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Microbiology > Herpes Virus Cards > Flashcards

Herpes Virus Cards Flashcards

1
Q

Front

A

Back

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2
Q

What is the genetic material of herpesviruses?

A

DNA virus

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3
Q

What is the incubation period of VZV?

A

10-21 days

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4
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Describe how VZV enters and replicates in the body

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Enters via respiratory tract/conjunctive; local replication in the upper airway and regional lymph nodes; primary viremia nad infection of lymphocytes and nerve cells

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5
Q

Describe how VZV progressed to a skin infection

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Primary viremia infects lymphocytes and nerve cells; VZV replicates, establishing a secondary viremia (fever) and skin infection (rash)

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6
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How does VZV modulate the immune system?

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VZV infects lymphocytes and inhibits MHC-I expression, thus turning on NK signals

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7
Q

How does interferon-alpha aid in controlling viral infection?

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IFN-alpha is produced locally in the skin late during a n infection and limits viral spread via blocking viral replication and decreasing virion assembly

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8
Q

How does shingles occur?

A

VZV establishes a latency in ganglia; when anti-VZV memory T cell activity drops with age, VZV re-activates and replicates

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9
Q

How does VZV establish latency?

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VZV establishes latency in a sensory nerve ganglion which is immunopriviledged

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10
Q

What are possible presentations of disseminated VZV?

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Hepatitis, pneumonia, encephalitis

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11
Q

What diseases does VZV cause?

A

Varicella (chickenpox) and Zoster (shingles), a reactivation disease

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12
Q

Describe the varicella rash

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Discrete papules –> vesicles with clear fluid –> cloudy fluid –> crusting at 5-7 days. Pt will have rash including all stages of vesicles at the same time. Involves the entire body. May be 200-500 vesicles!

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13
Q

What is the clinical presentation of shingles?

A

Vesicular rash along dematome, commonly on chest, pain, itching, sensitivity. Doesn’t cross midline.

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14
Q

What are the seasonal/climate associations with Varicella?

A

More often in late winter/spring, in temperate > tropical climates; may affect older individuals in warmer tropical climates, for an unknown reason

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15
Q

How infectious is VZV?

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Very. 90% secondary attack rate to susceptible household members.

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16
Q

What is the clinical presentation of chicken pox?

A

Itchy vesicular rash, central distribution, with 200-500 vesicles, possibly involving mucous membranes

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17
Q

Describe the epidemiology of zoster

A

Older (>45) or immunocompromised patients

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18
Q

Describe the zoster rash

A

Discrete varicella rash that coalesces; crusts by day 14; painful, does not cross midline and dermatomal

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19
Q

What is the most common complication of varicella?

A

Superinfection of vesicles (scratched open) with Staph aureus or strep pyogenes

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20
Q

Describe post herpetic neuralgia

A

Complication occuring in 20% of pts with zoster, most commonly in elderly. Results in pain that lasts months-years in response to touch and heat.

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21
Q

How is VZV diagnosed?

A

VZV is usually a clinical diagnoses based on symptoms and rash progression. May do PCR on vesicular fluid if atypical (e.g. varicella in previously immunized patient).

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22
Q

How are VZV antibody tests interpreted?

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IgG indicates previous infection or immunization. If IgG antibodies rise 4x, suggests recent acute infection (in non-immunized pt)

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23
Q

What is the basic treatment for VZV?

A

Prevention of secondary infection; antivirals in adults or immunocomromised patients

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24
Q

What antiviral is used to treat VZV?

