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Hannah's Intersystem > Skin and Soft Tissue Infections > Flashcards

Skin and Soft Tissue Infections Flashcards

1
Q

List 6 reasons skin is intrinsically resistant to infection

A 
Low water content
Low pH
Low temperature
High salt
Fats and fatty acids
Microbiota
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2
Q

What makes up the skin microbiota?

A

Mainly bacteria and some yeasts

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3
Q

List 7 microbes commonly found on the skin

A

Staphylococcus epidermidis
Staphylococcus aureus
Diptheroids (any corynebacterium besides Corynebacterium diphtheriae)
Streptococci
Gram negative bacilli (e.g. Pseudomonas)
Anaerobes (Gram - and +, e.g. Propionibacterium acnes)
Yeasts (e.g. Candida spp)

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4
Q

What are some common sites for anaerobes to reside?

A

In hair follicles and glands due to the lower O2

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5
Q

What areas of the skin have more bacteria and why?

A

Axilla, perineum, soles of feet and between toes, due to higher moisture

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6
Q

How many bacteria can be found on normal dry skin?

A

~1000 bacteria/cm2 (amount and composition of skin microbiota varies at different sites)

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7
Q

Give 5 examples of cutaneous manifestations of systemic infections

A 
Enteric fever "rose spots"
Petechiae in septicaemia
Rash in secondary syphilis
Scarlet fever
Toxic shock syndrome
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8
Q

What organism causes scarlet fever?

A

GAS

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9
Q

What organism causes toxic shock syndrome?

A

Staphylococci, streptococci (any bacteria producing toxic shock toxins)

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10
Q

Give 2 examples of fungi causing SSTI

A

Yeasts (e.g. Candida)

Filamentous fungi

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11
Q

Give 3 examples of bacteria causing SSTI. Which is most common?

A

S. aureus (most common cause of SSTI)
S. pyogenes
Clostridia

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12
Q

Give 3 examples of parasites causing SSTI

A

Leishmania
Schistosomes
Hookworms

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13
Q

Give 8 examples of viruses causing SSTI

A 
HSV
VZV
HPV
Measles
Rubella
Enteroviruses
Parvovirus B19
Molluscum contagiosum
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14
Q

What type of infection typically results in a compromised patient?

A

Polymicrobial infection with primary and opportunistic pathogens

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15
Q

What are the 3 types of SSTI? Give examples of each

A

Localised infections: folliculitis, abscess
Spreading infections: impetigo, cellulitis
Necrotising infections: fasciitis

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16
Q

What is folliculitis?

A

Infection of the hair follicle

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17
Q

What most commonly causes folliculitis? What is 1 other possible cause?

A

Most often due to blockage

May also result from direct inoculation of bacteria into hair follicle

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18
Q

What causes an abscess?

A

Progression of folliculitis to abscess (same original causes as folliculitis)

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19
Q

What is the most common causative organism in a case of folliculitis?

A

S. aureus

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20
Q

What is furunculosis?

A

Furuncle = abscess/boil

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21
Q

What is S. saprophyticus?

A

Urinary tract pathogen

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22
Q

What is the “definition” of S. aureus?

A

Coagulase +

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23
Q

Why does infection with S. aureus often recur?

A

Adaptive immune response is weak

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24
Q

How does staphylococcus enter damaged tissues?

A

Binds to cells and matrix via adhesins

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25
Q

How does staphylococcus evade the immune system and persist?

A

Inhibits chemotaxis
Inhibits phagocytosis
Resists killing if ingested by PMNs
Forms biofilm on biotic and abiotic surfaces (especially S. epidermidis)

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26
Q

How does staphylococcus inhibit chemotaxis and what effect does this have on the inflammatory process?

A

Via CHIPS, which blocks the complement receptor on cells and other proteins
Overall effect slows wound healing

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27
Q

How does staphylococcus inhibit phagocytosis?

A 
Capsule
Protein A
Staphylokinase
Complement inhibitors (SCIN)
Haemolysins
Leukocidins
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28
Q

How does protein A inhibit phagocytosis?

A

Binds Fc of Abs and prevents them activating host cells

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29
Q

What is the role of haemolysins and leukocidins?

