ID Flashcards

1
Q

Presentation Dengue fever

A
  1. Initial acute phase: Fever, severe headache (retro-orbital pain), malaise, severe joint and muscle pain, N&V
    Rash several days after fever onset
  2. Secondary severe phase (3-7 days after sx onset; ~ when fever starts to subside): haemmhoragic shock
    - > skin: petechiae, purpura, bruising
    - > bleeding from gums, nose, eyes
    - > intestinal and other internal bleeding
    - > thrombocytopaenia
    - > late eosinophilia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pertussis

A

‘whooping cough’
bacteria - bordatella pertussis

After 1 to 2 weeks and as the disease progresses, the traditional symptoms of pertussis may appear and include: Paroxysms (fits) of many, rapid coughs followed by a high-pitched “whoop” sound. Vomiting (throwing up) during or after coughing fits. Exhaustion (very tired) after coughing fits

  • often whooping cough occurs in 6mo-5 year olds. may be absent in older or younger people
  • may be dehydrated with conjunctival or facial petechiae from intense coughing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Live vaccines

A

Rotavirus
MMR
Varicella
IN influenza
BCG
Travel - yellow fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Immunology of vaccination

A

mimic response to infection without severe disease
Vaccine injection -> attracts dendritic cells, monocytes, neutrophils -> activation of those cells following Ag presentation -> migration of those cells to draining lymph node -> in LN you have activation of T and B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How do toxin-mediated vaccines work

A

High yield strain of C tetani is cultured to produce commercial toxoid which is harvested, purified and detoxified -> IgG levels correlate with protection

ex: tetanus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Conjugate vaccines - Mechanism
Benefits
Ex

A
  • A conjugate vaccine is a type of subunit vaccine which combines a weak antigen with a strong antigen as a carrier so that the immune system has a stronger response to the weak antigen.
  • Usefully for vaccines against bacteria which are protected by polysaccharide capsule
  • (The three most common causes of bacterial meningitis –
    • Neisseria meningitidis (the meningococcus A,C,W,Y)
    • Streptococcus pneumoniae
    • Haemophilus influenzae type b (Hib)

Benefits

  • T cell dependent
  • high serum levels IgG
  • produces long-lasting immune memory
  • Decreases carriage which produces broader herd immunity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Generation of B cell memory responses

A

Generated in response to T-dependent Ag in the germinal centres (spleen/lymph nodes) in parallel to plasma cells.

At their exit, they differentiate into memory B cells that transiently migrate through blood towards extrafollicular areas of spelln and nodes

Persist there as resting cells until re-exposed to their specific Ag

On secondary exposure, memory B cells readily proliferate and differentiate into plasma cells

-> secrete large amt of high affinity Ab that can be detected in serum a few days after boosting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Vaccine side-effects

inactivated vs activated

A

Inactivated

  • SE within 72 hours
  • Fever, local reaction

Live attenuated

  • Delated side effect
  • MMR: 5-14d (peak d10), fever, febrile convulsion (incr risk), rash
  • Varicella, rotavirus - fever, vomiting
  • Rotavirus -> intussusception (up to 7 days following first vaccine)

Anaphylaxis very rare (1 case per million vaccinated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Immune compromised individuals - how does this affect the vaccination schedule?

A

Live vaccines are generally CI as they can cause vaccine-related disease due to replication of the vaccine virus/bacteria

Includes BCG, oral typhoid, yellow fever, MMR, VZV
Rotavirus can be given except in case of intussusception

Household contacts should be vaccinated, incl with live vaccines (MMR, rotavirus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Tetanus Vaccination schedule

A

Vaccination
o Immunisations at 2,4,6 months then boosters at 18 months, 4 years and 10-15years
o Need 2x boosters to provide lasting immunity until middle age
o 10 year boosters no longer given but provides indication of how long immunity last (eg if treating someone > 10 years post booster, repeat booster)
o DTPa = childhood vaccine, increased doses of diphtheria and pertussis, dTpa = adult vaccine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Passive vs active immunisation

A
  • Passive immunisation = acquisition of PRE-FORMED antibodies
    • Natural: Ab transfer from mo to baby across placenta
    • Artificial: for example give HSV, hep B or varicella Ig to a pt after tehy are exposed to try to stop them developing the disease
  • Active immunisation = administration of an antigen to stimulate the body’s OWN immune response
    • via Infection
    • or via immunisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Types of vaccines
- examples

Effect on immunity

A

Whole organism vaccines

i. Attenuated (live)
ii. Inactivated (killed) - old pertussis

Subunit
(acellular pertussis, 13vPCV, HiB, HepB)

Recombinant protein (IPV, Hep A+B, Influenza)

Polysaccharide (pneum23V, men polysaccharide)

Conjugated

  • Rubella
  • HIB
  • pneumococcal 13
  • Men C

Toxoids (Diptheria, tetanus)

Viral vector (covid-19)

Live vaccines/replicative

  • self replicating
  • relatively long lasting immunity, mimics natural infx

Inactive/Nonreplicative

  • preformed Ag mass
  • relatively short lasting immunity, may require boosters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Vaccine adjuvant . what is it?

A

Traditionally based on whole bacteria (CFA) or bacterial cell walls (IFA)

  • Gives danger signal to immune system – stimulates TLR and PRR that turn on the immune response
  • Amplifies immune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What extra vaccines do these patients groups need to obtain?

  • Indigenous
  • Umnderlying medical conditions
A

Indigenous - Hep A (12mo), Tb and influenza >6mo

Underling medical conditions - pneumococcal (13v at 6mo, 23v at 4yo), influenza >6mo

Preterm- pneumococcal (13v at 6mo, 23v at 4yo), influenza >6mo, Hep B at 12 mo

*Note- give vaccines at chronological age (without correcting for prematurity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Largest R out of vaccinatable infectious diseases?

A

Measles R12-18
Pertussis R12-17

Note

  • Covid

–> alpha R 2.5

–> delta 5-7

–> omicron ?10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

HPV

  • disease
  • vaccine
  • vaccine schedule
A

Disease - risk of cervical cancer (high risk is 16, 18)
- most cleared within 12-24 mo but 10% persist

Vaccine is recombinant (virus-like particles) . Does NOT contain viral DNA and cannot cause infection.

3x doses at age 12-13yrs

  • ok if immunonocompromgsed
  • not if pregnant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which vaccine is CI in HIV pts regardless of CD4+ count?

A

BCG vaccine
Typhoid + polio oral live attenuated (use inactivated instead)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Varicella post exposure options

A

Active immunisation (Varicella vaccine) - for healthy hosts within 3-5 days of exposure if haven’t received the full (2) -dose series.

Passive immunisation (Varicella-specific Ab) 
- in immunocompromised if haven't received the full dose series 
OR if bone marrow transplant within 24 months or if requiring immunosuppression or having chronic GVHD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Effect of bone marrow transplant on immunity

A
  • Lose immunity to pathogens which they were previously immunised
  • Require immunisation against pneumococcus, HiB, tetanus etc
  • Avoid live vaccines for 24mo following HSCT (use inactive vaccines or passive immunisation when possible)
  • Live vaccines can be given >24mo following HSCT if there is no immunosuppression or GVHD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Indication for hep A vaccination

A

Travel to endemic areas in children >1yo

Almost universal seroconversion within 4 weeks of vaccination (repeat testing for seroconversion not indicated)

Single dose provides immunity for at least 1 year

Second dose recommended to prolong duration of protection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Least effective vaccine at providing long-lasting immunity

A

pertussis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Considerations for vaccination of patients with congenital heart disease

A
  • May have asplenia or functional hyposplenia
  • May have associated T cell deficiency
  • May have increased risk of deterioration/ collapse following immunisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Considerations for vaccination of oncology patients for those who have NOT completed primary vaccination vs those who HAVE COMPLETED primary vaccination

A

NOT completed primary vaccination
o Live vaccines contraindicated
- Those receiving immunosuppressive therapy
- Poorly controlled disease
o Administer to seronegative person 3 months after completion of chemotherapy if in remission
- Defer if recent IVIG
o Inactivated vaccines can be given however immune response suboptimal

COMPLETED primary vaccination
o Given a booster course following completion of treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How does the rotavirus vaccine work?

A

Live attenuated

Rotarix - 2,4 mo (Live attenuated human rotavirus vaccine)

-> Monovalent human G1P1A strain – protects against non-G1 serotypes on the basis of other shared epitopes

vs Rotatec 2,4,6 mo (Live attenuated pentavalent human–bovine reassortant rotavirus vaccine)

Prevents rotavirus gastroenteritis of any severity in 70% of those vaccinated + prevents SEVERE gastro req hospitalisation in 85-100% of those vaccinated

