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Myco-Viro > (1) Herpes, and Poxvirus > Flashcards

(1) Herpes, and Poxvirus Flashcards

1
Q

large group of virus that contains several important human viral pathogens

A

Herpesviridae

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2
Q

characteristic of HERPESVIRUSES

A
  • Double stranded DNA
  • Enveloped
  • Icosahedral symmetry
  • Linear
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3
Q

One outstanding property of herpesviruses

A

ability to establish lifelong persistent infections in their hosts

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4
Q

TOF

Herpesviridae undergo periodic reactivation

A

True

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5
Q

Herpesviridae reactivation happnes mostly to?

A

Already affected persons of Herpesviridae:
* elderly
* immunosuppressed individual

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6
Q

Herpesviridae

what is the second reactivation from latency of the virus called?

A

secondary infection or latent infection–latency

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7
Q

TOF

NOT ALL HERPESVIRIDAE have latency site

A

F (All)

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8
Q

HERPESVIRIDAE

once infected, they will remain ____ on that specific latency site

A

dormant

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9
Q

HERPESVIRIDAE

oh no i have a herpesviridae but its dormant, but i have low immunity now what will happen to me > __< uwu

A

REACTIVATED

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10
Q

Herpesviridae

TOF
Infect both warm and cold blooded animals

A

T

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11
Q

Infections of herpesviridae

A

mucocutaneous infection and even lifethreatening cancers

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12
Q

herpesviridae have become successful pathogens due to

A

latency and reactivation

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13
Q

Classification (herpesviridae)

Classification are mainly based on its?

A

biologic property

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14
Q

what are the subfamillies under herpesviridae

A
  • Alphaherpesviridae
  • Betaherpesviridae
  • Gammaherpesviridae
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15
Q

Herpesviridae: Subfamilies

Fast-growing virus (when tried to culture)

A

Alphaherpesviridae

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16
Q

Herpesviridae: Subfamilies

Slow growing virus (on culture)

A

Betaherpesviridae

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17
Q

Herpesviridae: Subfamilies

what infection does alphaherpesviridae have?

A

Cytolytic virus

causes lysis on the cell (damage the cell)

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18
Q

Herpesviridae: Subfamilies - Alpha

causes lysis on the cell (damage the cell)

A

Cytolytic virus

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19
Q

Herpesviridae: Alphaherpesviridae

site of latency

A

Neuron (CNS)

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20
Q

Herpesviridae: Subfamilies

enumerate the members of alphaherpesviridae

mnemonic: HeHeVading(ka)

A
  • Herpes simplex virus type 1
  • Herpes simplex virus type 2
  • Varicella-zoster virus
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21
Q

Herpesviridae: Subfamilies

what infection does betaherpesviridae harbor?

A

Cytomegalic virus

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22
Q

Herpesviridae: Subfamilies - Beta

enlargement of cell

A

Cytomegalic virus

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23
Q

Herpesviridae: Subfamilies - Beta

Site of latency

A

SECRETORY GLANDS and KIDNEYS

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24
Q

Herpesviridae: Subfamilies - Beta

enumerate the members

A
  • Cytomegalovirus
  • Human herpesvirus type 6
  • Human herpesvirus type 7
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25
Q

Herpesviridae: Subfamilies

what infection does gammaherpesviridae harbors?

A

Lymphoproliferative virus

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26
Q

Herpesviridae: Subfamilies - Beta

spread on lymphoid organs

A

Lymphoproliferative virus

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27
Q

Herpesviridae: Subfamilies - Gamma

Site of Latency

A

lymphoid tissues

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28
Q

Herpesviridae: Subfamilies - gamma

enumerate the members

A
  • Epstein- Barr virus
  • Kaposis sarcoma associated herpesvirus
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29
Q

Herpes Simplex Virus Type 1 (HSV-1)

Official name

A

Human Herpes Virus 1

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30
Q

Herpes Simplex Virus Type 1 (HSV-1)

Causes an infection to the?

A

UPPER PART OF THE BODY MOSTLY THE FACE AND MOUTH

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31
Q

Herpes Simplex Virus Type 1 (HSV-1)

Mode of transmission

A

Thru contact, usually involving infected saliva, skin lesions and oropharyngeal lesions

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32
Q

HSV-1: Pathogenesis

Transmitted by contact of a susceptible person with an ____ ____

Primary infection

A

excreting virus

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33
Q

HSV-1: Pathogenesis - Primary Infection

virus enter via?

