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DD unit 3 > common viral pathogens > Flashcards

common viral pathogens Flashcards

1
Q

What is a major characteristic of the Herpes

A

following primary infection, the vrius establishes a latent infection in the host and may reactivate at a later time

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2
Q

T or F: Reactivation is not always associated with disease

A

TRUE

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3
Q

What is the antiviral given for herpes and how does it work?

A

Acyclovir, inhibitor of viral DNA pol

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4
Q

How many Human herpes viruses (HHV) are there?

A

8

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5
Q

What are the HHV-1 and HHV-2?

A

Herpes simplex virus-1 (HSV1) and HSV2

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6
Q

HSV-1 and HSV-2 both cause what?

A

painful, clear fluid filled vesicles often with a red base on the skin at site of inoculation

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7
Q

What does HSV1 most commonly present as?

A

orofacial lesions

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8
Q

What does HSV2 most commonly present as?

A

genital lesions

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9
Q

T or F: HSV1 does not cause genital lesions

A

FALSE, it causes up to 40% of new genital infections

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10
Q

What is the incubation period of HSV1 and HSV2?

A

2-12 days (average of 4)

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11
Q

How are HSV1 and HSV2 trasmitted?

A

close contact with a person shedding virus at a mucosal surface. HSV penetrates susceptible mucosal surfaces or cracks in skin

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12
Q

T or F: primary infection of HSV can be symtomatic or asymptomatic

A

TRUE

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13
Q

T or F: primary infection of HSV is usually less severe that reactivation

A

FALSE

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14
Q

T or F: in immune competent hosts, HSV infection remains confined to site of contact, but immunocompromised hosts may spread to new areas

A

TRUE

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15
Q

When does Prmary HSV-1 infection usually occur?

A

childhood

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16
Q

Most common symptomatic sign of infection?

A

Gingivostomatitis (mouth ulcers), commonly associaed with fever and enlarged cervical nodes

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17
Q

What is Herpetic whitlow?

A

inoculation of HSV from oral secretions to fingers, often transmitted by mother’s kiss to injured finger of child.

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18
Q

What is herpes gladiotorum?

A

herpes from sports contact

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19
Q

What is genital herpes

A

sexually-trasmitted, with primary infection making vesicle/ulcers in genital area

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20
Q

How long do genital herpes lesions last?

A

10-14 days, usulaly very painful

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21
Q

How are genital herpes warts different from syphilis and chancroid?

A

syphilis are hard and painless ulcers, chancroid are soft painful ulcers associated with swollen inguinal lymph nodes

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22
Q

What is herpes keratitis?

A

HSV infection/inflammation of the cornea, distictive dendriric pattern, can be primary or reactivation

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23
Q

how does HSV get to cornea during reactivation

A

opthalmic branch of the trigeminal nerve

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24
Q

What is the most common cause of encephalitis in US?

A

HSV, and it can be primary or reactivation

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25
Q

Where is encephalitis by HSV usually located and what does it present with?

A

predilection for temporal lobes, often presents as psychiatric illnes

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26
Q

What is Neonatal HSV?

A

it is a serious disease transmitted to an infant perinatally, usually from exposure to maternal HSV1 or 2

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27
Q

What 3 different ways can Neonatal HSV present?

A

1) Skin, eye and mucous membrane disease 2) CNS disease 3) Disseminated

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28
Q

How does neonatal HSV skin, eye and muscous membrane disease present ?

A

leasons on skin, commonly at sites of trama (scalp, electrode site, wristband site, forceps site), eye lesions can lead to corneal ulcers and blindness

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29
Q

How does CNS neonatal HSV?

A

severe encephalitis, mortality with treatment about 30%, 75% of survivors with retardation, motor impairment, and/or learning disabilities

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30
Q

How does Disseminated neonatal HSV?

A

Widespread disease, including pneumonitis, hepatitis, DIC, with or without encephalitis, skin rash, or eye involvement. Most lethal, mortality with treatment 50%

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31
Q

What can you do for pregnant woman with HSV?

