- Shuffle
Toggle OnToggle Off
- Alphabetize
Toggle OnToggle Off
- Front First
Toggle OnToggle Off
- Both Sides
Toggle OnToggle Off
Front
How to study your flashcards.
Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key
Up/Down arrow keys: Flip the card between the front and back.down keyup key
H key: Show hint (3rd side).h key
PLAY BUTTON
PLAY BUTTON
248 Cards in this Set
- Front
- Back
|
which region has the largest prevalence of AIDS?
|
Sub-Saharan Africa
|
|
who are most new cases of AIDS in the US? (2)
|
blacks
hispanics |
|
who constitutes the largest transmission category in the US?
|
homosexuals
|
|
what is the tansmission rate among the uninfected vs the infected?
|
7% vs 2%
|
|
what is the only dsRNA virus?
|
reovirus, specifically rotavirus
|
|
what makes HIV a unique retrovirus?
|
it has 2 copies of ssRNA
|
|
what is gp120? (2)
|
a surface glycoprotein
the first molecule that attaches to the host cell |
|
how does gp120 avoid being detected?
|
heavy glycosylation
|
|
what does gp120 bind to? (2)
|
CD4 and CCR5
|
|
what is gp41? (2)
|
a transmembrane protein
most important molecule for viral entry |
|
what is matrix protein 17?
|
helps to maintain the viral structure and transport the viral genome to the host cell nucleus and assemble new virions
|
|
what is p24? (2)
|
a caspid protein
the first antigen the body will make an antibody to, therefore the p24 antibody is the best way to detect the presence of HIV in ELISA |
|
what are the 3 critical enzymes for HIV?
|
reverse transcriptase
integrase protease |
|
where is HIV-2 seen? (2)
|
west africa and india
|
|
how is hiv-2 different?
|
progression to AIDS is slower
|
|
what does gag code for? (3)
|
matrix, caspid, and nucleocaspid
|
|
if gag is mutated, what might we see?
|
drug resistance to drugs targeting p24
|
|
what does pol code for? (3)
|
the critical proteins
protease reverse transcriptase integrase |
|
if pol is mutated, what might we see?
|
resistance to protease inhibitors
|
|
what does env code for? (2)
|
gp120
gp41 |
|
what does tat code for?
|
positive regulator of transcription
|
|
what does rev code for?
|
regulator of viral expression
|
|
what is the regulator of viral expression?
|
transfers spliced and unspliced molecules from the nucleus to the cytoplasm
|
|
what does nef code for?
|
negative regulation factor
|
|
why is nef important?
|
the negative regulation factor is essential for the progression to AIDS
|
|
what does nef do? (2)
|
augments viral replication in vivo and in vitro
down-regulates CD4 and MHC class II |
|
why might someone be infected with HIV for 15 years and not progressing to AIDS?
|
a mutation in the nef protein
|
|
what type of mutation do non-caucasions usually have?
|
NEF
|
|
what type of mutation doe caucasions ususally have?
|
CCR5
|
|
what will macrophage-trophic viruses express?
|
CCR5 receptor
|
|
what will lymphocyte-trophic viruses express?
|
CXCR5
|
|
why are macrophages the 1st cells to be infected?
|
because of their strategic location at the mucosal surface
|
|
what is viral penetration mediated by?
|
fusion of viral gp41 with the host cell plasma membrane
|
|
what type of genetic material is synthesized and by what?
|
DNA copy synthesized by RNA dependent DNA polymerase
|
|
what does integrase do in HIV?
|
circularizes DNA and incorporates it into the host cell genome
|
|
when the host cell is activated, what happens? (3)
|
viral DNA is transcribed yielding messenger RNAs and viral genome RNA
|
|
what will NF-kappa-B do in HIV?
|
transcibes and translates Tat and Rev
|
|
what are tat and rev?
|
RNA proteins in HIV
|
|
what does Rev do in HIV?
|
regulates the number of RNA that will be transferred from the nucleus to the cytoplasm
|
|
what does tat do in HIV?
|
amplifies transription of viral RNA
|
|
what are the late proteins in HIV (3)?
|
gag, pol, env
|
|
what happens to the late proteins in HIV?
|
they are cleaved and assembled with genomic RNA into virions which bud from the cells
|
|
why do host cells lyse in HIV?
|
at some point the cell gets exhausted and dies after some time
|
|
what do NK cells mediate in HIV?