CI if previous history of intussusception or a congenital abnormality that may predispose to intussusception (ie mocker’s diverticulum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
BCG vaccine - efficacy - neonatal vaccination indications
Efficacy a. 80% protection in the first 15 years of life; reduces subsequently b. Greatest benefit in preventing **miliary tuberculosis** and **tuberculosis meningitis** in children, and pulmonary TB in adults c. Best efficacy in newborns and infants not previously exposed Neonatal vaccine indications a. Living in a house or family with a person with either current or past history of TB b. Household members who within the last 5 years have lived 6 months or longer in countries with high TB rates c. For first 5 years will be spending \>3 months in high-incidence country
26
Vaccines recommended in pregnancy and why?
* *DTP** in third trimester - more effective in reducing the risk of infant pertussis than maternal vaccination post partum * *Influenza** anytime during pregnancy - protects the mother, as pregnancy increases her risk of severe influenza, and also protects her newborn baby in the first few months after birth _Live vaccine deferred_ until after delivery - contraindicated
27
When can you vaccinate following blood products?
Live vaccines (MMR/VZV) specifically • 5 months after PRBC • 9-11months after IVIG This is because low levels of antibodies may be present in the blood product that may impair the immune response to the live vaccine.
28
1. How do penicillins work? 2. Which penicillin would you use for gram positive cover alone (oral and IV options) **without staph cover**? 3. Which penicillin would you use for **MSSA** cover? 4. Which would you use for **pseudomonas** cover? 5. Which would you use for **broad GP and GN cover including pseudomonas**? 6. **MRSA** cover
1. _Inhibit cell wall synthesis_ by **inhibiting binding of penicillin binding proteins** (irreversibly bind the binding site) 2. Oral – phenoxymethylpenicillin/penicillin V -\> amoxicillin, ampicillin; IV benpen/pen G 3. Fluclox or diclox 4. Ticarcillin, piperacillin 5. Amox/clav (augmentin), ticarc/clav (timentin), pip/taz (tazocin) 6. IV Vancomycin; PO clindamycin, bactrim, doxycycline, linezolid
29
Why do we avoid ceftriaxone in neonates?
Risk of **biliary sludging**
30
Which generation cefalosporins can cross BBB (give examples x3)
Third (ceftriaxone, ceftazidime, cefotaxime)
31
How do cephalosporins work?
Inhibit cell wall synthesis (target penicillin binding proteins and disrupt cross-linking of peptidoglycan to prevent formation of bacterial cell wall) IE - *same as penicillins,* but are **less susceptible to beta lactamase activity**
32
Which cefalosporins cover pseudomonas?
Ceftazidime (third gen) and cefepime (4th gen)
33
How is HIV transmitted to children?
Vertical transmission (transmission from mother to baby intero 5-10% chance, during labour/delivery 10-15% chance or via breastfeeding 5-20% chance)
34
What is the highest risk period for vertical transmission of HIV from mother to child?
During labour and delivery 10-15% risk (due to +++ secretions and blood)
35
How do you prevent transmission of HIV from mother to child?
1. Mother should be on **antiretroviral therapy** -\> suppression of viral load 2. **Post-exposure prophylaxis** for the infant within 4 hours of birth. - \> if very low risk setting, AZT monotherapy for 2 weeks - \> if low risk: AZT mono therapy for 4 weeks - \> if high risk (high viral load or you don't know anything about mother's treatment): combination therapy (AZT+3TC+NVP) 4. **Avoid BF** (note this is not a complete CI, excl BF \> mixed feeding)
36
Risk stratification for mother and baby for HIV transmission
V low risk - LOW/suppressed viral load (\<50copies/ml) & on cART \>10weeks (from 28 weeks GA) Low risk - low viral load \>= 36 weeks gestation. High risk - uncertainty about adherence or viral load or whether mother is on cART
37
When to commence cART for HIV pos mothers who are pregnant?
**By 28 weeks** gestation latest (at least 10 weeks prior to delivery)
38
Mode of delivery for HIV positive mothers
If viral low LOW (\<50copies/ml): NVD If \>400 copies/ml: C/S If 50-400 copies/ml: could do either. take other factors into consideration.
39
Diagnosis of HIV in children and teens
HIV serology (Ag and Ab)
40
Diagnosis of HIV in infants
1. HIV DNA **PCR** -\> at birth 50% sensitivity -\> **100% by 3 months** -\> 99.8% specificity at birth and 100% by 1 mo Ideally you do **serial testing x3 tests, last at 3months** (if neg then, considered neg for HIV)
41
HIV presentation
Initial non specific pres: - FTT - Dev delay - Encephalopatjy - B/L parotiditis - Fever - Lymphadenopathy - Hepatosplenomegaly - Oral candiasis Pregression of immunosuppression and progressive CD4 count - opportunistic infections (PJP, HSV, Tb, CMV, molluscum contagiosum)
42
Opportunistic infections
* PJP * Molluscum contagiosum * HSV * Tb * NTM (Non Tb mycobacterium) * Disseminated CMV * Oesophageal candiasis * HIV encephalopathy * Toxoplasmosis of brain * Recurrent bacterial pneumonia
43
Natural history of perinatal HIV
2 patterns 1. Rapid disease progression 2. Slower disease progression over 5-10 years (80-85% of patients in developed regions vs 55% in developing regions)
44
Pathophys of HIV infection of host
Enters via CD4 receptor -\> reverse transcription RNA into HIV DNA -\> uses cell's molecular mechanisms to transcribe HIV DNA into own cells' DNA (via 'integrase') -\> then it is transcripts into HIV RNA which then leaves cells to infect over cells
45
Treatment of paediatric HIV
2 nuclear reverse transcriptase inhibitors (NRTIs) + another agent (ie protease inhibitor, integrate inhibitor etc) Usually coformulated 2-3 drugs in one tablet, taken once a day = 'fixed dose combination pills'
46
Monitoring of HIV - aims in treatment
CD4 count (aim \>500 cells) Viral load (aim undetectable \<5o copies/ml)
47
What group has highest risk of drug resistance w HIV medications
Perinatally acquired HIV have much higher rates of resistance due to length of exposure and time
48
Morbidities assoc w long-term HIV
Metabolic (dislipidaemia, CV cx) Poor bone health Lower neurocognitive outcomes (school performance)
49
Infectious diseases w largest burden of morbidity and mortality
1. Influenza 2. HPV 3. Pneumococcal disease 4. Meningococcal disease 5. Shingles
50
MOA for Pfizer vaccine. What is the main SE and limitation for use in resource limited places?
mRNA based vaccine: encodes SARS-CoV2 spike protein, wrapped in lipid nanoparticles -\> incr expression and stimulation of neutralising Ab Needs storage at -60 to -80C Main SE - pericarditis esp in males after 2nd dose Currently all children \>=12yo eligible
51
R0 reproduction rate - what does this represent?
Mean number of infections generated during the infectious period of a single infected person
52
What is sepsis? main causes in chidren
systemic inflammatory response to a suspected infection Causes - s aureus - N meningititis - GAS - e coli
53
Toxic shock syndrome Definition Causes Presentation (what is the MAIN feature?)
Causes by super Ag from either * staph (Staph enterotoxin) * or group A strep (strep exotoxins A and B) - 60% culture + Features - HYPOTENSION is main feature! - fever - renal impairment - coagulpathy - maclar rash - soft tissue necrosis *(GAS)*
54
Pathophys of super Ags
- Super Ag overcomes binding between T cell MHCII and Ag presenting cell of -\> rapid non-specific activation of inflammatory response
55
Method of resistance and tx of MSSA
Beta lactase production - need fluclox or diclox or cefazolin (1st gen cephalosporin)
56
MRSA - method of resistance to methicillins
Carry a penicillin-binding protein, **PBP 2a** (encoded by genes *mecA and mec C*), that has a low affinity for all beta-lactam drugs other than those specifically designed to target it
57
VRSA mechanism of resistance to vancomycin
*VanA gene* resulting in **change in peptidoglycan target** and thus vancomycin resistance
58
N meningititis - what sort of bacteria is it? - methods of pathogenicity - treatment - who needs treatment
* _Gram neg diplococcus_ * **Encapsulated -** polysaccharide capsule for survival in blood. * Produces **endotoxin** which produces sepsis like picture Contains **factor H binding protein** - *inhibit C' cascade* and *alternative pathway* (critical for encapsulated organisms) **Pili** - enables adherence to and crossing BBB Treatment of meningitis - IV ceftriaxone Contact Prophylaxis - cipro (rifampicin in young children) - ceftriaxone in pregnancy Who needs prophylaxis? - all household contacts or day care contacts exposed within 10 days of index case illness onset - all healthcare contacts giving mouth to mouth or inadequate PPE within 10 days
59
Causes of **encephalitis**
Viral * HSV * Varicella (adolescents) * Enterovirus * Paraechovirus * Flu * Covid Bacterial - Mycoplasma pneumonia, Tb Fungal - Cryptococcal species Parasitic - Malaria, toxoplasma gondii Immune mediated Note 64% cases no pathogen identified
60
Presentation of encephalitis - General - Seizures is classic of what cause? - Drooling is classic of what cause? - Flaccid paralysis is classic of what cause? - Preceding pneumonia in what causes?
Inflammation of the _brain_ (vs meningitis- of the meninges) * Cognitive dysfunction * Behavioural changes * Seizures - classic of immune mediated * Drooling - classic of rabies * Flaccid paralysis - classic of enterovirus * Preceding pneumonia - in influenza or mycoplasma
61
CSF interpretation Normal Viral bacterial Tb Fungal
