CNS infections, HIV, tickborne illnesses Flashcards
most common CNS infection
meningitis
CNS infection involving parenchyma
encephalitis
very severe meningitis that may also involve parenchyma
meningoencephalitis
CNS infections (6)
meningitis, encephalitis, meningoencephalitis, brain abscess, subdural/epidural abscess, spinal canal abscess
acute neurologic disorders
focal: vascular (arterial or venous), traumatic
non-focal: meningitis (bacterial), toxic/metabolic
subacute neuro disorders (days)
focal: vascular (venous, brain abscess, spinal abscess, traumatic
non-focal: meningitis (bacterial or viral), encephalitis, autoimmune, toxic/metabolic
chronic (wks-months) neuro disorders
focal: brain abscess, tumor
non-focal: degenerative, toxic/metabolic
type of meningitis with most acute presentation
bacterial meningitis
time course for encephalitis
subacute (days)
meds that can cross the BBB in presence of inflammation
- penicillins
- 3rd/4th generation cephalosporins
- vancomycin
BBB function and integrity can be affected by:
- LPS
- multiple cytokines
3 major routes of infection:
- hematogenous
- contiguous
- ascending
majority of community-onset bacterial CNS infections
hematogenous
direct extension from neighboring anatomical sites
contiguous
typical route of infection for HSV or other virus
ascending
encapsulated organisms
Neisseria meningitidis, streptococcus pneumoniae, haemophilus influenzae, cryptococcus neoformans
Intracellular organisms
Listeria monocytogenes, enterovirus group, arbovirus group
organisms in systemic infections > CNS
staph aureus, HIV, Group B strep, mycobacterium tuberculosis
symptoms are caused by:
- increased P in intracranial/spinal canal space
- direct injury to nerve tissues
- inflammation
systemic signs, neck stiffness, Kernig’s sign/Brudzinski’s sign are all signs of:
inflammation
focal neuro deficit, seizure are signs of:
direct injury to nerve tissues
headache/back pain, altered mental status, visual disturbance are signs of:
increased P in intracranial/spinal canal space
lifting leg is
Kernig’s sign
lifting head and following lifting of knees is
Brudzinski’s sign
Question to ask all of the time:
Am I missing Bacterial meningitis??!!
nuchal rigidity, Kernig/Brudzinski signs, jolt accentuation are signs for
meningeal irritation
bulging of anterior fontanelle in infant & papilledema signify
intracranial HTN
‘Do Not Miss’ physical exam findings for CNS infection
meningeal irritation, intracranial hypertension, focal neurologic sign
single most important diagnostic test for meningitis
lumbar puncture
routine CSF tests to order
opening pressure; cell count with diff; glucose; total protein; gram stain; bacterial cultre
extra CSF tests
AFB smear/culture; fungal smear/culture; cryptococcal antigen; cytology; PCR of specific organism (HSV, enterovirus, tb)
when to administer antibiotics for suspected bacterial meningitis?
after PE, basic labs, blood culture and possibly 1 LP attempt; (if cannot get LP on first try or if need CT before LP, begin antibiotics immediately)
last resort diagnostic procedure for suspected CNS infection
brain/meningeal biopsy
major bacterial pathogens of meningitis:
strep pneumoniae, neisseria meningitidis, H influenzae, listeria monocytogenes, GBS, e coli
major viral pathogens of meningitis
HSV, enterovirus, arvovirus
fungal and Tb meningitis
cryptococcus neoformans, mycobacterium tb
classic triad for meningitis disease recognition:
nuchal rigidity, fever, altered mental status (at least 2 >95% frequency); vomiting and headache are other sign/symptoms
neonatal meningitis signs/symptoms
septic; consider meningitis for any febrile illness in newborn; body temp alteration (typically hyothermia), seizure, bulging fontanelle, nuchal rigidity, poor feeding
WBC count: 3000, mainly neutrophils,
bacterial meningitis
WBC count: 800, mainly mononuclear cells, glucose 50, protein 100
viral meningitis
meningitis patient presenting in august has a high likelihood of being caused by:
enteroviral meningitis
newborn meningitis micro:
group B strep, e. coli, listeria
microbio most common for 2-50 y.o. meningitis
s. pneumoniae, n. meningitidis
aerobic GNR can cause meningitis in what population
immune suppressed, elderly, neurosurgery patients
administration of meds
IV (can’t get into CNS with lower levels)
adjunctive therapy
steroids (decrease inflammation reaction in CSF)
> 80% encephalitis is caused by
idiopathic
most common known pathogens of encephalitis
viral: HSV, VZV, HHV6/7, arboviruses
bacterial causes of encephalitis
N. meningitidis (meningoenceph); l. monocytogenes (pure enceph)
“treatable” encephatlitis
HSV encephalitis
gold standard for HSV encephalitis diagnosis
HSV PCR on CSF (very sensitive and specific)
HSV encephalitis management
high-dose acyclovir; start immediately for suspected encephalitis
imaging for brain abscesss
CT w contrast; MRI gadolinium-enhanced T1 or diffusion-weighted image
severe sepsis
sepsis + hypoperfusion, hypotension (SBP
septic shock
severe sepsis + 1 of following:
ongoing hypotension despite volume resuscitation; need for vasopressors to maintain BP
refractory septic shock
hypotension despite vasopressor use
anti-inflammatory mediators in sepsis ‘cytokine storm’
IL-10, cortisol
pro-inflammatory mediators in sepsis ‘cytokine storm’
TNF-alpha, IL-6, IL-1Beta, C5a
what are mechanisms behind organ failure in sepsis?
