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FRACP 2023 Cram Homicrons Edition > Infectious Diseases > Flashcards

Infectious Diseases Flashcards

1
Q

Antibiotic classes: cell wall synthesis inhibitors

A

Beta lactams- Penicillins, cephalosporins, carbapenems
Peptidoglycan synthesis: vancomycin

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2
Q

Antibiotic classes: protein synthesis inhibitors (50S)

A

Macrolides (clarithromycin/azithromycin/erythromycin)
Chloramphenicol

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3
Q

Antibiotic classes: protein synthesis inhibitors (30S)

A

Tetracyclines (doxycycline/minocycline)
Aminoglycosides (getamicin/tobramycin/amikacin)

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4
Q

Antibiotic classes: DNA gyrase inhibitors

A

Quinolones- ciprofloxacin/norfloxacin

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5
Q

Antibiotic classes: mRNA synthesis inhibitors (DNA directed RNA polymerase)

A

Rifampicin

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6
Q

Antibiotic classes: disrupt DNA integrity

A

Metronidazole

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7
Q

Antibiotic classes: Inhibit folic acid synthesis

A

Trimethoprim/sulfonamides (sulfamethoxazole)

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8
Q

Is mild or severe pulmonary valve stenosis more likely to produce pulmonary valve dilatation

A

Mild- mechanism unknown, severe often treated earlier

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9
Q

Mechanism of toxin mediated disease with staph/strep?

A

Superantigen toxin allows the binding of MHC class II with T cell receptors resulting in polyclonal T cell activation - does NOT require processing by antigen presenting cells

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10
Q

Features of toxin mediated disease

A

Fever
Rash – sunburnt erythematous rash, blanching
Conjunctivitis
Mucous membrane changes
Hypotension
End organ damage

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11
Q

Why add clinda for toxin mediated disease

A

Toxin inhibition – this is immunomodulatory, inhibits toxin production AND host protein synthesis
Eagle effect – when bacteria reach stationary phase (not dividing as much), harder for penicillin to act as no PBP to act on (penicillin kills during dividing stage) 🡪 clindamycin overcomes this effect

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12
Q

Signs that make GAS phayngitis more likely than viral pharyngitis

A

> 4yrs
Tender lymphadenopathy
Pharyngotonsillitis
Scarlett fever rash

Temp >38
No cough/coryza/constitutional symptoms

Tonsilar exudate not helpful in differentiating

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13
Q

M type in strep that causes disease:

A

Types 1-4, 12, 28,tend to cause pharyngitis (type 12 only associated with GN)
Types 5, 49, 57, 60 = associated with skin disease + nephritogenetic

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14
Q

Risk factors for transmission of GBS

A

Primary risk factor is maternal GBS GU or GI colonisation
50% transmission without use of intrapartum antibiotic prophylaxis
Urine culture positive for GBS is a marker for heavy anovaginal colonisation
Delivery < 37/40
PROM
ROM > 18 hours before delivery
Chorioamnionitis
Maternal fever during labour
Early-onset GBS disease in previous pregnancy (routine prophylaxis)

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15
Q

What obstetric risk factors warrant intrapartum ABx (penicillin)?

A

Previous infant with EO-GBS
GBS bacteriuria
Spont onset of labour <37 weeks
ROM >=18 hours
Intrapartum fever >38 degrees
If any of the above are present intrapartum chemoprophylaxis indicated

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16
Q

Mechanism of bacterial toxin ‘tetanospasmin’ in C. Tetani

A

Toxin binds at the NMJ, enters motor nerve by endocytosis , exits motor nerve at spinal cord, enters spinal inhibitory interneurons 🡪 prevents release of glycine and GABA: this blocks normal inhibition of antagonistic muscles 🡪 contraction + unable to relax

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17
Q

Gram negative bacilli

A

H. Influenza
Pertussis
Cholera
E.Coli
Shigella
Legionella

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18
Q

Gram positive rods

A

Clostridium (tetani, botulinum, difficile)
Corynebacterium
Listeria
Nocardia
Bacillus Cereus

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19
Q

Gram positive cocci

A

Staph- MSSA, MRSA, CONS
Strep
- Group A: S. pyogenes, S. Pneumo
- Group B: S.Agalactiae
S. Viridians

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20
Q

Gram negative cocci

A

Moraxella
Neisseria
Yersinia

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21
Q

Gram negative rod

A

Salmonella
Campylobacter
Pseudomonas
Klebsiella

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22
Q

Leading cause of death in children <5?