**Normal values:** * Neuts 0 * Lymph \<22 * Protein \<1 * Glucose \>2 Bacterial * High pressure * Turbid colour * High protein * Low glucose * low glucose CSF:serum ratio * Positive gram stain * High WCC (\>500) * \>90% polymorphs Viral * Pressure normal or mildly incr * Clear * Low protein * Normal glucose (high glucose CSF:serum ratio) * Normal gram stain * High WCC (\<1000) * monocytes * can also have very high polymorphs Fungal * Fibrin web appearance * Normal protein * mildly low glucose * low glucose CSF:serum ratio * WCC moderately elevated (100-500) * monocytes
62
Classic presentation of tetanus
* Trismus (spasm of the jaw muscles, causing the mouth to remain tightly closed) * Opisthotonos (spasm of the muscles causing backward arching of the head, neck, and spine) * Spasms * Seizures * Autonomic instability
63
What bacteria causes tetanus (and type of bacteria) Pathophys of infection
Clostridium tetani - spore forming GP anaerobic bacillus From stool and soil Produces an exotoxin which is transported though peripheral nerves and INHIBITS ACH release from motor nerve end plates * binds at the NMJ, enters motor nerve, travels peripheral to spinal cord -\> acts on inhibitory neurons by preventing release of GABA and glycine -\> leads to contraction and rigidity
64
Tetanus treatment
Local tetanus Ig and excision of site of infection AND Systemic tetanus Ig and Metronidazole With ICU, benzos, Mg
65
Indications for tetanus prophylaxis w wounds
For minor clean wounds: - Don't need tetanus Ig. - For Tetanus vaccine if not fully immunised or if due for routine booster anyway (booster needs to be within 10 yrs) For **unclean and/or major** wounds: - Need _tetanus Ig_ - Also need vaccine If \>5 years since last booster
66
What kind or virus is RSV How does pavilizumab work? How does it spread?
Enveloped single stranded RNA virus - **G protein** required for **attachment** - **F protein** required for host cell **fusion** (_blocked by palivizumab_ thus _blocking cell fusion_) Droplet and contact spread
67
Risk factors for severe RSV
* Cyanotic heart disease * PPHN * Prematurity * Bronchopulmonary dysplasia (CLD) * Immunosuppression (BMT, lymphopaenia, HIV etc)
68
How does influenza bind/attach to epithelial cells? How does it escape from cells?
INfluenza contains 2 glycoproteins: * **Haemagglutinin (HA)** facilitates binding to respiratory epithelium, _entering cells_ * **Neuraminidase** enables the virus to be released from/_exit the host cell_ (target of influenza tx - inhibitors)
69
Highest risk for severe influenza
* \<5 * CF * Haem malignancy * Neurodevelopmental disability
70
Complications of influenza
* Secondary pneumonia (bacterial - s aureus) * Myositis * Reye syndrome (acute noninflammatory encephalopathy with fatty liver failure assoc w influenza, varicella and NSAID use) * Guillan barre syndrome (progressive bilateral ascending symmetric weakness starting at feet and hands) * Seizures * Necrotising encephalitis
71
Antiviral treatment for influenza - how does it work and indications for use
**Neuraminidase inhibitors** (zanamivir, _oseltamivir_, peramivir) trap influenza in host cells _Reduce duration of sx by 1 day_ in healthy adults Antiviral tx should be offered as early as possible to those: * For severe, complicated or progressive ilness * Children at HIGH risk of cx * Household contacts of those at high risk
72
S pneumonia - what type of bacteria is it?
Gram positive Diplococci Aerobic **ENCAPSULATED**! Capsule is pathogenic Asymptomiac carriage in 20-60% of children but can cause invasive disease
73
S pneumonia - vaccination schedule
2, 4, 6 and 12 mo (prevenar 13 = conjugate vaccine, includes 13 of the most invasive serotypes) indigenous and high risk children recieve the **23v vaccine at 4 years of age (booster 5 years later)**
74
RF for invasive pneumococcal disease
Immunodeficiency * Primary immunodeficiency * Prematurity * Transplant * HIV * Malignancy Other * Chronic disease (lung/kidneys/liver/lungs etc) * Sickle cell
75
MIC targets for s pneumonia susceptibility (CSF vs non-CSF) - what abx to use for sensitive, intermediate or resistant strains?
MIC * Non-CSF isolates **\<= 2** * CSF isolates **\<0.1** are susceptible to penicillins -\> note for *intermediate susceptibility:* still use penicillin but at higher dose Resistant: Ceftiraxone or vanc
76
Pertussis What type of bacteria is it? Pathophys of infection Presentation Treatment
Gram negative aerobic bacilli Secretes toxin -\> incr _bradykinin_ production and increases 1/2 life of bradykinin -\> stimulates cough receptors ('100 day cough') Note long incubation period (up to 3 weeks!) Coughing paroxysms, _mostly without fever_. often to point of vomiting. Tx w **Oral macrolides (azithromycin**. erythromycin avoided as it has been shown to incr rates of pyloric stenosis)
77
HIB what type of bacteria is it? Treatment
Gram negative coccobacillus Serotype B is the strain responsible for the majority of severe disease -\> cause of meningitis, sepsis, SA, epiglottis, empyema (many fewer cases now w vaccination) Treatment with **3rd generation cephalosporins** (ceftriaxone- meningitis cover)
78
Rotavirus infection what type of virus Pathophys of infection vaccination schedule treatment
Non enveloped dsDNA virus * damage to gut epithelium -\> mixed _osmotic, secretory, exudative_ diarrhoea * * Release of **5HT** -\> _vomiting_ and delayed gastric emptying * **PE2, IL6** -\> _fever_ Vaccination: live vaccine at **2, 4 months** * reduces hospitalisation and disease severity Mx - rehydration and monitoring of electrolytes. can supplement zinc
79
what is most common cause of SA in children \<4yo
**\<3mo:** Staph, E coli, **GBS** **\>3mo \<5yo: Kingella kingsae** * presents w unusual joints for SA * classically _lower ESR and CRP_ than s aureus infections * often culture negative (need to order DNA PCR instead) * rare cause of _endocarditis_ in children w heart disease
80
Measles - what sort of pathogen? What presentation ? Cx? Diagnosis?
RNA virus 4 Cs: Cough, coryza, conjunctivitis, koplick spots Fever, confluent rash (onset 3-5 days after symptoms begin), miserable Complications - *_encephalitis, myocarditis_* diagnosis: Measles IgM or PCR from throat or nasopharynx
81
Complications of varicella infection Treatment of varicella
Bacterial superinfection - **group A strep** Cerebellar ataxia Aseptic menigitis Incr stroke risk transverse stroke risk **IV or oral acyvlovir, valaciclovir**
82
Antiviral spectrum of activity
83
Treatment of neonatal/infant varicella exposure
84
Main causes sepsis in newborns (EOS) What is empiric treatment for this?
EOS - Group B strep - E coli - Listeria - HSV Mx - Benpen and gent - Benpen and cefotaxime
85
Main causes meningitis in toddlers What is empiric treatment
Bacterial 1. Strep pneumoniae 2. N meningitidis 3. Haemophilis influenza Viruses: enterovirus, HSV Treat with cefotaxime and acyclovir as empiric cover
86
What is the single most important factor in blood culture collection?
Blood volume -\> minimum 1 ml but should be ~ child's age in ml
87
Main causes of sepsis (not meningitic) in children \>3mo (not immunocompromised)
* S aureus * Strep pneumoniae * GAS * N meningitis (particularly in adolescents) Empiric treatment: ceftriaxone and flucloxacillin
88
Main causes of sepsis in immunocompromised patients eg oncology patients What is empiric treatment
Pseudomonas Candiasis Line site infections - Staph Amikacin and tazocin (piperacillin tazobactam) +/- vancomycin if high risk/very unwell
89
Neuraltamivit, peramivir, osteltamavir, zanamivir how do they work, what is their spectrum?
Neuraminidase inhibitors specific for influenza interferes with host cell release of complete viral particles
90
Valaciclovir and Aciclovir MOA Spectrum of action
Antiviral is converted by *viral thymidine kinase* to ACV MP then by host cell kinases to active product which _inhibits and inactivates HSV DNA polymerases_ Active against: * **HSV** * **VSV** NOT active against CMV * CMV viral thymidine kinase doesn't convert acyclovir to ACVMP very well
91
Ganciclovir and Valganciclovir MOA and spectrum of action
CMV as well as HSV, VZV Valganciclovir (PO form) an oral prodrug that is rapidly converted to ganciclovir (IV form) Ganciclovir MOA: inhibits viral DNA polymerases and disrupts DNA chain elongation
92
Foscarnet and Cidofovir Spectrum of action and MOA
MOA: pyrophosphate analog. Selectively inhibits the _pyrophosphate binding site on viral DNA polymerases._ *BROAD spectrum* **Foscarnet:** * HSV * VZV * *CMV* * *HHV6 and 7* * (NOT influenza) **Cidofovir** - all of the above PLUS: * Adenovirus * BK/JC
93
MOA azoles
Inhibits formation of fungal cell membrane via - inhibition of fungal enzyme (14alpha demethylase) that converts lanosterol to ergosterol (component of fungal cell membrane)
94
'fungins' Echinocandins MOA
Stop synthesis of gluten in cell wall via non competitive inhibition of the enzyme 1,3 beta gluten synthase
95
Polyenes (amphotericin, nystatin) MOA
Binds ergosterol in fungal membrane causing cell membrane to become leaky
96
what types of bacteria have a peptidoglycan cell wall?
Gram positive bacteria
97
What is MIC
Lowest concentration of abx that stops bugs from growing
98
Time above MIC - what abx
Antibiotics * Beta lactams (beta lactams, carbopenems, cephalosporins) * Macrolides (erythromycin, roxithromycin, azithromycin and clarithromycin) Method * Used as continuous infusion, give more often as bigger doses * * Goal is to _maximise duration of exposure_
99
Peak MIC what abx work via this?
**Aminoglycosides** (gentamicin, tobramycin etc) Goal is to _maximise concentrations_ - has long post-abs effect even after abx is withdrawn or level not
100
AUC/MIC (Area under curve over the MIC) What abx work according to this?
Fluoroquinolones (cipro) Vancomycin Azithromycin goal is to _maximise amount of drug_
101
What defines an ESBL? what do you treat them with?
=extended-spectrum beta lactamases Resistant to _3rd gen cephalosporins (ceftriazone, ceftaz, cefotax etc)_ and _broad spectrum penicillins_ Need **aminoglycocide** (gent; don't cross BBB) or **carbapenem/meropenem** (CNS cover)
