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Microbiology Exam V > Viral Infections of the Circulatory System > Flashcards

Viral Infections of the Circulatory System Flashcards

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1
Q

Epstein Barr Virus (Virology)

A 
Herpesviridae Family
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

Epstein Barr Virus (Pathogenesis)

A

Viral infection –> Viral genome remains separate and tags along –> Triggers cells to proliferate and produce antibodies (HETEROPHILE ANTIBODIES - antibodies to non-specific antigens) –> Immune response (T cells come in to take care of infected B cells) –> Latency –> Reactivation

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3
Q

Genes involved in EBV Carcinogenesis

A

1) Latent Membrane Protein 1 (LMP1)
- 6 transmembrane spanning domains
- CD40 homologue
- Constitutively Active Receptor (High proliferation, as they do not need a ligand)
- Increased Growth and Suppressed Apoptosis

2) Latent Membrane Protein 2 (LMP2)
- Increased Growth of B cells

3) Epstein Barr Virus Nuclear Antigen 1 (EBNA1)
- Transactivation of EBV transforming genes
- Inhibition of Apoptosis

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4
Q

Epstein Barr Virus (Clinical)

A

Transmission through SALIVA (Kissing Disease)
90% of population is seropositive

Primary infection:

1) Worldwide - before 5 years of age
2) United States - adolescence and early adulthood

Factors contributing to EBV associated cancers:

  • Immunosuppression (e.g. malaria)
  • Genetic predisposition
  • Environmental factors
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5
Q

Infectious Mononucleosis (Symptoms, Biochemical Marker, Epidemiology, Complication, Pathogenesis)

A

Fever, malaise, exudative pharyngitis, splenomegaly, tender lymphadenitis

BM: Heterophile antibodies

Epidemiology: Most common in young adulthood and in industrialized countries

Complication: Splenic rupture

Pathogenesis: Immune targeting of infected B cells

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6
Q

What is Mono commonly mistaken for, and what are the consequences?

A

Strep throat; patients develop a rash when treated with ampicillin antibiotics

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7
Q

Infectious Mononucleosis (Clinical Time Course)

A

Incubation: 2 months before onset of symptoms

3-5 days later: lymphadenopathy and hepatosplenomegaly

Fever peaks 5-10 days post onset of symptoms

See early antigens (EA) and viral capsid antigens (VCA) in early stages of infection

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8
Q

Infectious Mononucleosis (Diagnosis)

A

Mono Spot test:
-Heterophile antibodies- agglutinate sheep or horse RBC
(Negative = white; Positive = purple)

Antibodies to EBV:
-IgM to Viral Capsid Antigen (VCA) demonstrates primary EBV infection

  • DOWNEY CELLS*
  • Atypical T cells
  • Vacuoles
  • Altered nucleus
  • Indented cell margin
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9
Q

Oral Hair Leukoplakia

A

Immune suppressed populations (e.g. HIV patients with ~300 CD4 T-cell/mm3)

Active EBV replication (virus being shed and produced)

Treatment:

  • Antiherpetic drugs
  • Podophyllin resin
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10
Q

Burkitt’s Lymphoma

A

B-cell origin
Often presenting in the jaw of children (endemic form)

Highest incidence in Equatorial Africa

Most rapidly progressing human tumor

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11
Q

Burkitt’s Lymphoma (Disease)

A

Myc activates a bunch of cell cycle regulators (e.g. E2F) and leads to activation of the cell cycle from G1 to S

Co-factors:

  • Chronic malaria - endemic
  • Immune suppression
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12
Q

Hodgkin’s Disease

A

7600 new cases/yr in US
B-cell origin (like Burkitt’s Lymphoma)
Not linked to specific chromosomal translocation events (unlike Burkitt’s Lymphoma)

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13
Q

Hodgkin’s Disease (Patient Presentation)

A
  • Nontender, palpable, lymphadenopathy in neck supraclavicular, and/or axilla
  • Commonly enlargement of lymph nodes deep within CHEST (Mediastinal Adenopathy)
  • Approximately 1/3 of patients display fever, night sweats, and weight loss
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14
Q

Hodgkin’s Disease (Diagnosis and Treatment)

A
  • REED-STERNBERG CELL*
  • Large cell with two or more nuclei or nuclear lobes, each of which contains a large eosinophilic nucleolus

Treatment:

  • Radiotherapy or Chemotherapy
  • Localized Hodgkin’s Disease is cured in > 90% of patients
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15
Q

