Microbiology - Phase B - Second Term - half-assed job of second half

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Microbiology - Phase B - Second Term - half-assed job of second half
2014-05-29 18:22:35
Microbiology Phase Second Term 1st Half

Microbiology - Phase B - Second Term - 1st Half
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  1. What three drugs can you use to treat HSV?
    Oral acyclovir, famciclovir, valacyclovir

    the last two are prodrugs of the first
  2. Which of the HSV is sexually transmitted? Which one affects the face and which one affects the genitals
    HSV-2 is sexually transmitted

    HSV - 1 for the face and HSV-2 is more common in the genitals
  3. What is the ideal way to treat HSV-1 in someone with a recurrent infection?
    Get them to start taking acyclovir as soon as they feel the prodrome coming on
  4. Best way to test for HSV?
    Take a swab of the lesion and send for PCR
  5. If a mother tested positive for active HSV when in labour, what would you do?
    Caesarean Section
  6. A baby is born to a mom with HSV1, how to you treat baby?
    Send a serum HSV PCR and if it come back positive, start treating with po acyclovir immediately.
  7. When can you give VariZig in a VZV infection?
    Within 96 hours of exposure to VZV
  8. What is a good test to differentiate EBV from CMV
    Monospot test is positive for EBV, not for CMV. Otherwise these two look very similar
  9. How would you differentiate periorbital (preseptal) from orbital (postseptal) cellulitis?
    Orbital has: proptosis, impaired EOM, and impaired vision
  10. Classic triad of brain abscesses
    headache, fever, focal neurological deficits
  11. What are the three PE tests you would use for meningitis? Explain
    • Kernigs: bend knee up towards chest, does the patient flinch?
    • Brudzinski's: bend chin to chest, knees will jerk up to compensate
    • jolt test: headache worse when you shake your head.
  12. first line treatment for meningococcus?
  13. If you see a petichial rash, which type of meningitis would this make you think of?
    Neisseria menintides
  14. With regards to WBC#, WBC type, glucose, and protein. What CSF results would you expect to see for bacterial, TB (or fungal), viral, and brain abscesses
  15. You suspect a patient has HSV encephalitis. How would you confirm this (3) and how would you treat? Why is it important to diagnose this?
    Confirm with a LP and PCR for HSV; look for RBCs in CSF; also do an EEG or CT and look for temporal lobe involvement. Treat with IV acyclovir AS SOON AS YOU SUSPECT it is HSV encephalitis. Important to diagnose this because it is treatable.
  16. With regards to time course and severity, what is the difference between epidural and subdural abscesses?
    • epidural: slow
    • subdural: quick and is a surgical emergency
  17. Common neonate and adult bacteria that cause meningitis
    • neonate: GBS, E. Coli, Listeria
    • adult: S. pneumoniaea, Neiserria meningitidis (meningococcal), Listeria
  18. Meningitis empiric treatment for:
    -neonates (<1 mo)
    -and adults
    • neonates: ampicillin+cefotaxime
    • adults: vanco+ceftriaxone
  19. Two most common pathogens in skin and soft tissue infections
    GAS and staph. aureus
  20. What is the main/co-infection seen in impetigo? How do you treat?
    Usually caused by group A strep/Staph aureus. Treat with mupirocin ointment, amox/clavinuluate
  21. How is TEN/SJS different from SSSS?
    TEN/SJS usually in adults and caused by drug hypersens. SSSS usually in kids<6 and due to staph. aureus
  22. What is usually responsible for folliculitis/furuncle/carbuncle
    Staph Aureus
  23. How would you differentiate cellulitis from erysipelas? How does TMT differ?
    • For erysipelas:
    • organism: GAS
    • depth: dermis and lymph
    • Lesion morph: long and narrow (follow lymphatics)
    • Borders: sharp
    • Colour: bright red erythema
    • Peau d'orange present
    • TMT: penicillin or clindamycin

