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44 Cards in this Set
- Front
- Back
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what caused what was called "glandular fever"
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EBV
**causes mono and burkitts in some places **1-2 month incubation, polyclonal B cell proliforation |
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what is the hallmark of EBV infection
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poly clonal B cell proliforation
**1-2 month incubation, replication occurs in nose and reaches the LN |
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what are the sx of EBV infection
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EBC causes mono after a 1-2 month incubation. there is polyclonal B cell proliforation
**can replicate in nose nad LN, also can disseminate to liver nad spleen (hepatomegaly/splenomegaly) **prodrum of HA, fever, maliase **sore throat, lymphadenopathy, fever **WORRY that spenomagaly can rupture |
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are you jaundice with mono
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ya, EBV can disseminate to liver and spleen
hepatomegaly --> increased liver enzymes/jaundice Splenomagaly--> risk of rupture *we know EBV causes B cell proliforation but also t cells (downy cells) THIS is what causes pts sx |
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what replicates in EBV, B or T cells
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BOTH
B multiply first. Downy cells are the atypical T cells, T cells make the sx |
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whats teh micro stuff about EBV
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gamma herpesvirus
*enveloped, dsDNA **latent in throat, LN, blood cells can be EBV 1 or 2 |
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where can EBV infected cells hang out
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throat
LN blood EBV 1 and 2 |
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who gets a disease in which B cells have a polyclonal multiplicaiton but T cells cause sore throat, and hepatosplenomegaly
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college kids! kissing disease, spread through respiratory droplets
**1-2 month incubation **1:3 is asx!!!!! * relatively LOW infectious |
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ok so we know EBV like to hang in the throat, LN and blood in latency. what happens in latency
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the EBV genome integrates in host and replicates about 10 genes (contrast to HPV who in latency expresses little)
**can also have instances where there is NO LATENCY and the virus just replicates and replicates |
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tell me about dx of EBV
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can be hard, mono mimics other diseases
-will have downy (bad T cells) in circulation -heterophile AB bc of B cell proliforation (transient). RBC agglut in monospot -AB to EBV, these are PERMANENT |
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when testing for EBV in a case of IM what are heterophile AB what aboiut AB to EBV
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heterophile is bc of B cell polyclonal proliforation- these are TRANSIENT, show up in about a week and persist for a few months. these agglutinate in a monospot, may NOT be + in young kids
AB to EBV is PERMANENT. life long immunity **once we get a + monospot we confirm with IgM viral anticaspid |
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if you have a + monospot what is the FU
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+ monospot menas agglut by heterophile AB. may NOT be + in kids
FU with IgM anticapsid AG serology |
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tx for mono
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supportive
steroids are CONTROVERSY! |
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what are some complications of EBV
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1. jaundice
2. spleen rupture 3. rash after ampicillin tx 4. chronic infection, blood abnormalities 5. REACTIVATION DISEASE, chronic fatigue, malignancy? |
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how is EBV involved in cancers
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Burkits lymphoma
**its a MYC mutation, EBV helos but is NOT ESSENTIAL for BL Non Hodgkins lymphoma in HIV pts w/cyclocporin Hodgkins nasophayyngeal carcinoma |
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which cancer is assoicated with EBV
1. burkitts 2. hodgkins 3. non hodgkins 4. nasopharyngeal carcinoma |
**ALL of these!!!!
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what is teh most common infection of the fetus, waht else does it cause
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CMV
((causes death in HIV/Transplant pts, common in low SES |
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what virus replicates in fibroblasts, does it replicate anywhere else
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CMV
replicates in fibroblasts in citro and in epithelium in vivo! **makes owl eyes. characteristic CPE w/massive cell enlargement and intranuclear/intracytoplasmic inclusions |
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when do we see...
