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CRRAB II (Elaina) > Micro - - URT > Flashcards

Micro - - URT Flashcards

1
Q

methods cause disease - bacteria

A

toxin
host immune response
bacterial proliferation and invasion

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2
Q

methods cause disease - virus

A

cytopathic effect
host immune response
tumorigenesis

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3
Q

URTI

A

otitis externa/media, rhinitis, pharyngitis, epiglottis, laryngitis, croup, sinusitis

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4
Q

LRTI

A

bronchitis, bronchiolitis, influenza, pneumonia, TB

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5
Q

Anatomical features to defend against infection

A

Mucociliary lining of the nasal cavity, mucus contains antimicrobial compounds lysozyme and lactoferrin, and secretory IgA antibodies.
Change of direction of the airway from the sinuses to the pharynx
Alveolar macrophages eliminate microorganisms in the lungs
The ciliary elevator
Normal flora competition (Staphylococci)

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6
Q

obstacles to infection

A

Avoid/survive the mucus layers of the URT which would eventually lead to swallowing of the pathogen.
Must also avoid phagocytosis or be able to survive and/or multiply in the phagocytic cell.

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7
Q

Colonization facilitated by

A

adherence factors and immune evasion factors of the pathogenic microorganism.

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8
Q

Rhinitis pathogen

A

Usually rhinoviruses

adenovirus, coronavirus

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9
Q

rhinovirus characteristics

A

RNA - icosahedral nucleocapsid - nonenveloped - ss(+) nonsegmented (IV) - picornaviridae - rhinovirus

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10
Q

RNA - icosahedral nucleocapsid - nonenveloped - ss(+) nonsegmented (IV) - picornaviridae

A

rhinovirus (common cold 40-50%)

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11
Q

coronvirus characteristics

A

RNA - helical nucleocapsid - enveloped - ss(+) nonsegmented (IV) - coronaviridae - coronavirus

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12
Q

RNA - helical nucleocapsid - enveloped - ss(+) nonsegmented (IV) - coronaviridae

A

coronavirus (common cold 10%)

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13
Q

Influenza C virus characteristics

A

RNA virus - helical nuclecapsid - enveloped - ss(-) segmented (V) - orthomyxovirus - influenza (A, B, C)

C causes colds

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14
Q

RNA virus - helical nuclecapsid - enveloped - ss(-) segmented (V) - orthomyxovirus

Causes colds

A

Influenza C

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15
Q

Coxsackievirus A + B characteristics

A

RNA - icosahedral - nonenveloped - ss+ nonseg (IV) - picornaviridae - enterovirus - cox a/b

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16
Q

RNA - icosahedral - nonenveloped - ss+ nonseg (IV) - picornaviridae - enterovirus

A

cox a/b

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17
Q

parainfluenza virus characteristics

A

RNA - helical - env - ss(-) non (V) - paramyxovirus - parainfluenza

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18
Q

RNA - helical - env - ss(-) non (V) - paramyxovirus -

A

parainfluenza

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19
Q

adenovirus characteristics

A

DNa - icosahedral - nonenv - DS linear DNA (I) - adenoviridae - mastadenovirus

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20
Q

bugs for the common cold

A

rhinovirus
coronavirus

influenza C, cox A/B, parainf, adenovirus (summer + conj)

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21
Q

Most cases of sinusitis caused by

A

viruses

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22
Q

viral sinusitis resolves in

A

5-7 days, no med tx

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23
Q

viral sinusitis may predispose to

A

bacterial sinusitis (after cold, dental extractions, allergic rhinitis)

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24
Q

dx bacterial rhinosinusitis

A

beyond 7 days in adult, facial swelling or tooth pain

children - over 10-14 days or fever over 102, facial swelling/pain

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25
Q

common causes CA acute bacterial rhinosinusitis

A

Strep pneumo
H. influenzae

other: s. pyogenes, S. aureus, m. catarrhalis

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26
Q

fungal sinusitis

A

rare - after abx don’t work

aspergillus fumigatus (mechanical removal)

