Infectious diseases Flashcards
Positive vs negative sense viral RNA
Positive-sense viral RNA is similar to mRNA and thus can be immediately translated by the host cell. Negative-sense viral RNA is complementary to mRNA and thus must be converted to positive-sense RNA by an RNA polymerase before translation
eg. COVID is a positive sense single stranded RNA as a re most common viruses
Negative sense- rabies, ebola
MOA toxin mediated disease
Superantigen allows binding of MHC II with T cell receptiosn –> polyclonal T cell activation and overwhelming cytokine release
- doesnt need to be processed by APC and recognised by specific T cell receptor
Staph toxic shock syndrome
Exotoxin acts as superantigen which activates large number of T cells –> cytokine storm
Diagnostic criteria
- fever
- hypotension
-diffuse macular rash/erythema
- desquamation esp palms and soles 1-2 weeks after nset
- multisystem involvement: vomiting, diarrhoea, CK elevation/myalgia, AKI, liver failure, thrombytopenia, CNS involvement (confusion), hyperemia of mucous membranes
Usually no bacteremia
No locally invasive dieases
Rx: clindamycin + flucloxacillin +gent (as per RCH)
Streptococcal toxic shock syndrome
Exotoxins act as super antigens
- Isolation of GAS from normally sterile site
- Hypotension
- 2+ of: AKI, coagulopathy/thrombocytopenia, liver injury, ARDS, erythematous macular rash which may desquamate, soft tissue necrosis (nec fascittis, muositis or gangrene)
Higher rate of bacteremia
More progression to multiorgan failure and death than staph toxic shock
GIT symptoms and generalised erytheoderma less common
Rx: benpen + clindamycin
***1=bacteremia, pneumonia, osteomyelitis, septic arthritis, abscess, nec fascitis, meningitis etc
Most frequent source of infection is skin - cellulitis, varicella, burns
Staph
Gram pos
Aerobic
Catalase pos
Clusters
Staph aureus: coag positive
Staph epi: coagn neg
Coagulase neg Staph (CONS)
Staph epi
Causes infection in those with indwelling devices
Protective biofilm - resists phagocytosis
Rx: vanc
resistant to fluclox
Staph aureus toxins
Exotoxins: staph toxic shock syndrome
Exfoliatin - staph scalded skin syndrome
Enterotoxin- rapid food poisoning
Pathogenesis of MRSA
altered penicillin binding protein (PBP)
Rx: bactrim, clindamycin (Macrolide)
vanc, teicoplanin, ciprofloxacin
Strep
Gram pos cocci
Form strips
Catalase negative
GroupA= strep pyogenes (b hemolytic)
Group B= strep agalacitiae
Group D= enterococcus
Group E and F= Strep pneumonia and viridans (alpha haemolytic)
GAS tonsilitis more likely than viral if
Fever
Age >4 years
Tender enlarged cervical lymph nodes, esp if unilateral
NO cough or coryza
Absence of constitutional symtoms (headache, abdo pain)
Abssence of generalised lymphadenopathy or splenomegaly (EBV)
Group B strep in babies -transmission
20% women colanised
70% of infants born to colanised women become colanised
less than 1% develop GBS sepsis
Strep penumoniae
Gram pos
Diplococcus
Encapsulated
Catalase neg
Increased carriage in kids<2 years- more succeptible to disease
Resistance to beta lactams mediated by:
- mutations in penicillin binding proteins (able to pass these on via transposons)
- DO NOT PRODUCE BETA LACTAMASES
- resistance to macrolides mediated alteration to ribosomal target site and ATP efflux pumps
If intermediate resistance- can be overcoem with higher dose of penicillin
If high resistance/meningitis- need vancomycin + 3rd gen cephalosporin
Clostrodium tetani
Gram positive
Spore forming rod
Anaerobic
Causes toxin mediated disease- bacteria itself not invasive
Toxin binds NMJ- prevents GABA release –> muscle contraction and unable to relax
Trismus often first symptom
Opisthotonus- abn posturing
Rx: penicillin + tetanus immunoglobulin + immunisation
Management of tetanus exposure
All wounds other than clean minor wounds should be considered tetanus prone
