Microbiology GI Viruses Flashcards

1
Q

what are the two enteric viruses

A

rotavirus and norovirus

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2
Q

which of the enteric viruses mainly infects children

A

rotavirus

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3
Q

which of the enteric viruses mainly infects adult causing epidemic and endemic infections

A

norwalk (noro) virus

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4
Q

which virus is known to cause ulcers leading to inflammatory polyps and possibly obstruction of the colon

A

CMV

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5
Q

what three viruses are associated with immunocompromised pts resulting in acute inflammatory diarrhea

A

EBV, CMV, and HIV

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6
Q

wheel appearance

A

rota virus

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7
Q

what is the morphology of rota virus

A

icosahedral

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8
Q

what type is rota virus

A

double stranded segmented RNA

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9
Q

mild to severe diarrhea in INFANTS

A

rotavirus

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10
Q

VP1 of rotavirus

A

transcriptase

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11
Q

VP3 of rotavirus

A

mRNA capping

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12
Q

VP4 of rotavirus

A

hemagglutinin; surface protein involved in attachment

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13
Q

VP7 of rotavirus

A

induces the formation of neutralizing antibodies

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14
Q

what type of rotavirus is MOST COMMON in the united states ?

A

group A

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15
Q

pathogenesis of rotavirus

A

capsid of the virus protects it from stomach acid but the stomach acid partially digests and claves VP4 producing ISVP which can penetrate the cell and the ds-RNA is replicated and the VP’s are made and subsequently lyse the cell

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16
Q

function of NSP4 protein

A

part of rotavirus and promotes calcium influx into enterocytes resulting in secretion of water and loss of ions leading to watery diarrhea

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17
Q

immunity to rotavirus requires

A

IgA in the gut lumen

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18
Q

how is rotavirus transmittted

A

fecal oral transmission (it survives well on fomites and hands and there are frequent outbreaks in preschools, and daycare centers)

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19
Q

the Unitedstates has rotavirus outbreaks that commonly occur at what time of the year ?

A

WINTER

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20
Q

what is the method of choice for diagnosing rotavirus

A

direct detection of the viral antigen (EIA and latex agglutination)

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21
Q

what is the treatment for rotavirus

A

fluid and electrolyte replacement

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22
Q

how do you prevent rotavirus

A

2 live attenuated oral vaccines available which have a low risk of intussception

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23
Q

what type of virus is norovirus

A

positive sense, naked RNA virus

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24
Q

how are the noroviruses transmitted

A

fecal oral transmission

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25
Q

diagnosis of norovirus

A

RT-PCR in stool or emesis sample during outbreaks

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26
Q

treatment of norovirus

A

rehydration therapy, bismuth subslaicylate may reduce severity (peptobismol)

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27
Q

what type of virus is yellow fever virus

A

positive sense, single stranded, RNA enveloped virus

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28
Q

pathogenesis of yellow fever

A

kupffer cells are infected in 24 hours and can disseminate to the kidneys, lymph nodes, spleen, and bone marrow and can result in CONJUNCTIVAL INJECTION AND FACIAL FLUSHING during the viremic stage

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29
Q

symptoms of the toxic phase of yellow fever

A

jaundice, bleeding from the gums and venipuncture sites, black vomit (terminal phase is marked by delirium, stupor, and coma)

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30
Q

how do you prevent yellow fever virus

A

live attenuated vaccine, protective antibodies form in 7-10 day (protection last for at least 10 years)

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31
Q

yellow fever virus vaccine is effective in what patient population

A

HIV but must be greater than 200 ml

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32
Q

what type of virus is hepatitis A virus

A

picronavirus, negative RnA, naked, icosahedral, Vpg

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33
Q

what type of virus is hepatitis B

A

DNA, enveloped

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34
Q

what type of virus is hepatitis C

A

flavivirus, RNA enveloped

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35
Q

what type of virus is hepatitis D

A

delta virus, circular RNA enveloped

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36
Q

what type of virus is hepatits E

A

RNA, naked

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37
Q

which hepatitis viruses are fecal oral transission

A

A and E

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38
Q

which hepatitis viruses are transmitted via blood and body fluids

A

B through D

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39
Q

what are important sources of Hepatitis A virus

A

clams, oysters, mussels

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40
Q

what is the pathogenesis of HAV

A

the virus is ingested and then enters the blood stream via the GI tract, replicates in the hepatocytes and kupffer cells, released into bile, then stool

41
Q

what is the significance of IFN in HAV

A

it limits viral replication

42
Q

can HAV become a chronic infection

A

NO

43
Q

icteric phase of HAV

A

dark urine, pale stool
yellow eyes, abdominal pain
pruritus, arthralgia,s skin rash less frequent