A

Shigella gastroenteritis
- Fever, dysentry, HUS due to shiga toxin production

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23
Q

Bug associated with pontiac fever

A

Pontiac fever = fever, myalgia headache 🡪 self-limiting disease associated with legionella seroconversion

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24
Q

? ABx therapy in EHEC

A

Avoid ABx in EHEC infections- increases toxin release & HUS

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25
Q

RFs for N.Meningitides infection

A

Immunodeficiency
Complement deficiency (5-10,000x risk) – more likely to have recurrence
Current or future treatment with eculizumab (Mab against C5)
Functional or anatomic Asplenia
HIV
HSCT
Other = military, university students, indigenous

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26
Q

Signs of meningococcal sepsis early/late & complications

A
  • Rapid onset of symptoms (usually)
    Signs of sepsis
  • Fever, leg pain, altered conscious state (late)
  • Neck stiffness, headache, photophobia, bulging fontanelle (late sign>12 hours)
  • Rash: petechiae, purpura (late sign > 12 hours)

Complications:
Diffuse adrenal haemorrhage (Waterhouse-Friderichsen syndrome)
Renal failure, DIC, acidosis

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27
Q

Prophylaxis if exposed to meningococcal disease?

A

Prophylaxis should be given to contacts as soon as possible
Close household, intimate, and childcare contacts within 7 days prior to disease onset
Healthcare workers exposed to respiratory secretions (e.g. intubation without PPE)
,
Antibiotics
Infants < 1 month = rifampicin Q12H for 4 doses
Children > 1 month = rifampicin Q12H for 4 doses, OR ciprofloxacin single dose
Adults = ciprofloxacin single dose
Pregnant or contraindication to rifampicin = ceftriaxone IM single dose

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28
Q

RFs for non-typhoid salmonella infection

A

Risk factors
Neonates
HIV/AIDS or other immunodeficiency – especially IL-12
Malignancies
Haemolytic anaemia – including sickle cell disease, malaria
IBD, collagen vascular disease
Use of antacids

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29
Q

Extraintestinal manifestations of non-typhoid salmonella

A

Extraintestinal infections = skeletal system, meninges, intravascular sites
Associations with underlying illness
Reactive arthritis (HLA B27 +ve individuals)
Osteomyelitis (sickle cell disease)
Overwhelming bacteria ad multi-organ failure (HIV)
Toxic megacolon (IBD)

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30
Q

What bacterial infection is this rash associated with?
Features & Rx

A

Salmonella Typhae (rose spot rash)

Week 1 = fever (100%), abdominal pain, constipation OR diarrhoea (60%), headache, dry cough (30%), malaise, myalgia, epistaxis (25%), delirium

Week 2 = fever plateaus (39-50), symptoms ,progress, abdominal distension, delirium/ neuropsychiatric

Week 3 = symptoms progress, complications (intestinal perforation, intestinal hemorrhages, sepsis, myocarditis, abscesses)

Rx: azithromycin, ciprofloxacin

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31
Q

Complications of campylobacter infection?

A

Complications
Strong association with Guillian Barre Syndrome
?molecular mimicry between C. jejuni and GBS + Miller Fisher variant
Estimated rate of 1/3000 C. jejuni infections, stool culture +ve in > 25% of cases
Reactive arthritis
Typically migratory involving large joints and resolve without sequelae
More likely in HLA B27 +ve patients
5-40 days after onset of diarrhoea
Erythema nodosum
Irritable bowel syndrome

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32
Q

What bacterial infection is this caused by?

