Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

immunology > Week 5 > Flashcards

Week 5 Flashcards

1
Q

What is a primary infection?

A

First experience with virus

Typically presents much worse than a secondary infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is secondary infection?

A

Reactivated infection; renewal of viral replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is a latent infection?

A

Persistence of virus in a non-replicating state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a symptomatic infection?

A

infection with clinical signs and symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is an asymptomatic infection?

A

viral shedding without symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the three subfamilies of Herpesviridae?

A

Alpha, Beta, Gamma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the alpha viruses?

A

HSV-1, HSV-2, VZV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the beta viruses?

A

CMV, HHV-6, HHV-7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the gamma viruses?

A

EBV, KSV (HHV-8)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the characteristics of the alpha family?

A

short replication cycle then destroys host cells and spreads rapidly.

They become latent in sensory ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the characteristics of the beta family?

A

Long reproductive cycle
enlargement of infected cells
slow cell-to-cell spread

multiple non-ganglionic latency sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the characteristics of the gamma family?

A

Replicate in lymphoblastoid vells

latency in lymphoid tissue (EBV), monocytes and lymphocytes (HHV-8)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the lipid envelope of the HSV virus

A

The lipid envelope contains multiple surface glycoproteins

Glycoprotein G

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does HSV infect a host?

A

enters via skin-to-skin contact, mucous membrane contact, or openings in the skin (wound, burn, diaper rash)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What happens after HSV enters the host?

A

It replicates at the site of entry, destroys the cell, spreads rapidly, then becomes latent in sensory ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where is HSV-1’s latent site? HSV-2?

A

HSV-1: trigeminal ganglia

HSV-2: S2-S5 ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the clinical hallmarks of HSV?

A

fluid filled vesicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What type of cells are found in HSV lesions?

A

multinucleated giant cells and intranuclear inclusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

describe characteristics of HSV latency.

A
  • mediated by viral genes
  • maintained by T cell mediated immunity
  • viral genome is circular during activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Are antivirals effective against latent viruses?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What happens when HSV comes out of latency?

A

The DNA becomes linear and the virus travels back to the site of entry

Replication causes the cell to lyse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the reservoir for HSV?

A

humans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Are HSV clinical presentations typically more sever in the primary infection? How so?

A

Yes

illness severity
anatomic distribution
amount of virus in secretion
duration of shedding
no antibodies present
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Can HSV-2 be found above the belt? HSV-1 below the belt?

A

Yes and yes. However, they are generally associated as HSV-1 above the belt and HSV-2 below the belt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the common HSV-1 infections?

A

gingivostomatitis
cutaneous lesions
ocular infections
encephalitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the characteristics of herpes gingivostomatitis?

A 
Typically caused by HSV-1
more common at age 1-3
extensive oral +/- cutaneous lesions
Fever, irritability, tender adenopathy
Poor oral intake leading to dehydration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are characteristics of HSV cutaneous infections?

A 
Usually caused by HSV-1
Herpetic whitlow (lesions on fingers)
Herpes gladiatorum (wrestlers)
Scrum pox (rugby players)
Eczema herpeticum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are characteristics of HSV ocular infections?

A

Usually caused by HSV-1
Follicular conjunctivitis
Corneal involvement with dendritic ulcers
Recurrence may be sight threatening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are characteristics of HSV encephalitis?

A

Usually caused by HSV-1
Most common, sporadic form of encephalitis
Fever, headache, altered sensorium (state of consciousness)
Focal signs within the temporal lobe
Lumbar puncture will show CSF with RBCs, WBC, protein
- PCR CSF to diagnose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are characteristics of HSV genitalis?

A

Usually caused by HSV-2
Sexually transmitted
Genital, rectal, perirectal, proctitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the clinical presentations of HSV infections in immunocompromised hosts?

