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1
Q

Describe malaria types, lifecycle, features, diagnosis, chemoprophylaxis, and management

A

Lifecycle- infected anopheles injects sporozoites-> merozoites-> schizonts

Types- falciparum IP 1-4 weeks, causes cerebral malaria, shock and renal failure

  1. P malaria - persists in blood for over 20 years (no hypnozoites),
  2. Vivax- hypozoites, relapses
  3. Ovale - hypnozoites
  4. Knowlesi- zoonotic malaria mainly SE Asia .

Diagnosis- thick and thin film. Need 3 total negative to exclude .
False negatives occur if partially treated
ICT high specificity and sensitivity but doesn’t tell burden of disease.
Severe parasetemia over 2% in all except knowlsi is over 1%

Prophylaxis- doxycycline, mefloquine (contraindicated in neuropsy disorders, cardiac conduction defect), atorvaquone and proguanil

Mx- uncomplicated artemether and lumefantine (Riomet), quinine/doxycycline, atorvaquine+praguanil
If due to vivax and ovale- rest

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2
Q

Describe presentation, complications and management of typhoid fever

A

IP of 1-2 weeks, constipation, fever, hepatosplemeegaly, neuropsychiatric dc, relative bradycardia, rose spots (faint salmon coloured)

Complications- liver or spleen abscess, intestinal obstruction, endocarditis, bone and joint infection esp if grafts

Diagnosis- bone marrow biopsy lost sensitive

Mx- azithromycin, cipro, cef . If severe give sex
Chronic carriers have increased risk of gallbladder cancer

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3
Q

Dengue investigations

What’s its IP

A

Most specific is IgM but takes over 5 data, use NS1 antigen initially . Also seen pancytopenia
Critical to note IP of -10 days

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4
Q

Cause, intestinal and extraintestinal features of amoebiasis

A

Causes by entamoeba histolytica
Presents with dysentery, colitis, toxic megacolon, colonic lesions
Extracolonic are liver/brain/lung abscess , genitourinary diseaee

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5
Q

Diseases that scrub typhus cause

A

Rickettiosis, spotted fever and Rocky Mountain fever . Transmitted by anthropoid
Presents with sudden shakes, fevers, severe headache and Eschar

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6
Q

Describe meliodosis- cause, features, risks, diagnosis and management

A

Caused by burkholderia paeudomalle by inoculation
Most have underlying chronic infection like DM, outdoor or ATSI

Presents acute cases with upper lobe pneumonia . Subacutely with visceral abscess, OM, soft tissue abscess
Diagnosed on any culture of organism

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7
Q

How does schistosomiasis present and it’s diagnosis and management

A

3 phase- migratory phase which is swimmers itch
Acute phase aka katayama fever - eosinophils, hepatomegaly
Need to demonstrate worms in egg or poo
Mx- praziquantel

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8
Q

Describe leptospirosis it’s features, diagnosis and management

A

Febrile illness assoc with flooding , rats are main reservoirs
Features- conjunctival suffusion, jaundice, ARF, pulmonary haemorrhage, Weil’s disease (jaundice and ARF), leptospirosis pulmonary haemorrhage, mengintis, uveitis
Diagnosis- dark field urine exam, PCR, cultures
Mx- penicillin

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9
Q

Describe measles- infective period, complications and Ix and complications

A

Contagious for 5 days before rash appears
Prodtome of koplik spots, conjunctivitis then red maculopapular rash in face and spreading down
Ix- serum measles Ig, NP swan for culture.
Mx- Vit A, supportive , NEGATIVE pressure room (also for TH, VZV)
Complications- ADEM, SSPE

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10
Q

Hepatitis A and E presentation

A

Self limiting but highly contagious. Faecal oral. HepE can be severe in pregnancy

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11
Q

Main cause of travellers diarrhoea

Causes of acute and chronic travellers diarrhoea

A

ETEC in most cases

In acute watery- rotavirus most common in kids and norovirus most common in adults) Bloody diarrhoea EHEC, shigella, salmonella
Shortest IP for staph aureus then bacillus. Guardia takes 1-2 weeks- mx with metro or inidazole

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12
Q

Prevention advise and complications of Zika virus

A

Complications inc neurological like GBS, micro encephalopathy
Prevention- for male 6 months as per WHO (some say 3) and 2 for women - use contraception