102
What does ciprofloxacin NOT cover? what does it cover?
**Gram positives** (Enterococcus MRSA, MSSA, CONS) and **anaerobes** (Good Gram Neg cover - pseudomonas, enterobacter and atypicals)
103
What subclasses fall under beta-lactams what bug is resistant to all of these?
penicillins cephalosporins carbapenems MRSA is resistant to ALL of these - req vanc which is a glycopeptide
104
What bugs don't penicillins cover?
C diff MRSA Pseudomonas (except for tazocin ) Atypicals
105
What bugs don't cephalosporins cover?
Enterococcus!!! MRSA (except ceftaRoline) C diff Atypical
106
What bugs don't carbapenems cover?
C diff MRSA Enterococcus Atypical Pseudomonas is covered (except with erbapenem)
107
Bioavailability of vancomycin
``` Zero oral availability IV only (except given oral in c diff BECAUSE it is not absorbed) ```
108
Major toxicity with vancomycin
AKI
109
How do you treat red man syndrome
SLOW vancomycin infusion (is NOT an allergic reaction)
110
Major toxicity w daptomycin
Rhabdomyolysis - needs weekly CK check whilst using
111
Linezolid major toxicity
peripheral neuropathy and bone marrow suppression w extended use (peripheral neuropathy is irreversible - particularly optic nerve)
112
Glycopeptides (vancomycin, daptomycin, teicoplanin and linezolid) what do they cover?
Treats GP bugs including MRSA NO coverage of gram negatives, atypicals or anaerobes (except vanc for c diff)
113
Fluoroquinolones (cipro, levofloxacin, moxifloxacin)
GN (Enterobacteracae and psueudomonas) + atypicals Moxiflox also covers GP and anaerobes
114
Tetracyclines give example what is it used for?
doxycycline . good oral bioavailability MRSA -\> used often for MRSA skin infections in community. Not reliable for GN coverage
115
What bugs is clindamycin active against? What is its main toxicity?
Used for strep, CONS, MSSA (not reliable for MRSA anymore) Toxicities: GI upset, c diff colitis
116
What bugs is metronidazole active against?
Anaerobes incl c diff
117
What is the limitation of nitrofurantoin in urinary infections?
CAN ONLY BE USED FOR SIMPLE UTIS. Cant be used for pyelo (or infections outside urinary tract) as concentrates in urine, doesn't get to kidneys well Covers UTI bugs (ie gram negative rods)
118
Trimethoprim-sulfamethoxazole coverage
GNR coverage (e coli, proteus, klebsiella ie main UTI organisms) Streptococcus, MRSA, CONS, MSSA as well -\> covers pretty much everything *except pseudomonas and e faecium*
119
MRSA - resistance to what abx? - what do you use to treat it?
- res to: beta lactams except ceftaroline - treat w vancomycin
120
VRE Res to? treat with?
res to vancomycin treat with daptomycin, linezolid
121
ESBL resistant to? treat with?
is an enterobacteriaeceae species (GNR) res to pencillins, cephalosporins treat w carbapenems
122
CRE res to? treat with?
is an enterobacteriaeceae species (GNR) res to all beta lactams treat with new inhibitor combinations (ceftaz-avibactam, tigecycline, polymixins)
123
Ceftriaxone break points (MIC) for Non-CNS infx CNS infx
Non-CNS infx \<= 1 sens CNS infx \<= 0.5 sens
124
Penicillin break points (MIC) for PO and IV (Non-CNS infx CNS infx)
PO sens \<=0.06 IV - CNS \<= 0.06 - Non CNS \<= 2
125
What gram positive abx don't cover enterococcus?
cephalosporins clindamycin TMP-SMX
126
Does gentamicin penetrate CSF?
No
127
Ix of Abx active against C diff
Ix - 2 step process 1. PCR: if neg, no c diff. If pos, go onto step 2 (to determine colonisation vs infection) 2. EIA immunoassay for toxin antigen protein: if positive, confirms acute infection. If negative, colonisation. Tx * Mild-mod infx: PO metronidazole * Sevre infx: PO vanc
128
What abx has biliary slugging as a possible SE
Ceftriaxone
129
bugs assoc w line infections
S aureus CONS
130
bugs assoc w chemo induced mucus membranes/mucositis related sepsis
Strep viridans
131
Bugs assoc w colitis-induced sepsis
E coli Pseudonomas enterococcus candida
132
Neutropaenia related infections (pre-engraftment phase **day 0-30** when really **neutropenic**)
* Staph, Strep species * Gram NEG bacilli * HSV * Candida from gut * Aspergillus from air, inhaled
133
Post-engraftment related infections (impaired cellular and humeral immunity, **NK cells recover first**, then CD8 T cells gradually increasing - no Cd4 t cells and B yet)
Viral and fungal mostly (Rather than bacterial) * CMV, HSV * Resp and enteric viruses * EBV * HHV6 * Pneumocystits * Candida * Aspergillus
134
Late phase infections assoc w impaired cellular and humeral immunity (**B cells and CD4 T cells deplete** but numbers gradually recovering and repertoire diversifying)
**Encapsulated bacteria Varicella zoster virus** CMV HSV Resp, interim viruses HHV EBV Pneumocystis and aspergillis (opportunistic)
135
what cephalosporins cover pseudomonas?
Cefepime CEftazidime
136
Max blood vol in paed vs adult BC bottles What is the consequence of too much volume?
paed- max 4 ml adult - max 10ml Too much blood reduces sensitivity of result
137
Most common causes of febrile neutropaenia
1. Bacterial infection 2. Viral URTI/LRTI 3. Fungal 4. UTI 10% - may be asymptomatic given neutropenic so won't have pyuria. needs treatment regardless
138
Causes of prolonged feb neut (fever \>3-5d)
untreated bacterial infection - are they missing anaerobic cover? ie on cefepime with GI sx? -\> source control issue? abscess? New or reactivated (if HSCT) viral infection? Invasive fungal disease
139
High risk phases of ALL treatment for feb neut /infection
Induction Consolidation Delayed intensification (low risk in maintenance and interim maintenance phases)
140
High risk groups for feb neut
AML Relapsed Acute leukaemia High risk ALL Allogenic HSCT Acute or chronic GVHD
141
Investigations for prolonged feb neut
Blood culture x2 (incl 1 from each lumen) with first or any new fevers (after being afebrile) Viral molecular tests (NOT serology) Fungal - consider galactomannan (aspergillus) Imaging - CTCAP - PET CT or MRI BAL if pulmonary infiltrates on imaging
142
Mould active antifungals
Liposomal amphotericin Voriconazole Posaconazole Echinocandin
143
Signs of fungal infection on chest CT
1. NOdules 2. Halo sign (area of ground glass attenuation surrounding pulm nodule or mass)a 3. Air crescent 4. Cavitation
144
Causes of diffuse lung infiltrates (pneumonitis) on CT chest
Non-infectious - neoplastic process - radiotherapy - anti-neoplastic agents (cylophosphamide, MTx, bleomycin, immunotherapy) Viral Atypical pneumonia - **mycoplasma or chalmydia or legionella** Other - **PJP!!**
145
Presentation of PJP in cancer patients -what should you check?
Fever *Non productive cough* Tachypnoea Dyspnoea **Hypoxaaemia Quiet sounding chest** CT chest - **diffuse pulm infiltrates** **_Ask about bactrim compliance!!_**
146
Patient with probable/confirmed invasive pulmonary infection - what should you investigate and why?
Need to image the brain because many cancer patients present asymptomatically
147
What do u treat CMV with?
Ganciclovir
148
Candida aura - what sort of infection does it cause - how is it acquired? - first line tx
**Bloodstream infections** are the most frequently reported infections. Infections have crude mortality of 30–60%. Acquisition is generally **healthcare-associated** and risks include underlying chronic disease, immunocompromise and presence of indwelling medical devices assoc w antimicrobial resistance first line tx its **echinocandids**
149
What do u treat HSV and VZV with?
acyclovir (NOT active against CMV)
150
Treatment of EBV
NO antiviral treatment is useful. Key is to reduce immunosuppression
151
Treatment of HHV6
Ganciclovir Foscarnet second line
152
Infections associated with humeral abnormalities (hyposplenism, GVHD, hypogammaglobulinaemia)
Antibodies play an essential role in protection of the sinopulmonary tract and mucosal surfaces. -\> Recurrent **otitis media, sinusitis, and pneumonia** Encapsulated bacteria * Strep pneumonia * Haemophilus influenza Chronic diarrhea * Giardia lamblia * Salmonella enterica * Campylobacter jejuni * Rotavirus Classic ex is an infant whose susceptibility to infections arises at **four to nine months of age**, when protective levels of the maternal antibodies have waned (transplacental IgG t/f in utero).
153
Fever in returned traveller from Vietnam Chills Headache Myalgia Arthralgias M/P rash Diagnosis? how to confirm the diagnosis?
DENGUE fever - first week of illness serum viral DNA (PCR) or ns1 Ag will be positive. - second week and later serology IgM then IgG will be positive
154
What bugs cause enteric fever?
Salmonella typhae and salmonella paratyphae
155
What are the top 5 more common causes for fever in returned travellers
Malaria Dengue Chikungynya Enteric fever Rickettsial diseases
156
Exposure to freshwater in returned traveller w fever - ddx?
Schistosomiasis Leptospirosis
157
Exposure to unpasteurised dairy products in returned traveller w fever - ddx?
Brucellosis Listeriosis Campylobacter
158
Bird contact in returned traveller w fever - ddx?
Psittacosis Avian influenza
159
Mosquito bites in returned traveller w fever - ddx?
Malaria Dengue Chikungunya Zika virus Japanese encephalitis Yellow fever Filariasis
160
Soil-skin contact (bare feet) in returned traveller w fever - ddx?
CLM Hookworm Strongyloides
161
Unprotected sex in returned traveller wfever - ddx?
HIV Hep B STIs Zika virus
162
Raw or undercooked food in returned traveller w fever - ddx?
Food born viruses and bacteria Intestinal parasites Listeriosis Cholera
163
Hx of animal bite in returned traveller w fever - Ddx?
Rabies Rat-bite fever Herpes B (bitten or scratched by an **infected macaque monkey,** or have contact with the monkey’s eyes, nose, or mouth)
164
Dengue fever incubation period and natural history
Biphasic reaction Short incubation period - exposure -\> sx within 14 days. - 1st phase is general viral syndrome (viraemia pre IgM/IgG) with mild haem lab findings - 2nd phase is severe illness w shock, bleeding/haemmhorage and end-organ impairment (not all patients will progress to this phase)
