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Block 6 Week 4 > DNA viruses- Verma > Flashcards

DNA viruses- Verma Flashcards

1
Q

What are the three types of enveloped DNA viruses?

A

pox, herpes, hepadna

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2
Q

What are the four types of nake capsid DNA viruses?

A

polyoma
papilloma
adeno
Parvo (SS)

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3
Q

What kind of virus is the human herpes virus?

A

enveloped DNA virus

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4
Q

What are the three types of alpha herpes virus?

A

VZV
HSV-1
HSV-2

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5
Q

What are the three types of beta-herpesvirus?

A

CMV
HHV-6
HHV-7

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6
Q

What are the 2 types of gamma-herpesvirus?

A

KSHV

EBV

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7
Q

What happens after the primary infection of herpesvirus?

A

you get latent or persisten infection

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8
Q

When will you get reactivation of herpesvirus?

A

during immunosuppresion

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9
Q

Both primary herpesvirus infection and reactivations are likely to be more serious in (blank) patients.

A

immunocompromised

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10
Q

Herpesvirus encode their own (blank) which are targets of anti-viral drugs.

A

DNA polymerase

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11
Q

How does herpesvirus enter the cell?

A

receptor-mediated endocytosis

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12
Q

How does herpesvirus replicate?

A 
receptor mediated endocytosis
viral DNA translocates to nucleus
transcription via cellular RNA polymerase
IE-> regulatory
E- enzymes for DNA rep
L-> structural
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13
Q

What is the Herpes simplex virus?

A

HSV-1 and HSV-2

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14
Q

HSV-1 and HSV-2 show latency in (blank)

A

neurons (latency associated with transcripts)

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15
Q

How do you know someone has herpes simplex virus 1 versus herpes simplex virus 2?

A

antigenicity and location of lesions

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16
Q

In HSV-1 where will you see lesions?

A

mouth, eye, skin (above the waist) CNS (encephalitis), disseminate to viscera in immunocompromised people

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17
Q

IN HSV-2 where will you see lesions?

A

vesicular lesions below the waist (especially genitals), CNS (meningitis), neonates and doesnt disseminate to viscera in immunocompromised people

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18
Q

What diseases are associated with HSV-1?

A

gingivostomatosis
herpes labialis (cold sores)
encephalitis

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19
Q

Who primarily gets gingivostomatitis?

A

children

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20
Q

What are the symptoms of gingivostomatitis?

A

fever, irritabiity, and vesciular lesions in the mouth. THe primary disease is more severe than the recurrences

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21
Q

What is characteristic of herpes labialis (cold sores)?

A

reucrrent form-characterized by the crops of vesices at the mucocutaneous junctions of the lips or nose

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22
Q

What is characteristic of encephalitis?

A

necrotic lesion in the temporal lobe. Fever, headache and seizures

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23
Q

What are the 2 types of HSV-2 diseases?

A

genital herpes

neonatal herpes

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24
Q

What is characteristic of genital herpes?

A

painful vesicular lesions on the genitals.
lesions are more severe in primary disease than in recurrences
primary infection present with fever
asymptomatic infections (some people have antibody to HSV-2 but have no history of disease)

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25
Q

What is charachteristic of neonatal herpes?

A

contact with vesicular lesions within the birth cana

varies from severe disease (encephalitis) to milder local lesions (skin, eye, mouth) to asymptomatic infection

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26
Q

How is HSV-1 transmitted?

Where do symptoms show?

A

through saliva

face

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27
Q

How is HSV-2 transmitted?

Where do symptoms show?

A

sexual contact

genital area

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28
Q

How can you get HSV-2 in the oral region and HSV-1 on the genitals?

A

oral-genital sexual practices

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29
Q

(blank) percent of people in the US are infected with HSV-1 and (bank) percent have recurrent herpes labialis

A

50-60%

40%

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30
Q

Most primary infections by HSV-1 occur when?

A

childhood (evidenced by early antibodies)

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31
Q

When does HSV-2 appear?

A

at age of sexual activity

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32
Q

How can you diagnose HSV through the lab?