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13
Q

Describe how Lyme diseaee presents , cause, and major cause of death

A

Caused
By borrelia burgdorferi spread by ticks
Classical erythema chronic migrans (bulls eye) rash is itself diagnostic . Mx- doxy

Cause of death many cases heart block

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14
Q

Describe how influenza presents and basis if its medications , distinguish causes of pandemics and epidemics , who is suitable for post exposure prophylaxis and the highest risk groups

A

Main antigens are haemaglutinin which binds to body’s surfaces and neuraminidase which cleaves the virus allowing to be unleashed into host

Mx options are neuraminidase inhibitors (1st kind being oseltamivir, 2nd line zanamivir). M2 inhibitors used for influenza A only- they include amatidine and rimantadine
New drug boloxavir is a selective inhibitor of endonuclease which blocks influenza proliferation by blocking mRNA

Treatment should be within 48 hours or if severe within 4 days

Antigenic shift cause pandemics (due to genetic reassortment- only influenza A causes pandemics) whilst antigenic drift cause epidemics due to point mutations in HA and NA

Highest risk in first two trimesters of pregnancy and obesity

Post exposure prophylaxis only for long term care facilities, HIV/HSCT, pregnant

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15
Q

If TB in patient in flight , who would you screen

A

If flight more than 8 hours and within 2 rows of affected patient

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16
Q

Most common extrapulmonary site of TB

A

TB lymphadenitis

Extra pulmonary TB not infection risk

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17
Q

Investigations for TB

A

Need 3 sputum specimens at least 8 hours apart inc at least one early morning specimen for AFB, and mycobacterium culture
Diagnosis established by isolation of the bacteria from sputum/BAL/tissue/pleural fluid OR Positive PCR (NAA)
Note AFB smear alone inadequate

For latent we do so tuberculin skin test and interferon gamma release assay aka quantiferon. IFNgamma tests for cytokine released by TB sensitised WBCs
Note these only test for TB exposure- can not exclude disease or latency in their absence, and can not diagnose latent vs active in their presence
TSST looks at IFN released by T cells, type 4 hypersensitivity. If BCG vaccinated need to be over to diagnosis, in close contacts over 5mm adequate and in patients with RFs over 10mm needed

It has lower specificity to quantiferon if BCG vaccinated.

If pleural or pericardial TB- need tissue diagnosis

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18
Q

Management of standard TB as well as MDR, XDR
And SE of treatment
Mx of latent TB

A

Std is isoniazid, rifampicin, ethambutol, pyrazinamine for pulmonaryband extrapulmonary TB
For latent- isoniazid OR rifampicin

If isoniazid resistant- 2 months of above and 7 months of above except isoniazid

If MDR- means resistant to at least isoniazid and rifampicin - bedaquiline, quinolone, linezolid for 18-20 months.

Note rifampicin resistance is highly predictive of MDR

If XDR- resistant to rifampicin, quinolone AND an injectible (these are kanamycin, amikacin)

Steroids used for TH meningitis/pericarditis and IRIS
IF TB meningitis- mozifloxacin used instead of ethambutol due to better CSF penetration.

SE of antiTB meds- ethambutol causes optic neuropathy and vision loss and high ALT
Isoniazid causes hepatitis, rash, neuropathy (due to increased excretion of pyridoxine/B6- thus give with it )
Pyrazinamixe- main cause of drug induced hepatitis

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19
Q

Most common NTM in Aus

A

MAC

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20
Q

If screened positive for TB and about to start TNFa for RA what do you do?