165
Patient returns from travelling to rural village in nepal. 5 days on return he feels sick w fatigue and fevers. 5 days onwards he has ongoing fever. What is the most likely diagnosis and how is it tranasmitted? tx
Enteric fever (salmonella typhae/paratyphae) Acquired via faecal-oral transmission. Sx: can be a mild illness with low grade **fever, headache, fatigue, malaise**, loss of appetite, cough, **constipation** and **skin rash** or rose spots to in some cases, a fatal complications such as _intestinal perforations,_ _gastrointestinal hemorrhages_, encephalitis and cranial neuritis Ix w blood cultures Tx cipro or azithromycin (or IV ceftriaxone)
166
Enteric fever - what is the incubation period - Clinical presentation - where in world is it found - complications - diagnosis - treatment
Short - within 14 days Clinical features - **Febrile with RELATIVE BRADYCARDIA** (not tachycardic w fever) - Non specific sx: high grade persistent fever, headache, malaise, myalgia, cough, anorexia, nausea - Altered bowel habits **(constipation** \> diarrhoea), hepatosplenomegaly - Cx: GI bleeding, intestinal perforation, chronic carriage - Diagnosis via blood culture -\> isolation from culture. - Can also do faecal culture and PCR (not diagnostic though as may be carrier) Found in SE asia (indonesia, india) Tx : **IV ceftriaxone and/or oral/IV azithromycin**. Note that persistent fever isn't a sign of treatment failure.
167
Traveller returned from 3 week Uganda 10 days ago. Fever, headache, myalgia, no rash Whats the diagnosis?
Malaria until proven otherwise as this is an endemic region! Malaria should be actively ruled out in all travellers returning from endemic regions.
168
Malaria Where is it found? What is the incubation period?
Found subsaharan africa, PNG, solomon islands Incubation period is VARIABLE! Up to a couple of months post exposure.
169
Severe Malaria clinical presentation and treatment
Severe sx: - jaundice - oliguria - resp distress - severe anaemia - hypoglycaemia - vomiting - AKI - impaired consciousness treatment - IV artesunate +/- IV guanine if acquired in SE asia due to resistance patterns (thailand, cambodia, vietnam, laos, myanmar)
170
How do Malaria P vivax and ovale cause recurrence in disease?
sporozoites become dormant Hypnozoiticide -\>relapse P viva and P ovale infection months or years after initial infection
171
Malaria presentation
Headache, fever, chills (often cyclical every few days) Initial sx 10-14 days after infection Haemolytic anaemia due to destruction of RBCs -\> fatigue, headaches, jaundice, splenomegaly ``` If complicated (most commonly w P falciparum) - Mental status changes/encephalitis if brain affected +/- liver, lungs, kidneys, spleen ```
172
How do you investigate for Malaria?
Serial (x3) thick and thin blood film (needs 3 neg films for ruling out) - diagnostic confirmation - species differentiation (more than one parasite per red blood cell = falciparum) - parasite density rapid diagnostic test
173
Prevention vs Treatment of uncomplicated malaria
Prevention w doxycycline Treatment w Artemether/iumefantrine for P falciparum For P vivax or ovale need primaquine or efanoquine
174
What consideration has to be made before starting primaquine as treatment for P vivax malaria?
Consider G6PD testing as primaquine can cause haemolytic in G6PD deficiency individuals
175
Fever conjunctivitis and cough with later onset rash diagnosis? what is the r0 for this condition and when do outbreaks occur?
Measles r0 18 unvax population outbreaks when \>10% of population are susceptible
176
Nonspecific febrile illnesses with spotty scabbed rash and lymphadenopathy Just back from African, has been to game park wearing shorts What is the diagnosis? How is it transmitted? Where is it found? How to diagnose? How to treat?
Rickettsia 'spotted fevers' (eschar at bite site) carried by vectors ticks, fleas, lice common in african countries in travellers w outside exposures Diagnosis with PCR on eschar swab/biopsy or blood (days 1-5) or serology from day 6 on Treat w doxycycline
177
Fever, dry cough, lethargy, abdo pain and eosinophilia on return from East Africa (2 weeks ago) what the diagnosis and how is it transmitted?
Schistosomiasis (type of worm/helminth) - High prevalence in subsaharan africa Transmitted via freshwater contact - enters circulation, matures into adult form in liver, then travels to vesical/mesenteric plexus and lays eggs -\> inflammation and fibrosis
178
Clinical presentation/Stages of schistomiasis infection
Initially get 'swimmers itch' 2. acute schistosomiasis: get fevers, child, cough, myalgia, arthralgia, rash, abdo pain, lymphadenopathy, diarrhoea and EOSINOPHILIA - serology negative at this stage 3. Chronic - haematuria and portal hypertension, hepatosplenomegaly, pulmonary HTN, eosinophilia - serology positive at this sage - urine, stool microscopy may be positive in high count infections
179
treatment of schistosomiasis
Praziquantel
180
Covid virus and mechanism of infection
Single stranded RNA virus with spike protein on the membrane spike protein connect to ACE2 protein on human cell -\> fusion or endocytosis of viral particle -\> release of viral venome -\> translation of viral polymerase protein -\> RNA replication -\> translation of viral structural proteins and genome -\> formation of mature visions which exocytose from host human cell to then infect other cells
181
R0 mumps presentaiton?
10 flu-like prodrome followed my parotiditis (uni or bilateral) +/- trismus
182
r0 varicella
16
183
Malaria life cycle
``` Infected mosquito (sporozoite in mosquito's salivary gland) -\> mosquito bite: injection of sporozoites -\> travel to liver and infects human liver cell: A) P falciparum/malariae/knowlesi: multiply asexually and mature into merozoites whilst host cells lie. B) P vivax and ovale enter into dormant phase (=hyponozoites) ``` Merozoites enter into blood, invading RBCs - \> vivax prefers reticulocutes - \> falciparum and ovale invade RBCs of all ages Inside RBCs merozoites undergo asexual reproduction 1st stage: ring form trophozoite 2nd stage: late trophozoite 3rd stage: schizont. grows by digesting Hb and leaves behind hemozoin (brown gunk) then replicates via mitosis Merozoites released into blood to further invade RBCs OR may undergo gametogeny -\> divide to produce M or F gametes which remain inside RBCs and can be ingested by mosquitos blood meal Sexual reproduction within mosquito
184
Memorise (p falciparum and P vivax)
Malaria stages in blood film
185
P falciparum vs vivax in terms of disease severity, incubation period
P falciparum - high levels in blood stage (multiple parasites per blood cell). causes severe disease (inv CNS), shorter incubation period (10-14 d) vs p vivax - milder disease but can be RECURRENT. longer incubation period 2-3 weeks.
186
Pakistan refugee with progressive erythematous papule to nodule to ulcerating lesion, enlarging over time Painless what is the diagnosis?
Cutaneous leishmaniasis confirmed on biopsy
187
Phillipines playing Barefoot in sand/dirt Itchy snakelike/serpigenous rash systemically well what's the diagnosis? treatment?
Caused by contact w dog/cat faeces = CLD (cutaneous larva migrans) treatment w oral albendazole or ivermectin
188
Hx exposure to sheep RUQ and vomiting US -\> cyst w several internal membranes in liver w normal CXR What is the diagnosis, causative agent and transmission route and treatment?
Dx: Hydatid cyst (echinoccus granulosus) Transmission: Faecal oral transmission (ingestion of parasite-egg containing food) OR close contact w infected animals Other commonly affected site is the lungs. Tx: albendazole (surgery only if 'complicated' ie rupture or compressive effect) Cx - compressive effect, anaphylaxis w rupture.
189
Cause of eosinophilic meningitis in returned traveller. life cycle of this pathogen
Angylostrogylus cantonesis -\> larvae infect snails and slugs are intermediate hosts -\> ingested by humans (accidental hosts) OR by rats -\> eggs hatch in LUNGS and are passed on in rat faeces and go on to infect more snails/slugs
190
Life cycle of dengue virus
Invasion of macrophages and multiplication within then Migration to lymph nodes -\> amplification of infection in macrophages, monocytes and dissemination throughout lymphatic system Virus travels through body (viraemia) within 24 hrs Macrophages -\> IFNs, cytokines, chemokines, TNF etc recruited =\> flu like sx and pain as well as inflammatory response including leaky blood vessels -\> low BP/shock and reduction of blood flow to organs = organ dysfunction. infection of bone marrow leads to insufficient plt production =\> clotting defects and risk of bleeding.
191
What pathogen is known to cause secondary bacterial infections post varicella (chickenpox) infection
Strep progenies (GAS)
192
What is the causative organism and treatment for: mild presentation of septic arthritis in child under 5 yo with mild rise in inflammatory markers
Kingella Kingae. Not does not always grow on culture (BC or aspirate) Usually susceptible to beta lactams but not always so generally treat w cefazolin or augmentin.
193
Q fever - what is the infectious agent? - what exposure is a RF? - How is it transmitted? - Symptoms - Cx - Ix - Treatment
Caused by the bacterium Coxiella burnetii (spore producing GNB Exposure to cattle, sheep and goats other wild animals Transmitted via inhalation of aeroloised spores in the air or dust, by drinking unpasteurised milk or direct contact with tissue or body fluids of infected animals (main host) Sx onset 2-3 weeks after infection Causes flu-like illness w high fevers (NO rash) +/- Atypical pneumonia +/- hepatitis Small number of ppl go on to develop chronic disease Chronic disease - chronic cough, intermittent fevers and/or headaches +/-rarely endocarditis Ix: PCR or serology Mx: doxycycline .
