ID Flashcards
Presentation Dengue fever
- Initial acute phase: Fever, severe headache (retro-orbital pain), malaise, severe joint and muscle pain, N&V
Rash several days after fever onset - 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
Pertussis
‘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
Live vaccines
Rotavirus
MMR
Varicella
IN influenza
BCG
Travel - yellow fever
Immunology of vaccination
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 do toxin-mediated vaccines work
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
Conjugate vaccines - Mechanism
Benefits
Ex
- 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
Generation of B cell memory responses
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
Vaccine side-effects
inactivated vs activated
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)
Immune compromised individuals - how does this affect the vaccination schedule?
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)
Tetanus Vaccination schedule
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
Passive vs active immunisation
- 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
Types of vaccines
- examples
Effect on immunity
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
Vaccine adjuvant . what is it?
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
What extra vaccines do these patients groups need to obtain?
- Indigenous
- Umnderlying medical conditions
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)
Largest R out of vaccinatable infectious diseases?
Measles R12-18
Pertussis R12-17
Note
- Covid
–> alpha R 2.5
–> delta 5-7
–> omicron ?10
HPV
- disease
- vaccine
- vaccine schedule
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
Which vaccine is CI in HIV pts regardless of CD4+ count?
BCG vaccine
Typhoid + polio oral live attenuated (use inactivated instead)
Varicella post exposure options
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
Effect of bone marrow transplant on immunity
- 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
Indication for hep A vaccination
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
Least effective vaccine at providing long-lasting immunity
pertussis
Considerations for vaccination of patients with congenital heart disease
- May have asplenia or functional hyposplenia
- May have associated T cell deficiency
- May have increased risk of deterioration/ collapse following immunisation
Considerations for vaccination of oncology patients for those who have NOT completed primary vaccination vs those who HAVE COMPLETED primary vaccination
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 does the rotavirus vaccine work?
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)
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
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
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.
- How do penicillins work?
- Which penicillin would you use for gram positive cover alone (oral and IV options) without staph cover?
- Which penicillin would you use for MSSA cover?
- Which would you use for pseudomonas cover?
- Which would you use for broad GP and GN cover including pseudomonas?
- MRSA cover
- Inhibit cell wall synthesis by inhibiting binding of penicillin binding proteins (irreversibly bind the binding site)
- Oral – phenoxymethylpenicillin/penicillin V -> amoxicillin, ampicillin; IV benpen/pen G
- Fluclox or diclox
- Ticarcillin, piperacillin
- Amox/clav (augmentin), ticarc/clav (timentin), pip/taz (tazocin)
- IV Vancomycin; PO clindamycin, bactrim, doxycycline, linezolid
Why do we avoid ceftriaxone in neonates?
Risk of biliary sludging
Which generation cefalosporins can cross BBB (give examples x3)
Third (ceftriaxone, ceftazidime, cefotaxime)
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
Which cefalosporins cover pseudomonas?
Ceftazidime (third gen) and cefepime (4th gen)
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)
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)
How do you prevent transmission of HIV from mother to child?
- Mother should be on antiretroviral therapy -> suppression of viral load
-
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) - Avoid BF (note this is not a complete CI, excl BF > mixed feeding)
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
When to commence cART for HIV pos mothers who are pregnant?
By 28 weeks gestation latest (at least 10 weeks prior to delivery)
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.
Diagnosis of HIV in children and teens
HIV serology (Ag and Ab)
Diagnosis of HIV in infants
- 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)
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)
Opportunistic infections
- PJP
- Molluscum contagiosum
- HSV
- Tb
- NTM (Non Tb mycobacterium)
- Disseminated CMV
- Oesophageal candiasis
- HIV encephalopathy
- Toxoplasmosis of brain
- Recurrent bacterial pneumonia
Natural history of perinatal HIV
2 patterns
- Rapid disease progression
- Slower disease progression over 5-10 years (80-85% of patients in developed regions vs 55% in developing regions)
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
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’
Monitoring of HIV
- aims in treatment
CD4 count (aim >500 cells)
Viral load (aim undetectable <5o copies/ml)
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
Morbidities assoc w long-term HIV
Metabolic (dislipidaemia, CV cx)
Poor bone health
Lower neurocognitive outcomes (school performance)
Infectious diseases w largest burden of morbidity and mortality
- Influenza
- HPV
- Pneumococcal disease
- Meningococcal disease
- Shingles
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
R0 reproduction rate - what does this represent?