- hypoperfusion
- coagulopathy
- programmed cell death/apoptosis
- oxygen utilization/metabolism
warm shock
early, increased CO can still compensate for decreased peripheral VR; bounding pulses; warm flushed skin; cap refill
cold shock
later; CO cannot compensate for decreased peripheral VR; weak pulses, cold clammy skin; cap refill delayed; low ScvO2
why patients with warm shock demonstrate perfusion of skin despite hypoperfusion to vital organs
redistributive shock
elevated lactate is a sign of
anaerobic respiration, often result of hypoperfusion
types of shock
cardiogenic, hypovolemic, redistributive (sepsis)
coagulopathy at IV sites, elevated glucose, elevated lactate are examples of:
organ failure in sepsis
Management of sepsis (2 interventions):
- Source control - treat infection appropriately and immediately (antibiotics, surgical therapy or complete drainage of pus)
- institute resuscitation to optimize tissue perfusion IMMEDIATELY; vasopressors if needed
staph epidermidis signifies:
likely contaminant
staph aureus likely signifies ____ bacteremia
continuous
minimize false negatives when diagnosing bacteremia with blood cultures by:
obtaining cultures prior to starting antibiotics
minimize false positives by:
proper technique/skin antiseptic prior to draw; avoid drawing cultures through intravascular cath (one set should be via direct venipuncture site); >1 bl culture set
examples of continuous bacteremia (endovascular)
- endocarditis 2. infection of vascular graft
bacteria that have surface proteins making adhere to host proteins
staph and strep
bacteria not common in endocarditis due to lack of adherence abilities
e. coli; very common bacteremia but not endocarditis
cause of 32% of IE
staph aureus
main bacteria in IVDU IE
60-70% staph aureus; 15-20% strep and enterococci; likely multiple organisms
splinter hemorrhages indicative of:
endocarditis
Osler’s nodes
painful, late stage endocarditis
Janeway lesions
painless, flat, endocarditis
RNA + HIV test means
acute HIV infection; initiate care
if RNA - HIV test,
initial serologic assay was false +
HIV 1/2 immunoassay is positive, then do ___
HIV-1/HIV-2 differentiation immunoassay
if differentiation immunoassay is HIV-1 and HIV-2 negative, then do ___
HIV RNA
time from HIV infection to clinical AIDS without effective therapy:
9.8 years
CD4 count of direct HIV symptoms (PCP/PJP)
> 500 cells/mm3
toxo, histo, MAI, CMV CD4 count
thrush, zoster CD4 count
200-500; infections associated with mild-moderate immune defects
skin conditions in HIV infected patients are related to:
CD4 count (seborrheic dermatitis ~600, herpes zoster ~500; eosinophilic folliculitis
common manifestations when CD4 > 500 cells/mm3
primary HIV infection (acute HIV, HIV mono); PGL; aseptic meningitis; HIV CNS disease; ITP; depression
signs and symptoms seen when CD4 > 500 are due to:
HIV infection itself (not immunosuppression)
when are HIV levels the highest?