A 
More recurrent infections
More prolonged
More progressive and destructive
More widespread
  - Liver, lungs, esophagus, brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Name 5 methods that can be used to diagnose HSV infections

A

1) Biopsy may indicate histological features of infection
2) DFA (direct fluorescent antibody) test that labels antibodies specific to HSV with dye
3) PCR
4) Viral culture
5) Serology (Look for HSV antibody in the serum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the typical antiviral therapy used for HSV infections?

A

acyclovir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are some strategies to prevent HSV infections?

A

1) Avoid contact
- Horizontal (person-to-person)
- Condoms, antivirals
- Vertical (mother-to-child)
- C-section, antivirals

2) Prophylactic therapy
3) vaccination is the holy grail but one does not exist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the 3 classical clinical presentations of neonatal HSV infections?

A

1) Skin, eye, mucosal (SEM) disease
- important to rapidly diagnose via DFA to prevent progression

2) Disseminated disease
- Presents with sepsis, liver dysfunction, coagulopathy resulting in hemorrhage, respiratory distress, encephalitis

3) CNS disease
- Lethargy, irritability, fever, SEIZURES
- Culture CSF and perform PCR
- Be sure to look at temporal lobe!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are some strategies to prevent infections in the fetus and newborn?

A
  • vaccinate before pregnancy
  • treatment during pregnancy
  • avoidance during or after delivery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are some strategies to prevent infections in the fetus and newborn?

A
  • vaccinate before pregnancy (BEST)
  • treatment during pregnancy
  • avoidance during or after delivery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the mechanism of fever?

A

IL-1, IL-6, TNF, and IFN act on the hypothalamus to increase body temperature

Can be caused by a crap ton of things

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What can cause fever?

A

Again, a crap ton of things

infection
neoplasms
allergies
immune disorders
etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is FUO?

A

Fever of undetermined origin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are some microbiologic characteristics of EBV?

A
  • gamma 1 herpesviridae
  • dsDNA
  • Multiple surface glycoproteins
  • virus-specific antigens:
    • viral capsid antigen (VCA)
    • Early antigens (EA)
    • Nuclear antigens (EBNA)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How is EBV typically transmitted?

A

Usually via oral transfer of saliva

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Describe the pathogenesis of EBV

A

1) EBV colonizes the epithelium in the oropharynx, including tonsils and salivary glands.
2) There, it replicates and infects B cells by binding to CD21R and enters the cell
3) If it enters the lytic phase,, EBV produces a homologue to IL-10, which inhibits Th1 cells. Inhibition of Th1 cells inhibits IFN secretion and activation of macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are clinical presentations of EBV?

A

non-specific symptoms with atypical lymphocytes (lots of cytosol including some granulation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What two cells does EBV infect?

A

epithelial in the oropharynx and B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

When does EBV proceed to the lytic phase? Latent phase? Does the cell lyse?

A

Typically, when EBV infects epithelial cells, it proceeds directly into the lytic phase and lyses the cell

Typically, when EBV infects B cells, it proceeds directly into the latent phase and enters lytic phase at a later time, which may or may not lyse the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the symptom of mononucleosis?

A

MONO

fever, pharyngitis, and adenopathy

Known as the “kissing disease” and it typically makes you tired.

48
Q

What occurs when EBV infects a B cell and enters the latent phase?

A

The DNA becomes circular and attaches to the host DNA with the help of EBNA-1. This allows for the virus DNA to be replicated during cell proliferation

49
Q

What occurs when EBV leaves the latent phase and enters the lytic phase?

A

The circular DNA becomes linear, which transforms the cell and causes mass proliferation

50
Q

What are some diseases of reactivated EBV infections?

A
  • Burkitt lymphoma
  • Nasopharyngeal carcinoma
  • Hodgkin’s lymphoma
  • CNS lymphoma
  • Oral hairy leukoplakia
  • Post-transplant lymphoproliferative disease
51
Q

Are lytic genes expressed in EBV-associated cancers?