Mean number of infections generated during the infectious period of a single infected person
What is sepsis?
main causes in chidren
systemic inflammatory response to a suspected infection
Causes
- s aureus
- N meningititis
- GAS
- e coli
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)
Pathophys of super Ags
- Super Ag overcomes binding between T cell MHCII and Ag presenting cell of -> rapid non-specific activation of inflammatory response
Method of resistance and tx of MSSA
Beta lactase production
- need fluclox or diclox or cefazolin (1st gen cephalosporin)
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
VRSA mechanism of resistance to vancomycin
VanA gene resulting in change in peptidoglycan target and thus vancomycin resistance
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
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
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
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
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
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
Tetanus treatment
Local tetanus Ig and excision of site of infection
AND
Systemic tetanus Ig
and Metronidazole
With ICU, benzos, Mg
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
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
Risk factors for severe RSV
- Cyanotic heart disease
- PPHN
- Prematurity
- Bronchopulmonary dysplasia (CLD)
- Immunosuppression (BMT, lymphopaenia, HIV etc)
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)
Highest risk for severe influenza
- <5
- CF
- Haem malignancy
- Neurodevelopmental disability
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
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
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
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)
RF for invasive pneumococcal disease
Immunodeficiency
- Primary immunodeficiency
- Prematurity
- Transplant
- HIV
- Malignancy
Other
- Chronic disease (lung/kidneys/liver/lungs etc)
- Sickle cell
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
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)
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)
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
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
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
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
Antiviral spectrum of activity
Treatment of neonatal/infant varicella exposure
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
Main causes meningitis in toddlers
What is empiric treatment
Bacterial
- Strep pneumoniae
- N meningitidis
- Haemophilis influenza
Viruses: enterovirus, HSV
Treat with cefotaxime and acyclovir as empiric cover
What is the single most important factor in blood culture collection?
Blood volume
-> minimum 1 ml but should be ~ child’s age in ml
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
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
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
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
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
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
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)
‘fungins’
Echinocandins
MOA
Stop synthesis of gluten in cell wall via non competitive inhibition of the enzyme 1,3 beta gluten synthase
Polyenes (amphotericin, nystatin) MOA
Binds ergosterol in fungal membrane causing cell membrane to become leaky
what types of bacteria have a peptidoglycan cell wall?
Gram positive bacteria
What is MIC
Lowest concentration of abx that stops bugs from growing
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
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
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
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)
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)
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
What bugs don’t penicillins cover?
C diff
MRSA
Pseudomonas (except for tazocin )
Atypicals
What bugs don’t cephalosporins cover?
Enterococcus!!!
MRSA (except ceftaRoline)
C diff
Atypical
What bugs don’t carbapenems cover?
C diff
MRSA
Enterococcus
Atypical
Pseudomonas is covered (except with erbapenem)
Bioavailability of vancomycin
Zero oral availability IV only (except given oral in c diff BECAUSE it is not absorbed)
Major toxicity with vancomycin
AKI
How do you treat red man syndrome
SLOW vancomycin infusion (is NOT an allergic reaction)
Major toxicity w daptomycin
Rhabdomyolysis - needs weekly CK check whilst using
Linezolid major toxicity
peripheral neuropathy and bone marrow suppression w extended use (peripheral neuropathy is irreversible - particularly optic nerve)
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)
Fluoroquinolones (cipro, levofloxacin, moxifloxacin)
GN (Enterobacteracae and psueudomonas) + atypicals
Moxiflox also covers GP and anaerobes
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
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
What bugs is metronidazole active against?
Anaerobes incl c diff
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)
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
MRSA
- resistance to what abx?
- what do you use to treat it?
- res to: beta lactams except ceftaroline
- treat w vancomycin
VRE
Res to?
treat with?
res to vancomycin
treat with daptomycin, linezolid
ESBL
resistant to?
treat with?
is an enterobacteriaeceae species (GNR)
res to pencillins, cephalosporins
treat w carbapenems
CRE
res to?
treat with?
is an enterobacteriaeceae species (GNR)
res to all beta lactams
treat with new inhibitor combinations (ceftaz-avibactam, tigecycline, polymixins)
Ceftriaxone break points (MIC) for
Non-CNS infx
CNS infx
Non-CNS infx <= 1 sens
CNS infx <= 0.5 sens
Penicillin break points (MIC) for
PO
and IV (Non-CNS infx
CNS infx)
PO sens <=0.06
IV
- CNS <= 0.06
- Non CNS <= 2
What gram positive abx don’t cover enterococcus?
cephalosporins
clindamycin
TMP-SMX
Does gentamicin penetrate CSF?
No
Ix of Abx active against C diff
Ix - 2 step process
- PCR: if neg, no c diff. If pos, go onto step 2 (to determine colonisation vs infection)
- EIA immunoassay for toxin antigen protein: if positive, confirms acute infection. If negative, colonisation.