|
attack of HIV specific cytotoxic T cells
|
|
what does ADCC do in HIV?
|
kills antibody identified cells
|
|
what do B cells do in HIV?
|
not directly damaged, but in order for the B cells to be functional they need help from the Th2 cells which are also under attack so they become useless
|
|
what is Acute retroviral syndrome and how does it manifest?
|
the fist sign of HIV, in which the patient suffers from flu-like symptoms and is usually considered to be a cold or flu
|
|
what is the symptomatic stage of HIV? (2)
|
opportunistic infection or malignancies
|
|
what are 4 opportunistic infections in HIV?
|
candida
pneumocystis CMV toxo |
|
what are 4 malignancies in HIV?
|
kaposi sarcoma
burkitt's lymphoma cervical carcinoma anal carcinoma burkitt lymphoma NHL |
|
what may lead people to be a long-term non-progressor?
|
a NEF or CCR5 mutation
|
|
how is viral load expressed?
|
in mL
|
|
how is CD4 cell count expressed?
|
in microL or mm^3
|
|
what is the CDC definition of AIDS? (2)
|
patient has to be HIV+ and CD4 count below 200
OR patients who are HIV+ with a total T cell count less than 14% |
|
What are 4 differential diagnosis possibilities of AIDS?
|
mono
secondary syphillis acute early hep B or A influenza |
|
how do you know if a patient has a CMV form of mono?
|
the heterophile test will be negative
|
|
what is diagnostic method 1 for AIDS?
|
symptoms are consistent with acute retroviral syndrome
negative HIV ELISA within past 6 months positive HIV ELISA at current testing |
|
what is diagnostic method 2 for AIDS?
|
symptoms are consistent with acute retroviral syndrome
negative HIV ELISA at current testing High HIV RNA titer at current testing |
|
Is PCR qualitative or quantitative?
|
qualitative
|
|
is RT-PCR qualitative or quantitative?
|
quantitative
|
|
what type of diagnostic method would you use for a baby born to a mother with HIV and why?
|
PCR
you already know the baby will have the antibodies, you want to know if the baby has the viral RNA |
|
what type of diagnostic method would you use for a patient you are treating and want to know if they have gotten better or not?
|
RT-PCR
|
|
why does ELISA have to be confirmed with western blot?
|
because ELISA is a highly sensitive test so it can give false positives
|
|
if viral serology is negative, what might the differential diagnosis include? (5)
|
idiopathic CD4+ lymphocytopenia
Sjogren syndrome sarcoidosis lymphoma congenital immunodeficiency syndromes |
|
how can vertical transmittion be avoided? (5)
|
elective c section
28 weeks onward go on AZT given NRTI inhibitor at delivery babes given anti-retrovirals for a week no breast feeding |
|
how do you treat post-exposure prophylaxis?
|
give at least 2 drugs for 2-3 months
|
|
what is the initial immune response to HIV? (3)
|
antibodies to the envelope protein
antibodies to the cytotoxic T cells antibodies to the HIV core protein |
|
how does the body lose ground against HIV?
|
when the envelope protein changes, the antibodies against it become useless; as the antibodies adjust, the virus has time to change even further
|
|
why do viruses have so many mutations?
|
because they do not have a good proof reading system
|
|
what are 4 ways HIV evades the immune system?
|
rapid multiplication
high mutation rate (antigenic variation) elimination of CD4 T cells misdirected and exhausted B cell response |
|
how does strep pneumonia avoid the immune system?
|
uses a capsule to avoid phagocytosis
|
|
how does mycobacterium tb avoid the immune system?
|
by blocking lysosome fusion with the phagosome it avoids antibody and complement opsonization
|
|
how does listeria monocytogenes avoid the immune system?
|
it escapes the phagosome
|
|
what is an important side effect of INH + Pyridoxine?
|
strong peripheral neuropathy
|
|
what does HAART do?
|
does not cure but controls retroviral replication
|
|
when is the HAART goal achieved?
|
when the plasma viremia level drops below detectable levels (50mL or less)
|
|
what is the recommended agent for TB prophylaxis?
|
INH + pyridoxine
|
|
according to the books, when should HAART begin? (2)
|
Any patient with symptoms of when CD4 count falls below 200
|
|
in practice, when should HAART begin?
|
when CD4 hits 350
|
|
what is ATRIPLA?