Nasopharyngeal Carcinoma

A 
Originates in the nasopharynx
Epithelial cell cancer
Symptoms:
-Facial pain
-Fullness in sinuses and throat
-Hearing loss
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16
Q

EBV Neoplasms (Treatment and Prevention)

A

Chemotherapy and Radiation

Cofactors:

  • Genetics
  • Diet
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17
Q

Post-Transplantation Lymphoproliferative Disorder (PTLD)

A
  • 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

Diagnosis: look for EBV in the tissues

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18
Q

Post-Transplantation Lymphoproliferative Disorder (PTLD) (Diagnosis and Treatment)

A

Diagnosis:

  • Histological analysis of tissue
  • Detection of EBV genomes (in situ hybridization)

Treatment:

  • 1st Reduce Immunosuppression
  • 2nd Treatment with Rituximab (mouse human chimeric anti-CD20 antibody)
  • 3rd conventional chemotherapy
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19
Q

Cytomegalovirus (CMV) (Virology)

A 
Herpesviridae family
Enveloped
dsDNA
Viral replication
1) Mucosal epithelium
2) Viremia
Latency in MONOCYTE
Reactivation is rarely symptomatic in immunocompetent individuals (Shedding the virus without knowing it)
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20
Q

Cytomegalovirus (CMV) (Clinical)

A

Transmission:
-Saliva, Breast Milk, Urine, Fomites, Sexual Contact

Viral Diagnosis:

  • 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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21
Q

Cytomegalovirus (CMV) (Antivirals: 1st and 2nd Lines of Defense)

A

1st

  • Gancyclovir: converted to viral polymerase inhibitor by CMV enzymes (IV or oral)
  • Valganciclovir: converted to gancyclovir within the body. Increased bioavailability. (Oral)
  • **Toxicity- bone marrow toxicity and drug-related neutropenia

2nd

  • Cidofovir: converted to viral polymerase inhibitor by cellular enzymes. MORE TOXIC than gancyclovir (IV)
  • Foscarnet: direct inhibitor of the CMV polymerase. Renal toxicity. (IV)
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22
Q

CMV Infectious Mono-like Illness

A

Incubation 20-60 days
Symptoms duration 2-6 weeks
-Fever, fatigue, pharyngitis (non-exudative, usually), Abnormal T cells (DOWNEY CELLS), no heterophile antibody production

Etiology: Primary infection with CMV

Young Children = asympatomatic, but shed virus for long periods of time (months to years) in saliva and urine

Adults = symptomatic

23
Q

Cytomegalic Inclusion Body Disease

A

CONGENITAL INFECTION

Symptoms:

  • Hepatosplenomegaly***
  • Jaundice***
  • Petechiae/Rash***
  • Microcephaly
  • Growth Retardation
  • Inguinal hernias
  • Chorioretinitis
24
Q

Cytomegalic Inclusion Body Disease (Epidemiology and Infection)

A
  • Most common congenital viral infection*
  • 30,000 children per year in US

30-50% women childbearing age seronegative for CMV
1-4% of these women will be exposed during pregnancy
Risk of transmission from primary CMV infection during pregnancy = 33%

25
Q

Cytomegalic Inclusion Body Disease (Prevention and Treatment)

A

Prevention (primarily for seronegative pregnant women)

  • Interrupt CMV transmission in bodily fluids (children are frequent shedders of CMV)
    1) Handwashing
    2) Avoid sharing drinks and toothbrushes with young children
    3) Avoid contact with saliva when kissing a child
  • NO VACCINES*

Treatment:
-Maternal treatment with CMV immunoglobulin during pregnancy (currently under investigation)

26
Q

CMV in Immunosuppressed Populations

A
  • Most important/common pathogen complicating ORGAN TRANSPLANT*
  • AIDS patients present with CMV diseases usually with highly advanced disease (CD4 counts between 50 and 100 cells/uL)
  • Spiking fever (100-104 F)
  • Sources: Transplanted organ, reactivation of latent CMV
27
Q

CMV in Immunosuppressed Populations (Transplant Recipients)

A

CMV pneumonitis (Symptoms)

  • Fever
  • Hypoxia
  • Interstitial lung infiltrates (interstitial opacities on CXR)

GI Tract (Symptoms)

  • Diarrhea
  • Abdominal Pain
  • Nausea
  • Vomiting
  • Complication: perforation and hemorrhage of GI epithelium*

GRAFT VS HOST DISEASE

28
Q

CMV in Immunosuppressed Populations (AIDS Patients)

