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Bacterial Pathogenesis > Midterm 1 > Flashcards

Midterm 1 Flashcards

1
Q

Innate immunity components

A

Skin resource competition, mucosal surfaces, phagocytes, cytotoxic cells

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2
Q

Mucosal surface types

A

GI, respiratory, urogenital, conjunctiva (eyes)

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3
Q

Phagocyte purpose and types

A

Ingest and kill bacteria
Monocytes = blood, develop into macrophages
Macrophages = Stuck in tissue (liver, lymph, etc.)
PMNS/Neutrophils = Abundant in blood, 1st to infection

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4
Q

Cytotoxic cell types

A

CD8+ T Cells = deliver toxic granules (specific)
NK (Natural T-Killer) = deliver toxic granules (variety)

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5
Q

WBC count

A

Range 4500-10000/uL, leukocytes in blood

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6
Q

Granulocytes

A

Mostly phagocytic neutrophils, some eosinophils and few histamine releasing basophils

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7
Q

Agranulocytes/PBMC

A

Mostly lymphocytes (B-T-NK) and some monocytes

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8
Q

Mast cells

A

Not technically granulocytes (fixed in tissue) but have granules and release histamines - found in connective tissue

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9
Q

Complement purpose and production

A

Produced in liver, recruit phagocytes, facilitate phagocytosis and stimulate inflammation

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10
Q

C3a purpose

A

Recruit phagocytes, vasodilation (move phagocytes), anaphylatoxin (histamine release from mast cells)

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11
Q

C3b purpose

A

Phagocyte uptake and opsonization, bind to bug and recognized by phagocytes

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12
Q

C5a purpose

A

Like C3a, vasodilation, recruitment and anaphylatoxin

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13
Q

C5b-C6-C9 complex

A

MAC (Membrane attack complex) forms membrane pores and kills Gram -

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14
Q

Classical complement pathway

A

Ab driven, IgG binds to Ab on variable bug surface, C1 binds and starts complement cascade, C3 cleaved into C3a and C3b, MAC forms pores and kills Gram -

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15
Q

Where does C5b bind

A

LPS

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16
Q

Where do C6-C9 bind

A

Membrane with C5

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17
Q

Alternate complement pathway

A

C3b driven, C3 is hydrolyzed to C3a and C3b, C3b binds to LPS Or TA, C3b further stimulated to cleave C3

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18
Q

Mannose binding lectin pathway

A

Lectins bind to mannose and other sugars on bug, stimulate C3 cleavage, MBL binding clumps bacteria and allows elimination via phagocytes

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19
Q

Control of complement

A

Factor H binds to C3b to form complex, degraded by factor I

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20
Q

Gram - bacteria

A

Inner and outer membrane, small cell wall, LPS attached to OM

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21
Q

Gram + bacteria

A

Cytoplasmic membrane, large cell wall, LTA attached to membrane and TA attached to cell wall

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22
Q

Phagocytosis mechanism

A

Engulfed into phagosome, fusion with lysosome

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23
Q

PAMPs

A

Pathogen associated molecular patterns recognized by phagocytes like LPS, LTA, and flagella, which stimulate TLRs and cytotoxic cell production

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24
Q

Phagocyte activation

A

LPS bind to LPS binding protein, LPS-LBP complex bind to CD14 receptors and activate TLR4. PMNs released from marrow, margination inside blood vessels, extravasation to squeeze into tissue, oxidative burst

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25
Q

What causes septic shock

A

Not enough oxygen because of hypoperfusion (low blood flow)

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26
Q

Stage 1 sepsis / organ dysfunction

A

Acute SOFA score change, respiration, coagulation, liver, CNS, kidneys, and GCS motor responses

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27
Q

Stage 2 septic shock

A

Complement cascade and vasodilation, cytokine production, disseminated intravascular coagulation (DIC), hemorrhaging, MODS (multiple organ dysfunction syndrome bc of low blood flow and ARDS (acute respiratory distress syndrome) bc of lung inflammation/ leaking leads to death

