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Micro 7 > Viral Inf of Circ, Lymph, and Res > Flashcards

Viral Inf of Circ, Lymph, and Res Flashcards

1
Q

Epstein Barr Virus – Virology

A
  • Herpesviridae family member
  • Enveloped
  • dsDNA virus
  • Uses C3d component of complement system for attachment and entry.
  • Replication in epithelial and B-cells.
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2
Q

Heterophile Antibodies

A

random antibodies produced by B-cells “animal antibodies”

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3
Q

Latent Membrane Protein 1 (LMP1)

A
  • Genes Involved in EBV Carcinogenesis
  • 6 transmembrane-spanning domains
  • CD40 Homologue
  • Constitutively Active Receptor
  • Increased Growth and Suppressed Apoptosis
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4
Q

Latent Membrane Protein 2 (LMP2)

A
  • Genes Involved in EBV Carcinogenesis

- Increased Growth of B cells

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5
Q

Epstein Barr Virus Nuclear Antigen 1 (EBNA1)

A
  • Genes Involved in EBV Carcinogenesis
  • Transactivation of EBV transforming genes
  • Inhibition of Apoptosis
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6
Q

Epstein-Barr Virus - transmission:

A

-saliva

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7
Q

Infectious Mononucleosis - causative agent:

A

Epstein-Barr Virus

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8
Q

Infectious Mononucleosis -

A
  • Symptoms: fever, malaise, exudative pharyngitis, splenomegaly,tender lymphadenitis
  • Biochemical Marker: Heterophile antibodies
  • Epidemiology:Most common in young adulthood in industrialized countries.
  • Complication: splenic rupture
  • Pathogenesis: immune targeting of the infected B cells.
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9
Q

ampicillin and mono results in

A

a rash!

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10
Q

Infectious Mononucleosis Clinical Time course

A
  • 2 months for symptom onset
  • fever, malaise, fatigue
  • lymphadenopathy and hepatosplenomegaly
  • pharyngitis - pretty severe
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11
Q

Infectious Mononucleosis - serologic

A

-can first detect: EA = EBV Early Antigen (lytic)
and VCA = EBV Viral Capsid Antigen (lytic)
-later can detect: EBNA = Epstein Barr Nuclear Antigen (latent)

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12
Q

Infectious Mononucleosis - diagnosis

A
  • Antibodies to EBV: IgM to Viral Capsid Antigen (VCA) demonstrates primary EBV infection.
  • Mono Spot test: Heterophile Antibodies : agglutinate sheep or horse RBC.
  • -Downey Cells: Atypical T cell; Vacuoles; Altered Nucleus; Indented Cell Margin
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13
Q

Infectious Mononucleosis: Treatment & Prevention

A
  • No human vaccine approved yet.
  • Rest and Hydration
  • Anti-virals (acyclovir) inhibit the viral polymerase, but have little impact on the outcome of clinical illness.
  • Avoid strenuous activity to avoid splenic rupture.
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14
Q

Oral hairy leukoplakia

A
  • EBV Manifestations
  • Active EBV replication =white patches on tongue
  • Primarily Immunocompromised, e.g., HIV infection.
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15
Q

Oral hairy leukoplakia treatment

A
  • Antiherpetic drugs

- Podophyllin resin

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16
Q

Burkitt’s Lymphoma

A
  • EBV Manifestations
  • B-cell origin
  • Often presenting in the jaw of children (endemic form)
  • specific chromosome translocation (8 to 14) = overtranscription of myc gene –> cell cycle regulator = cell proliferation
  • Co-factors: Chronic Malaria – endemic & Immune Suppression
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17
Q

Hodgkin’s Disease info/pateint presentation

A
  • EBV Manifestations
  • Not linked to specific chromosomal translocation events.
  • Patient presentation:Nontender, palpable, lymphandenopathy in neck supraclavicular, and/or axilla. Commonly enlargement of lymph nodes deep within chest (medistinal adenopathy). Approximately 1/3 of patients display fever, night sweats, and weight loss
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18
Q

hallmark of Hodgkins disease

A

-Reed-Sternberg cell: a large cell with two or more nuclei or nuclear lobes, each of which contains a large eosinophilic nucleolus

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19
Q

Hodgkin’s Disease treatment

A
  • Treatment with radiotherapy and/or chemotherapy.