194
What is the causative agent of this congenital syndrome? Severe microcephaly with PARTIALLY collapsed skull Thin cerebral cortices w subcortical calcification Eye changes - macular scarring and focal retinal mottling Uni or bilateral clubfoot Severe early hypertonia
Zika virus
195
In what stages of sphilis infection are risk of perinatal transmission highest?
Primary (risk highest) or secondary syphilis (moderate risk) 70-100% transmission Latent and tertiary syphilis - minimal/negligile risk of congenital infectiion
196
Syphillis - name of infectious agent - presentation - diagnosis - treatment
Agent: treponema pallidum * Hepatosplenomegaly * Rash - erythematous maculopapular or bullous lesions, followed by desquamation of peripheries * Snuffles (highly infectious secretions) Other: lymphadenopathy, hepatosplenomegaly. pancytopaenia, pneumonitis, osteitis, oedema Diagnosis via ***serology*** ***-*** *Antibodies have to be positive to be infected* * - if RPR and VDRL are also positive = syphilis of any stage* * - if RPR and VDRL are negatibev = primary or latent syphilis* * - neg serology but pos RPR and VDRL = false pos. no syphilis.* Treatment w IV **penicillin**
197
What condition is advantageous/protective against malaria and why?
Sickle cell anaemia - protective against malaria because RBCs lack the duffy Ag that is required for malaria virus to infect host RBC Thalassaemia and G6PD - leads to increased oxidative stress in red blood cells, this may in turn have a negative influence on the parasite/destruction of parasite infected RBCs For this reason these conditions Are selected for in regions where malaria is endemic (subsaharan africa)
198
WHy/how does p falciparum cause severe malarial illness
In severe falciparum malaria, parasitized red cells may obstruct capillaries and postcapillary venules, leading to local hypoxia and the release of toxic cellular products. Obstruction of the microcirculation in the brain (cerebral malaria) and in other vital organs is thought to be responsible for severe complications.
199
What mechanism is responsible for the periodic burst of fever/chills/illness in malaria?
periodic febrile response is caused by rupture of mature schizonts
200
Parvovirus B19 When is it most contagious? What is the classic presentation? Ix (and limitation) and tx
Most contagious in the few days preceding rash - this is when the viraemia peaks. Affects SCHOOL AGED children (5-14 days) Non-specific **viral prodrome (fever, headache, myalgia**) followed by **'erythema infectiosum' rash about 1 week later** (cheeks and papular-pruritic glove and sock syndrome to hands/feet) diagnosis w serology (note IgM stays positive for up to 3 mo) Mx- supportive
201
What haematological change might you see in a child w parvovirus B19
assoc aplastic anaemia (dip in reticulocyte counts)
202
what is the most common virus assoc w febrile convulsions (and rash with high fevers)
HHV6 = '6th disease' (5th disease is parvovirus B19) * classic presentation is fever followed by macular rash to **torso** _as fever wanes_
203
presentation and mx of HHV6
**Roseola of infancy or '6th disease'** Affects children aged 1-2years of age Presentation: high fevers and convulsions for 3-5 days +/- diarrhoea As fever subsites, rash evolves Mx: supportive. ganciclovir if immunocompromised (risk of encephalitis, marrow suppression, interstitial penumonitis)
204
Presentation of rubella and when does viral shedding occur relative to this?
Presentation: Prodrome eye pain, conjunctivitis, headache, fever, malaise and tender lymphadenopathy Forchheimer sign - petechiae on softpalate (20%) - see photo 50% asymptomatic Rash on face, trunk, hands and feet (viral shedding 5 days pre to 4 days post rash)
205
Koplick spots - are a sign of what?
Measles.
206
What are the 4 'Cs' of measles presentation how does this relate to the viraemia?
Cough Coryza Conjunctivitis 'Koplik' spots (white spots in oral mucosa) - these are associated with viraemia Rash develops days 4-7 of illness, starting on FACE Serology will be positive 4-14 days after rash If investigating before this, do PCR on throat or nose swab
207
Mx of measles
Supportive \<6mo - Human Ig if immunocompromised or mum unimmunised/seroneg 6-18mo - Vaccinate if \<2 doses of vaccine Notifiabe disease - vaccinate susceptible contacts if within 72 hrs - if unvaxxed, exclude from school for 14 days
208
Complications of varicella/chicken pox
Bacterial infection (GAS) pneumonia Aseptic meningitis or encephalitis Post-infectious cerebellar ataxia Reye syndrome (encephalopathy, liver dysfunction) Varicella zoster (shingles) - incr risk if varicella \<2yo
209
CMV in children (not congenital infection) presentation (When not asymptomatic), mx and tx
Prolongued fever, lymphadenopathy, hepatitis for up to 4 weeks cx - anaemia, thrombocytopenia, pneumonitis and meningoencephalitis and CMV retinitis Diagnosis: PCR and serology (IgM) Tx: ganciclovir or foscarnet in immunocompromised or in immunocompetent if severe disease
210
7yo w sore throat (enlarged coated tonsils and erythematous pharynx), fatigue/malaise, fever 2 weeks, lymphadenopathy and splenomegaly (can have LUQ pain) with fine rash to torso Diagnosis?
EBV infectious mononucleosis Fine rash is assoc w amoxycillin use in EBV Diagnosis w monospot or serology
211
what malignancy is ebv assoc with?
lymphoma (Burkitts and hodgkins)
212
Hand foot and mouth disease What is the presentation what age group does it affect what virus causes this
Children \<5yo Spread via F/O route Sore t**hroat, fever** and _papulovesiscular_ lesions to **palms, soles and oral mucosa**. can also be on **buttocks and genitals**. Caused by coxsackie viruses (also echoviruses and enteroviruses) Cx: aseptic meningitis, encephalitis ?neurodevelopmental changes
213
Tx Hep B
* Tenofovir (inhibition of viral polymerase) * Lamivudine (inhibits reverse transcriptase of hepatitis B virus) * pegylated IFN alpha
214
**Hep B serology** * acute * vs chronic infection * vs past infection * vs immunisation
Acute infection: * **HBsAg** around 4 weeks post infection * Anti-**HBc IgM** * **HBV PCR +** * +/- HBeAg (if high viral load, high infectivity) Chronic * **HBsAg** (chronic if present **_\>6mo_**) * Anti-**HBc IgG** * **HBeAg** (level indicative of infectivity) * ***Anti-HBe Ab** = LOW infectivity* Past infection * **Anti-HBs Ab** (=immunity, either due to vaccination or resolution of infection) * **_HBc IgG_** Immunised * **Anti-HBs Ab** (=immunity) * *_NO anti-Hbc Ab_*
215
Indication for administration of Hep B Virus Ig (HBIG) at birth
* Babies born to mothers who are HepBsAg+ AND HepBe Ag+ (HBe Ag indicates high infectivity * Give Ig Within 72 hours * Presence of maternal anti-HBe Ab = low infectivity, just give Hep B vaccine within 12 hours
216
Multisystem inflammatory syndrome in children (MISC/P-MIS) presentation ix findings complications mx
Post infectious phenomenon post covid 19 infection (onset 2-6 weeks POST acute infection) * Persistent fever * inflammation (rise in inflammatory markers) * evidence of single or multi organ dysfunction May fulfil full or partial criteria for kawasaki disease need to exclude other microbial causes (bacterial sepsis, staph or strep shock syndromes, infections assoc w myocarditis SARS Cov2 PCR may often be NEG (bc is post-infectious phenomenon) Cx: _●Shock_ – 32 to 76 percent ●Mucocutaneous findings (red or swollen lips, strawberry tongue) – 27 to 76 percent ●Criteria met for complete Kawasaki disease (KD) (table 2) – 22 to 64 percent ●**Myocardial dysfunction** (by echocardiogram and/or elevated troponin or brain natriuretic peptide [BNP]) – 51 to 90 percent ●Arrhythmia – 12 percent ●Acute respiratory failure requiring noninvasive or invasive ventilation – 28 to 52 percent ●Acute kidney injury (most cases were mild) – 8 to 52 percent _●Serositis_ (small pleural, pericardial, and ascitic effusions) – 24 to 57 percent ●Hepatitis or hepatomegaly – 5 to 21 percent ●_Encephalopathy, seizures, coma, or meningoencephalitis_ – 6 to 7 percent Ix - High CRP, ESR, ferritin, procalcitonin, D-dimer, pro-BNP, troponin. LYMPHOPENIA but neutrophilia, thrombocytopaenia Treat w **IVIG**, **aspirin,** pulse **steroids** and **biologics** (ankinra, infliximab, tociluzimab)
217
What is the most common cause of occult bacteraemia in australisian children? (bacteria in blood with no focus of infection and you aren't that unwell)
Strep pneumonia
218
Out of hep B, hep C and HIV, which is highest risk of transmission w needle stick injury?
hep B 30% \> hep C 3%\> HIV 0.3%
219
Incubation period of hep B
45-160 days (**mean 90 days** or 3 months)
220
What proportion of acute hepatitis B infections in children progress to fulminant hepatitis?
1%
221
What age groups of patients classically do/do not display symptoms of hep B infection
Age infection directly correlates with risk of symptomatic disease * Infants **infected perinatally** (_vertical transmission_ from mo) usually are **aymptomatic** * Risk incr w duration of exposure to maternal _HBsAg_ and particularly _HBeAg_ * *​90% become carriers* * Age 1-5: 5-15% symptomatic * Age \>5: 33-50% syptomatic
222
What is the most important determinant of chronic hep B infection in children?
Age at infection is inversely related to likelihood of progression to chronic illness * 90% perinatal HBV infections become chronic (but less likely to be symptomatic) * 25-50% age 1-5 * 6-10% in older children/adults (most likely to be symptomatic)
223
Which serological marker of HepB correlates/is indicative of viral load? Why is this important in the pregnancy period?