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28
Q

Early therapy for sepsis

A

Early antibiotics but symptoms are non-specific, no effective therapy to stop shock

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29
Q

Supportive therapy for sepsis

A

Ventilators to support oxygen, fluid administration and vasopressors/epinephrine to constrict vessels and bronchodilation by inducing fight/flight response

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30
Q

IgG

A

Best at opsonization and toxin neutralization, smallest, most abundant, can cross placenta, in the blood and LRT

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31
Q

IgM

A

Best at activating complement via classical pathway, pentamer, in blood

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32
Q

sIgA

A

Best at trapping bug in mucin, toxin neutralization, secreted into mucosa NOT in blood

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33
Q

IgE

A

Binds to mast cells and basophils to stimulate histamine release and vasodilation like C3a and C5a, located below epithelial surfaces NOT in blood

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34
Q

Antibody timing

A

IgM produced by immature B cells quickly to activate complement, IgG produced after a week and is very specific

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35
Q

Macrophage/T cell activation mechanism

A

MHC (Major histocompatibility complex)

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36
Q

MHC II

A

Ag complex on APC surface stimulate CD4+ Th cells, Th1 produces interferon gamma and activates Mac/CD8+ T cells, Th2 produces interleukin 4 and stimulates Ab production

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37
Q

MHC I

A

Ag complex on nucleated cells stimulates CD8+ T cells to release toxins into infected host cells with perforin to make pores and granzymes inducing apoptosis

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38
Q

CHO capsules

A

Bind directly to B cell surfaces produce antibody, no Th cell activation, cant be engulfed unless opsonized, babies cant make antibodies to CHO

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39
Q

Bacterial endotoxin

A

LPS

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40
Q

Bacterial protein toxins

A

AB exotoxins, membrane disrupting toxins, SAgs (superantigens)

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41
Q

Clostridium classification

A

Gram +, spore forming, anaerobe, in soil

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42
Q

What causes botulism

A

BoNT (Botulinum neurotoxin) produced by C. botulinum

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43
Q

BoNT feature

A

Most toxic known toxin, biowarfare agent

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44
Q

Botulism pathogenesis

A

Spores germinate in food and replicate, bug produce toxin which is ingested and enters blood, BoNT causes symptoms, flaccid paralysis, respiratory and heart failure

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45
Q

BoNT mechanism

A

Cleaves SNARE proteins at vesicles in nerve endings of PNS, prevents acetylcholine release, no muscle activation

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46
Q

BoNT serotypes

A

ABEF humans, CDE animals

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47
Q

Botulism symptoms

A

Appear within 1-3 days, slurred speech, double vision, vomiting

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48
Q

Botulism treatment/prevention

A

No vaccine, treatment with ventilator and HBAT antitoxin from horse, prevention is to boil canned food

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49
Q

Infant botulism

A

Ingest bee honey with spores, GI tract colonization and produce BoNT

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50
Q

Wound botulism

A

Spores enter wound, colonization, BoNT produced

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51
Q

Treatment for colonization botulism

A

Antibiotics for bacteria in addition to antitoxin

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52
Q

Botox

A

Uses low dose of BoNT

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53
Q

What causes tetanus

A

TeNT (Tetanus neurotoxin), NOT contagious person to person

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54
Q

Tetanus reservoir

A

Spores in soil, animal feces and intestine

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55
Q

Tetanus transmission

A

Spores to wound

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56
Q

Tetanus pathogenisis

A

Spore enters wound, bug colonizes and produces TeNT, which enters bloodstream, respiratory failure and death

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57
Q

TeNT mechanism

A

Cleave SNARE proteins in CNS inhibitory neurons, muscle always active and uninhibited

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58
Q

Tetanus symptoms

A

Spastic paralysis, lockjaw, respiratory failure and death at high rates

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59
Q

Tetanus treatment

A

TIG (tetanus immune globin) from human immunized donor, antibiotics, vaccinate with toxoid