A

NO LYTIC GENES ARE EXPRESSED IN EBV-ASSOCIATED CANCERS, ONLY LATENT GENES WITH DIFFERENT PATTERNS

52
Q

What are the clinical presentations of Burkitt lymphoma? Describe endemic and sporadic

A

The ENDEMIC (African) VARIANT is an 8:14/8:22 translocation involving the c-myc oncogene (just one of the few variants, but all involve the c-myc gene).

can involve the jaw/facial bones, GI, and/or GU

SPORADIC VARIANT is typically not associated with EBV and is seen in the ileocecal region

53
Q

What do Burkitt’s lymphoma cells look like on slides?

A

“Starry sky” lipid droplets inside of the cell

54
Q

What are the clinical presentations of nasopharyngeal carcinoma?

A

Common in Southern China and native North Americans

Genome expresses EBNA-1 and LMP-1 latent gene products

55
Q

What are the clinical presentations of Hodgkin’s lymphoma?

A

Patients have EBV antibody

nodular sclerosis (scarring of lymph nodes)

56
Q

What are the clinical presentations of CNS lymphoma?

A

Typically occurs in patients with advanced T cell immunosuppression, particularly in patients with HIV/AIDS

  • headache
  • focal neurological symptoms
  • neuropsychiatric symptoms
  • seizures
57
Q

What can bee seen on MRI in patients with CNS lymphoma?

A

lesion(s) on in the periventricular white matter

58
Q

What does CSF analysis show in CNS lymphoma?

A

elevated intracranial pressure
elevated protein
lymphocytic pleocytosis

59
Q

What are the clinical presentations of Post-transplant lymphoproliferative disease?

A

B cell proliferation due to immunosuppression following organ transplantation (immunosuppression tells EBV to become active)

60
Q

What are the clinical presentations of oral hairy leukoplakia?

A

White patches on the margin of the tongue caused by EBV replication

firm, does not scrape off

typically seen in patients with HIV/AIDS

61
Q

What does the varicella zoster virus cause?

A

chicken pox and shingles

62
Q

What is the classification of VZV?

A

DNA virus

alpha herpesviridae

63
Q

What are immune privileged sites?

A

tissues that are in part protected from the immune system, as inflammation can

(Brain, nerves, eyes, testes, placenta/fetus)

64
Q

Describe VZV pathogenesis

A

1) VZV infects the respiratory tract and/or conjunctiva
2) Virus replicates in the upper airway and regional lymph nodes
3) Primary viremia results in infection of lymphocytes and nerve cells
4) replication causes secondary viremia leading to clinical symptoms such as fever and malaise
5) infection of skin results in a vesicular rash. Zoster rash occurs in a dermatome pattern

65
Q

Who is at high risk for disseminated disease (VZV)?

A

Individuals with HIV or who are receiving chemotherapy

66
Q

Who is at high risk for shingles?

A

older patients who naturally lose memory T cell loss

67
Q

Describe the progression of varicella rash

A

papules -> vesicles with clear fluid -> vesicles with cloudy fluid (T cells) -> crusting

68
Q

Describe the progression of VZV rash

A

papules -> vesicles with clear fluid -> vesicles with cloudy fluid (T cells) -> crusting

69
Q

What are the clinical manifestations of Varicella? Zoster?

A

Varicella

  • Itchy vesicular rash that has a central distribution primarily on the trunk
  • Because VZV is viremic, it can result in hepatitis, encephalitis, pneumonitis

Zoster
- Painful vesicular rash with a dermatomal distribution

70
Q

How are VZV infections diagnosed?

A

typically by observing clinical presentations (vesicles). However, these tests can be used:

PCR > Stains/fluorescents > antibody tests > culture (doesn’t culture well)

71
Q

How is VZV treated?

A

symptom control is mainstay of treatment, but anti-viral therapy is indicated in adolescents, adults, and immunocompromised

72
Q

Describe vaccination for varicella. Who should not receive this vaccination?

A

Live attenuated vaccine that is given alone or with MMR (MMRV)

immunocompromised or pregnant women should not receive this vaccine

73
Q

Describe the zoster vaccination and who gets it. What is given to those who cannot receive the vaccine?