- Can be cured in over 90% of patients

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20
Q

Nasopharyngeal Carcinoma info/symptoms

A
  • EBV Manifestations
  • Originates in the nasopharynx.
  • Epithelial cell cancer.
  • Symptoms: Facial pain; Fullness in sinuses and throat; Hearing loss
  • Cofactors: Genetics & Diet
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21
Q

Nasopharyngeal Carcinoma - treatment and prevention:

A

Nasopharyngeal carcinomas are treated through chemotherapy and radiation treatment regimens.

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22
Q

Post-transplantation Lymphoproliferative Disorder (PTLD) - what is it info/symptoms

A
  • EBV Manifestations
  • Abnormal proliferation of lymphoid cells in a transplant patient.
  • Symptoms: fever, fatigue, weight loss, or progressive encephalopathy
  • Benign or Malignant
  • EBV infection at time of transplant = major risk factor.
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23
Q

Post-transplantation Lymphoproliferative Disorder (PTLD)- diagnosis

A
  • Histological analysis of tissue.

- Detection of EBV genomes (in situ hybridization)

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24
Q

Post-transplantation Lymphoproliferative Disorder (PTLD) - treatment

A
  • 1st Reduce Immunosuppression
  • 2nd Treatment with Rituximab (mouse human chimeric anti-CD20 antibody.)
  • 3rd conventional chemotherapy
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25
Q

Cytomegalovirus Disease presentation in patients

A
  • depends on patient demographics
  • normal immune status indiv: asymptomatic carrier or mono-like symptoms (distinct from EBV bc heterophile AB negative& no EBV antigens)
  • baby of seronegative mother: prior to birth –> cytomegalic inclusion disease
  • immunodef/AIDS population: Multisite symptomatic disease
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26
Q

Cytomegalovirus (CMV) -Virology

A
  • Herpesviridae family
  • Enveloped
  • dsDNA
  • Viral Replication: 1. Mucosal epithelium 2. Viremia (highest risk of spread to others)
  • Latency in monocyte
  • Reactivation is rarely symptomatic in immunocompetent individuals.
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27
Q

Cytomegalovirus (CMV) - transmission

A
  • Saliva
  • Breast milk
  • Urine
  • Fomites
  • Sexual contact
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28
Q

Cytomegalovirus (CMV) - diagnosis

A
  • Detection of viral DNA or virus culture from diseased tissue.: Note: Virus may be shed from urine or saliva for months to years after acute infection. Not necessarily diagnostic of acute.
  • Seroconversion: ***Timing and multiple samples needed to differentiate recent from current infection.
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29
Q

Cytomegalovirus (CMV) - treatment

A

—1st—
-Gancyclovir: converted to viral polymerase inhibitor by CMV enzymes (i.v. or oral).
-Valganciclovir: converted to gancyclovir within the body. Increased bioavailability. (oral)
-Toxicity: Bone marrow toxicity, drug-related neutropenia.
—2nd—
-Cidofovir: converted to viral polymerase inhibitor by cellular enzymes. More toxic than gancyclovir.(i.v.)
-Foscarnet: direct inhibitor of the CMV polymerase. renal toxicity. (i.v.)
(ACYCLOVIR AND VALACYCLOVIR = NO GOOD)

30
Q

Cytomegalovirus (CMV) - symptoms

A 
-Mono-like: most mild outcome of CMV infection
Fever
Fatigue
Pharyngitis (usually non exudative)
Abnormal T cells
No heterophile antibody production
(ONLY PRIMARY INF WITH CMV)
31
Q

Cytomegalic Inclusion Body Disease - symptoms

A

-Cytomegalovirus (CMV) manifestation
-Most common with primary infections
-Hepatosplenomegaly
Jaundice
Petechiae/Rash

32
Q

Cytomegalic Inclusion body Disease - treatment/prevention

A
  • Prevention (primarily for seronegative pregnant women)
  • Interrupt CMV transmission in body fluids (children are frequent shedders of CMV)
  • Handwashing
  • Avoid sharing drinks and toothbrushes with young children
  • Avoid contact with saliva when kissing a child
  • Treatment
  • Maternal treatment with CMV immunoglobulin during pregnancy (currently under investigation)
33
Q

