Infectious Diseases Flashcards
Antibiotic classes: cell wall synthesis inhibitors
Beta lactams- Penicillins, cephalosporins, carbapenems
Peptidoglycan synthesis: vancomycin
Antibiotic classes: protein synthesis inhibitors (50S)
Macrolides (clarithromycin/azithromycin/erythromycin)
Chloramphenicol
Antibiotic classes: protein synthesis inhibitors (30S)
Tetracyclines (doxycycline/minocycline)
Aminoglycosides (getamicin/tobramycin/amikacin)
Antibiotic classes: DNA gyrase inhibitors
Quinolones- ciprofloxacin/norfloxacin
Antibiotic classes: mRNA synthesis inhibitors (DNA directed RNA polymerase)
Rifampicin
Antibiotic classes: disrupt DNA integrity
Metronidazole
Antibiotic classes: Inhibit folic acid synthesis
Trimethoprim/sulfonamides (sulfamethoxazole)
Is mild or severe pulmonary valve stenosis more likely to produce pulmonary valve dilatation
Mild- mechanism unknown, severe often treated earlier
Mechanism of toxin mediated disease with staph/strep?
Superantigen toxin allows the binding of MHC class II with T cell receptors resulting in polyclonal T cell activation - does NOT require processing by antigen presenting cells
Features of toxin mediated disease
Fever
Rash – sunburnt erythematous rash, blanching
Conjunctivitis
Mucous membrane changes
Hypotension
End organ damage
Why add clinda for toxin mediated disease
Toxin inhibition – this is immunomodulatory, inhibits toxin production AND host protein synthesis
Eagle effect – when bacteria reach stationary phase (not dividing as much), harder for penicillin to act as no PBP to act on (penicillin kills during dividing stage) 🡪 clindamycin overcomes this effect
Signs that make GAS phayngitis more likely than viral pharyngitis
> 4yrs
Tender lymphadenopathy
Pharyngotonsillitis
Scarlett fever rash
Temp >38
No cough/coryza/constitutional symptoms
Tonsilar exudate not helpful in differentiating
M type in strep that causes disease:
Types 1-4, 12, 28,tend to cause pharyngitis (type 12 only associated with GN)
Types 5, 49, 57, 60 = associated with skin disease + nephritogenetic
Risk factors for transmission of GBS
Primary risk factor is maternal GBS GU or GI colonisation
50% transmission without use of intrapartum antibiotic prophylaxis
Urine culture positive for GBS is a marker for heavy anovaginal colonisation
Delivery < 37/40
PROM
ROM > 18 hours before delivery
Chorioamnionitis
Maternal fever during labour
Early-onset GBS disease in previous pregnancy (routine prophylaxis)
What obstetric risk factors warrant intrapartum ABx (penicillin)?
Previous infant with EO-GBS
GBS bacteriuria
Spont onset of labour <37 weeks
ROM >=18 hours
Intrapartum fever >38 degrees
If any of the above are present intrapartum chemoprophylaxis indicated
Mechanism of bacterial toxin ‘tetanospasmin’ in C. Tetani
Toxin binds at the NMJ, enters motor nerve by endocytosis , exits motor nerve at spinal cord, enters spinal inhibitory interneurons 🡪 prevents release of glycine and GABA: this blocks normal inhibition of antagonistic muscles 🡪 contraction + unable to relax
Gram negative bacilli
H. Influenza
Pertussis
Cholera
E.Coli
Shigella
Legionella
Gram positive rods
Clostridium (tetani, botulinum, difficile)
Corynebacterium
Listeria
Nocardia
Bacillus Cereus
Gram positive cocci
Staph- MSSA, MRSA, CONS
Strep
- Group A: S. pyogenes, S. Pneumo
- Group B: S.Agalactiae
S. Viridians
Gram negative cocci
Moraxella
Neisseria
Yersinia
Gram negative rod
Salmonella
Campylobacter
Pseudomonas
Klebsiella
Leading cause of death in children <5?
Shigella gastroenteritis
- Fever, dysentry, HUS due to shiga toxin production
Bug associated with pontiac fever
Pontiac fever = fever, myalgia headache 🡪 self-limiting disease associated with legionella seroconversion
? ABx therapy in EHEC
Avoid ABx in EHEC infections- increases toxin release & HUS
RFs for N.Meningitides infection
Immunodeficiency
Complement deficiency (5-10,000x risk) – more likely to have recurrence
Current or future treatment with eculizumab (Mab against C5)
Functional or anatomic Asplenia
HIV
HSCT
Other = military, university students, indigenous
Signs of meningococcal sepsis early/late & complications
- Rapid onset of symptoms (usually)
Signs of sepsis - Fever, leg pain, altered conscious state (late)
- Neck stiffness, headache, photophobia, bulging fontanelle (late sign>12 hours)
- Rash: petechiae, purpura (late sign > 12 hours)
Complications:
Diffuse adrenal haemorrhage (Waterhouse-Friderichsen syndrome)
Renal failure, DIC, acidosis
Prophylaxis if exposed to meningococcal disease?
Prophylaxis should be given to contacts as soon as possible
Close household, intimate, and childcare contacts within 7 days prior to disease onset
Healthcare workers exposed to respiratory secretions (e.g. intubation without PPE)
,
Antibiotics
Infants < 1 month = rifampicin Q12H for 4 doses
Children > 1 month = rifampicin Q12H for 4 doses, OR ciprofloxacin single dose
Adults = ciprofloxacin single dose
Pregnant or contraindication to rifampicin = ceftriaxone IM single dose
RFs for non-typhoid salmonella infection
Risk factors
Neonates
HIV/AIDS or other immunodeficiency – especially IL-12
Malignancies
Haemolytic anaemia – including sickle cell disease, malaria
IBD, collagen vascular disease
Use of antacids
Extraintestinal manifestations of non-typhoid salmonella
Extraintestinal infections = skeletal system, meninges, intravascular sites
Associations with underlying illness
Reactive arthritis (HLA B27 +ve individuals)
Osteomyelitis (sickle cell disease)
Overwhelming bacteria ad multi-organ failure (HIV)
Toxic megacolon (IBD)
What bacterial infection is this rash associated with?
Features & Rx
Salmonella Typhae (rose spot rash)
Week 1 = fever (100%), abdominal pain, constipation OR diarrhoea (60%), headache, dry cough (30%), malaise, myalgia, epistaxis (25%), delirium
Week 2 = fever plateaus (39-50), symptoms ,progress, abdominal distension, delirium/ neuropsychiatric
Week 3 = symptoms progress, complications (intestinal perforation, intestinal hemorrhages, sepsis, myocarditis, abscesses)
Rx: azithromycin, ciprofloxacin
Complications of campylobacter infection?
Complications
Strong association with Guillian Barre Syndrome
?molecular mimicry between C. jejuni and GBS + Miller Fisher variant
Estimated rate of 1/3000 C. jejuni infections, stool culture +ve in > 25% of cases
Reactive arthritis
Typically migratory involving large joints and resolve without sequelae
More likely in HLA B27 +ve patients
5-40 days after onset of diarrhoea
Erythema nodosum
Irritable bowel syndrome
What bacterial infection is this caused by?
Ecthyma gangrenosum- Pseudomonas
What bacteria causes this skin lesion
Burkholderia Psuedomallei (meliodosis)
Dx on this CXR
PJP pneumonia
- Bilateral, symmetric, reticular (interstitial), or granular opacities
- Initially perihilar 🡪 peripherally (apical areas spared until last)
Complications = pneumatocoeles, pneumothorax (may be bilateral)
Dx on this CXR
ABPA
Hypersensitivity disease from immunologic sensitization to aspergillus antigens:
Starts with non-invasive colonization of bronchial airways
Persistent inflammation + hypersensitivity response
Immunologic responses lead to wheezing, infiltrates, bronchiectasis and fibrosis
What is Ponchet’s disease
MTB osteitis
Well defined sclerotic margins on X-ray
Thick , inflammatory synovium 🡪 invades articular surface
More common in school age group
Spinal TB 🡪 vertebral body destruction, deformity
Side effects of TB treatment
Rifampicin
Inducer of liver enzymes
Orange secretions
Hepatitis
Influenza-like reaction
Thrombocytopaenia
Pruritis
Isoniazid
Hepatitis – particularly if >35 years, comorbid alcohol intake – check LFTs prior to starting treatment
Asymptomatic mild elevation of serum liver enzymes < 5 x normal 🡪 do not stop treatment
Immediate hypersensitivity reaction
Peripheral neuritis – prevented by B6, increased risk with poor nutrition
Haematological problems
Pyrazinamide
Hepatotoxic
Arthralgia
GIT upset
Pruritis
Rash
Ethambutol
Optic neuritis – particularly colour + acuity
GIT disturbance
Hypersensitivity
Management of baby with TB pos mother?