A

Same live attenuated virus as varicella, but given at a higher concentration to people 60+

immunoglobulins are given to immunocompromised patients who can’t receive the vaccine

74
Q

What can cause vesicular rashes?

A 
VZV
Herpes
Enterovirus
staph a bullous impetigo
insect bites
contact dermatitis
75
Q

define epidemic

A

rapid spread of infection in a city, state or entire country over a short period of time

76
Q

define pandemic

A

an epidemic that spreads across boarders, even worldwide, affecting large numbers

77
Q

Describe the structure of the influenza virus

A 
orthomyxovirus family
ssRNA (-) sense
segmented genome
enveloped
  - Hemagglutin (HA)
     - binds sialic acid receptors for viral entry
     - agglutinates RBCs
     - antigenic (neutralizing)
  - Neuraminidase (NA)
     - cleaves sialic acid to release virus
     - degrades mucin
     - antigenic (non-neutralizing)
78
Q

What is antigenic drift (relate to influenza)?

A

small mutations in HA or NA

79
Q

What is antigenic shift (relate to influenza)?

A

complete mutations in HA or NA

Only occurs in type A

80
Q

Describe the pathogenesis of influenza

A

1) spreads via large droplets or contaminated surfaces
2) NA degrades protective mucus
3) HA binds to sialic acid receptors and enters cell
4) virus uncoats
5) genome moves to the nucleus
6) mRNAs are created for protein synthesis and for genetic material for new virions
7) Virions are assembled in the cytoplasm
8) Virions are released via budding when NA cleaves saliac acids
9) viral replication results in cell destruction

81
Q

What are the clinical manifestations of influenza (incubation period, type of onset and symptoms, period of infectiousness)

A

incubation is 1-4 days

abrupt onset of fever, myalgias, headache, pharyngitis, rhinorrhea, cough, fatigue

infectious for 3-5 days after symptom onset

82
Q

What are potential complications of influenza?

A
  • Primary pneumonia leading to respiratory failure
  • secondary bacterial pneumonia
  • Reye’s syndrome
83
Q

What is Reye’s syndrome?

A

Rare potential complication of influenza that occurs in children that is characterized by:

  • fever
  • rash
  • encephalopathy
  • liver failure
84
Q

What are the common methods used for diagnosing influenza?

A

nasopharyngeal aspirate or swab then:

viral culture
- gold standard but takes 10 days

Direct fluorescent antibody
- 1-4 hours

PCR
- most sensitive and specific and takes 1-6 hours

rapid antigen detection
- most rapid (<30 min) but can show false negatives

85
Q

Name two adamantanes. What are their mechanisms and SAEs?

A

Amantadine and Rimantadine

Influenza A M2 ion channel inhibitor that prevents viral uncoating

CNS and anticholinergic effects. teratogenic

86
Q

Name two neuraminidase inhibitors. What are their mechanisms and SAEs?

A

Oseltamivir and Zanamavir

Influenza A and B NA inhibitor that prevents the release of virions from cell

N/A

87
Q

Describe the population at risk for influenza

A

infants
- no maternal IgG after 6 months and IgA from milk doesn’t protect against influenza

elderly

immunocompromised

obese individuals

pregnant women
- produce more Treg

88
Q

Describe the types of influenza vaccines

A

trivalent or quadravalent conjugate vaccine

live attenuated nasal spray
- do not give to pregnant women or immunocompromised

89
Q

What are the warnings and contraindications of influenza vaccination?

A

may cause:

  • Guillain Barre syndrome
  • allergic reaction

contraindication
- if you’ve had a sever reaction to the vaccine in the past, don’t get it

90
Q

define vaccine antigen

A

the molecule in the vaccine that an antibody response should be generated against

91
Q

define adjuvant

A

substance that non-specifically activates the immune system - added to vaccines to enhance the immune response

92
Q

define vaccine titer

A

a measure of amount of antibody made to a vaccine antigen

93
Q

What are the 5 different types of vaccines?