44
Q

how do you diagnose HAV

A

ELISA for anti-HAV IgM

45
Q

vaccine for HAV

A

killed AV vaccine given at 2years of age and with HBV vaccine to adults

46
Q

HBV is member of

A

hepadnaviruses

47
Q

how does HBV replicate

A

via reverse transcriptase and replicates via an RNA intermediate

48
Q

stable vironions of HBV are called

A

Dane particles

49
Q

virions of HBV contain

A

DNA
DNA poly (RT and ribonuclease activity)
protein kinase

50
Q

most common cause of pediatric gastroenteritis

A

rotavirus

51
Q

double stranded segmented RNA genome that is naked

A

rotavirus

52
Q

cruise ships

A

noro virus

53
Q

what is the mosquito responsible for yellow fever

A

aedes aegypto

54
Q

what causes the symptoms of Hepatitis viruses

A

immune response against the virus

55
Q

RNA intermediate

A

HBV

56
Q

enzyme associated HBV

A

RNA dependent DNA polymerase

57
Q

core antigen

A

we make antibodies to this in HBV

58
Q

E antigen

A

important to tell us if the pt is actively makingthe virus

59
Q

S antigen

A

binds hepatocytes, decoy viruses, marker for chronic disease and leads to immune complex diseases

60
Q

replicates through an RNA intermediate

A

hepatitis B virus

61
Q

only hepatitis virus that has DNA

A

hepatitis B

62
Q

attachment to hepatocytes is mediated by _____in the hepatitis B Virus

A

HbSAg

63
Q

what causes fulminant hepatitis

A

HDV (delta agent)

64
Q

what is the signifiance for neutralizing Ab (nAb)

A

nAb made against HbsAg and later in infection, large amount of HbsAg in the serum can block nAb which limits the capacity to resolve the infection. immune complexes can form btween HbsAg and nAb (type III hypersensitivity reaction causing vasculitis, arthralgia, rash, and renal damage)

65
Q

who is at risk for HBV

A

medical personnel
sexual promiscuity, IV drug abuse
babies born to chronic HBV positive mothers

66
Q

after 6 months it is concere

A

chronic or resolved

67
Q

Positive HbsAg

A

early disease

68
Q

positive HbcAb, HbsAg, and HbeAg

A

acute disease

69
Q

positive HbcAb, HbsAg and HbeAb

A

chronic passive (must be more thatn 6 months)

70
Q

positive HbvAb, HbsAg, HbeAg

A

chronic active

71
Q

positive HbcAb, HbsAg

A

resolved

72
Q

positive HbsAb

A

vaccinated

73
Q

HbsAg

A

indicates infection and if present it means you have the actively replicating virus, if present for greater than 6 months then you have chronic infection

74
Q

AbsAb indicates

A

resolution or immunity

75
Q

Hbs window is time between

A

HbsAg not detected

HbsAb cannot be detected yet so you must measure HBcAb

76
Q

HbeAg

A

correlates with active viral replication and is present during acute disease and active chronic disease

77
Q

HBeAb

A

usually ordered in chronic infections

78
Q

HBcAb

A

first antibody to appear, presence indicates recent infection used during window period, both IgM and IgG Ab present

79
Q

if E antigen is present

A

active chronic infection

80
Q

what do you give for hepatitis B post exposure prophylaxid

A

immune globulin

81
Q

chronic HBV is treated with drugs targeting what

A

the polymerize

82
Q

what are the two drugs used to treat chronic HBV

A

HIV RT inhibitors and IFN-alpha for at least four months

83
Q

what does IFN-alpha do

A

activate protein kinase that inactivates EF2

84
Q

what can you get if you give immune globulin

A

serum sickness (type three hypersensitivity)

85
Q

what does the subunit vaccine contain for HBV

A

HBsAg

86
Q

type of virus is hepatitic C

A

positive sense RNA genome that is enveloped

87
Q

type of hepatitis for hepatitic C

A

chronic

88
Q

HCV replication

A

coats itself with LDL and VLDL an uses these receptors for uptake into hepatocytes, it also binds CD81 (tetraspanin)

89
Q

treatment for HCV

A

recombinant INF-alpha, ribavarin, “ivir”

90
Q

responsible for 40% of fulminant hepatitis infections

A

hepatitis D

91
Q

a viral parasite

A

hepatitis D

92
Q

what is essential for the packaging of HDV

A

HBsAg

93
Q

genome of HDV

A

small, single stranded RNA genome, cicular

94
Q

responsibility of ribozyme in HDV replication

A

cleaves delta Ag to promote association of genome with HbsAg to form the virion

95
Q

when you get infected with both viruses (HBV and HDV at the same time) this is called

A

coinfection (less severe than superinfection)

96
Q

superinfection

A

infected with HDV AFTER HBV infection and is a more rapid and severe progression

97
Q

HEV is a

A

norovirus

98
Q

how is HEV transmitted

A

fecal oral usually contaminated water

99
Q

Hepatitis E is important in one patient population

A

pregnant patient