Tx
- Mild-mod infx: PO metronidazole
- Sevre infx: PO vanc
What abx has biliary slugging as a possible SE
Ceftriaxone
bugs assoc w line infections
S aureus
CONS
bugs assoc w chemo induced mucus membranes/mucositis related sepsis
Strep viridans
Bugs assoc w colitis-induced sepsis
E coli
Pseudonomas
enterococcus
candida
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
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
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)
what cephalosporins cover pseudomonas?
Cefepime
CEftazidime
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
Most common causes of febrile neutropaenia
- Bacterial infection
- Viral URTI/LRTI
- Fungal
- UTI 10% - may be asymptomatic given neutropenic so won’t have pyuria. needs treatment regardless
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
High risk phases of ALL treatment for feb neut /infection
Induction
Consolidation
Delayed intensification
(low risk in maintenance and interim maintenance phases)
High risk groups for feb neut
AML
Relapsed Acute leukaemia
High risk ALL
Allogenic HSCT
Acute or chronic GVHD
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
Mould active antifungals
Liposomal amphotericin
Voriconazole
Posaconazole
Echinocandin
Signs of fungal infection on chest CT
- NOdules
- Halo sign (area of ground glass attenuation surrounding pulm nodule or mass)a
- Air crescent
- Cavitation
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!!
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!!
Patient with probable/confirmed invasive pulmonary infection - what should you investigate and why?
Need to image the brain because many cancer patients present asymptomatically
What do u treat CMV with?
Ganciclovir
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
What do u treat HSV and VZV with?
acyclovir (NOT active against CMV)
Treatment of EBV
NO antiviral treatment is useful.
Key is to reduce immunosuppression
Treatment of HHV6
Ganciclovir
Foscarnet second line
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).
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
What bugs cause enteric fever?
Salmonella typhae
and salmonella paratyphae
What are the top 5 more common causes for fever in returned travellers
Malaria
Dengue
Chikungynya
Enteric fever
Rickettsial diseases
Exposure to freshwater in returned traveller w fever - ddx?
Schistosomiasis
Leptospirosis
Exposure to unpasteurised dairy products in returned traveller w fever - ddx?
Brucellosis
Listeriosis
Campylobacter
Bird contact in returned traveller w fever - ddx?
Psittacosis
Avian influenza
Mosquito bites in returned traveller w fever - ddx?
Malaria
Dengue
Chikungunya
Zika virus
Japanese encephalitis
Yellow fever
Filariasis
Soil-skin contact (bare feet) in returned traveller w fever - ddx?
CLM
Hookworm
Strongyloides
Unprotected sex in returned traveller wfever - ddx?
HIV
Hep B
STIs
Zika virus
Raw or undercooked food in returned traveller w fever - ddx?
Food born viruses and bacteria
Intestinal parasites
Listeriosis
Cholera
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)
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)
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)
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.
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.
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.
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)
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
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
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
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
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
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
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
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
Clinical presentation/Stages of schistomiasis infection
Initially get ‘swimmers itch’
- acute schistosomiasis: get fevers, child, cough, myalgia, arthralgia, rash, abdo pain, lymphadenopathy, diarrhoea and EOSINOPHILIA
- serology negative at this stage - Chronic - haematuria and portal hypertension, hepatosplenomegaly, pulmonary HTN, eosinophilia
- serology positive at this sage
- urine, stool microscopy may be positive in high count infections
treatment of schistosomiasis
Praziquantel
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
R0 mumps
presentaiton?
10
flu-like prodrome followed my parotiditis (uni or bilateral) +/- trismus
r0 varicella
16
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
Memorise (p falciparum and P vivax)
Malaria stages in blood film
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.
Pakistan refugee with
progressive erythematous papule to nodule to ulcerating lesion, enlarging over time
Painless
what is the diagnosis?
Cutaneous leishmaniasis
confirmed on biopsy
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
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.
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
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.
What pathogen is known to cause secondary bacterial infections post varicella (chickenpox) infection
Strep progenies (GAS)
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.
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
.
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
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
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
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)
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.
What mechanism is responsible for the periodic burst of fever/chills/illness in malaria?
periodic febrile response is caused by rupture of mature schizonts
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
What haematological change might you see in a child w parvovirus B19
assoc aplastic anaemia (dip in reticulocyte counts)
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
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)
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)
Koplick spots - are a sign of what?
Measles.
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
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
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
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
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
what malignancy is ebv assoc with?
lymphoma (Burkitts and hodgkins)
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 throat, 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
Tx Hep B
- Tenofovir (inhibition of viral polymerase)
- Lamivudine (inhibits reverse transcriptase of hepatitis B virus)
- pegylated IFN alpha
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
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
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)
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
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%
Incubation period of hep B
45-160 days (mean 90 days or 3 months)
What proportion of acute hepatitis B infections in children progress to fulminant hepatitis?