A

Give isoniazid for 1 months then start TNFa

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21
Q

Main causes of meningitis in young adults and elderly

A

Young adults- neisseria meninitis (gram neg diplococci) then strep pneumonia (gram pos diplococci)

In elderly- strep pneumonia then neisseria then listeria (gram pos bacilli)
Post head injury- pseudomonas, acinobactet, strep, MRSA

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22
Q

Commonest viral cause of meningitis

A

Enterocirus inc coxsacxhie and polio

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23
Q

CSF in viral vs TB/cryptococcal/fungal

A

Viral shows normal sugars and high protein with high lymphocytes

TB/cryptococcal/TB shows high lymphocytes and low glucose

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24
Q

Empirical management of TB

A

Dex within 30 mins and ceftriaxone

If over 50 yrs OR pregnant OR low immunity OR high alcohol= ceftriaxone AND benpen

If neurosurg or head injury= vanc and cefepime/ceftazidine

If suspecting strep pneumo as cause based on pneumococcal antigen positive, suspected OM/sinusitis, gram pos diplococci in stain= vanc, cef and dex

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25
Describe directed therapy in the case of N meningitis, strep pneumo, listeria, GBS, Hib
N meningitis= benpen If susceptible otherwise ceftriaxone ``` Strep pneumo= cont dex, until MIC returns cont cef and vanc. If MIC <0.125 - benpen . If 0.125-1= cef If over 1= cef AND vanc or moxiflocacin Listeria- benpen GBS- benpen Hib- benpen or cef If penicillin allergy vanc and cipro ```
26
Presentation and management of cryptococcal meningitis
In immunocompromksed due to neoformans in normal gathi Causes cerebral lesions Mx- induction with amphotericin AND flucytosine - then continue flucanazole
27
Cause of esoniphilic meningitis
Angiostrongyloids and gnathostoma- mx corticosteroids and anthelmintic
28
Cause of Mallaret syndrome and its management
It’s reccurrent benign lymphocytic meningitis | Caused by HSV2 . Mx- mostly none. If needed oral valaciclovir
29
Cause of HSV encephalitis and treatment
HSV1 | IV aciclovir
30
When is chemo prophylaxis indicated and what do you give
Indicated if close household contact with meningitis (over 8 hours within 7 days prior to sx)- single dose cipro. If pregnant- IM ceftriaxone Only need to give prophecies for N meningitis (and serious HiB)
31
If a male presents with recurrent meningitis but CH50 normal what’s cause
Properidin deficiency (X linked - properin needed to stabilise C3 concertise in alternate pathway)
32
What’s a unique feature of listeria meningitis
Presents in immunocompromosed and with neuro sx like seizures and strokes and palsies
33
Why do we give dex in meningitis
As strep pneumo causes hearing loss and neurological complications and to reduce mortality
34
List the minor and major dukes criteria for infective endocarditis
Major is 2 positive blood cultures with typical organisms Persistent bacterimia Positive serology for coxielle (Q fever) Positive echo (vegetation, abscess, new regurg) Minor are Predisposing heart disease or IVDU Fever over 38 Vascular or immunological phenomenon Microbiological evidence not fitting major criteria Definitive IE needs 2 major and 1 minor and 5 minor
35
What’s the most common valvular lesion in IE
MVP
36
Empiric Management of native and prosthetic valve IE inc typical organisms for each
For native- suspect staph then strep viridens, coag neg staph, enterococcus, strep Bovis, HACEK MX= benpen, fluclox and gent Prosthetic calicoes- in first 2 months after prosthesis, coag neg organisms most common (skin), and after that same as native bugs MX= Fluclox, vanc, gent
37
Directed therapy for strep viridens, staph aureus, HACEK, Q fever
Strep viridens - benpen and gent (or benpen for 4 weeks) MSSA- fluclox MRSA- vanc +/-fusidix acid Enterococcus- gent and ampicillin Q fever- doxy, rifampicin and hydrochloromine HÁČEK- amoxicillin or benpen
38
Complications post IE
Heart failure secondary to AR/MR leading to cardiogrnic shock, embolisatipn, perianular extension of infection (MONITOR ECG for worsening heart block), splenic abscess and mycotic aneurysm
39
Endocarditis prophylaxis | What’re the high risk procedures and high risk conditions needing prophylaxis
High risk conditions- prosthetic heart valve, prior IE, cardiac transplant with subsequent development of cardiac valvulopathy, congenital heart disease IF it involved an unrepaired cyanosis defect or repaired defect with prosthetic material High risk procedures are dental extraction/implants/existing disease, resp: invasive ENT/resp tract procedure GIT/genitourinary- IF abscess, obstruction or infection
40
Class I indications for surgery in IE
Valve stenosis/regular causing heart failure AR/MR with raised LVEDP Fungal organisms, heart block/abscess, prosthetic valve endocarditis
41
Definition, causes and management of culture negative endocarditis
3 neg BCs after 7 days- due to fastidious organisms like Q fever etc. if post dental- think strep family Mx with combination of vanc and ceftriaxone
42
Diagnostic criteria for ARF
Preceding GAS 2-4 weeks before with 2 major and 2 minor JONES Major= JONES= Migratory polyarthritis, oslers nodes, syndenham chorea, erythema marginatum , subcutaneous nodules Minor criteri= LEAF mnemonic = Long PR, Elevated ESR, Arthralgia, Fever
43
Commonest valvular lesion in RHD
Mitral regurg which progresses to MS | More likely if carditis occurred during ARF
44
Other than rhd, what’s another sequele of ARF
Jaccoud arthropathy- loosening and lengthening of periarticular tendons in hands, feet
45
Management of ARF
Benzathine penicillin
46
Secondary prophylaxis post ARF or RHD
If no RHD- prevent GAS giving benzathine penicillin for min 10 years or until 2- yrs (whichever is longer) If developed moderate RHD- continue till 35 years If severe- 40 yrs If cardiac surg- lifelong Annual yearly dental check for all ARF
47
Describe presentation and management of buruli ulcer
Chronic disease due I mycobacterium ulcerans- affects bone and skin. Starts as painless nodule or diffuse painless swelling Mx- rifampicin and either clarithromycin/moxifloxacin
48
What syndrome does gonorrhoea cause
Fitz Hugh Cuits syndrome
49
Describe the phases of presentation of syphilis , diagnosis and issues with diagnostic tests
Chancre is painless punched out ulcer Secondary syphilis is seen 6-8 weeks post in half, where macupapular rash develops on face/palm/soles, condylomata., fever Latent syphilis- patient asymptomatic but blood tests positive. Most diagnosed here. Tertiary syphilis due to immune destruction with tissue harbouring - inc aortic incompetence due to aneurysm, meningovascular syphilis Diagnosis - nontreponemal(cardiolipin) inc RPR and VDRL, and if positive then treponemal (TPPA). Once a positive treponemal it remains positive for life- thus not used to monitor progress or detect repeat infection. Both tests can be negative early on Non treponemal takes 3 years to disappear after treatment . BUT if the RPR titre rises 4 fold post during this time, it suggests re-infection Causes of false positive nontreponemal tests- APPS, SLE, HIV, TB
50
Types and presentation of vaginitis
Candida - with OCP, steroids, abx. White cheesy discharges and itch . Acidic. Mx with fungal pessary and oral clotrimazole Trichomonas are mostly STI, offensive vaginal discharge - mx metronidazole Bacterial vaginitis is in sexually actively women fishy greenish thin vaginal discharge . Acidic, diagnoses on whiff test and clue cells seek
51
List the roles of each of the 5 key antiherpes drugs and their major SE
1. Acyclovir- to treat HSV and VZV. IV prep goes to CNS (thus first line in HSV encephalitis). SE- Nephrotoxicity 2. Cidofovir- for CMV retinitis in HIV infected patients. SE: neohrotoxicity 3. Ganciclovir- IV ganciclovir (or its oral prodrug valganciclovir) for active CMV 4. vanganciclovir is main agent for CMV prophylaxis in solid organ transplant and stem cell when used Oral valganciclovir is converted to ganciclovir. SE- bone marrow suppression 5. Valacyclovir- treats genital herpes and VZV. Can be used for prophylaxis against RENAL transplant against CMV
52
Describe role of antiviral prophylaxis in the two types of transplants