A

CMV Retinitis

  • Blurred vision, “Floaters”, White Lesions -> Lesions with irregular, white necrotic border
  • Diagnosis –> Pupil dilation and ophthalmoscope exam

GI Tract

CMV pneumonitis

29
Q

CMV in Immunosuppressed Populations (Prevention and Treatment)

A

Organ Transplant Prevention:

  • Donor matching (e.g. seronegative transplant to a seronegative donor)
  • Prophylaxis or preemptive therapy with antivirals
  • CMV immunoglobin

AIDS Prevention: Maintenance therapy with antivirals when reaching a threshold level of CD4+ T-cells (~100)

Treatment indications: Immunocompromised patients with severe disease are treated with IV antivirals

30
Q

Viral Myocarditis

A

Inflammation of middle muscular layer of the heart, leading to ventricular dysfunction

  • Most prevalent in adult MEN
  • Symptoms
    1) Typical presentation
  • Shortness of breath
  • Exercise intolerance
  • Fatigue
    2) Sometimes also
  • Chest pain, abdominal pain, palpitations, syncope
    3) May mimic myocardial infarction
31
Q

Viral Myocarditis (Etiology)

A

1) Most US myocarditis cases are associated with a viral infection
- Adenoviruses (types 2 and 5)
- Enteroviruses (Coxsackievirus B)
- Parvovirus (B19)*
- HHV-6*

Other viruses include:

  • Echovirus
  • Influenza virus
  • Mumps virus
32
Q

Viral Myocarditis (Diagnosis, Treatment, Prognosis)

A

Diagnosis:

  • High index of suspicion in patients with CHF OF UNKNOWN ORIGIN
  • Chest radiograph, electrocardiogram, endomyocardial biopsy (Nucleic acid based test on the biopsied material may reveal viral cause)

Treatment:

  • Manage symptoms of CHF and arrhythmias
  • Mild disease –> Bed rest and observation

Prognosis:

  • 50% full cardiac function restored
  • 25% display ECG or CXR abnormalities w/o symptoms
33
Q

Mumps (Symptoms)

A

Swollen, tender PAROTID GLANDS
Sometimes accompanied by submandibular gland swelling
Prodrome of malaise and anorexia (1-2 days)

34
Q

Mumps (Characteristics)

A

Paramyxoviridae family
-ssRNA
One serotype
Incubation period: 14-18 days
Age of onset usually between 5-14 years (in pre-vaccine era)
20% of infections are ASYMPTOMATIC
Complications:
-Meningitis (15% of mumps cases)
-Orchitis (testicular inflammation) common in postpubertal male. Rarely affects fertility.
-Deafness in 1/20,000 mumps cases
-Myocarditis (EXTREMELY RARE, BUT OFTEN FATAL)

35
Q

Mumps (Virology)

A

1) silent entry into respiratory tract
2) spread to local lymph nodes
3) primary viremia (in bloodstream)
4) spread to salivary glands, testes, ovaries, pancreas, CNS
5) viremia (in bloodstream)
6) generalized spread to salivary and other glands, and to other body sites including the KIDNEYS
7) viremia (in bloodstream)

Incubation period: steps 1-6 (~19 days)

Disease period: step 7 (~day 20)

36
Q

Mumps (Diagnosis and Treatment)

A

Diagnosis:

  • According to the CDC guidelines, the case definition for mumps is an “acute onset of unilateral or bilateral tender, self-limited swelling of the parotid or other salivary gland lasting more than 2 days and without apparent other cause”
  • Assays to detect viral genomes or serological tests are available

Treatment:
-Uncomplicated cases usually resolve within 10 days

37
Q

Mumps (Transmission and Prevention)

A

Transmission:
Direct contact- respiratory droplets, saliva, fomites

Prevention:
***LIVE ATTENUATED VACCINE***
Part of MMR and MMRV vaccine combinations
IM injection
Routine vaccination for children
38
Q

Mumps (MMR/MMRV Vaccine Schedule in Children)

A

1st dose 12-15 months (MMR + Varicella - Preferred) or MMRV

2nd dose 4-6 years (MMRV)

39
Q

Mumps (Vaccination in Adults)

A

1 dose for all adults (78% effective)

2 doses for those at HIGH RISK for mumps exposure (at least 28 days apart) (88% effective)

  • Healthcare workers
  • International travelers
  • Students at post-high school educational institutions
40
Q

Where is Mumps most prevalent?

