Microbiology - Phase B - Second Term - half-assed job of second half
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. What would you like to do?
What three drugs can you use to treat HSV?
Oral acyclovir, famciclovir, valacyclovir
the last two are prodrugs of the first
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
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
Best way to test for HSV?
Take a swab of the lesion and send for PCR
If a mother tested positive for active HSV when in labour, what would you do?
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.
When can you give VariZig in a VZV infection?
Within 96 hours of exposure to VZV
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
How would you differentiate periorbital (preseptal) from orbital (postseptal) cellulitis?
Orbital has: proptosis, impaired EOM, and impaired vision
Classic triad of brain abscesses
headache, fever, focal neurological deficits
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.
first line treatment for meningococcus?
If you see a petichial rash, which type of meningitis would this make you think of?
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
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.
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
Common neonate and adult bacteria that cause meningitis
- neonate: GBS, E. Coli, Listeria
- adult: S. pneumoniaea, Neiserria meningitidis (meningococcal), Listeria
Meningitis empiric treatment for:
-neonates (<1 mo)
- neonates: ampicillin+cefotaxime
- adults: vanco+ceftriaxone
Two most common pathogens in skin and soft tissue infections
GAS and staph. aureus
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
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
What is usually responsible for folliculitis/furuncle/carbuncle
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
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)
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!!!!
TMT of clostridial soft tissue infections
pen G and clindamycin
What are the red flags that would make you suspect a serious soft tissue infection (9)
- -pain out of proportion
- -systemic toxicity
- -multicolored lesions
- -skin necrosis
- -areas of numbness and crepitus
- -dishwater pus, foul smelling
- -RF's: diabetes, devitalized tissues
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)
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
What is the best diagnostic test for OM
technitium bone scan
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
What is the general treatment of OM?
surgical drainage and Abx treatment according to the gram stain
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
What usually causes non-gonococcal arthritis?
S. aureus (60%); Strep (15%); pneumococcus (5%)
What would you expect to see on a synovial fluid aspirate in septic arthritis?
elevated WBC's; elevated protein; decreased blood glucose
What do you usually see in people with reversible pulpitis?
intermittent pain that can be elicited by thermal changes (cold drink)
At what age should parents introduce tooth brushing with a low fluoride toothpaste?
What can pulpitis progress to? When do you need to give Abx before a referral? what types?
Give Abx if cellulitis is present. Give amox/clav or clindamycin
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)
What cardiovascular diseases are associated with periodontal disease?
Define gingivitis and periodontitis
gingivitis: inflammation of gums without loss of supportive bone
Periodontitis: loss of supportive bone due to gingivitis
How do you treat gingivitis? peridontitis?
ging: Chlorhexidine, or a mouth wash
periodontitis: mechanical debridement, if this fails then use doxycycline or metronidazole
List some common pathogens in cystitis
- SEEKS PP mnemonic
- Staph. saprophyticus
- E coli
- Proteus Mirabilis
What are three common treatments for uncomplicated UTI's
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)
Pyuria is considered how many WBC's on microscopy?
Someone comes in with burning on urination, other than testing for a UTI, what would you do?
Test for STI
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
What are the indications for doing microscopic urinalysis?
- leuk esterase is ++ or more
- protein is ++ or more
- hemoglobin is ++ or more
How do you treat chlamlydia and gonorrhea?
ceftriaxone and azithromycin
Describe the clinical picture for pyelonephritis
- -fever and chills
- -flank pain (CVA tenderness)
- -frequency and urgency
What is the most common serious medical complication in pregnancy?
How do you treat and E. Coli renal abscess?
ceftriaxone and ciprofloxacin
What would make a UTI "complicated" (5)?
- -renal problems
What two groups SHOULD receive tmt for asymp. bacteruria?
- -pregnant women (prevent pyelonephritis)
- -people about to undergo an invasive urologic investigation
When is an infection considered nosocomial (time line)?
Sx onset 72 hours after admission OR 5 days after discharge
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
What is the most common nosocomial infection?
Why do you not want to treat asymp. bacteriuria?
only leads to more CAB, with more resistant organisms. DOES NOT PREVENT INFECTION!
Three main modifiable RF's for CAUTI
- -prolonged cath
- -disconnection of drainage system
- -poorly trained inserter
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
What is the most common nosocomial blood stream pathogen?
