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60 Cards in this Set

  • Front
  • Back
What is Nuchal rigidity?
Restriction in flexion of the neck (concern for CNS infection)
Pleocytosis
Increase cells in the CSF
AST
Liver enzyme (hepatocellular inflammation)
moreulae
Tinny inclusions within the cytoplasm of cells.
Pancytopenia
All blood cells are low
Leukopenia
Low white cells
what does a morulae in a vacule tell us?
that it is in the cytoplasm.
Which disease has central nervous system involvment? (confusion)
HME
What causes HME?
(Human Monocytic Ehrlichiosis)
Ehrlichia chafeensis
HGA
Human granulocytic anaplasmosis
What causes HGA
Anaplasma phagocytophilum
CNS involvement uncommon in
HGA
meningitis or meningoencephalitis is a neurologic manifestation of
HME (Human Monocytc Ehrlichiosis)
HEE
human ewingii ehrlichiosis
What is the target cell for
E. ewingii
Nuetrophils
Test to differentiate HGA from HEE
PCR
HGA vector
Ixodes scapularis
HME vector
Amblyomma americanum
Ixodes scapularis transmits
Anaplasma phagocytophilum
Amblyomma americanum (lone star tick) transmits
Ehrlichia chafeensis
What is the drug of choice for ehrlichiosis and anaplasmosis?
Doxycycline
should see a huge improvement in 24 hours
what will doxycycine not treat?
babesiosis
How do Ehrlichia and Anaplasma enter the cell
through receptor-mediated endocytosis
(glycophosphoinositol anchored receptor)
Where do Ehrlichia and Anaplasma multiply
within endosomes
Cardinal features of CNS infection (20% cases)
Nuchal rigidity, confusion, fever
Pleocytosis and elevated protein in CSF
Abnormal -> this patient has CNS disorder
Monocytes cytoplasm
Bluish – no granulocytes
Nucleus takes up a lot of space
Epidemiology of HME
Southeast/central (ambyloma americanum – lone star tick)
Epidemiology of HGA
North (ixodes scapularis)
If patients don’t respond to Doxycycline
Possibly coinfected with babesiosis
If someone is pregnant use
Rifampin
Atypical lymphocytes
Lots of basophilic cytoplasm
Nucleus is elongated
Ratio of nucleus to cytoplasm
Mononucleosis S/S
Posterior cervical lymph nodes, age, atypical lymphocytes, splenomegaly (common), pharyngitis
Group A strep
No atypical lymphocytes
No splenomegaly
Confirm diagnosis of Group A strep
Throat swab – culture
Rapid strep test
CMV
2nd most common Infectious mononucleosis
Risk factors for CMV
Daycare (exposure to children less than 2 yo) /immunocompromised
Difference between CMV and EBV
Higher AST (disseminated disease compared to EBV) -> prolonged fever

Less prominent localized (less lymphadenopathy)
EBV affects which cells
Epithelial
B cells
HIV
Diffuse and non tender lymphadenopathy*
Mucocutaneous ulcers*
Rash (all can present with rash)
Other risk factors
Laboratory tests for EBV
Atypical lymphocytes
Monospot test
Heterophile antibody cross agglutinates with horse RBC
Sensitivity 75%
Specificity – if it is negative even in infection (early in infection b/c body hasn’t made antibodies)
Management of EBV
Rest, supportive care
Intervene: airway/autoimmune hemolytic rxn use prednisone
Acylovair – no role currently
Common complications with EBV
Meningitis/encephalitis
Ruptured spleen (3 wks can’t participate in non contact sport/4 wks for contact activity)
EBV
Oral hairy leukoplakia (differential oral thrush)
Happens on side of tongue not scrapable easily like candidasis.
Cancers associated with EBV
Nasal pharyngeal carcinoma (asia, china)
Burkitts lymphoma (africa)
Hodgkin’s lymphoma/hairy cell leukemia (US)
HIV 1
T tropic – primarily affects T cell lines (receptor uses CCR4)
M tropic - ** most common infection of cells is through macrophages. (uses CCR5 receptor)
Dual tropic
*assay can tell you which one the pt is infected with.
Oral candidasis
Not oral hairy leukoplakia b/c not on side of tongue/scraping possible
CCR5 receptors
Have genetic variance
Life cycle of HIV
Affects mucosal surface
DC goes to lymph nodes and starts to infect CD4 cells
Step 1 : attachment, CD4 and chemokine receptor depending on HIV virus type
Step 2: uncoating
Step 3: RT (two major classes NRTI and NNRTI – nucleoside RT inhibitor and non nucleoside)
Step 4: integration
Integrase enzyme
Step 5: proviral transcription
Step 6: Translation
Step 7: protease cleavage
Protease inhibitor stops the making of protein (another class of drugs)
Step 8: assembly, maturation, release
Tests for HIV acute
HIV RNA – PCR*
p24 antigen (ELISA?)
Immunoflorescent assay
Confirm HIV diagnosis via
Western Blot measures
Proteins gp160/120/p24/POL/GAG/ENV
ARS
Acute retroviral syndrome : flu like
Fever (slightly prolonged), chills, Sore throat, myalgias, arthralgias, headache, malaise, nausea, rash more likely in HIV than others.

*ARS is not common clinical scenario, HIV pts come in with extremely low CD4 count.
Initial test for HIV
ELISA (both HIV 1 and 2)
CD4+ Tcell
Normal: 800-1000
When is HIV considered AIDS
CD4+ lower than 200 cells/micro l
When would you start Tx for an AIDS patient?

antiretroviral therapy (ART)
AIDS defining illness – oral candidasis is one of them.
CD4 = 350-500
Pregnant women – start ART regardless of CD4 count b/c risk of transmission is high
HIV associated nephropathy
Hep B co infection – also treat for Hep B
Major side effects of NRTI (Nucleoside/Nucleotide Reverse Transcriptase Inhibitors)
Bone marrow suppression
Peripheral neuropathy
Pancreatitis
Abacavir – hypersensitivity
NNRTI (Non-Nucleoside Reverse Transcriptase Inhibitors) side effects
Lots of drug-drug interaction
Severe skin rash
Hepatitis
Rapid resistance if dose missed. ***
PI (Protease Inhibitors) side effect
Parestehsias
Hypertriglyceridemia
Hypercholesterolemia
*so not good for 45 yo diabetic