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2 and FINAL Microbiology Oral/Med > Final > Flashcards

Final Flashcards

1
Q

treatment for influenza?

A

Tamiflu

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2
Q

difference between influenza A and B?

A

A= H1N1; causes drifting; use amanthadine to target M2 protein

B= does NOT cause a shift; use TAMIFLU; targets the NA (nerve an…) on 6th segment

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3
Q

How much A and how much B in influenza injections?

A

2-3 A

1 B

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4
Q

Epstein Barr is?

LMPs?

A

Herpes

 latent membrane proteins (LMPs) 1 and 2 have oncoprotein-like activity
 Epstein-Bar-encoded RNA (EBER) molecules, EBER-1 and EBER-2 may also have roles in oncogenics

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5
Q

HBD vs HBV

HBD= hep D
HBV= hep B
A

HBD NEEDS HBV either prier or as a co-infection!

need HBV surface antigen to create capsid

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6
Q

rubella vs toga virus transmission?

A
  • rubella is person to perspn

* togo is via insect; ALPHA

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7
Q

Varicella zoster means?

A 
varicella= chickenpox
zoster= shingles later on
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8
Q

five childhood exanthems?

their associations?

A

1) Measles – paramyxovirus Measles virus
2) Rubella – a Toga virus, Rubella virus
3) Chickenpox – a Herpes virus, Varicella Zoster
4) Roseola – a Herpes virus, Herpes 6, 7
5) Fifth disease – Parvovirus B19

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9
Q

Measles as childhood exanthem example?

A

a paramyxovirus Measles virus

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10
Q

Rubella as childhood exanthem example?

A

a Toga viridea (an alpha form of Rubella virus)

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11
Q

Chickenpox as childhood exanthem example?

A

Herpes virus, Varicella Zoster

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12
Q

Roseola as childhood exanthem example?

A

a Herpes virus, Herpes 6, 7

**T-cells affected, mild, asymptomatic

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13
Q

Fifth disease as childhood exanthem example?

A

Parvovirus B19

*circulating!

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14
Q

Hemagglutination

A

Presence of virus in secretions; RBCs binding to other RBC’s

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15
Q

Hemadsorption

A
  • presence of hemagglitinin protein on cell surface

* RBC’s binding to something else (cell, virus, surface, etc.)

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16
Q

Inhibition of hemadsorption

A

identification of influenza type and strain

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17
Q

hemagglutinin

A

attachment protein, fusion protein, target of antibody for hemadsorption!!!

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18
Q

neuraminidase

Targeted by?

A

cleaves sialic acid and promotes virus release or entry ENZYME
*• targeted by zanamivir (Relenza) and oseltamivir (Tamiflu)

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19
Q

what is the MOST common oportunistic when working with AIDS?

A

Pneumocytisis jerovecii

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20
Q

Pneumocytisis jerovecii

*only fungi to what?

A

life threatening due to pnemonia

  • ONLY fungi to react to antibodies
  • oppotunistic bacteria
  • MOST common opportunist for AIDS
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21
Q

when does Pneumocytisis jerovecii take over?

A

when CD4 T-cells fall below 200

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22
Q

why is piconarvirus genome cruciform structure importtant?

A

allows the genome it to function as mRNA right away once it enters cytoplasm of cell! Needs no processing

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23
Q

describe 5’ and 3’ end of piconarvirus genome?

A

5’ end
o Vpg -functions as primer for RNA-dependent RNA polymerase as it becomes uridylated
o IRES =Internal ribosome entry site on 5’ end allows for translation in a 5’ cap independent manner

3’ end
o polyA tail

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24
Q

measles transportant? type of virus?

A

circulating immune compex= suppresent!

*Paramyxovirus

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25
Q

paravirus B19 targets?

A

RBC precursors and my cause anemia or other blood diseases

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26
Q

retrovirius

A

HIV
Immunosuppression
*has an RNA genome that must be reverses into DNA

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27
Q

HPV is RNA or DNA?

A

DNA

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28
Q

What have long incubation periods?

A

AIDS and HIV = years!

Hep B, rabies, or papilloma= 50+ days

29
Q

incubation means?

A

the time it takes to have infection and then have symptoms show

30
Q

what are classic cold viruses?

A

1) rhinovirus
2) common coronavirus
3) adenovirus

31
Q

which common cold virus does NOT produce a cough?

A

rhinovirus

32
Q

SARS and MERS

A

more serious coronavirus that causes sudden ACUTE respiratory syndrome

  • Sars= china
  • Mers= middle east
  • *AT HIGHER TEMPERATURE! Need 37 degrees! (not 33 like classic cold viruses)
33
Q

name antiviral agents

A

1) Guanosine analogs
2) Acyclovirs
3) Protease inhibitors
4) Tamiflu
5) interferons

34
Q

Acyclovirs depends on?

A

thimadine kinase

35
Q

Protease inhibitors target?

A

proteases

Ex: HIV

36
Q

Guanosine analogs are modified by?

A

modified by kinase to get phosphorylated

*modified= guanacina analog to STOP viral replication

37
Q

big problem with interferons?

A

they are natural antiviruses; so we need to make sure they are NOT broken down quickly (pegalated?)

38
Q

rabies is always?

A

fatal unless treated

  • neorulogical phase= indicative
  • proldone phase= too late, must have vaccines during incubation
39
Q

ebola requires what level of isolation?

A

level 4

40
Q

candida infection causes infection where?
effect on immune system?
dental relation example?

A

oropharyngeal infection

  • immunosuppressin
  • denture wearers= denture stomatitis
41
Q

viruses that cause grave concern during pregnancy? and why?

