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M2 B3 Microbiology > 1. Herpetic Stomatitis & Infectious Esophagitis > Flashcards

1. Herpetic Stomatitis & Infectious Esophagitis Flashcards

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1
Q

HSV Structure

A

Large
Linear dsDNA
No polymerase

Icosahedral core > Nucleocapsid > Tegument > Lipoprotein envelope

Tegument: regulatory proteins (transcription & translation)
- used for viral replication

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2
Q

HSV Properties

A

Replicates in nucleus > intranucleur inclusions

Obtains envelope by budding from nuclear membrane

Causes latent infections:

  • Asymptomatic period (latent state) > Acute disease
  • Provoking agent/immunosuppression > reactivates HSV replication > disease

After HSV infects > latency-associated transcripts (noncoding & regulatory RNAs) are synthesised > suppresses viral replication > initiates & maintains latent state

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3
Q

HSV family members

A

Alpha: (1ry - Epithelial / Latent - Neurons)

- HSV1 (cranial)
- HSV2 (lumbar/sacral)
- VZV (cranial/thoracic)

Beta: (1ry & Latent - variety of tissue)
-CMV (Monocytes)

Gamma: (1ry & Latent - Lymphoid cells)

- EBV (B Lymphocytes)
- HV8 (uncertain)
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4
Q

HSV1 Primary infection

A

Ginivostomatitis

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5
Q

HSV1 Usual latency site

A

cranial sensory ganglia

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6
Q

HSV1 Recurrent infection [3]

A
  • Herpes labialis
  • Encephalitits
  • Keratitis
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7
Q

HSV1 Route of transmission

A
  • Respiratory secretions & saliva
  • Direct contact with virus vesicle
  • Oral-genital sex
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8
Q

HSV1 giant cell [Yes/No]

A

Yes

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9
Q

HSV1 Fetal/Neonatal [Yes/No]

A

No

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10
Q

VZV Primary infection

A

Varicella

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11
Q

VZV Usual latency site

A

Cranial/thoracic sensory ganglia

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12
Q

VZV Recurrent infeciton

A

Zoster

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13
Q

VZV Route of transmission

A

Respiratory secretions

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14
Q

VZV giant cell [Yes/No]

A

Yes

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15
Q

VZV Fetal/Neonate [Yes/No]

A

No

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16
Q

CMV Primary infection

A
  • Congenital infection ( in utero)

- Mononucelosis

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17
Q

CMV Usual latency site

A

Monocytes

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18
Q

CMV Recurrent infection

A

Asymptomatic shedding

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19
Q

CMV Route of transmission [4]

A
  • Intrauterine infection
  • Transfusions
  • Sexual contact
  • Secretions (e.g. saliva & urine)
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20
Q

CMV giant cell [Yes/No]

A

Yes

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21
Q

CMV Fetal/Neonate [Yes/No]

A

Yes

22
Q

EBV Primary infection

A

Infectious mononucleosis

23
Q

EBV Usual latency site

A

B lymphocytes

24
Q

EBV Recurrent infection

A

Asymptomatic shedding

25
Q

EBV Route of transmission

A

Respiratory secretions & saliva

26
Q

EBV giant cell [Yes/No]

A

No

27
Q

EBV Fetal/Neonatal [Yes/No]

A

No

28
Q

HSV1 Pathogenesis

A

Initial: (childhood)
Replicates in skin/mucous membranes > Retrograde axonal flow > Latent in Trigemnial ganglia (viral DNA in cytoplasm)
Reactivated by
-Sunlight, Hormonal changes, Trauma, Stress, Fever
Migrates down neuron > replicates in skin > lesions

  • Lesions = vesicle (infectious) w/serous fluid filled w/virus particles & cell debris
  • Multinucleated giant cells: base of herpesvirus lesions
  • Cell-mediated immunity
29
Q

HSV1 Clinical Findings

A 
1- Gingivostomatitis
2- Herpes labialis
3- Keratoconjunctivitis
4- Encephalitits
5- Herpetic whitlow
6- Herpes gladiatorum
7- Eczema herpeticum
8- Disseminated infections
9- Erythema multiforme
30
Q

1- Gingivostomatitis

A
  • 1rily in children
  • fever, irritability & vesicular lesions in mouth
  • 1ry disease is more sever & lasts longer than recurrences
  • lesions heal spontaneosly in 2-3 weeks
  • many children are asymptomatic
31
Q

2- Herpes labialis (fever blisters/cold sores)