CMV in Immunosuppressed Populations

A

-Most important and common viral pathogen complicating organ transplant. Highest risk – 1- 4 mo. following transplant.
-AIDS patients present with CMV diseases usually with highly advanced disease
-CD4 counts between 50 and 100 cells/μL
Spiking Fever (100- 104 ºF)
-Sources: Transplanted Organ, reactivation of latent CMV

34
Q

CMV in transplant recipients:

A

-CMV pneumonitis -Symptoms: Fever; Hypoxia; Interstitial Lung Infiltrates
-GI tract -Symptoms: Diarrhea; Abdominal Pain
Nausea; Vomiting –> Complication: perforation and hemorrhage of GI epithelium
-Graft vs. Host Disease

35
Q

CMV in AIDS patients

A
  • —-CMV Retinitis: Symptoms: Blurred Vision; “Floaters”; White lesions –> Lesions with irregular, white necrotic border
  • Diagnosis: Pupil dilation and ophthalmoscope examination
  • —GI tract
  • —CMV pneumonitis
36
Q

Limiting CMV spread

A
  • Organ transplant prevention
  • Donor matching
  • Prophylaxis or preemptive therapy with antivirals
  • CMV immunoglobin
  • AIDS Prevention: Maintenance therapy with antivirals when reaching a threshhold level of CD4+ T-cells.
  • Treatment Indications: immunocompromised patients with severe disease are treated with I.V. antivirals.
37
Q

Myocarditis definition

A

inflammation of the middle muscular layer of the heart wall leading to ventricular dysfunction.

38
Q

Viral Myocarditis - who is most likely to get and symptoms:

A
  • Most prevalent in adult men.
  • Typical presentation: Shortness of breath; Exercise intolerance; Fatigue
  • May mimic cardial infarction
39
Q

most common viral genome found within myocarditis tissue:

A

historicaly: -adenoviruses (especially types 2 &5) -enteroviruses (especially coxsackievirus B)
more recently: B19 parvovirus & HHV-6

40
Q

Viral Myocarditis - diagnosis

A
  • High index of suspicion in patients with congestive heart failure of unknown origin.
  • Chest Radiograph, electrocardiogram, endomyocardial biopsy.
  • Nucleic acid based test on the biopsied material may reveal viral cause.
41
Q

Viral Myocarditis - management/treatment

A
  • Manage symptoms of CHF and arrhythmias

- Mild disease –> bed rest and observation

42
Q

Mumps - symptoms

A
  • Swollen, tender parotid glands
  • Sometimes accompanied by submandibular gland swelling.
  • Prodrome of malaise and anorexia (1-2 days).
43
Q

Mumps virus - virology

A
  • Paramyxoviridae family.
  • ssRNA genome.
  • One serotype
  • Incubation period is 14-18 days.
  • Age of onset usually between 5-14 years. (in pre-vaccine era)
  • 20% of infections are asymptomatic.
44
Q

Mumps virus - complications

A
  • Meningitis (15% of mumps cases)
  • Orchitis (testicular inflammation) common in postpubertal males. Rarely affects fertility.
  • Deafness in 1/20,000 mumps cases.
  • Myocarditis (extremely rare, but often fatal)
45
Q

Mumps virus - lifecycle:

A
  • entry into respiratory tract
  • spreads into local lymph nodes
  • primary viremia established
  • sperad to salivary glands, teste,ovaries, pancreas, CNS
  • more viremia
  • generalized spread to other body sites including kidneys
  • more viremia
46
Q

Mumps virus - diagnosis

A

-swelling of parotid gland or other salivary gland without any other reason is enough

47
Q

Mumps virus - treatment

A

if uncomplicated will resolve on its own

48
Q

Mumps Virus - transmission

A
  • Direct contact
  • respiratory droplets
  • saliva
  • contaminated fomites
49
Q

Mumps Virus - prevention

A
  • live attenuated – Intramuscular

- recommended for all children

50
Q

MMRV vaccine consists of and dosing schedule:

