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312 Cards in this Set
- Front
- Back
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"Tropisms"
definition? |
attractions to certain tissues
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"Tropisms"
determine? |
which body sites microorganisms colonize
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"Tropisms"
influence? |
normal flora (many other thigns do this too)
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Viruses:
size? |
0.02-0.3 um (micrometers)
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Viruses:
can reproduce independently or require host? |
host required
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Viruses:
outer cover chiefly includes? |
proteins
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Viruses:
outer cover possibly includes? |
lipids
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Viruses:
core contains? |
RNA & DNA
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Viruses:
RNA & DNA replication process? (3 parts) |
1.separates from outer cover
2.replicates inside host cell 3.process requires specific enzymes |
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RNA viruses:
replicate their nucleic acid where? |
cytoplasm
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DNA viruses:
replicate their nucleic acid where? |
nucleus
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Fate of host cell post viral replication?
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cell death
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Latency:
described as? with example? beneficial to virus how? |
asymptomatic viral infection
herpes simplex may facilitate spreading between hosts |
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Human infecting viruses spread via 4 methods?
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1. respitory excretions
2. enteric (small intestine) excretions 3. sexually 4. blood |
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Oncogenic Virus exs?
(viruses that produce tumors) (name 5) |
1.Human T-lymphotrophic virus-1
2.Epstein-Barr virus 3.Hepatitis B 4.Hepatitis C 5.Human herpesvirus 8 |
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Oncogenic virus #1:
what is it & what does it result in? |
Human T-lymphotropic virus-1
--> leukemia, lymphoma |
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Oncogenic virus #2:
what is it & what does it result in? |
Epstein-Barr --> causative agent for mononucleosis;
malignancies such as nasopharyngeal carcinoma in Asians and Burkitt's lymphoma in South Africans Hodgkin lymphoma & lymphomas among immuno-suppressed pts |
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Oncogenic virus #3:
what is it & what does it result in? |
Hepatitis B --> jaundice, hepatocellular carcinoma, cirrhosis, fulminant (sudden & severe) hepatitis
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Oncogenic virus #4:
what is it & what does it result in? |
Hepatitis C --> jaundice, liver failure, cirrhosis, hepatocellular carcinoma
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Oncogenic virus #5:
what is it & what does it result in? |
Herpesvirus 8 --> Kaposi's sarcoma, primary effusion lymphomas and Castleman dz (a lymphoproliferative disorder)
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Slow (months to years)viruses include?
(name 3) |
1. subacute sclerosing panencephalitis (d/t measles)
2. progressive rubella panencephalitis (d/t rubella) 3. progressive multifocal leukoencephalopathy |
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what is subacute sclerosing panencephalitis?
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Rare complication of measles in which the measles infection passes to the brain and remains there in an inactive state but causing increasingly terrible problems
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What is progressive rubella panencephalitis?
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Rare complication of rubella (German measles) where there is a gradual infection of CNS causing inflammation of the brain
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What is progressive multifocal leukoencephalopathy(PML)?
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Progressive multifocal leukoencephalopathy (PML) is caused by the reactivation of a common virus in the central nervous system of immune-compromised individuals. Polyomavirus JC (often called JC virus) is carried by a majority of people and is harmless except among those with lowered immune defenses.
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What are 2 dzs with traits like viruses but are not acutual viruses?
What are they caused by? |
1. Creutzfeld-Jacob dz
2. bovine spongirom encephalopathy both d/t PRIONS |
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Dx methods:
name 1 slow & 3 rapid? also, use light or electron micorscopy? |
SLOW = serologic
RAPID = culture, viral Ag, and PCR (Polymerase chain reaction) use electron micros |
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Remember what PCR is?
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Polymerase chain reaction (PCR) is a biochemistry and molecular biology technique[1] for enzymatically replicating DNA without using a living organism, such as E. coli or yeast. Like amplification using living organisms, the technique allows a small amount of DNA to be amplified exponentially. As PCR is an in vitro technique, it can be performed without restrictions on the form of DNA, and it can be extensively modified to perform a wide array of genetic manipulations.
PCR is commonly used in medical and biological research labs for a variety of tasks, such as the detection of hereditary diseases, the identification of genetic fingerprints, the diagnosis of infectious diseases, the cloning of genes, paternity testing, and DNA computing. |
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Tx / Prevention:
(name 2 classes) |
1. Antiviral dx
2. interferons |
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Antivirals best against:
(3 viral listings) |
Herpes 8
Respitory HIV |
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Interferons used for:
(name 3) |
1. Hep B
2. Hep C 3. HPV |
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Vaccines work by stimulating what kind of immunity?
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ACQUIRED immunity
(her notes say 'innate' immunity but that consists of only generalized defenses like macs, pmns, skin, etc. & NOT memory lymphocytes (see Rho packet IIA) |
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Viral vaccines in general use?
(name 10) |
influenza, measles, mumps, poliomyelitis, rabies, rubella, hep A, hep B, varicella, yellow fever
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Viral vaccines given to high-risk groups only (ex: military)?
(name 2) |
smallpox, adenovirus
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Dosing Igs used for what 2 things?