acute IV infection
T or F: HIV antibody wil be + in HIV mono
F: HIV antibody testing is usually negative in early HIV mono; may need RNA levels
primary HIV infection
HIV-mono, acute HIV; presents 1-12 weeks post-exposure and lasts 1-8 weeks
signs/symptoms of acute HIV infection:
non-specific, flu-like, mono symptoms, derm
CD4 count of infections related to impaired immune surveillance, not life threatening, respond to therapy
200-500
community acquired pneumonia, oral hairy leukoplakia, seborrheic dermatitis, oral/vaginal candidiasis, recurrent oral/genital HSV, shingles, NH lymphoma, sarcoma, TB
common manifestations of CD4 200-500
oral hairy leukoplakia CD4 level
doesn’t come off; 200-500
oral candidiasis (thrush)
comes off in chunks; 200-500 CD4 level
pneumocystitis carinii pneumonia, cryptosporidium parvum
CD4 100-200
CD4
toxoplasmosis, cryptococcus, CMV (
CDC definition of AIDS
CD4
cotton wool spot in retina, retinitis in HIV/AIDS patients, likely caused by ____
CMV/ Cd4 likely
ketchup on scrambled eggs
CMV; (retina with hemorrhage along blood vessels and inflammation)
severe IRIS therapy
stop ART and begin steroids; (Immune reconstitution inflammatory syndrome)
IRIS is associated with:
low CD4, unrecognized OI, high microbial burden, starting HAART close to OI therapy; local and systemic inflammation may occur
HIV infection clinical category A
mono-asymptommatic-PGL
HIV infection clinical category B
symptommatic
HIV infection clinical category C
AIDS indicators
OI
PCP, toxoplasmosis, HPV, HSV, VZV, CMV; in most people, reactivate due to immunosuppression
best predictor of rate of HIV clinical disease
HIV viral load; (better than CD4 count)
predictor of CD4 decline
VL
antiretroviral drug classes (4):
RT inhibitors (NRTI, NNRTI); protease inhibitor; integrase inhibitor; fusion and entry inhibitor
disease from Borrelia burgdorferi
Lyme disease
disease from Babesia microti
babesiosis
disease from anaplasma phagocytophilum
granulocytic anaplasmosis
disease from ehrlichia chaffeensis
monocytic ehrlichiosis
disease from rickettsia rickettsii
rocky mountain spotted fever
associated with deer ticks, rash erythema chronicum migrans (ECM), most common tickborne infection in US
Lyme Disease (spirochete Borrelia burgdorferi)
tickborne disease prevalent on western coast and E/SE US + Wisconsin/minnesota
Lyme disease
Lyme disease tick on West coast
Western blacklegged tick (ixodes pacificus)
Geographic location for deer tick (ixodes scapularis)
east/se USA/wisconsin/minnesota
Lyme disease vector
nymph
Borrelia burgdorferi transmission (vector)
ixodes scapularis nympths = majority; ixodes pacificus
primary reservoir for borrelia burgdorferi
small rodents
3 sites of dissemination in secondary stage of lyme disease
1)dermatologic; 2) cardiac (AV conduction abn) 3)neurologic (Bell’s palsy, aseptic meningitis)
migratory, regcurrent oligoarticular arthritis in knee or confusion and peripheral neuropathy indicate
tertiary stage of lyme disease
oral drug for lyme disease
doxycycline; amoxicillin, cefuroxime
IV drug for lyme disease
ceftriaxone
ixodes scapularis is vector for:
lyme disease and babesiosis and ehrlichiosis
protozoal parasite of RBC
babesiosis (babesis microti)
Treatment for babesiosis
Azithromycin + atovaquone; or Quinine + clindamycin
diagnosis of babesiosis
PCR or blood smear
organism and vector that cause HGA
organism: ixodes tick
vector: anaplasma phagocytophilum
have intracellular rickettsi-like organisms infecting WBC
anaplasmosis, ehrlichiosis
organism and vector that cause HME
organism: ehrlichia chaffeensis (arkansas) (lone star tick): SE USA
vector: ambylomma americanum
incidence of HGA is highest in what parts of USA
same as Lyme, babesiosis (western coast, e, s/e USA)
incidence of HME is highest in what parts of USA:
SE
leukopenia, increased bands, thrombocytopenia, increased LFTs, possibly morulae indicate:
ehrlichiosis, anaplasmosis
indications for doxycycline:
lyme disease, ehrlichiosis, anaplasmosis, RMSF
RMSF organism and vector:
organism: rickettsia rickettsii
vector: dermacentor variabilis-dog tick & dermacentor andersoni-wood tick
RMSF populations:
kids
pathogenesis of RMSF can lead to:
organ failure (endothelial dysfunction>extravasation>clotting factor activation; poor perfusion, edema, organ failure
periorbital edema may indcate
RMSF (early)
only tickborne illness where doxy is not indicated
babesiosis
clinically diagnosed tickborne illness that does not require further testing
Lyme disease
ixodes scapularis can transmit what organisms?
Borrelia burgdorferi, anaplasma phagocytophilum, babesia microti
febrile + Bell’s palsy + tick bite
Lyme disease (disseminated, 2nd stage)