Debride necrotic tissue as anaerobic conditions can promote growth
If 3+ doses of vaccine and <5 years since last done- no further treatment
If 3+ doses of vaccine and >5 years since last dose- booster vaccine (unless clean minor wound, then dont need a booster)
If <3 doses or uncertain, OR >10 years since last dose- TIG and booster (unless clean minor wound then just vaccine)
Clostrodium botulinum classical neonatal presentation
(Gram + rod, anaerobe, spores +)
Symmetrical flacid descending paralysis beginning with CRANIAL NERVES
found in honey- dont given <12 mo/age
Treatment of C.diff
PO/IV metronidazole if mild
PO vancomycin if severe
Antibiotics increasing risk of C. diff
quinolones
cephalosporins
clindamycin/lincomycin
amoxicillin/augmentin
Clindamycin has the HIGHEST risk
Listeria
Gram positive rod
Anaerobic
Catalase positive
Produces ENDOTOXIN (only gram + bacteria to produce endotoxin, rest produce exotoxin)
INTRACELLULAR- needs T cells
Found in soft cheeses, unpasturised milk, undercooked meat
Causes septicemia and meningitis in neonates
Gives a distinctive rash in neonatal sepsis
Penicillin OR Ampicillin +/- aminoglycoside
*cephalosporins not effective
Bordetella pertussis
Gram neg bacillus
Highly infectious
No long term immunity from initial infection/vaccination
- immunity wanes 3-5 years after vaccination
Catarrhal phase 1-2 weeks of URTI symptoms
Paroxysmal phase with 2-8 weeks of cough/insp whoop/post tussive vomiting without other URTI/LRTI symptoms
- complications: pneumonia, seizures, encephalopathy, apnoea
Convalsecnt phase
> 70% of household contacts commonly infected
Consider in infants presenting with apnoea/cynosis/BRUE/gagging/gasping
Rx: azithomycin in babies, azithro or clindamycin in kids
neisseria contact prophylaxis
kids- rifampicin
adults- ciprofloxacin
pregnant women - ceftriaxone
enterococci are intrinsically resistant to …
cephalosporins
- low affinity of cephalosporins to enterococcal PBP
Beta lactam resistance is mediated by..
- alteration of target site PBP
- inactivation by bacterial enzyme (penicillinase, cephalosporinase, beta lactamase)
- removal of drug by efflux pump (usually pseudmonas)
Extended spectrum beta lactamase
Produced by GN bacteria (eg Klebsiella, E.coli)
Resistant to cephalosporins, penicillins, aminoglycocides, RETAIN succeptibiluty to carbapenem (meropenem, imipenem)
AND beta lactam inhibitor (clavulanate) can block this resistance
Neonatal chlamydia trachomatis conjunctivitis
GN intracellular coccobacillus (gonorrhoea= diplococcus)
Presents 5-15 days of life (typically later than gonorrhoea)
chemosis of conjunctiva
oedema of eyelids
discharge - may be mucopurulent
Pharyngitis, otits media and PNEUMONIA usually after 8 weeks
Untreated0 can cause corneal scarring (blindness)
Rx: azithromycin/erythromycin
**risk pyloric stenosis with macrolides first weeks of life
Neonatal neisseria gonorrhoea conjunctivitis
GN diplococcus
Presents within first week of life (usually D2-5)- earlier than chlamydia
Clasically hyper purulent discharge (more than chlamydia) w eyelid swelling
Complications: corneal ulceration, perforation, blindness
Rx: IV cefotaxime, eye irrigation
measles exposure in unvaccinated child
Immunocompetant infant age 6-12 mo who has not yet been vaccinated (MMR usually given at 12 mo)- give MMR within 72 hours of exposure
Immunoglobulin if vaccine is contraindicated, or if succeptible but didnt receive vaccine within 72 hours of exposure
Considered to be immune if have had one dose of measles containing vaccine
*cant give MMR within 3 mo of IM immunoglobuln
Subacute sclerosing pan encephalitis
occurs 5-10 years after measles infection (not vaccine strains)
rogressive neurological deterioration occurs, characterized by behavior change, intellectual problems, myoclonic seizures, blindness, ataxia, and eventually death.