A

Ecthyma gangrenosum- Pseudomonas

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33
Q

What bacteria causes this skin lesion

A

Burkholderia Psuedomallei (meliodosis)

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34
Q

Dx on this CXR

A

PJP pneumonia
- Bilateral, symmetric, reticular (interstitial), or granular opacities
- Initially perihilar 🡪 peripherally (apical areas spared until last)

Complications = pneumatocoeles, pneumothorax (may be bilateral)

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35
Q

Dx on this CXR

A

ABPA
Hypersensitivity disease from immunologic sensitization to aspergillus antigens:
Starts with non-invasive colonization of bronchial airways
Persistent inflammation + hypersensitivity response
Immunologic responses lead to wheezing, infiltrates, bronchiectasis and fibrosis

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36
Q

What is Ponchet’s disease

A

MTB osteitis
Well defined sclerotic margins on X-ray
Thick , inflammatory synovium 🡪 invades articular surface
More common in school age group
Spinal TB 🡪 vertebral body destruction, deformity

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37
Q

Side effects of TB treatment

A

Rifampicin
Inducer of liver enzymes
Orange secretions
Hepatitis
Influenza-like reaction
Thrombocytopaenia
Pruritis

Isoniazid
Hepatitis – particularly if >35 years, comorbid alcohol intake – check LFTs prior to starting treatment
Asymptomatic mild elevation of serum liver enzymes < 5 x normal 🡪 do not stop treatment
Immediate hypersensitivity reaction
Peripheral neuritis – prevented by B6, increased risk with poor nutrition
Haematological problems

Pyrazinamide
Hepatotoxic
Arthralgia
GIT upset
Pruritis
Rash

Ethambutol
Optic neuritis – particularly colour + acuity
GIT disturbance
Hypersensitivity

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38
Q

Management of baby with TB pos mother?

A
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39
Q

Complications of mycoplasma infection

A

Complications
Skin lesions = SJS, erythema multiform
Neurologic complications = meningoencephalitis, transverse myelitis, aseptic meningitis, cerebellar ataxia, Bell palsy, deafness
Haematologic complications = haemolysis (DAT +ve ) , cold antibody mediated disease

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40
Q

Phases of leptospirosis?

A
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41
Q

What parasite causes this infection?

A

Leishmaniasis, common in refugee populations, various Rx options, no good evidence

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41
Q

What parasite causes this infection?

A

Leishmaniasis, common in refugee populations, various Rx options, no good evidence

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42
Q

Summarise causes of acute/chronic schistosomiasis & symptoms

A

Asymptomatic
Pruritic rash – swimmer’s itch

Acute schistosomiasis = Katayama syndrome
Serum-sickness like syndrome manifested by acute onset of fever, cough, chills sweating, abdominal pain, lymphadenopathy, hepatosplenomegaly and eosinophilia

Chronic schistosomiasis

Genitourinary disease
Cause = S. haematobium
Can result in infertility, increases risk of HIV infection
Microscopic or macroscopic haematuria

Gastrointestinal disease
Cause = S. mansoni, S japnoicum, S intercalatum, S mekongi
Chronic or intermittent abdominal pain, poor appetite, diarrhoea
Chronic ulceration resulting in bleeding and IDA

Hepatosplenic
Cause = S. mansoni, S japnoicum, S intercalatum, S mekongi
Non-fibrotic granulomatous inflammation around trapped eggs in the presinusoidal periportal spaces of the liver
Can develop into periportal fibrosis

Pulmonary
Cause = S. mansoni, S japoncium, S haemtobium
Eggs lodge in pulmonary arterioles and produce pulmonary endarteritis 🡪 pulmonary hypertension and cor pulmonale

CNS disease = neuroschistosomiasis
Can involve spinal cord or brain
May result in single or multiple intracerebral lesions

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42
Q

Summarise causes of acute/chronic schistosomiasis & symptoms

A

Asymptomatic
Pruritic rash – swimmer’s itch

Acute schistosomiasis = Katayama syndrome
Serum-sickness like syndrome manifested by acute onset of fever, cough, chills sweating, abdominal pain, lymphadenopathy, hepatosplenomegaly and eosinophilia

Chronic schistosomiasis

Genitourinary disease
Cause = S. haematobium
Can result in infertility, increases risk of HIV infection
Microscopic or macroscopic haematuria