A

broken skin or mucous membrane

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34
Q

HSV-1: Pathogenesis - Primary Infection

TOF
Viral replication occurs first at the site of infection

A

True

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35
Q

HSV-1: Pathogenesis - Primary Infection

location of the initial lesion

A

Site of infection, characteristic lesion can be seen (produced during primary infeciton)

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36
Q

HSV-1: Pathogenesis - Primary Infection

The virus then spreads locally and short- termed ____ occurs.

A

Viremia

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37
Q

HSV-1: Pathogenesis - Primary Infection

during the period of viremis, what happens to the virus?

A

disseminated in the body

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38
Q

HSV-1: Pathogenesis - Primary Infection

virus invades the? and this is where the latency is established

A

local nerve endings

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39
Q

HSV-1: Pathogenesis

Site of letency

A

Trigeminal Nerve Root Ganglion

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40
Q

HSV-1: Pathogenesis

TOF

Viral persistence in the infected ganglia lasts for the quarter of life Of the host

A

False (last for the lifetime of the host)

Reactivates when immunocompromised

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41
Q

HSV-1: Clinical Manifestation

enumerate all clinical manifestation

A
  • Oropharyngeal disease
  • Keratoconjunctivitis
  • Genital Herpes
  • Skin infection
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42
Q

HSV-1: Clinical Manifestation

enumerate the disease under oropharyngeal disease

A
  • Gingivostomatitis
  • Herpes labialis
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43
Q

HSV-1: Clinical Manifestation

common manifestation of Gingivostomatitis

A

Gingivitis

“singaw”

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44
Q

HSV-1: Clinical Manifestation

signs for Gingivitis are noticed when?

A

immune system lowers and stressed

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45
Q

HSV-1: Clinical Manifestation

Adult manifestations for Gingivostomatitis

A

Pharyngitis and tonsilitis

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46
Q

HSV-1: Clinical Manifestation

TOF

gingivostomatitis is asymptomatic?

A

F (nakita mong may mga lesions sa mouth)

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47
Q

HSV-1: Clinical Manifestation

Gingivostomatitis occurs commonly on?

A

young children (ages 1-5)

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48
Q

HSV-1: Clinical Manifestation

Gingivostomatitis involves the?

A
  • Mouth area
  • Mucal (or buccal-check trans) cavity
  • gingival mucosa
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49
Q

HSV-1: Clinical Manifestation

Recurrent lesion of the eyes

A

Keratoconjunctivitis

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50
Q

HSV-1: Clinical Manifestation

keratoconjunctivitis appears as?

A

dendritic keratitis or corneal ulcer

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51
Q

HSV-1: Clinical Manifestation

TOF

Vesicle on the labia can also be seen

A

F (eyelids)

hindi eyelids ng puthy

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52
Q

HSV-1: Clinical Manifestation

what are produced with keratoconjunctivitis?

A

pus

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53
Q

HSV-1: Clinical Manifestation

TOF

there is no recurrent issue for keratoconjunctivitis

A

F there is, it can result to permanent impairment or blindness

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54
Q

HSV-1: Clinical Manifestation

genital herpes are characteriz by?

A

vesiculo-ulcerative lesion for male and female

The sores and lesions are very painful

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55
Q

HSV-1: Clinical Manifestation

Skin infection manifestation virus portal of entry are?

A

Broken skin

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56
Q

HSV-1: Clinical Manifestation

signs and symptoms for skin infection

A

Herpetic Whitlow - can be seen on fingers

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57
Q

HSV-1: Clinical Manifestation

herpetic whitlow are common with?

A

healthcare personnel handling the patient without wearing proper PPE

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58
Q

HSV-1: Clinical Manifestation

other variation for skin infection

A
  • Herpes gladiatorum (wrestler)
  • Eczema herpeticum (eczema)
  • CNS (meningitis and encephalitis)
  • Neonatal herpes
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59
Q

Herpes Simplex Virus Type 2 (HSV-2) are also called as?

A

Genital herpes and Neonatal herpes

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60
Q

Herpes Simplex Virus Type 2 (HSV-2)

may also cause

A

aseptic meningitis

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61
Q

Herpes Simplex Virus Type 2 (HSV-2)

TOF

can also cause Cervical cancer

A

T (but most common with papilloma virus)

62
Q

Herpes Simplex Virus Type 2 (HSV-2)

Latency site

A

sacral ganglion

63
Q

Herpes Simplex Virus Type 2 (HSV-2)

official name

A

Human Herpesvirus 2

64
Q

Herpes Simplex Virus Type 2 (HSV-2)

Causes an infection to what part of the body

A

LOWER PART OF THE BODY, MOSTLY IN THE GENITALS, also causes VIRAL STD

65
Q

Herpes Simplex Virus Type 2 (HSV-2)

mode of transmission

A

sexually or from a maternal genital infection to a newborn

66
Q

Herpes Simplex Virus Type 2 (HSV-2)

primary infection

A

Same with HSV-1 just recall sa trans

67
Q

Lab Diagnosis: HSV-1 and HSV-2

specimens used

A
  • Aspirate from Vesicle
  • Scraping from base of ulcer
  • Respiratory samples
  • Serum/CSF for antibody
68
Q

Lab Diagnosis: HSV-1 and HSV-2

enumerate the lab diagnosis

A
  1. Direct Micrscopic Examination
  2. Cell culture
  3. Serology
  4. Molecular Assay
69
Q

Lab Diagnosis: HSV-1 and HSV-2

what smear is used for Direct microscopic examination

A

Tzanck Smear

70
Q

Lab Diagnosis: HSV-1 and HSV-2

scraping from the base (the lesion) of the vesicles stained with giemsa

A

Tzanck Smear

Screening method

71
Q

Lab Diagnosis: HSV-1 and HSV-2

After staining you can observe inclusion under direct microscopic examination

A

Multinucleated giant cell with cowdry inclusion

72
Q

Lab Diagnosis: HSV-1 and HSV-2

what is the disadvantage of direct microscopic

A

Cannot distinguish between Herpes simplex virus type (HSV -1 & -2) and Varicella-zoster virus

inclusion can be seen from these 3 members

73
Q

Lab Diagnosis: HSV-1 and HSV-2

what if tzank smear was only ordered by the physician, what other basis can be used for diagnosis

A

signs and symptoms

74
Q

Lab Diagnosis: HSV-1 and HSV-2

TOF

HSV is easy to cultivate and Inoculation of tissue cultures is used for viral isolation.

A

Ture

75
Q

Lab Diagnosis: HSV-1 and HSV-2

what is used for cell culture?

A

SHELL VIAL CULTURE

76
Q

Lab Diagnosis: HSV-1 and HSV-2

  • Replication of virus occurs after 24 hours of incubation with fluorescent antibodies
  • incubated with fluorescent antibodies
  • will be observed with fluorescent microscope
A

Cell culture: shell vial culture

77
Q

Lab Diagnosis: HSV-1 and HSV-2

what will be the cytopathic effect under cell culture?

A

GIANT CELLS.BALLOONING OF CELLS

78
Q

Lab Diagnosis: HSV-1 and HSV-2

for serology how many days are before it the infection of antibodies start to appear

A

4 to 7

79
Q

Lab Diagnosis: HSV-1 and HSV-2

in serology the infection peak after?

A

2 to 4 weeks of infection

80
Q

Lab Diagnosis: HSV-1 and HSV-2

Detection methods under serology:

A
  • neutralization
  • immunofluorescence
  • enzyme-linked immunosorbent assay (ELISA)
81
Q

Lab Diagnosis: HSV-1 and HSV-2

disadvantage of serology

A

Diagnostic value is limited due to antigen sharing Of HSV - 1 and HSV -2

little to no differentiation

82
Q

Lab Diagnosis: HSV-1 and HSV-2

most sensitive

A

Molecular assay

83
Q

Lab Diagnosis: HSV-1 and HSV-2

what molecular assay technique can be used?

A

PCR - Sensitive and Specific

84
Q

Management: HSV-2

this the drug of choice for most situations at present. It is available in a number of formulations:

A

Acyclovir

85
Q

Management: HSV-2

oral only, more expensive than acyclovir.

A

Famciclovir and valacyclovir

86
Q

Management: HSV-2

idoxuridine, trifluorothymidine, Vidarabine (ara-A). is an example of?

A

Other older viral agents

highly toxic and is suitable for topical use for opthalmic infection only

87
Q

Varicella-Zoster Virus (VZV)

Official name?

A

Human Herpesvirus 3

88
Q

Varicella-Zoster Virus (VZV)

TOF

morphologically identical to HSV with no known animal host

A

T

89
Q

Varicella-Zoster Virus (VZV)

mode of transmission

A

Spread by airborne droplets and by direct contact with infected individual

90
Q

Varicella-Zoster Virus (VZV) Pathogenesis

  1. inhaled and infected in mucosal cell in the nose and throat
A

Droplets

91
Q

Varicella-Zoster Virus (VZV) Pathogenesis

Droplets →

A

Respiratory tract (Upper)

92
Q

Varicella-Zoster Virus (VZV) Pathogenesis

Respiratory tract →

A

Lymphatics - will have a viremia and will spread and infect in the lymphatic (lymph nodes)

93
Q

Varicella-Zoster Virus (VZV) Pathogenesis

Lymphatics →

A

Liver, Spleen, Reticuloendothelial system

94
Q

Varicella-Zoster Virus (VZV) Pathogenesis

where does it reac the secondary viremia?

