FRACP 2023 Cram Homicrons Edition > Infectious Diseases > Flashcards

Infectious Diseases Flashcards

(124 cards)

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1
Q

Antibiotic classes: cell wall synthesis inhibitors

A

Beta lactams- Penicillins, cephalosporins, carbapenems
Peptidoglycan synthesis: vancomycin

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2
Q

Antibiotic classes: protein synthesis inhibitors (50S)

A

Macrolides (clarithromycin/azithromycin/erythromycin)
Chloramphenicol

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3
Q

Antibiotic classes: protein synthesis inhibitors (30S)

A

Tetracyclines (doxycycline/minocycline)
Aminoglycosides (getamicin/tobramycin/amikacin)

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4
Q

Antibiotic classes: DNA gyrase inhibitors

A

Quinolones- ciprofloxacin/norfloxacin

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5
Q

Antibiotic classes: mRNA synthesis inhibitors (DNA directed RNA polymerase)

A

Rifampicin

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6
Q

Antibiotic classes: disrupt DNA integrity

A

Metronidazole

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7
Q

Antibiotic classes: Inhibit folic acid synthesis

A

Trimethoprim/sulfonamides (sulfamethoxazole)

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8
Q

Is mild or severe pulmonary valve stenosis more likely to produce pulmonary valve dilatation

A

Mild- mechanism unknown, severe often treated earlier

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9
Q

Mechanism of toxin mediated disease with staph/strep?

A

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

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10
Q

Features of toxin mediated disease

A

Fever
Rash – sunburnt erythematous rash, blanching
Conjunctivitis
Mucous membrane changes
Hypotension
End organ damage

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11
Q

Why add clinda for toxin mediated disease

A

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

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12
Q

Signs that make GAS phayngitis more likely than viral pharyngitis

A

> 4yrs
Tender lymphadenopathy
Pharyngotonsillitis
Scarlett fever rash

Temp >38
No cough/coryza/constitutional symptoms

Tonsilar exudate not helpful in differentiating

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13
Q

M type in strep that causes disease:

A

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

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14
Q

Risk factors for transmission of GBS

A

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)

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15
Q

What obstetric risk factors warrant intrapartum ABx (penicillin)?

A

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

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16
Q

Mechanism of bacterial toxin ‘tetanospasmin’ in C. Tetani

A

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

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17
Q

Gram negative bacilli

A

H. Influenza
Pertussis
Cholera
E.Coli
Shigella
Legionella

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18
Q

Gram positive rods

A

Clostridium (tetani, botulinum, difficile)
Corynebacterium
Listeria
Nocardia
Bacillus Cereus

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19
Q

Gram positive cocci

A

Staph- MSSA, MRSA, CONS
Strep
- Group A: S. pyogenes, S. Pneumo
- Group B: S.Agalactiae
S. Viridians

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20
Q

Gram negative cocci

A

Moraxella
Neisseria
Yersinia

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21
Q

Gram negative rod

A

Salmonella
Campylobacter
Pseudomonas
Klebsiella

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22
Q

Leading cause of death in children <5?

A

Shigella gastroenteritis
- Fever, dysentry, HUS due to shiga toxin production

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23
Q

Bug associated with pontiac fever

A

Pontiac fever = fever, myalgia headache 🡪 self-limiting disease associated with legionella seroconversion