**HBeAg positive -** very high viral load = *highly infectious* Important because viral load dictates risk of vertical transmission to baby. IE higher the maternal viral load, higher the risk of transmission to bub. In absence of immunoprophylaxis, risk is 90%. in presence of immunoprophylaxis (HBV Ig and vaccine), risk is 5-30%
224
What tests do you order to SCREEN for hep B virus (IE at immigrant health clinic) Further investigations if positive screen result?
1. HBsAg (infection) 2. HBsAb (immunity - either due to past infection or immunisation. 3. HBcAb (clarifies if immunity due to infection as *not present if vaccinated*) If HBsAg positive, go on to order further serology - HBcAb IgM and IgG (acute vs chronic infection) - HBeAg (?infectivity) - HBV DNA (?viral load)
225
What condition carries the highest burden of chronic disease?
Congenital **CMV infection** Then FASD Then Downs syndrome Then spina bifida
226
In what trimester is risk of CMV vertical tramission highest? and what about severe disease?
Risk of transmission lower in first trimester of pregnancy however risk of serious sequelae is much higher (and risk of transmission is highest in third trimester but risk of serious disease is lowest) Overall RIsk: Primary maternal infection -\> 30% risk of congenital CMV (85% asymp, 15% symptomatic) vs reactivation maternal infection \<1% of congenital infection
227
Presentation of congenital CMV infection Investigation? Treatment?
IUGR Microcephalis Petechial rash due to thrombocytopaenia Jaundice HSM Other: SNHL (all infants failing hearing test need to be screened for CMV) Intracranial calcifications Chorioretinitis Ix: Urine CMV PCR is most sensitive (more so than PCR on blood or saliva) Tx: ganciclovir -\> improves CNS disease (neurodevelopment and hearing loss) -\> evidence is to treat all cases of CNS disease and symptomatic patients. not asymptomatic pts as can cause neutropenia and unknown effects on fertility.
228
HSV - in what situations is risk of transmission to baby highest in pregnancy?
Highest risk of transmission in unrecognised ROM in a woman with primary HSV (infected maternal secretions) -\> women with recurrent symptomatic disease (lesions) at time of delivery have LOWER RISK of transmission than women with no lesions/asymptomatic shedding because of Ab passage to baby and institution of preventative regimens (C/S)
229
Presentation of congenital HSV infection what is treatment?
May present in 1st week of life - 1/3 will NOT have vesicular rash/skin lesions - Pneumonitis (classically day 5) - hepatitic - DIC - meningoencephalitis - long term neurodevelopmental problems Tx w acyclovir (improves neurodevelopmental outcomes)
230
Features of congenital varicella syndrome
Limb hypoplasia/abnormalities Dermatomal scarring Microcephaly Cataracts Prematurity Low birth weight
231
what congenital infection is mot likely to cause macrocephaly?
toxoplasmosis (hydrocephalus)
232
4cs of congenital toxoplasmosis infection presentation what is the main long-term consequence we worry about?
Cerebral Calcifications HydroCephalus Chorioretinitis Convulsions Although most newborns are asymptomatic Cx/sequelae - ocular disease (chorioretinitis)
233
Toxoplasmosis - how is it transmitted - how common is it
Parasites Cat poo or ingestion of undercooked meat from pigs/sheet etc RARE in australia (but common in other parts of the world with 1/3 people colonised) Risk of congenital infection is highest w primary infection later on in pregnancy (but more likely to be asymptomatic)
234
What congenital infection is this rash associated with?
Congenital rubella syndrome (blueberry muffin rash) due to extra medullary haematopoesis Also CMV
235
Congenital rubella syndrome
Ears: SNHL Eyes: Cataracts Heart: Congenital heart disease (pulm stenosis or PDA) Skin: Blueberry muffin rash (petechial/purpuric rash) Bones: radiolucent bone lesions at metaphyses
236
Tx of rheumatic fever
National recommendations for secondary prophylaxis in ARF are IM benzathine penicillin every 28 days for 10 years or until 21 years old (whichever is longer). For ARF with moderate rheumatic heart diseases is is for 19 years or until 35 years old (whichever is longer). With severe rheumatic heart disease or post surgery it is up to 40 years or lifelong.
237
Main cause of neonatal mastitis
S aureus
238
Treatment of head lice
Topical benzyl alcohol Knit combing Hot wash bedding Prophylactic treatment of bedmates Stay home from school
239
How long can lice survive on fomites?
24 hrs
240
How long can lice survive on fomites?
24-48 hrs
241
Scabies presentation
Intense intractable itch Nodules and pustules at most intense sites of itch, may also be crusted/scaly Common site: axillary folds, webs of fingers, volar aspect hand/wrist, belt line, penis, areola RF: overcrowding, poor heigine/nutrtion, homelessness, dementia
242
Diagnosis and treatment of scabies
Skin scraping and fluorescein stain OR S scabiei DNA PCR Mx: topical permethrin or benzyl benzoate +/- oral ivermectin
243
TB pathophysiology/stages of infection Define each: * primary tb * granuloma * ghon focus * ghon complex * ranke complex * miliary tb
Acid-fast bacilli (rods) - bright on ziehl neelsen stain Strict aerobe 1. Inhaled -\> lungs -\> localised infection in lower lobes = Primary Tb (infection soon after exposure to Tb) - \> mild-flu like illness or asymtpatomic at this stage 2. Granuloma formation: immune system walls off the infection to stop spread 3. Ghon focus: caseous necrosis inside granuloma (tissue death) 4. Ghon Complex: Spread to adjacent hilarity lymph nodes with caseation there as well as in the focus 5. Ranke complex: calcification of ghon complex 6a. Mycobacterium may then be completely killed off by immune system 6b. OR if may remain dormant in Ghon complex and can become activated again when immunocompromised (ex: HIV, malnutrition, ageing) 7. Re-activation -\> spread to UPPER LOBES -\> cavitation -\> dissemination of mycobacterium through airways and lymph channels to other parts of lungs and to the rest of the body = Systemic Miliary TB
244
Mantoux test What is it? How does it work? What are its limitations?
Purified protein derivative intradermal skin test for Tb _1st line for children \<5yo_ (as false negs with qfn gold) - Small localised reaction within 42-48 hours in response to intradermal purified protein. - Large area of induration = POSITIVE test (\>= 5mm if immunocompromised, \>= 10mm if RF for TB, \>= 15mm if no Tb RF and immunocompetent) - POS test = previously exposed at some point. Doesn't differentiate between ACTIVE vs LATENT disease. - False positives w BCG vaccination and non-Tb Mycobacterium (not specific for Tb) - False negatives if immunocompromsied/on steroids etc
245
Quanteferon Gold test What does it test for and how? What are its benefits/limitations?
IFN gamma release assay Alternative to mantoux test for screening test for M. Tb (NOT for chlidren \<5yo as false negs can occur) - Evidence in blood specific to M. Tb - pt doesn't have to return for test to be read at later date - Unlikely to be falsely positive due to BCG vaccine
246
Stages of Tb investigation - what comes next if screening w Mantoux or QFN gold is positive?
1. CXR +/- CT chest if resp sx and normal CXR Sputum or BAL (_NG aspirate from children \<6_ as unable to give sputum sample) -\> Culture, Z-N stain and PCR for M. Tb
247
Tx for Tb - Latent infection - Active infection
LATENT: 9months of Isoniazid ACTIVE = **RIPE** - Rifampin - Isoniazid - Pyrazinamide - Ethambutol
248
How infective is childhood Tb relative to adult Tb?
Childhood TB (\<10yo) is rarely contagious because: - Children with active TB usually have a low bacterial load - Children are less able to generate the tussive forces needed to aerosolise bacilli - Young children with pulmonary TB rarely have cavitating disease. - Young children swallow rather than expectorate sputum Older children (\> 10 years) and adolescents may present with cavitatory TB and are commonly infectious.
249
M Tb: How does childhood disease progression compare w that of adults?
Most children contain the infection resulting in what is commonly referred to as ‘latent TB infection’ (LTBI), but the risk of developing active disease remains lifelong. -\>**Progression to TB disease** occurs _more commonly_ in children than in adults (due to less developed immune system) and the risk of is greatest in the first 24 months following infection. ---\> Following exposure, the risk of progression to TB disease is highest in young children ( \<5 years, especially \<2 years). -\> Children are _more likely_ to develop **disseminated or non-pulmonary TB** disease than adults; infants are particularly prone to miliary TB and TB meningitis (associated with a poorer outcome than localised disease)
250
GAS: What type of bacteria? What are its virulence factors?
Encapsulated Gram positive cocci 'Strep Pyogenes' Produce Streptolysin O and S cause haemolysis Streptococcal pyrogenic exotoxins - superAg.
251
Pathophys of super antigens
1. Streptococcal Pyrogenic Exotoxins (A and C are super Ags) -\> cause haemolysis 2. Staphylococcal enterotoxins (SE) 3. Enterotoxogenic E. coli (ETEC) enterotoxin Pathophys - \> don't need to be eaten and processed/displayed on Ag presenting cells (macrophages) to generate a T cell immune response - \> the SuperAg binds directly w Class II MHC molecule on surface of macrophage which then interacts with T cell receptor -\> Massive recruitment (300x) of T cell populations -\> Cytokine storm and Toxic Shock syndrome TSS - widespread systemic vasodilation -\> shock - \> poor perfusion of vital organs
252
Infections caused by Strep pyogenies (GAS)
Strep throat/pharyngitis +/- Scarlet fever (associated purpuric rash resulting from haemolysis) Impetigo (epidermis) Erysipelas (upper dermis) Cellulitis (lower dermis) Necrotising fasciitis Acute Rheumatic fever as post-infectious complication
253
Causes of impetigo
Staph aureus Strep pyogenes
254