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1. passive artificial immunity
2. postexposure (rabies, hep) |
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HIV:
is what kind of virus? |
retrovirus, actually there are 2 similar retroviruses called HIV-1 & HIV-2
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HIV:
actions? (name 3) |
1. destroys CD4+ (which affects Th1 & Th2)
2. Impairs CMI(cell-mediated immunity) 3. increase risk of infections & cancers |
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HIV:
type of virus and what it does? |
retrovirus - enveloped RNA virus, replication via reverse transcription to make DNA that integrates into host cell genome
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HIV:
dx via? |
Abs or Ag testing
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HIV:
when dx change to AIDS? |
# CD4+ is x<200uL(microliters) = AIDS
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what is another major retrovirus and what does it cause?
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Human T-lymphotropic virus (HTLV) 1 & 2 -- causes t-cell leukemias and lymphomas
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HTLV transmitted how?
(2 ways) |
breastfeeding & sex
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enough tangents --back to HIV
which HIV is less virulent? |
HIV-2
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HIV:
transmission? |
body fluids with free virions
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HIV:
transmission mom to baby what routes? |
transplacentally or perinatally 30-50% of cases;
via breastmilk infants that had not been infected before have a 75% chance of infxn |
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HIV:
risk post-cutaneous stick, treated & untreated? |
untreated -- 1/300
treated -- 1/1500 |
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HIV:[pathophysiology now continued on"nutshell slide"
(#25)after previous digressions] --so the reverse transcriptase has copied HIV RNA and produced proviral DNA, what is this copying prone to and what does it result in? |
prone to errors resulting in frequent mutations
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HIV: pathophysio cont:
Proviral DNA only NOW enters the nucleus & gets integrated into host DNA using what? |
HIV integrase
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HIV: pathophysio cont:
so the proviral DNA is being duplicated with the host's DNA and is transcribed to viral RNA, ultimately being translated to HIV proteins. What envelope glycoproteins are affected? |
glycoproteins 40 & 120
(gotta know it, came up with Rho & Sokolovah also) |
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HIV: pathophysio cont:
HIV proteins are assembled into what and this is done where? |
into VIRIONS and this happens at the inner cell memebrane whereupon they subsequently bud to the surface
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HIV: pathophysio cont:
how many virions produced per host cell? (tens, hundreds, or thousands) |
thousands of virions are made per host cell
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HIV: pathophysio cont:
What HIV enzyme cleaves viral proteins after budding, thereby making the new virion an infectious form? |
protease
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HIV: pathophysio cont:
1/2 life of a virion? |
6 hours
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HIV: pathophysio cont:
in moderate to heavy infections, approximately how many virions are being created and destroyed daily? |
108 virions
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HIV: pathophysio cont:
For what's discussed thusfar, what 2 factors would you isolate as contributing most to HIV's resistance to host immunity and Abx therapies? |
1. high degree of viral replication occurring
2. high frequency of transcription errors |
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HIV: pathophysio cont:
main consequence of HIV infxn? |
impairment of the immune system, specifically loss of CD4+T lymphocytes which drive cell-mediated immunity and mildly influence humoral immunity
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HIV: pathophysio cont:
so what leukocyte is actually being depleted by HIV? |
CD4+ T lymphocyte
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HIV: pathophysio cont:
infected CD4+ 1/2 life? |
2 days
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HIV: pathophysio cont:
What is the normal CD4+ count per uL (microliter) anyway? |
750/uL
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HIV: pathophysio cont:
At what CD4+ level is does immunity begin to get affected? |
x<500/uL
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HIV: pathophysio cont:
At what CD4+ level is does immunity get grossly affected resulting in AIDS? |
x<200/uL
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HIV: pathophysio cont:
How is humoral immunity affected? What befalls the Ab producing B cells? What does this result in systemically? |
hyperplasia of the B cells, which results in lymphadeno-
pathy and increased secretion to already encounterd Ags (hyperglobulinemia) |
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HIV: pathophysio cont:
Re: Total Ab levels behaving in 2 contrary ways in early stages of dz, what are they? |
1st - SURGE of IgG & IgA against previous Ags
2nd - DEPLETION of all Abs, including responses to new threats |
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HIV: pathophysio cont:
Risk & severity of opportunistic infxns, AIDS, & AIDS-related Ca determined by what? |
1. CD4+ count
2. pt's exposure to potentially opportunistic pathogens |
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HIV: pathophysio cont:
without tx, % risk of HIV -> AIDS increases by how much every year? |
1st 2-3 years of infxn = 1-2%
subsequent years = 5-6% |
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HIV: early signs & sx:
may be asymptomatic or if sx develop, how specific are they? |
nonspecific
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HIV:
Nonspecific sxs associated with primary infxn are called what syndrome? |
acute retroviral syndrome
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HIV:
Acute retroviral syndrome sxs include? |
fever, rash, malaise, rash, lymphadenopathy, occasionally aseptic meningitis
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HIV:
initial infxn often mistaken for what? (name 2) |
infectious mononucleosis
& benign viral syndromes |
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HIV:
Detection to HIV Abs sensitive and specific except for during the initial few _____. |
weeks, detection not specific 1st few weeks
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HIV:
Which test is used as a screening (hence it is less sensitive and specific)? What HIV Ag does it look for? |
ELISA (enzyme-linked immunosorbent assay);
looks for p24HIV Ag |
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HIV:
Which test used after a + ELISA b/c it is more specific? |
Western blot
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HIV:
True or false, newer and rapid testing of saliva and blood allow instant results? |
true
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HIV:
What do you test for to determine infxn the first few weeks before ELISA will show results? What body fluid do you use? Is this test sensitive, specific, or both? |
plasma can be tested for HIV RNA. "The nucleic acid amplification assays used are sensitive and specific".
