Micro Lectures Flashcards

1
Q

What is an acute lytic viral infection?

A

Real world definition = viral infection that results in the production of progeny virus and lysis of the infected cell

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2
Q

Acute clinical symptoms are the result of:

A

Either tissue destriction due to virus replication, or side effects of the host immune system (e.g. inflammation, tissue damage)

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3
Q

Examples of disease from acute lytic viral infections:

A

Time course: 3-14 days

Symptoms can include: fever, fatigue, vomiting, diarrhea, hemorrhage etc.

Successful immune response clears infection

e.g. flu, norovirus, ebola

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4
Q

What is a chronic lytic viral infection?

A

Productive viral infection in a subset of cells

Continual infection/ re-infection cycle

Ongoing shedding of virus from infected cells that does not immediately result in cell lysis

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5
Q

Chronic Focal Infection:

A

◦A subset of “carrier cells” produces virus

◦Infects neighboring cells

◦Initial cells replaced by new cells

◦Newly infected cells reinitiate the process

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6
Q

Chronic Diffuse Infection:

A

◦Both infected cells and virus continue to replicate

◦Cells are not lysed by virus

◦Cells continue to shed virus for their life span

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7
Q

Hepatitis C Virus causes a ____ infection. Elaborate.

A

Chronic Lytic Infection

◦Chronically infects hepatocytes in 80% of patients

◦Persistent lytic replication result in progressive liver disease

◦Culminates in cirrhosis &/or hepatocellular carcinoma (approx. 30 years)

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8
Q

The main difference between acute lytic and chronic infections is the ______

A

time to clear the virus

◦Acute infection <2 weeks

◦Chronic infection persist for weeks/months/years

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9
Q

What is latency?

A

Presence of viral nucleic acid in the absence of pre-formed infectious virus that has the ability to re-initiate lytic replication

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10
Q

Chronic vs. latent infection:

A

Both involve persistence of viral nucleic acid

Both may involve a period of clinical latency (infection in the absence of disease)

Difference is in the molecular state of the virus:

  • Latent infections do not produce infectious virus
  • Chronic infections involve continual production of new viral particles
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11
Q

For latent viruses, the viral genome is maintained as ____ in DNA viruses and ___ in RNA viruses

A

Maintained as DNA in both cases!

Both RNA and DNA viruses can establish latency.

Viral genomes can be integrated into host genome (provirus) or

Viral genomes can be maintained as extra-chromosomal DNA (episome)

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12
Q

Provirus:

A

Viral genomes are integrated into host genome

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13
Q

Episome:

A

Viral genomes maintained as extra-chromosomal DNA

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14
Q

Rhinovirus (cause of common cold) infection is best described as:

A. Acute lytic

B. Chronic lytic

C. Latent

A

Acute lytic

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15
Q

Untreated HIV infection is best described as:

A. Acute lytic

B. Chronic lytic

C. Latent

A

Chronic Lytic

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16
Q

Characteristics of herpesviruses:

A

Herpesvirus genomes are linear ds DNA

Viral DNA is in an icosahedral core

Virus particle is enveloped in a lipid membrane

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17
Q

EBV is latent in ____ cells. CMV is latent in ____ cells.

A

EBV is latent in lymphoid (esp. B) cells. CMV is latent in various cells.

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18
Q

How is EBV transmitted?

A

Exchange of saliva

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19
Q

Describe the infection process of EBV:

A

Transmitted via exchange of saliva

Initially infects epithelial cells in the oropharynx

Spreads to the blood; infects B-cells via CD21 complement receptor

Early 1° infection usually asymptomatic

Clinically apparent as infectious mononucleosis when 1° infection occurs later (among adolescents & young adults)

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20
Q

Clinical signs and symptoms of infectious mono:

A

Clinical signs & symptoms include fatigue, fever, sore throat, lymphadenopathy

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21
Q

Define mononucleosis:

A

Mononucleosis = proliferation of ‘mononuclear’ cells (lymphocytes, not monocytes)

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22
Q

In EBV infection, infected B cells are recognized by _____

A

cytotoxic T-cells

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23
Q

What is indicated by this blood smear?

A

Cells on the left are atypical lymphocytes characteristic of EBV infection.