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60
Q

Tetanus vaccine

A

Inactivated TeNT toxoid, part of DTaP

61
Q

Model for membrane disrupting toxin

A

C. perfringens

62
Q

C. perfringens disease

A

Gas gangrene, infection of muscle tissue and production of carbon dioxide from bug, 100% fatal w/ no treatment

63
Q

C. perfringens reservoir

A

Soil, human and animal intestine

64
Q

C. perfringens pathogenesis

A

Spore enters wound and bug colonizes, alpha toxin disrupts membrane, necrosis, spread, death

65
Q

C. perfringens alpha toxin

A

Phospholipase disrupts phospholipid bilayer

66
Q

C. perfringens treatment

A

Surgery

67
Q

Superantigen purpose

A

Aggressively activate host immune response

68
Q

Staphylococcal menstrual TSS (toxic shock syndrome)

A

Old superabsorbent tampons promoted anaerobic bug growth, produce TSST1 (toxic shock syndrome toxin) which entered blood and caused fever, shock, possible organ failure and death

69
Q

Streptococcal TSS (toxic shock syndrome)

A

S. pyogenes growth in wound, bacteria enter bloodstream, release SpeA (S. pyogenes exotoxinA) leading to organ failure and death

70
Q

Superantigen mechanism

A

Normally MHC-II+antigen complex binds to T cell to stimulate specific response, superantigen toxins bind conserved regions of T cell receptors and MHCII and cause cytokine storm/massive immune response

71
Q

Diphtheria classification

A

Gram + club, no spores

72
Q

Diphtheria nickname

A

The strangler bc of neck swelling

73
Q

Original dog sled race

A

Delivering the horse antitoxin to Alaska

74
Q

Diphtheria reservoir

A

Human asymptomatic carriers

75
Q

Diphtheria transmission

A

Aerosols

76
Q

Diphtheria pathogenesis

A

Aerosols or contact, throat colonization, form adherent pseudo membrane, produce DT which enters bloodstream which causes respiratory and heart failure

77
Q

Diphtheria toxin

A

AB toxin binds to HB-EGF (Heparin binding epidermal growth factor) precursor and ADPR EF2 to kill cell

78
Q

DT target

A

Heart/organs, since HB-EGF is present in many cell types

79
Q

Diphtheria treatment

A

DAT (diphtheria antitoxin) on unbound toxin and antibiotics

80
Q

Diphtheria vaccine

A

DT toxoid elicits IgG response, part of the DTaP series

81
Q

DT conjugate vaccines

A

Link DT to CHO capsules to give effective antibody response

82
Q

Hib characterization

A

Gram - rod causing infant meningitis

83
Q

Hib transmission

A

Aerosols causing colonization of oropharynx

84
Q

Hib disease

A

Infant meningitis and pneumonia

85
Q

Hib vaccine

A

Hib CHO capsule linked to DT toxoid

86
Q

Immunotoxins

A

DT A fragment linked to antibodies that recognize only cancer antigens

87
Q

Yersinia characterization

A

Gram - rod w/ capsule

88
Q

Y. enterocolitica disease

A

Appendectomy in children / general food poisoning

89
Q

Y. enterocolitica transmission

A

Contaminated food/water

90
Q

Y. enterocolitica pathogenesis

A

Diarrhea caused by YST (Yersinia stable toxin) and growth in mesenteric (abdominal) lymph nodes causing inflammation

91
Q

Y. pestis defining characteristic

A

Causes black death, DIC black skin lesions

92
Q

Y. pestis reservoir

A

Wild rats

93
Q

Y. pestis transmission

A

Infected fleas, direct contact with fluids, aerosols

94
Q

Bubonic plague

A

Flea feeds on infected rodent, inject into human, growth in lymph nodes

95
Q

Septicemic plague

A

Progressed stage of bubonic plague, enter and multiply in blood, infect multiple organs