    • For Cellulitis:
    • Organism responsible: GAS and staph
    • depth: dermis and subcut. fat
    • lesion morph: circular
    • borders: hazy
    • Colour: pink
    • No peau d'orange
    • TMT: cloxacillin or cefazolin
  24. How would you differentiate type I and II Necrotizing Fasciitis? difference in Abx
    • Type I:
    • Flora: anaerobes and facultative anaerobes (mostly GNB)
    • Progression: rapid
    • Crepitus: 25%
    • Abx: pip/tazo

    • Type II:
    • Flora: mostly GAS
    • Progression: very rapid
    • Crepitus: absent
    • Abx: clindamycin (static) THEN penicillin (-cidal)
  25. What are the slam dunk things you would see in a patient with necrotizing fasciitis? What is the first thing you should do with a patient that shows up with these?
    crepitus, pain out of proportion, HIGH FEVER, point of entry. SURGICAL DEBRIDEMENT!!!!
  26. TMT of clostridial soft tissue infections
    surgical debridement

    pen G and clindamycin
  27. What are the red flags that would make you suspect a serious soft tissue infection (9)
    • -pain out of proportion
    • -rapid
    • -systemic toxicity
    • -multicolored lesions
    • -bullae
    • -skin necrosis
    • -areas of numbness and crepitus
    • -dishwater pus, foul smelling
    • -RF's: diabetes, devitalized tissues
  28. What organism is responsible for hematogenously spread OM? Where is it seen? Who gets it
    • Staph Aureus
    • Location: metaphyses of long bones (children); vertebral bodies (IVDU's)
  29. What are the three etiologies of OM? Who gets each? What is primarily responsible for each?
    • 1. Acute hematogenous: children and IVDUs
    • 2. secondary to contiguous infection: adults with recent trauma or joint replacement
    • 3. Vascular insufficiency: adults 50+ with diabetes or peripheral vascular disease.

    Staph aureus for first two. 3 usually is polymicrobial
  30. What is the best diagnostic test for OM
    technitium bone scan
  31. List 6 classic associations in OM (insult->bug)
    • 1. IVDU > sternoclavicular osteo (s. aureus)
    • 2. foot puncture-> pseudomonas
    • 3. foreign bodies-> CONS (S. epidermidis)
    • 4. sickle cell anemia -> salmonella
    • 5. Animal bites -> Pasturella multocida
    • 6. human bites -> mixed, including anaerobes
  32. What is the general treatment of OM?
    surgical drainage and Abx treatment according to the gram stain
  33. How do you differentiate gonococcal from non-gonococcal septic arthritis
    Gonococcal: 15-35, migratory, tenosynovitis, petichiae or purpura, usually elevated WBCs

    Nongonococcal: older, monoarticular, usually knee, LOTS of WBC's, no skin manifestation
  34. What usually causes non-gonococcal arthritis?
    S. aureus (60%); Strep (15%); pneumococcus (5%)
  35. What would you expect to see on a synovial fluid aspirate in septic arthritis?
    elevated WBC's; elevated protein; decreased blood glucose
  36. What do you usually see in people with reversible pulpitis?
    intermittent pain that can be elicited by thermal changes (cold drink)
  37. At what age should parents introduce tooth brushing with a low fluoride toothpaste?
    two years
  38. What can pulpitis progress to? When do you need to give Abx before a referral? what types?
    periapical abscess->cellulitis

    Give Abx if cellulitis is present. Give amox/clav or clindamycin
  39. When would you hospitalize a patient with a tooth infection and put them on IV Abx?
    facial swelling, fever, and trismus (inability to open jaw)
  40. What cardiovascular diseases are associated with periodontal disease?
    • atherosclerosis
    • endocarditis
  41. Define gingivitis and periodontitis
    gingivitis: inflammation of gums without loss of supportive bone