A

give acyclovir or valacyclovir to treat lesions, If leasions at time of delivery, C-section is recommended

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32
Q

T or F: skin vesicle on a neonate less than 1 month of age is a medical emergency

A

TRUE, assume HSV, treat fast with acyclovir

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33
Q

What does HSV do after primary infection and how does it do it?

A

establishes latent infection by traveling up sensory nerve ending and axon to sensory ganglia

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34
Q

Where does orofacial latent HSV establish?

A

trigeminal ganglia

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35
Q

Where does genital latent HSV establish?

A

sacral ganglia

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36
Q

how long does a latent infection last?

A

That shit’s for life

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37
Q

how does reactivation of HSV happen?

A

get stimuli (stress, sunlight, illness, menstration, immunosuppression), goes back down axon, makes lesion (more localized and heal faster)

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38
Q

T or F: reactivated lesions are not infectious

A

FALSE, people even shed for a period after it heals

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39
Q

T or F: reactivation may produce no lesion

A

TRUE, virus still sheds and this is how 70% of transmissions occur

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40
Q

how can you confirm HSV lesion?

A

Tzanck smear, viral culture, direct IFA, PCR

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41
Q

What is HHV-3?

A

Varicella Zoster Virus (VZV)

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42
Q

Varicella Zoster Virus (VZV) causes what 2 clinical syndromes?

A

chicken pox (varicella), and Shingles (herpes zoster or zoster)

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43
Q

T or F: varicella is a clinical manifestation of primary infection with VZV

A

TRUE, common childhood disease

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44
Q

How is VZV transmitted?

A

primarily respiratory via droplet or aerosolized secretions, or contact with lesions

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45
Q

What is the incubation period of VZV

A

10-21 days

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46
Q

How does Varicella present?

A

starts w/ fever, malaise, headache, +/- cough. Then generalized itchy vesicular rash, first on trunk, spread to face and limbs, appear in waves of lesions, illness lasts 7 days.

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47
Q

What are the stages of the classic rash of chicken pox?

A

appears in crops or waves, first blister or vesicle, then pustule, then scab.

48
Q

Give a general pathogenesis of Primary VZV infection

A

entry via respiratory tract, goes to lymphoid system, replicated for 2-4 days, then primary viremia, 4-6day initial inoculation, replicates in liver and spleen and other, secondary viremia spread to skin causing rash

49
Q

What complications arise with primary VZV?

A

secondary infections ( group A strep +/- necrotizing fasciitis), pneumonia, encephalitis or encephalomyelitis, hepatits, congenital varicella, adolescents and adults more severe, pregnant woman and immunocompromised patients have higher morbidity and mortality

50
Q

Varicella treatment

A

Uncomplicated varicella is self-limited disease, no specific treatment. Acyclovir can resolve chicken pox faster if presents early, immunocompromised always receive treatment

51
Q

How can prevent we prevent VZV?

A

Live attenuated varicella vaccine (VAR) given in 2 doses (once at 12-15 months, booster at 4-6 years), but can causes disease in pregnant and immunocompromised. Can be used post-exposure in certain unimmunized kids

52
Q

Where does VZV remain latent

A

cranial, dorsal root and/or trigeminal ganglia

53
Q

T or F: VZV is the ONLY herpesvirus that does NOT have asymptomatic viral shedding

A

TRUE

54
Q

T or F: VZV reactivation forms a dermatomal rash

A

TRUE

55
Q

T or F: Herpes Zoster or shingle occurs in 90% of people

A

FALSE, 30%

56
Q

T or F: shingles is a primary infection of VZV

A

FALSE, reactivation

57
Q

symptoms of shingles

A

radicular pain from site where shingles will erupt in a few days, leasions in a single dermatome that do not cross midline, may itch but are very painful, 2 weeks to heal

58
Q

What is post-herpetic neuralgia (PHN)?

A

debilitating neuropathic pain that can last weeks to months after reactivation of VZV

59
Q

how do you diagnose VZV?

