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CRRAB II > Upper Respiratory Tract Infections > Flashcards

Upper Respiratory Tract Infections Flashcards

1
Q

Rhinoviruses initiate infections how?

A

–Binding ICAM-1 on upper respiratory tract epithelial cells. Replicates in these cells without killing host cells.

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2
Q

What causes increased ICAM-1 production and exudate in rhinovirus infections? What does this do?

A

Local inflammation. Increases ability of virus to spread and causes further infection. Exudate can block air passageways (can cause bacterial sinusitis or otitis media)

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3
Q

What type of immunity do ind. acquire after rhinovirus infection?

A

IgA to the rhinovirus serotype after infection

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4
Q

Rhinoviruses clinical presentation

A

Common cold (50% of common cold cases)

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5
Q

Rhinovirus classification

A
  • -RNA virus
  • -Icosahedral nucleocapsid
  • -Nonenveloped
  • -SS(+) non-segmented genome (Clase IV)
  • -Picornaviridae
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6
Q

Paramyxoviridae (Parainfluenza) classification

A
  • -RNA virus
  • -Helical nucleocapsid
  • -Enveloped
  • -SS(-) non-segmented genome (Class V)
  • -Paramyxoviridae
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7
Q

Parainfluenza clinical presentation

A

Children: croup and pneumonia
Adults: common cold (moderately severe)

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8
Q

Parainfluenza general info

A

Viral fusion (F) surface proteins common to all paramyxoviridae. Disease/tissue damage from cytopathic effects of virus and immune response to infection.

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9
Q

Viral fusion (F) surface proteins

A
  • -On all paramyxoviridae

- -Cause infected cells to form multinucleate giant cells

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10
Q

Parainfluenza pathology

A
  • -Inhaled through aerosols
  • -Infect larynx mucosa via contact of hemaglutinin envelope protein w/sialic acid on cell surfaces (endocytosis occurs).
  • -Viral neurominidase envelope protein help cleaving hemagglutinin bound to sialic acid.
  • -Infection progresses downward to tracheal and bronchial epithelium–>inflammation and swelling of mucous membranes–>narrowing of lumen and obstruction of inspiration–>croup. an invade lower respiratory tact and cause pneumonia.
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11
Q

What allows for infection of mucosa in parainfluenza, influenza C, and adenovirus viruses

A

Contact of viral hemagglutinin (HA) envelope protein w/sialic acid on cell surfaces

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12
Q

Viral neurominidase envelope protein

A

Important for cleaving hemagglutinin bound to sialic acid allowing for viral spread in parainfluenza and influenza C viruses

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13
Q

Diagnosis of parainfluenza viruses

A

Usually based on symptoms. Anti-hemagglutination antibodies can be confirmed through lab testing

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14
Q

Treatment of parainfluenza viruses

A

Supportive care (cool mist, oxygen in severe cases). Corticosteroids

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15
Q

Coronavirus classification

A
  • -RNA virus
  • -Helical nucleocapsid
  • -Enveloped
  • -SS(+) non-segmented genome (class IV)
  • -Coronaviridae
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16
Q

Why do coronaviruses have the name corona?

A

Club-shaped viral proteins projecting out of viral envelope look like corona surrounding sun

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17
Q

What is the 2nd most common cause of the common cold?

A

Coronaviruses (10-20%)

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18
Q

SARS

A

Rapidly progressive viral pneumonia that presents with fever, dyspnea, cough that can progress to respiratory failure and death. Causes by SARS coronavirus

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19
Q

Coronavirus clinical presentation

A

Common cold

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20
Q

Pathology of coronavirus

A
  • -Inhaled through respiratory aerosols–>infection of upper respiratory tract cells
  • -3 day asymptomatic incubation period.
  • -6-7 day length of common cold.
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21
Q

Influenza C virus classification

A
  • -RNA virus
  • -Helical nucleocapsid
  • -Enveloped
  • -SS (-) non-segmented genome (class V)
  • -Orthomyxoviridae
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22
Q