96
Q

Pneumonic plague

A

Human aerosols can infect, severe pneumonia, bloody sputum

97
Q

Plasmids in all Yersinia

A

pYV (plasmid yersinia virulence) T3SS, injectisome to secrete toxins into host, repress inflammatory genes and inhibit phagocytosis

V antigen activate IL-10 to repress inflammation

98
Q

Y. pestis specialized plasmids

A

pPla (plasminogen protease activator), converts plasminogen to plasmin and allows disemination from bite source [CLOT BUSTING like Tpa for heart attacks]

pMT (murine toxin) F1 antiphagocytic protein capsule, phospholipase D promotes flea colonization

99
Q

Staph. aureus classification

A

Gram+ coccus, hemolytic with yellow colonies

100
Q

Staph. aureus diseases

A

Most common cause of sepsis, most are skin infections. Also causes SE (food toxicosis), systemic infection and toxicosis

101
Q

Staph. aureus reservoir

A

Normal skin flora, GI and URT, infected animals

102
Q

Staph. aureus transmission

A

Close contact, occasionally from animals

103
Q

Staph. aureus blocking opsonic phagocytosis

A

Alpha toxin/hemolysin pore forming toxin to ADAM-10, leucocidin pore forming toxin to Mac complement receptor, staphylokinase degrades complement and antibody and converts plasminogen to plasmin, protein A binds to IgG-Fc

Nuc staphylococcal nuclease degrades NETs (traps)
Polysaccharide capsule blocks opsonization

104
Q

Staph. aureus disemmination

A

Hyaluronidase cleaves hyaluronic acid to increase tissue spread

105
Q

Staph. aureus superantigens

A

SE (staphylococcal enterotoxin) causes food poisoning, SE-TSS produced systematically and SEB is a biowarfare agent

TSST1 causes menstrual and non menstrual toxic shock

106
Q

MRSA

A

Methicillin resistant Staph. aureus, vancomycin used instead, acquired in hospital and community

107
Q

VRSA

A

Vancomycin resistant Staph. aureus

108
Q

Streptococci classification

A

Gram + aerobic coccus

109
Q

Streptococci identification

A

RBC alpha (partial), beta (complete), or gamma (no) hemolysis

Lancefield cell wall carbohydrate grouping (GAS,GBS, etc.)

110
Q

S. pyogenes classification

A

GAS, forms chains beta hemolysis, causes strep throat and skin infections

111
Q

S. pyogenes / GAS reservoir

A

Mouth/throat and other parts of the body

112
Q

S. pyogenes / GAS transmission

A

Person to person nasal/saliva in crowded conditions

113
Q

S. pyogenes / GAS diseases

A

Skin infection, flesh eating disease, strep throat, middle ear, scarlet fever, pneumonia, meningitis

114
Q

S. pyogenes / GAS cytokine degradation

A

C5a protease (ScpA) inhibit phagocyte recuitment

115
Q

S. pyogenes / GAS blocking opsonic phagocytosis

A

M proteins bind to Fc of IgG, Streptolysin lyse macrophages, Sda1 DNAse degrade NETs, hyaluronic acid capsule

Streptokinase clot busting like Ppla
SpeA causing TSS and scarlet fever

116
Q

S. pyogenes/ GAS dissemination

A

Cleave hyaluronic acid to penetrate tissue and increase lesion

117
Q

Rheumatic fever (RF)

A

Caused by M epitopes reacting with heart in some untreated GAS infections, need to treat strep throat with antibiotics

118
Q

PSGN

A

Post-streptococcal glomerulonephritis, GAS epitopes Ag-Ab complexes react and damage kidney glomeruli

119
Q

Rapid Strep Test

A

Throat swab to detect GAS Lancefield CHO, backup throat culture PCR/NAAT takes days

120
Q

S. pyogenes / GAS prevention & treatment

A

Hand washing, sanitation, treatment with antibiotics

121
Q

S. agalactiae / GBS characterization

A

Leading cause of neonatal meningitis, alpha beta or gamma hemolytic, forms chains