A

clinically, if unclear do direct IFA, PCR, viral culture

60
Q

How do we tream shingles?

A

acyclovir within 48-72 hrs or PPX with recurrent shingles. For PHN give NSAIDs, opiates, and occasionally corticosteroids

61
Q

T or F: Cell mediated immunity (CMI) to VZV is an important determinant in who is at risk for shingles

A

TRUE, low CMI =higher risk

62
Q

HHV-4 is what?

A

Epstein Barr Vrisu (EBV)

63
Q

how common is EBV?

A

95% have it by 40 years of age

64
Q

T or F: Primary infection with EBV is often symtomatic

A

FALSE

65
Q

how is EBV transmitted?

A

contact with saliva

66
Q

infectious mononucleosis is caused by what?

A

EBV

67
Q

symptoms of Infectious mono

A

Fever, sore throat, swollen lymph nodes, fatigue

68
Q

signs of Infectious mononucleosis

A

Exudative tonsillitis, enlarged cervical nodes (often posterior cervical), splenomegaly and/or mild hepatomegaly

69
Q

how long til infectious mononucleosis resolves?

A

4-8 weeks

70
Q

Where does EBV infect and spread to?

A

infects nasopharyngeal epithelium, cell lysis causes spread to lymphoid tissue and salivary glads

71
Q

Where does EBV go dormant/latent?

A

nasopharyngeal epithelium and B cells

72
Q

T or F: reactivation is commonly found intermittently in saliva and occurs without symptoms

A

TRUE

73
Q

how is diagnosis of infectious mononucleosis done?

A

typically clinical, but can see atypical lymphocytes in peripheral blood smear, serology tests: IgM to viral capsid antigen (VCA), IgG to VCA is prior infection

74
Q

monospot/heterophile tests

A

after acute infection of EBV, 75%-90% of patients develop antibodies that cross-react and agglutinate RBCs. This detects antibodies that bind RBC

75
Q

What cancers in EBV associated with?

A

Burkitt’s lynphoma, Hodgkin’s lynphoma, Nasopharyngeal carcinoma, lymphoproliferative disease

76
Q

How do you treat EBV?

A

fluids, antipyretics, steroids (lymphode swelling threatens bloodflow. Reduce immunosuppression in the immunocompromised

77
Q

What is HHV-5?

A

cytomegalovirus (CMV)

78
Q

how is CMV spread?

A

infected body fluids contact (blood, organ, secretions, urine, tears, perinatally, inutero)

79
Q

what is the prevalence of CMV?

A

90% in developing countries, 50-80% in developed countries

80
Q

Where does CMV infect?

A

spithelial cells of salivary glands or genital tract. Likely viremia shortly after. Intermittent viral shedding also seen

81
Q

T or F: almost all CMV primary infections come in a mononucleosis-like syndrome

A

FALSE, this does happen but more often is asymptomatic

82
Q

T or F: primary infection of CMV in immunocompromised persons is serious and can infect most organs

A

TRUE, can cause retinitis and colitis

83
Q

Where is CMV latent?

A

monocytes and lymphocytes

84
Q

T or F: Reactivation in persons with normal immune systems is asymptomatic

A

TRUE, but virus is still being shed in fluids

85
Q

What is congenital CMV syndrome?

A

mom gives CMV to baby in utero. Leads to low birthweight, microcephaly, hearing loss, mental impairment, hepatosplenomegaly, skin rash (blueberry muffin spots), jaundice, chorioretinitis. Most often asymptomatic

86
Q

What affects the severity of CMV disease and where does it hit?

A

severity parallels the degree of impairment of cell-mediated immunity. Can be general febrile syndrome or organ-specific

87
Q

Serology with pos IgM and IgG for CMV means what?

A

recent reactivation

88
Q

Tissue histology of CMV infection

A

Infected cells have “owl’s eye” (intranuclear inclusion bodies) and Intracytoplasmic inclusions

89
Q

Treatment of CMV

A

In immunocompromised treat with gancyclovir, Ig in pregers, gancyclovir in infants maybe

90
Q

What is RSV?