Lymphocyte on the right is normal.

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24
Q

Hemoatologic characteristics of EBV:

A

◦Lymphocytosis during primary infection

◦High % of atypical lymphocytes

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25
Q

Immunologic diagnosis of EBV:

A

◦Heterophile antibodies (literally against an antigen from another species) = used to define antibodies against poorly-defined or cross-reacting antigens

  • –detected with monospot test, positive within 2 weeks of illness
  • –non-specific, false positives and false negatives possible
  • –does not confirm EBV infection

◦EBV-specific antibodies (IgM early, IgG later)

  • –VCA = viral capsid antigens
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26
Q

How is EBV treated?

A

Acyclovir is generally not effective against EBV

There is no vaccine against EBV

No kissing?

Basically don’t treat it.

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27
Q

X-linked lymphoproliferative syndrome:

A

Children with this disease are susceptible to severe, life-threatening mono (>70% mortality rate by age 10)

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28
Q

Hairy leukoplakia:

A

EBV associated disease

Whitish, nonmalignant lesions on the tongue

Immunocompromised pts, especially AIDS

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29
Q

Burkitt’s Lymphoma:

A

EBV-associated disease

Endemic in Africa and New Guinea

Sporadic in US and Western Europe

HIV-associated

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30
Q

EBV establishes latency as ____ in the ____ of infected B cells.

A

EBV establishes latency as episomal DNA in the nucleus of infected B cells.

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31
Q

Latently-infected EBV cells produce an increase in ____, resulting in uncontrolled proliferation

A

IL-10

32
Q

What two groups of genes (broad) are mutated in cancer?

A

tumor suppressors (inhibit cell cycle progression)

proto-oncogenes (stimulate cell cycle progression - normal to have proto-oncogene; mutant is oncogene)

33
Q

How is CMV transmitted?

A

Transmitted transplacentally, also via saliva, genital secretions, transfusions & transplants

34
Q

CMV causes the formation of ___ cells with _____

A

CMV causes the formation of giant cells with intranuclear inclusions

35
Q

What is the most common cause of congenital abnormalities in the US?

A

CMV

36
Q

CMV pathogenesis:

A

Primary infections in kids and adults are usually asymptomatic

In developing fetus (during mom’s 1° infection in 1st trimester), cytomegalic inclusion disease causes defects in many organs

Maintains latency in many cell types for many years

Latently infected cells have unstable MHC-I, so aren’t well recognized by CD8+ T-cells

37
Q

Latently infected CMV cells have unstable ____, so they aren’t well recognized by ____ cells.

A

Latently infected CMV cells have unstable MHC-1, so they aren’t well recognized by CD8+ T cells.

38
Q

CMV clinical findings:

A

“Blueberry muffin” lesions in neonates (not CMV-specific)

Heterophile-negative mono in immunocompetent adults

Pneumonia, esophagitis & hepatitis in transplant patients

Intestinal infections in AIDS patients leads to severe colitis & diarrhea

Also causes retinitis in AIDS patients

39
Q

CMV treatment/prevention:

A

Acyclovir is not effective, but ganciclovir and valgancyclovir are moderately effective in treatment of pneumonia and retinitis

No vaccine

Sero-matching blood and organs for transplantation for CMV-seronegative recipients

40
Q

Which of the following best describes heterophile antibodies used for diagnosis of infectious mononucleosis?

A. Specific for EBV viral capsid antigens

B. Develop during latent infection with EBV

C. Can be present in other conditions

A

Can be present in other conditions

By definition, heterophile means to other things, so they’re actually also associated in other conditions too. They’re not specific for the virus, they just develop in the presence of this infection.

41
Q

Why are heterophile antibodies associated with infectious mono caused by EBV and not CMV?

A

EBV infects B cells, which causes them to aberrantly proliferate and produce antibodies.

CMV doesn’t infect the B cells.

42
Q

What is the cell wall of fungi composed of?

A

Chitin and B glucans

43
Q

What is contained in the cell membrane of fungi?

A

Ergosterol

44
Q

Fungal proteins contain _____

A

Mannose

45
Q

What is a yeast?

