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Bacterial Pathogenesis > Midterm 2 > Flashcards

Midterm 2 Flashcards

1
Q

Pseudomonas pathogen type

A

Opportunistic, leading cause of HAI

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2
Q

Who Pseudomonas affects most

A

Fibrosis patients, CFTR mutation, MDR PA with salty mucin

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3
Q

Pseudomonas reservoir

A

Soil, water, plants

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4
Q

Pseudomonas transmission

A

Healthcare workers/equipment, burn and surgery wounds

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5
Q

Pseudomonas diseases

A

Fibrosis patients, burns and wounds, skin, eye and ear, HAI

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6
Q

Pseudomonas binding pathogenesis

A

Pili opportunistic binding (flu expose URT/upper respiratory tract receptors), LPS bind to chloride channels in LRT/lower respiratory tract

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7
Q

Pseudomonas dissemination pathogenesis

A

Elastase degrades complement and elastin lung protein, ExoS ADPR G proteins to disrupt PMN, ExoA ADPR EF2 like DT, NA cleaves sialic acid, phospholipase degrades surfactants

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8
Q

CF test

A

Sweat test, high sweat because salt balance is off

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9
Q

Pseudomonas resistance

A

Intrinsic barrier to antibiotics by forming biofilm

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10
Q

Special pseudomonas protocol

A

No fruits or veggies to hospital patients

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11
Q

Pertussis past

A

One of the most frequent diseases prior to vaccination

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12
Q

Pertussis reservoir

A

Human aerosols

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13
Q

Pertussis transmission

A

Air droplets

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14
Q

Pertussis diseases

A

Infants (whooping cough), Adults mild cough, Complications (secondary bacterial pneumonia)

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15
Q

Pertussis catarrhal stage

A

Colonization first 2 weeks, very contagious, runny nose, fever, cough, bug recovered from culture, antibiotics help

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16
Q

Pertussis toxemic stage

A

2-8 weeks, whooping cough, bug is gone, symptoms due to toxin PT, antibiotics don’t help

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17
Q

Pertussis convalescent stage

A

Gradual recovery (months), susceptible to secondary infection

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18
Q

Pertussis pathogenesis

A

Inhalation, attachment to ciliated cells, paralyze ciliated cells, toxins inflame RT and stop clearing of mucus

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19
Q

Pertussis adhesins

A

PT A1B5, and FHA (filamentous hemagglutinin) binds ciliated cells like PT

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20
Q

Pertussis toxins

A

PT ADPR Gi to increase cAMP (reduce phagocyte killing), introduce own ACase to increase cAMP, tracheal cytotoxin damages ciliated cells, lethal toxin necrosis

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21
Q

PT mechanism

A

Normally Gs activates ACase, all deactivated by Gi, when Gi is ADPR then the system isn’t inhibited

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22
Q

Pertussis testing/detection

A

Culture 1st 2 weeks, PCR 1st 4 weeks, serology Ab test 2+ weeks

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23
Q

Pertussis prevention

A

DTaP vaccine uses PT & FHA, Tdap booster every 10 years, Tdap booster every pregnancy

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24
Q

Anthrax

A

Large cells with infectious spores (bioterror)

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25
Q

Anthrax reservoir

A

Soil

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26
Q

Anthrax transmission

A

Spores from animals/products (NOT human-human)

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27
Q

Cutaneous anthrax information

A

Most common, spores enter wound, germination, lesion develops with edema (rarely highly fatal septicemia)

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28
Q

GI anthrax information

A

Very rare, ingest spores from contaminated meat, invade mucosa and lymphatic system, high death rate

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29
Q

Inhalation anthrax information

A

Infection 1wk-2mo of inhalation, germination in Macs, bacteria in bloodstream, septic shock and high death rate

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30
Q

Anthrax capsule

A

Anti phagocytic (PGDG) poly gamma d glutamic acid resistant capsule

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31
Q

Anthrax toxin

A

2A1B, protective antigen binds up to 3 A portions, lethal toxin causes lethal effects w cell lysis and cytokine storm, and edema factor causes edema in cutaneous anthrax w/ own ACase

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32
Q

Anthrax treatment

A

60 days, ensure all spores germinated, antibiotics good if early, antitoxin to PA (protective antigen)

