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Skin, Blood, Lymph > Bacterial Skin Infections II > Flashcards

Bacterial Skin Infections II Flashcards

1
Q

Clostridium perfringens General

A

-Gram (+) bacilli, Anaerobic, Spore forming, non‐Fasciitis

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2
Q

Clostridium perfringens Pathogenesis

A

TOXIN production:exotoxin (alpha, phospholipase, hemolysins, collagenase), NECROSIS -fascitis, gas gangrene

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3
Q

Cutaneous Anthrax general

A

Black eschar within 12‐36 hours – No pus – painless • Generalized toxic effects – as bacilli spread to lymphatics – septicemia • Edema

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4
Q

Bacillus anthracis General

A

– Gram (+), spore forming, encapsulated rods – found in soil, water, air & vegetation -Bioterorism

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5
Q

Bacillus anthracis Pathogenesis/Virulence factors

A

-polyglutamic acid capsule –exotoxin components that enter the cell: protective Ag (PA), 2 NZ components (edema factor (adenylate cyclase) and lethal factor (endoprotease/MAPKK)

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6
Q

Enterococcus faecalis General

A

-catalase negative,lancet or bullet shaped, survive high salt and bile concentrations

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7
Q

Enterococcus faecalis Sources/Transmission

A

Catheter, normal flora, person to person via fecal oral route

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8
Q

Enterococcus faecalis Virulence

A

-resistant to Optochin (P disk). -MANY ways to be antibiotic resistant

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9
Q

Enterobacter cloacae General

A

Gram (‐) motile bacillus, glucose fermenter, lactose fermenter, MacConkey agar -ornithine decarboxylase‐positive, urease negative

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10
Q

Enterobacter cloacae Virulence/Resistance

A

Enotoxin

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11
Q

Enterobacter cloacae Sources/transmission

A

-Nosocomial pathogen -Common in pts with recurrent infections, instrumented, anatomical defects

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12
Q

Acinetobacter baumanni General

A

-pleomorphic aerobic Gram (‐) rod – Gram stain similar to H. influenzae, Strictly aerobic, Nonfermenting, Nonfastidious, Nonmotile, Catalase‐positive, Oxidase‐negative

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13
Q

Acinetobacter baumanni Sources/Transmission/Risk Factors

A

-nosocomial pathogen,catheter, normal flora, survive on dry inanimate surfaces(1‐5 months) • biofilm on glass or plastic surfaces advanced age • immune suppression, major trauma or burn injuries, invasive procedures • previous administration of antibiotics

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14
Q

Acinetobacter baumanni Virulence

A

-INHERENT MULTI DRUG RESISTANCE -Fimbriae, LPS, Biofilm Enzymatic (degradation: β‐lactams, cephalosporins, modification and/or efflux),Nonenzymatic (Changes in outer membrane proteins, Multidrug efflux pumps,Alterations in affinity or binding of penicillin‐binding proteins -Endotoxin: targeted (TLR4)

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15
Q

Acinetobacter baumanni Treatment

A

experimental treatment: LpxC‐1 blocks LPS synthesis & TLR4‐induced inflammatory cytokine cascade is shut down

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16
Q

Acinetobacter baumanni Clinical Manifestations

A

Pneumonia,meningitis,Peritonitis, SURGICAL SITE INFECTION, SKIN INFECTION

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17
Q

Shewanella sp. General

A

-unusual cause of disease in humans,emerging infection • often IDed wrong as Pseudomonas • Gram negative bacillus, oxidase+, catalase+, non‐fermenter, H2S+

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18
Q

Shewanella sp. Clinical Manifestations

A

-soft tissue chronic infections -cellulitis, abscesses, bacteremia, wound or burn infection

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19
Q

Shewanella sp. Source/Risk factors

A

-ubiquitous: foods, sewage, fresh & salt water -hepatobiliary disease, peripheral vascular disease, poor hygiene, low socioeconomic status

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20
Q

Aspergillus sp. General

A

-Fungus -hyphae, septae & branch at 45° angles, silver stain

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21
Q

Aspergillus sp. Clinical Manifestations

A

Endocarditis

22
Q

Candida albicans General

A

-Fungus -budding yeast

23
Q

Candida albicans Source/Transmission

A

-Nosocomial infection -Catheter, broad spectrum antibiotics -Diabetic, immunosuppressed