    Periodontitis: loss of supportive bone due to gingivitis
  42. How do you treat gingivitis? peridontitis?
    ging: Chlorhexidine, or a mouth wash

    periodontitis: mechanical debridement, if this fails then use doxycycline or metronidazole
  43. List some common pathogens in cystitis
    • SEEKS PP mnemonic
    • Staph. saprophyticus
    • E coli
    • Enterobacter
    • Klebsiella
    • Serratia
    • Pseudomonas
    • Proteus Mirabilis
  44. What are three common treatments for uncomplicated UTI's
    • TMP-SMX
    • fluoroquinolone
    • nitrofurantoin
  45. Describe what you commonly see on a UA dipstick when someone has a UTI
    • increased Leukocyte esterase (WBC marker)
    • increased nitrates (bacterial marker)
    • increased urine pH (Proteus infections)
    • hematuria (seen with cystitis)
  46. Pyuria is considered how many WBC's on microscopy?
  47. Someone comes in with burning on urination, other than testing for a UTI, what would you do?
    Test for STI
  48. What is the difference between first void and midstream urine collection?
    first void: first pee of the day, urethral contents have built up overnight

    midstream: reflects bladder contents
  49. What are the indications for doing microscopic urinalysis?
    • leuk esterase is ++ or more
    • protein is ++ or more
    • hemoglobin is ++ or more
  50. How do you treat chlamlydia and gonorrhea?
    ceftriaxone and azithromycin
  51. Describe the clinical picture for pyelonephritis
    • -fever and chills
    • -flank pain (CVA tenderness)
    • -N/V
    • -frequency and urgency
  52. What is the most common serious medical complication in pregnancy?
  53. How do you treat and E. Coli renal abscess?

    ceftriaxone and ciprofloxacin
  54. What would make a UTI "complicated" (5)?
    • -renal problems
    • -diabetes
    • -catheter
    • -pregnancy
    • -immunosuppression
  55. What two groups SHOULD receive tmt for asymp. bacteruria?
    • -pregnant women (prevent pyelonephritis)
    • -people about to undergo an invasive urologic investigation
  56. When is an infection considered nosocomial (time line)?
    Sx onset 72 hours after admission OR 5 days after discharge
  57. Define the following nosocomial infection acronyms: HAP, VAP, NHP, CAUTI, CAB, BSI, CLABSI, SSI, CDI/CDAD, ARO
    Hospital-acquired pneumonia, ventilator-acquired pneumonia, nursing home pneumonia, catheter associated UTI, catheter-associated bacteriuria, blood stream infection, central line associated BSI, surgical site infection, C diff infection/associated disease, Abx resistant organism
  58. What is the most common nosocomial infection?
  59. Why do you not want to treat asymp. bacteriuria?
    only leads to more CAB, with more resistant organisms. DOES NOT PREVENT INFECTION!
  60. Three main modifiable RF's for CAUTI
    • -prolonged cath
    • -disconnection of drainage system
    • -poorly trained inserter
  61. When is a catheter needed (6)?
    • 1) urinary retention/blockage
    • 2) need to accurately measure urine output
    • 3) Some surgery: urologic, long duration, large vol infusion
    • 4) incont patients with sacral or perianal injuries
    • 5) prolonged immobilizations
    • 6) end of life care if needed
  62. What is the most common nosocomial blood stream pathogen?
  63. Describe and differentiate catheter infections. How would you deal with each
    • 1) Exit site: localized infection, no systemic signs, DO NOTHING
    • 2) Tunnel infection: infection travels along outside of cath, erythema and tend. on line pathway, REMOVE and REPLACE at other site. Systemic Abx
    • 3) Catheter Contam: Periph blood cultures neg, cathater cultures positive, asymp., do nothing
    • 4) Cath colon: same as 3, Abx lock
    • 5) CABSI: periph and line cultures +ve, sepsis signs, IV Abx and removal (if possible), if no removal then us Abx lock
  64. List 4 common nosocomial pathogens and methods of spread?
    • 1) C. Diff: extended Abx use, wash with soap and water
    • 2) Pseudomonas: loves aqueous environments
    • 3) ARO's (MRSA, ESBL): overuse of Abx, only treat if symptomatic
    • 4) Norovirus: long term care homes usually, fecal to oral transmission (high viral load in feces)
  65. 3 general groups of causes for bacterial conj.
    • 1) skin and resp flora: staph, strep, haemophilus
    • 2) neonatal: Chlamydia and gonococcus (AN EMERGENCY!!)
    • 3) C. trochamonis - most common cause of blindness worldwide
  66. Most common cause of viral conjunctavitis? What is usually associated with it
    adenovirus, URTI
  67. With regards to Sx, discharge, follicles/papillae, tmt, and public health concerns; compare viral, bacterial, and allergic conjunct.
    • 1) viral: Sx-red, itchy; discharge-watery; follicles, supportive, droplet and contact precautions
    • 2) bacterial: morning crust and less itchy, pus, no follicles/papillae, topical Abx, contact/droplet
    • 3) allergic: itching, mucoid discharge, papillae (vasculature), mast cell stabilizer, no concerns
  68. What is the characteristic thing you see in HSV keratitis? How do you treat it? what should you NOT do?
    • -corneal dendrites under fluorescent stain
    • -antivirals (oral acyclovir, topical ganciclovir)
    • -DONT GIVE steroids until you know that the antiviral is working, otherwise the infection will TAKE OFF!
  69. When you see a patient with shingles and involvement of THIS area you should check for dendritic ulcers (note dendritic ulcers in both HSV and HZV)
    -tip of the nose for HZV
  70. What are the key risk factors for fungal keratitis (4)?
    • -steroid eye drops
    • -contact with organic matter (farmers)
    • -use of soft contact lenses
    • -immunocompromised
  71. Main causes of meningitis in children (6mo - 6 years)
    • SHEN
    • S. pneumoniae
    • H. influenzae
    • Enteroviruses
    • Neiseria menigitides (outbreaks)
  72. How do you differentiate orbital from periorbital (preseptal) cellulitis? Which one is an emergency?
    preseptal is anterior to the orbital septum