A
  • Crops of vesicles at mucocutaneous junction of lips/nose

- Milder & recurrences appear at same sites

32
Q

3- Keratoconjunctivitis

A
  • Corneal ulcers & lesions of conjunctival epithelium

- Recurrences > scarring & blindness

33
Q

4- Encephalitis

A

-fever, headache, nausea, & vomiting
-focal neurological defects - medial temporal lobe:
(smell, vision, memory, hemiparesis, ataxia, hyperreflexia)
-Seizures, Altered mental status, Behavioral changes
-Meningeal signs (nuchal rigidity & photphobia)
-CSF analysis:
(high protein, lymphocytic pleocytosis, normal glucose)

34
Q

5- Herpetic whitlow

A
  • Pustular lesion of slin/finger/hand

- In medical personnel (lesion contact)

35
Q

6- Herpes gladiatorum

A
  • Vesicular lesions on head/neck/trunk

- Wrestlers & other close body contact people

36
Q

7- Eczema herpeticum (Kaposi’s varicelliform eruption)

A

Vesicular lesions at site of atopic dermatitis (eczema) in children

37
Q

8- Disseminated infections

A

Esophagitis & pneumonia in immunocompromised w/ depressed T-cell function

38
Q

9- Ereythema multiforme

A

-Rash (target/bull’s eye lesion)
-Macular/papular lesions occur symmetrically on trunk/hands/feet
(Rash due to immune reaction)

39
Q

Lab diagnosis

A 
1- Cell culture
2- Tzanck smear
3- PCR
4- Neonatal Diagnosis
5- Serologic tests
40
Q

1- Cell culture

A
  • Isolation of virus from lesion > Cytopathic effect (1-3 days)
  • Virus is identified by:
    1) Fluorescent antibody staining of infected cells
    2) ELISA - virus glycoproteins
  • Monoclonal antibody against glycoprotein G for HSV1 vs HSV2
41
Q

2- Tzanck smear

A
  • Rapid presumption diagnosis of skin lesions

- Detect multinucleated giant cells using Giemsa stain

42
Q

3- PCR

A

-Rapid diagnosis of herpes encephalitis
-Detect HSV DNA in spinal fluid
(more sensitive than viral culture)

43
Q

4- Diagnosis of neonatal herpes

A
  • Viral culture

- PCR

44
Q

5- Serological test

A 
Neutralisation test (for 1ry - increase in titer)
(not for recurrent since antibodies are available/rarely increase)
45
Q

CMV Properties

A
  • Similar to other HV
  • Antigenically different
  • Single serotype
  • Natural host: human
  • Forms giant cells (cytomegalo)
46
Q

CMV Transmission

A
  • Early in life: aross placenta, bith canal, & breast milk
  • Young children: saliva
  • Later in life: sexually, blood transfusions, & organ transplant
47
Q

CMV Pathogenesis

A
  • Fetal infection can cause cytomegalic inclusion disease > multinucleated giant cells w/intranuclear inclusions.
  • Many organs affected & widespread congenital abnormalities
  • Fetus infected if virus isn’t neutrailised by mother w/ 1ry infection
  • Congenital abnormalities if during trimester
  • Enters latent in monocytes > reactivated in immunocomprimisation
  • Can persist in kidney for years
  • Reactivation of CMV in cervical > fetal infections
48
Q

CMV mechanisms for longer latent period state

A

1- Unstable MHC I > viral antigens aren’t displayed > not killed by Tc cells
2- Micro RNAs prevent MHC I synthesis > …
3- Synthesise chemokine receptor > prevent signalling
4- Infection inhibit T cells > immunsuppresion

49
Q

CMV Clinical findings

A

1- CMID: microcephaly, seizures, deafness, jaundice, & purpura (blueberry muffin)
2- Hepatosplenomegaly
3- Excrete CMV in urine for years
4- Immunocompetent adults > heterophil(-ve) mononucleosis fever, lethargy, & abnormal lymphocytes in peripheral blood smears
5- Immunicomprimised > (renal/bone marrow transplants) systemic infection e.g. pneumonitis, esophagitis, & hepatitis
6- AIDS: intestinal tract > colitis w/diarrhea / retinitis > blindness

50
Q

CMV Lab diagnosis

A

1- Culturing w/immunofluorescent antibody > 72 hrs
(to test susceptibility to ganciclovir)
2- Flourescent antibody & Histologic staining (basophilic owl’s eye in giant cells/urine/tissue)
3- Fourfold or greater in antibody titer
4- PCR of CMV DNA/RNA
5- CMV antigenemia (pp65 protein from CMV nucleocapsid in blood leukocytes via immunofluorescence assay)

M2 B3 Microbiology (5 decks)

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