Gastrointestinal disease
Cause = S. mansoni, S japnoicum, S intercalatum, S mekongi
Chronic or intermittent abdominal pain, poor appetite, diarrhoea
Chronic ulceration resulting in bleeding and IDA

Hepatosplenic
Cause = S. mansoni, S japnoicum, S intercalatum, S mekongi
Non-fibrotic granulomatous inflammation around trapped eggs in the presinusoidal periportal spaces of the liver
Can develop into periportal fibrosis

Pulmonary
Cause = S. mansoni, S japoncium, S haemtobium
Eggs lodge in pulmonary arterioles and produce pulmonary endarteritis 🡪 pulmonary hypertension and cor pulmonale

CNS disease = neuroschistosomiasis
Can involve spinal cord or brain
May result in single or multiple intracerebral lesions

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43
Q

Main concerns with congenital symptomatic cCMV?

A

Main concerns of symptomatic cCMV infection 30,31
– Early mortality (first 3 months) rate between rate 5-10%
– Neurological sequelae of microcephaly (35–50%), seizures (10%), chorioretinitis (10–20%), developmental delay (70%)
– Sensorineural hearing loss (SNHL, 25–50%), with progression expected in about half (mainly in the first 2 years of life)

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44
Q

Treatment for cCMV

A

If symptomatic or isolated HL on NBHS.

Valgancyclovir 6mo, start at <30d.
Monitor LFTs & neutrophil count

Follow up:
Hearing until 6yrs
Paeds review 3-6mo until 2, then until 6
Opthal: annually until 6

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45
Q

Congenital infection likely to cause these CrUSS findings?

A

CMV

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46
Q

Risk of infection/congenital rubella syndrome with primary vs reactivation?

A

1-12wks: infection80%, congenital defects 85%
13-16wks: infection 55%, congenital defects 35%
17-30wks: infection 35%, defects rare
31-36wks: infection 60-100%, defects rare

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47
Q

Risk of infection/congenital toxoplasmosis with primary vs reactivation?

A

First Tri: low risk infection, high risk of severe damage if infected 34-85%

Second tri: intermediate risk infection/severity

Third tri: high risk infection, low risk damage

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48
Q

Spectrum of symptoms in congenital syphillis

A

Transplacental spread
Abortion
Fetal death
Hydrops fetalis
Preterm labour
IUGR
Congenital syphilis
Early features
Wide spectrum, including fulminant sepsis
Maculopapular rash on back, legs, palms, soles
Bullous/ desquamation
Rhinitis snuffles 1/52-3/12
Lymphadenopathy + HSM
Osteitis
Jaundice, pancytopenia, edema
Untreated, late features
Facial features = frontal bossing, saddle nose, short maxilla, protruberant mandible
Ophthal = interstitial keratitis, chorioretinitis, secondary glaucoma, corneal scarring, optic atrophy
Ears = SNHL
Oropharynx = Hutchinson teeth, mulberry molars, perforation of hard palate
Cutaneous = rhagades, gummas
CNS = ID, arrested hydrocephalus, seizures, paresis
Skeletal = saber shins (anterior bowing), Higoumenakis sign (enlargement of sternoclavicular portion of clavicle), Clutton joints (painless arthritis), scaphoid scapula

49
Q

What TORCH infection causes this skin lesion?

A

Foetal Varicella Syndrome
Risk of transmission <0.55% <12wks, 1.4% 12-28%, >28wks no cases reported

50
Q

Diagnosis on CSF stain (India Ink)

A

Cryptococcus- halo sign on india ink as dye unable to penetrate capsule

51
Q

Differentiate foetal varicella syndrome (congenital) or neonatal varicella

A

Neonatal varicella
Mortality is very high
Risk is highest for mothers who develop varicella from five days prior 🡪 2 days afterward
Infants generally symptomatic by first week – second week of life
Treatment = ZIG 🡪 50% will still develop varicella but it is usually mild
Then treated with acyclovir 10 mg/kg tds if lesions develop

Congenital varicella syndrome
0.4% of infants < 13 weeks of gestation
2% of infants 13-20 weeks of gestation
Features
Cicatricial skin scarring
Limb hypoplasia
Neurologic features: microcepahly, cortical atrophy, seizures, mental retardation ,
Eyes – chroioretinitis, micropthalmai, cataracts
Renal – hydroureter + hydronephrosis
ANS abnormalities
Maternal treatment with Varicella IgG / Aciclovir – benefit unknown

52
Q

What is the monospot test?
What does it test for, what are false positives and false negatives?