    • orbital has: proptosis, impaired EOM, and impaired vision
    • Periorbital doesn't have these

    Orbital is an emergency. it is life and vision threatening
  73. What are some of the complications in orbital cellulitis (4)?
    • -subperiosteal abscess
    • -cavernous sinus thrombosis
    • -meningitis/brain abscess
    • -ischemic retinopathy
  74. List and briefly define 4 periocular infections
    • Hordeum (stye): infected eyelash follicle (painful)
    • Chalazion: enlarged meibonian gland (painless)
    • Blepharitis: infection of eyelid margins
    • Dacrocystitis: infection of lacrimal duct area
  75. What is the most common culprit and clinical signs (5) of endophthalmitis?
    • -candida
    • -eye pain/photophobia, decreased visual acuity, conj. injection, corneal edema/opafication, hypopyon (pus in anterior chamber)
  76. How do you treat endophthalmitis?
    • -urgent referral!
    • -blood cultures to see if there is sepsis
    • -empiric Abx
  77. Most common causes of retinitis in
    1) immunocomp (3)
    2) normal (3)
    • 1) CMV, herpes viruses, toxoplasma
    • 2) TB, syphillis, toxoplasma
  78. three most common causes of meningitis in neonates
    • -GBS
    • -E. Coli
    • -Listeria
  79. how would you differentiate aseptic meningitis from encephalitis?
    encephalitis: decreased LOC, altered cerebral status (focal findings, behavior, personality changes)
  80. How would you differentiate viral and bacterial meningitis (4)?
    • -CSF: lymphocytes, normal glucose, mildly elevated protein in viral
    • -C reactive protein higher in bacterial
    • -Viral has milder Sx with slower onset
    • -viral is more in summer and fall
  81. What are the most common pathogens in a brain abscess (2)?
    • anaerobes
    • aerobic gram positive cocci (both staph and strep species)
  82. In an immunocompromised host, what are three common causes of brain abscess?
    • toxoplasma
    • cryptococcus
    • aspergillus
  83. how would you treat a brain abscess?
    • 1) surgical drainage
    • 2) get microbial Dx
    • 3) Steroids if there is decreased LOC or increased pressure (dexamethasone)
    • 4) Abx
  84. Why can cranial neuropathies happen in both meningitis/cerebritis and brain abscesses?
    • meningitis/cerebritis: inflammation of SA space
    • brain abscess: increased ICP
  85. What considerations do you need to make with regards to Drug, duration, and delivery when treating a brain abscess?
    • Drug: bacterialcidal (brain sucks at killing these on its own)
    • duration: long (the bugs have low metabolic state)
    • Delivery: high dose with good BBB penetration
  86. List six commonly used Abx used in the tmt of meningitis and what they treat
    • Penicillin: oral strep
    • metronidazole: good against anaerobes, good BBB penetration
    • Cloxacillin: MSSA
    • Vanco: MRSA (shitty BBB pen)
    • Cefotaxime/ceftriaxone: gram +ve and -ve aerobes
    • ceftazidime: pseudomonas
  87. What are five common Sx you will see with someone with meningitis?
    fever, headache, nuchal rigidity, N/V, photophobia
  88. How long before you should get Abx into a patient that you suspect has bacterial meningitis?
    20 minutes from when they come into the hospital
  89. 4 most common causes of meningitis in an adult (6-60)
    • S. pneumoniae
    • N. meningitides
    • Enteroviruses
    • HSV
  90. What empiric Abx choices would you make in a patient with meningitis that is:
    -2 month - 50
    • < 1 month: ampicillin + cefotaxime or aminoglycoside (e.g. gent.)
    • 2month - 50: Vanco + cefotaxime or ceftriaxone
    • >50: add ampicillin to the above
  91. 4 Sx that can help you differentiate encephalitis from encephalopathy
    encephalitis often has: fever, headache, focal signs