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27
Q

sinusitis tx

A

nasal saline washes and steam!
mapap, decong, mucolytics?

abx tx = augmentin (amox) or azithro

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28
Q

mechanism augmentin

A

Inhibit cross-linking of peptidoglycan by transpeptidase (D-al-D-al spot)

+ clavulanate = block penicillinase

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29
Q

mechanism azithromycin

A

MACROLIDE
Bind 23S of 50S to prevent translocation - Binds to 50S ribosomal RNA near the peptidyltransferase center blocking peptide chain elongation.

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30
Q

most common cause pharyngitis

A

viruses cause 90% adults, 75% kids (rhino, corona, adeno, parainflu, influ A/B, RSV, EBV)

bacteria - s. pyogenes

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31
Q

virulence factors S. pyo for pharyngitis

A

when S. pyogenes attaches to the mucosal epithelial cells using its M protein, lipoteichoic acid, and fibronectin-binding protein (protein F). Capsule is composed of hyaluronic acid (HA) and prevents phagocytosis by macrophages. Invasion virulence factors include protease and hyaluronidase.

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32
Q

symptoms pharyngitis viral and bact

A

Fever, sore throat, edema, and hyperemia of the tonsils and pharyngeal walls

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33
Q

viral pharyngitis sxs

A 
Conjunctivitis
Cough
Hoarseness
Inflammation of the mucus membrane
Diarrhea
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34
Q

bac pharyngitis sxs

A

5-15 yo
fever, severe pain
Ha, N/V, abdomnal pain
red tonsils w/o exudate and enlarged tender cervical lymph nodes

NOT definitive

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35
Q

tx S. pyo pharyngitis

A

antibiotics (penicillin or erythromycin for those allergic to penicillin) to block the development of glomerulonephritis and rheumatic fever.

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36
Q

dx S pyo phar

A

rapid strep test (antigen detection)

culture takes 1-2 days but is most accurate

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37
Q

s. pyo characteristics

A 
Gram +
cocci
catalase -
B hem
bacitracin sensitive
Group A - S. pyogenes
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38
Q 
Gram +
cocci
catalase -
B hem
bacitracin sensitive
Group A
A

S. pyogenes

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39
Q

other disease associated with S. pyogenes pharyngitis

A

Scarlet fever

exotoxins ssa, speA, speC (superantigens)

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40
Q

S. pyo uses ______ to get rid of oxgyen radicals

A

peroxidase (makes 2H2O but no O2 so no bubbles like catalase)

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41
Q

Diptheria causes

A

pharyngitis

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42
Q

symptoms unique to diptherria

A

thick grey membrane covering back of through

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43
Q

C. diphtheriae characteristics

A

bacteria - gram + - bacilli - non-spore forming - non-motile - c. diphth

44
Q

bacteria - gram + - bacilli - non-spore forming - non-motile

A

Corynebacterium diphtheriae

45
Q

toxins diphtheria

A

A-B toxin (A = active, B = binding)
genes from a lysogenized phage
If toxin reaches blood stream –> myocarditis, neuritis

46
Q

vaccine diphtheria

A

DTaP

47
Q

cultured diphtheria on

A

Potassium tellurite (turns black)

48
Q

croup

A

laryngotracheobronchitis

viral

49
Q

sxs croup

A

“Bark-like” cough, fever of 38-39C (100.4-102.2F), restlessness, and shortness of breath. Typically begins with a mild URI with general cold-like symptoms and cough that lasts 2 to 3 days that is followed by a harsh, bark-like cough. Respiratory stridor (noisy breathing) usually occurs at night
watch for respiratory distress