A

College campuses

41
Q

Kaposi’s Sarcoma

A

Cutaneous lesions

  • Pink, purple, or brown in color
  • Usually non-painful
  • Can become CONFLUENT (grow together as one)
  • Increased proliferation of ENDOTHELIAL CELLS

Cases with Visceral Lesions
-Weight loss or fever

Histology
-Spindle morphology of cell

Highly associated with IMMUNOSUPPRESSION

42
Q

Kaposi’s Sarcoma (Classic vs Endemic)

A

Classic KS:

  • RARE disease
  • Middle Eastern or Mediterranean descent
  • Few lesions
  • Rarely life threatening

Endemic KS

  • Equatorial KS
  • Two forms
    1) Presents like Classic KS
    2) Aggresive form in pre-pubescent children, often fatal within 3 years
43
Q

Kaposi’s Sarcoma (Transplan- vs. AIDS-related)

A

Transplant-related:

  • Immune suppression after organ transplant
  • Lesions often resolve when immunosuppressive therapy is discontinued/modified

AIDS-related:

  • Often more widespread lesions than other KS forms
  • May include other symptoms (lymph node swelling, fever, weight loss)
  • Often fatal when lung involvement occurs
44
Q

Human Herpes Virus 8 (HHV-8) (Virology)

A

Also called Kaposi’s Sarcaoma-associated herpesvirus (KSHV)
Enveloped
dsDNA genome
Latent state in KS lesions
Contains several homologues of cellular genes

45
Q

Human Herpes Virus 8 (HHV-8) (Transmission and Associated Diseases)

A

Sexual
Needle sharing

Immune deficiency substantially increases the risk of developing KS

Other HHV-8 associated diseases:

  • Castleman’s Disease
  • Primary effusion lymphomas
46
Q

Human Herpes Virus 8 (HHV-8) (Prevention and Treatments)

A

Prevention of HHV-8 Transmission:

  • Safe sex
  • Limit needle sharing

Treatments for KS:

  • Controlling immune deficiency
  • NOT herpes antivirals because virus is in the LATENT state in KS lesions
  • Chemotherapy, radiation, and/or surgery
47
Q

Adult T-Cell Lymphoma (ATL)

A 
T-cell origin
Clinical presentation
-Lymphadenopathy
-Hepatosplenomegaly
-Hypercalcemia (***UNIQUE***)
-Skin infiltration of tumor cells (papules, plaques, tumors, ulcers)

Most common in southern Japan, Caribbean, and Central Africa

48
Q

Adult T-Cell Lymphoma (ATL) (Diagnosis)

A
  • FLOWER CELLS*

- Can be confirmed by the detection of antibodies to Human T-cell leukemia virus 1 (HTLV-1)

49
Q

HTLV-1 Associated Myelopathy (HAM)/Tropic Spastic Paraparesis

A

Caused by HTLV-1

***Demyelination of neurons within the spinal cord
Likely an AUTOIMMUNE DISEASE
Highest incidence in adult women

Symptoms:

  • Stiff gait
  • Lower extremity weakness, back pain
  • Incontinence
  • 1/3 of patients are bedridden at 10 years post diagnosis
50
Q

Human T-Cell Leukemia Virus I (HTLV-I)

A 
Human T-cell Leukemia Virus I/Human T-cell Lymphotropic Virus I
-Infects CD4 and CD8 positive cells
***Retrovirus***
-Enveloped
\+ssRNA genome
-Reverse transcription
51
Q

Human T-Cell Leukemia Virus I (HTLV-I) (Clinical)

A

Mainly in Japan, Central Africa, and Caribbean

  • **Approximately 1/20 develop adult T cell leukemia (ATL)
  • Time between infection and ATL development is approximately 30 years
  • CHILDHOOD TRANSMISSION = greatest risk for ATL

Cell-associated Virus (attached to cell; has to bring cell along with it in order to cause infection)

52
Q

Human T-Cell Leukemia Virus I (HTLV-I) (Transmission)

A

Nursing
Blood transfusion
Sexual Transmission (Male –> Female more efficient)

53
Q

Human T-Cell Leukemia Virus I (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

54
Q

Examples of HHV-8 Genes involved in cancer (vGPCR, vIL-6, K4, K4.1, K6, vFLIP, LANA)

A

vGPCR –> IL-8 homologue

vIL-6 –> IL-6 homologue

K4, K4.1, K6 –> ChemoKine homologue

vFLIP –> FLIP homologue involved in apoptosis protection

LANA –> Maintains viral latency and binds to p53

Microbiology Exam V (6 decks)

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