All solid organ transplants with either donor or receipient CMV pos gets valganciclovir prophylaxis (if CMV for both negative we give valacyclovir for HSV prophylaxis without testing ) If haem stem cell transplant- monitor routinely to see if patient develops CMV PCR positive to avoid marrow suppression
53
List the steps of HIV invasion
Binding/attachment to CD4 receptor Fusion (HIV envelopes CD4) Reverse transcription (HIV’s reverse transcriptase converts its RNA to DNA and enters our CD4 nucleus) Integration - HIVs integrase allows viral DNA to integrate into CD4 Replication Assembly Budding- by HIV proteases
54
WHO stages of HIV
Primary HIV, clinical stage 1 (persistent generalised lymphadenopathy), stage 2 (weight loss of under 10%), stage 3 (weight loss over 10%, oral candidiases, oral hairy leukaemia), stage 4 is HIV wasting syndrome
55
Diagnostic tests for HIV
Antigen p24 year HIV ELISA (combined Ag/Ab test) HIV viral load for monitoring Also do genotype testing baseline for all
56
Main cause of death in treated HIV
Non aids malignancy then CVD
57
What’re the management options in HIV | What’re their key SEs
Start for all NRTI- tenofovir, lamivudine, abacavir, SE- mitochondrial toxicity presenting as peripheral neuropathy, pancreatitis , lipoatrophy (subcut fat wasting), hepatic steatosis, lactic acidosis Tenofovir causes Fanconi syndrome and ATN and low BMD Abacavir causes hypersensitivity with fever/malaise NNRTI- etavirenz SE- vivid dreams, rash, teratogenic Protease inhibitor- ritonavir Integrase inhibitor- raltegravir, dolutegravir Most on 2NRTI and an integrase inhibitor
58
Management of HIV and hepB coinfection
Tenofovir, embricitabine
59
Why do we add low dose ritonovir
To increase ART potency, improves its pharmacokinetics (and reduce pull burden)
60
What’s a critical test before starting abacacir and why
HLA5701 to reduce risk of abacavir hypersensitivity (need to wait for this)
61
Which ART increase CVS risk
Abacavir and protease inhibitors
62
Define treatment success in HIV
Viral load suppression is goal- under 200
63
Define virological failure and virological rebound in HIV
Failure is when HIV RNA is above 200 after 24 weeks on ART | Virological rebound is repeat detection over 200 after suppression
64
What do you do if drug resistance suspected and likely cause
Most due to noncompliance, do genotype testing again
65
Drugs to avoid with ritonavir
Ritonovir is P450 inhibitor- don’t give simvastatin or lovastatin (causes rhabdo) or Midaz (increases sedation) Tenofovir and ritonovir both relatively c/I in TB patients due to interactions with rifampicin
66
Who gets preexposure prophylaxis for HIV and with what
High risk like MSM, transgender, partner HIV pos Tenofovir and embricitabine
67
When and what to give as post exposure prophylaxis
2 drugs if source HIV status unknown but anal sex with MSM or high prevalence country 3 drugs if source HIV positive with unknown viral load or high viral load (if suppressed VL- no treatment!) If needle stick in health care worker- treat whilst awaiting results, or source cannot be identified continue PEP in high risk situations . Start within 1-2 hours, no point after 72 hours
68
How to manage a pregnant woman on ART for HIV
Maternal CD4 over 500 confers lowest risk of transmission If mum is HIV infected- continue ART If pre delivery material VL inadequate or unknown give intrapartum zidovudine. And give baby ART within 6 hours and continue for 4 weeks C section only if VL over 400 at 36 weeks. Breastfeed if good VL
69
What’re the only situations where we don’t start ART in HIV
If cryptococcal meningitis, CNS TOXO, TB meningitis as higher risk of ITIS and in CNS infections no place for inflammatory markers to go
70
When to start ART in TB -HIV patient
If TB AND CD4 over 50- don’t start ART for 4-8 weeks of TB treatment If TB and CD4 under 50- ART at 2-4 weeks
71
When do we suspect MAC and what do we give as prophylaxis in HIV patients
Once CD4 under 50 give azithromycin
72
CNS mass lrsions in AIDS
Toxo, primary CNS lymphoma, PML, TB
73
What’re AIDS defining malignancies
NHL, kaposi’s sarcoma, cervical cancer and cryptococcal infections
74