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24
Q

? ABx therapy in EHEC

A

Avoid ABx in EHEC infections- increases toxin release & HUS

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25
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
26
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
27
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
28
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
29
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)
30
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
31
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
32
What bacterial infection is this caused by?
Ecthyma gangrenosum- Pseudomonas
33
What bacteria causes this skin lesion
Burkholderia Psuedomallei (meliodosis)
34
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)
35
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
36
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
37
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
38
Management of baby with TB pos mother?
39
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
40
Phases of leptospirosis?
41
What parasite causes this infection?
Leishmaniasis, common in refugee populations, various Rx options, no good evidence
41
What parasite causes this infection?
Leishmaniasis, common in refugee populations, various Rx options, no good evidence
42
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
42
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
43
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)
44
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
45
Congenital infection likely to cause these CrUSS findings?
CMV
46
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
47
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
48
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
49
What TORCH infection causes this skin lesion?
Foetal Varicella Syndrome Risk of transmission <0.55% <12wks, 1.4% 12-28%, >28wks no cases reported
50
Diagnosis on CSF stain (India Ink)
Cryptococcus- halo sign on india ink as dye unable to penetrate capsule
51
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
52
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
53
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
54
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
55
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
56
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
57
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
58
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
59
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'
60
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%
61
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)
62
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
63
Antibiotic treatment for Listeria
GP rod Penicillin Ampicillin Aminoglycoside (think pEOS cover)
64
Diptheria treatment?
GP rod Acute Mx: Antitoxin Antibiotics : erythromycin / penicillin Prophylaxis for contacts with erythromycin / IM benpen
65
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
66
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)
67
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
68
Abx for strep pneumoniae?
Penicillin Third generation cephalasporin Vancomycin Clindamycin Clarithromycin/erythromycin Bactrim Linezolid
69
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
70
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
71
What virus enters the cell via integrins?
HSV
72
What virus enters the cell via sialylated glycans (SA)?
Enterovirus
73
What virus enters the cell via cell adhesion molecules on CD4?
HIV
74
What virus enters the cell via ACE2?
COVID
75
Virulence proteins in rotavirus?
NSP1 protein = interferon antagonist NSP4 protein =enterotoxin/viral replication.
76
Risk of intussuception post rotavirus vaccination?
1 in 20-100,000
77
TORCH infection MOST LIKELY to have hearing loss?
Rubella 90% CMV 35% (but more common)
78
TORCH infection MOST LIKELY to have retinopathy?
Toxoplasmosis
79
TORCH infection MOST LIKELY to have hydrocephalus?
Toxoplasmosis
80
TORCH infection MOST LIKELY to have microcephaly?
CMV Zika virus
81
TORCH infection MOST LIKELY to have intracranial calcifications?
Toxoplasmosis Zika virus CMV
82
TORCH infection MOST LIKELY to have hepatosplenomegaly?
Most - Rubella - CMV - Syphillis - Toxoplasmosis less common
83
TORCH infection MOST LIKELY to have cardiac defects?
Rubella
84
Congenital Rubella Sx
Cardiac defects SNHL/deafness HSM Cataracts +/- retinopathy, microcephaly, calcifications (First tri)
85
CMV Sx
Microcephaly, CNS calcifications (periventricular) Immediate or delayed SNHL- 35%
86
Congenital Herpes Sx
Multi-system failure Rash Neonatal seizures Transmission greatest intrapartum if active genital lesions
87
Congenital parvovirus Sx
Hydrops, death (First tri)
88
Congenital syphillis infection
Chorioretinitis Neuro symptoms Osteochondtritis/ abnormal epiphyses Maculopapular rash and abnormal nails HSM
89
Congenital VZV Sx
Skin & muscle defects IUGR Limb abnormalities/arthrogryposis
90
Congenital Zika Sx
Microcephaly, calcifications, ID (First tri)
91
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
92
First time HSV genital infection in labour?
If early- prophylactic antivirals from 36wks, spec for active lesions Late- same as above but consider LUSCs
93
Neonatal herpes Sx
1. Skin/eyes/mouth: - Vesicular lesions or atypically pustular or bullous lesions - Corneal ulceration, keratitis Mouth: - Ulceration, palate, tongue 2. 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
94
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
95
Examples of DNA viruses
dsDNA Enveloped: HSV, EBV, VZVm hep B Non-enveloped: adenovirus, HPV ssDNA
96
Dx:
Cutaneous larva migrans
97
Dx?
Loiasis
98
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
99
Most common bacterial cause of IE?
Strep viridians >90% - Enterococcus & staph aureus Increase in HACEK organisms – Haemophilus, Actinobacillus, Cardiobacterium, Eikenella and Kingella
100
Stages of trachoma?
101
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
102
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
103
Prevention of malaria
Avoidance - Nets, sprays, clothing Meds - AP (malarone) - Mefloquine - Doxycycline >8yrs Note – sickle erythrocytes, HbF and ovalocytes are resistant to plasmodium falciparum
104
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
105
What is the most common AIDS defining illness?
PJP- 50% of cases - Low grade fever/^RR - Bilat perihilar interstital infiltrates on CXR
106
Prophylaxis for HIV exposed neonate?
Zidovudine - reverse transcriptase inhibitor + 2x other agents
107
Medications used to treat HIV
1. Reverse transcriptase inhibitors - Zudovudine - Lactic acidosis, hepatic steatosis, lipodystrophy 2. Protease inhibitors - Ritonavir, tipranivir - High BSL/TG, lipdystrophy 3. Fusion/CCR4 blockers - Entuvirtide (blocks GP1) - Maraviroc (blocks CCR4) 4. Integrase i nhibitors - Raltegavir- GI upset/LFT derangement
108
Vector for schistosomiasis
Infection with blood fluke Carried by aquatic snails Haematuria Increased risk of bladder Ca/anaemia Rx: praziquantel
109
Vector for Onchocerciasis
Black flies - endemic in Sub-Saharan Africa Rx: Ivermectin
110
Hep B serology: HbsAg + Anti HbS & HbC -
1) acute early infection 2) transient positivity post vaccine (18-52d)
111
Hep B serology: HbsAg - Anti HbS + HbC + - IgM -
Previous infection
112
Hep B serology: HbsAg + Anti HbS - HbC + - IgM -
Chronic HB+BV
112
Hep B serology: HbsAg - Anti HbS + HbC - - IgM -
Previous immunisation
113
Hep B serology: HbsAg + Anti HbS - HbC + -IgM +
Acute HBV
114
Hep B serology: HbsAg - Anti HbS +/- HbC + -IgM +
Acute HBV which is resolving
115
Hep B serology: HbsAg - Anti HbS +/- HbC + -IgM +
Acute HBV which is resolving
116
Urease positive organisms (PUNCH)
Proteus Ureaplasma Nocardia Cryptococcus (fungus) H.Pylori
117
Encapsulated organisms (SHINE SKiS)
Strep Pneumoniae H.Influenzae Neisseria Meningitides E.Coli Salmonella Klebsiella GBS
118
Catalase positive (CATS BeeN PLACES)
Candida (fungus) Aspergillus (fungus) T
119
Catalase positive (CATS BeeN PLACES)
Cat(alase) B.Cepacia Nocardia Pseudomonas Listeria Aspergillus (fungus) Candida (fungus) E.Coli Staph/Serratia
120
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
121
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
FRACP 2023 Cram Homicrons Edition
flashcards
Decks in class (29)
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