A

-Mumps
-Measles
-Rubella
-Varicella
2 doses 12-15mo and 4-6 years

51
Q

mumps vaccine for adults

A
  • all adults one done

- 2 doses for high risk exposure

52
Q

Kaposi’s Sarcoma (KS) lesion info

A
  • –Cutaneous Lesions:
  • Pink, Purple, or Brown in Color
  • Usually non-painful
  • Can become confluent (combine into one giant lesion)
  • Increased proliferation of endothelial cells.*
  • –Cases with visceral lesions: Weight loss or fever
  • –Histology: Spindle morphology of cells
53
Q

Kaposi’s Sarcoma (KS) - Classic type

A

rare
middle eastern or miditerranean
few lesions
-not life threatening

54
Q

Kaposi’s Sarcoma (KS) - endemic type

A
  • equatorial africa
  • Presents like Classic KS
  • Aggressive form in pre-pubrescent children, often fatal within 3 years
55
Q

Kaposi’s Sarcoma (KS) - transplant related type

A
  • Occurs in individuals whose immune systems have been suppressed following organ transplant.
  • Often lesions resolve when immunosuppressive therapy is discontinued (or modified).
56
Q

Kaposi’s Sarcoma (KS) - AIDS related type

A
  • Often more widespread lesions than other KS forms.
  • May include other symptoms
  • Lymph node swelling
  • Fever
  • Weight loss
  • Often fatal when lung involvement occurs
57
Q

Kaposi’s Sarcoma (KS) - what casuses it?

A

Herpes virus 8 (HHV-8)

58
Q

Human Herpes Virus 8 (HHV-8) - Virology

A

(-causes Kaposi’s Sarcoma)

  • Enveloped
  • dsDNA genome
  • Latent state in KS lesions
  • Contains several homologues of cellular genes.
59
Q

Human Herpes Virus 8 (HHV-8) - transmission

A

-blood borne - needle, sex

60
Q

HHV-8 – Treatment and Prevention

A
  • Prevention of HHV-8 transmission: Safe sex practices; Limit needle sharing
  • Treatments for KS: Often controlling immune deficiency higher priority that treating KS.;Not herpes antivirals because virus is in the latent state in KS lesions.; Treatment can be with chemotherapy, radiation, and/or surgery.
61
Q

Adult T-cell Lymphoma (ATL) - what virus? Presentation?

A
  • caused by human t-cell lymphoma virus-1
  • T-cell origin
  • –Clinical presentation:—
  • Lymphadenopathy
  • Hepatosplenomegaly
  • Hypercalcemia
  • Skin infiltration of tumor cells: Papules; Plaques; Tumors; Ulcers
62
Q

Adult T-cell Lymphoma (ATL) appearance in cells:

A

“flower cells!”

63
Q

Adult T-cell Lymphoma (ATL) - who gets most, where most prevalent?

A
  • Disease most common in southern Japan, the Caribbean, and Central Africa.
  • Median age of onset = 55 years
64
Q

Adult T-cell Lymphoma - dagnosis:

A

Serology: antibodies to Human T-cell leukemia virus 1 (HTLV-I).

65
Q

HTLV-1 Associated Myelopathy (HAM)/Tropic Spastic Paraparesis - what happens? what virus?

A
  • caused by human t-cell lymphoma virus-1
  • Demyelination of neurons within the spinal cord.
  • Likely autoimmune disease
66
Q

HTLV-1 Associated Myelopathy (HAM)/Tropic Spastic Paraparesis - who is affected most? symptoms?

A
  • Highest incidence adult women
  • Symptoms: Stiff gait ; Lower extremity; weakness, back pain; Incontinence; 1/3 patients bedridden at 10 yr post diagnosis
67
Q

Human T-cell Leukemia Virus I (HTLV-I) - virology

A

-Infects CD4 and CD8 positive cells
-Retrovirus
-Enveloped
+ssRNA genome
-Reverse transcription

68
Q

HTLV Life Cycle

A
  • gets in via glut1 receptor
  • reverse transcriptase to make dsDNA from its +ssrNA
  • integrate into genome
  • transcribed = mRNA and protein
  • maturation step with budding
69
Q

HTLV-I - transmission

A
  • Nursing
  • Blood transfusion
  • Sexual transmission (Male to Female more efficient)
70
Q

HTLV-I – Treatment and Prevention

A
  • Nursing discouraged in endemic areas.
  • Screening the blood supply
  • Reduce unprotected sex
  • Treatment with combined chemotherapy, however limited effectiveness.

Micro 7 (6 decks)

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