A

Single-celled form of fungi

Divides by fission

46
Q

Hyphae can be ___ or ____

A

septate (see divisions between cells) or aseptate (cells divide without forming a cell wall in between - looks like a giant ribbon)

47
Q

Conidia:

A

Fungal spores

48
Q

Germ tubes are associated with:

A

Candida

49
Q

Polyenes:

A

Antifungal agent - binds ergosterol and forms pores in the membrane. BUT can also bind to cholesterol in mammalian cells.

E.g. Amphotericin B, nystatin

50
Q

Azoles:

A

Antifungals that target ergosterol synthesis

e.g. fluconazole, itraconazole, ketoconazole

51
Q

Echinocandins:

A

B-glucan synthesis inhibitors

e.g. Caspofungin, micafungin, anidulafungin

52
Q

Pyrimidine analogues:

A

Can be used to treat fungal infections

e.g. 5FU, which inhibits fungal thymidine synthesis (side effects = bone marrow suppression and pancytopenia)

53
Q

Virtually all fungal pathogens induce ____ production by phagocytes, leading to further production of ___ and ___ responses.

A

Virtually all fungal pathogens induce IL-12 production by phagocytes, leading to further production of IFN-gamma and Th1 responses.

54
Q

How do fungi induce complement?

A

Stimulate mannose-binding lectin pathway

(opsonization by C3b increases phagocyte clearance, especially of yeast)

55
Q

___ immunity is particularly important in fighting fungal infections

A

T cell-mediated adaptive immunity

(antibodies don’t seem super important; AIDS patients are super prone to fungal infections)

56
Q

List two important yeasts:

A

Candida

Cryptococcus

57
Q

List 3 important Mold families:

A

Aspergillus

Zygomycetes (Mucor & Rhizopus)

Fusarium

58
Q

List 4 important dimorphics:

A

Histoplasma

Blastomyces

Coccidioides

Paracoccidioides

59
Q

Opportunistic fungi:

A

Candida albicans

Cryptococcus neoformans

Aspergillus

Mucor & Rhizopus

Pneymocystis jirovecii

60
Q

Associate india ink stain with what fungi?

A

Cryptococcus neoformans

61
Q

Specific risk factors for Candidiasis:

A

Surgery

Acute renal failure

Total parentral nutrition (e.g. central venous catheter)

62
Q

Specific risk factors for Cryptococcosis:

A

C. neoformans - exposure to bird droppings

C. gatii - exposure to plant debris

63
Q

Specific risk factors for Aspergillosis and Mucormycosis:

A

Hematologic malignancy

Cytotoxic chemo

64
Q

What patient population is affected by endemic mycoses?

A

These fungi can cause disease in normal hosts, but are worse in immunocompromised

65
Q

What is the characteristic disease associated with this slide and region?

A

Histiocytosis

Found around Ohio River valley

Characteristic yeast cells in macrophages on smear

Often associated with bats/attics (spooky)

66
Q

How is Histoplasma diagnosed?

A

Antigen detection (ELISA urine and/or serum test)

Antibody test is retrospective

Microscopy is low sensitivity

Culture takes a long time

67
Q

What is the characteristic disease associated with this location and smear?

A

Blastomyces

Often Blastomyces dermitidis - affects skin

Also - Blastomyces forms encapsulated yeast with Broad-Based Budding. Can also spread to Bones!

68
Q

Blastomyces generally arises after exposure to ____

A

The environment (DIRT especially)

69
Q

How is Blastomyces diagnosed?

A

Microscopy (low sensitivity)

Culture (may take 6 weeks)

Antigen detection (EIA with urine, serum, or BAL; may cross-react with Histo or other fungi)

70
Q

What fungi is associated with this geographic region and smear?

A

Coccidioides

(see cocci spherule in lung tissue)

71
Q

What funal infection is indicated by this location and smear?

A

Paracoccidioides

See budding yeast around cells

72
Q

What is the most likely cause of this gram stain (left) and positive germ tube assay (right)

A

Candida albicans

Yeast will actually gram stain, but they’re bigger and oval-shaped

73
Q

What type of hyphal structure is most consistent with mucormycosis?

A

Aseptate

74
Q

Aspergillus and Fusarium form ___ hyphae

A

Septate

75
Q

Mucor and Rhizopus (Zygomycetes) form ___ hyphae

A

nonseptate