50
Q

common pathogens croup

A 
Parainfluenza virus (any time of year).
Influenza virus (more in winter/early spring)
Respiratory syncytial virus infections (more in winter/early spring).
51
Q

tx croup

A

self-limiting, symptomatic usually

severe: cs, nebulized epi, oxygenation/ventilation

52
Q

RSV characteristics

A

virus - helical - env - ss(-) nonseg (IV) - paramyxovirus - pneumovirus - Respiratory Syncytial virus

53
Q

virus - helical - env - ss(-) nonseg (IV) - paramyxovirus - pneumovirus -

A

RSV

54
Q

Most common causes of pneumonia in young children

A

RSV

parainfluenza virus

55
Q

most common causes of conjunctivitis

A

H. influenza
Adenoviruses
S. pneumoniae

56
Q

multinucleated cell that can result from multiple cell fusions of uninuclear cells

A

syncytium

57
Q

vaccine RSV

A

F proteins on the surface of the virus cause the cell membranes on nearby cells to fuse. Palivizumab is a humanized monoclonal antibody (IgG1κ) produced by recombinant DNA technology, directed to an epitope in the A antigenic site of the F protein of RSV.

58
Q

epiglottitis cause

A

Caused by beta-hemolytic streptococci - group A (most frequent), B, C or Haemophilus influenzae type b (Hib), but possibly others.

59
Q

tx epiglottitis

A

secure airway
broad-spectrum second- or third-generation cephalosporins in combination with penicillinase-resistant penicillin is typical empiric therapy

60
Q

differences between croup and epiglottitis

A

ep - sudden onset, drooling

croup - gradual, no drool

61
Q

rhinovirus pathogenesis

A

binding to ICAM-1 on URT epi cells - replicates in epi cells and spreads w/o killing host cells

pathogenesis from host response –> inc. ICAM-1 –> spread & exudate –> blocks –> bacterial predisposition

62
Q

Parainfluenza virus has ____ surface proteins which cause infected cells to form multinucleate giant cells

A

viral fusion (F)

disease from cytopathic effects of virus and immune response

63
Q

clinical presentation parainf

A

children - croup & pneumonia

adults - common cold (mod severe)

64
Q

pathogenesis parainfluenza virus

A

infect larynx mucose via HA w/ sialic acid on cell surface – endocytosis – NA cleaves HA/sial – viral spread (same as influ) downward

obstruction – croup, down to LRT = pneumonia

65
Q

coronavirus clinical presentation

A

2nd most common cause of the common cold (~rhinovirus)

SARS is a coronavirus too (fever, dyspnea, cough –> viral pneumonia to resp. failure and death)

66
Q

pathology corona virus

A

Inhaled through respiratory aerosols leading to infection of upper respiratory tract cells. 3-day asymptomatic incubation period. 6 to 7 day length of common cold symptoms.

67
Q

influenza C vs. A/B

A

Genome has seven RNA segments (Influenza A and B viruses has eight RNA segments). Much less virulent than the influenza A and B virus types, many infections are asymptomatic. There is no animal reservoir for influenza B and C viruses → no antigenic shifts. Unresponsive to amantadine or rimantadine.

68
Q

clinical presentation influe C

A

common cold

69
Q

pathogenesis influe C

A

Inhaled through aerosols. Infects the larynx mucosa via contact of the viral (HA) envelope protein with sialic acid on cell surfaces (leads to endocytosis). The viral neurominidase (NA) envelope protein is important for cleaving HA bound to sialic acid, this permits viral spread.

Virus replication in host cells can lead to death of the host cell leading to tissue damage and disease. The immune response to infection also contributes to disease via production of IL-1 and IFN-γ.

70
Q

Cox A + B clinical presentation

A

More common infections in Coxsackie A – herpangia and hand-foot-and-mouth disease.

More common in Coxsackie B – pleurodynia, myocarditis, and pericarditis.

Common in both Coxsackie A and B – aseptic meningitis, paralysis, and upper respiratory tract infections (common cold).