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
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)
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
Most common cause of viral conjunctavitis? What is usually associated with it
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
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!
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
What are the key risk factors for fungal keratitis (4)?
- -steroid eye drops
- -contact with organic matter (farmers)
- -use of soft contact lenses
Main causes of meningitis in children (6mo - 6 years)
- S. pneumoniae
- H. influenzae
- Neiseria menigitides (outbreaks)
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
What are some of the complications in orbital cellulitis (4)?
- -subperiosteal abscess
- -cavernous sinus thrombosis
- -meningitis/brain abscess
- -ischemic retinopathy
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
What is the most common culprit and clinical signs (5) of endophthalmitis?
- -eye pain/photophobia, decreased visual acuity, conj. injection, corneal edema/opafication, hypopyon (pus in anterior chamber)
How do you treat endophthalmitis?
- -urgent referral!
- -blood cultures to see if there is sepsis
- -empiric Abx
Most common causes of retinitis in
1) immunocomp (3)
2) normal (3)
- 1) CMV, herpes viruses, toxoplasma
- 2) TB, syphillis, toxoplasma
three most common causes of meningitis in neonates
how would you differentiate aseptic meningitis from encephalitis?
encephalitis: decreased LOC, altered cerebral status (focal findings, behavior, personality changes)
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
What are the most common pathogens in a brain abscess (2)?
- aerobic gram positive cocci (both staph and strep species)
In an immunocompromised host, what are three common causes of brain abscess?
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
Why can cranial neuropathies happen in both meningitis/cerebritis and brain abscesses?
- meningitis/cerebritis: inflammation of SA space
- brain abscess: increased ICP
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
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
What are five common Sx you will see with someone with meningitis?
fever, headache, nuchal rigidity, N/V, photophobia
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
4 most common causes of meningitis in an adult (6-60)
- S. pneumoniae
- N. meningitides
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
4 Sx that can help you differentiate encephalitis from encephalopathy
encephalitis often has: fever, headache, focal signs
encephalopathy often has: progressive decrease in LOC
five Sx of HSV encephalitis
Fever, headache, physchiatric Sx, Seizures, vomiting
If you see a ring-enhancing lesion in the brain of an immunocompromised patient, what do you think it is.
Tmt for candidemia in:
- non-neut: fluconazole, enchinocandin
- neutropenic: lipid amp B (need something fungicidal), enchinocandin
What does it mean when a yeast is "germ tube +ve"?
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?
-higher flucanazole treatments with intravitreal amp B shots if that doesn't help
What type of meningitis is common in aids patients?
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
- 1. recent neutropenia (>10 days)
- 2. recent allo SCT
- 3. immunosuppressants
- 4. inherited immunodeficiency
- Clinical1. dense lesions on CT +/- halo sign, air crescent sign, cavity
- 1. direct test (culture)
- 2. Indirect test: galactomannan (cell wall component in aspergilliosis) or beta-glucan antigen in plasma
What is first line treatment for someone with aspergillioses
- IV voriconazole for most patients
- liposomal AMP-B for some patients
How does Amp B work?
binds to ergosterol on the fungal cell membrane and causes holes
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
what is the first line treatment for candidiasis?
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
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
How do you treat Infectious Mononucleosis?
- -supportive tmt,
- -add steroids if there is resp compromise due to enlarged tonsils, hematological complications, neurological complications
Describe the heme and neuro complications of patients with infectious mononucleosis
- Heme: hemolytic anemia, splenic rupture, aplastic anemia, cytopenias
- Neuro: meningitis, encephalitis
Risk Factors for CMV infection (2)
- -premature infant
How do you get EBV and CMV (6)?
- Horizontal transmission:
- -sexual secretions
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
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
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)
What is the clinical picture for congenital CMV (5)?
- -cerebral palsy
- -dev. delay
- -sensoryneuro hearing loss
7 clinical syndromes for HSV
- Oro-facial HSV
- genital disease
- neonatal HSV
- CNS disease (encephalitis and meningitis)
- HSV keratitis
- disseminated infection
- dermatologic disease
What do you see in primary HSV oro-facial disease. What about secondary (recurrent) disease
- -gingivostomatitis: oropharyngeal vesicles, cervical adenopathy
- -cold sores (remember that you want to treat during the prodrome)
Clinical manifestations of neonatal HSV (3)
- 1) 1/3 skin, eye, and mouth disease
- 2) 1/3 CNS disease
- 3) 1/3 disseminated disease
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
What would you use for recurrent HSV prophylaxis? When (5 indications)?