Influenza C general info

A
  • -7 RNA segments (A and B have 8)
  • -Less virulent than a type
  • -Many infections asymptomatic
  • -No animal reservoir for B and C
  • -Unresponsive to amantadine or rimantadine
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23
Q

Clinical presentation of influenza C

A

Common cold

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24
Q

Pathology of Influenza C

A
  • -Inhaled through aerosols–>infects larynx mucosa via viral hemagglutinin envelope protein w/sialic acid–>viral neurominidase envelope cleaves HA bound to sialic acid allowing for viral spread
  • Similar to parainfluenza viruses
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25
Q

Can Influenza C virus replication in host cells cause cell death?

A

-Virus replication in host cells can lead to death of host cell causing tissue damage and disease

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26
Q

Does immune response to Influenza C contribute to disease?

A

Yes. IL-1 and IFN-y contribute.

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27
Q

Diagnosis of influenza C.

A
  • -Patient symptoms

- -Lab confirmation through rapid antigen test on nasopharyngeal swab and detect HA type via RBC agglutination test.

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28
Q

Treatment for influenza C

A

Supportive (acetaminophen, hydration, rest).

No vaccine is available

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29
Q

Coxsackievirus A and B classification

A
  • -RNA virus
  • -Icosahedral nucleocapsid
  • -Nonenveloped
  • -SS(+) non-segmented genome (class IV)
  • -Picornaviridae
  • -Enterovirus
30
Q

Clinical presentation of coxsackieviruses A and B

A
  • -Coxsackie A: herpangia and hand, foot and mouth disease more common
  • -Coxsackie B: pleurodynia, myocarditis, pericarditis
  • -Common in both: common cold! paralysis, aseptic meningitis
31
Q

Coxsackieviruses pathology

A
  • -Fecal-to-oral or aerosol transmission. More common in summer and fall
  • -Can travel in GI and infect mucosal epithelial cells (low pH resistant). Replicates adn causes viremia to infect and destroy skin and mucosal epithelium (group A herpangia, or common cold in both types)
32
Q

Coxsackievirus diagnosis

A

Isolate virus, serology

33
Q

Coxsackievirus treatment

A

Supportive. Can give anti-inflammatory agents for symptomatic infections. No antivirals or vaccines available.

34
Q

Adenovirus classification

A
  • -DNA virus
  • -Icosahedral nucleocapsid
  • -Nonenveloped
  • -DS linear DNA (group I)
  • -Adenoviridae (mastadenovirus)
35
Q

Adenoviruses get their name from what?

A

Latent virus can be found in tonsillar adenoids following infection

36
Q

Adenovirus clinical presentation

A

Common cold, conjunctivitis, hemorrhagic cystitis, gastroenteritis

37
Q

Adenovirus pathology

A

–Spread by aerosol, fecal-oral, direct contact–>bind via hemmagglutinin–>enters and lyses mucosal cells of upper respiratory tract (causes rhinitis and sore through)

38
Q

Diagnosis of adenovirus

A

Isolate virus in cell culture, serology

39
Q

Adenovirus treatment

A

Vaccine of liver viruses of specific serotypes (only used in military)

40
Q

Streptococcus pyogenes classification

A
  • -Bacteria
  • -G+ cocci
  • -Catalase -
  • -Beta hemolytic
  • -Bacitracin sensitive
  • -ASO +
  • -Anti-streptolysin O antibodies
41
Q

Strep pyogenes virulence factors

A
  • -Streptokinase
  • -M protein
  • -Hyaluronidase
  • -DNase
42
Q

DNase

A

Breaks down DNA

43
Q

Streptokinase

A

Converts plasminogen to plasmin and causes fibrinolysis

44
Q

M protein

A

Resists phagocytosis

45
Q

Hyaluronidase

A

Breaks down connective tissue

46
Q

Clinical presentation of strep pyogenes

A

Pharyngitis, impetigo, erysipelas, cellulitis

47
Q

Strep pyogenes pathology (related to pharyngitis)

A

May be part of normal flora of skin or oropharynx in some people
–Can be transmitted through respiratory droplets or food–> adhere and colonize pharyngeal epithelial cells via pili on surface of bacteria–>localized inflammation and sore throat w/enlarged cervical lymph nodes.