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HIV:
What assays are used for determining prognosis and monitoring tx? |
quantitative plasma HIV RNA assays
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HIV:
Hematologic abnormalities and what kind of biopsies are helpful for evaluating syndromes (like lymphomas & cancers) as well as infxns? |
Hematologic abnormalities and bone marrow biopsies are used
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HIV:
Describe most pts' marrow: _____cellular despite peripheral ______. |
normocellular or hypercellular marrow despite peripheral cytopenia, reflecting peripheral destruction
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HIV: MUST KNOW THIS ONE
COMMON NEUROLOGICAL SYNDROMES OF HIV/AIDS are? (name 5 and what they are from) |
1.dementia--cryptococcal
2.meningitis--cytomegalovirus 3.encephalitis--primary CNS 4.lymphoma--progressive multi-focal 5.leukoencephalopathy--TB meningitis 6.focal encephalitis--toxoplasma encephalitis |
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HIV:
Prognosis via? (name 2) |
CD4+ count (short term)
plasma viral RNA (long term) |
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HIV:
And remind me what the normal CD4 count is again? |
x>500uL
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HIV: prognosis cont.
for every 3-fold increase in viral load, mortality over the next 2-3 years increases how much? |
50% increase
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HIV: tx: NOT ON NOE TEST
HAART what does it mean? |
highly active anti-retroviral therapy
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HIV: tx: NOT ON NOE TEST
HAART what does it try to do? (name 2) |
1. reduce plasma HIV RNA levels
2. increase CD4+ lymphocyte counts |
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HIV: tx: NOT ON NOE TEST
IRIS what does it mean? |
immune reconstitution inflammatory syndrome
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HIV: tx: NOT ON NOE TEST
IRIS when does it occur? |
it's a serious rxn to HAART,
clinical deterioration despite rising CD4+ counts d/t subclinical opportunistic infxns or residual microbial antigens |
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HIV: tx: NOT ON NOE TEST
NRTIs what are they? |
nucleoSide reverse transcriptase inhibitors--they are phosphorylated to active metabolites that compete for incorporation INTO viral DNA
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HIV: tx: NOT ON NOE TEST
nRTIs what are they? (this is not a type-o) |
nucleoTide reverse transcriptase inhibitors--
they do the same as NRTIs but do not need to be phosphorylated into position |
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HIV: tx: NOT ON NOE TEST
PIs what are they? |
protease inhibitors -- stop the viral enzyme crucial to maturation of HIV variants after budding from host cells
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HIV: tx: NOT ON NOE TEST
FIs what are they? |
block binding of HIV to CD4+ lymphocyte receptors that is reqd for HIV to enter cells
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HIV: tx: NOT ON NOE TEST
Stopping tx and interrupting doses of rx creates resistance to rx how? |
makes mutations more likely
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HIV: tx: NOT ON NOE TEST
NRTIs what are they? |
nucleoSide reverse transcriptase inhibitors--they are phosphorylated to active metabolites that compete for incorporation INTO viral DNA
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HIV: tx: NOT ON NOE TEST
nRTIs what are they? (this is not a type-o) |
nucleoTide reverse transcriptase inhibitors--
they do the same as NRTIs but do not need to be phosphorylated into position |
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HIV: tx: NOT ON NOE TEST
PIs what are they? |
protease inhibitors -- stop the viral enzyme crucial to maturation of HIV variants after budding from host cells
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HIV: tx: NOT ON NOE TEST
FIs what are they? |
block binding of HIV to CD4+ lymphocyte receptors that is reqd for HIV to enter cells
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HIV: tx: NOT ON NOE TEST
Stopping tx and interrupting doses of rx creates resistance to rx how? |
makes mutations more likely
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HIV: tx: NOT ON NOE TEST
Give an AIDS pt immune-stimulating herbs to kick some viral ass! Good idea? |
Hell no! b/c replication occurs once immune system activated
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HIV: tx: NOT ON NOE TEST
My AIDS pt has lymphadenopathy, I'd better flush their lymph system and massage those nodes! Good idea? |
If you want to kill your pt!
