Microbiology Flashcards

1
Q

Epstein-Barr virus

A

Icosahedral, enveloped, double-stranded DNA virus
Uses CD21 as receptor, transmitted via saliva
Infectious mononucleosis
Later on, polyclonal and monoclonal B-cell lymphomas and oral hairy leukoplakia

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2
Q

Mechanism of EBV

A

Proliferation/activation of CD8+ T cells - kill B cells and limit proliferation of B cells
T-cell response is required for controlling infection but also contributes to clinical disease
Latency in memory B cells

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3
Q

When does EBV reactivate?

A

When memory B-cell hosting latent virus is activated

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4
Q

How does EBV cause cancer?

A

In absence of T cells, EBV can immortalize B cells

IL-10 analogue inhibits TH1 response, stimulates B-cell growth

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5
Q

What does B cell activation cause?

A

Production of an IgM antibody (heterophile Ab) to the Paul-Bunnell antigen
Overall immune response - mono
Lack of effective immune control - lymphoma, hairy cell leukoplakia

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6
Q

What cancers can be caused by EBV?

A
Burkitt Lymphoma
B cell lymphoma
Hodgkin lymphoma
Nasopharyngeal carcinoma
X-linked lymphoproliferative disease
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7
Q

Symptoms of mono

A

4-6 wk incubation
Fever, fatigue, lymphadenopathy, exudative pharyngitis, splenomegaly
May have erythematous rash

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8
Q

Complications of mono

A

Laryngeal obstruction, splenic rupture, neurological complications (Meningioencephalitis, Guillain-Barre)

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9
Q

Hairy oral leukoplakia

A

Opportunistic EBV infection in AIDS patients
Infection of epithelial cells
Characterized by lesions of the mouth

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10
Q

Diagnosis of EBV

A

Blood counts - lymphocytosis w/ more than 10% atypical lymphocytes
Heterphile antibody test most common

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11
Q

EBNAs

A

EBV Nuclear Antigens - first to appear, seen in all infected and transformed cells
Anti-EBNA develops late in infection

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12
Q

What does presence of Anti-EBNA suggest?

A

Past EBV infection
Reactivated EBV
Burkitt’s Lymphoma
Nasopharyngeal Carcinoma

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13
Q

Cytomegalovirus

A

Double-stranded linear DNA virus
Lymphotrophic virus - only replicates in human cells
Latent infection in mononuclear lymphocytes

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14
Q

How does CMV replicate?

A

Activation of transcription factors, NF-kB, and SP1

Replicates in kidney and secretory glands

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15
Q

Pathology of CMV infection

A

Suppression of cell-mediated immunity allows recurrence and severe disease
Prevents antigen presentation to CD8 and CD4 T cells; viral protein blocks NK cell attack

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16
Q

Neonatal CMV

A

Most common viral cause of congenital disease
Fetus infected via blood (primary infection) or by virus ascending from cervix (recurrence)
Low birth weight, thrombocytopenia, microcephaly, jaundice, hepatosplenomegaly, Blueberry muffin rash

17
Q

What is special about CMV mono?

A

Heterophile antibody isn’t present

18
Q

CMV in Immunocompromised patients

A

Pneumonia (can be fatal if not treated)

19
Q

CMV in AIDS patients

A

Retinitis, colitis, esophagitis

Diarrhea, weight loss, anorexia, fever

20
Q

CMV in organ transplants

A

Often reactivated in recipients due to immunosuppression

Responsible for most kidney transplant failures

21
Q

Diagnosis of CMV

A

Owl’s eye inclusion
ELISA, PCR
Seroconversion good marker for primary infection

22
Q

Treatment of CMV

A

Ganciclovir (Drug of choice)

Cidofovir, Foscarnet