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
common causes CA acute bacterial rhinosinusitis
Strep pneumo H. influenzae other: s. pyogenes, S. aureus, m. catarrhalis
26
fungal sinusitis
rare - after abx don't work aspergillus fumigatus (mechanical removal)
27
sinusitis tx
nasal saline washes and steam! mapap, decong, mucolytics? abx tx = augmentin (amox) or azithro
28
mechanism augmentin
Inhibit cross-linking of peptidoglycan by transpeptidase (D-al-D-al spot) + clavulanate = block penicillinase
29
mechanism azithromycin
MACROLIDE Bind 23S of 50S to prevent translocation - Binds to 50S ribosomal RNA near the peptidyltransferase center blocking peptide chain elongation.
30
most common cause pharyngitis
viruses cause 90% adults, 75% kids (rhino, corona, adeno, parainflu, influ A/B, RSV, EBV) bacteria - s. pyogenes
31
virulence factors S. pyo for pharyngitis
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.
32
symptoms pharyngitis viral and bact
Fever, sore throat, edema, and hyperemia of the tonsils and pharyngeal walls
33
viral pharyngitis sxs
``` Conjunctivitis Cough Hoarseness Inflammation of the mucus membrane Diarrhea ```
34
bac pharyngitis sxs
5-15 yo fever, severe pain Ha, N/V, abdomnal pain red tonsils w/o exudate and enlarged tender cervical lymph nodes NOT definitive
35
tx S. pyo pharyngitis
antibiotics (penicillin or erythromycin for those allergic to penicillin) to block the development of glomerulonephritis and rheumatic fever.
36
dx S pyo phar
rapid strep test (antigen detection) | culture takes 1-2 days but is most accurate
37
s. pyo characteristics
``` Gram + cocci catalase - B hem bacitracin sensitive Group A - S. pyogenes ```
38
``` Gram + cocci catalase - B hem bacitracin sensitive Group A ```
S. pyogenes
39
other disease associated with S. pyogenes pharyngitis
Scarlet fever exotoxins ssa, speA, speC (superantigens)
40
S. pyo uses ______ to get rid of oxgyen radicals
peroxidase (makes 2H2O but no O2 so no bubbles like catalase)
41
Diptheria causes
pharyngitis
42
symptoms unique to diptherria
thick grey membrane covering back of through
43
C. diphtheriae characteristics
bacteria - gram + - bacilli - non-spore forming - non-motile - c. diphth
44
bacteria - gram + - bacilli - non-spore forming - non-motile
Corynebacterium diphtheriae
45
toxins diphtheria
A-B toxin (A = active, B = binding) genes from a lysogenized phage If toxin reaches blood stream --> myocarditis, neuritis
46
vaccine diphtheria
DTaP
47
cultured diphtheria on
Potassium tellurite (turns black)
48
croup
laryngotracheobronchitis | viral
49
sxs croup
“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
common pathogens croup
``` Parainfluenza virus (any time of year). Influenza virus (more in winter/early spring) Respiratory syncytial virus infections (more in winter/early spring). ```
51
tx croup
self-limiting, symptomatic usually | severe: cs, nebulized epi, oxygenation/ventilation
52
RSV characteristics
virus - helical - env - ss(-) nonseg (IV) - paramyxovirus - pneumovirus - Respiratory Syncytial virus
53
virus - helical - env - ss(-) nonseg (IV) - paramyxovirus - pneumovirus -
RSV
54
Most common causes of pneumonia in young children
RSV | parainfluenza virus
55
most common causes of conjunctivitis
H. influenza Adenoviruses S. pneumoniae
56
multinucleated cell that can result from multiple cell fusions of uninuclear cells
syncytium
57
vaccine RSV
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
epiglottitis cause
Caused by beta-hemolytic streptococci - group A (most frequent), B, C or Haemophilus influenzae type b (Hib), but possibly others.