A

1) Rubella virus
- –can replicate in placenta

2) Cytomegalovirus= herpes
- –most common cause for congenital defects
- –present in 15% of stillborn babies

42
Q

which common cold virus is the worst?

A

adenovirus

43
Q

what type of virus is rhinovirus?

A

picornavirus (cruciform shape, translates RNA right away)

44
Q

what 5 viruses commonly contribute to the development of cancers?

A

1) human papilloma viruses
2) EBV*
3) retroviruses (HTLV)*
4) Adenoviruses
5) hepatitis B virus*

  • = same thing
45
Q

describe the parts to HPV?

A

o E5 stabilizes epidermal growth factor receptor – leads to more cell growth

o E6 target p53 protein – this a major tumor suppressor protein

o E7 targets retinoblastoma protein (Rb) – major protein for cell cycle arrest at G1 of cell cycle

46
Q

Adenoviruses target?

A

E1a and E1b target p53 and Rb

47
Q

Hepatitis B virus causes what cancer?

A

primary hepatocellular carcinoma (Hepatitis C virus can also cause this)

48
Q

what viruses whose infected cells lead to multiple giant cells?

A

1) paramyxoviruses (entire group)

2) herpes simplex viruses

49
Q

mumps, Koplik’s spots and measles virus is what type of virus?

A

paramyxoviruses

50
Q

paramyxoviruses leading to giant cells?

A
  • -F protein promotes the fusion that causes the formation of multinucleated cells
  • -Respiratory Syncytial Virus – multinucleated cells in respiratory epithelium
  • -Mumps – multinucleated cells when grown in monkey kidney cells
  • -Parainfluenza viruses – in epithelial cells of upper respiratory tract
  • -Measles – in upper respiratory tract and urinary sediment
51
Q

herpes simplex viruses leading to giant cells?

A

seen under diagnostics using the Tzanck smear, these multinucleated cells also contain Cowdry type A inclusion bodies specific to HSV

52
Q

what are the viruses that exhibit classic latency?

A

herpes virus
retroviruses
HPV

53
Q

herpes virus hides in latency in what cells?

A

1) 1 and 2 in neurons
2) ebv in memory b-cells
3) 6 and 7 in t-cells
4) 8 in lymphocytes and b-cells

54
Q

Koplik’s spots

A
  • buccal area around 1st and 2nd molar near Stenson duct (possible by conjunctiva or vagina)
  • usually precede the measles rash and may be seen for the first day or two after the rash appears
  • lesions are small (grains of salt around red halo for 24-48 hrs)
55
Q

kaposi sarcoma

-found in what two cancers?

A
  • most common cancer in Africa
  • Human Herpes virus-8 (HHV8)
    1) primary effusion lymphomoans (rare B-cell lymphoma)
    2) AIDS can also have Kaposi sarcoma due to opportunisitic neoplasias
56
Q

herpangina caused by?

classic finding is?

A

-caused by coxsackievirus A (picornaviruses)
-not related to a herpesvirus infection
-fever, sore throat, pain on swallowing, anorexia, and vomiting characterize this disease
-*classic finding is vesicular ulcerated lesions around the soft palate and uvula
(maybe around hard palate)
-can be recovered from lesions or feces -self-limited and requires only symptomatic management

57
Q

pneumocystis is what type of infection?

A

HI opportunistic infection

58
Q

cryptococcosis is the most common cause of? manifests as? mimics?

A

*causes fungal meningitis
*manifests as tumors anywhere in the body
*mimics molluscum cantagiosum
(occurs in patients with defective cellular immunity; AIDS)

59
Q

Cause of chronic mucocutaneous candidiasis?
describe their lesions?
often got how?

A

 deficient Th17 is development or response= rare T-lymphocyte defects to Candida
 Severe lesions that are disfiguring and granulomes
 Often got by catheters, liver patients at high risk

60
Q

names of viral intracellular inclusions (5)

A

1) Molluscum contagiosum
o Molluscum bodies in keratinocytes

2) Rabies Virus
o Negri bodies in certain nerve cells

3) HSV-1 and HSV-2
o Cowdry type A intranuclear inclusion bodies

4) Cytomegalovirus
o “owl’s eye” basophilic intranuclear inclusion body

5) Poxviruses
o Guarnieri bodies (virus assembly factory)

61
Q

what are arboviruses?

symptoms due to?

A

o ssRNA viruses
o Arthropod-borne virus! From female mosquitoes or arachnids!
o symptoms due to large production of interferons and cytokines
o cell-mediated immunity important in resistance, but also important in the disease

62
Q

Togavirus and Flavivirus are types of what virus?

A

arboviruses

63
Q

Togavirus vs Flavivirus

A

Togavirus
 Alphavirus; arboviruses
 Rubivirus; rubella virus (German measles)
 “little red” respiratory virus

Flavivirus
 Hepaciviridae; Hep C virus

64
Q

HIV targets what cells?

A

CD4 T-cell and macrophages

65
Q

HIV cellular receptor?

A

CD4 with CCR5 or CXCR4

o gp120 and gp41 binds to CD4 and CCR5 (coreceptor) which is expressed on myeloid and CD4 T cells
—during chronic infection, the env gene mutates so that gp120 binds to CXCR4, which is expressed primarily on T-cells

66
Q

first sign of measles?

A

Kopliks spots!

67
Q

Hep B (HBV) is an incomplete _____ virus?

A

dsdna

68
Q

CD55 is in association with what viruses?

A

Adenoviruses and coxsachie

2 and FINAL Microbiology Oral/Med (14 decks)

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