24
Q

Clostridium tetani General

A

-Gram‐positive rods – Spore‐forming – Strict anaerobes

25
Q

Clostridium tetani Clinical Manifestations

A

-WOUND INFECTIONS -tonic muscle spasms & hyperflexia

26
Q

Clostridium tetani Pathogenesis

A

Neurotoxin

27
Q

-Gram (+) bacilli, Anaerobic, Spore forming, non‐Fasciitis

A

Clostridium perfringens General

28
Q

TOXIN production:exotoxin (alpha, phospholipase, hemolysins, collagenase), NECROSIS -fascitis, gas gangrene

A

Clostridium perfringens Pathogenesis

29
Q

Black eschar within 12‐36 hours – No pus – painless • Generalized toxic effects – as bacilli spread to lymphatics – septicemia • Edema

A

Cutaneous Anthrax general

30
Q

– Gram (+), spore forming, encapsulated rods – found in soil, water, air & vegetation -Bioterorism

A

Bacillus anthracis General

31
Q

-polyglutamic acid capsule –exotoxin components that enter the cell: protective Ag (PA), 2 NZ components (edema factor (adenylate cyclase) and lethal factor (endoprotease/MAPKK)

A

Bacillus anthracis Pathogenesis/Virulence factors

32
Q

-catalase negative,lancet or bullet shaped, survive high salt and bile concentrations

A

Enterococcus faecalis General

33
Q

Catheter, normal flora, person to person via fecal oral route

A

Enterococcus faecalis Sources/Transmission

34
Q

-resistant to Optochin (P disk). -MANY ways to be antibiotic resistant

A

Enterococcus faecalis Virulence

35
Q

Gram (‐) motile bacillus, glucose fermenter, lactose fermenter, MacConkey agar -ornithine decarboxylase‐positive, urease negative

A

Enterobacter cloacae General

36
Q

Enotoxin

A

Enterobacter cloacae Virulence/Resistance

37
Q

-Nosocomial pathogen -Common in pts with recurrent infections, instrumented, anatomical defects

A

Enterobacter cloacae Sources/transmission

38
Q

-pleomorphic aerobic Gram (‐) rod – Gram stain similar to H. influenzae, Strictly aerobic, Nonfermenting, Nonfastidious, Nonmotile, Catalase‐positive, Oxidase‐negative

A

Acinetobacter baumanni General

39
Q

-nosocomial pathogen,catheter, normal flora, survive on dry inanimate surfaces(1‐5 months) • biofilm on glass or plastic surfaces advanced age • immune suppression, major trauma or burn injuries, invasive procedures • previous administration of antibiotics

A

Acinetobacter baumanni Sources/Transmission/Risk Factors

40
Q

-INHERENT MULTI DRUG RESISTANCE -Fimbriae, LPS, Biofilm Enzymatic (degradation: β‐lactams, cephalosporins, modification and/or efflux),Nonenzymatic (Changes in outer membrane proteins, Multidrug efflux pumps,Alterations in affinity or binding of penicillin‐binding proteins -Endotoxin: targeted (TLR4)

A

Acinetobacter baumanni Virulence

41
Q

experimental treatment: LpxC‐1 blocks LPS synthesis & TLR4‐induced inflammatory cytokine cascade is shut down

A

Acinetobacter baumanni Treatment

42
Q

Pneumonia,meningitis,Peritonitis, SURGICAL SITE INFECTION, SKIN INFECTION

A

Acinetobacter baumanni Clinical Manifestations

43
Q

-unusual cause of disease in humans,emerging infection • often IDed wrong as Pseudomonas • Gram negative bacillus, oxidase+, catalase+, non‐fermenter, H2S+

A

Shewanella sp. General

44
Q

-soft tissue chronic infections -cellulitis, abscesses, bacteremia, wound or burn infection

A

Shewanella sp. Clinical Manifestations

45
Q

-ubiquitous: foods, sewage, fresh & salt water -hepatobiliary disease, peripheral vascular disease, poor hygiene, low socioeconomic status

A

Shewanella sp. Source/Risk factors

46
Q

-Fungus -hyphae, septae & branch at 45° angles, silver stain

A

Aspergillus sp. General

47
Q

Endocarditis

A

Aspergillus sp. Clinical Manifestations

48
Q

-Fungus -budding yeast

A

Candida albicans General

49
Q

-Nosocomial infection -Catheter, broad spectrum antibiotics -Diabetic, immunosuppressed

A

Candida albicans Source/Transmission

50
Q

-Gram‐positive rods – Spore‐forming – Strict anaerobes

A

Clostridium tetani General

51
Q

-WOUND INFECTIONS -tonic muscle spasms & hyperflexia

A

Clostridium tetani Clinical Manifestations

52
Q

Neurotoxin

A

Clostridium tetani Pathogenesis

Skin, Blood, Lymph (22 decks)

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