Describe HIV-associated neurocognitive disorders (HAND)
Prev called HIV encephalitis - marked by subcortical dysfunction (unlike AD) with reduced attention, concentration , depression, memory)
75
Of those hospitalised pneumonia’s commonest cause
Pseudomonas aeroginosa (gram neg bacilli)
76
What’re the extra hepatic manifestations of hep C
Mixed cryoglobuliemia , DM in 70%, NHL, MALT, lichen planus, thyroid dysfunction, Sjogrens
77
Diagnosis for HCV
1st do HCV Ab, if pos do HCV PCR (confirms active infection) and if positive viral load and genotype testing in all
78
What’s quasispecies and implications
Quasispecies is presence of different strains in infected host Causes viral persistence, reduced response to IFN, harder to develop vaccines
79
Main cause of cirrhosis in Aus
Hep C
80
Management of hepatitis C
All Options are 1. NS3/4A- protease inhibitors (high risk of resistance thus not used alone). End in “previr” NS5A end in “avir” NS5B end in “buvir” Combo options are 12 weeks of sofosbuvir and velpatasvir Alternative is 8 weeks of glecaprevir and pibrentasvir (give for 12 weeks if cirrhosis, 8 weeks otherwise)
81
Which drugs are contraindicated with DAA
Amiodarone (causes heart block) and carbamazepine
82
Which drug contraindicated in renal failure
Cannot use sofosbuvir when GFR under 30
83
How to manage hep C in pregnancy y
Ideal to avoid for 6 months before and after Very low perinatal transmission If mum is positive test baby at 15-18 months
84
Management of treatment resistant hep C
These likely have resistance and need triple therapy | Sofosbuvir, velparasvir and voxillaprevir
85
Post exposure prophylaxis for hep C
Usually none! If source is HCV At and Ab positive AND detectable viral load- test patients HCV Ab and viral load immediately, 2 months and 6 months and if positive then treat
86
Phases of hep B disease
Phase 1 is immune tolerance and phase 2 is immune clearance (eAg positive in both, starting to become eAb positive) Phase 3 is immune control and phase 4 is immune escape
87
Interpret cause HBsAg positive, HBeAg neg, HBeAb positive
Inactive carrier
88
Interpret In known HEP B there’s an increase in HBV DNA and ALT
Deactivation
89
Interpret HBsAg neg, HBsAb neg, HBcAb pos
Infection resolved long time ago (most likely) Recovering from acute (time between sAg loss and sAb development) Passive transfer in kids False positive result Occult HBV! (Need viral load done to confirm)
90
Interpret HBsAg neg, HBsAb pos and HBcAb pos
Immune due to infection (recovered)
91
Interpret HBsAg neg, HBsAb pos, HBcAb neg
Immunised
92
Interpret | HBsAg pos, HBsAb neg, HBcAb pos , HBcIgM Ab pos
Active infection (sAg was ages 3-4 months to disappear- if remains chronic infection)
93
Interpret HBsAg pos, HBsAb neg, HBcAb pos, HBcIgM neg
Chronic infection
94
What’s pre-core mutant, core mutants
PreCore mutant production of HBeAg positive but preserves HBcAb Core mutant is reduced HBeAg but unregulated HBcAb Suspect as cause when eAg neg but high viral DNA load and high ALT
95
How does occult HBV present
Absent HBsAg but HBV DNA present | Same risk of cirrhosis as nonoccult infections
96
Post exposure prophylaxis in hep B
If vaccinated and known responder- Nil If known non responder - if source neg then nill, but if source pos or unknown give HB immunoglobulin and follow up for seroconversion If source HBsAg over 10- treat as responder and no treatment
97
If HbsAg pos and about to start ritux what do you do
Give prophylactic lamivudine or entacavir immediately and continue for 6 weeks post cessation of immunisation Some even treat if sAb pos and cAb pos even if sAg neg as can still reactivate
98
WHen do we treat Hep B
If HBV DNA over 2000 AMD ALT high with biopsy showing moderate fibrosis If HBV DNA over 20,000 and ALT twice the ULN Compensated cirrhosis, particulate if HBV DNA over 2000 All decompensated cirrhosis
99
Best time to treat
Immune clearance and escape phases (where highest risk of cirrhosis)
100
Three options for management of Hep B
Nucleoside analogues - entecavir, lamivudine (high resistance) , telbivudine Nucleotide analogues- tenofovir, Cytokines - pegylated infterferon - cannot use if decompensated liver