Symptoms progress through the following 4 stages:
Stage 1: There may be personality changes, mood swings, or depression. This stage may last up to 6 months.
Stage 2: This stage may involve jerking, muscle spasms, seizures, loss of vision, and dementia.
Stage 3: Jerking movements are replaced by writhing (twisting) movements and rigidity. At this stage, complications may result in blindness or death.
Stage 4: Progressive loss of consciousness into a persistent vegetative state. Death usually occurs as a result of fever, heart failure, or the brain’s inability to control the autonomic nervous system.
which common childhood pathogens DO NOT mandate school exclusion
HSV gingivostomatitis
CMV
EBV/glandular fever
Head lice as long a treated before school
Hep B + C /HIV as long as wounds covered
Molloscum contagiosum
Roseola
Parvo B19
what is the mechanism of strep pneumoniae resistance to penicillins
alterations of penicillin binding site
–> reduced affinity of PBP to antibiotic
NO BETA LACTAMASES
Risk vertical transmission form mum with first primary HSV
50% if no prior exposure to HSV (seroneg)
25% if first episode non primary (ie new serotype, but exposed to another serotype- partial protection)
<5% if recurent HSV
what is high risk neonatal HSV
mother with primary infection close to delivery or infant born vaginally with active disease to mother with no prior history of genital HSV
need to swab (PCR) at birth and bloods + LP + IV acyclovir
management bub with low risk neonatal HSV
includes mother with recurrent infection, and primary infection seroconverted well prior to delivery, surface swabs should be collected at 24-26 hrs hrs of life (eye, throat, rectum, umbi, rectum, urine). If any swabs positive OR evidence noenatal HSV, perform CSF and serum HSV PCR and start IV acyclovir
how long is someone with chickenpox contagious for?
contagious from 24-48 hours before the rash appears and until all the vesicles have crusted over
most common side effect of hep b treatment w ribavarin
ribavarin (part of triple therpy)
most common A/E is hemolytic anemia
POSITIVE TB RESULT
· 5mm or more is positive in
o An HIV-positive person
o Persons with recent contacts with a TB patient
o Persons with nodular or fibrotic changes on chest X-ray consistent with old healed TB
o immunocompramised
10 mm or more is positive in :
o Recent arrivals (less than five years) fromhigh-prevalence countries
o Children less than four years of age, or children and adolescents exposed to adults in high-risk categories
· 15mm or more is positive in:
Persons with no known risk factors for TB
false positive mantaux test
nontuberculosis mycobacteria
previous BCG
**Can use IGRA to differentiate in kids 5+ years
false negative mantaux test
very recent TB infection
EBV infection
recent live virus vaccine eg mmr
sarcoidosis
Hodgkins lymphoma
corticosteroid use
malnutrition
HIV
which antibiotics have concentration dependant killing
aminoglycosides
fluroquinolones eg ciprofloxacin
Max bacteriocidal activity achieved when antibiotic concentraiton much higher than MIC (10x)
+ post antibiotic effect
Cmax/MIC= aminoglycoside, quinolone
Area under curve /MIC= quinolone, aminoglycosides, vanc
Which antibiotics have time dependant killing
beta lactams, vancomycin, macrolides, clindomycin
T>MIC
Max kill rate at 2-4 x MIC
No post antibiotic effect so need frequent dosing
need to be >MIC for >40% of time to have bacteriocidal effect
first generation cephalosporins
cefazolin
cephalexin
Cover gram pos + few GN (kingella kingae, some klebsiella pneumonia, some E.coli)
used for surgical prophylaxis and skin/soft tissue infections
second gen cephalosporins
cefoxitin - anaerobic cover, used for surgical prophylaxis in abdominal surgery
cefaclor - causes serum sickness
Cefuroxime - CAP if penicillin allergy
third gen cephalosporins
ceftriaxone
cefotaxime
GP- MSSA, strep pneumo, strep viridans
Broad spectrum GN activity
as with 1st gen + h. influenaze, e.coli, klebsiella, proteus, neisseria, serratia
A/E: biliary sludging, calcium precipitation
3rd gen extended - ceftazadime. ADDS PSEUDOMONAS COVER (but worse GP cover)
fourth gen cephalosporins
Cefepime
Adds pseudomonas cover
5th gen cefalosporin
