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M2 | Microbiolgy > Herpetic stomatitis & Infectious Esophagitis > Flashcards

Herpetic stomatitis & Infectious Esophagitis Flashcards

1
Q

Mention the similar structures of all HSV family

A
  • Large viruses with Icosahedral core surrounded by lipoprotein envelope
  • linear double stranded DNA
  • No polymerase
  • Has tegument :
  • that is located between nucleocapsid & envelope
  • play role in viral replication by regulatory proteins ( transcription & translation factors )
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2
Q

Mention the important properties of HSV family

A
  • Replicate in nucleus & form intranuclear inclusions
  • Budding from nuclear membrane let it obtain an envelope
  • Cause Latent infection:
    1. Acute disease —-> asymptomatic period (latent state)
  1. Provoking agent or immunosuppression —> reactivation of HSV replication——> cause disease
  2. After HSV infects neurons ——> latency-associated transcripts are synthesized——-> suppress viral replication ——> initiate & maintain latent state
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3
Q

What is the mode of transmission of Herpes Simplex Virus-1 ?

A
  • Saliva ( mostly primary infection occur during childhood )
  • oral- genital sex
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4
Q

During latency in HSV 1 where is the viral DNA located ?

A

Cytoplasm ( NOT integrated into

nuclear DNA)

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5
Q

Explain the pathogenesis of HSV 1

A

Virus replicates in skin or mucous membrane at initial site of infection ——> migrates up neuron by retrograde axonal flow ——-> latent in trigeminal ganglia

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6
Q

What factors reactivate HSV 1 ?

A
  1. sunlight
  2. hormonal changes
  3. trauma
  4. stress
  5. fever
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7
Q

How do HSV 1 reactivation occur ?

A

Previous factors will migrate down neuron ——> replicates in skin —-> lesions

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8
Q

Describe the lesion of HSV 1

A
  • Skin lesion contains vesicles filled of serous fluid with virus particles & cell debris
  • Multinucleated giant cells : base of herpesvirus lesions
  • Cell-mediated immunity: limiting herpesviruses
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9
Q

What happens if the vesicles of HSV 1 ruptures ?

A

virus can be transmitted to other individuals

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10
Q

State all the clinical findings / diseases caused by HSV 1

A

1- Gingivostomatitis

2- Herpes labialis

3- Keratoconjunctivitis

4- Encephalitis

5- Herpetic whitlow

6- Herpes gladiatorum ( on fingers & fingertips)

7- Eczema herpeticum (Kaposi’s varicelliform eruption)

8- Disseminated infections

9- Erythema multiforme

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11
Q

A patient has vesicles on his upper lip at the mucocutaneous junction . What is the clinical finding & it’s caused by which virus ?

A

Herpes labialis
Caused by HSV 1

  • Note : Milder & recurrences frequently reappear at the same site
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12
Q

Corneal ulcers & lesions of conjunctival epithelium ; that could cause blindness due to reoccurrence

A

Keratoconjunctivitis

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13
Q

What is Gingivostomatitis?

A
  • Cause Fever, irritability & vesicular lesions in mouth
  • Primarily in children and many of them are asymptomatic
  • Primary disease is more severe & lasts longer than recurrences
  • Lesions heal spontaneously in 2 to 3 weeks
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14
Q

Which HSV 1 finding cause :

Esophagitis & depressed T-cell pneumonia function ?

A

Disseminated infections

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15
Q

What is Kaposi’s varicelliform eruption ?

A

It’s another name for Eczema herpeticum ; caused by HSV 1
It’s determined by its Vesicular lesions at site of atopic dermatitis
(eczema) in children

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16
Q

Vesicular lesion found on the head, neck & trunk

A

Herpes gladiatorum

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17
Q

Herpes gladiatorum occurs to which group of people?

A

Wrestlers & others who have close body contact

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18
Q

A physician developed Pustular lesion in her hand after contact with patient’s lesions. What is the clinical finding?

A

Herpetic whitlow

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19
Q

Mention the indications of Encephalitis

A
  1. Fever, headache , nausea & vomiting

2- altered sense of smell & loss of vision, memory loss

3- hemiparesis, ataxia, hyperreflexia

  • Point #2 & 3 are examples of Focal neurological deficits affecting medial temporal lobe

4- Seizures , Altered mental status & Behavioral changes

5- Meningeal signs —-> nuchal rigidity & photophobia

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20
Q

What is the CSF analysis of Encephalitis due to HSV 1

A
  • High protein level
  • Lymphocytic pleocytosis
  • Normal glucose levels
21
Q

State features of Erythema multiforme

A
  • “ target” or “bull’s eye” lesion ( rash a central red ring ) due to immune-mediated reaction to HSV antigens
  • Macular or papular lesions on the trunk , hand & feet symmetrically occurring
22
Q

What are all the diagnosis that could be done for HSV 1 ?

A

1- Cell culture

2- Tzanck smear

3- PCR

4- Diagnosis of neonatal herpes

  • Viral cultures or PCR assay

5- Neutralization test ( Serologic test)

23
Q

Which test is useless to diagnose HSV 1 and why ?