59
tx epiglottitis
secure airway broad-spectrum second- or third-generation cephalosporins in combination with penicillinase-resistant penicillin is typical empiric therapy
60
differences between croup and epiglottitis
ep - sudden onset, drooling croup - gradual, no drool
61
rhinovirus pathogenesis
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
Parainfluenza virus has ____ surface proteins which cause infected cells to form multinucleate giant cells
viral fusion (F) disease from cytopathic effects of virus and immune response
63
clinical presentation parainf
children - croup & pneumonia | adults - common cold (mod severe)
64
pathogenesis parainfluenza virus
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
coronavirus clinical presentation
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
pathology corona virus
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
influenza C vs. A/B
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
clinical presentation influe C
common cold
69
pathogenesis influe C
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
Cox A + B clinical presentation
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
pathogenesis cox a/b
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
adenovirus clinical presentaion
respiratory tract infection (common cold), conjunctivitis, hemorrhagic cystitis, gastroenteritis.
73
path adenovirus
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
why tx s. pyo
glomerulonephritis and rheumatic fever
75
vf of s. pyo that promote spread of infection
``` streptokinase (converts plasminogen to plasmin → fibrinolysis) M protein (resists phagocytosis) hyaluronidase (breaks down connective tissue) DNase (breaks down DNA). ```
76
clinical presentation s. pyo
pharyngitis, impetigo, erysipelas, cellulitis
77
diagnosis s. pyo
Gram (+) cocci, throat or skin culture, β-hemolytic, bacitracin sensitive, ASO +, anti-streptolysin O antibodies present.
78
tx s. pyo
Penicillin G
79
second most common cause of bacterial pneumonia in patients w/ COPD behind nontypeable H. influe
M. catarrhalis
80
VF M. catarrhalis
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
Clinical presentation of M. catarrhalis
otitis media, sinusitis, pneumonia
82
Pathology M. Cat
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
M cat diagnosis
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
tx M cat
amoxicillin-clavulanate (95% of strains produce beta-lactamase), second and third generation cephalosporins, TMP-SMX.
85
second gen ceph name
cefoxitin
86
third gen ceph name
ceftriaxone
87
pathology C. dip
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
Diagnosis C. dip
Gram (+) rod, aerobic, may look like “Chinese letters” under the microscope, black colonies on potassium tellurite.
89
tx c dip
Antitoxin, penicillin or erythromycin. Prophylaxis = DTaP vaccine, with boosters.
90
mech erythromycin
Bind 23S of 50S to prevent translocation - Binds to 50S ribosomal RNA near the peptidyltransferase center blocking peptide chain elongation.
91
S. pneumo clinical presentation
Major cause of community acquired pneumonia. Other systemic infections caused by S. pneumoniae include osteomyelitis, septic arthritis, and endocarditis, meningitis.
92
s. pneumo virulence factor - asplenic/vaccine related
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
pathology s. pneumo
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
Diagnosis S. pneumo
Gram (+) diplococcic, α-hemolytic, catalase (-), susceptible to optochin. Quellung reaction.
95
tx s pneumo
Penicillin or cephalosporins, except vancomycin for meningitis. Preventative = Pneumovax – vaccine with capsular polysaccharides.
96
Hib vs. non-typeable
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
Hib greatest risk
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
H. inf non-typeable most often occurs in
“Non-typeable” H. influenzae pneumonia occurs most often in adults with COPD or recent influenza viral infection.
99
Clinical presentation Hib
Local = epiglottitis, otitis media, pneumonia. Systemic = meningitis, septic arthritis, cellulitis.
100
Pathology Hib
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
Diagnosis Hib
Gram (-) microorganism, requires hemin (X factor) and NAD (V factor) on chocolate agar. Immunofluorescence, + Quellung test (capsule).
102
tx Hib
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
ceftriaxone MOA
Cell wall inhibitor, binds to penicillin binding protein
104
AE ceftriaxone
interacts with ca-meds to form crystals in lungs and kidneys
105
RSV path
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
RSV F protein
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).