Ceftaroline
Adds cover for MRSA
which gram pos bacteria is not covered by any cephalosporin
enterococcus
Staph aureus mechanism of resistance
beta lactamases (penicillinase)
Antibiotic of choice is flucloxacillin/methicillin /vancomycin
Staph becoming resistant to many other penicillins
Thus need to use augmentin or piptaz to overcome (contain a beta lactamase inhibitor)
cephalosporins (1st and 2nd gen) also have MSSA cover and are resistant to the penicillinase produced by staph aureus
which cefalosporins have pseudomonas cover
ceftazadime
cefepime
which class of bacteria have intrinisic resistance to vancomycin
gram negatives
Vanc only effective on GP as it acts on the bacterial cell wall, which in GN is beneath a lipid layer and cant be reached by vancomycin
to which class of antibiotics dos p.aeruginoas have intrinsic resistance to
most cephalosporins except ceftazadime and cefepime
Antibiotic choice for enterococci
e. faecalis- penicillin, amoxicillin
e.faecium - vancomycin
NO CEPHALOSPORINS
to which antibiotic are Strep pyogenes universally succeptible to
penicillin
and mostly macrolides
to which antibiotic are neisseria meningidites universally succeptible to
ceftriaxone, rifampicin and ciprofloxacin (all these are used in contact prophylaxis as well!)
Increasing resistance to penicillins
antibiotics of choice for strep pneumoniae
if very unwell/meningitis
Ceftriaxone (+ vancomycin if GP cocci in CSF)
high risk of resistance to penicillins
meningitis antibiotic choices
<2 months: ampicillin + cephotaxime
- amp covers listeria + GBS
- cef covers strep pneumoniae
> 2 months: cefotax/ceftriaxone + vanc if GP cocci in CSF
At what MIC is a bacteria considered sensitive to strep penumoniae
<0.5 for cephaosporins
<0.06 for penicillins
At what MIC is a bacteria considered resistant (meningitis) to strep pneumoniae
For both penicillins/cephalosporins
Bacteria must have MIC < 0.06 /<0.5 to be considered sensitive. Anything above this is resistant
At what MIC is a bacteria considered resistant (non meningitis) to strep pneumoniae
benzylpenicillin + cefotaxime R>2
>1 = intermediate succeptibility
can be overcome with higher antibiotic dose
Which antibiotic would be 1st line for strep pyogenes
Flucloxacillin if cellulitis
Penicillin if invasive
abscess treatment
incision and drainage
not antibiotics
how do anti staph penicillins work
different side chain which reduces access of beta lactamase enzyme to PBP
what are the major adverse effects of flucloxacillin
allergy
Bone marrow suppression at high dsoes
hepatotoxicity
interstitial nephritis
MRSA treatment
clindamycin
bactrim
erythromycin/doxycycline
rifampicin
vancomycin esp MRSA bacteremia/ endocarditis
lincomycin
what is the mechanism of penicillin resistance in MRSA
altered receptor binding site PBP2a
Wont bind to any beta lactam drug so MRSA is resistant to all penicillins and cephalosporins
not beta lactamase
examples and MOA of macrolide antibiotics
eg azithromycin, erythromycin, clarithromycin
MOA- inhibit protein synthesis by targeting the 50S ribosomal subunit
used to treat legionella, chlamydia, mycoplasma , pertussis, non tuberculosis mycobacteria
azithro- h. influenzae
A/E: QT prolongation
Clarythromycin and erythromycin are inhibitors of CYP450 and therefore can lead to toxicity of other drugs that are metabolised in the liver
MOA and examples of lincosamides
clindamycin
lincomycin
Active against Gram pos and anaerobes (except b. fragilis and c. diff)
NO GRAM NEG cover
Active against MSSA, MRSA, and strep pneumoniae
Used for staph and strep toxic shock (clinda) as adjuvant
related to macrolides (same MOA) for if antibiotic is sensitive to one, it should be sensitive to the other
MOA of aminoglycosides
Bind 30S subunit of ribosome –> impair protein synthesis
MOA of quinolones
Impair action of DNA gyrase (topoisomerase) - impairs DNA synthesis
MOA rifampicin
impairs action of RNA polymerase –> impairs RNA synthesis
which antibiotics act on the 50S subunit
macrolides
licosamides:clindamycin /lincomycin
–> impair protein synthesis
which antibiotics bind to 30S ribosome subunit
tetracyclines eg doxycycline
aminoglycosides
A/E aminoglycosides
nephrotoxicity (uusally reversible)