|
a combination of 3 HIV medicines
efavirenz (sustiva) emtricitabine (emtriva) tenoforvir (viread) |
|
what is the MOA of NRTIs?
|
structurally similar to purine and pyrimidine components of the viral nucleic acid
NRTIs get incorporated into the growing DNA chain and block the completion of the DNA strand |
|
what type of drug is zidovudin (azt)?
|
NRTI
|
|
what type of drug is stavudin (D4T)?
|
NRTI
|
|
what type of drug is larnivudin (3TC)?
|
NRTI
|
|
what type of drug is didanosine (ddI)?
|
NRTI
|
|
what type of drug is zalcitabine (ddC)?
|
NRTI
|
|
what type of drug is nevirapine?
|
NNRTI
|
|
what type of drug is delavirdine?
|
NNRTI
|
|
what type of drug is efavirenz?
|
NNRTI
|
|
what type of drug is saquinavir?
|
protease inhibitor
|
|
what type of drug is ritonavir?
|
protease inhibitor
|
|
what type of drug is indinavir?
|
protease inhibitor
|
|
what type of drug is nelfinavir?
|
protease inhibotor
|
|
how do protease inhibitors work?
|
prevent packaging of viral proteins in the virion
|
|
how does the herpes virus evade the immune system?
|
persists in the host cells without dividing to avoid the immune system recognition
|
|
how does strep pneumonia, influenza virus, and HIV avoid the immune system?
|
use antigenic variation to avoid memory response
|
|
how does neisseria, strep pneumonia, and haemophilis influenza avoid the immune system?
|
expresses IgA protease to avoid IgA neutralization
|
|
how does EBV avoid the immune system?
|
inhibits host cell expression of LFA-3, ICAM-1 to block adhesion of CTL to infected cells
|
|
how do herpes simplex and CMV avoid the immune system?
|
inhibits host cell class I expression to block CTL recognition
|
|
how does mycobacterium leprae avoid the immune system?
|
stimulates Th2 response to suppress Th1 response
|
|
what type of vaccine is contraindicated in AIDS?
|
live vaccines
|
|
what is a major consideration in immunizing AIDS pts?
|
is T cell numbers are low, will the patient even be able to benefit from an immunization?
|
|
is the pneumococcal vaccine advised in AIDS?
|
yes, every 5 years
|
|
is the influenza vaccine advised in AIDS?
|
yes, the inactivated vaccine annually
|
|
is the hepatitis B vaccine advised in AIDS?
|
yes, 3 injection sites if not immune
|
|
if the hepatitis A vaccine advised in AIDS?
|
yes, with a 2 injection series with underlying liver disease and no immunity
|
|
is the tetanus-diptheria vaccine advised in AIDS?
|
yes, every 10 years
|
|
is MMR advised in AIDS?
|
not if CD4 is less than 200, otherwise per routine
|
|
is oral poluomyelitis vaccine advised in AIDS?
|
nope
|
|
is the oral typhoid vaccine advised in AIDS?
|
no
|
|
is the BCG vaccine advised in AIDS?
|
no
|
|
is the varicella-zoster advised in AIDS?
|
no, use herd immunity
|
|
is the yellow-fever vaccine advised in AIDS?
|
no
|
|
when do you begin prophylaxis for pneumocystis jiroveci in AIDS?
|
when CD4<200
|
|
what do you use for prophylaxis for pneumocystis jiroveci in AIDS?
|
TMP-SMX
|
|
when do you begin prophylaxis for mycobacterium avium complex in AIDS?
|
when CD4<50
|
|
when do you begin prophylaxis for toxoplasmosis in AIDS?
|
when CD4<100 and positive anti-toxo IgG assay
|
|
when do you begin prophylaxis for tb in AIDS?
|
with induration >5mm
|
|
what do you use for prophylaxis for mycobacterium avium complex in AIDS? (3)
|
azithromycin
clarithromycin ethambutol |
|
what do you use for prophylaxis for toxoplasmosis in AIDS?
|
TMP-SMX
|
|
what are 2 second line AIDS drugs?
|
fusion inhibitors
integrase inhibitors |
|
how do fusion inhibitors work?
|
inhibit gp41 from fusing with the host membrane
|
|
what is an example of a fusion inhibitor?
|
enfuviritide (fuzeon)
|
|
what is an example of an integrase inhibitor?
