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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
Can Influenza C virus replication in host cells cause cell death?
-Virus replication in host cells can lead to death of host cell causing tissue damage and disease
26
Does immune response to Influenza C contribute to disease?
Yes. IL-1 and IFN-y contribute.
27
Diagnosis of influenza C.
- -Patient symptoms | - -Lab confirmation through rapid antigen test on nasopharyngeal swab and detect HA type via RBC agglutination test.
28
Treatment for influenza C
Supportive (acetaminophen, hydration, rest). | No vaccine is available
29
Coxsackievirus A and B classification
- -RNA virus - -Icosahedral nucleocapsid - -Nonenveloped - -SS(+) non-segmented genome (class IV) - -Picornaviridae - -Enterovirus
30
Clinical presentation of coxsackieviruses A and B
- -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
Coxsackieviruses pathology
- -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
Coxsackievirus diagnosis
Isolate virus, serology
33
Coxsackievirus treatment
Supportive. Can give anti-inflammatory agents for symptomatic infections. No antivirals or vaccines available.
34
Adenovirus classification
- -DNA virus - -Icosahedral nucleocapsid - -Nonenveloped - -DS linear DNA (group I) - -Adenoviridae (mastadenovirus)
35
Adenoviruses get their name from what?
Latent virus can be found in tonsillar adenoids following infection
36
Adenovirus clinical presentation
Common cold, conjunctivitis, hemorrhagic cystitis, gastroenteritis
37
Adenovirus pathology
--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
Diagnosis of adenovirus
Isolate virus in cell culture, serology
39
Adenovirus treatment
Vaccine of liver viruses of specific serotypes (only used in military)
40
Streptococcus pyogenes classification
- -Bacteria - -G+ cocci - -Catalase - - -Beta hemolytic - -Bacitracin sensitive - -ASO + - -Anti-streptolysin O antibodies
41
Strep pyogenes virulence factors
- -Streptokinase - -M protein - -Hyaluronidase - -DNase
42
DNase
Breaks down DNA
43
Streptokinase
Converts plasminogen to plasmin and causes fibrinolysis
44
M protein
Resists phagocytosis
45
Hyaluronidase
Breaks down connective tissue
46
Clinical presentation of strep pyogenes
Pharyngitis, impetigo, erysipelas, cellulitis
47
Strep pyogenes pathology (related to pharyngitis)
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
Strep pyogenes treatment
Penicillin G or erythromycin (if penicillin allergy)
49
Moraxella catarrhalis classification
- -Bacteria - -G- - -Hydrolyzes tributyrin - -produces DNase - -Reduces nitrate and nitrite - -Doesn't ferment sucrose, glucose, maltose, or lactose
50
Moraxella catarrhalis clinical presentation
Otitis media, sinusitis, pneumonia
51
Moraxella catarrhalis virulence factors
- -Specialized pili for attachement to mucosal surface - -Antigenic variation to avoid host immune response - -Endotoxin - -Capsule - -DNase
52
Moraxella catarrhalis pathology
--Colonizes nasopharynx and then spreads to mucosal surfaces. Can release endotoxin at the mucosal surfaces and stimulate inflammatory response
53
Can G- or G+ release endotoxin?
G-
54
Treatment of Moraxella catarrhalis?
Amoxicillin-clavulanate, 2nd and 3rd gen. cephalosporins, TMP-SMX
55
Corynebacterium diphtheriae classification
Bacteria, G+, bacilli, non-spore forming, non-motilic, black colonies on K+ tellurite. Look like "Chinese letters" under microscope
56
Corynebacterium diphtheriae toxin
Carried by phage, so only lysogenic organisms can cause disease
57
Corynebacterium diphtheriae clinical formation
Local=formation of sudomembrane, airway obstruction. Systemic=myocarditis and polyneuritis
58
Corynebacterium diphtheriae pathology
Enters nasopharynx by respiratory droplets--> gray, fibrous exudate created (composed of bacterial cells, WBCs and necrotic mucosa).
59
Diphtheria toxin
AB toxin ribosylates EF-2 and prevents protein synthesis in all cells--> ult. effects include cardiac issue and nervous system issues.
60
Diphtheria treatment
Antitoxin, pencillin, erythromycin. Prophylaxis =DTaP vaccine w/boosters
61
Strep pneumoniae classification
Bacteria, G+ cocci, catalase -, alpha hemolitic, bile esculin negative, optochin sensitive, Quellung +, capsule antiphagocytic
62
How does strep pneumo evade host?
IgA proteases and by capsule formation.
63
Strep. pneumo treatment
Penicillin or cephalosporins. Use vanco for meningitis. Preventative pneumovax vaccine
64
Haemophilus influenzae type B classification
Bacteria, gram -, requires hemin (X factor) and NAD (V factor) on chocolate agar, coccobacilli, pleomorphic. + quellung test
65
Hib clinical presentation
Local= otitis media, epiglottitis, rhinosinusitis, pneumonia. Systemic= meningitis, septic arthritis, cellulitis
66
Hib virulence factors
IgA protease (protects from secretory IgA)
67
Respiratory syncytial virus classification
Helical nucleocapsid, SS- nonsegmented, paramyoxviridae, pneumovirus
68
RSV virulence factors
G surface protein, F surface protein.
69
G surface protein
Important for RSV attachment to host cells
70
F surface protein
Causes RSV infected cells to fuse (form syncytia)

CRRAB II (13 decks)

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