    encephalopathy often has: progressive decrease in LOC
  92. five Sx of HSV encephalitis
    Fever, headache, physchiatric Sx, Seizures, vomiting
  93. If you see a ring-enhancing lesion in the brain of an immunocompromised patient, what do you think it is.
  94. Tmt for candidemia in:
    non-neutropenic adults
    neutropenic adults
    • non-neut: fluconazole, enchinocandin
    • neutropenic: lipid amp B (need something fungicidal), enchinocandin
  95. What does it mean when a yeast is "germ tube +ve"?
    C. albicans
  96. If you see white spots on the retina of someone with candidemia, what is it? And how would you treat it initially? What if that doesn't work?
    Candida retinitis


    -higher flucanazole treatments with intravitreal amp B shots if that doesn't help
  97. What type of meningitis is common in aids patients?
  98. In order for someone to have a probable diagnosis of aspergilliosis you need one host factor (4), one clinical criterion (3), AND one mycological criterion. List them
    • HOST
    • 1. recent neutropenia (>10 days)
    • 2. recent allo SCT
    • 3. immunosuppressants
    • 4. inherited immunodeficiency

    • Clinical
    • 1. dense lesions on CT +/- halo sign, air crescent sign, cavity

    • Mycological
    • 1. direct test (culture)
    • 2. Indirect test: galactomannan (cell wall component in aspergilliosis) or beta-glucan antigen in plasma
  99. What is first line treatment for someone with aspergillioses
    • IV voriconazole for most patients
    • liposomal AMP-B for some patients
  100. How does Amp B work?
    binds to ergosterol on the fungal cell membrane and causes holes
  101. When should you use lipid AmpB?
    • 1) refractory to conventional AmpB
    • 2) patient intolerant to AmpB
    • 3) renal dysfunction
    • 4) selected difficult to treat pathologies
  102. what is the first line treatment for candidiasis?
  103. What fungal infection would you be thinking in the following scenarios:
    1)Returned from Phoenix
    2) visiting lake country of northeastern ontairo
    3) recently moved from Indiana, or from the St. Lawrence area

    Treatment for all three
    • 1) Coccidioidomycosis
    • 2) Blastomycosis
    • 3) Histoplasmosis