A

MONOSPOT – tests for Heterophile antibody, usually +ve after 2-9 weeks after infection

Heterophile antibodies = agglutinate cells from species different from those in the source serum
Heterophile – reacts with proteins across species line

False +ve = CMV, hepatitis, influenza, malaria, rubella, lymphoma, pancreatic tumour, RA, SLE< serum sickness etc

False –ve = 25% in first week of illness
High rate of false negative in very young ages

53
Q

Indications for Pavlivizumab?

A

Palivizumab = monoclonal antibody
Given monthly during peak seasons
For high risk children
CLD
Congenital heart disease if < 2
Extremely premature < 28 weeks
Given IM monthly for five doses
Discontinue if admitted with RSV infection

54
Q

Indications for Pavlivizumab?

A

Palivizumab = monoclonal antibody
Given monthly during peak seasons
For high risk children
CLD
Congenital heart disease if < 2
Extremely premature < 28 weeks
Given IM monthly for five doses
Discontinue if admitted with RSV infection

55
Q

What bugs constitute ESCAPPM? What is their method of resistance

A

Enterobacter, Serratia, Citrobacter, Acinetobacter/ Aeromonas, Proteus, Providentia, Morganela
Hydrolyse penicillins, cephalosporins, AND resistant to beta lactamase inhibitors (enzyme = AmpC beta-lactamase)
Usually chromsomally encoded
Are also inducible 🡪 may be initially sensitive on testing
Usually require treatment with carbapenems / cefepime / SHORT course of beta lactam

56
Q

ESBL mechanism of action

A

Extended spectrum beta lactamase
- found exclusively in Gram-negative organisms: primarily in Klebsiella pneumoniae, Klebsiella oxytoca, and Escherichia coli. also in Acinetobacter, Burkholderia, Citrobacter, Enterobacter, Morganella, Proteus, Pseudomonas, Salmonella, Serratia, and Shigella spp.
arose by amino acid substitutions that allowed narrower spectrum enzymes to attack the new oxyimino-beta-lactams

57
Q

Thick vs thin smear malaria testing?

A

Thin smear: small amount of blood, cells remain intact- examine type of parasite/density

Thick smear: screening test to see if parasite present (can also estimate parasite density)

RDT- looks for histadine rich protein 2, plasmodium LDH & aldolase- can identify parasite but not density

58
Q

Child with itchy (non tender) purulent/vesicular otitis externa- pathogen?

A

Varicella (painless)

Bacterial- 90% gram positive
- S.Epidermis, S.Aureus
- P.Aeruginosa also common

Sx: +++ear pain, itch, discharge +/- conductive hearing loss

59
Q

Natural history of HIV

A

Early (seroconversion): fever/rash/lymphadenopathy
= First marker to appear gp41 and p24 antibodies

Latent: (seroconversion - 6mo): asymptomatic, HIV infiltrates lymphoid tissue, high rates of T cell destruction/turnover
= viral load (HIV RNA count) most important predictor in this phase

Late phase (>6mo): IgG positive from 6mo onwards- persists for life, IgM insensitive marker
= CD4 counts best predictor of disease

AIDS- once has ‘aids defining illness’

60
Q

What are AIDS defining illnesses?

A
  • Invasive candida/cryptococcus
  • CMV/HSV/toxoplasmosis
  • PJP (50% of illnesses diagnosed in first 1yr of life)
  • MAC
  • Cervical cancer, lymphoma, Kaposi sarcoma

CD4+ count <15%

61
Q

Systemic features of Yersinia gastroenteritis?

A

Acute febrile gastro +
- Pseudoappendicitis (lymphadenopathy)
- Erythema nodosum (30%)
- Reactive arthritis (30%)- large weight bearing joints

(more prevalent in HLAB27 tissue type)

62
Q

Clostridium Difficile treatment?

A

GP rod
Antibiotic induced diarrhoea (fluoroquinolones, cephalasporins, clindamycin)- during/months after ABx

Self limiting watery diarrhoea to pseudomembranous colitis

Dx: C.Diff toxin on stool/histo

Mild: PO/IV metronidazole
Severe: PO Vancomycin

63
Q

Antibiotic treatment for Listeria

A

GP rod

Penicillin
Ampicillin
Aminoglycoside

(think pEOS cover)

64
Q

Diptheria treatment?

A

GP rod

Acute Mx:
Antitoxin
Antibiotics : erythromycin / penicillin
Prophylaxis for contacts with erythromycin / IM benpen

65
Q

Tetanus acute treatment

A

Clean wound, excise devitalised tissue

Penicillin

Tetanus immunoglobulin AND immunization booster

Immunoglobulin neutralises toxin, but needs to be given prior to toxin reaching the spinal cord
Can give IVIG if tetanus immunoglobulin not available, but dosages unknown

Exposure to toxin alone does not induce immunity 🡪 need to give vaccine

Muscle relaxants

66
Q

Treatment of pt w/ tetanus prone wound

A

If >=3 doses of vaccine and <5 years since last dose – do not require any further treatment

If >=3 doses of vaccine and >5-10 years since last dose – booster vaccine

If <3 doses or uncertain – TIG + booster (unless minor wound)

67
Q

Difference between prevenar 13/23?

A

Prevenar 13 = pneumococcal CONJUGATE vaccine
Provides T cell immunity, reduces nasopharyngeal colonization

Reduce nasopharyngeal carriage of vaccine serotypes by up to 60-70%

Pneumovax 23 = pneumococcal POLYSACCHARIDE vaccine
Contains more capsular types of strep pneumoniae

Induces limited immune response in children < 2 years of age + immunosuppressed patients

68
Q

Abx for strep pneumoniae?

A

Penicillin
Third generation cephalasporin
Vancomycin

Clindamycin
Clarithromycin/erythromycin

Bactrim

Linezolid

69
Q

Mode of resistance in strep pneumo

A

B lactams- altered PBP, can be overcome by ↑ dose
Macrolides - altered RNA binding (ermB), expels drug (mefA)
Fluoroquinosoles- spontaneous/altered binding

70
Q

Most common organisms causing primary peritonitis, ABx Rx?

A

Strep pneumoniae 60-77%
Other streptococcus 15%
Gram negative rods (E.Coli) 10-25%
Haemophilus influenzae
Enterococcus spp.

Rx:
Ampicillin or Amoxicillin
Gentamicin
Metronidazole
~14d

71
Q

What virus enters the cell via integrins?

A

HSV

72
Q

What virus enters the cell via sialylated glycans (SA)?

A

Enterovirus

73
Q

What virus enters the cell via cell adhesion molecules on CD4?

A

HIV

74
Q

What virus enters the cell via ACE2?

A

COVID

75
Q

Virulence proteins in rotavirus?

A

NSP1 protein = interferon antagonist
NSP4 protein =enterotoxin/viral replication.

76
Q

Risk of intussuception post rotavirus vaccination?

A

1 in 20-100,000

77
Q

TORCH infection MOST LIKELY to have hearing loss?

A

Rubella 90%
CMV 35% (but more common)

78
Q

TORCH infection MOST LIKELY to have retinopathy?

A

Toxoplasmosis

79
Q

TORCH infection MOST LIKELY to have hydrocephalus?

A

Toxoplasmosis

80
Q

TORCH infection MOST LIKELY to have microcephaly?

A

CMV
Zika virus

81
Q

TORCH infection MOST LIKELY to have intracranial calcifications?

A

Toxoplasmosis
Zika virus
CMV

82
Q

TORCH infection MOST LIKELY to have hepatosplenomegaly?

A

Most
- Rubella
- CMV
- Syphillis

  • Toxoplasmosis less common
83
Q

TORCH infection MOST LIKELY to have cardiac defects?