Complications of mycoplasma infection
Complications
Skin lesions = SJS, erythema multiform
Neurologic complications = meningoencephalitis, transverse myelitis, aseptic meningitis, cerebellar ataxia, Bell palsy, deafness
Haematologic complications = haemolysis (DAT +ve ) , cold antibody mediated disease
Phases of leptospirosis?
What parasite causes this infection?
Leishmaniasis, common in refugee populations, various Rx options, no good evidence
What parasite causes this infection?
Leishmaniasis, common in refugee populations, various Rx options, no good evidence
Summarise causes of acute/chronic schistosomiasis & symptoms
Asymptomatic
Pruritic rash – swimmer’s itch
Acute schistosomiasis = Katayama syndrome
Serum-sickness like syndrome manifested by acute onset of fever, cough, chills sweating, abdominal pain, lymphadenopathy, hepatosplenomegaly and eosinophilia
Chronic schistosomiasis
Genitourinary disease
Cause = S. haematobium
Can result in infertility, increases risk of HIV infection
Microscopic or macroscopic haematuria
Gastrointestinal disease
Cause = S. mansoni, S japnoicum, S intercalatum, S mekongi
Chronic or intermittent abdominal pain, poor appetite, diarrhoea
Chronic ulceration resulting in bleeding and IDA
Hepatosplenic
Cause = S. mansoni, S japnoicum, S intercalatum, S mekongi
Non-fibrotic granulomatous inflammation around trapped eggs in the presinusoidal periportal spaces of the liver
Can develop into periportal fibrosis
Pulmonary
Cause = S. mansoni, S japoncium, S haemtobium
Eggs lodge in pulmonary arterioles and produce pulmonary endarteritis 🡪 pulmonary hypertension and cor pulmonale
CNS disease = neuroschistosomiasis
Can involve spinal cord or brain
May result in single or multiple intracerebral lesions
Summarise causes of acute/chronic schistosomiasis & symptoms
Asymptomatic
Pruritic rash – swimmer’s itch
Acute schistosomiasis = Katayama syndrome
Serum-sickness like syndrome manifested by acute onset of fever, cough, chills sweating, abdominal pain, lymphadenopathy, hepatosplenomegaly and eosinophilia
Chronic schistosomiasis
Genitourinary disease
Cause = S. haematobium
Can result in infertility, increases risk of HIV infection
Microscopic or macroscopic haematuria
Gastrointestinal disease
Cause = S. mansoni, S japnoicum, S intercalatum, S mekongi
Chronic or intermittent abdominal pain, poor appetite, diarrhoea
Chronic ulceration resulting in bleeding and IDA
Hepatosplenic
Cause = S. mansoni, S japnoicum, S intercalatum, S mekongi
Non-fibrotic granulomatous inflammation around trapped eggs in the presinusoidal periportal spaces of the liver
Can develop into periportal fibrosis
Pulmonary
Cause = S. mansoni, S japoncium, S haemtobium
Eggs lodge in pulmonary arterioles and produce pulmonary endarteritis 🡪 pulmonary hypertension and cor pulmonale
CNS disease = neuroschistosomiasis
Can involve spinal cord or brain
May result in single or multiple intracerebral lesions
Main concerns with congenital symptomatic cCMV?
Main concerns of symptomatic cCMV infection 30,31
– Early mortality (first 3 months) rate between rate 5-10%
– Neurological sequelae of microcephaly (35–50%), seizures (10%), chorioretinitis (10–20%), developmental delay (70%)
– Sensorineural hearing loss (SNHL, 25–50%), with progression expected in about half (mainly in the first 2 years of life)
Treatment for cCMV
If symptomatic or isolated HL on NBHS.
Valgancyclovir 6mo, start at <30d.
Monitor LFTs & neutrophil count
Follow up:
Hearing until 6yrs
Paeds review 3-6mo until 2, then until 6
Opthal: annually until 6
Congenital infection likely to cause these CrUSS findings?
CMV
Risk of infection/congenital rubella syndrome with primary vs reactivation?