101
If hep b induced decompesated cirrhosis how to manage
Use combination of nucleoside and nucleotide
102
Management of hep B and C coinfection
Tenofovir and lamivudine
103
Management of Hep B in pregnancy
Avoid even if in treatment If have to use (high viral load esp eAg pos) use tenofovir or lamivudine in 3rd trimester All infants born to mothers of HBsAg pos should get HBIG within 12 hours and be vaccinated
104
WHich of hep B or C cause cancer and which cause transmission after needle stick
Both Hep B
105
Describe Hep D
RNA virus that coinfection with hep B , HBV DNA is low in chronic HDV as HDV suppresses the HBV Compared to coinfection (when both occur at same time) if HDV in setting of chronic HBV more likely liver failure
106
Most aggressive virus causing hepatitis
Hep D
107
Management of Hep D
Pigialated interferon alpha for at at least 48 weeks , most relapse Transplant only cure
108
Main cause of Hep E
Pig meat | Mostly in immunocompromoser
109
Gram positive (purple) bugs can be classified into cocci and bacilli/rods
Cocci- catalase positive are subdivided into coagulase positive (staph aureus) and coag neg staph epi (form biofilm) Catalyse neg form alpha (strep viridens), beta (GAS, group b is strep agalactrae, Strep bovis (causes endocarditis and colon cancer) Entercocci - all intrinsically resistant to cephalosporins- faecalis (penicillin susceptible, not virulent) and fascium (bad, most VRE) Bacilli/rods inc clostridium, bascillus, listeria (intrinsically resistant to cephalosporins), Nocardia (pos modified acid fast)
110
``` Gram negatives (pink) divided into cocci and bacilli/rods List them ```
Cocci- neisseria Bacilli inc enterics (E coli, Klebsiella which are intrinsically resistant to amoxicilllin, proteas, campylobacter , shigella, vibrio cholera), fastidious (haemophilus, legionella, Morexella, HACEK which are mx with ceftriaxone ), environmental (like pseudomonas, burkholderia), ESCAPPM (inc enterobacter which are inducible to 3rd gen cephalosporins)
111
What’re the atypical
Chlamydia, coxiella brunetti, rickettsia, mycoplasma, spirochittes like treponemal
112
Which bugs are intrinsically resistant to cephalosporins | And amoxicillin
Resistant to amoxicillin with klebsiella Listeria and all enterococcus are resistant to cephalosporins
113
What antibiotics are community or nmMRSA sensitive to
Vanc, Bactrim, clindamycin
114
List the 7 groups of drugs under beta lactams
Penicillin (benpen, piptaz etc), cephalosporin, beta lactamase inhivitors, cephalosporin, vanc, teicoplanin, carbopenem, and monobactams (aztreonem)
115
Distinguish between Aug and piptaz in what they cover
Both cover gram hey and entero and anaerobes but piptaz also covers psuedomonas
116
What happens to the coverages of cephalosporins as we progress generations
We lose gram pos and gain gram neg cover
117
How’s teicoplanin different to vanc
Both glycopeptides but teicoplanin also covers VRE-VanB
118
DIfference between meropenem and entapenem
Both carbopenems covering ESBL, but ertapenem is once daily dose but has no pseudomonas cover
119
Which beta lactam doesn’t need renal adjustment
Cephalosporins
120
How is the killing different between beta lactams and aminoglycosies
Beta lactams kill based on time above MIC, aminoglycosides kill on AUC/max conc
121
List the 5 protein synthesis inhibitors and their subclasses
Aminoglycosides (gent, tobramycin, streptomycin), tetracyclines (doxy), macrolide (inc azithromycin, erythromycin, clarithromycin), linocosamide (clindamycin), linezolid
122
List the two DNA synthesis inhibitors and their subclasses
Fluroquinilions (cipro and moxi) and metro
123
Main SEs with fluroquinilones
QT pronlgation, tendon rupture, retinal detachment , strong association with C diff
124
Main indication got amikacin
CPE
125
List the 4 major mechanisms antibiotics use for resistance and list examples
1. Antibiotic inactivation- haemophilus, staph, ESCAPM, ESBL, beta lactamases 2. Alteration of antibiotic target sites - such as PBP sites - strep pneumonia, coag neg strep, MRSA, N meningitis 3. Decreased permeability - seen in enterobactera, psuedomonas to trimethoprim, vanc and sulphonamides 4. Antibiotic efflux- seen with pseudomonas, linezolid