1%
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
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)
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%
What tests do you order to SCREEN for hep B virus (IE at immigrant health clinic)
Further investigations if positive screen result?
- HBsAg (infection)
- HBsAb (immunity - either due to past infection or immunisation.
- 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)
What condition carries the highest burden of chronic disease?
Congenital CMV infection
Then FASD
Then Downs syndrome
Then spina bifida
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
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.
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)
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)
Features of congenital varicella syndrome
Limb hypoplasia/abnormalities
Dermatomal scarring
Microcephaly
Cataracts
Prematurity
Low birth weight
what congenital infection is mot likely to cause macrocephaly?
toxoplasmosis (hydrocephalus)
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)
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)
What congenital infection is this rash associated with?
Congenital rubella syndrome (blueberry muffin rash)
due to extra medullary haematopoesis
Also CMV
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
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.
Main cause of neonatal mastitis
S aureus
Treatment of head lice
Topical benzyl alcohol
Knit combing
Hot wash bedding
Prophylactic treatment of bedmates
Stay home from school
How long can lice survive on fomites?
24 hrs
How long can lice survive on fomites?
24-48 hrs
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
Diagnosis and treatment of scabies
Skin scraping and fluorescein stain
OR S scabiei DNA PCR
Mx: topical permethrin or benzyl benzoate +/- oral ivermectin
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
- Inhaled -> lungs -> localised infection in lower lobes = Primary Tb (infection soon after exposure to Tb)
- > mild-flu like illness or asymtpatomic at this stage - Granuloma formation: immune system walls off the infection to stop spread
- Ghon focus: caseous necrosis inside granuloma (tissue death)
- Ghon Complex: Spread to adjacent hilarity lymph nodes with caseation there as well as in the focus
- 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
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
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
Stages of Tb investigation - what comes next if screening w Mantoux or QFN gold is positive?
- 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
Tx for Tb
- Latent infection
- Active infection
LATENT: 9months of Isoniazid
ACTIVE = RIPE
- Rifampin
- Isoniazid
- Pyrazinamide
- Ethambutol
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.
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)
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.
Pathophys of super antigens
- Streptococcal Pyrogenic Exotoxins (A and C are super Ags) -> cause haemolysis
- Staphylococcal enterotoxins (SE)
- 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
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
Causes of impetigo
Staph aureus
Strep pyogenes
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
Sx of acute rheumatic fever
Major critera = ‘JONES’
- Joint inflammation (migratory poly arthritis)
- Heart damage (new murmurs)
- Nodules (elbows, knees, forearms)
- Erythema marginatum (rash)
- 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
Treatment of group a streptococcal infections
Penicillin G (cef or azith if penicillin allergy)
Mechanism of staph aureus resistance against beta lactams
make betalactamases which disable beta lactam abx by breaking their beat lactam ring
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
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
What conditions are associated w chronic mucocutaneous fungal disease/candiasis?
T1DM
hypothyroidism, hypoparathyroidism, hypoadrenism
Enterobius vermicularis - what is the colloquial name
Pinworms
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)
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)
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)
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
MMR vaccine schedule
12 and 18 mo
meningococcal vaccine schedule
12 months (ACWY)
Additional mening B vaccine a 2,4,6,12 months for INDIGENOUS australians
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)
Prevention of GBS in mothers with RF for GBS
receiving antibiotics in labour
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)
official name of ‘group B strep’
Streptococcus Agalactae
what is the commonest cause of fungal meningitis in immunocompromised patients
Cryptococcus neoformans
- india ink stain -> halo (capsulated)
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
Which form of heptitis carries the highest risk of progression to chronic lvier disease, cirrhosism HCC?
- Hep D SUPER-infection in someone w Hep B (chronic infection carries 70% risk of cirrhosis)
- Hepatitis C (much rarer in children; vertical TRANSMISSION)
- Rate CLD is 50%
- Cirrhosis is 25%
- HCC is 15%
- 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%
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%)
-
CO-infectino with HBV
Molluscum contagiosum
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
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.)
Spot diagnosis?
Diptheria
Formation of characteristic grey pseudomembrane
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
what tests to order for diagnosis of GAS infection?
Anti-DNAse B (more specific)
ASOT
Treatment candiadasis
Fluconazole
Voriconazole
Amphotericin B if bloodstream infection/immunocompromised due to azole resistance in some strains of candida
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).
most common cause infectious myocarditis/pericarditis/cardiomyopathy
Coxsackie B -> can cause dilated cardiomyopathy and fulminant congestive cardiac failure
What VIRLA infection can mimic the presentation of kawasaki disease?
Adenovirus
- pharngitis
- conjuncivities
- cervical lymphadenopathy
+/- febrile convulsion
What infection is assoc w erythema multiforme?
HSV
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)
