher mortality: Staph or strep toxic shock syndrome?
A: Strep 30% vs. staph <5%

Q: How do you differentiate STaph scalded skin syndrome and Staph toxic shock syndrome?
A: Scalded skin do not show hypotension or organ dysfunction

Q: DDx of toxic shock syndrome
A: Rocky mountain spotted fever
Leptospirosis
Meningococcaemia
SJS
TEN
Kawasaki

Q: Treatment of Toxic shock syndrome
A: Remove nidus of infection
Mero + Vanc + Lincomycin (as for nec fasc)
IVIG if fails to improve

Q: Which patient groups are most at risk of strep toxic shock syndrome?
A: Older and <1yo with necrotising fasciitis

Q: Treatment of strep toxic shock syndrome
A: PipTaz 4.5g QID or Meropenem 1g TDS + Lincomycin 600mg IV TDS
Add vanc if MRSA risk
Once GAS confirmed
 - Change to Pen G 4 million U q4h + Lincomyin

Q: Treatment of tickborne rickettsial infection
A: Doxycycline 100mg BD for 7 days

Q: DDx of zoonotic encephalitis
A: Japanese encephalitis
Bartonella henselae (cat scratch)
Brucella canis
Borelliosis
Coxiella burnetii
Listeriosis
Leptospirosis
Toxoplasmosis

Q: Presentation of Q fever
A: Pneumonia
Meningoencephalitis
Pericarditis
Myocarditis
Endocarditis
Granulomatous hepatitis

Q: Consequences of transplacental toxoplasmosis
A: Chorioretinitis
Hydrocephalus
Hepatosplenomegaly
Thrombocytopaenia

Q: Define mrMRSA
A: Methicillin + 3 or more classes of non-beta-lactam antibiotic

Q: Define nmMRSA
A: Methicillin + <3 classes of non-beta-lactam antibiotic

Q: Most common clone of mrMRSA?
A: EMRSA-15: Penicillin, cipro, macrolides/lincosamide resistant

Q: Which drug is mrMRSA susceptible to?
A: Potentially only vancomycin
Some variants (EMRSA-15) are susceptible to bactrim and rifampicin

Q: Mechanism of methicillin resistance in staph aureus?
A: pbp-2a less affinity for penicillins, cephalosporins and carbapenems
Not a beta-lactamase (therefore beta-lactamase inhibitors not effective)

Q: What is Panton-Valentine leucocidin (PVL)?
A: Toxin produced by some CA-MRSA resulting in more purulent, surgically drainable collections and recurrent boils

Q: Primary HSV-1 infection
A: Gingivostomatitis and pharyngitis

Q: Primary HSV-2 infection
A: Genital ulcers

Q: Is topical aciclovir effective for primary HSV-1 and HSV-2?
A: No. Need systemic oral or IV antiviral

Q: HSV-1 recurrence presents as?
A: Recurrent herpes labialis, herpetic whitlow, herpes gladiatorum, Bell's palsy and herpes keratitis

Q: HSV-2 recurrence presents as?
A: Recurrent genital ulcers

Q: When is PEP recommended for sexual exposure to known HIV positive?
A: All except oral intercourse (unless mucous membrane breached or viral load KNOWN to be undetectable)

Q: When is PEP indicated in unknown HIV status exposure?
A: If source MSM or high-prevalence country
Not recommended for oral sex, mucous membrane exposure or discarded needlestick injury

Q: What is the RASP tool?
A: Risk assessment stratification protocol to determine approximate risk of HIV seroconversion following exposure

Q: How is RASP tool organised?
A: Total score (Z) = Source population (A) x Inoculum type (B) x Method of transmission (C)
Basic risk = 1/Z
Total risk = 1/Z x Volume of inoculum score (D)

Q: As per RASP, when is PEP indicated?
A: >1/1000 risk = Definitely
1/1000 to 1/10 000 = Recommended but optional
1/10 000 to 1/100 000 = Not recommended but optional
<1/100 000 = Not indicated

