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week 2 lec 2 Flashcards

1
Q

normal epidermis is colonized by what commensal bacteria after birth

A

Coagulase-negative Staphylococci (Staph epidermidis)

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2
Q

most common purulent skin infection and what its caused by

A

pyoderma from staph aureus

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3
Q

what can cause staphylococcal skin infections

A

Immunosuppressive disorders, diabetes, atopic dermatitis, preexisting tissue injury (surgical sites, burns)

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4
Q

which staph is commensal and which is pathogenic

A

Staph epidermidis – mostly commensal

Staph aureus- commensal and aggressive/ pathogenic
–> MRSA- methicillin resistance staph aureus

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5
Q

risk factors for staph soft tissue infection

A

lack IL-17

defective neutrophil function or # (cancer, chemo, genes)

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6
Q

pathogenesis of staph soft tissue infection (3)

A
  1. pore-forming toxins (i.e. alpha and gamma toxin) –> lyse neutrophils and macrophages
  2. phenol-soluble modulins –> lyse leukocytes and erythrocytes
  3. exfoliative toxins (from bacteriophages) –> serine proteases target desmosomal cadherin –> intraepithelial bullae (skin) OR staphylococcal-scalded skin syndrome (systemic)
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7
Q

staph superantigens examples

A

I.e. toxic shock syndrome toxin 1, enterotoxins…

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8
Q

staph superantigens nonspecifically activate

A

T cells via HLA-2 on APCs and beta-subunit of TCR –> CD4+ T cells activated

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9
Q

what does toxic shock syndrome toxin 1 (TSST-1) rxn cause

A

high fever, hypotension, scarlet fever-like rash, desquamation of skin, multiorgan dysfunction

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10
Q

staph- neutrophil evasion

what does protein A block?

A

(expressed on surface of S. aureus)–> blocks antibody-mediated phagocytosis by both neutrophils and macrophages

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11
Q

staph- neutrophil evasion

what does staphylococcal nuclease destroy?

A

destroys neutrophil extracellular traps

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12
Q

staph- neutrophil evasion

what does catalase, alkyl hydroperoxidase reductase and staphyloxanthin inhibit?

A

inhibit ROS-mediated killing of S. aureus

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13
Q

staph- neutrophil evasion

what does staph-superantigen-like 5 and 11 block?

A

block P-selecting and ICAM-1 which normally allow neutrophils to adhere to the endothelium and enter tissue

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14
Q

staph- neutrophil evasion

what does chemotaxis inhibitory proteins (CHIPS) or staphopain A (ScpA) block?

A

block complement receptors and CXCR2 neutrophil-
attracting chemokines

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15
Q

what (antimicrobial peptides) AMPs fight against staph?

A

Beta-defensins 2 and 3, cathelicidin, RNase 7

–> bacteriostatic or bactericidal activity

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16
Q

which neutrophils via PRRs fight against staph?

A

TLR-2 –peptidoglycan and lipoproteins
NOD-2 –muramyl dipeptide

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17
Q

staph has a pore forming toxin that helps promote neutrophil recruitment and fight against the bacteria. how?

A

Staph’s pore-forming toxin actually activate caspase-1 and result in activation of IL-1Beta –> promote neutrophil recruitment

IL-17 also for neutrophil recruitment

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18
Q

what do the exfoliative toxins in staph aureus cause

A

blistering skin disorders

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19
Q

what are the 2 exfoliative toxins in staph and what do they cause

A

ET-A causes bulleux impetigo (localized)

ET-B causes staphylococcal scalded-skin syndrome (SSSS) (cutaneous tenderness and widespread superficial blistering)

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20
Q

what is the mechanism of action of exfoliative toxins in staph aureus

A

ETs are serine proteases that bind to cell adhesion molecule desmoglein-1 –> loss of cell-cell adhesion between stratum spinous and granulosum –> making it easy to blister

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21
Q

how do staph exfoliative toxins worse

A

bind desmoglein-1 (cell adhesion molecule) and cause loss of cell adhesion and easy blistering

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22
Q

common cause of superficial purulent skin infections

A

group A streptococcus (GAS) (i.e. strep pyrogens)

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23
Q

local and invasive problems from group A strep

A

local: impetigo, ecthyma, intertrigo

invasive: erysipelas, cellultiis, necrotizing fasciitis, deep tissue necrosis –> sepsis, shock, multi organ failure, death

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24
Q

a group A strep infection can trigger an immune mediated disease like

A

Guttate psoriasis, acute rheumatic fever, rheumatic heart disease, glomerulonephritis