    Treat with an oral azole to start. Treat with IV amp B in severe disease
  104. What causes Infectious mononucleosis? What are the clinical features? best test?
    • -usually due to acute EBV infection
    • -Classic triad: fever, sore throat, and lympadenopathy
    • -additional features: lymphocytosis with atypical lymphocytes, fatigue, hepatosplenomegaly

    Best test is the monospot (heterophil) test
  105. How do you treat Infectious Mononucleosis?
    • -supportive tmt,
    • -add steroids if there is resp compromise due to enlarged tonsils, hematological complications, neurological complications
  106. Describe the heme and neuro complications of patients with infectious mononucleosis
    • Heme: hemolytic anemia, splenic rupture, aplastic anemia, cytopenias
    • Neuro: meningitis, encephalitis
  107. Risk Factors for CMV infection (2)
    • -Immunocomp
    • -premature infant
  108. How do you get EBV and CMV (6)?
    • Horizontal transmission:
    • -blood
    • -saliva
    • -urine
    • -breastmilk
    • -sexual secretions
    • -transplant
  109. What does a CMV infection look like in adults? How can you differentiate from Infectious Mononucleosis?
    Looks alot like infectious mononucleosis clinically. However, it will come up as negative on the monospot test
  110. How do you investigate for congenital CMV?
    • urine for viral culture
    • urine/saliva/serum for PCR
    • Serology: IgM - congenital infection; IgG - passive transfer from mom OR congenital infection
  111. How do you treat CMV? when to use antivirals? Which antivirals?
    • Treat the same as infectious mononucleosis (support +/- steroids)
    • use antivirals if recurrent infection or immunocomp (ganciclovir/valganciclovir)
  112. What is the clinical picture for congenital CMV (5)?
    • -microcephaly
    • -cerebral palsy
    • -dev. delay
    • -sensoryneuro hearing loss
    • -petichiae/purpura
  113. 7 clinical syndromes for HSV
    • Oro-facial HSV
    • genital disease
    • neonatal HSV
    • CNS disease (encephalitis and meningitis)
    • HSV keratitis
    • disseminated infection
    • dermatologic disease
  114. What do you see in primary HSV oro-facial disease. What about secondary (recurrent) disease
    • Primary
    • -gingivostomatitis: oropharyngeal vesicles, cervical adenopathy
    • -pharyngitis
    • -esophagitis
    • Secondary:
    • -cold sores (remember that you want to treat during the prodrome)
  115. Clinical manifestations of neonatal HSV (3)
    • 1) 1/3 skin, eye, and mouth disease
    • 2) 1/3 CNS disease
    • 3) 1/3 disseminated disease
  116. What are the 6 indications for using IV acyclovir for HSV
    • -severe disease (cannot eat or swallow)
    • -aseptic meningitis
    • -HSV encephalitis
    • -autonomic dysfunction
    • -neonatal HSV
    • -disseminated disease
  117. What would you use for recurrent HSV prophylaxis? When (5 indications)?
    • what: acyclovir, valacyclovir, famciclovir (last two are prodrugs of acyclovir)
    • Indications:
    • ->6 recurrences/year
    • -systemic complications
    • -affect job performance
    • -discordant couples with HSV2
    • -pregnancy
  118. How is VZV transmitted
    respiratory route
  119. Describe the timeline of infection for VZV
    • primary infection: chickenpox (incubation period is 10-21 days, contateous 2 days before and 5 days after appearance of rash)
    • Reactivation infection: shingles (can cause post herpetic neuralgia in old people)
  120. How do you treat VZV infection
    young, immunocompetent: supportive therapy like anthistamines, tylenol for fever, abx if secondary infection, oatmeal bath