ototoxicity (usually irreversible)
Ciprofloxacin
fluroquinolone
Impairs DNA replication by binding to DNA gyrase
Only PO antibiotic with pseudomonal cover
Covers most DN, some staph/strep activity but unreliable
pseudomonas wounds and ear infections
cystic fibrosis, neisseria contact prophylaxis
A/E: achilles tendon rupture
Nitroimidazole
Metronidazole
Affects DNA replication
Covers:
anaerobes eg bacteroides fragillis
C. diff
Protozoa: trichomonas vaginalis, giardia, entamoeba histolytica
Bactrim
trimethoprim inhibits DNA synthesis via antifolate acitvity
Sulfamethoxazole inhibits production of folic acid needed for DNA synthesis
used for:
PJP
MRSA
Nocardia
UTI- covers E.coli + ESBL
MOA vancomycin
Glycopeptide
Interferes with cross linking of glycopeptide cell wall
Bacteriocidal against most, bacteriostatic against enterococci
ESBL
E.coli and klebisella
Resistant to penicilins, cephalosporins, but are succeptible to carbapenems
Inhibited by beta lactamase inhibitos (eg clavulanic acid) - but dont use this for treatment, high resistance
Enzymes are aquired via plasmids
Rx: carbopenem +/- aminoglycosides
what is the non antibiotic use of macrolides
azithromycin modulates airway inflammation in cystic fibrosis
Management congenital toxoplasmosis
ii. <=18 weeks – spiramycin
1. Goal is to prevent vertical transmission to fetus
iii. >= 18 weeks – pyramethamine + sulfadiazine + folinic acid
Neonatal
i. Treatment = Pyrimethamine + sulphadiazine +/- spiramycin for one year
ii. Add steroids if evidence of eye disease
Neurodevelopmenta, opthal, audiolgy f/u
which drug prevents relapse in plasmodium vivax malaria
primiquine
but test for g6pd first!
during which trimester is risk congenital toxo the highest
third trimester is highest risk of transmission
but risk of congenita abnormalities highest with infection in first trimester
what is the most common presentation of congenital toxo
85% normal at birth
of these, 85% will have chorio retinitis
hearing loss 10-30%, dev delay 20-75%
Treatment neonatal herpes simples
IV acylovir
14 days if skin/eyes/mouth
21 days if CNS/disseminated
when is the risk to bub of neonatal HSV highest
primary maternal infection
ie mums with recurrent genital hsv/primary infection but seroconversion well before labour , even if born through a canal with active lesions, is much lower risk than if lesions detected at time of birth w primary HSV/no prev history of HSV
- if high risk, need to do LP/bloods/swabs treat with IV acylovir
- if low risk, just take swabs 24-36 hours of life and only treat if becomes symptomatic
what antibiotics cover neonatal GBS and e.coli
penicilllin + aminoglycoside
clues to congenital syphilis
rhinitis “snuffles”
bone things -osteochondritis/periostitis/periosteal reaction
rash with desquamation of hands and feet
hepatomegaly+/- spelenomegaly, jaudice
congenital syphilis testing
Non trepomonal tests= screening
Sensitive but not specific
- corrolate with disease acitvity, can be used to monitor progress
eg RPR, VDRL
Treponemal tests= TPPA/TPHA
detect syphilis specific antibodies -“reactive” or “non reactive”
usually remain positive for life
if suspect congenital syphilis- take bloods from mum and baby. If the baby’s titre is four times the mother’s titre, then it is considered positive
diagnosis congenital syphilis
Serology- RPR, TPPA
LP
skin lesions/rhinitis fluid - microscopy for spirochites
Rx congenital syphilis
10 days IV benzylpenicillin
management of neonates born to mum with Hep B
tenofovir
defining features congenital rubella
SNHL
Cataracts ‘cardiac- PA stenosis, PDA
treatment of neonates born to mothers with HIV
All- zidovudine at least 4 weeks
high risk-
add lamivudine + nevirapine OR raltegravir
ie 2 x NRTIs + NNRTI OR integrase inhibitor
when is the highest ris of congenital varicella
maternal varicella in 2nd trimester
low risk if in firts trimester
NO risk in 3rd trimester
management if mum develops chickenox 2-28 days post delivery
give baby ZIG if prem <28 weeks<1kg within 96 hours
If baby develops varicella:
Admit
if mid disease and ZIG given on time, no treatment, observation only
If severe disease or ZIG>24 hours after birth, treat with IV acyclovir