A

Serological tests such as Neutralization test

Because many adults already have circulating antibodies & recurrences rarely cause rise in antibody titer

24
Q

Rapid diagnosis for herpes encephalitis is …..

A

PCR ; it detects HSV DNA in spinal fluid

25
Q

How is cell culture performed for HSV 1 ?

A

Virus is identified by :

1- Fluorescent antibody staining of infected cells

2- Enzyme-linked immunosorbent assay (ELISA): virus glycoproteins

26
Q

How many days does it take for the Cytopathic effect of isolated virus from a lesion ?

A

1 to 3 days

27
Q

How to distinguish between HSV 1 & HSV 2

A

ELISA test ——> by using monoclonal antibody against glycoprotein G

28
Q

Which test detects multinucleated giant cells using

Giemsa stain in HSV 1 ?

A

Tzanck smear

29
Q

State the main properties of Cytomegalovirus

A
  • It’s Structurally & morphologically similar to other herpesviruses
  • It is antigenically different than other herpesviruses
  • Single serotype
  • Natural hosts: Humans
  • Giant cells are formed ——-> cytomegalo
30
Q

How CMV is transmitted in young children?

A

Via saliva

31
Q

How CMV is transmitted later in life ?

A
  1. Sexually ( semen & cervical secretions)
  2. Blood transfusions
  3. Organ transplants
32
Q

How CMV is transmitted early in life ?

A
  1. Across placenta
  2. Birth canal
  3. Breast milk
33
Q

What is cytomegalic inclusion disease ?

A
  • A fetus infection by CMV characterized by multinucleated giant cells with intranuclear inclusions
  • Many organs are affected
  • Widespread congenital abnormalities
34
Q

How cytomegalic inclusion disease occur ?

A

When primary infection occurs in pregnant woman who has no antibodies to neutralize virus before it infect fetus

  • If pregnant woman has antibodies against virus then the fetus will NOT be infected
35
Q

When & how does the congenital abnormalities appear in fetus with cytomegalic inclusion disease ?

A

When : During 1st trimester

How: development of organs occurs
& death of precursor cells result in ——> congenital defects

36
Q

CMV enters latent state in monocytes & reactivated when ……………..?

A

When cell - mediated immunity is decreased

37
Q

Reactivation of CMV from latent state in cervical cells will cause …?

A

Infection of newborn during passage through the birth canal

38
Q

CMV can persist for years in which organ/s ?

A

Kidneys

39
Q

What are the mechanisms pulled by CMV to maintain longer latent state ?

A
  1. CMV encode MicroRNAs:
    ——> binds to & prevent translation of cell’s mRNA for class 1 MHC
    ——> prevents viral proteins from being displayed on infected cell & not killed by cytotoxic T cells
  2. Assembly of MHC class I ——> the viral peptide complex is unstable in CMV infected cells —-> viral antigens is not displaced on cell surface & not killed by cytotoxic T cells
  3. Also encodes protein that function as chemokine receptor —-> preventing chemokines from serving as signal for host immune cells to migrate to site of CMV infection
  4. Has immunosuppressive effect that —-> inhibits T cells
40
Q

What are the clinical findings for infants during gestation with CMV infection?

A
  1. microcephaly
  2. seizures
  3. deafness
  4. thrombocytopenia
  5. jaundice
  6. Purpura “ blueberry muffin “
  7. Hepatosplenomegaly
  8. Excrete CMV in urine for several years
41
Q

What are the clinical findings of CMV in Immunocompetent adults ?

A
  1. heterophil- negative mononucleosis fever
  2. Lethargy
  3. Abnormal lymphocytes in peripheral blood smears
42
Q

What are the clinical findings of CMV In immunocompromised patients?

A

Eg.Renal & bone marrow transplants

Systemic CMV infection——> eg. pneumonitis esophagitis & hepatitis

43
Q

What does CMV cause for AIDS patients ?

A
  • CMV infects intestinal tract—-> colitis with diarrhea

* CMV causes retinitis ——> blindness

44
Q

What are all the diagnosis performed for CMV ?

A
  1. Culturing
  2. Fluorescent antibody & Histologic staining
  3. Fourfold or greater rise in antibody titer
  4. PCR
  5. CMV antigenemia ( by immunofluorescence assay)
45
Q

Which protein in immunofluorescence assay test identifies CMV ?

A

pp65 protein ( located in nucleocapsid of CMV) it’s identified in blood leukocytes

46
Q

Which fluids are obtained to examine the DNA & RNA of CMV ?

A

PCR test is used to identify the DNA or RNA in tissue or body fluids

For CMV fluids are obtained from spinal fluid & amniotic fluid

47
Q

What does the Fluorescent antibody & Histologic staining identify?

A

Basophilic intranuclear inclusions oval

“owl’s eye” in giant cells in urine & tissue

48
Q

How is culturing performed for CMV diagnosis?

A
  • Culturing is coupled with the use of immunofluorescent antibody
  • used to determine susceptibility to ganciclovir
  • diagnosis in 72 hours is preferred

M2 | Microbiolgy (17 decks)

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