- what: acyclovir, valacyclovir, famciclovir (last two are prodrugs of acyclovir)
- ->6 recurrences/year
- -systemic complications
- -affect job performance
- -discordant couples with HSV2
How is VZV transmitted
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)
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
When do you give VariZIG to someone that is exposed? (5)
- -within 96 hours of contact
- -newborns if mothers develop chickenpox around time of delivery
- -premature babies
Usually you cannot give the varicella vaccine (live attenuated) in immunocompromised persons. What are the two exceptions to this rule?
When do you give the zoster vaccine?
- -in healthy people greater than 60
- - do not use in immunocompromised people (live virus)
If you see red, rapidly growing streaks in someones skin what should you be thinking
cutaneous lava migrans
If someone has "resistant scabies" what do they usually have?
-poor adherance to the treatment regimen-poor treatment of close contacts
What pharm tmt can be used both for scabies and lice
Describe where the following fall on the bacterial flow chart in T. Notes:
viridens group strep
- 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
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)
Definition of AIDS (3)
- 1) HIV +ve plus CD4 < 200
- 2) HIV plus indicator diseases
- 3) HIV status unknown plus more specific indicator diseases
What is the greatest risk in transmission of HIV?
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
How to test for HIV?
- 1) EIA: detects IgG abs
- 2) if positive, confirm with western blot
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)
Describe the "cascade of care" plot
4 considerations when choosing an antiretroviral regimen
- 1) liklihood of adherence
- 2) tolerability
- 3) Drug-drug interactions
- 4) long-term and short term toxicities
Who should be given HAART?
Any HIV positive patient who wants it.
3 correlations in OI's
- correlated with
- 1) CD4 counts
- 2) geographic location
- 3) treatment status
3 aids defining malignancies
- -kaposi's sarcoma (HHV8)
- -NHL (EBV)
- -cervial cancer (HPV)
If you see a white plaque on the side of the tongue and the buccal mucosa what should you be thinking?
oral hairy leukoplakia
Most common cause of dysphagia in HIV patients
What is a severe and potentially life threatening fatal complication of NRTI treatment of HIV?
lactic acidosis (severe diarrhea can occur)
what is the single most common cause of symptomatic pancreatitis in HIV infected patients?
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
Worldwide, what is the most common and most deadly OI in HIV?
In saskatchewan, what is the most likely mode of HIV transmission in
- 1) IVDU
- 2) secondary to infected mother
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
Should you give live attenuated MMR and varicella vaccines in HIV positive kids?
yes, benefits outweigh the risks
When do you start primary prophylaxis in HIV patients (for what?) when do you stop prophylaxis?
- 1) CD4<200 - PJP (PCP)
- 2) CD4<100 - toxoplasma encephalitis
- 3) CD4 < 50 - disseminated MAC
stop ALL of these when CD4 > 200
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
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
3 important parisotologic concepts pertaining to helminth infections
- 1) Migration
- 2) worm burden
- 3) autoinfection
How do you get toxoplasma? (3)
- 1) cat's poop
- 2) blood transfusion
- 3) steak tartare
What must you rule out in a traveller that comes back with a fever? A key finding
MALARIA!! a key finding is thrombocytopenia
If someone has a travel history and a non-healing ulcer, what should you be thinking of?
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
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)
If you see eosinophilia, what should you look for?
TISSUE INVASIVE helminths
What is the criteria for SIRS (systemic inflammatory response syndrome) (4)
- T<36 or T>38
- WBC < 4 or >12; or 10% bands
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
3 specific therapies that reduce mortality
- -early goal directed therapy
- -early Abx therapy
- -lung protection/ventilation therapy
How do you treat dermatophytes?
azoles are first line oral and systemic (tinea capitus and nail probs) treatments
How to treat onychomycosis (2)
If you are considering an invasive bacterial infection and cannot test the relavent site. What should you ALWAYS do?
get blood cultures
Why combine abx? (3)
- 1) broaden spectrum of activity
- 2) prevent emergence of resistance
- 3) additive or synergistic effects
Describe the major classes of drugs and where they act
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
What are 4 abx you do NOT need to give intravenously
fluoroquinolones, clindamycin, septra, metronidazole
What would you like to do?
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