A

virus isolation and growth in culture (most definitive)
PCR-rapid diagnosis of encephalitis :detects DNA in spinal fluid
Serology-> for primary infection
Tzanck smear

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33
Q

What is this:

base of vesicles are stained with Giesma stain. Multinucleated giant cells

A

Tzanck smear

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34
Q

How do you treat encephalitis caused by HSV-1 and HSV-2?

A

Acyclovir (acycloguanosine, zovirax)

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35
Q

How should you treat HSV-1 that is resistant to acyclovir?

A

with foscarnet

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36
Q

What is used to treat genita herpes?

A

valcyclovir and famciclovir

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37
Q

What can you do to prevent the spread of HSV-1 or HSV-2?

A

avoid vesicular lesions and if pregnant have a C-section if active lesions are present

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38
Q

A 20y old women present to the university health clinic with painful vesicular lesions on the vulva and perineum. She has not felt well the past week and complains of pain on urination. During the history, you find out that she has had unprotected sex with three different partners the past month. On physical examination, she has a low-grade fever and lymphadenopathy. You swab a vesicular lesion and submit the specimen to the laboratory to confirm your diagnosis. What is this?

A

HSV-2

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39
Q

What is varicella-zoster virus (HHV-3)?

A 
Chicken pox (primary infection) 
shingles (reactivation)
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40
Q

What does the primary infection of varicella result in?

A

chickenpox

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41
Q

What is the incubation period of varicella?

A

14-21 days

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42
Q

What is the clinical presentation of varicella?

A

fever, lymphadenopathy, and widespread vesicular rash

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43
Q

Complications with varicella are rare but occures more frequently in (blank) and (Blank) patients, it includes what three disease?

A

adults and immunocompromised

viral pneumonia, encephalitis and hemorrhagic chickenpox

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44
Q

What is herpes zoster?

A

shingles

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45
Q

Who usually gets shingles?

A

people over the age of 50

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46
Q

How does herpes zoster (shingles) work?

A

the latent virus reactivates in sensory ganglion and tracks down the sensory nerve to the appropriate segment

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47
Q

What areas of the body will herpes zoster create major problems?

A

in the eye and face

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48
Q

Which people should not get shingles cuz it will unbelievable awful for them?

A

immunocompromised patients

reactivation may occur mutiple times with severe complications

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49
Q

How do you treat varicella and herpes zoster?

A

with prevention; vaccines (varivax for varicella) and zostavax for zoster

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50
Q

Who should get varivax?

Who should get zostavax?

A

recommended in 1-12 years children

people over 60

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51
Q

What medications can reduce the duration of varicella/shingles in aduls?

A

acyclovir, famciclovir, valcyclovir

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52
Q

How can you diagnose varicella/shingles?

A

Cytology-Direct IFA, PCR (most sensitive)
Virus Isolation (difficult to isolate, virus very labile)
Serology: antibody titers are normally low

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53
Q

A 55y old women undergoing chemotherapy for metastatic breast cancer is seen by her oncologist because of ithcy, burning blisters on her rib cage that began 3 days earlier as a tingly or numb sensation. Physical examination reveals an otherwise healthy patient with vesicular eruptions along a thoracic dermatome.
What is this?

A

shingles!

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54
Q

What is epstein barr virus (HHV4)?

A

causes infectious mononucleosis, B-cell lymphoma and nasopharyngeal carcinoma (NPC)

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55
Q

What are the antigens found on epstein barr virus?

A 
Viral capsid antigen (VCA)
Early antigens (EA)
Nuclear antigens (EBNA)
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56
Q

How can epstein barr virus present?

A

Infectious mononucleosis
Nasopharyngeal carcinoma
African Burkitt’s lymphoma
Post-transplant lymphoproliferative disease (PTLD)
Oral Hairy Leukoplakia-(whitish non-malignant hairy surface on the lateral side of the tongue)

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57
Q

What does infectious mononucleosis present like?

A

infection in children is subclinical

fatigue, fever, sore throat

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58
Q

How is EBV transmitted?