A

Liver, Spleen, Reticuloendothelial system

95
Q

Varicella-Zoster Virus (VZV) Pathogenesis

after the secondary viremia what will happen

A

sign and symptoms will occur:

  • Fever
  • malaise
  • Headached
  • Sore throat
96
Q

Varicella-Zoster Virus (VZV) Pathogenesis

and with the period of second viremia which records a virus on blood, what formation can be seen?

A

Vesicle progression (formation) – SKIN LESIONS

97
Q

Varicella-Zoster Virus (VZV) Pathogenesis

what involves with the skin lesions?

A
  • Macules
  • Papules
  • Vesicles
  • Pustules
  • Crusts
98
Q

Varicella-Zoster Virus (VZV) Pathogenesis

And when the immune system is strong enough, what happens

A

infection will be eliminated and the “tirang” virus will be dormant or latent in the Dorsal root of ganglia

99
Q

Varicella-Zoster Virus (VZV) Pathogenesis

site of latency?

A

Dorsal root of ganglia

100
Q

VZV Clinical manifestation (findings)

Enumerate the disease manifestation

A
  1. Varicella
  2. Herpes Zoster
101
Q

VZV Clinical manifestation (findings)

Commonly called as CHICKENPOX “bulotong”

A

Varicella

102
Q

VZV Clinical manifestation (findings)

Varicella’s Incubation period is between

A

10-21 days

103
Q

VZV Clinical manifestation (findings)

what are the earliest symptoms of varicella

A
  • malaise and fever (occurs in 2nd viremia)
  • quickly followed by Rash on trunk, face, limbs, buccal, and pharyngeal mucosa
104
Q

VZV Clinical manifestation (findings)

Varicella’s successive fresh vesicles appear in

A

crops

105
Q

VZV Clinical manifestation (findings)

TOF

Successive fresh vesicles appear in crops, so that all stages of macules, papules, vesicles, and crusts may be seen at one time

A

True

106
Q

VZV Clinical manifestation (findings)

complications

A
  • Rare in normal children
  • Varicella pneumonia
107
Q

VZV Clinical manifestation (findings)

Commonly called as SHINGLES

A

Herpes Zoste

VZV Clinical manifestation (findings)

108
Q

VZV Clinical manifestation (findings)

Herpes zoster is characterized by

A

skin vesicles,often on one side of the body (characteristic)with severe pain around the skin lesions

109
Q

VZV Clinical manifestation (findings)

complication may include:

A
  • CNS disorders
  • eye problems (ophthalmic zoster)
  • facial paralysis
110
Q

VZV Clinical manifestation (findings)

Immunity to Varicella Zoster Virus, can be acuqired by?

A
  • Previous infection confers lifelong immunity to varicella
  • if Vaccinated
111
Q

Lab Diagnosis: VZV

specimens

A
  • Aspirate from Vesicle
  • Scraping from base of ulcer
112
Q

Lab Diagnosis: VZV

Same method like HSV-1 & -2

A

check direct micrscopic and cell culture ty

113
Q

Lab Diagnosis: VZV

what is the main difference for Cytopathic effect of VZV from HSV-1 and -2

A

HAIR LIKE PROJECTIONS/ THREAD LIKE on the ballooning parts

114
Q

Lab Diagnosis: VZV (Serology)

  • recent primary infection
  • first antibody produced during primary infections
A

VZV IgM

115
Q

Lab Diagnosis: VZV (Serology)

  • past infection and immunity
A

VZV IgG

116
Q

Lab Diagnosis: VZV (Serology)

Rise in specific antibody titer is detected by either

A
  • fluorescent antibody
  • enzyme immunoassay
117
Q

Lab Diagnosis: VZV (Serology)

preferred methoid for diagnosis of VZV encephalitis

A

PCR - molecular assay

118
Q

VZV: Treatment, Prevention and Control

TOF

Vaccination is possible?

A

T (live attenuated varicella vaccine)

Antibodies induced after vaccination persist for at least 20 years

119
Q

VZV: Treatment, Prevention and Control

DRUG OF CHOICE

A

Acyclovir

120
Q

Epstein - Barr Virus (EBV)

Official name

A

Human Herpesvirus 4

121
Q

Epstein - Barr Virus (EBV)

discovered by?