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25
risk factors for strep
environmental: hygiene, poverty, corwding pre-existing condition: tissue damage and inflammation i.e. eczema and fungal infections
26
where to non-GAS species (other strep, not group A) infect
areas with poor blood flow (e.g., ischemia or venous stasis).
27
which strep are linked to skin infections
D and E
28
what is the protein that differentiates the 200 subtypes of GAS (group A strep)
m-protein
29
M-protein in strep inhibits immune defesnes by
bindings regulators of complement system --> no activation of classical and alternative path inhibit antibody-medicted phagocytosis by binding Fc region of IgG inflammation via TLR-2 on monocytes --> increase IL-6, IL-1 beta and TNFalpha
30
where can m protein of strep bind on keratinocytes
fibronectin and CD46
31
2 pore forming toxins in strep
steptolysin O and steptolysin S
32
steptolysin O vs steptolysin S these strep pore-forming toxins act on
O= large pore formation cause apoptosis of neutrophils, macrophages and epithelial cells S= cytolytic against neutrophils, lymphocytes, erythrocytes and platelets (inflammation, vascular injury and necrosis)
33
what is the strep superantigen? effect?
Strep pyrogenic exotoxin serotype A, C, G to M, mitogenic exotoxin SMEZn non-specifically activates T cells
34
Streptococcal Pyrogenic Exotoxins (superantigen) causes what
streptococcal toxic shock syndrome, scarlet fever, erysipelas and invasive presentations
35
how does strep do neutrophil invasion?
make antioxidants (glutathione peroxidase, superoxide dismutase) to inhibit ROS mediated killing nuclease A and DNase Sda1 breakdown neutrophil extracellular traps
36
how does the immune system respond to strep?
AMPs made by keratinocytes (beta-defensins 1 and 3, cathelicidin) neutrophil recruitment (TLR-2 peptidoglycan and lipoproteins and NOD-2 for muramyl dipeptide) type 1 IFN response (TLR-9 activation --> oxidative burst) adaptive T and B response (but so many M proteins and types of strep that immunity to 1 type doesnt protect against others)
37
super antigenic toxins from which bacteria
staph aureus or group A strep
38
super antigenic toxins lead to a cytokine storm of which cytokines? what does this cause?
TNF alpha, IL-1, IL-6 Capillary leak syndrome and other systemic problems (i.e., toxic shock syndrome)
39
do super antigenic toxins need APCs to exert effects on T cells
no
40
where to super antigenic toxins bind on APCs?
HLA-2 but outer walls so recognition is not specific to HLA-2 or T cell receptor = greater T cell response
41
how do super antigenic toxins cause cutaneous manifestations?
increase # of T cells with CLA (skin homing) *cutanoeus lymphocyte-associated antigen
42
pseudomonas aeruginosa characteristics
gram negative rod in aqeusous envo sweet grape odor blue green color oxidase positive non lactose fermenting obligate aerobic bacteria likes warm (42 celcisu)
43
primary cutaneous infections from pseudomonas aeruginosa
Green nail syndrome, toe web infection, folliculitis, hot-foot syndrome, external otitis, perichondritis
44
pseudomonas in immunocompromised patietns
bacteria and ecthyma gangrenosum
45
how can pseudomonas aeruginosa get into skin
if damage i.e. infection, catheter, trauma
46
what factors in pseudomonas aeruginosa degrade skin and parts of immune system
alkaline protease, protease IV, elastase
47
what does pseudomonas aeruginosa release after contacting the host
exoenzymes ExoS --> TLR’s --> TNF-alpha production ExoT --> binds adenosine diphosphate ribosyltransferase ExoU --> damages cell membranes ExoY --> binds adenylate cyclase
48
other factors in pseudomonas aeruginosa
Exotoxin A --> interferes with protein synthesis! cell death Procyanin --> pro-inflammatory and oxidative effects LPS --> activates TLR4 --> septic shock mediator Quorum sensing --> intercellular signaling to coordinate gene transcription and possible biofilm formation
49
pseudomonas aeruginosa pathogenic feature
makes alginate to scavenge free radicals, impair phagocytosis, inhibit neutrophil chemotaxis, inhibit complement activation biofilm production (protect against antibiotics and AMPs)
50
how do pseudomonas aerguinoa be antibiotic resistnant
Multidrug efflux pumps (pump it out), beta-lactamases (breakdown the antibiotic), downregulation of porins on the outer membrane (then antibiotic can’t get in)
51
pathogenesis of pseudomonas aeruginosa
1. green nail syndrome 2. toe web infection 3. folliculitis and hot-foot syndrome --> all if it water 4. external otitis 5. bacteremia (in bloodstream) and ecthyma gangrenosum (veins and arteries then to skin invasion- inside out)
52
how do you get Bacteremia and Ecthyma Gangrenosum from psuedomonas aeruginosa
Hospitalized patients with neutropenia, hematological malignancy or low CD4+ count
53
what are dermatophytoses and what do they thrive on
fungal infections that use keratin (spores adhere to it and change gene expression) fungi releases proteases, lipases and ceramidases to digest through the keratin interfere with keratinocyte proliferation and cell mediated immunity
54
immune response to dermatophytes
mannan (fungal component) activates TLR (causes keratinocyte proliferation, AMP secrete, pro-inflammatory cytokine) delayed-hypersensitivity- Th1 and Th17 to clear fungus