management if mum develops chickenox >7 days before delivery
No ZIG needed
management if mum develops chickenox -7 days before - 2 days after delivery
ZIG within 24 hours
treat infant with acyclovir if they develop chickenpox only if prem <28 weeks, severe disease or initial ZIG delayed past 24 hours
What is a kerion
an inflammatory, pus-filled sore (abscess) that sometimes oozes. Kerions form when your immune system overreacts to the fungal infection ringworm (tinea corporis). They most often appear on your scalp,
what is a herpatic whitlow
HSV infection
painful vesicle on finger, usually tip
indications bacterial prophylaxis for endocarditis
prosthetic valves
previous endocarditis
RHD
CHD- unrepaired cyanotic, inc palliative shunts
or repaired cyanotic CHD within 6 months
Latent TB
Latent TB
- Evidence of TB infection without disease
- Diagnose by positive skin test (>5mm with close contact) or IGRA and absnce of CXR changes or symptoms of disease
- Need to evaluate all contacts of confirmed TB cases
- treatment if to both prevent disease, especially disseminated disease, but also reduce risk of reactivation later in life
TPT is strongly recommended in the following risk groups:
* Young children (<5 years) who have been in close contact with a case of bacteriologically confirmed TB irrespective of initial TST. If TST positive, complete TPT course. If TST negative on initial screening, commence TPT and review with repeat TST at three months from break of contact. If break-of- contact TST is negative, TPT may be ceased.
- Older children and adolescents who have been in contact with TB and have evidence of infection
- Children with co-morbidities such as HIV or diabetes at risk of TB infection.
- Children in whom corticosteroid or immunosuppressive therapy (including anti-TNF therapy) is contemplated.
Treatment: 3 months isoniazid PLUS rifampicin OR 6 months with isoniazid OR 4 months rifampicin
TB testing in kids <5 years
: Tuberculin skin tests are the preferred test in children under 5 years. Some disadvantages of the tuberculin skin test include false positives from previous BCG vaccination or exposure to non-tuberculous mycobacteria. However, IGRA does not perform well in children and is not recommended in children less than 5 years old.
Gastric aspirates to obtain sputum for acid fast bacilli are used in children with suspected pulmonary TB- dont do for latent TB
Signs suggestive of HIV
weight loss
chronic diarhroea
prolonged fever
Lymphadenopathy 2 + sites
HSM
recurrent/persistant URTI
Parotitis
candidiasis
disseminated varicella
opportunistic infection s
at what point should kids with HIV be treated
The WHO recommends initiating ART for all infants, children, and adolescents living with HIV, regardless of WHO clinical stage and/or CD4 count
All kids <1 year need to receive PJP prophylaxis
what would be the first test used to detect early HIV
HIV RNA (viral load) usually positive 1-2 weeks post exposure
p24 antigen soon after (average 16 days)
Ab/Ag testing likely to be positive at ~4 weeks
highest risk time HIV transmission
at or around deliver
smaller risk in utero transmission
BF gives smallest risk
Most common treatment regime for kids >3 kgs
2 x NRTIs (zidovudine, lamivudine) + integrase inhibitor (dolutegravir)
TST/IGRA
IGRA more sensitive
but shouldn’t be used in kids <5 years. (frequent false neg) - less likely to have false pos
TST can be false neg or false pos
Remember a negative test doesnt rule out disease
Positive test can tell you TB infection but not disease
False negative result:
- Host related (eg severe infection, malnutrition, malignnacy, corticosteroid use)
- PPD related (eg improper storage, delayed administration after laoding syringe)
- Administration related (eg subcutaneous injection rather than intra dermal)
Mantous method: measure swelling (not redness)
Positive if >10 mm (not HIV infected) or >5 mm (HIV infected)
PCR (Xpert) not as sensitive as culture but establishes rifampidin resistance
definition latent TB
Asymptomatic child with postive TST but normal CXR
definition Tb disease
child with positive TST, symptomatic, and abnormal CXR or MTB cultures/PCR positive
TST interpretation
Treatment of latent TB - who to treat ?
