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