this will spread the dz! |
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HIV: tx: NOT ON NOE TEST
Side effects of AIDS tx? (name 4) |
anemia
pancreatitis hepatitis glucose intolerance |
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HIV: tx: NOT ON NOE TEST
HAART side effects? |
osteopenia
osteoperosis |
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HIV: tx: NOT ON NOE TEST
Abacavir what is it? What makes it different from the others? |
part of HAART,
can be fatal if reintroduced to pt who had fever or rash from it before, and has now stopped rx tx for short time |
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Herpesvirus:
MUST KNOW CHART how many types? |
1. herpes simplex virus 1(human herpes virus 1)
2. herpes simplex virus 2(human herpes virus 2) 3. varicella zoster virus(human herpes virus 3) 4. Epstein-Barr virus(human herpes virus 4) 5. Cytomegalovirus(human herpes virus 5) 6. Human herpesvirus 6 7. Human herpesvirus 7 8. Kaposi sarcoma-related herpesvirus(human herpes virus 8) |
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Herpesvirus:
only 1 can survive outside the body & thus aerosol transmission, which one? |
varicella zoster virus (VZV)
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Herpesvirus:
which 3 are linked to malignancy? |
EBV, CMV, & HHV8
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herpes simplex virus 1(human herpes virus 1)
manifests how & where? |
face, genitals, encephalitis, labialis, (and in immune compromised pts-- esophagitis, pneumonia, hepatitis)
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herpes simplex virus 2(human herpes virus 2)
manifests how & where? |
genital, neonatal, (and in immune compromised pts--- hepatitis, disseminated infxn, aspetic meningitis)
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varicella zoster virus(human herpes virus 3)
manifests how & where? |
chicken pox, herpes zoster (shingles)
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Epstein-Barr virus(human herpes virus 4)
manifests how & where? |
linked to malignancy:
infectious mono, hepatitis, encephalitis, nasopharyngeal carcinoma, (and if pt immunocompromised, lymphoproliferative syndromes & oral hairy leukoplakia) |
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Cytomegalovirus(human herpes virus 5)
manifests how & where? |
linked to malignancy:
infectious mono, hepatitis, congenital cytomegalic inclusion dz (and if immune compromised, retinitis, pneumonia, colitis) |
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Human herpesvirus 6
manifests how & where? |
roseola infantum, otitis media with fever, encephalitis
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Human herpesvirus 7
manifests how & where? |
roseola infantum
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Kaposi's sarcoma-associated herpes virus
(human herpesvirus 8) manifest how & where? |
linked to malignancy:
causative role in Kapsoi's sarcoma and AIDS associated non-Hodgkin lymphomas of lungs, pericardium, an abdominal cavity |
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Varicella Zoster Virus (VZV):
manifestation as chicken pox: description of course? (name 4 aspects to ) |
1.acute
2.systemic 3.begins as mild constitutional sxs 4.followed by skin lesions |
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Varicella Zoster Virus (VZV):
manifestation as chicken pox: description of skin lesions? (name 4 aspects to) |
macules
papules vesicles are tear drop shaped crusting |
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Varicella Zoster Virus (VZV):
manifestation as chicken pox: sxs present how soon after exposure? |
11-15 days after exposure
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Varicella Zoster Virus (VZV):
manifestation as chicken pox: who is at risk for complications? |
adults
newborns immunocompromised |
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Varicella Zoster Virus (VZV):
manifestation as chicken pox: how would you describe this phase of the virus? |
acute invasive phase
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Varicella Zoster Virus (VZV):
manifestation as chicken pox: spread how? communicable when? |
infected droplets, very communicable, mostly during prodrome and early stages,
from 48 hours BEFORE first skin lesions appear until the final lesions have crusted |
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Varicella Zoster Virus (VZV):
manifestation as chicken pox: indirect transmission through carriers possible? |
no
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Varicella Zoster Virus (VZV):
manifestation as chicken pox: prevalence when? |
winter, early spring, in 3-4 year cycles
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Varicella Zoster Virus (VZV):
manifestation as herpes zoster (shingels): how would you describe this phase of the virus? |
reactivation of the latent phase
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Signs and symptoms of chickenpox (varicella) in immunocompetent child.
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Rarely severe. mild headache (HA), moderate fever, malaise, and lesions.
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Signs and Symptoms of varicella in pt's >10yrs.
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Prodrome is more likely after 10 yrs of age and more severe in adults.
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Describe the pathognomonic lesion of varicella (chickenpox).
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Lesions which progress to papules, then teardrop vesicles, often intensely itchy, on red bases.
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On what Mucous membranes may the ulcerated lesions of varicella appear?
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Oropharynx, upper resp tract, palpebral conjunctiva, rectal and vaginal mucosa.
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Describe time line of lesion appearance, progression, and remission.
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New lesions usu stop by the 5th day, majority are crusted by 6th day, and disappear in < 20 days after onset.
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If diagnosis is uncertain what can be done to confirm varicella?
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Laboratory confirmation can be performed, using skin scraping.
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Who is at risk for severe, fatal varicella infection?
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Adults with depressed T-cell immunity (lymphoreticular malignancy), those taking corticosteroids or chemo.
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What is primary concern regarding the intense itching of chickenpox, & the risk of the pt scratching it?
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Secondary bacterial infection.
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For reliefe of severe itch what can be done?
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Use of wet compresses, systemic antihistamines, colloidal oatmeal baths
(avoid large doses of systemic and topical antihistamines as they can cause encephalopathy). |
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How long does naturally acquired immunity protect you from future varicella infections?
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Naturally acquired immunity is lifelong post varicella infx.
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Who should be vaccinated against varicella according to our notes?
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All healthy children and susceptible adults, esp. women of child-bearing age, and adults with underlying chronic medical conditions.
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What type of preparation is the varicella vaccination?
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Live attenuated vaccine.
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Who Should not get the varicella vaccine?
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Vaccination is contraindicated in pts with moderate to severe concurrent illnes, immunocompromised, pregnant, those on steroids, kids being given salicylates.
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If a compormised pt contracts varicella what can be done to help attenuate the infection?
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Post exposure vaccination, or IM administration of varicella-zoster immune globulin (VZIG)
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Cytomegalovirus is also known as?
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CMV and Human Herpesvirus Type 5.
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An infection with CMV has a similar course as what other infection?
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CMV is similar to infectious mononucleosis but lacks severe pharangitis.
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How is CMV transmitted?
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Transmitted via blood, body fluids, or translplanted organs, transplacentally or during birth.
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What percentage of adults have had CMV infection?
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60-90%
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Describe the range of affects CMV can have during congenital infection.
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Congenital infection affects range from asymptomatic to abortion, stillbirth, or postnatal death.
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CMV mononucleosis, or CMV hepatitis may present with what signs?