Treatment of children and adolescents with TB infection and no evidence of TB disease is known as tuberculosis preventive treatment (TPT), and is indicated because:
· it greatly reduces the risk of developing disease in the years immediately after acquiring the infection (Martinez et al. 2020), including of severe disease in young children;
· the lifelong risk of developing TB can be reduced substantially, especially as the risk of re-infection in a low TB-endemic setting is extremely low; and
· TPT is very well tolerated in children and adolescents and serious adverse events are rare
Therefore, TPT is recommended for otherwise healthy children and young people who have a positive TST or IGRA and no evidence of TB disease.
TPT is strongly recommended in the following risk groups:
· Young children (<5 years) who have been in close contact with a case of bacteriologically confirmed TB irrespective of initial TST. If TST positive, complete TPT course. If TST negative on initial screening, commence TPT and review with repeat TST at three months from break of contact. If break-of- contact TST is negative, TPT may be ceased.
· Older children and adolescents who have been in contact with TB and have evidence of infection
· Children with co-morbidities such as HIV or diabetes at risk of TB infection.
Children in whom corticosteroid or immunosuppressive therapy (including anti-TNF therapy) is contemplated.
Options for LTB treatment
3 months isoniazid PLUS rifampicin OR 6 months with isoniazid OR 4 months rifampicin
isonazid can be used as monotherapy for 6 mo if contraindication to rifampicin OR
rifampicin monotherapy for 4 months if hepatotoxicity from isonazid
Treatment active TB disease
c. Traditional 6 month course= 2 months RIPE 4 months RI
d. Shortened 4 month regimen for non severe, smear negative disease= 2 months RIPE 2 months RI
i. Rifampicin = sterilizing activity to eradicate persistent subpopulations
ii. Isoniazid = bactericidal agent with high activity
iii. Pyriazinamide = agent to kill extracellular microbes in acid vacuoles
iv. Ethambutol = agent to reduce risk of development of resistance
main side effects TB treatment
isonazid- hepatitis
(keep treating unless >5 x ULN)
peripheral neuritis - risk reduced with B6
Which antibiotics have pseudomonas aeriginosa cover
Ceftazidime
Cefepime
Piptaz
Ciprofloxacin
Tobramycin,amikacin
Colistin
Carbopenems
how long is varicella contagious for
incubation period is 10-21 days
contagious 1-2 days before rash onset until all lesions are crusted over or until no new lesions appear for 24 hours (approx 5 days)
how long is measles contagious for
incubation period ~ 12 days from exposure to initial prodroma symptoms
rash occurs 2-4 days after prodrome (~2 weeks after exposure)
measles is infectious 4 days before to 4 days after rash onset (CDC)
gram negative bacilli
Kingella Kingae –> rx: cefazolin
erysipelas
cellulitis caused by a toxin of strep pyogenes
abrupt onset of a striking red rash with a clear line of demarcation
classic “butterfly” rash
ramsey hunt syndrome
presents with bells palsy
herpes zoster of the ear
diagnosis of rotavirus
ELISA/PCR
minimal leuks in stool
diagnosis of congenital syphilis
Darkfield microscopy of nasal discharge or moist skin lesions may reveal the spirochaetes. They are too small to be visualised by traditional microscopy. These are thin, motile spirals which move back and forward on their longitudinal axis. If these are not seen, it does not exclude the diagnosis as previous antibiotic use may kill the active spirochaetes.