|
raltegravir (isentress)
|
|
what 2nd line AIDS drug must be given in combination with other drugs?
|
integrase inhibitors
|
|
how does integrase inhibitor work?
|
inhibits the integrase protein from HIV DNA from meshing with healthy cell DNA
|
|
what is merovoc?
|
CCR5 antagonist
|
|
what is the problem with waiting until the CD4 count drops to admin HAART?
|
once the CD4 drops other manifestations of AIDS begin to develop (i.e. opportunistic infections) that you must treat as well
|
|
why should you never use a protease inhibitor by itself?
|
single use leads to selection of the resistant strains resulting in progression to AIDS whereas RTIs require 3 or 4 independent mutations
|
|
what is a thyroid complication associated with HAART?
|
elevated TSH with normal T3 and T4 (normally T3 and T4 would go down)
|
|
what 2 HAART drugs is an elevated bilirubin associated with?
|
indinavir
atazanavir |
|
what 4 hematological complications are associated with AZT?
|
macroxytosis
anemia thrombocytopenia neutropenia |
|
what are 5 ways a retrovirus can transform a cell into a malignant one?
|
utilizing the cell machinery for a long period of time which transforms it into a malignant cell
integrating into the host cell genome insertional mutagenesis (activating a proto-oncogene) expression of transgenes frame shift mutations |
|
what are transgenes?
|
new genes that activate trancription factors in the cell which activate proliferation
|
|
what do you need for kaposi sarcoma?
|
co-infection of HIV and HHV-8
|
|
what virus in addition to HIV causes kaposi sarcoma?
|
HHV-8
|
|
what will a kaposi sarcoma look like and what will its color depend on?
|
amber red or deep purple
color depends on whether it is an artery or vein that is affected |
|
in kaposi sarcoma, what induces prolioferation of endothelial cells?
|
VEGF, induced by tat
|
|
what can kaposi sarcoma tumor be confused for?
|
basillary angiomatosis
|
|
how can you differentiate between basillary angiomatosis and kaposi sarcoma?
|
basillary angiomatosis is caused by bartonella henslease which is associated with cats
|
|
what favors the malignant transformation of kaposi sarcoma cells?
|
HHV-8
|
|
what 2 things will you see in later tumor formations of kaposi sarcoma?
|
spindle shaped cells
neovascilargenesis |
|
where is burkitt lymphoma prevalent?
|
west africa
|
|
if something looks like burkitt lymphoma but is in asia, what is it?
|
nasopharyngeal carcinoma
|
|
how does EBV gain access to the b cell in burkitt lymphoma?
|
via CD21 which is the EBV receptor on the b cell
|
|
how are latent B cells activated?
|
HIV
|
|
what 2 HPV types will cause cervical and anal carcinoma?
|
16 and 18
|
|
when does HPV replication increase?
|
when host cellular immunity decreases
|
|
what 2 things does HPV do to cellular replication?
|
induces cellular replication while simultaneously disregulating replication
|
|
how often should HIV+ individuals be screened for precancerous conditions in the cervix or anus?
|
2x/year
|
|
what 2 things will you look for in a pelvic exam for cervical and anal carcinomas?
|
cervical intraepithelial neoplasia
koilocytes |
|
what are koilocytes?
|
abnormal cell with a large nucleus surrounded by a perinuclear halo
|
|
when should you begin prophylaxis for CMV?
|
CD4<50
|
|
when should you begin prophylaxis for cryptococcus?
|
CD4<50
|
|
what causes progressive multifocal encephalopathy and will appear as white sclerotic plaques?
|
JC virus in HIV
|
|
how will JC virus in HIV present?
|
progressive multifocal encephalopathy and will appear as white sclerotic plaques
|
|
why is toxo a commonly encountered problem in HIV?
|
because 50% of the US population is seropositive for toxo
|
|
what is the invasive form of toxo?
|
tachyzones/trophozoite
|
|
what is the infective form of toxo?
|
oocyst
|
|
what is the number 1 source of toxo?
|
undercooked pork
|
|
where does toxo undergo sexual and asexual development?
|
in the GI tract of the cat
|
|
how is toxo excreted from the cat?
|
as an immature oocyst
|
|
when do problems arise for humans with toxo infections?
|
when it gets into circulation and can enter the brain
|
|
what are 3 problems seen if a baby is exposed to toxo early in utero?
|
CNS problems
hepatitis pneumonia |
|
how is toxo presented when the baby is exposed later on in utero?
|
won't present until the 2nd or 3rd decade of life
blindness (chorioretinitis) retardation strabismus |
|
how will immunocompetent adults present with toxo infection?
|
similar to mono
|
|
how will immunocompromised present with toxo infection? (4)
|
encephalopathy which will present as
meningoencephalitis diffuse encephalopathy mass lesion |
|
what is the definitive sign of toxo?
|
ring enhancing lesion in the brain
|
|
what percent of AIDS patients will get toxo?
|
50%
|
|
of those AIDS patients exposed to toxo, what percent will die?
|
90%
|
|
how is toxo treated?
|
sulfonamide + pyrimethamine
|
|
how is toxo treated in pregnant women?
|
replace pyrimethanine with spiromycin
|
|
what toxo treatment is effective against both encysted and trophozoite forms?
|
atrovaquone
|
|
what parasite will cause intractable diarrhea?
|
crytosporidium gastroenteritis
|
|
how can you ID cryptosporidium cysts?
|
they will be acid-fast positive
|
|
what is the morphology of cryptosporidium?
|
spherical structures arranged in rows along the microvilli of epithelial cells
|
|
what are 3 other AFB parasites that cause diarrhea?
|
isospora
cyclospora microsporidium |
|
where does crytosporidium go through sexual differentiation?
|
in human intestines
|
|
what form of crytosporidium are males?
|
microgametes
|
|
what form of cryptosporidium are females?
|
macrogametes
|
|
which form of cryptosporidium can auto-infect?
|
thin walled oocyst
|
|
which form of cryptosporidium can infect outside the body?
|
thick walled oocyst
|
|
why doesn't cryptosporidium need a second host?
|
becuase both sexual and asexual life cycles occur in humans
|
|
how does cryptosporidium cause intractible diarrhea?
|
affects the jejunum to prevent absorption which leads to deficiencies
leads to atrophied villi with widened crypts |
|
how do you treat cryptosporidium?
|
only way is to improve CD4 count; there is no cure
|
|
what is the most common site of infection for mycobacterium avium complex?
|
blood
|
|
how will you know a patient has mycobacterium avium complex and not TB?
|
TB screening will be negative
TB will not have diarrhea |
|
how will you treat mycobacterium avium complex?
|
azithromycin or other macrolide
|
|
what is the main mainfestation of mycobacterium avium complex? (2)
|
cavitary pulmonary lesion that has disseminated
diarrhea |
|
how do you diagnose mycobacterium avium complex?
|
blood culture
|
|
how is mycobacterium kansasii similar to TB? (2)
|
symptoms will be similar
PPD positive |
|
how will you treat mycobacterium kansasii?
|
traditional TB drugs
|
|
how will you differentiate mycobacterium kansasii from TB?
|
mycobacterium kansasii is unique because it is photochromogenic (produces a pigmented colony in the presence of light)
|
|
how is pneumocystis carinii a unique fungus and what 2 implications does this have?
|
does not have ergasterol on cell membrane
therefore we cannot treat it with a traditional antifungal harder to stain |
|
how will pneumocystis carinii stain?
|
with silver stain
|
|
what is the epidemiology of pneumocystis carinii?
|
ubiquitous (we've already developed an infection)
|
|
where will pneumocystis carinii epidemics be found? (3)
|
hospitalized infants
elderly nursing home residents malnourished infants |
|
what type of response will immunocompetent individuals develop to pneumocystis carinii? (2)
|
cell mediated
humoral response |
|
where do pneumocystis carinii spores attach and what implication does this have?
|
spores attach to the alveolar walls so sputum samples will be useless
|
|
what is a long lasting effect of pneumocystis carinii?
|
the alveolar walls become thickened and scarred, preventing the free passage of oxygen
|
|
what are 3 symptoms of pneumocystis carinii?
|
SOB
tachypnea non-productive cough |
|
what does pneumocystis carinii require for diagnosis?
|
requires a living creature
|
|
what will you see on a CXR for pneumocystis carinii?
|
interstitial pneumonia
linear opacities with hazy ground glass appearance |
|
what type of sample should you use for pneumocystis carinii diagnosis? (2)
|
BAL or biopsy
|
|
what type of stain can you use for pneumocystis carinii with BAL?
|
wright
giemsa papanicolaou |
|
what type of stain can you use for pneumocystis carinii with biopsy? (2)
|
methenamine stain
silver stain |
|
how will pneumocystis carinii appear on biopsy?
|
honeycomb appearance
|
|
what is cryptococcus neoformans?
|
a unique fungus that is a respirator pathogen but will present with menigneal encephalitis
|
|
what is an important virulence factor in cryptococcus neoformans?
|
polysaccharide capsule (GXM)
|
|
why is it problematic that cryptococcus neoformans is thymus independant?
|
it does not require T cells to develop an immune response so no memory will be developed because you need T cells to induce class switching in B cells; you'll only get IgM which cannot induce a memory response
|
|
how will cryptococcus neoformans grow? (3)
|
at body temperature
on a variety of media colony morphology resembles bacteria |
|
what type of stain will show the thick capsule of cryptococcus neoformans?
|
indian ink
|
|
where will cryptococcus neoformans be found?
|
soil contaminated with pigeon droppings
|
|
when does cryptococcus neoformans begin replicating?
|
as soon as it enters the blood stream
|
|
what does cryptococcus neoformans produce that allows it to replicate inside the macrophage?
|
melanin which prevents oxidative injury
|
|
if cryptococcus neoformans encysts in the brain, how will it present?
|
headache
seizures loss of consciousness (key symptom) |
|
what is the latex agglutination test?
|
looks for the antigen rather than the antibody
|
|
what can latex agglutination test be used for? (4)
|
strep pneumonia
haemophilis influenza neisseria meningitis cryptococcus neoformans |
|
how is cryptococcus neoformans treated? (3)
|
amphotecerin B in combination with flucytosine or fluconazole
|
|
what percent of cryptococcus neoformans patients suffer from residual damage?
|
50%
|
|
what is the number one cause of in-utero infections in the US?
|
CMV
|
|
how does CMV become latent?
|
uses the mononuclear cell
|
|
what is the key morphological feature of CMV?
|
basophilic internuclear inclusion body with a large halo
|
|
what percent of adults are sero positive for CMV?
|
50%
|
|
how is CMV transmitted?
|
close personal contact
sexual contact transfusion organ transplant vertical transmission |
|
what does CMV infect?
|
eye
CNS liver |
|
what does CMV do in an infected cell?
|
remains in a non-replicating and non-infectious form
|
|
what is the difference between CMV iinfection in monocytes vs lymphocytes?
|
monocytes - replication is very slow
lymphocytes - cell becomes quiescent |
|
who are susceptible to reactivation in CMV?
|
organ transplants
AIDS chemotherapy |
|
what is a blueberry muffin baby (3) and what is it associated with?
|
associated with CMV
jaundice thrombocytopenic purpora yellow and red will turn blue |
|
how does CMV present? (4)
|
blueberry muffin baby
chorioretinitis microcephaly gastroenteritis |
|
what will acute CMV infections present like?
|
mono
|
|
in what population is CMV pneumonia the #1 cause of pneumonia?
|
bone marrow transplant
|
|
what is the key feature of CMV?
|
chorioretinitis
|
|
how do you prevent CMV?
|
anti-CMV globulin
|
|
what 3 drugs are used for CMV treatment?
|
gancyclovir
foscarnet cidofovir |
|
what is the MOA of gancyclovir?
|
inhibits DNA polymerase
|
|
what is a side effect of gancyclovir?
|
bone marrow suppression
|
|
what is most effective in decreasing the mortality of CMV pneumonia?
|
combination of gancyclovir and immuno-globulins
|
|
what is the MOA of foscarnet?
|
inhibits DNA polymerase
|
|
what is a side effect of foscarnet?
|
nephrotoxic
|
|
what is cidofovir used for?
|
retinitis
|
|
what three things indicate the presence of HIV? How many must be present to make an official diagnosis?
|
GP120
GP41 p24 must have 2/3 |
|
what is the normal ratio of CD4:CD8?
|
2:1
|
|
what happens to the CD4:CD8 ratio in AIDS?
|
reverses; becomes 1:2
|
|
what are two physical findings of meningitis?
|
kernig's sign
brugniskis |
|
If a patient was seropositive for toxo and then became infected, which immunoglobulin will increase?
|
IgG
|
|
If a patient was seronegative for toxo and then became infected, which immunoglobulin will increase?
|
IgM
|