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Acute febrile illness, with elevated aminotransferases, atypical lymphocytosis, and splenomegaly.
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List some of the complications of CMV in the immunocompromised pt.
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mortality, retinitis, ulcerative disease of the colon with abpain & GI blding, esophageal bld, odynophagia.
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Because of the above info about who gets what type of infection who would you suspect has CMV?
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1)healthy people with mononucleosis-like symptoms
2)immunocompromised pts with GI, CNS or retinal symptoms 3) newborns with systemic disease. |
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CMV can be excreted for how long from the body?
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It can be excreted for months or years after infection, therefore, if you find it you aren't necessarily looking at an acute infection.
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Treatment of severe CMV is typically with what?
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Ganciclovir and other antiviral drugs.
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Laboratory dx of severe CMV may involve what studies?
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Cultures, serology, biopsy, or antigen or nucleic acid detection.
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When we say Herpes Simplex Virus we are talking about which HSV infections?
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Human herpesviruses 1 and 2.
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Typical presentation of HSV 1 and 2?
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Recurrent infection affecting the skin, mouth, lips, eyes, and genitals.
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Common severe infections of HSV 1 and 2 include?
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Encephalitis, Meningitis, neonatal herpes, and in immunocompromised pts, disseminated infection.
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Describe lesions of HSV 1 and 2.
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Mucocutaneous clusers of small painful vesicles on an erythematous base.
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What tests can confirm HSV 1 or 2 dx?
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culture, PCR, direct immunofluorescene, or serology.
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Treatment is usually symptomatic, but in severe cases what class of drugs may be used? Give 3 common drugs used for HSV 1 and 2.
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Antiviral drugs, such as acyclovir, valacyclovir, or famciclovir.
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Can both HSV 1 and 2 cause oral or genital infection?
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Yes both HSV 1 and 2 can cause oral and genital infectin.
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Most often HSV 1 causes what 3 specific infections?
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Gingivostomatitis, Herpes Labialis, Herpes Keratitis.
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HSV 2 usually causes lesions where?
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Genital area.
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Viral shedding occurs during what phases of the viral outbreak?
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From prodrom, through active lesion, and may continue even when lesions are not apparent.
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After active infection HSV can remain dormant then periodically emerge, where does the virus hide during latency?
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Remains dormant in nerve ganlia.
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Recurrent herpetic injury are precipitated by what factors?
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Overexposure to sunlight, febrile illnesses, physical and emotional stress, immunosuppression.
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Over time do HSV 1 and 2 out breaks occur more or less often? Are they more or less sever?
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Recurrent eruptions are generally less severe and generally occur less frequently over time.
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What is Herpetic whitlow?
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A swollen, painful, erythematous lesion of the distal phalanx, which results from inoculation of HSV through the skin and is most common in health care workers.
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What is the most common ulcerative sexually transmitted disease in "developed" countries?
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HSV 2; although 10-30% involve HSV 1.
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What is Herpes simplex keratitis?
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HSV infection ofthe corneal epithelium.
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What is Neonatal herpes simplex?
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Infection of HSV that developes in the neonate.
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Dx of HSV is by what methods?
|
Usually just by characteristic lesions, also by Tzanck test, by culture, and by seroconversion.
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Treatment of HSV 1 and 2 involves?
|
Palliative expecially for just mucocutaneious, antivirals (oral and topical).
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Herpes Zoster is known by what two other names?
|
Shingles and
Acute Posterior Ganglionitis. |
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What is the antecedent condition that leads to Herpes Zoste?
|
It is an infection that results when varicella zoster virus reactivates from its latent state in a posterior dorsal root ganglion.
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Describe the common symptomotology of Shingles.
|
Symptoms usu begin with pain along the affected dermatome, followed in 2 to 3 days by a vesicular eruption that is usually diagnostic.
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Treatment of Acute Posterior Ganglionitis (herpes zoster) is usu with what?
|
Antiviral drugs and possibly corticosteroids.
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Who is most likely to contract herpes zoster?
|
Dr. Noe says that there are no clear cut precipitants but that the stats say that the old, young, and immunocompromised are most at risk.
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Chicken pox and Herpes Zoster are caused by the same human herpesvirus type, which type is it?
|
Human Herpesvirus Type 3
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What is Postherpetic neuralgia?
|
A condition occuring most often in the elderly in which persistent pain may last for months, years, or permanently.
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What is Geniculate Zoster?
|
A Herpes Zoster infection results from involvement of the geniculate ganglion.
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Consequences of Geniculate Zoster?
|
Ear pain, facial paralysis, vertigo; vesicles in the external auditory canal, taste lost in anterior 2/3 of tongue.
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Ophthamlic herpes Zoster results from involvement of which ganglion?
|
The Gasserian Ganglion, with eruption in and around the eye, this is the opthalmic division of CN 5.
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What is Hutchison's sign?
|
Vesicles on the tip of the nose, indicative of involvement of the nasociliary branch (often with ocular disease).
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Can you get intraoral zoster?
|
Yes, but it is uncommon.
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When do you suspect an infection with Herpes Zoster?
|
When a pt presents with the characteristic rash and with pain in a dermatomal distribution.
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Treatment of Herpes Zoster may include what for the pain?
|
Wet compresses sooth, but systemic analgesics are often necessary.
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Tx Herpes Zoster infections with what type of drugs?
|
Antivirals, but only effective if given with in 72 hours, and is best if given in the prodromal phase.
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Infectious mononucleosis is caused by what virus?
|
Epstein-Barr virus (EBV)
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Mononucleosis/EBV is categorized as whattype of human herpesvirus?
|
Human herpes virus type 4.
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EBV is characterized by what typical signs and symptoms?
|
Fatigue, fever, pharyngitis, lymphadenopathy.
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How long may these s/s last?
|
Weeks or months.
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What are some of the severe complications of EBV?
|
Splenic rupture, neurologic syndromes, are rare.
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Dx of EBV is by what means?
|
Dx is clinical, or with heterophil antibody testing.
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Treatment for EBV is?
|
EBV treatment is just supportive.
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What percentage of children under 5 are infected with EBV?
|
50%
|
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|
What cells are infected by EBV?
|
B cells; morpholoically abnormal (atypical) lymphocytes develop, mainly from CD8+ T cells.
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From what oriface does EBV shed?
|
Get your mind out of the gutter - the answer is oropharynx.
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|
How is EBV transmitted?
|
Blood products, or more likely from KISSING; almost never from environmental sources.
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EBV is associated with what diseases?
|
1) Burkitt's lymphoma
2)certain B-cell tumors in immunocompromised patients 3) Nasopharyngeal carcinoma |
|
|
Allopaths don't agree but what other syndrome does EBV cause?
|
Chronic Fatigue Syndrome.
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|
What characterizes Chronic Active EBV.
|
Fever, Interstitial pneumonitis, pancytopenia, and uveitis.
|
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|
What complications are typical of EBV?
|
Although recovery is usually complete, complications can be dramatic: neurologic, splenic rupture, respiratory, hepatic.
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Mononucleosis looks a lot like grp A beta-hemolytic streptococci except that???
|
Mononucleosis presents with posterior cervical or generalized adenopathy and hepatosplenomegaly.
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|
Mono. looks like CMV except that?
|
CMV doesn't present with pharyngitis like Mono.
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What is the typical prognosis and treatment of Mononucleosis?
|
Infectious Mononucleosis is usually self-limited. Duration of illness varies, the acute phase lasts about 2 wks. Treatment is supportive.
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|
How does Dr. Noe say to treat EBV post sequeli syndrome?
|
Id the triggering event, id the initial signs and symptoms then treat with: Medical mushrooms, NAC, homeopathic nosoides.
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Roseola infantum is know by what other two names?
|
Exanthem Subitum; and
Pseudorubella |
|
|
What type of human herpesvirus causes Roseola infantum?
|
Type 6, or less commonly HHV-7
|
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|
Who is affected by Roseola infantum?
|
infants and young children are affected.
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How do you diagnose and treat Roseola infantum?
|
dx is clinical, and treatment is symptomatic.
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|
How does Roseola infantum present?
|
High fever, and a rubelliform eruption occurs during or after defervescence. Localizing s/s are absent.
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Despite the "classic" presentation of Roseola infantum what percentage of cases present in this way?
|
Only 30% of the cases have the classic presentation.
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Give three other names for Measles.
|
Rubeola
Morbilli 9-Day Measles |
|
|
How would you characterize the contagious nature of measles?
|
Highly contagious.
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|
What s/s characterize a measles infection.
|
This viral infection is common in children, it presents with fever, cough, coryza, conjunctivitis, enamthem (Koplik's spots), and a maculopapular rash.
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|
Dx of measles is based on what?
|
Clinical presentation.
|
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|
How do you treat measles?
|
Treatment is supportive.
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|
According to the notes how effective is the measles vaccination?
|
Highly effective vaccination.
|
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|
How many cases of measles occur worldwide?
|
30-40 million, with 800,000 deaths primarily in children.
|
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|
How many cases of measles occur in the US annually?
|
100 to 300 cases occur annually.
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|
How is measles spread and when is it most communicable?
|
Spread very easily via airborne droplets during the prodromal phase and early eruptive stage.
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|
What is the pathognomonic of a Measles infection?
|
Koplik's spots which appear 2 to 4 days incubation period.
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|
Other major s/s of measles include?
|
a "Confluent Diffuse Macular Rash" begins as small red spots,grows lrgr,spreads & blends - forming patches.
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Monkeypox is more mild than, but otherwise nearly indistinguishable from what other Orthopoxvirus?
|
Smallpox virus.
|
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|
How do you treat monkeypox?
|
Treatment is support. Report all cases to public health authorities.
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|
Mumps is also called?
|
Epidemic Parotitis because it is an infection of the parotid gland.
|
|
|
Complications of mumpus include?
|
Orchtis, meningoencephalitis,and pancreatitis.
|
|
|
What is a dx of mumps based on?
|
Clinical presention.
|
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|
How is mumps spread?
|
Spread by droplets or via saliva.
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|
What do they say about the mumps vaccination?
|
It is highly effective.
|
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|
While parotid gland swelling is the most common sign of mumps what other organs can be involved?
|
Testicals (orchitis), ovaries (oophoritis), meningies, pancrease, prostate, nephrons, myocardium, mastitis
|
|
|
How is Mumps treated?
|
Treatment of mumps and its complications is supportive.
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Rubella, give two other names for Rubella.
|
German Measles; 3-Day Measles.
|
|
|
What are the common characteristics of a Rubella infection?
|
Adenopathy, rash, sometimes constitutional symptoms that are usu. mild and brief.
|
|
|
When is the worst time to contract Rubella?
|
Infection during early pregnancy can cause spontaneous abortion, stillbirth, or congenital defects, i.e. Rubella is teratogenic.
|
|
|
How is Rubella treated?
|
Treatment is usually unnecessary.
|
|
|
As always what do they say about the Rubella vaccination?
|
It is effective.
|
|
|
How is Rubella spread?
|
Respiratory Droplets via close contact or through the air.
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|
|
The rash characteristic of Rubella begins on what part of the body usually?
|
The Face and neck, then moves to the trunk, then the extremities.
|
|
|
There is a characteristic pharyngeal injection at the onset of what infection?
|
Rubella.
|
|
|
What is the worst case scinario regarding an infection with Rubellss?
|
Progressive Rubella Panencephalitis, a neurological disorder in kids.
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|
Give another name for Smallpox.
|
Variola is another name for this infection.
|
|
|
What is the main concern regarding outbreaks of Smallpox (Variola?
|
Bioterrorism.
|
|
|
How is an infection with Smallpox (Variola) characterized?
|
Severe constitutional symptoms, and a characteristic pustualar rash.
|
|
|
Is the smallpox vaccine part of the standard vaccine schedule?
|
No, because of its risks the vaccination to this infection is given selectively.
|
|
|
Name the virus that the WHO declared eradicated in the natural world.
|
Smallpox (Variola). Last case in 1977.
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|
How are Respiratory Viruses categorized?
|
These infections can be classified by the causative virus, they are generally classified clinically according to syndrome (common cold, croup, etc.).
|
|
|
True or False: each respiratory virus causes only one specific syndrome.
|
False. Although specific pathogens commonly produce characteristic clinical s/s, each is capable of causing any of the viral resp syndroms
|
|
|
In what ways may an Adenovirus infection manifest?
|
Most are asymptomatic, or any one of many of adenoviruses may cause a specific syndrome resulting in keratoconjuctivitis, pharyngitis, fever, bronchiolitis (peds), pneumonia (peds).
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|
|
The Common Cold, aka?
|
Upper Respiratory Infection.
|
|
|
Characterize the common cold.
|
An acute, usually afebrile, self limited viral infection involving upper respiratory symptoms, such as rhinorrhea, cough, and sore throat.
|
|
|
What is the most common viral cause of the common cold?
|
Rhinovirus, of which an one of 100+ serotypes could be responsible.
|
|
|
What other viruses are responsible for causing the common cold?
|
Coronavirus, influenza, parainfluenza, and respiratory syncytial virus.
|
|
|
Most common seasons for URIs (upper resp infections, aka the common cold)is what?
|
Fall and Spring. Less common during winter.
|
|
|
How are URIs spread?
|
Most efficiently spread by direct person-to-person contact; and also by large-particle aerosols.
|
|
|
What is the "most potent deterrent to URIs?
|
The presence of specific neutralizing antibodies in the serum and secretions, induced by previous exposure to the same or a closely related virus is the best deterrent to these infections.
|
|
|
Typical s/s to expect with an UPI (common cold).
|
sore throat, sneezing, rhinorrhea, nasal obstruction, malaise, NO fever if infx is d/t rhinovirus or coronavirus, cough.
|
|
|
purulent sinusitis and otitis media in the context of an URI would suggest what about the infection?
|
Either d/t progression ofthe URI viral infection itself, or to a secondary bacterial infection.
|
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|
Think anyone will read the cards this far back?
|
Hell no!
|
|
|
Wonder if Alexis is disturbed that I don't capitalize the answers I type?
|
probably
|
|
|
Influenza:
(Flu, Grip, Grippe) Signs & sxs? (name 7 -hint-many are common cold sxs) |
fever, cough, h/a, malaise, sudden chills, muscle aches, coryza
|
|
|
Influenza:
(Flu, Grip, Grippe) What is coryza? |
acute catarrhal inflam of nasal mucous membranes accompanied by acute nasal discharge
|
|
|
Influenza:
(Flu, Grip, Grippe) Populations most @ risk among epidemics? |
institutionalized, extreme ages, cardiopulmonary insuff, late in pregnancy
|
|
|
Influenza:
(Flu, Grip, Grippe) Classified as Types? |
Influenza A (harshest), B, C(which does not cause influenza illness)
|
|
|
Influenza:
(Flu, Grip, Grippe) Name the 2 glycoproteins most which bind to sialic acid of host cells, allowing for viral penetration? |
HA (Hemagglutinin)
NA (Neuraminidase) |
|
|
Influenza:
(Flu, Grip, Grippe) Mutations of what glycoproteins allow for frequent mutations of viral strains? |
HA & NA
|
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|
Influenza:
(Flu, Grip, Grippe) Epidemics occur in the US every ______, and are associated with which classification? |
2-3 years, Influenza A
|
|
|
Influenza:
(Flu, Grip, Grippe) Epidemics occur in the US every 3-5 years are associated with which classification? |
Influenza B
|
|
|
Influenza:
(Flu, Grip, Grippe) Spread how? (name 3 ways) |
airborne
person-to-person contaminated items |
|
|
Influenza:
(Flu, Grip, Grippe) Late Signs & Sxs in respitory tract & cough? (name |
LOWER respitory infxn
cough becomes persistant, rapsy, & productive |
|
|
Influenza:
(Flu, Grip, Grippe) Dx (general non-definitive)? |
made when influenza known to be in community, rapid tests are controversial
|
|
|
Influenza:
(Flu, Grip, Grippe) Dx (definitive) requires what? |
culture of nasopharyngeal swabs, aspirate, or Ab titers
--this requires several days |
|
|
Influenza:
(Flu, Grip, Grippe) Incubation period? |
1-4 days, usu 24 hrs
|
|
|
Influenza:
(Flu, Grip, Grippe) Recovery typically? |
1-2 weeks,
|
|
|
Influenza:
(Flu, Grip, Grippe) Influenza-related ________ can be fatal in susceptible people? |
influenza-related pneumonia
|
|
|
Influenza:
(Flu, Grip, Grippe) Vaccinations may be helpful if performed how often? |
annually
|
|
|
Avian influenza:
(Bird Flu) Linked to which Influenza classification? |
Influenza A
|
|
|
Avian influenza:
(Bird Flu) All of the following strains have caused human infxn (H5N1, H7N7, H7N3, H9N2) but most human infxns are d/t which one? |
H5N1
|
|
|
Avian influenza:
(Bird Flu) Has some human-to-human transmission been implicated yet? |
Yes, in the Netherlands
|
|
|
Avian influenza:
(Bird Flu) True/False: If suspected in a pt, you are required by law to culture & send to CDC? |
No way Jose! Culture is forbidden b/c they don't know enough about it, though you do have to contact CDC
|
|
|
Parainfluenza Virus:
What do they cause? |
ACUTE RESPITORY infxns
|
|
|
Parainfluenza Virus:
What population do they target most? |
kids
|
|
|
Parainfluenza Virus:
Are one of several viruses contributing to common cold (URI)? |
yes
|
|
|
Parainfluenza Virus:
These are specifically what viruses & with how many types? |
Paramyxoviruses types 1-4
|
|
|
Parainfluenza Virus:
What do all types of paramyxoviruses share? |
antigenic cross-reactivity, which is similarity of ag so much that an ab made specifically for one will also engage the second ag
|
|
|
Parainfluenza Virus:
May manifest as common cold, influenza-like, or pneumonia-like with _____as most common severe manifestation? |
croup
|
|
|
Parainfluenza Virus & croup:
Parainfluenza # _____ probably causes croup? |
Parainfluenza 1
|
|
|
Parainfluenza Virus & croup:
Croup is a childhood dz affecting what ages & where in the respitory system? |
Croup (laryngotracheobronchitis) is an URI affecting 6-36 months
|
|
|
Parainfluenza & croup:
Croup hallmark? |
stridor, seal bark, resonant barking cough, diff breather
|
|
|
Respitory Syncytial Virus (RSV):
Causes URI or LRI? |
lower respitory infxn
|
|
|
RSV:
Presents as asymtomatic, mild or severe? |
could be all 3
|
|
|
RSV:
Is an RNA virus classified as a _______virus (hint--think lung_ |
a pneumovirus
|
|
|
RSV:
True or false: Is ubiquitous infecting almost all children by age 4? |
true
|
|
|
RSV:
Immune response does not what? |
protect against reinfection so almost 1/2 people exposed become infected
|
|
|
RSV:
Outbreaks occur when? |
annually in winter & early spring
|
|
|
Human Metapneumovirus (hMPV):
similar to RSV in many ways but much lower incidence. so is it a URI or LRI? asymptomatic, mild, or sevre? occurs when? |
LRI
could be any form of severity winter & early spring |
|
|
RSV & hMPV:
signs & sxs? (name 2) |
bronchiolitis & pneumonia (must know)
also, apnea for RSV in x<6months or afebrile common cold in healthy adults |
|
|
RSV & hMPV:
Tx & prevention? |
O2, hydration, abx only if infxn in chest
corticosteroids & bronchodilators not helpful |
|
|
Severe Acute Respitory Syn:
(SARS) Caused by what kind of virus and is it new or old? (hint--the virus is mexican) |
CORONAvirus (SARS-CoV)this thing is so new it is unrelated to any known huamn or animal coronaviruses
|
|
|
Severe Acute Respitory Syn:
(SARS) Spread how? Incubation how long? |
respitory droplets
2-10 days |
|
|
Severe Acute Respitory Syn:
(SARS) Results in ______-like illness? |
influenza-like illness with fever, cough, chills, rigor,
|
|
|
Severe Acute Respitory Syn:
(SARS) URI sxs common or uncommon? Sxs are specific or nonspecific? |
uncommon URI sxs
sxs are nonspecific so difficult to know SARS is the problem |
|
|
Severe Acute Respitory Syn:
(SARS) Progressive sxs include? (name 3) |
dyspnea, hypoxemia, ARDS (acute respitory distress syn)
|
|
|
Severe Acute Respitory Syn:
(SARS) Can any serologic or PCR tests be used for clinical management? |
no
|
|
|
Severe Acute Respitory Syn:
(SARS) Tx? |
supportive, no effective remedies yet
|
|
|
Severe Acute Respitory Syn:
(SARS) pts placed in what kind of room? |
negative pressure
|
|
|
Severe Acute Respitory Syn:
(SARS) Protocol for people exposed to pts with SARS? |
*if sxs absent - continue activities as normal
*if sxs like fever or resp present - limilt activity *if sxs do not progress to SARS criteria in 72 hours - return to normal activity |
|
|
If you have actually read all these fucking cards, please take the time to edit the "answer" side of this card by adding your name to the list of pioneers----you have just hiked the Appalachian Trail
|
We actually read all your fucking viral cards:
am I truely the only one? These cards were great! Penelope |