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33
Q

Anthrax bioterror

A

Release anthrax spores into the environment or infect livestock and transmit with infected carcasses

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34
Q

Anthrax Pasteur vaccine

A

Inject live strain into livestock and 5 doses of IM shots with boosters for military of PA

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35
Q

TB general information

A

Gram + like, acid fast +, white plague, only in humans

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36
Q

TB reservoir

A

Only humans

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37
Q

TB transmission

A

Highly contagious droplets/aerosols

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38
Q

LTBI information

A

Not infectious and no symptoms, skin test positive but nothing else

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39
Q

TB disease information

A

Highly infectious, skin test +, X-ray +, sputum +, cough fever, weight loss

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40
Q

TB predisposing factor

A

HIV knocks out CD4+ T cells, TB takes advantage

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41
Q

Primary TB pathogenesis

A

Inhale droplets into lung aveoli, invade Macs, body CD4+ T cell response, formation of tubercule (usually LTBI)

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42
Q

Primary TB disease information

A

5% of total cases, usually pulmonary, occasionally EPTB, and even more rarely military TB with cancer like tubercule formation

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43
Q

Secondary TB information

A

5-10% of LTBI cases, tubercules break down and infectious again, rarely EPTB

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44
Q

TB virulence factors

A

Resistant and waxy cell wall, has mycolic acid fatty acid chains, cord factor sticking cells together, Wax D. Also LAM (lipoarabinomannan) cell wall glycolypid which modifies phagosome

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45
Q

TB diagnosis

A

Acid fast test heat/acidify bacteria (need many bugs/doesnt separate other myobacteria), NaOH sputum culture (slow generation time), PPD TST (skin test with boiled protein extract look for hard raised bump), TB blood test (most accurate, IGRA [interferon gamma release assay])

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46
Q

TB treatment

A

For LTBI INH for 9 months, for disease INH + RIF (RNA Pol Inhibitor) + EMB + PZA for 9 months, all targeting cell wall synthesis, XDR and MDR TB can form if not full course

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47
Q

TB vaccine

A

BCG live attenuated vaccine with M. bovis, scar formation administered in some countries to protect kids

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48
Q

Cholera general information

A

Curved rod, gram -, flagella, causes “blue death”, hella diarrhea and rapidly fatal

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49
Q

Cholera reservoir

A

Water/humans/shellfish

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50
Q

Cholera transmission

A

Fecal/oral, NOT direct, poop water

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51
Q

Cholera severity

A

10% severe, generally cleared after a week

52
Q

Cholera pathogenesis

A

Ingested and adheres to small intestine, produces cholera toxin (CT) and acts on mucosal cells causing huge diarrhea and dehydration/circulatory collapse

53
Q

Cholera symptoms

A

Typically very fast (<1 day), extreme thirst, cramps and blue skin, liquid stool and shock, rice water stool

54
Q

Cholera adherence

A

Tcp (toxin coregulated pilus) binds to small intestinal mucosa, NA, CT

55
Q

Cholera toxin

A

5B1A, ADPR Gs, binds to mucosal surfaces

56
Q

Cholera toxin mechanism

A

ADPR Gs to not allow Gi to inhibit the production of ACase, raise cAMP, phosphorylation of chloride ion channel, chloride/K+ leaves and so does water

57
Q

Cholera treatment

A

Rehydration, necessary to have glucose included for uptake

58
Q

Cholera vaccine

A

VAXCHORA live attenuated vaccine with deleted A portion, given to travelers

59
Q

C. diff general information

A

Gram +, forms spores, causes watery diarrhea and colitis, very resistant to most things other then bleach

60
Q

C. diff risk factors

A

Long term antibiotics (colon microbiome depletion)

61
Q

C. diff reservoir

A

Spores in air, soil, water, human and animal intestine

62
Q

C. diff transmission

A

Fecal-oral, spore ingestion, contaminated surfaces

63
Q

C. diff diseases

A

Pseudomembranous colitis, toxic megacolon, colon rupture

64
Q

C. diff pathogenesis

A

Ingested spores, germination and colonization of colon, produce TcdA and TcdB, diarrhea and ulceration, sepsis and death