A

1) inactivated/killed
2) toxoid (inactivated toxin)
3) subunit
4) conjugate
5) live, attenuated

94
Q

How are inactivated vaccines created? examples?

A

made by inactivating the whole pathogen by heat or by chemicals

polio vaccine
hepatitis A vaccine
rabies vaccine

95
Q

How are toxoid vaccines created? examples?

A

inactivate the toxin by heat or chemical

tetanus
diphtheria

96
Q

How are subunit vaccines created? examples?

A

made by isolating or making a specific component of a pathogen. MUST be mixed with an adjuvant

Hep B
HPV
Pertussis
Influenza
Pneumococcal polysaccharide
meningococcal polysaccharide
97
Q

How are conjugate vaccines created? examples?

A

Conjugate a carbohydrate to a protein to enhance immune response

H. influenza
Pneumococcal conjugate
Meningococcal conjugate

98
Q

How are live, attenuated vaccines created? examples?

A

grow virus in another animal. Over time, the virus becomes worse at growing in humans

Measles
Mumps
Rubella
Varicella
Rotavirus
Influenza (nasal spray)
Polio (oral)
Yellow fever
Bacille Calmette Guerin (BCG for TB)
99
Q

What are two problems with live, attenuated vaccines?

A

1) If given to immunocompromised patients, the attenuated virus can be pathogenic
2) The attenuated virus can revert back to wild-type form to become pathogenic

100
Q

Describe T cell dependent antibody production

A

Small antigens that are recognized by B cells are presented to T cells, which result in activation and potential class switching. This results in B cell memory

101
Q

Describe T cell independent antibody production

A

Long, repeating carbohydrates cross-link B cell receptor causing activation. No B cell memory

102
Q

Describe how conjugate vaccines help create a T cell dependent response

A

Conjugate vaccines connect a carbohydrate to a protein, which creates a T cell dependent response, resulting in B cell memory

103
Q

What is meningitis? what are its associated symptoms?

A

inflammation of the meninges

fever, headache, stiff neck, and potential petechia

104
Q

What is encephalitis? what are its associated symptoms?

A

inflammation of the brain parenchyma

fever, altered mental status, and seizures

105
Q

What is meningoencephalitis? what are its associated symptoms?

A

inflammation of both the meninges and the brain parenchyma

fever, headache, stiff neck, altered mental status, and seizures

106
Q

What is myelitis? What are its associated symptoms?

A

Inflammation of the spinal cord

flaccid paralysis and sensory loss

107
Q

What is a positive Kernig’s test?

A

Pain associated with quadricep flexion (indicates inflamed meninges)

108
Q

What is a positive Brudzinski test?

A

Pain associated with flexion of the head (indicates inflamed meninges)

109
Q

What indicates bacterial meningitis?

A

CSF shows:

high PMNs, low glucose, and high protein

110
Q

What is aseptic meningitis?

A

inflammation of the meninges and a bacterial source is not to blame

111
Q

What are the 3 possible outcomes when collecting CSF for suspicion of meningitis

A

If no WBC in CSF, consider alternative diagnoses

If WBC present but no bacterial growth = aseptic meningitis

If WBC present and bacterial growth = bacterial meningitis

112
Q

If no bacteria grow in culture, what could be the cause of aseptic meningitis?

A

1) bacteria that don’t grow on standard media
2) virus
3) fungi
4) parasites
5) antibiotics given to patient before lumbar puncture could make it look like aseptic when really septic meningitis

113
Q

How does aseptic meningitis present in CSF analysis?

A 
WBC: normal
Glucose: normal/low
Protein: normal/high
gram stain: negative
culture: no growth
114
Q

What are Arboviruses? What do they commonly cause?

A

Arthropod borne viruses

encephalitis

115
Q

What is the most common cause of viral meningitis?

A

enterovirus

immunology (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions