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52 Cards in this Set

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Cytomegalovirus
-HHV5

-has the largest genome of the HHVs

-the most prevalent cause of congenital infections
What does CMV lead to?
-heterophile negative infectious mononucleosis (milder version of heterophile + infectious mono)

-infections of multiple organs in AIDS pts

-organ rejections
Lab diagnosis (cytomegalic cell)
-"owl's eye" basophilic intranuclear inclusion body:
such infected cells can be found in any tissue of the body or in urine and are thought to be infected epi cells

***50% OF ADULTS IN THE US HAVE CMV, IN MOST CASES SHEDDING IS ASYMPTOMATIC
Where is CMV found?
-saliva
-urine
-blood
-throat washings
-tears
-tit milk
-man juice
-shit
-vag secretions
-transplant tissues
How is CMV transmitted?
-orally and sexually
-in blood transfusions
-tissue transplants
-in utero
-at birth and by nursing
FDA approved treatment of CMV
-Acyclovir
-Ganciclovir
-Valganciclovir
-Cidofovir
-Foscarnet

-passive administration of CMV serum Igs is commonly used for prevention or treatment of CMV disease following organ transplant
Yellow Fever:

Clinical symptoms
-pt may be viremic for 3-6 days prior to symptoms

-initially fever and chills, severe headache, back pain, general muscle aches, nausea fatigue, and weakness

-phase may be followed by a short period of symptom remission
What is the toxic phase of Yellow Fever?
-in 15% of pts, the next phase

-fever returns w/ headaches, back pain, nausea, vomit, ab pain, fatigue

-Hepatic coagulopathy produces hemorrhagic symptoms:
1. hematemesis (black vomit)
2. Epistaxis, gum bleeding, and petechial and purpuric hemmorhages (bruising)
Treatment and control of Yellow Fever
-no specific medication for treatment:
-may take analgesics with acetaminophen and NOT asprin**
-rest, fluids

-Live, attenuated vaccine available-->highly effective
Yellow Fever Live Virus Vaccine
-single dose confers immunity for 10 or more years

-booster dose every 10 yrs for people living in high risk areas

-Adults and children > 9 months can take this vaccine
Dengue
-sudden onset of fever, severe headache, myalgias, arthralgias, leukopenia, thrombocytopenia and hemorrhagic manifestations

-occasional shock and hemorrhage--> leading to death
Dengue Prevention
-is key

-medical personnel still unclear how best to treat hemorrhagic cases

-transmitted by mosquito bites

-abolish mosquito breeding grounds including no stagnant water, proper disposal of garbage
Dengue Prevention for travelers
-Risk of indoor mosquito bites is reduced by use of
1. Air conditioning or screens on windows and doors
2. Proper application of mosquito repellents containing 20-30% DEET
-I personally prefer 100% DEET nothing fucks with you
Ebola and Marburg Viruses
-Filoviradae Family

-enveloped, helical capsid, - ssRNA
Ebola and Marburg Viruses Symptoms
-rash on trunk (early stages)

-pts bleed from their orifices, their mucus membranes

-MASSIVE internal and external hemorrhage

-Mortality rate 25-100%
Ebola and Marburg Viruses

Transmission
-direct contact with an infected person or with their bodily fluids

-handling dead gorilla carcases
*Laura is a high risk individual

-eating infected primate meat

-->02/03 Ebola epidemic in C. Africa
Lassa Fever


General Information
Arenaviridae Family

-enveloped, beaded NC, -ssRNA
Lassa Fever

Transmission
-Inhalation of infected aerosols of rat droppings, urine, hair etc

-eating food contaminated with the above

-95% of infected pregos suffer abortions
***noted
Colorado Tick Fever

General Information
-carried to humans by wood tick Dermacentor Andersoni
(which bacterial disease does this tick also cause....)

-Reoviradae family, Coltivirus genus

-naked, icosahedral capsids (2), dsRNA segments
Coltivirus

General Information
-multiplies in arthropods (ticks) and vertebrates (humans)

-Hosts: ground squirrels, porcupines, chipmunks, and mice of the genus Peromyscus
Coltivirus

Clinical Symptoms
-biphasic fever and conjunctivitis

*Fever is nearly always present
-a fever pattern noted in about half the cases is "saddleback" fever which is suggestive of diagnosis
Coltivirus

Clinical Symptoms continued...
*rash is infrequent
-macular, maculopapular, and petechial
-distribution is often truncal (more acral rash in RMSF)

-rash is short lived (diff than RMSF)

-Petechiae occur in rare cases and may be complicated by thrombocytopenia
RMSF
*Rash appears on the palms and soles

-later becomes generalized and may become hemorrhagic

-microscopy using DFA of skin lesion biopsy allows confirmation within hours
Colorado Tick Fever

Diagnosis
-Rash appears on trunk and is short lived

-immunoflourescent staining of blood smears to test for viral Ags on the surface of RBS

-Serology:ELISA to test for IgM or IgG levels in acute and convalescent sera
Colorado Tick Fever

Pathogenesis and Immunity
-infects erythroid precursors

-persists in adult RBCs and this protects the virus from being cleared (immune evasion)

-first 10 days - high levels of interferon

-viremia can persist for wks/months which promotes transmission to the tick vector
Colorado Tick Fever

Epidemiology
-western and NW areas of the US and Canada, where the wood tick is found

-tick AKA Rocky Mt wood tick

-acquire the virus by feeding on an infected host and transmit it to a new host in its saliva, during feeding
Colorado Tick Fever

Treatment, Prevention, and Control
-Supportive treatment (acetaminophen and analgesics)
-Protective clothing
-Avoid tick infested areas
-Remove ticks before they bite
-NO vaccine
-DO NOT donate Blood (virus is transmissible via blood)
HIV

General Information
-member of the:

1. Retroviridae family

2. Lentivirus genus
HIV-1
Virulence: High

Ability to transmit: High

Prevalence: Global

Purported Origin: Chimps

***causes the majority of HIV infections globally
HIV-2
Virulence: Low

Ability to transmit: Low

Prevalence: West Africa

Purported Origin: Sooty Mangabey
GP120 and CD4 Receptor
-GP120 binds to the CD4 receptor

-CD4 is a glycoprotein expressed on the surface of T-help cells, T-reg cells, monocytes, macros, and dendritics

HIV induced immunosuppression (AIDS) results from a reduction in CD4 and T cells
What are the coreceptors for M-Troic and T-Tropic Strains?
-RT lacks proof reading abilities, resulting in ~5 errors/genome

-this genetic instability is responsible for emergence of new strains during disease
HIV

Symptoms
-initial symptoms could subside after 2-3 weeks

-Virus replication in the lymph nodes

-->May be asymptomatic or persist as generalized lymphadenopathy for years
What are indicative of AIDS
-Oppurtunistic infections

-fungal, bacterial, protozoal, viral
-oppurtunistic neoplasias
What to look for when trying to diagnose HIV?
-bc the CD4 counts are so variable some HC providers prefer to look at CD4% which refer to total lymphocytes

***This % is > stable than the CD4 cell number
***Normal range between 20-40%
Corresponding Values for CD4 count and CD4%
>500 ~ 29%

20-500 ~ 14 - 28%

<200 ~ <14%
So, CD4 counts or CD4%?
-some HC providers start agressive ART when CD4% < 15% even if the CD4 count is high

-CD4% < 14% indicates serious immune damage, it is a sign of AIDS in ppl with HIV infection

CD4% is a predictor of HIV disease progression
CD4:CD8 as a correlate of HIV
CD4:CD8 ratio:
-healthy ratio is .9 - 1.9, indicating 1-2 CD4 cells per CD8 cell

-ppl with HIV, ratio drops, indicating more CD8 cells than CD4 cells
What do official treatment guidelines in the US suggest regarding CD4 counts?
-bc they are such an important indicator of the strength of the immune system CD4 counts should be monitored every 3-4 months
Testing for HIV
-ELISA on blood is the most common tests: looks for Abs to HIV

A + reaction is confirmed by Western Blotting
Specimens used: blood, oral fluid (not saliva), urine
Why do does HIV cause anigenic drift of gp120 and heavy glycosylation of gp120?
-in order to evade immune detection
Why do does HIV infect lymphocytes and macrophages?
-to inactivate key players of immune response
Why do does HIV inactivate CD4 T cells?
-loos of major activator of the immune response and the DTH response

kinda like HIV is the terminator and John Connor is the CD4 T Cell, there can be no resistance if HIV is successful in inactivating CD4 T cells
How does one reduce risk of perinatal transmission of HIV?
1. Taking combination therapy during preggers and taking AZT during labor and birth

2. C section

3. Administering AZT to newborn for up to 6 weeks after birth

4. using formula milk, milk bank milk instead of breast feeding
Control of HIV
-know the antiviral drugs that can limit disease progression in HIV infected pts

-know why HIV protease is important

-know what the standard of care is for therapy
HTLV

General information
-retroviridae family

-oncovirinae subfamily

-adult acute T-cell lymphocyte leukemia (ATLL)

-HTLV-1 associated myelopathy (neurologic)
HTLV

Transmission
-long latency period (30+ yrs)

-spreads through blood transfusion, sex, breast feeding

-infects T cells: CD4 + Th and DTH Tcells
HTLV

Clinical Syndromes
-usually asymptomatic

-ATLL is a neoplasia of CD4 helper T cells

-T cells express high levels of IL-2R

-Acute ATLL is usually fatal within one year
HTLV


Epidemiology
-Endemic to southern Japan, found in the Carribean and among blacks in the SE U.S.
(this sounds racist, Maya is Indian right? so is Krishna and he is racist so at least he wont forget this one)

-Okinawa: 35% are seropositive
HTLV

Transmission
From mom to child (placenta/milk)

-making whoopi (throwback term)

-Blood transfusions

-IV drug use (shared needles)
HTLV

Treatment and Control
-AZT and INF

-no current approved treatment

-Abs against the IL-2R (tagged w/ toxins/radiations)

-sexual precautions, screening of blood

***maternal screening needs to be implemented
Maya's closing statement:

Know which viruses are latent

Know which vaccines you can give to pregos
MAKE A CHART