55
dermatophytid reaction is
inflammatory dermatitis at a distance site from primary infection -delayed hypersensitive, eruption is polymorphic
56
criteria to establish dermatophytid (ID) eruption
1. dermatophytosis is on another body part 2. no fungal elements in ID eruption 3. ID eruption goes away once primary dermatophyte infection clears
57
Onychomycosis
fungal infection of nail
58
common causes of onychomycosis
90% caused by Trichophyton rubrum and T. interdigitale, Candida spp are often culprits of fingernail infections
59
tine barbae
fungal infection of the beard
60
causes of tinea barbae
zoophilic strains of T. interdigitale, T. verrucosum
61
tinea corporis AKA ringworm
dermatophytosis of glabrous skin (except palms, soles and groin)
62
tinea corporis AKA ringworm cause
T. rubrum Head, neck and arms
63
tinea cruris
Dermatophytosis of groin, genitalis, pubic area, perineal and perianal skin
64
causes of tinea cruris
T. rubric and Epidermophyton floccosum
65
tinea pedis and tinea mannum
Dermatophytosis of feet (pedis) or palmar and interdigital areas of hands (mannum)
66
pathogen for tinea pedis and tinea mannum
T. rubric, T. interdigitale and Epidermophyton floccosum
67
measles
Highly contagious, single-stranded, enveloped RNA virus of the Paramyxoviridae family
68
how are measles transmitted
person- person (contact or airborne respiratory droplets)
69
Koplik spots, fever, cough, coryza, conjunctivitis with possible severe complications of pneumonia and encephalomyelitis in which disease
measles
70
rubella
Enveloped positive-stranded RNA virus of the Togaviridae family
71
family for measles vs rubella
rubella- togaviridae family measles- paramyxoviridae family
72
how is rubella trasnmitted
direct or nasopharynx droplets
73
features of rubella
Enlarged cervical, suboccipital and postauricular lymph nodes rash
74
rubella and immunity
lifelong
75
erythema infectious aka fifth disease is causesd by which virus and what does it look like?
parvovirus B19 (Parvoviridae, no envelope, single-stranded DNA virus) slapped cheeks
76
Erythema Infectiosum - Parvovirus B19
cheek rash then lacy eruptions on extremities, polyarthritis, papular purpuric glove and sock syndrome
77
what is the crisis that can be caused by Erythema Infectiosum - Parvovirus B19
Transient aplastic crisis – can infect and destroy erythroid progenitor cells
78
Human Herpesvirus 6 (HHV-6) causes what in infants
Exanthem subitum/ roseola infantum, 6th disease fevers (usually no rash in kids)
79
what is true for all herpesviruses
Chronic infection with latent stage and possibility to reactivate
80
what causes Human Herpesvirus 6 (HHV-6)
Herpesviridae family, double-stranded DNA
81
where does Human Herpesvirus 6 (HHV-6) replicate in the body and get transmitted
replicate in salivary glands and trasmitted through saliva
82
herpes simplex virus- where does it infect
1st infects skin or mucosa then to local nerve ends and ganglia to be latent and reactivated
83
types of herpes simplex virus and where they infect
HSV-1 oral HSV-2 genital
84
symptoms of herpes simplex virus
Most primary infection are asymptomatic, and most transmission occurs during asymptomatic shedding
85
herpes simplex virus pathogenesis depends on
immune function/ competence IFN and TLR2 mutations increase lesions or encephalitis dendritic cells and CD8+ T cells localize to sites of reactivation humeral immunity to reduce viral titers at inoculation sites
86
varicella herpes zoster virus is what initially and upon reactivation turns into what
chicken pox --> shingles
87
varicella herpes zoster virus spread?
highly contageous chicken pox on face and scalp then spread to trunk rose coloured macules to papules
88
how does shingles present (reactivation of Varicella Herpes Zoster Virus)
unilateral dermatomal pain and rash postherpetic neuralgia
89
how does varicella herpes zoster virus (chicken pox) enter the body?
mucosa of respiratory tract and oropharynx disseminated via blood and lymph
90
how long to show sx of chicken pox
10-14 days after infection --> larger viremia (post replication)
91
which sensory nerves and ganglia does chicken pox (Varicella Herpes Zoster Virus) travel
trigeminal nerve, spinal sensory ganglia T1-L2
92
how does chicken pox (Varicella Herpes Zoster Virus) circulate
via lymphocytes
93
to end and go into latency for Varicella Herpes Zoster Virus (chickenpox) infection what is needed
T cell mediated immunity
94
how does Varicella Herpes Zoster Virus get reactivated
T cell mediated immunity fails spread in ganglion neuropathic pain destroy neurons and sensory nerves spread antidromically via sensory nerve and into skin endings --> zoster vesicles
95
human papillomavirus type
DNA virus of the Papillomaviruses, nonenveloped, double stranded DNA virus
96
many types of human papillomavirus.. which are high risk for malignancy
E6 and E7 proteins have oncogenic effects
97
what does human papillomavirus infect
keratinocytes replicate when in basal epidermal keratinocytes (E6 and E7 proteins for amplification)
98
human papillomavirus causes what skin symptoms
Common warts: HPV-2, 27, 57 and HPV-4 and HPV-1 Butcher’s warts (wet meat handling) - HPV-7

BMS250 (52 decks)

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