A

Acyclovir (at a higher dose than for HSV) or Famciclovir as an alternative

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25
What is the mechanism of action and resistance for acyclovir?
Acyclovir inhibits viral DNA polymerase; virus may mutate thymidine kinase
26
What is the treatment of zoster?
Antivirals (acyclovir) to speed resolution of rash and decrease post-herpetic neuralgia, plus pain management
27
What type of vaccine is the varicella vaccine?
Live attenuated
28
How is the varicella vaccine given?
Primary immunization at 1 year old and booster at 4-6 years old
29
What type of vaccine is the zoster vaccine?
Live attenuated, with a higher concentration of varicella virus than in the varicella vaccine
30
How is the zoster vaccine given?
Routine immunization at 60yo or greater; most effective in 60-69yo
31
How can you prevent/treat VZV in an immunocompromised host?
Immunoglobulins (VariZIG) for post-exposure management + acyclovir early in infection
32
Describe the HSV rash
Vesicular and crusting rash, localized or in small groups, painful
33
Describe the variola virus rash
Vesicular and pustular rash on the entire body; lesions will be all at the same stage of progression
34
Describe the coxsackie virus rash
Combination of papules, pustules and vesicles localized on the hand, foot, mouth, and buttocks (hand food mouth disease); possibly with fever
35
Describe the etiology and characteristics of bullous impetigo
Etiology: Staphylococcus aureus; rash: fluid-filled bullae, non-itchy
36
What are the characteristics of alpha-herpesviruses? Name three alpha-herpesviruses
HSV1, HSV2, VZV. These have short reproductive cycle, rapid culture growth, latency in sensory ganglia, and destruction of infected cells.
37
What are the characteristics of beta-herpesviruses? Name three.
CMV, HHV6, HHV7. These have a long reproductive cycle, slow culture spread, non-ganglionic latency, and enlargement of infected cells.
38
What is the presentation of roseola?
Highmulti-day fever, fussiness, diarrhea, lymphadenopathy followed by erythematous morbiliform rash on the trunk, spreading to face/extremities
39
Which subgroup of HHV6 causes most disease?
HHV-6B
40
What property allows HHV6 to be transmitted vertically?
In latency, HHV6 may integrate into telomeres and become germ-line
41
What are the neurological symptoms of HHV6?
HHV6 infects astrocytes and glial cells, causing seizures in primary illness and encephalitis in reactivation disease
42
What are common complications of HHV6?
Usually no complications; may have febrile seizures (in pts 6mo-6yo)
43
Which patients are most likely to have HHV6 reactivation?
Bone marrow and solid organ transplant patients
44
What is the treatment for HHV6?
Sympomatic treatment in healthy patients; antivirals (acyclovir) in immunocompromised
45
What cells does HHV7 infect?
CD4+ T cells and other tissues
46
How is HHV7 transmitted?
Respiratory secretion (persistent salivary infectious burden) from asymptomatic people
47
What is the clinical presentation of HHV7?
Similar to HHV6 (high fever --> rash) but febrile seizures may be more severe
48
Where is body temperature regulated?
Thermoregulatory center in the hypothalamus
49
Name four endogenous pyrogens
IL-1, IL-6, TNF-alpha, IFN
50
What are adverse effects of a fever?
Induction of sepsis, increase in oxygen demand/consumption, stress on CV and neurological tissue
51
What are beneficial effects of a fever?
Recruitment of Increased antigen presentation, antibody production, cytokine production, lymphocyte proliferation; inhibition of pathogen growth and increased antimicrobial susceptibility
52
What causes diurnal variation in temperature?
Serum cortisol release from the adrenal glands in a diurnal pattern
53
What is the definition of FUO?
Temperature above 38.3/101.0 on multiple occasions for >3 weeks, with no diagnosis after >1 week evaluation
54
What are the characteristics of gamma herpesviruses? Name two.
EBV, HHV8. These replicate in lymphoblastoid cells. Latency sites are lymphoid tissue (EBV) or monocytes/B lymphocytes (HHV8)
55
Describe the microbiology (shape, surface markers, etc) of EBV
dsDNA genome, enveloped, with multiple surface glycoproteins
56
Name the three EBV-specific antigens
Viral capsid antigen, early antigen, and nuclear antigens
57
How does EBV suppress the immune system?
In the lytic phase, it produces an IL-10 homologue that inhibits Th1 response/release of IFN-gamma and macrophage activation
58
What are reactive/atypical lymphocytes?
Large reactive lymphocytes that appear in EBV, CMV, and viral hepatitis
59
How is EBV transmitted?
Saliva, infecting epithelium of oropharynx
60
What immune response leads to the symptoms of primary EBV infection?
CD8+ T cell proliferation
61
What is the clinical triad of mononucleosis?
Fever, pharynitis, adenopathy
62
What are possible causes of mononucleosis syndrome?
EBV, but also CMV, HIV, viral hepatitis, rubella, parvovirus, influenza, secondary syphilis, bacteremia, rickettsia, coccidiomycosis, malaria, toxoplasmosis. Also drug reaction, malignancy, drug reaction. Basically everything!
63