71
Q

pathogenesis cox a/b

A

Fecal-to-oral or aerosol transmission possible. Can travel in the GI tract (low pH resistant) and infect the mucosal epithelial cells. From here it replicates and spreads to cause viremia to infect and destroy several other cell types including: skin and mucosal epithelium (Group A) → form vesicles which can lead to herpangina (red oropharynx vesicles, fever, sore throat), hand-foot-and-mouth disease; heart and pleural surfaces (Group B) → pleurodynia, myocarditis, and pericarditis; meninges and anterior horn motor neurons (Group A or B) → aseptic meningitis, paralysis.

72
Q

adenovirus clinical presentaion

A

respiratory tract infection (common cold), conjunctivitis, hemorrhagic cystitis, gastroenteritis.

73
Q

path adenovirus

A

Spread by aerosol, fecal-oral route, or direct contact → binds via hemmagglutinin → enters and lyses mucosal cells of: the upper respiratory tract which causes rhinitis and a sore throat. This infection can progress to the lower respiratory tract causing atypical pneumonia. The virus can also infect the conjunctiva causing conjunctivitis. It can also infect the bladder causing hemorrhagic cystitis → hematuria and dysuria. In young children in can also infect the gastrointestinal tract leading to gastroenteritis with non-bloody diarrhea.

74
Q

why tx s. pyo

A

glomerulonephritis and rheumatic fever

75
Q

vf of s. pyo that promote spread of infection

A 
streptokinase (converts plasminogen to plasmin → fibrinolysis)
M protein (resists phagocytosis)
hyaluronidase (breaks down connective tissue)
DNase (breaks down DNA).
76
Q

clinical presentation s. pyo

A

pharyngitis, impetigo, erysipelas, cellulitis

77
Q

diagnosis s. pyo

A

Gram (+) cocci, throat or skin culture, β-hemolytic, bacitracin sensitive, ASO +, anti-streptolysin O antibodies present.

78
Q

tx s. pyo

A

Penicillin G

79
Q

second most common cause of bacterial pneumonia in patients w/ COPD behind nontypeable H. influe

A

M. catarrhalis

80
Q

VF M. catarrhalis

A

specialized pili that allow for the attachment of the microorganism to the mucosal surface, antigenic variation to evade host immune responses, endotoxin, and capsule.

81
Q

Clinical presentation of M. catarrhalis

A

otitis media, sinusitis, pneumonia

82
Q

Pathology M. Cat

A

Normally colonizes the nasopharynx and then spreads to the mucosal surfaces. At the mucosal surfaces it can release endotoxin (think Gram (-) = endotoxin) and stimulate an inflammatory response.

83
Q

M cat diagnosis

A

Gram -, diplococci, fastidious, oxidase +,
Biochemical features that can aid in diagnosis = hydrolyzes tributyrin, produces DNase, reduces nitrite and nitrate, does not ferment sucrose, glucose, maltose, or lactose.

84
Q

tx M cat

A

amoxicillin-clavulanate (95% of strains produce beta-lactamase), second and third generation cephalosporins, TMP-SMX.

85
Q

second gen ceph name

A

cefoxitin

86
Q

third gen ceph name

A

ceftriaxone

87
Q

pathology C. dip

A

Enters the nasopharynx by respiratory droplets and creates a gray fibrinous exudate (pseudomembrane) composed of bacterial cells, WBCs, and necrotic mucosa. This membrane may be life-threatening by blocking airways. The bacteria also secrete diphtheria toxin (AB toxin the ADP ribosylates EF-2 and prevents protein synthesis in all cells) – ultimate toxin effects include cardiac issues (arrhythmia and myocarditis) and nervous system issues (cranial and peripheral nerve palsy).

88
Q

Diagnosis C. dip

A

Gram (+) rod, aerobic, may look like “Chinese letters” under the microscope, black colonies on potassium tellurite.

89
Q

tx c dip

A

Antitoxin, penicillin or erythromycin. Prophylaxis = DTaP vaccine, with boosters.