A

Rubella

84
Q

Congenital Rubella Sx

A

Cardiac defects
SNHL/deafness
HSM
Cataracts

+/- retinopathy, microcephaly, calcifications
(First tri)

85
Q

CMV Sx

A

Microcephaly, CNS calcifications (periventricular)
Immediate or delayed SNHL- 35%

86
Q

Congenital Herpes Sx

A

Multi-system failure
Rash
Neonatal seizures

Transmission greatest intrapartum if active genital lesions

87
Q

Congenital parvovirus Sx

A

Hydrops, death
(First tri)

88
Q

Congenital syphillis infection

A

Chorioretinitis
Neuro symptoms
Osteochondtritis/ abnormal epiphyses
Maculopapular rash and abnormal nails
HSM

89
Q

Congenital VZV Sx

A

Skin & muscle defects
IUGR
Limb abnormalities/arthrogryposis

90
Q

Congenital Zika Sx

A

Microcephaly, calcifications, ID
(First tri)

91
Q

Management of pregnancy if previous HSV (2>1)

A

Consider use of suppressive antiviral therapy from 36 weeks

Careful speculum examination in labour

No active lesions 🡪 vaginal delivery
Active lesions 🡪 management of newborn as below

92
Q

First time HSV genital infection in labour?

A

If early- prophylactic antivirals from 36wks, spec for active lesions

Late- same as above but consider LUSCs

93
Q

Neonatal herpes Sx

A
  1. Skin/eyes/mouth:
    - Vesicular lesions or atypically pustular or bullous lesions
    - Corneal ulceration, keratitis
    Mouth:
    - Ulceration, palate, tongue
  2. CNS/disseminated
    - Seizures
    - Unexplained sepsis
    - Low platelets, elevated LFTs, DIC
    - Respiratory distress
    (disseminated earlier, CNS later)

Septic workup
IV aciclovir- 2wks SEM, 3 wks disseminated

94
Q

Examples of RNA viruses

A

Positive-sense single-stranded RNA virus:
Enveloped:
- Dengue
- COVID
- MERS/SARS
- Rhinovirus
- Aids
- Rubella
- Hep C
Non enveloped: HepA, cold, polio

Negative sense single strandres RNA
Enveloped: Ebola/rabies, flu, measles, mumps

95
Q

Examples of DNA viruses

A

dsDNA
Enveloped: HSV, EBV, VZVm hep B
Non-enveloped: adenovirus, HPV

ssDNA

96
Q

Dx:

A

Cutaneous larva migrans

97
Q

Dx?

A

Loiasis

98
Q

Sx/Mx Strongyloidiasis

A

Strongyloidiasis
- Autoinfective nematode (can enter via any organ)
- Larva currens (serpiginous lesions that move rapidly) on trunk and buttocks
- Eosinophilia 10-70%

  • Bronchopneumonia, abscesses
  • Diarrhoea/PLE
  • Pericardial effusion
  • Hepatomegaly/abscess
  • Gram neg sepsis from enteric bacteria

IgG only positive in chronic phase
Larvae in stool higher in acute

Rx: ivermectin (prophylaxis) or albendazole

99
Q

Most common bacterial cause of IE?

A

Strep viridians >90%
- Enterococcus & staph aureus

Increase in HACEK organisms – Haemophilus, Actinobacillus, Cardiobacterium, Eikenella and Kingella

100
Q

Stages of trachoma?

A
101
Q

Types of malaria and findings on thick/thin smear

A

Transmitted by anopheles mosquito
Falciparum
- Most common
- Most likely to cause severe/CNS disease
- Ring trophozoites on thick blood smear

Ovale
- Latent, can reactivate and cause infection
- Causes splenomegaly
- 48h fevers, hypnozoite

Vivax
- Can hide in liver & relapse up to 5yrs after
- 48h fevers, hypnozoite
- Mainly Asia

Malariae
- Nephrotic syndrome
- 72h fevers

102
Q

Treatment of malaria

A

Falciparum
1. AL (coartem/riamet)
2. AP (malarone)
3. Quinine + clinda

Vivax, ovale, malariae, knowlesi
1. Chloroquine/HCQ/AL
2. Primaquine (hypnozoites)

Severe: IV artesunate > IV quinidine > IV AL

103
Q

Prevention of malaria

A

Avoidance
- Nets, sprays, clothing

Meds
- AP (malarone)
- Mefloquine
- Doxycycline >8yrs

Note – sickle erythrocytes, HbF and ovalocytes are resistant to plasmodium falciparum

104
Q

Rates of vertical HIV transmission & ways to prevent.