48
Q

Strep pyogenes treatment

A

Penicillin G or erythromycin (if penicillin allergy)

49
Q

Moraxella catarrhalis classification

A
  • -Bacteria
  • -G-
  • -Hydrolyzes tributyrin
  • -produces DNase
  • -Reduces nitrate and nitrite
  • -Doesn’t ferment sucrose, glucose, maltose, or lactose
50
Q

Moraxella catarrhalis clinical presentation

A

Otitis media, sinusitis, pneumonia

51
Q

Moraxella catarrhalis virulence factors

A
  • -Specialized pili for attachement to mucosal surface
  • -Antigenic variation to avoid host immune response
  • -Endotoxin
  • -Capsule
  • -DNase
52
Q

Moraxella catarrhalis pathology

A

–Colonizes nasopharynx and then spreads to mucosal surfaces. Can release endotoxin at the mucosal surfaces and stimulate inflammatory response

53
Q

Can G- or G+ release endotoxin?

A

G-

54
Q

Treatment of Moraxella catarrhalis?

A

Amoxicillin-clavulanate, 2nd and 3rd gen. cephalosporins, TMP-SMX

55
Q

Corynebacterium diphtheriae classification

A

Bacteria, G+, bacilli, non-spore forming, non-motilic, black colonies on K+ tellurite. Look like “Chinese letters” under microscope

56
Q

Corynebacterium diphtheriae toxin

A

Carried by phage, so only lysogenic organisms can cause disease

57
Q

Corynebacterium diphtheriae clinical formation

A

Local=formation of sudomembrane, airway obstruction. Systemic=myocarditis and polyneuritis

58
Q

Corynebacterium diphtheriae pathology

A

Enters nasopharynx by respiratory droplets–> gray, fibrous exudate created (composed of bacterial cells, WBCs and necrotic mucosa).

59
Q

Diphtheria toxin

A

AB toxin ribosylates EF-2 and prevents protein synthesis in all cells–> ult. effects include cardiac issue and nervous system issues.

60
Q

Diphtheria treatment

A

Antitoxin, pencillin, erythromycin. Prophylaxis =DTaP vaccine w/boosters

61
Q

Strep pneumoniae classification

A

Bacteria, G+ cocci, catalase -, alpha hemolitic, bile esculin negative, optochin sensitive, Quellung +, capsule antiphagocytic

62
Q

How does strep pneumo evade host?

A

IgA proteases and by capsule formation.

63
Q

Strep. pneumo treatment

A

Penicillin or cephalosporins. Use vanco for meningitis. Preventative pneumovax vaccine

64
Q

Haemophilus influenzae type B classification

A

Bacteria, gram -, requires hemin (X factor) and NAD (V factor) on chocolate agar, coccobacilli, pleomorphic. + quellung test

65
Q

Hib clinical presentation

A

Local= otitis media, epiglottitis, rhinosinusitis, pneumonia. Systemic= meningitis, septic arthritis, cellulitis

66
Q

Hib virulence factors

A

IgA protease (protects from secretory IgA)

67
Q

Respiratory syncytial virus classification

A

Helical nucleocapsid, SS- nonsegmented, paramyoxviridae, pneumovirus

68
Q

RSV virulence factors

A

G surface protein, F surface protein.

69
Q

G surface protein

A

Important for RSV attachment to host cells

70
Q

F surface protein

A

Causes RSV infected cells to fuse (form syncytia)

CRRAB II (13 decks)

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