1. owl eyes 2. downy cells |
1. owl eyes, CMV (fetus and HIV/transplants)
2. Downy: EBV, (mono and burkitts) |
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does EBV/CMS have seasonality
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NOPE
EBV: kissing, seen in 17-25 CMV: seen in fetus, HIV, transplants, low SES HIGH in africa and NY. common in young and old |
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NY and africa have high infrections of what
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CMV
**person to person transmission, more common in low SES and CROWDS. common in old and young |
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where is the CMV virus in pp;l
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blood
saliva seman urine DONOR ORGANS SEXUALLY TRANSMITTED (EBV can also sometimes be sexually transmitted) |
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are ppl coming in with CMV infections a lot
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NO. MOST INFECTIONS ARE SUBCLINICAL
**significant disease in immunosuppressed and congenital infections. |
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what is the WORST situation for a CMV infection
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PRIMARY infection in immunocomprimised host. also bad for a mom to get primary infection when preggo
**most infections are subclinical. BUT prevalent in immunosuppressed (old, youmg, HIV) **no sx in healthy ppl in primary, reactivation or reinfection |
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if your 60 yo has mono like sx, have they been kissing 17 yo?
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nope, its prble CMV NOT EBV
**negative heterophile AB w/atypical lymphs (owl eyes) **latent infection ARE established with both EBV and CMV |
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what happens to the babe if a preggo mom gets CMV
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more risk with primary infectino of mom rather than a reactivation
**range from asx child to full scale CMV inclusion disease **KIDS ARE HUGE CMV RESEVOIRE |
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whats the risk of CMV w/transplant
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2% for blood transfusion
70-90% for liver/kidney/heart **bad bc its SUPER common so lots of donors have it but the recipient is immunosuppressed so will ofter die bc of it |
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what are the 3 sx of CMV in HIV pts
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retinitis
GI CNS penumonia |
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who gets CMV related retinitis, GI, CNS, and penumonia
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HIV pts SUPER COMMON in this population
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whats the dx for CMV
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the owl eyes no heterophile AB
**in moms the CMV is tested as part of the TORCH series |
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what is an underappreciated risj of CMV infection in adults
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KIDS!!!
we know about crowding and transplants but KIDS are just crawling in CMV recal CMV is in blood, saliva, seman,urine |
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your pt has signs of hep but is NEGATIVE for A B AND C, they are also heterophile AB negative. what can it be
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CMV
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tx of CMV
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ganciclovir, fomivirsen
Ig **get transplant pts through initial phase **contrast to ebv which has sx tx TOWNE VACCINE 125, live attenuated |
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what is the live attenuated towne vaccine for
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CMV
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whats the micro with MUMPS
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paramyxovirus
ssRNA - sense enveloped viral spikes with hemagglutinin and neuraminidase |
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does CMv EBV or MUMPS have envelope with hemagglutinin and neurominidase
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MUmps
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what are some common sx of mumps besides parotid swelling/infection
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spreads to CNS to cause fever, HA, vomit
*permanent damage is RARE **30-40% are ASX!!! |
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whats the dx of mumps
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Clinical: febrile kid with parotosis
HA assay w.culture for lab dx **commonly is ASX |
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is mumps or EBV Highly infectious
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mumps, humas are only resevoire
**viral shedding BEFORE sx onset *single serotype is known |
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what was the prevalence of mumps before vaccination began
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super common, super infectious
common in Jan-May |
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why do we vaccinate against mumps if its asx often adn can cause some non permanent changes in CNS like HA and fever
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can cause Orchitis (testicular swelling). can appear in absense of other signs/sx
seen in like 30%! can also replicate in kidney, mild renal impaiment |
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what is associated with testicular swelling
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mumps, can happen w/o parotitis
mumps can also cause renal impairment |
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mumps tx
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sx, better to prevent with vaccine (MMR)
**get LIFE LONG IMMUNITY, cant be used in pts w/egg allergies |
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what was the great mumps outbreak
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its when vaccinated ppl got mumps, the MMR is LEAST effective for mumps
2006 – over 3, 000 cases were reported, centered in the Midwest, with most cases in vaccinated patients Investigation revealed the vaccine is effective against the G strain responsible for the outbreak This outbreak may have revealed systematic failure in our MMR vaccination method and the need for a routine third boosting Outbreaks continue to be reported, typically linked to foreign travel and non-receipt of vaccine |