65
Q

TcdA and TcdB mechanisms

A

Largest known toxins, UDP glycosylate G proteins, block Rho GTPase activity, different B portions recognize different epithelial cell surfaces, result in disruption of tight junctions and increase inflammatory response

66
Q

C. diff testing

A

ELISA Ab test for A and B in feces, NAAT for toxin gene in stool (PCR)

67
Q

C. diff treatment

A

Antibiotics, oral vancomycin, FMT (fecal microbiome transplant)

68
Q

C. diff prevention

A

Contact precaution (wash hands), bleach contaminated surfaces, avoid unnecessary antibiotics

69
Q

Kleb. pneumoniae information

A

Gram -, principally extracellular, carbapenem resistant

70
Q

Kleb. pneumoniae risk factors

A

Ventilators, catheters, IV, long term antibiotics

71
Q

Kleb. pneumoniae reservoir

A

human intestine and oropharynx

72
Q

Kleb. pneumoniae transmission

A

Person to person, NOT air, usually medical device/contaminated hands

73
Q

Kleb. pneumoniae diseases

A

Pneumonia, UTI, sepsis

74
Q

Kleb. pneumoniae pneumonia pathogenesis

A

Colonize oropharynx, inhalation and biofilm growth in lung, pneumonia and lung scarring, bacteremia and sepsis

75
Q

Kleb. pneumoniae virulence (HV strains)

A

Hypercapsule (77 types), pili biofilm formation, LPS block C1 binding and inflammatory response, siderophore iron scavenging proteins

76
Q

Kleb. pneumoniae diagnosis

A

Respiratory panel PCR

77
Q

Kleb. pneumoniae treatment

A

Bug is carbapenem resistant due to outer membrane alterations and efflux pump up-regulation and (ESBL) extended spectra beta lactate enzymes which break down penicillins

78
Q

Salmonella general info

A

Gram -, motile rod with flagella, food poisoning and typhoid fever, many variants

79
Q

(NTS) Non-typhoidal salmonella information

A

Largest food borne bacterial disease cause

80
Q

NTS reservoir

A

Human and animal intestinal tract

81
Q

NTS transmission

A

Contaminated food and water

82
Q

NTS disease

A

Food poisoning

83
Q

NTS symptoms

A

12-72h after infection diarrhea, cramping, fever for up to 1 week and asymptomatic carrier for up to 3 months

84
Q

NTS pathogenesis

A

Ingestion, invade enterocytes, replicate in macrophage

85
Q

NTS virulence

A

Pef (plasmid encoded fimbriae) adhesin which bind to microvilli, Salmonella pathogenicity islands (T3SS) invade cells, SPI-1 mucosal invasion and SPI-2 systemic survival produces SpvB toxin which ADPR actin to dusrupt cytoskeleton

86
Q

S. typhi special feature

A

Found only in humans

87
Q

S. typhi reservoir

A

Human intestine/gallbladder and shellfish

88
Q

S. typhi transmission

A

Poop contaminated food/water

89
Q

S. typhi symptoms

A

Sustained high fever, stuporous state, body aches, flushed appearance, diarreah

90
Q

S. typhi asymptomatic carriers

A

Around 5% of affected, carriers for months-years

91
Q

S. typhi disease

A

Typhoid fever

92
Q

Typhoid fever incubation phase

A

Ingestion, growth in macrophages in MLN (lymph nodes), 1 -3 weeks

93
Q

Typhoid fever systemic period

A

Septicemia intestinal ulcers, typhoid toxin LPS shock

94
Q

Typhoid fever asymptomatic period

A

Live in gallbladder, shed bugs for years, hard to clear with antibiotics (targeting to gallbladder)

95
Q

S. typhi virulence

A

Typhoid toxin A1B2, (hybrid of PT/CDT)
A1-PltA=pertussis-like toxin ADPR unknown target
A2-CdtB (cytolethal distending toxin)=DNAse activity
B-PltB=Binds only to human glycoprotein target

Antiphagocytic Vi (virulence) capsule

96
Q

S. typhi prevention

A

Water sanitation

97
Q

S. typhi treatment

A

Antibiotics

98
Q

S. typhi vaccine

A

Live attenuated oral for travelers, Vi capsule IM shot

99
Q

Diarrheagenic E. coli information

A

Gram -, flagellated rod
O antigen = LPS
H antigen = Flagella
K antigen = capsule
Top 6 pathogen for death because of resistance