How does EBV establish infection?
It infects epithelial cells and B cells via binding the CD21 receptor. It then enters a lytic or latent phase.
64
What occurs during an EBV lytic phase?
Linearization of circular EBV genome and production of infectious virions using viral DNA polymerase.
65
When does EBV lytic phase occur?
In epithelium, this occurs right after entry. In B cells, this occurs usually after reactivation from latent phase (a small % are immediately in the lytic phase).
66
What occurs in the EBV latent phase?
Viral circular DNA is integrated into the host cell; few proteins are expressed (immune evasion); uses host cell DNA polymerase; cell aquires the capacity to proliferate indefinitely
67
How is EBV latency maintained during host c ell division?
Epstein-Barr Nucleic Acid-1 binds viral episome to host chromosome to maintain virus in nucleus of B cell
68
What occurs during an EBV reactivation phase?
Viral gene expression using host DNA polymerase; apparently unlimited and unregulated growth
69
Describe T cell activity during different stages of EBV
T cells control EBV infection not only in lytic/reactivation but also during latency. T cell disorders are associated with lymphoproliferative syndromes.
70
What are 6 EBV-associated malignancies?
Burkitt lymphoma, nasopharyngeal lymphoma, Hodgkin's lymphoma, CNS lymphoma, post-transplant lymphoproliferative disease, and oral hairy leukoplakia
71
Which EBV genes are associated in EBV malignancies?
Latent genes; no lytic genes are expressed
72
Describe clinical presentation of endemic Burkitt lymphoma
Jaw, facial bones, GI, GU involvement
73
Describe the epidemiology of endemic Burkitt lymphoma
Associated with EBV, appears in malaria endemic regions (malaria = reduced resistance to EBV)
74
What is the common genetic mutation in endemic Burkitt lymphoma?
8:14 or 8:22 translocation of c-myc
75
Describe sporadic Burkitt lymphoma
Rare lymphoma, not associated with EBV, more commonly in the ileocecal region
76
Describe the histology of Burkitt lymphoma
Intracytoplasmic lipid droplets or "starry sky"
77
What is the epidemiology of nasopharyngeal carcinoma?
More common in Southern China, native North Americans
78
What genes are expressed in nasopharyngeal carcinoma?
EBNA-1, LMP-1 (latent EBV genes)
79
Does EBV play a role in Hodgkin lymphoma?
Maybe. EBV antibodies or DNA may be present, especially in aggressive Hodgkin lymphoma
80
What are the clinical symptoms of CNS lymphoma?
Headache, focal neurological deficits, seizure, neuropsychiatric symptoms
81
What is the MRI finding in CNS lymphoma?
1+ homogenously enhancing lesions in periventricular white matter
82
What is the CSF finding in CNS lymphoma?
Elevated intracranial pressure, elevated protein, high WBC, predominantly lymphocytes
83
In which patients is CNS lymphoma most common?
Pts with HIV/AIDS (DC4
84
What is the histology of CNS lymphoma?
Neoplastic lymphoid cells (pale, with mitoses) that are 3-4x larger than normal lymphocytes, arranged in a perivascular distribution; may have EBV genomes
85
How does post-transplant lymphoproliferative disease develop?
Following organ transplant, immunosuppression and T cell depletion prevent control and lead to B cell proliferation
86
What is oral hairy leukoplakia?
Cutaneous lesion involving lingual epithelium commonly found in HIV patients; It is not premalignant; results from over-replication of EBV (not cell dysfunction due to infection)
87
How do you tell oral thrush apart from oral hairy leukoplakia?
OHL is firm and will not scrape off, usually affecting the lateral tongue; thrush is candida and will scrape off, usually affecting buccal mucosa. Both are associated with immunosuppressed states, although OHL is more specific for HIV infection.
88
How do you treat OHL?
Antiviral therapy to target excessive EBV replication or HAART to target underlying HIV immunosuppression
89
What is the "monospot" diagnostic test?
An IgM heterophile antibody (induced by external antigen) with an affinity for sheep and horse RBC. Positive after 1 week and up to 3-6 months, but not positive during the incubation period.
90
How is acute EBV infection diagnosed?
Mononucleosis syndrome plus positive monostop heterophile antibody test
91
What is the specificity/sensitivity of the monospot test?
High specificity (rule in). False negatives during incubation, but 4yo) than in teens and adults (>80%). False positives may occur in HIV, lymphoma and lupus.
92
Describe the pattern of antibodies to EBV viral capsid antigen
Anti-VCA present during illness; IgM appears first and disappears after 3 months; IgG appears second but persists
93
Describe the pattern of antibodies to EBV early antigen
IgG to EA may appear early in clinical illness (not always) and dispapears after recovery; may be present in reactivation
94
Descibe the pattern of antibodies to EBV nuclear antigens
Anti-NA are expressed during latency (6-12 weeks) and persist indefinitely
95
What is the antibody pattern of EBV reactivation?
Negative IgM VCA; Positive IgG VCA, EA, NA

Microbiology (9 decks)

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