A

by saliva (greater than 90% of infected people shed virus for life)

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59
Q

At least (blank) percent of population is infected by age 30

A

70%

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60
Q

(blank) and (blank) people are at high risk for lymphoproliferative disorders.

A

AIDS and immunodeficient

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61
Q

How does the esptein barr virus spread throughout the body?

A

the infection occurs in oropharynx and spreads to blood to infect B lymphocytes

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62
Q

What is the immune response to EBV infection?

A

IgM antibody to VCA
IgG antibody to VCA persists for life.
IgM for acute infection and IgG for prior infection

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63
Q

What will a productive infection cause antibodies to make?

A

antibodies to VCA-MA-EA and when cell lysis occurs then to EBNA

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64
Q

If you are looking at blood, how do you know you are looking at EBV?

A

30% are atypical lymphocytes (enlarged nucleus and vaculoated cytoplasm)

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65
Q

How can you diagnose EBV?

A

hematologically
immunologically (heterophile antibody, EBV antibody)
PCR

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66
Q

What is heterophile antibody for?

A

for early diagnosis of Infectious mononucleosis

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67
Q

What is oral hairy leukoplakia?

A

whitish non-malignant hairy surface on the lateral side of the tongue caused by EBV

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68
Q

Can you use acyclovir on EBV?

Is there a vaccine for EBV?

A

No :( this is very limited activity

N0 :(

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69
Q

A 19y old college student presents to the student health clinic complaining of fever, fatigue and sore throat that developed about a month ago after spring break. Physical examination shows pharyngitis, cervical and axillary lymphadenopathy, and splenomegaly. Laboratory test show atypical lymphocytes and positive for heterophile antibody.
What is this?

A

EBV

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70
Q

What is the most common viral cause of congenital birth defects?

A

Cytomegalovirus (HHV5)

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71
Q

What kind of pathogen is cytomegalovirus and who does it sneak into?

A

opportunistic pathogen in immunocompromised patients

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72
Q

What can cytomegalovirus (HHV5) cause?

A

pneumonia, retinitis, and colitis in immunocompromised patients such as recipients of bone marrow.

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73
Q

Where is latency of cytomegalovirus found?

A

in stromal cells of the bone marrow

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74
Q

At what age can you get cytolomegalovirus?

A

any age, at birth you get congenital cytolomegalovirus that will effect .5-2.5% of all newborns in the US

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75
Q

How can you transmit CMV in children?

A

saliva

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76
Q

How can you transmit CMV in adults?

A

sexually

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77
Q

Risk for serious birth defects is extremely high for infants born to whom?

A

mothers with primary CMV infection during pregnancy

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78
Q

What wil you find in immune competent adults with CMV?

A

heterophile negative mononucleiosis fever and the presence of abnormal lymphocytes

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79
Q

What three inflammatory diseases occur in immune compromised individuals with CMV?

A

pneumonitis, retinitis, hepatitis

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80
Q

How do you treat CMV?

A

ganciclovir and foscarnet

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81
Q

How do you diagnose CMV?

A

histologicaly
w/ antibodies, probes, PCR
cell culture-easy

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82
Q

Is there a vaccine for CMV?

A

no

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83
Q

How do you prevent disseminated CMV infections in organ transplant patients?

A

a high titer immune globulin (cytogam)

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84
Q

What causes Roseola infantum?

A

HHV-6 and 7

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85
Q

What is the main target of HHV-6 and 7?

A

T lymphocyte, although B lymphocytes may be infected

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86
Q

HHV-6 and HHV-7 share limited nucelotide homology and antigenic (blank). SO how are they related to each other?

A

cross-reactivity

similiar to how HSV1 and HSV2 are

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87
Q

Where do you find HHV-6 and HHV-7?

A

it is ubiquitous worldwide

88
Q

How do you transmit HHV-6 and HHV-7?

A

through saliva and breast feeding

89
Q

By the time of (blank), 90-99% of the population becomes infected by both viruses

A

adulthood

90
Q

When is the earliest you can get HHV6 and HHV7 infection? Why?