1-12wks: infection80%, congenital defects 85%
13-16wks: infection 55%, congenital defects 35%
17-30wks: infection 35%, defects rare
31-36wks: infection 60-100%, defects rare
Risk of infection/congenital toxoplasmosis with primary vs reactivation?
First Tri: low risk infection, high risk of severe damage if infected 34-85%
Second tri: intermediate risk infection/severity
Third tri: high risk infection, low risk damage
Spectrum of symptoms in congenital syphillis
Transplacental spread
Abortion
Fetal death
Hydrops fetalis
Preterm labour
IUGR
Congenital syphilis
Early features
Wide spectrum, including fulminant sepsis
Maculopapular rash on back, legs, palms, soles
Bullous/ desquamation
Rhinitis snuffles 1/52-3/12
Lymphadenopathy + HSM
Osteitis
Jaundice, pancytopenia, edema
Untreated, late features
Facial features = frontal bossing, saddle nose, short maxilla, protruberant mandible
Ophthal = interstitial keratitis, chorioretinitis, secondary glaucoma, corneal scarring, optic atrophy
Ears = SNHL
Oropharynx = Hutchinson teeth, mulberry molars, perforation of hard palate
Cutaneous = rhagades, gummas
CNS = ID, arrested hydrocephalus, seizures, paresis
Skeletal = saber shins (anterior bowing), Higoumenakis sign (enlargement of sternoclavicular portion of clavicle), Clutton joints (painless arthritis), scaphoid scapula
What TORCH infection causes this skin lesion?
Foetal Varicella Syndrome
Risk of transmission <0.55% <12wks, 1.4% 12-28%, >28wks no cases reported
Diagnosis on CSF stain (India Ink)
Cryptococcus- halo sign on india ink as dye unable to penetrate capsule
Differentiate foetal varicella syndrome (congenital) or neonatal varicella
Neonatal varicella
Mortality is very high
Risk is highest for mothers who develop varicella from five days prior 🡪 2 days afterward
Infants generally symptomatic by first week – second week of life
Treatment = ZIG 🡪 50% will still develop varicella but it is usually mild
Then treated with acyclovir 10 mg/kg tds if lesions develop
Congenital varicella syndrome
0.4% of infants < 13 weeks of gestation
2% of infants 13-20 weeks of gestation
Features
Cicatricial skin scarring
Limb hypoplasia
Neurologic features: microcepahly, cortical atrophy, seizures, mental retardation ,
Eyes – chroioretinitis, micropthalmai, cataracts
Renal – hydroureter + hydronephrosis
ANS abnormalities
Maternal treatment with Varicella IgG / Aciclovir – benefit unknown
What is the monospot test?
What does it test for, what are false positives and false negatives?
MONOSPOT – tests for Heterophile antibody, usually +ve after 2-9 weeks after infection
Heterophile antibodies = agglutinate cells from species different from those in the source serum
Heterophile – reacts with proteins across species line
False +ve = CMV, hepatitis, influenza, malaria, rubella, lymphoma, pancreatic tumour, RA, SLE< serum sickness etc
False –ve = 25% in first week of illness
High rate of false negative in very young ages
Indications for Pavlivizumab?
Palivizumab = monoclonal antibody
Given monthly during peak seasons
For high risk children
CLD
Congenital heart disease if < 2
Extremely premature < 28 weeks
Given IM monthly for five doses
Discontinue if admitted with RSV infection
Indications for Pavlivizumab?
Palivizumab = monoclonal antibody
Given monthly during peak seasons
For high risk children
CLD
Congenital heart disease if < 2
Extremely premature < 28 weeks
Given IM monthly for five doses
Discontinue if admitted with RSV infection
What bugs constitute ESCAPPM? What is their method of resistance
Enterobacter, Serratia, Citrobacter, Acinetobacter/ Aeromonas, Proteus, Providentia, Morganela
Hydrolyse penicillins, cephalosporins, AND resistant to beta lactamase inhibitors (enzyme = AmpC beta-lactamase)
Usually chromsomally encoded
Are also inducible 🡪 may be initially sensitive on testing
Usually require treatment with carbapenems / cefepime / SHORT course of beta lactam
ESBL mechanism of action
Extended spectrum beta lactamase
- found exclusively in Gram-negative organisms: primarily in Klebsiella pneumoniae, Klebsiella oxytoca, and Escherichia coli. also in Acinetobacter, Burkholderia, Citrobacter, Enterobacter, Morganella, Proteus, Pseudomonas, Salmonella, Serratia, and Shigella spp.
arose by amino acid substitutions that allowed narrower spectrum enzymes to attack the new oxyimino-beta-lactams
Thick vs thin smear malaria testing?