    in pregnant women and people with shingles: give acyclovir and others from that class
  121. When do you give VariZIG to someone that is exposed? (5)
    • -within 96 hours of contact
    • -immunocompromised
    • -pregnant
    • -newborns if mothers develop chickenpox around time of delivery
    • -premature babies
  122. Usually you cannot give the varicella vaccine (live attenuated) in immunocompromised persons. What are the two exceptions to this rule?
    • ALL
    • HIV
  123. When do you give the zoster vaccine?
    • -in healthy people greater than 60
    • - do not use in immunocompromised people (live virus)
  124. If you see red, rapidly growing streaks in someones skin what should you be thinking
    cutaneous lava migrans
  125. If someone has "resistant scabies" what do they usually have?
    -poor adherance to the treatment regimen-poor treatment of close contacts
  126. What pharm tmt can be used both for scabies and lice
  127. Describe where the following fall on the bacterial flow chart in T. Notes:
    Staph aureus
    viridens group strep
    S. pyogenes
    C. botulin
    • 1) Staph aureus: gram +ve, cocci in clusters, aerobic, catalase positive, coagulase +ve
    • 2) viridens group strep: gram +ve, cooci in lines, catalase +ve, alpha hemolytic
    • 3) S. pyogenes: same as above, but beta hemolytic
    • 4) C. botulin: gram positive, bacilli, anaerobic
    • 5) Listeria: gram +ve bacilli, aerobic, box car
  128. Difference between gram +ve and -ve bacteria (4)
    • Gram -ve have:
    • -thin peptidoglycan layer
    • -no teichoic acid
    • -high lipid content, which decolourizes gram stain
    • -lots of lipopoly saccharide (lipid A is an endotoxin)
  129. Definition of AIDS (3)
    • 1) HIV +ve plus CD4 < 200
    • 2) HIV plus indicator diseases
    • 3) HIV status unknown plus more specific indicator diseases
  130. What is the greatest risk in transmission of HIV?
    viral load
  131. 4 uses of antiretrovirals to reduce HIV transmission
    • 1) pre exposure prophylaxis (PeEP)
    • 2) Post-exposure prophylaxis (PEP)
    • 3) prevention of mother to child transmission
    • 4) treatment as prevention
  132. How to test for HIV?
    • 1) EIA: detects IgG abs
    • 2) if positive, confirm with western blot
  133. Name the conditions where you need to test for HIV (because they have an AIDS prevalence of > 0.1 %) (8)
    • 1) STI's
    • 2) Unexplained fever
    • 3) Candidemia
    • 4) invasive pneumococcal disease
    • 5) Seborrheic dermatitis
    • 6) Heps B and C
    • 7) unexplained leukopenia/thrombocytopenia > 4 weeks
    • 8) Mono-like illness
    • (there are more, but these seem to be the high yield ones)
  134. Describe the "cascade of care" plot
  135. 4 considerations when choosing an antiretroviral regimen
    • 1) liklihood of adherence
    • 2) tolerability
    • 3) Drug-drug interactions
    • 4) long-term and short term toxicities
  136. Who should be given HAART?
    Any HIV positive patient who wants it.
  137. 3 correlations in OI's
    • correlated with
    • 1) CD4 counts
    • 2) geographic location
    • 3) treatment status
  138. 3 aids defining malignancies
    • -kaposi's sarcoma (HHV8)
    • -NHL (EBV)
    • -cervial cancer (HPV)
  139. If you see a white plaque on the side of the tongue and the buccal mucosa what should you be thinking?
    oral hairy leukoplakia
  140. Most common cause of dysphagia in HIV patients
    candida esophagitis
  141. What is a severe and potentially life threatening fatal complication of NRTI treatment of HIV?
    lactic acidosis (severe diarrhea can occur)
  142. what is the single most common cause of symptomatic pancreatitis in HIV infected patients?
    medication-related pancreatitis
  143. Describe the types of resp conditions you see at the following CD4 counts:
    1) < 400 (1)
    2) < 200 (2)
    3) < 50 (3)
    • 1) kaposi's sarcoma
    • 2) PJP (PCP); atypical TB
    • 3) disseminated MAC; CMV pneumonia; fungal pneumonia
  144. Worldwide, what is the most common and most deadly OI in HIV?
  145. In saskatchewan, what is the most likely mode of HIV transmission in
    1) adult
    2) child
    • 1) IVDU
    • 2) secondary to infected mother
  146. If there is an HIV positive mother, why do we use PCR to test for HIV in the first 18 months rather than serum testing?
    can get a false positive if you test serum because of maternal Abs to HIV. PCR detects true virus
  147. Should you give live attenuated MMR and varicella vaccines in HIV positive kids?
    yes, benefits outweigh the risks
  148. When do you start primary prophylaxis in HIV patients (for what?) when do you stop prophylaxis?
    • start:
    • 1) CD4<200 - PJP (PCP)
    • 2) CD4<100 - toxoplasma encephalitis
    • 3) CD4 < 50 - disseminated MAC