Q: Mortality rate of severe malaria with treatment
A: 5-30%

Q: What proportion of people exposed to TB in droplets actually become infected?
A: 30%

Q: What proportion of patients develop active reactivation (post-primary) TB?
A: 10%

Q: What is the rate of post-primary/reactivation TB in children and HIV + patients?
A: 20%

Q: What proportion of TB infected patients suffer reactivation within 2 years?
A: 5%

Q: What is the risk of reactivation TB if HIV+ per year?
A: 5-10%

Q: Pupils in botulism?
A: Fixed and dilated

Q: Phases of yellow fever infection
A: Period of infection (after 3-5 days incubation)
Period of remission (for 48 hours)
period of intoxication (15% of patients)

Q: What causes hot tub cellulitis?
A: Pseudomonas

Q: Reservoir of schistosomiasis
A: Freshwater snails

Q: 3 major species of schistosomiasis
A: S. mansoni (GI)
S. japonicum (GI)
S. haematobium (GU)

Q: Bladder features of schistosomiasis
A: Eosinophilic granulomas
Chronic ulceration
pseudopolyps
Increased risk of cancer

Q: Katayama fever presentation
A: Acute schistosomiasis syndrome
 - Fever, headache, urticaria, chills, myalgia, diarrhoea, abdo pain
Eosinophilia

Q: Treatment of schistosomiasis
A: Katayama fever - Prednisone 50mg/day for 5 days + Praziquantel
Chronic infection - Praziquantel

Q: Which patients are at risk of Brucellosis?
A: Feral pig hunters
Overseas travellers/migrants exposed to unpasteurised dairy products in countries where brucellosis occurs in cattle/goats/sheep

Q: Which symptoms is specific for brucellosis in fever of unknown origin?
A: Significant depression

Q: Management of brucellosis?
A: Doxycycline + Gentamicin

Q: How does cat scratch disease present?
A: Blister/papule at site of scratch or bite followed by painful regional lymphadenopathy in about 2 weeks
Flu-like illness
Fever of unknown origin

Q: Treatment of cat scratch disease
A: Azithromycin
Rifampicin added if invasive liver, spleen, eye, CNS disease

Q: How does Q fever present?
A: Acute flu-like illness, mild pneumonia in most cases
Minority suffer hepatitis, acute endocarditis
Minority suffer persistent localised infection

Q: How is Q fever diagnosed?
A: Serology

Q: Treatment of Q fever?
A: Doxycycline

Q: Clinical signs of catheter-related infection
A: Invasive line and no other source for BSI
Suppurative
Metastatic infection
Haemodynamic instability
Clinical signs of sepsis during catheter use
BC positive for S. aureus, S. epi or Candida
Clinical improvement within 24 hours of removal

Q: When should long-term CVL/PICC be removed?
A: Septic shock
Persistent bacteraemia despite 72 hours of antimicrobials
Metastatic infection
Suppurative thrombophlebitis

Q: When should catheter-related infection be covered for Candida?
A: TPN
Long-term broad-spec Ab
Haematological malignancy
Transplant
Femoral catheter
Candida colonisation at multiple sites

Q: Are steroids beneficial in zoster?
A: May reduce pain of rash and postherpetic neuralgia
Thought to be most beneficial in elderly as most at risk of post-herpetic neuralgia

Q: What causes most death in ebola?
A: Diarrhoeal volume losses

Q: When are ebola patients infective?
A: Only once symptomatic

Q: How does ebola present?
A: Fever, fatigue, headache, vomiting, diarrhoea, anorexia
Diffuse maculopapular rash
Leukopaenia, thrombocytopaenia, transaminitis +- DIC

Q: Three phases of yellow fever
A: Period of infection (3-4 day viraemia)
Period of remission
Period of intoxication (MODS)

Q: Seroprevalence of HIV in MSM in Australia?
A: 11%

Q: Risk factors for Fournier's
A: Age, DM, alcoholism, cirrhosis, immunosuppression, cancer