Thin smear: small amount of blood, cells remain intact- examine type of parasite/density
Thick smear: screening test to see if parasite present (can also estimate parasite density)
RDT- looks for histadine rich protein 2, plasmodium LDH & aldolase- can identify parasite but not density
Child with itchy (non tender) purulent/vesicular otitis externa- pathogen?
Varicella (painless)
Bacterial- 90% gram positive
- S.Epidermis, S.Aureus
- P.Aeruginosa also common
Sx: +++ear pain, itch, discharge +/- conductive hearing loss
Natural history of HIV
Early (seroconversion): fever/rash/lymphadenopathy
= First marker to appear gp41 and p24 antibodies
Latent: (seroconversion - 6mo): asymptomatic, HIV infiltrates lymphoid tissue, high rates of T cell destruction/turnover
= viral load (HIV RNA count) most important predictor in this phase
Late phase (>6mo): IgG positive from 6mo onwards- persists for life, IgM insensitive marker
= CD4 counts best predictor of disease
AIDS- once has ‘aids defining illness’
What are AIDS defining illnesses?
- Invasive candida/cryptococcus
- CMV/HSV/toxoplasmosis
- PJP (50% of illnesses diagnosed in first 1yr of life)
- MAC
- Cervical cancer, lymphoma, Kaposi sarcoma
CD4+ count <15%
Systemic features of Yersinia gastroenteritis?
Acute febrile gastro +
- Pseudoappendicitis (lymphadenopathy)
- Erythema nodosum (30%)
- Reactive arthritis (30%)- large weight bearing joints
(more prevalent in HLAB27 tissue type)
Clostridium Difficile treatment?
GP rod
Antibiotic induced diarrhoea (fluoroquinolones, cephalasporins, clindamycin)- during/months after ABx
Self limiting watery diarrhoea to pseudomembranous colitis
Dx: C.Diff toxin on stool/histo
Mild: PO/IV metronidazole
Severe: PO Vancomycin
Antibiotic treatment for Listeria
GP rod
Penicillin
Ampicillin
Aminoglycoside
(think pEOS cover)
Diptheria treatment?
GP rod
Acute Mx:
Antitoxin
Antibiotics : erythromycin / penicillin
Prophylaxis for contacts with erythromycin / IM benpen
Tetanus acute treatment
Clean wound, excise devitalised tissue
Penicillin
Tetanus immunoglobulin AND immunization booster
Immunoglobulin neutralises toxin, but needs to be given prior to toxin reaching the spinal cord
Can give IVIG if tetanus immunoglobulin not available, but dosages unknown
Exposure to toxin alone does not induce immunity 🡪 need to give vaccine
Muscle relaxants
Treatment of pt w/ tetanus prone wound
If >=3 doses of vaccine and <5 years since last dose – do not require any further treatment
If >=3 doses of vaccine and >5-10 years since last dose – booster vaccine
If <3 doses or uncertain – TIG + booster (unless minor wound)
Difference between prevenar 13/23?
Prevenar 13 = pneumococcal CONJUGATE vaccine
Provides T cell immunity, reduces nasopharyngeal colonization
Reduce nasopharyngeal carriage of vaccine serotypes by up to 60-70%
Pneumovax 23 = pneumococcal POLYSACCHARIDE vaccine
Contains more capsular types of strep pneumoniae
Induces limited immune response in children < 2 years of age + immunosuppressed patients
Abx for strep pneumoniae?
Penicillin
Third generation cephalasporin
Vancomycin
Clindamycin
Clarithromycin/erythromycin
Bactrim
Linezolid
Mode of resistance in strep pneumo
B lactams- altered PBP, can be overcome by ↑ dose
Macrolides - altered RNA binding (ermB), expels drug (mefA)
Fluoroquinosoles- spontaneous/altered binding
Most common organisms causing primary peritonitis, ABx Rx?
Strep pneumoniae 60-77%
Other streptococcus 15%
Gram negative rods (E.Coli) 10-25%
Haemophilus influenzae
Enterococcus spp.
Rx:
Ampicillin or Amoxicillin
Gentamicin
Metronidazole
~14d
What virus enters the cell via integrins?