A

Primary route of paediatric infection
- 30-40% intrauterine
- 60-70% intrapartum
- post partum (breast feeding) = least common

With prophylaxis <2% infection rate
- Mat ART
- Elective C/S
- Formula fed (if developed country)
- PEP if at risk

50% mortality rate if untreated

105
Q

What is the most common AIDS defining illness?

A

PJP- 50% of cases
- Low grade fever/^RR
- Bilat perihilar interstital infiltrates on CXR

106
Q

Prophylaxis for HIV exposed neonate?

A

Zidovudine
- reverse transcriptase inhibitor
+ 2x other agents

107
Q

Medications used to treat HIV

A
  1. Reverse transcriptase inhibitors
    - Zudovudine
    - Lactic acidosis, hepatic steatosis, lipodystrophy
  2. Protease inhibitors
    - Ritonavir, tipranivir
    - High BSL/TG, lipdystrophy
  3. Fusion/CCR4 blockers
    - Entuvirtide (blocks GP1)
    - Maraviroc (blocks CCR4)
  4. Integrase i nhibitors
    - Raltegavir- GI upset/LFT derangement
108
Q

Vector for schistosomiasis

A

Infection with blood fluke

Carried by aquatic snails
Haematuria
Increased risk of bladder Ca/anaemia

Rx: praziquantel

109
Q

Vector for Onchocerciasis

A

Black flies
- endemic in Sub-Saharan Africa

Rx: Ivermectin

110
Q

Hep B serology:
HbsAg +
Anti HbS & HbC -

A

1) acute early infection
2) transient positivity post vaccine (18-52d)

111
Q

Hep B serology:
HbsAg -
Anti HbS +
HbC +
- IgM -

A

Previous infection

112
Q

Hep B serology:
HbsAg +
Anti HbS -
HbC +
- IgM -

A

Chronic HB+BV

112
Q

Hep B serology:
HbsAg -
Anti HbS +
HbC -
- IgM -

A

Previous immunisation

113
Q

Hep B serology:
HbsAg +
Anti HbS -
HbC +
-IgM +

A

Acute HBV

114
Q

Hep B serology:
HbsAg -
Anti HbS +/-
HbC +
-IgM +

A

Acute HBV which is resolving

115
Q

Hep B serology:
HbsAg -
Anti HbS +/-
HbC +
-IgM +

A

Acute HBV which is resolving

116
Q

Urease positive organisms
(PUNCH)

A

Proteus
Ureaplasma
Nocardia
Cryptococcus (fungus)
H.Pylori

117
Q

Encapsulated organisms
(SHINE SKiS)

A

Strep Pneumoniae
H.Influenzae
Neisseria Meningitides
E.Coli
Salmonella
Klebsiella
GBS

118
Q

Catalase positive
(CATS BeeN PLACES)

A

Candida (fungus)
Aspergillus (fungus)
T

119
Q

Catalase positive
(CATS BeeN PLACES)

A

Cat(alase)

B.Cepacia
Nocardia

Pseudomonas
Listeria
Aspergillus (fungus)
Candida (fungus)
E.Coli
Staph/Serratia

120
Q

Risk factors for HSV encephalitis?

A

Risk factors for HSV encephalitis:
* Presence of vesicles and/or seizures in
infant
* Mucous membrane ulcers in infant
* Hypothermia in infant
* Maternal history of genital HSV lesions
(absence of this history is not reassuring)
* Leukopenia or thrombocytopaenia in infant
* Deranged liver function tests (consider
checking for liver function tests if HSV is
suspected) and/ or coagulopathy
* CSF pleocytosis with negative gram stain
in infant

121
Q

Pseudomonas resistance mechanism

A

Altered porin expression is a mechanism for bacteria to prevent antibiotics from entering the cell.

It has been noted that Pseudomonas aeruginosa develops mutations in the OprD gene during therapy

FRACP 2023 Cram Homicrons Edition (29 decks)

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