A

acquired after the age of 4 months when the effect of maternal antibody wears off

91
Q

Primary (blank) is associated with roseola infantum, a classic diease of childhood

A

HHV-6

92
Q

What happens with HHV-6 after you get infected?

A

A spiking fever develops over a period of 2 days followed by a mild rash.

93
Q

How do you diagnose HHV-6 and HHV-7?

A

IgM and IgG

94
Q

A 9 month old infant is seen in a pediatric practice with a history of irritability and a fever of 103oF for 3 days followed by appearance of a generalized erythematous maculopapular rash on the neck and truck. The infant was treated symptomatically and recovered within a few days without complications

A

This is Roseola infantum caused by HHV-6

95
Q

What is HHV8?

A

Kaposi sarcome herpesvirus

96
Q

What is Kaposi’s sarcoma herpesvirus associated with?

A

castleman’s disease and primary effusion lymphomas

97
Q

Most patients with KS have antibodies against (blank)

A

HHV-8

98
Q

The seroprevalence of HHV8 is (blank) among the general population but (blank) in groups susceptible to KS, such as homosexuals

A

low

high

99
Q

A 28y old homosexual man is seen by a dermatologist with complaints of bluish-purple spots on his chest and thigh. History is significant for feeling tired and intermittent diarrhea for the past year and unprotected sex with multiple partners. Physical examination reveals generalized lymphadenopathy. A biopsy of a lesion is submitted to confirm the diagnosis.
What is this?

A

Kaposi’s sarcoma herpesvirus: HHV8

100
Q

In 18th centry, this virus accounted for 7-12% of deaths in england

A

pox virus

101
Q

Has smallpox been eradicated?

A

yes

102
Q

Pox virus is a category (blank) select agent

A

A

103
Q

The virion paricle of the pox virus is….?

A

ds DNA genome and DNA dependent RNA polymerase

104
Q

Where does the pox virus replicate?

A

in the cytoplasm

105
Q

How many serotypes does the pox virus have?

A

one, this is why we can have a successful vaccine for it

106
Q

How do you transmit pox virus?

A

respiratory aerosol or by direct contact with virus

107
Q

What does the small pox virus infect?

A

upper respiratory tract-lymph node-blood vessels (primary viremia)

108
Q

When pox virus is messing with the internal organs and the virus reenters blood and is exposed in the skin, what is this called?

A

secondary viremia

109
Q

What is the rash in small pox due to?

A

replication of virus in the skin

110
Q

What is the incubation period of the pox virus?

A

7-14 days

111
Q

What is the clinical presentation of the pox virus?

A

fever, malaise

rash worst on the face and extremities

112
Q

How do you diagnose pox virus?

A

culturing virus, viral antigens

113
Q

Disease is eradicated by the global use of (blank)

A

live attenuated vaccine

114
Q

Why was the vaccine successful for small pox?

A

single serotype, and no animal reservoir

115
Q

How do you give the small pox vaccine?

A

intra-dermally, forms vesicles

116
Q

Exposed individuals can be immunized up to (blank) days POST infection and be protected from small pox!!! AMAZING

A

4 days

117
Q

How can you treat small pox?

A

vaccine immune globulins-high titer antibodies- treat complications

118
Q

What does molluscum contagiosum virus cause?

A

small papule of the skin or mucus membrane. This are painless, non-itchy and non-inflamed lesions

119
Q

Where do the lesions of molluscum contagiosum virus most commonly occu?

A

on trunk, genitalia, proximal extremities

120
Q

Do the lesions of molluscum contagiosum virus occur in lines or clusters?

A

clusters

121
Q

What is the incubation period of lesions of molluscum contagiosum virus?

A

2-8 weeks

122
Q

How do you diagnose molluscum contagiosum virus?

A

clinically cuz the virus is not culturalable

123
Q

A 9y old boy is seen in a pediatric practice with a chief complaint of multiple lumps on his face that have persisted for 2 weeks. Physical examination reveals multiple painless, flesh-colored, nodule on the face and trunk without signs of inflammation. What is this?

A

molluscum contagiosum virus

124
Q

What is the structure of HBV (hepatitis B virus)?