100
Q

ETEC (enterotoxigenic E. coli)

A

Traveler’s diarrhea, human/animal reservoir, noninvasive

101
Q

ETEC virulence

A

Noninvasive, small intestine adherence, LT (heat labile toxin) ADPR Gs, ST (heat stable toxin) activates GCase, increase cGMP for water release, no inflammatory response

102
Q

EAEC (enteroaggregative E. coli)

A

Persistent watery diarrhea in children, human only reservoirs

103
Q

EAEC virulence

A

Noninvasive but clump aggregation, EAST (EA stable toxin) activates GCase like ST, hemolysin like toxin, no inflammatory response

104
Q

EPEC (enteropathogenic E. coli)

A

Watery/bloody diarrhea, human reservoir, moderately invasive

105
Q

EPEC virulence

A

EAF (EPEC adherence factor), intimin (glue) no microvilli at binding sites, pedestal under bacteria, no diarrheal toxin, disrupt signal transduction

106
Q

EHEC (enterohemorrhagic E. coli) / STEC

A

Shiga toxin producing E. coli, livestock reservoir

107
Q

EHEC virulence

A

Moderately invasive, intimin, Shiga toxin (A1B5) stops protein synthesis by cleaving 28s RNA, only human receptor

108
Q

EHEC diseases

A

HC (hemorrhagic colitis) causes bloody diarrhea and HUS (hemolytic uremic syndrome) causes kidney/organ failure with bloody urine

109
Q

EIEC (enteroinvasive E. coli)

A

Dysentery, bloody and mucous diarrhea, human reservoir

110
Q

EIEC virulence

A

Very invasive, colon adherence, spread laterally to adjacent cells, no diarrheal toxin, damage due to mucosal destruction

111
Q

Types of ExPEC (extraintestinal pathogenic E. coli)

A

UPEC (urpopathogenic E. coli), NMEC (neonatal meningitis E. coli), SEPEC (sepsis associated E.coli)

112
Q

Cause of UTIs

A

90% of the time, UPEC

113
Q

UTI/UPEC reservoir

A

Colon and vaginal colinzation

114
Q

UTI/UPEC transmission

A

From colon or vagina or sex, most common in women due to anatomy

115
Q

Community acquired UTI/UPEC pathogenesis

A

Ascending infection, urethra (urine discharge), bladder (cystitis), ureters (tubes), kidneys (pyelonephritis and sepsis)

116
Q

HAI UTI/UPEC pathogenesis

A

Ascending infection due to catheter restricting fast flow and rarely hematogenous UTI from blood infection

117
Q

UPEC adhesion

A

Pap pili (pyelonephritis associated pili) for uroepithelial cell adhesion and mountain climbing, type 1 pili bind to bladder cells and promote invasion, Tamm-Horsfall protein/uromodulin (THP) most abundant urine protein to clear type 1 pili by binding, S fimbriae (sfa) bind intestinal epithelial cells

118
Q

Other UPEC virulence

A

Hemolysin (HlyA) pore forming toxin causes damage in pyelonephritis and promotes invasion, LPS fatty acid bind O antigen core, mediates bladder colonization, resistance to hydrophobic antibiotics and toxins, siderophores, and K1 sialic acid capsule

119
Q

UPEC prevention

A

Wipe front to back, pee after sex, cranberry juice prevent type 1 pili binding

120
Q

UPEC treatment

A

Antibiotics, but disrupt normal colon/vagina flora, and spermicides inhibit lactobacillus

121
Q

NMEC disease

A

Leading cause of infant meningitis

122
Q

NMEC reservoir

A

Human GI/vagina

123
Q

NMEC transmission

A

Like GBS, prenatal due to trauma or procedure, early onset due to exposure during delivery, and late onset due to caregivers or invasive devices

124
Q

NMEC virulence

A

S fimbriae adhesion to EC components, IbeABC allows crossing of blood brain barrier, siderophores, and K1 sialic acid capsule

125
Q

NMEC treatment

A

Antibiotics (no vaccine)

Bacterial Pathogenesis (3 decks)

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