A

Respiratory Syncytial Virus

91
Q

T or F: RSV is in the paramyxoviridae family

A

TRUE

92
Q

What is the structure, genome, and important proteins of RSV?

A

Enveloped virus with ssRNA genome, 2 important proteins: G-protein for viral attachemtn to host and F-protein allows fusion of infected cells to neighboring cells to form syncytia

93
Q

What kind of infections does RSV cause?

A

acute respiratory disease. Bronchiolitis (children <1 yr of age), Viral pneumonia (young children and elderly, Upper respiratory tract infection (children and adults)

94
Q

T or F: Primary infection is usually symptomatic

A

TRUE, lasts 7-21 days

95
Q

How is RSV trasmitted?

A

contact with droplets on environmental surfaces or objects

96
Q

T or F: RSV is the most frequent cause of bronchiolitis and viral pneumonia in young children and infants

A

TRUE

97
Q

T or F: reinfection with RSV is normally asymptomatic

A

FALSE, can be but usually looks like a cold

98
Q

how does RSV Bronchiolitis present?

A

URI with congestion, sore throat, fever. Cough deepens and becomes more prominent. Lower resp. tract develops with increase RR, retraction, and wheezing. Mucus and inflammation can block airways

99
Q

T or F: Wheezing in child <2 yrs is most likely bronchiolitis

A

TRUE

100
Q

Give pathogenesis of RSV

A

enters through mucosa of eye and nose, cell-cell transer leading to lower respiratory infection, syncytia, Bronchiolitis

101
Q

Which infants are at high risk for severe RSV bronchiolitis?

A

Premature infants (<32 weeks gestation), chronic lung disease, congenital heart disease

102
Q

how is RSV diagnosed?

A

usually clinical, rapid test (not very sensitive), Viral culture, Serlogy, Direct fluorescent antibody

103
Q

What is treatment for RSV?

A

primarily supportive, Ribavirin is the only antiviral that works (use is controversial

104
Q

T or F: RSV has no licensed vaccine

A

TRUE, but there is a monoclonal RSV F-protein antibody

105
Q

What family is Rotavirus a part of?

A

Reoviridae

106
Q

What is the structure, genome, and important proteins of rotavirus?

A

dsRNA virus with segmented genome (reassortment), several serotypes, 5 strains are responsible for more than 90% of rotavirus disease

107
Q

What does rotavirus cause?

A

leading single cause of severe diarrhea and/or gastroenteritis in infants and young children worldwide

108
Q

Is there a vaccine for Rotavirus?

A

yup, since 2006. before is was very common

109
Q

How is Rotavirus transmitted?

A

Fecal oral is the most common

110
Q

Why is Rotavirus so infectious?

A

kids excrete 100 billion rotavirus particles per mL of feces (infectious at just 10-100 particles) it survives on fingers for 60 min

111
Q

Clinical characteristics of rotavirus

A

incubation of 2 days, then vomiting, watery diarrhea, freq also fever, addominal pain, lasts 3-8 days

112
Q

pathogenesis of rotavirus

A

infects mature absorptive epithelial cells or enterocytes in proximal 2/3 of illem. Cell death. Regen of villi takes 7-10 days

113
Q

describe immunity in Rotavirus infection

A

1st infection => severe gastroenteritis. Subsequent infection milder or asymptomatic (incomplere immunity develops after infection, protects against symptoms but not disease.

114
Q

diagnosis of rotavirus

A

ELISA on stool sample, or the rest of the typical diagnostics

115
Q

how is Rotavirus treated?

A

no antivirals, supportive care given.

116
Q

how many vaccines are available for rotavirus?

A

2 oral, live-attenuated.

117
Q

T or F: Herpetic whitlow is an occupational hazard for doctors, dentist, and nurses

A

TRUE

DD unit 3 (5 decks)

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