HSV
What virus enters the cell via sialylated glycans (SA)?
Enterovirus
What virus enters the cell via cell adhesion molecules on CD4?
HIV
What virus enters the cell via ACE2?
COVID
Virulence proteins in rotavirus?
NSP1 protein = interferon antagonist
NSP4 protein =enterotoxin/viral replication.
Risk of intussuception post rotavirus vaccination?
1 in 20-100,000
TORCH infection MOST LIKELY to have hearing loss?
Rubella 90%
CMV 35% (but more common)
TORCH infection MOST LIKELY to have retinopathy?
Toxoplasmosis
TORCH infection MOST LIKELY to have hydrocephalus?
Toxoplasmosis
TORCH infection MOST LIKELY to have microcephaly?
CMV
Zika virus
TORCH infection MOST LIKELY to have intracranial calcifications?
Toxoplasmosis
Zika virus
CMV
TORCH infection MOST LIKELY to have hepatosplenomegaly?
Most
- Rubella
- CMV
- Syphillis
- Toxoplasmosis less common
TORCH infection MOST LIKELY to have cardiac defects?
Rubella
Congenital Rubella Sx
Cardiac defects
SNHL/deafness
HSM
Cataracts
+/- retinopathy, microcephaly, calcifications
(First tri)
CMV Sx
Microcephaly, CNS calcifications (periventricular)
Immediate or delayed SNHL- 35%
Congenital Herpes Sx
Multi-system failure
Rash
Neonatal seizures
Transmission greatest intrapartum if active genital lesions
Congenital parvovirus Sx
Hydrops, death
(First tri)
Congenital syphillis infection
Chorioretinitis
Neuro symptoms
Osteochondtritis/ abnormal epiphyses
Maculopapular rash and abnormal nails
HSM
Congenital VZV Sx
Skin & muscle defects
IUGR
Limb abnormalities/arthrogryposis
Congenital Zika Sx
Microcephaly, calcifications, ID
(First tri)
Management of pregnancy if previous HSV (2>1)
Consider use of suppressive antiviral therapy from 36 weeks
Careful speculum examination in labour
No active lesions 🡪 vaginal delivery
Active lesions 🡪 management of newborn as below
First time HSV genital infection in labour?
If early- prophylactic antivirals from 36wks, spec for active lesions
Late- same as above but consider LUSCs
Neonatal herpes Sx
- Skin/eyes/mouth:
- Vesicular lesions or atypically pustular or bullous lesions
- Corneal ulceration, keratitis
Mouth:
- Ulceration, palate, tongue - CNS/disseminated
- Seizures
- Unexplained sepsis
- Low platelets, elevated LFTs, DIC
- Respiratory distress
(disseminated earlier, CNS later)
Septic workup
IV aciclovir- 2wks SEM, 3 wks disseminated
Examples of RNA viruses
Positive-sense single-stranded RNA virus:
Enveloped:
- Dengue
- COVID
- MERS/SARS
- Rhinovirus
- Aids
- Rubella
- Hep C
Non enveloped: HepA, cold, polio
Negative sense single strandres RNA
Enveloped: Ebola/rabies, flu, measles, mumps
Examples of DNA viruses
dsDNA
Enveloped: HSV, EBV, VZVm hep B
Non-enveloped: adenovirus, HPV
ssDNA
Dx:
Cutaneous larva migrans
Dx?
Loiasis
Sx/Mx Strongyloidiasis
Strongyloidiasis
- Autoinfective nematode (can enter via any organ)
- Larva currens (serpiginous lesions that move rapidly) on trunk and buttocks
- Eosinophilia 10-70%
- Bronchopneumonia, abscesses
- Diarrhoea/PLE
- Pericardial effusion
- Hepatomegaly/abscess
- Gram neg sepsis from enteric bacteria
IgG only positive in chronic phase
Larvae in stool higher in acute
Rx: ivermectin (prophylaxis) or albendazole
Most common bacterial cause of IE?
Strep viridians >90%
- Enterococcus & staph aureus
Increase in HACEK organisms – Haemophilus, Actinobacillus, Cardiobacterium, Eikenella and Kingella
Stages of trachoma?