    stop ALL of these when CD4 > 200
  149. What are the first line drugs for the following HIV-related OI's:
    1) Pneumocystis (PCP)
    2) tocoplasma encephalitis
    3) disseminated MAC
    4) oral candidiasis
    • 1) Septra
    • 2) pyrimethamine+sulfadiazine+leucovorin
    • 3) azithromycin
    • 4) fluconazole
  150. What are the three take home points about OI's in HIV
    • 1) they are less common now that HAART is around
    • 2) common infections are still more likely that OI, but they may be presenting atypically
    • 3) need to treat the OI AND start HAART
  151. 3 important parisotologic concepts pertaining to helminth infections
    • 1) Migration
    • 2) worm burden
    • 3) autoinfection
  152. How do you get toxoplasma? (3)
    • 1) cat's poop
    • 2) blood transfusion
    • 3) steak tartare
  153. What must you rule out in a traveller that comes back with a fever? A key finding
    MALARIA!! a key finding is thrombocytopenia
  154. If someone has a travel history and a non-healing ulcer, what should you be thinking of?
  155. 3 findings that make you suspect toxocara. difference from Trichinella?
    • 1) young kid (<5) who like to play in sandbox
    • 2) eosinophilia
    • 3) loss of red reflex

    Trichinella is less common than this and affects children and adults equally
  156. What are 2 take home points on strongyloides
    • 1) most patients are asymptomatic
    • 2) infection can persist for many years because of autoinfection (some Korean war vets still have it)
  157. If you see eosinophilia, what should you look for?
    TISSUE INVASIVE helminths
  158. What is the criteria for SIRS (systemic inflammatory response syndrome) (4)
    • HR>90
    • RR>20
    • T<36 or T>38
    • WBC < 4 or >12; or 10% bands
  159. Define sepsis, severe sepsis, and septic shock
    • Sepsis: SIRS + confirmed infection
    • Severe Sepsis: Sepsis + one or more organ failures (decreased LOC, tachycard, low O2 sats, etc) but DOES respond to fluid boluses
    • Septic Shock: severe sepsis that does NOT respond to fluid boluses of crystalloid
  160. 3 specific therapies that reduce mortality
    • -early goal directed therapy
    • -early Abx therapy
    • -lung protection/ventilation therapy
  161. How do you treat dermatophytes?
    azoles are first line oral and systemic (tinea capitus and nail probs) treatments
  162. How to treat onychomycosis (2)
    • Terbinafine
    • itraconazole
  163. If you are considering an invasive bacterial infection and cannot test the relavent site. What should you ALWAYS do?
    get blood cultures
  164. Why combine abx? (3)
    • 1) broaden spectrum of activity
    • 2) prevent emergence of resistance
    • 3) additive or synergistic effects
  165. Describe the major classes of drugs and where they act
  166. describe the 4 catogories of chronic lyme disease. What is the only one that has been adequately studied?
    • Category 1: Sx of unknown cause, no Bb infection
    • Cat 2: Sx of illness other than lyme disease, no Bb infection
    • Cat 3: Sx on unknown cause, anti-Bb Abs with no objective findings of lyme disease
    • Cat 4: post lyme disease syndrome, clear Hx of previous lyme disease
  167. What are 4 abx you do NOT need to give intravenously
    fluoroquinolones, clindamycin, septra, metronidazole