126
What’re the virulence determinants in nmMRSA
Panton Valentine leukocidin (causes WBC destruction and tissue necrosis) - causes skin and soft tissue infections Alpha hemolysin, phenol soluble modulator
127
Distinguish VISA vs VRSA
Both MRSA but VRSA are not susceptible e to vanc (MIC over 16) VISA mainly seen in dialysis patients or those with infected foreign bodies receiving frequent vanc- associated with thickener cell wall . VRSA - associated with van genes from VRE Mx- linezolid (DAPTO DOES NOT WORK) ASSUME when MRSA patients don’t get better on vanc
128
What antibiotic has been a risk for VRE
Metro used in aspiration pneumonia symptoms
129
Which Abx use increase ESBL risk
Fluroquinilones
130
Which bacteria mainly cause ESBL
Klebsiella but also R coli, salmonella etc
131
Two types of CPE and their management
Klebsiella pneumonia CPE- mx ceftazidine-avabactam, colistin-polymixin Metallobetalactamase- aztreonam and colistin
132
Type A vs Type B ADR
TYpe A is non immune | Type B is T cell or IgE mediated hypersensitivity
133
Of the cephalosporins which is safest in penicillin allergic patients
Cefazolin as no common side R chain
134
MAangement of different types of osteomyelitis
If long bone- fluclox If vertebral - ceftriaxone and vanc
135
Management of two types of necrotising fasciitis
Type 1 involves poly microbes whilst T2 is mainly GAS MX- surgical exploration, meropenem, clindamycin and Vanc, and IVIG suspected
136
What’re the 3 phases post transplant and which organisms predominate in each
In preengraftment phase - mostly bacteria and candida In post engraftment it’s CMV, BK, fungi Phase 3 is late phase where we see encapsulated bacteria, CMV, VZV, pneumocystis
137
Commonest infections after solid organ transplant under 1 month, 1-6 months and over 6 months
Under 1 month- associated with surgery like MRSA, candida, catheter , wound In 1-6 months- CMV, HBV, BK, TB After 6 months- pneumonia, aspergillus, CMV HSV, moulds
138
Commonest infections after solid organ transplant under 1 month, 1-6 months and over 6 months
Under 1 month- associated with surgery like MRSA, candida, catheter , wound In 1-6 months- CMV, HBV, BK, TB After 6 months- pneumonia, aspergillus, CMV HSV, moulds
139
WHats the new antiviral agent used for CMV prophylaxis
Letermovir
140
There are 4 major classes of antifungal agents. List examples of them and their mechanism
1. Azoles- inhibit CYP450 and thus ergosterol which interferes with membrane synthesis Inc imidazole group (ketocomazole and clotrimazole) and thiazoles (fluconazole, voriconazole, posaconazole and itraconazole) 2. Polyenes- inc amphotericin B (new prep is liposomal amphotericin B aka ambisome which are also membrane inhibitors 3. Echinocandins inc capsofungin and These inhibit fungal cell wall synthesis 4. Flucystine Inhibit DNA synthesis
141
First line management for invasive aspergillosis, candidemia, prophylaxis and cryptococcal meningitis
For candida echinocandins used If stable can use fluconazole too For cryptococcal- induced with flucystosine and ambisome For invasive aspergillosis- voriconazole For prophylaxis- posaconazole
142
MAnagemrn of MAC
Clarithromycin/azithromycin, rifampicin, ethambutol
143
Gold standard for pertussis diagnosis
Culture from NP is gold standard
144
Gold standard for diagnosis of invasive aspergillosis
Galactomannan (cell wall of aspergillus)- more accurate than BAL BUT often we do both
145
In C diff what does a positive culture but negative toxin mean
Colonisation
146
Management of meliodosis
Ceftazidime , carbopenem
147
What’re the live vaccines
BCG, encephalitis, MMRV, zoster, typhoid, yellow fever
148
WHen do you treat an asymptomatic candida UTI
If neutropenic or urological procedure
149
How do BK and adenovirus present in renal vs haem transplant
Cause tubulointestinal nephritis and urethral stenosis in kidney transplant In bone marrow transplant cases haemorrhagic cystitis CLB can cause myelitis and radical it is as well - and with diarrhoea can mimic GVHD (thus biopsy sometimes needed or CMV PCR)

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