A

small enveloped DNA virus-DsDNA

125
Q

Viral particles of HBV are resistant to what?

A

low pH, freezing, moderate heating (this hinders disinection)

126
Q

What does the envelope of HBV contain?

A

surace antigens (HBsAg) which are used for diagnosis

127
Q

What are 2 other important antigens of HBV other than HBsAg?

A

HBcAG

HBeAG

128
Q

What are the only natural hosts of HBV?

A

humans

129
Q

What are the three main modes of transmission for HBV?

A

blood, sexual and perinatal (mother to newborn)

130
Q

HBV is prevalent in (blank) users

A

IV drug

131
Q

HBV is worldwide but prevalent in (blank)-high incidence of hepatocellular carcinoma

A

asia

132
Q

(blank) vaccine is the first to prevent human cancer

A

HBV

133
Q

Many HBV infections are (blank) and can be detecte dby HBsAG?

A

asymptomatic

134
Q

HBV can cause acute hepatitis, what are the symptoms of this?

A

fever, fatigue, nausea, pain associated with hepatomegaly

135
Q

(blank) occurs in 5-10% of the people infected with HBV

A

Chronic hepatitis

136
Q

One third of chronic hepatitis patients caused by HBV will develop what?

A

cirrhosis and liver failure

137
Q

80% of cases of (blank) are due to chronic HBV infection.

A

primary hepatocellular carcinoma (HCC)

138
Q

How do you diagnose HBV?

A

biochemical (liver enzymes)

and serological tests

139
Q

What is IgM antibody to HBcAg and indicator of

A

acute infection of HBV

140
Q

HbsAg antibody is associated with (blank) infection

A

chronic

141
Q

Is there a treatment for acute hepatitis B?

A

no

142
Q

How do you treat chronic hepatitis B?

A

interferon alpha, lamivudine, adefovir, or entecavir

143
Q

How can you get immunized against HBV?

A

with recombinant HBsAg vaccine

144
Q

Neonates born to HBsAg (+) mothers are given (blank)

A

HBV IgG

145
Q

A 29y old man with a history of injection drug use is seen by an internist with complaints of fever, fatigue, nausea loss of appetite, joint pain and abdominal soreness for the past few weeks, he reports that his urine is dark and his skin looks yellowish. On examination, he is jaundiced, with an enlarged and tender liver, subsequent laboratory tests were positive for elevated liver enzymes and serum bilirubin. Serologic tests was positive for HBsAg and IgM anti-HBc.

A

HBV

146
Q

Approx. (bank) people worldwide are infected by Hep D virus

A

15 million

147
Q

What is the structure of Hep D?

A

small circular enveloped RNA genome

148
Q

When will HDV propagate?

A

Ony in the presence of HBV

149
Q

HBV and HDV are transmitted through the (blank) so the person is co-infected

A

same route

150
Q

What does HDV do?

A

codes for delta agent which surrounds the genome.

151
Q

Where is delta agent present?

A

blood, semen, vaginal secretions

152
Q

Replication of the delta agent leads to (blank) damage

A

liver

153
Q

How can you tell if HDV is present?

A

detecting RNA genome, delta antigen or anti-HDV antibodies

154
Q

A 45y old male is seen in the medical clinic with complaints of fatigue, anorexia, nausea, vomiting and low grade fever for the past 5 days. In the morning, he noticed his urine was dark and stools were clay-colored. On examination, his liver was enlarged and tender. He recently returned from a week-long trip to Nepal.
What is this?

A

HEV (hepatitis E virus)

155
Q

What are symptoms of HEV?

A 
dark colored urine
clay colored stools
hepatitis
trip to nepal
fecal-oral route pathogen
156
Q

IS adenovirus enveleoped or naked?

A

Naked

157
Q

Where do you find adenovirus?

A

upper and lower respiratory tract disease (pharyngitis, conjuctivitis, common cold and pneumonia)

158
Q

How many different serotypes are there of adenovirus?

A

50

159
Q

What are the clinical manifestations of adenovirus?

A

pharyngo-conjuctival fever (adenovirus type 3 and 7)-fever, pharyngitis, conjuctivitis and cervical adenopathy

160
Q

What is responsible for this:
Pneumonias and common cold- all ages
conjunctivitis (pink eye)-all ages
Acute respiratory disease (types 4 and 7)-all ages
Kerato-conjunctivitis (types 8, 19 and 37)-adults
Acute gastroenteritis (types 40 and 41)-infants and young children

A

adenovirus

161
Q

What types of adenovirus cause acute respiratory disease?

A

4 and 7

162
Q

What types of adenovirus cause kerato-conjunctivitis?

A

8,19,37

163
Q

What types of adenovirus cause acute gastroenteritis?

A

40 and 41

164
Q

How does the adenovirus work?

A

infects epithelial cell lining of oropharynx, respiratory and intestinal tract and causes cytotoxic damage

165
Q

How is the adenovirus spread?

A

aersol, close contact or fecal oral route

166
Q

What is important for resolving an infection caused by adenovirus?

A

antibody

167
Q

How can you identify the idenovirus?

A

cultures, or direct antigen detection (serology) and PCR

168
Q

Is there a specific antiviral therapy for adenovirus?

A

no

just wash your hands

169
Q

A 9-year-old girl is seen in a pediatric practice with conjunctivitis and sore throat that has continued for 3 days. On examination, the child has a fever; pharyngitis, conjunctival redness, watering, pain and cervical adenopathy. A rapid strep test is negative. You collect a conjunctival and pharyngeal swab for viral culture and antigen detection.

What is this?

A

adenovirus

170
Q

HPV causes (blank)

A

papillomas (benign tumors of squamos cells)

171
Q

Which HPV types cause carcinoma of cervix, penis and anus?

A

16 and 18

172
Q

WHich virally encoded genes are implicated in carcinogenesis of HPV? How come?

A

E6 and E7

cuz they inhibit tumor suppressor genes

173
Q

How can you get warts (skin and planter warts) from HPV?

A

HPV 1-4

174
Q

How can you get Anogenital warts from HPV?

A

HPV6 and HPV11

175
Q

HPV can give you laryngeal papilloma in young children, what are these?

A

benign head and neck tumors

176
Q

Carcinoma of the uterine cervix, penis and anus are caused by what HPV strandS

A

16 and 18

177
Q

HPV is very (resistant/responden) to inactivation

A

resistant

178
Q

How can you get infected with HPV?

A

breaks in skin/sexual intercourse, infant passing through infected birth canal

179
Q

Planter/flat warts are common in who?

A

young children/middle aged adults

180
Q

What is the most prevalently sexually transmitted infection in the world?

A

HPV (20 million infected in US, 6 million new genital cases per year)

181
Q

(Blank) occur in young children/middle aged adults

A

laryngeal papillomas

182
Q

HPV is present in (blank) percent of all cervcal cancers

A

99.7%

183
Q

What are all the high risk HPV strains?

What are the low risk?

A

16,18,31,45

6 and 11

184
Q

What will happen if HPV infects and replicats within the squamos epithelium?

A

general warts

185
Q

What will happen if HPV infects and replicates within the mucous membranes ?

A

genital, oral & conjuctival papilomas

186
Q

HPV 16 and 18 create cervical carcinomas contain (Blank)

A

integrated DNA

187
Q

E6/E7 are oncogenes- they inactivate cellular growth supressors which are (blank and blan)

A

p53 and RB

188
Q

How do you diagnose HPV?

A

microscopic examination. DNA molecular probes/PCR

189
Q

How do you treat HPV?

A

Podophylin/interferon/cidofovir

Liquid nitrogen for skin warts (surgical removal or treated with salicylic acid)

190
Q

What are the vaccines you can get against HPV and what do they protect against?

A

gardasil: 6,11,16,18
Cervarix: 16 and 18

191
Q

A 25y old women presents to her gynecologist with complaints of itching, burning and tenderness in the genital area. The patient is sexually active but with no history of sexually transmitted disease. Physical examination is significant for for flesh-colored papules on the labia and vulva. A pap smear is performed to check for cervical abnormalities. WHat is this?

A

genital warts

HPV 6 and 11

192
Q

Tell me about the parvovirus?

A

Parvirus B19 is very small non-enveloped ssDNA virus. Only one serotype. Virus replicates in the nucleus

193
Q

What can parvovirus cause??

A

1 erythema infectiosum (slapped cheek syndrome, fifth disease)

194
Q

What does 1 erythema infectiousum look like?

A

bright red rash prominent on cheeks accompannied by low grade fever, runny nose and sore throat

195
Q

Several Children in a kindergarten class were seen at a pediatric practice with a bright red rash on the cheeks. All children were in a good physical condition, other than mild fever and some abdominal rash. The rashes resolved over 1 to 2 weeks without specific treatment. What is this?

A

1 erythema infectiosum

196
Q

What are the three types of polyomaviridae viruses and whom do they affect?

A

JC virus and BK virus infects humans

SV40, a monkey virus can also infect humans

197
Q

Is polyomavirus bigger or somaller than papilloma?

A

smaller (genome 5kb)

198
Q

What can JC virus cause?

A

Progressive multifocal leukoencephalopathy (PML)

199
Q

What is progressive multifocal leukoencephalopathy?

A

fatal demyelinating disease of white matter (involves multiple areas of the brain)
Affects visual field and results in blindness, weakness, dementia, and patients die wtihin 6 months. Mostly occurs in AIDS patients

200
Q

What can BK virus cause?

A

nephropathy and graft loss in immune suppressed renal transplant patients

201
Q

Antibodies to JC virus are found in (blank) of normal human sera.

A

75%

202
Q

BK virus infection is (blank)

A

widespread

203
Q

In immune compromised individuals, latent virus is (blank) to cause disease

A

reactivated

204
Q

Polyomavirus persists in the (blank) cells, and is excreted in the urine

A

kidney cells

205
Q

How do you diagnose polyomavirus?

A

PCR from CSF

206
Q

How do you treat polyomavirus?

A

no treatment but cidofovir may be beneficial

207
Q

A 69y old man with complaints of speech and vision abnormalities and decreasing mental function is referred to a neurologist. The patient has a 3y history of chronic lymphocytic leukemia that is being treated with chemotherapy. MRI reveals multiple focal areas of demyelination.
What is this?

A

Progressive multifocal leukoencephalopathy caused by JC

208
Q

A 34y old male presented to the ER with gait disorder of about 2 months. A series of laboratory tests were ordered that came out to be either negative of within normal limits. His condition got progressively worse over the next few weeks. MRI revealed patchy lesions in the white matter of the brain. Past medical history was significant for HIV+ immunoassay, CD+ count of 10 and viral load of 500,000.
What is this?

A

Progressive multifocal leukoencephalopathy

209
Q

What are prions?

A

a unconventional slow virus that lacks nucleic acid and creates degenerative disorders of the brain

210
Q

What do prions cause?

A

transmissible spongiform encephalopathies which cause spongiform degeneration.

211
Q

What is caused by ingesting or handing brain tissue; occured in new guinea tribes people

A

KURU

212
Q

How long is the incubation period of Kuru?

A

can exceed 50 years

213
Q

What is caused by iatrogenic transmission by corneal transplant, brain electrodes, or growth hormone, OR mutation in germ cells, or can be caused sporadicly?

A

Creutzfeldt Jakob Disease

214
Q

(blank) are the cause of transmissible spongiform encephalopathies such as creutzfeldt-jakob disease.

A

Prions

215
Q

What all can create prions?

A 
familial
sporadic
iatrogenic
vCJD
Kuru
Human 
Feline encephalopaty
chronic wasting disease of deer and elk
bovine spongiform encephalopathy (BSE)
mink encephalopathy
scrapie
216
Q

A 67y old previously healthy women was referred to a neurologist because of a 2-month history of increased dementia manifested as confusion, memory loss, and bizarre behavior. On physical examination , she exhibited ataxia and slurred speech. Hematologic studies were normal.

What is this?

A

creutzfeldt jakob disease

Block 6 Week 4 (9 decks)

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