122
Q

GBS reservoir

A

Human GI tract and vagina

123
Q

GBS transmission

A

Prenatal, early, and late onset

124
Q

Prenatal GBS

A

Invasive procedure or pregnancy trauma, bloodstream invasion

125
Q

Early onset GBS

A

Exposure during delivery

126
Q

Late onset GBS

A

From caregivers or invasive devices

127
Q

GBS vagina colonization

A

Nisin protease cleaves Lactobacillus nisin and allows colonization, beta hemolysin aids colonization

128
Q

GBS virulence

A

Beta protein binds factor H to degrade C3b, C5a peptidase, beta hemolysin stimulates meningitis, sialic acid capsule binds immune cell lectins to downregulate immune response and C3b opsonization

129
Q

GBS urine culture

A

Treat asymptomatic bacteriuria early in pregnancy

130
Q

GBS late pregnancy test

A

Vaginal and rectal swab, IAP (intrapartum antibiotic prophylaxis) if positive right before delivery

131
Q

GBS meningitis diagnosis

A

Blood or spine tap culture/PCR

132
Q

GBS treatment

A

Antibiotics, no vax

133
Q

Enterococcus / GDS characteristics

A

leading cause of hospital/nosocomial bacteremia, very hardy, inherently resistant, Gram +, nonhemolytic, clot buster

134
Q

Enterococcus reservoir

A

Colon in humans and animals

135
Q

Enterococcus transmission

A

Fecal/oral and direct contact with contaminated surfaces and fluids

136
Q

Enterococcus diseases

A

Nosocomial bacteremia, UTI, pneumonia, surgical infection

137
Q

Enterococcus virulence

A

Cytolysin membrane disruptor, gelatinase E degrades E-cadherin in tight junction, hyaluronidase, polysaccharide capsule

138
Q

Enterococcus antibiotic resistance

A

VRE (vancomycin resistant enterococcus) in hospitals, necessitate specific protocol

139
Q

Enterococcus diagnosis

A

Bile/optochin resistance (differentiation from S. pneumoniae) and PCR

140
Q

S. pneumoniae / pneumococcus classification

A

Similar to enterococcus, alpha hemolytic, no Lancefield classification

141
Q

S. pneumoniae / pneumococcus danger

A

Kills more people than vaccine preventable diseases combined, most common cause of community acquired pneumonia, causes middle ear infections in children

142
Q

S. pneumoniae / pneumococcus reservoir

A

Human nasopharynx as normal flora

143
Q

S. pneumoniae / pneumococcus transmission

A

Aersosols

144
Q

S. pneumoniae / pneumococcus diseases

A

INFLAMMATION, most common cause of bacterial pneumonia, infant meningitis, ear infections, MID EAR TO NASOPHARYNX PATH

145
Q

S. pneumoniae / pneumococcus pathogenesis

A

Adherence to nasopharynx, inhalation into lung, replication, pneumonia, incite inflammation and generate pus, bacteremia and meningitis, septic shock

146
Q

S. pneumoniae / pneumococcus virulence

A

CpbA (choline binding protein) for adherence, CHO capsule binds Factor H, proinflammatory thick cell wall, pneumolysin inflammatory pore forming cytotoxin, NA cleaves sialic acid, sIgA protease, autolysin

147
Q

S. pneumoniae / pneumococcus tests

A

Quellung test capsule serotyping via Ab+bug capsule swelling, bile and optochin test, UAT (urinary antigen test) for cell wall components, NAAT/PCR

148
Q

S. pneumoniae treatment

A

Antibiotics with steroids because of autolysin releasing inflammatory components

149
Q

S. pneumoniae vaccines

A

Prevnar 13 or 15 for children, DT linked to capsule serotypes, PCV20 for elderly, PPSV23 old design without DT linkage

Bacterial Pathogenesis (3 decks)

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