Post-infectious phenomenons (2) associated w GAS infections
Acute rheumatic fever: Streptococcal bacterial 'M protein' is similar to myosin and glycogen of muscle and smooth muscle cells -\> confused by host immune system -\> type II sensitivity reaction -\> IgM and IgG against heart muscle, valves and pericardium (=\> myocarditis, endocarditis, pericarditis) Post-strep GN - commonly after impetigo - type III sensitivity reaction -\> Ag-Ab complexes form that deposit in BM of glomerulus -\> C' activation -\> kidney damage -\> oedema and haematuria
255
Sx of acute rheumatic fever
Major critera = 'JONES' 1. Joint inflammation (**migratory poly arthritis)** 2. Heart damage (new murmurs) 3. Nodules (elbows, knees, forearms) 4. Erythema marginatum (rash) 5. Sydenham's chorea (rapid involuntary movement of face and hands) Minor - raised ESR, CRP - fever - arthralgia - prolongued PR interval - h/o rheumatic fever/rh heart disease
256
Treatment of group a streptococcal infections
Penicillin G (cef or azith if penicillin allergy)
257
Mechanism of staph aureus resistance against beta lactams
make betalactamases which disable beta lactam abx by breaking their beat lactam ring
258
MOA beta lactam abx
Disrupt/disable penicillin binding proteins expressed by bacteria Thus PBP cannot work to make peptidoglycan -\> bacteria can't make cell wall -\> cell wall becomes leaky and bacteria dies Methods of resistance - Penicillin resistant: Make beta-lactamase which destroys the beta lactam ring - Methicillin resistance: Encode special PBPs that can't be easily disabled by beta lactam abx
259
Method of resistance of staph aureus against methicillin
Encode special penicillin binding proteins (make peptidoglycan in cell walls) that are unable to be disabled by abx
260
What conditions are associated w chronic mucocutaneous fungal disease/candiasis?
T1DM hypothyroidism, hypoparathyroidism, hypoadrenism
261
‎Enterobius vermicularis - what is the colloquial name
Pinworms
262
What antibiotics should a person with G6PD avoid?
Nitrofurantoin Cotrimoxazole (Bactrim/septra) Antimalarials (quinine, chloroquine, primaquine) Due to risk of haemolysis (blood film ft target cells, bit cells, spherocytes and some fragmented cells)
263
Listeria monocytogenes - transmission (to mother and to baby) and risk to baby
Transmitted to mother via food, especially unpasteurised dairy products contaminated by infected farm animals, soft cheeses, prepared deli meats and refrigerated meat spreads. Transmitted to baby either in-utero or intrapartum Transmission highest in the 3rd trimester; maternal listeriosis in 2nd and 3rd trimester results in 40 to 50 per cent fetal mortality. Transmission in 1st and 2nd trimester commonly causes M/C and foetal death in utero. Intrapartum transmission can present as EOS (mortality rate 20-40%) or LOS (mortality rate 0-20%) - typically meningitis (or pneumonia, conjunctivitis etc)
264
a) Which virus is most recognised as a suppressor of bone marrow erythropoietic activity? b) Which patients are most susceptible to this BM suppression when infected w parvovirus?
a) Parvovirus B19 b) Patients w hereditary anaemias (sickle cell, hereditary spherocytosis etc with reduced RBC lifespans as they are heavily dependent or erythropoiesis)
265
Differences between staph and strep toxic shock syndrome
Strep - Often w bacteraemia/septicaemia ie patients sicker - Other cx include ARDS, DIC, renal failure - higher mortality Staph - bacteraemia/septicaemia uncommon
266
MMR vaccine schedule
12 and 18 mo
267
meningococcal vaccine schedule
12 months (ACWY) Additional mening B vaccine a 2,4,6,12 months for INDIGENOUS australians
268
rotavirus vaccine schedule -risk of intussusception
2 and 4 months Risk of intussusception is 1 in 20,000-100,000 (risk of developing severe rotavirus GE is much higher than this if unvaccinated)
269
Prevention of GBS in mothers with RF for GBS
receiving antibiotics in labour
270
Agents responsible for OM/SA in the following age groups - neonates - toddlers - children/adolescents - non immunised - sickle cell disease
Neonates (\<6mo): Group B strep Infants 6mo-4years: kingella kingae Children \>4years: staph aureus Other situations - Non-immunised: consider H influenzae - Sickle cell disease: consider salmonella (asplenism -\> susceptible to encapsulated bacteria)
271
official name of 'group B strep'
Streptococcus Agalactae
272
what is the commonest cause of fungal meningitis in immunocompromised patients
Cryptococcus neoformans - india ink stain -\> halo (capsulated)
273
what is the most common cause of viral hepatitis? transmission/incubation/clinical illness and serology
**Hep A Virus** * **Transmission** - faecal oral route * **Incubation** - 2 weeks * **Malaise Prodrome** (2 wks; _HAV in stool_) - flu-like illness (malaise, N&V, diarrhoea, headaches); N bili but _AST elevated_ and urine bilirubin and urobilinogen incr * **Jaundice** (2-4wks; _anti-HAVIgM pos_) - cholestatic jaundice _(elevated AST, ALP, bilirubin)_, pruritis, mild hepatosplenomegaly * Rare cx: fulminant hepatic failure, myocarditis, arthritis, renal failure * **Recovery phase:** ALT normal, IgM decr and _IgG increases_ * self-limiting; supportive only * No carrier state Serology: Serum ALT is first to rise with viraemia
274
Which form of heptitis carries the highest risk of progression to chronic lvier disease, cirrhosism HCC?
1. Hep D SUPER-infection in someone w Hep B (chronic infection carries 70% risk of cirrhosis) 2. Hepatitis C (much rarer in children; vertical TRANSMISSION) * Rate CLD is 50% * Cirrhosis is 25% * HCC is 15% 3. Hepatitis B chronic/carrier status is more common in children but risk of cirrhosis etc is less than HCV * Cirrhosis is 2-3% (incr risk with higher viral load) * HCC is \<1%
275
What is the significance of hepatitis D virus
* Can only cause infection in presence of Hep B virus * **CO-infectino** with HBV * -\> high risk of **ACUTE hepatitis**, SEVERE sx * **SUPER-infectino** in someone already infected w HBV * -\> higher risk of **CHRONIC hepatitis**, **fulminant hepatitis** and/or progression to **cirrhosis (70%)**
276
Molluscum contagiosum
277
Traveller returned from India within the week p/w sudden onset fever, skin rash and swollen, sore, stiff joints whats the diagnosis?
**Chikungunya virus** * Transmission via mosquito bites * The incubation period ranges from 3 to 12 days. * Short duration of illness, 3-4 days Sx: The onset is usually abrupt and the acute stage is characterized by sudden onset with **high-grade fever**, **severe arthralgias**, myalgias, and **skin rash**. **_Swollen tender joints and crippling arthritis_** are usually evident. Cx: Several neurological, ocular, and *hemorrhagic* manifestations of fulminant *hepatitis*
278
Returned from India (or anywhere in tropics) with sudden onset fevers, myalgias, headahce and this eye sign (see photo) . Had been fresh water swimming. Whats the diagnosis? Cx of such infection?
**leptospirosis** (urine/faeces of infected rats, cattle -\> water; transmitted to humans mostly via fresh water swimming) Sx: abrupt onset of **fever, rigors, myalgias, and headache** in 75 to 100 percent of patients. **_-\> Conjunctival suffusion_** (pic) in a patient with a nonspecific febrile illness should raise suspicion for the diagnosis of leptospirosis - complicated by renal failure (non-oliguric w hypoK, hypoNa) - uveitis - hemorrhage - ARDS with pulmonary hemorrhage - myocarditis - rhabdomyolysis. (See 'Clinical features' above.)
279
Spot diagnosis?
Diptheria Formation of characteristic grey pseudomembrane
280
Returned traveller rfom hiking in north america p/w this rash (localised), fever, chills and malaise. Diagnosis?
* **Lyme disease** = bacterial infection **Boriella Burgdorferi** * From tick bite * early signs/sx (3-30d after tick bite) * Erythema migrans rash (bulls eye at site of tick bite * constitutional/flu like sx * disseminated disease (days to months after exposure) * meningitis * cranial neuropathy * carditis -heart block, myopericarditis * arthritis * Ix: elevated CRP, ALT, AST, CK * diagnosis via enzyme specific immunoassay or IgM and/or IgG western blot * tx: doxycycline
281
what tests to order for diagnosis of GAS infection?
Anti-DNAse B (more specific) ASOT
282
Treatment candiadasis
Fluconazole Voriconazole Amphotericin B if bloodstream infection/immunocompromised due to azole resistance in some strains of candida
283
Treatment of dental infections
Penicillins Treatment usually involves tooth extraction +/- incision and drainage. Dental registrar referral is required for: * Fever in the setting of suspected dental abscess * facial cellulitis/ swelling * Fast patient until dental review * Adequate analgesia * Consider OPG (discuss with ED consultant or dental registrar); Generally children under 3 years are not able to cooperate for OPG. * Antibiotics - IV penicillin or oral amoxicillin (if well enough for discharge).
284
most common cause infectious myocarditis/pericarditis/cardiomyopathy
Coxsackie B -\> can cause dilated cardiomyopathy and fulminant congestive cardiac failure
285
What VIRLA infection can mimic the presentation of kawasaki disease?
Adenovirus - pharngitis - conjuncivities - cervical lymphadenopathy +/- febrile convulsion
286
What infection is assoc w erythema multiforme?
HSV
287
Management of penicillin allergy - what alternative abx to use?
* In confirmed penicillin allergy (skin test positive), other penicillins should be avoided * Third generation cephalosporins can be employed in patients with a history of non-immediate or non-life-threatening allergy to penicillin * Carbapenems can be employed in patients with a history or immediate penicillin allergv -\> \<1% rate of cross-reactivity * In the case of severe T-cell mediated delayed reactions such as DRESS SJS/TEN antibiotic class avoidance is preferred (-\> clindamycin)