90
Q

mech erythromycin

A

Bind 23S of 50S to prevent translocation - Binds to 50S ribosomal RNA near the peptidyltransferase center blocking peptide chain elongation.

91
Q

S. pneumo clinical presentation

A

Major cause of community acquired pneumonia. Other systemic infections caused by S. pneumoniae include osteomyelitis, septic arthritis, and endocarditis, meningitis.

92
Q

s. pneumo virulence factor - asplenic/vaccine related

A

Asplenic patients are especially susceptible because they are unable to clear Ab-coated organisms (give Pneumovax). Capsule is antiphagocytic and make sthe bacteria Quellung (+). The capsule sugars serve as the antigens for the Pneumovax vaccine.

93
Q

pathology s. pneumo

A

Spread by respiratory droplets and colonizes the nasopharynx epithelium (especially if clearance is hindered by viral infection, allergy, or smoking. Evades host defenses by capsule formation (escapes phagocytosis) and IgA proteases.
May spread to the middle ear and the sinuses after initial infection and stimulate inflammation which leads to otitis media and sinusitis.
May also travel to the alveoli and stimulate inflammation eventually leading to lobar pneumonia.
If the host lacks anti-capsular IgG then invasive strains enter the lung lymphatics followed by the bloodstream which leads to the seeding of infection in the meninges followed by local inflammation.

94
Q

Diagnosis S. pneumo

A

Gram (+) diplococcic, α-hemolytic, catalase (-), susceptible to optochin. Quellung reaction.

95
Q

tx s pneumo

A

Penicillin or cephalosporins, except vancomycin for meningitis. Preventative = Pneumovax – vaccine with capsular polysaccharides.

96
Q

Hib vs. non-typeable

A

Encapsulated organisms such as H. influenzae type B (Hib) are frequently invasive whereas non-encapsulated organisms such as “non-typeable” H. influenzae colonize locally.

97
Q

Hib greatest risk

A

Hib poses a great risk to asplenic patients because the spleen in the primary organ to eliminate opsonized bacteria. Hib causes meningitis most commonly in children after the maternal Ab protection has declined and before they have developed their own Abs.

98
Q

H. inf non-typeable most often occurs in

A

“Non-typeable” H. influenzae pneumonia occurs most often in adults with COPD or recent influenza viral infection.

99
Q

Clinical presentation Hib

A

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

100
Q

Pathology Hib

A

protected from secretory IgA by IgA protease. Colonizes the upper respiratory tract which leads to local inflammation and epiglottitis and otitis media. Avoids phagocytosis with its capsule and invades the submucosa and spreads by the blood stream. Can seed the CNS, large joints, or soft tissue (especially facial) which can lead to meningitis, septic arthritis, and cellulitis.

101
Q

Diagnosis Hib

A

Gram (-) microorganism, requires hemin (X factor) and NAD (V factor) on chocolate agar. Immunofluorescence, + Quellung test (capsule).

102
Q

tx Hib

A

Third generation cephalosporin (ceftriaxone).

Preventative = Hib vaccine (against the capsule polysaccharide of type B strain conjugated to the diphtheria toxoid), rifampin prophylaxis for close contacts.

103
Q

ceftriaxone MOA

A

Cell wall inhibitor, binds to penicillin binding protein

104
Q

AE ceftriaxone

A

interacts with ca-meds to form crystals in lungs and kidneys

105
Q

RSV path

A

Attaches to bronchiolar and alveoli epithelium via protein G on viral envelope which can lead to lower respiratory tract infections and necrosis and inflammation of the bronchioles → mucous obstruction of airway → bronchiolitis and wheezing. Inflammation can also occur in the alveoli → pneumonia. Recurrent infection builds IgA immunity against further infection.

106
Q

RSV F protein

A

F surface protein causes infected cells to fuse (form syncytia).

Preventative = Synagis (F antigen vaccine) to prevent infection in high-risk infants (premature, lung disease, heart disease).

CRRAB II (Elaina) (7 decks)

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