A

Epstein & colleagues

122
Q

Epstein - Barr Virus (EBV)

TOF

Common in almost all parts of the world with more than 69% of adults are seropositive

A

F (90%)

123
Q

Epstein - Barr Virus (EBV)

Mode of transmission

A

Contact with oropharyngeal secretions (respiratory secretion)

124
Q

Epstein - Barr Virus (EBV)

Infects what cell

A

B cells (C3)

125
Q

Epstein - Barr Virus (EBV)

Site of latency

A

B-Cells/ B-lymphocytes

126
Q

Epstein - Barr Virus (EBV)

pls check the process of pathogenesis

A

,/,

127
Q

EBV: Clinical manifestation

enumerate the disease

A
  • Infections mononucleosis (IM)
  • Malignancies
128
Q

EBV: Clinical manifestation

Also called as: Kissing disease or Glandular fever

A

Infections Mononucleosis (IM)

129
Q

EBV: Clinical manifestation

common in?

A

adolescence and adults (15 to 25 years of age)

130
Q

EBV: Clinical manifestation

Infections mononucleosis are usually a ____ disease with flu-like signs and symptoms

A

Self limiting

131
Q

EBV: Clinical manifestation

TOF
Complications are not rare

A

F (rare)

but may be serious if present such as: splenic rupture, meningoencephalitis, pharyngeal obstruction and neurological complications

132
Q

EBV: Clinical manifestation

what are the way to diagnose IM

A

Hematology — blood smear and staining

133
Q

EBV: Clinical manifestation

Diagnosis of IM using hematolgy, what presence should be on the peripheral blood smear

A

Atypical Lymphocytes of ‘DOWNEY CELLS’

(activated b-cells “skirt like” or “fried egg like cytoplasm)

134
Q

EBV: Clinical manifestation

Diagnosis of IM: TOF

Positive on HETEROPHILE ANTIBODIES

A

T

135
Q

EBV: Clinical manifestation

what is being detected for antibodies with IM?

A

EBV antibodies

136
Q

EBV: Clinical manifestation

what are the malignancies

A
  • Burkitt’s lymphoma
  • Nasopharyngeal carcinoma
  • Hodgkin’s disease
  • Non - Hodgkin’s disease
  • Chronic interstitial pneumonitis
  • Gastric carcinoma
137
Q

Lab Diagnosis: EBV (isolation)

EBV may bve isolate from the

A

saliva, peripheral blood, or lymphoid tissue

138
Q

Lab Diagnosis: EBV (isolation)

how are the isolate can be retrieved

A

by immortalization of normal human lymphocyes commonly obtained from umblical cord blood

139
Q

Lab Diagnosis: EBV (isolation)

TOF
this technique is seldom performed due to the time consuming process

A

T

140
Q

Lab Diagnosis: EBV (Serology)

Detects?

A

EBV antibodies

141
Q

Lab Diagnosis: EBV (Serology)

Detects EBV antibodies thru

A
  • ELISA
  • Immunoblot assays
  • Indirect immunofluorescence tests
142
Q

Lab Diagnosis: EBV (Serology)

if u see this card check

A

check the typical pattern of the antibody response with primary EBV infection

143
Q

Lab Diagnosis: EBV (Serology)

Early acute infection: Rise in the VCA (viral capsid antigen)

A

VCA IgM

144
Q

Lab Diagnosis: EBV (Serology)

weeks after early infection:

A

VCA IgG

145
Q

Lab Diagnosis: EBV (Serology)

Approx. 1 month of infection

A

Antibodies against Early antinges (EA)

146
Q

Lab Diagnosis: EBV (Serology)

Approx. months after early acute infection:

A

EBNA (epstein barr nuclear antigens) IgG

147
Q

Lab Diagnosis: EBV (agglutination)

During Infectious mononucleosis infection most patients develop transient ____ ____ that agglutinate sheep cells.

A

heterophil antibodies

148
Q

Lab Diagnosis: EBV (agglutination)

Main disadvantage

A

presence Of heterophil antibodies is not specific to Infectious mononucleosis cause Other diseases such as serum sickness also produces heterophil antibodies.

149
Q

Lab Diagnosis: EBV (agglutination)

TOF

DEFINITIVE, not specific with infection mononucleos

A

F (Not definitive)

150
Q

Lab Diagnosis: EBV

what molecular assay can be used

A

Quantitative PCR - determine viral progession

151
Q

EBV: Treatment, Prevention and Control

Drug of Choice

A

Acylovir

152
Q

EBV: Treatment, Prevention and Control

vaccine?

A

walang Avail

Myco-Viro (5 decks)

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