Types of malaria and findings on thick/thin smear
Transmitted by anopheles mosquito
Falciparum
- Most common
- Most likely to cause severe/CNS disease
- Ring trophozoites on thick blood smear
Ovale
- Latent, can reactivate and cause infection
- Causes splenomegaly
- 48h fevers, hypnozoite
Vivax
- Can hide in liver & relapse up to 5yrs after
- 48h fevers, hypnozoite
- Mainly Asia
Malariae
- Nephrotic syndrome
- 72h fevers
Treatment of malaria
Falciparum
1. AL (coartem/riamet)
2. AP (malarone)
3. Quinine + clinda
Vivax, ovale, malariae, knowlesi
1. Chloroquine/HCQ/AL
2. Primaquine (hypnozoites)
Severe: IV artesunate > IV quinidine > IV AL
Prevention of malaria
Avoidance
- Nets, sprays, clothing
Meds
- AP (malarone)
- Mefloquine
- Doxycycline >8yrs
Note – sickle erythrocytes, HbF and ovalocytes are resistant to plasmodium falciparum
Rates of vertical HIV transmission & ways to prevent.
Primary route of paediatric infection
- 30-40% intrauterine
- 60-70% intrapartum
- post partum (breast feeding) = least common
With prophylaxis <2% infection rate
- Mat ART
- Elective C/S
- Formula fed (if developed country)
- PEP if at risk
50% mortality rate if untreated
What is the most common AIDS defining illness?
PJP- 50% of cases
- Low grade fever/^RR
- Bilat perihilar interstital infiltrates on CXR
Prophylaxis for HIV exposed neonate?
Zidovudine
- reverse transcriptase inhibitor
+ 2x other agents
Medications used to treat HIV
- Reverse transcriptase inhibitors
- Zudovudine
- Lactic acidosis, hepatic steatosis, lipodystrophy - Protease inhibitors
- Ritonavir, tipranivir
- High BSL/TG, lipdystrophy - Fusion/CCR4 blockers
- Entuvirtide (blocks GP1)
- Maraviroc (blocks CCR4) - Integrase i nhibitors
- Raltegavir- GI upset/LFT derangement
Vector for schistosomiasis
Infection with blood fluke
Carried by aquatic snails
Haematuria
Increased risk of bladder Ca/anaemia
Rx: praziquantel
Vector for Onchocerciasis
Black flies
- endemic in Sub-Saharan Africa
Rx: Ivermectin
Hep B serology:
HbsAg +
Anti HbS & HbC -
1) acute early infection
2) transient positivity post vaccine (18-52d)
Hep B serology:
HbsAg -
Anti HbS +
HbC +
- IgM -
Previous infection
Hep B serology:
HbsAg +
Anti HbS -
HbC +
- IgM -
Chronic HB+BV
Hep B serology:
HbsAg -
Anti HbS +
HbC -
- IgM -
Previous immunisation
Hep B serology:
HbsAg +
Anti HbS -
HbC +
-IgM +
Acute HBV
Hep B serology:
HbsAg -
Anti HbS +/-
HbC +
-IgM +
Acute HBV which is resolving
Hep B serology:
HbsAg -
Anti HbS +/-
HbC +
-IgM +
Acute HBV which is resolving
Urease positive organisms
(PUNCH)
Proteus
Ureaplasma
Nocardia
Cryptococcus (fungus)
H.Pylori
Encapsulated organisms
(SHINE SKiS)
Strep Pneumoniae
H.Influenzae
Neisseria Meningitides
E.Coli
Salmonella
Klebsiella
GBS
Catalase positive
(CATS BeeN PLACES)
Candida (fungus)
Aspergillus (fungus)
T
Catalase positive
(CATS BeeN PLACES)
Cat(alase)
B.Cepacia
Nocardia
Pseudomonas
Listeria
Aspergillus (fungus)
Candida (fungus)
E.Coli
Staph/Serratia
Risk factors for HSV encephalitis?
Risk factors for HSV encephalitis:
* Presence of vesicles and/or seizures in
infant
* Mucous membrane ulcers in infant
* Hypothermia in infant
* Maternal history of genital HSV lesions
(absence of this history is not reassuring)
* Leukopenia or thrombocytopaenia in infant
* Deranged liver function tests (consider
checking for liver function tests if HSV is
suspected) and/ or coagulopathy
* CSF pleocytosis with negative gram stain
in infant
Pseudomonas resistance mechanism
Altered porin expression is a mechanism for bacteria to prevent antibiotics from entering the cell.
It has been noted that Pseudomonas aeruginosa develops mutations in the OprD gene during therapy