VDRL is a non-treponemal test which should be taken from the baby and the mum. If the baby’s titre is four times the mother’s titre, then it is considered positive.
RPR is also a non-treponemal test with similar sensitivity (up to 90%) and specificity (approx. 50%) to VDRL. The tests are used interchangeably but it is important to do the same test in both mother and child. Therefore, don’t do VDRL in the mother and RPR in the child or vice versa. Choose one test and use for both.
most common viral cause. of myocarditis
coxachie B viruses
also give meningo-encephalitis
breastfeeding if mum varicella positive
BF not contraindicated unless there are active lesions on the breast
Herpes viruses
HHV1 = HSV1
HHV2= HSV2
HHV3= varicella zoster
HHV4= EBV
HHV5= CMV
HHV6 = Roseola
HHV7 =
HHV8= Karposis sarcoma
acute cerebellar ataxia associated with which virus
varicella
prophylaxis for snail ingestion
ALBENDAZOLE - up to 1 week post exposure
Angiostrongylus cantonesis (rat lung worm) –> eosinphilic meningitis
visceral leishmaniasis
leishmaniasis amastigotes are transmitted by sandflies
visceral, mucaneous and mucosal forms
cutaneous- large sores (crater)
Visceral: weight loss, present with massive hepatomegaly /- splenomegaly and generalised lymphadenopathy. Often coexists with HIV
onchocercasis (river blindness)
onchocerca volvus transmitted by infected blackfly
introduce filarial larvae into bite wound
microfilarei in the skin and lymphatics
cause pruritis, dermatitis, subcutaneous nodules
ocular lesions can progress to blindness
chagas disease
trypanosoma cruzi via infected triatomine bug “kissing bug”
mostly asymtomatic
complications of chronic chagas disease: arrythmias, cardiomyopathy, dilated oesophagus or colon
most common organism causing bacteria tracheitis
staph aureus
what to do about hematuria during a febrile illness
repeat urine mcs with GP when well
if in association with abdominal pain, consider calculus, puyelonephritis
if with bloody diarrhoa, consider hemolytic uraemic syndrome
if macroscopic haematuria, HTN, oedema —> consider nephritis and do a glomeurlonephritis screen
PREP
Tenofovir disoproxil and emtricitabine (Truvada) is the only PBS listed medication for PrEP. If taken correctly it is 99% effective at preventing HIV transmission. It should be considered in those at risk of HIV (e.g. men who have sex with men (MSM) who have a sexual partner with HIV and a detectable viral load, men or women who have casual anal sex without condoms with MSM, or a woman whose partner is HIV positive and is planning natural conception). It is recommended to complete HIV and STI testing, as well as assess renal function, prior to prescribing PrEP and at three month intervals whilst taking PrEP, and to also provide information regarding safe sex.
antibiotic treatment for brain abscess
cef + metronidazole
gent doesnt cross the BBB
presentation of roseola (HHV-6)
common viral illness in children <2yo. Classically this causes a sudden high fever, which may be associated with coryza. As the fever subsides (after 2-5 days) a rash which is erythematous, raised and blanching may develop primarily on the trunk, but often extending to the limbs.
Parvo B19 presentation
‘slapped cheek’ or Erythema Infectiosum. This illness is common in primary school children and is characterised by an initial viraemia which most commonly causes fever, coryza, headache, and diarrhoea. This is followed 2-5 days later by the typical ‘slapped cheek’ rash. This rash may progress to a lacy exanthem on the torso over the subsequent two days. Complications of parvovirus infection include arthritis/arthralgia, which is more common in older children and may persist for weeks, as well as aplastic anaemia in children with chronic haemolysis. Infection during pregnancy may cause hydrops in the developing fetus.
dengue transmission is via…
aedes aegyptes mosquito
tse tse flies transmit
trypanosomiasis
sandflies transmit
leishmaniasis
differentiating between lymphadenitis caused by mycobacterium avium and bartonella henslae
Mycobacterium: slowly enlarging, NON TENDER, usually cervical. pink/purple hue, can develop draining sinus. Systemically well
Bartonella: PAINFUL, more rapidly enlarging, can have systemic involvement, usually axillary, often hx cat scratch
Rx with azithromycin or bactrim