A

Inhibits phagocytosis by killing neutrophils

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30
Q

Give an example of an important leukocidin

A

Panton-Valentine leukocidin

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31
Q

Describe the resistance profile of S. aureus

A

~90% are resistant to penicillin

Increasing % are resistant to methicillin and other antimicrobials (MRSA)

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32
Q

What is the difference between CA-MRSA and HA-MRSA?

A

Differences in genes, e.g. PV leukocidin
CA-MRSA more virulent
Different spectrum of disease (CA-MRSA causes aggressive abscesses which can invade to produce pneumonia, affects young people)

33
Q

What is impetigo?

A

An infection of the epidermis characterised by bullous (blistered), crusted or pustular lesions

34
Q

What is the causative organism in impetigo?

A

S. aureus and/or GAS (often both)

35
Q

What organism causes bullous impetigo?

A

S. aureus

36
Q

What is erysipelas?

A

A rapidly spreading erythematous infection (usually of face, legs or feet) with well-defined border, plus pain and fever
Potentially serious

37
Q

What is cellulitis?

A

Similar to erysipelas but involves subcutaenous fat

Potentially serious

38
Q

What is the causative organism in erysipelas/cellulitis?

A

Most often GAS
Cellulitis has wider range of causative organisms including S. aureus and other environmental organisms (e.g. Vibrio spp but not cholerae)

39
Q

When does anaerobic cellulitis occur?

A

When tissue is devitalised

40
Q

What is necrotising fasciitis?

A

Rapidly spreading infection along fascial planes which disrupts the blood supply, leading to necrosis (as well as myonecrosis and gangrene in severe cases)

41
Q

What are some common causes of necrotising fasciitis?

A

GAS

Anaerobes (including Clostridium spp)

42
Q

What is the most common cause of gas gangrene?

A

Clostridia (especially C. perfringens)

43
Q

How are streptococci classified?

A

According to type of haemolysis they produce on blood agar

Further classified into Lancefield groups (A-T)

44
Q

What is GAS?

A

S. pyogenes

45
Q

What is GBS?

A

S. agalactiae

46
Q

What are the Lancefield groups which contain pathogens?

A

A, B, C, D, G

47
Q

What is the basis of Lancefield grouping?

A

Dependent on type of CHO in cell wall

48
Q

List 5 structural virulence determinants of GAS

A 
M-protein
Capsule
Lipoteichoic acid
Cell wall CHO
Other surface Ags
49
Q

What is the M-protein? What is the clinical signifiance of the M-protein?

A

A structural virulence determinant of GAS; can be used to classify GAS by M-type (low numbered are generally more virulent)
Immunity can be M-type specific (can get multiple infections with GAS of different M-types)

50
Q

List 5 enzymes which act as virulence determinants for GAS. What are their roles?

A 
Streptokinase (fibrinolysin)
Hyaluronidase (spreading)
C5a peptidase
SpeB (protease)
DNAses
51
Q

List 3 toxins which act as virulence determinants for GAS. What are their roles?

A

Streptolysins (haemolysins)
Leukocidins
Superantigens (e.g. SpeA)

52
Q

What virulence factors are involved in the adhesion and colonisation of GAS?

A

Lipoteichoic acid
Fibronectin-binding proteins
M-protein

53
Q

How do GAS invade?

A

Mechanism unknown

Invade into or between cells

54
Q

List 4 ways GAS evades innate immunity

A

M-protein and capsule are anti-phagocytic
Leukocidal toxins kills phagocytes
DNAse overcomes NETS
C5a peptidase

55
Q

What is NETS?

A

Neutrophil Extracellular Traps: fibres (composed of fibrin and other granular material) extrude and form a net around the neutrophil to trap microorganisms

56
Q

List 3 mechanisms by which GAS cause tissue damage

A

Directly via cytolethal toxins and enzymes
Superantigens (causing toxic shock syndrome)
Activation of autoimmunity

57
Q

Describe the morphology and classification of Clostridia

A

Gram+ rods

Anaerobes

58
Q

What makes Clostridia so difficult to remove from the environment?

A

Forms hardy spores (especially C. tetani - spores can be seen under the microscope; C. perfringens will only form spores if the going is very tough)

59
Q

What is the typical mechanism of wound colonisation in the case of clostridial infection?

A

Spores (usually) or vegetative bacteria from environment, gut or vaginal microbiota colonise wound

60
Q

Under what conditions does clostridial infection take hold?

A

Clostridia germinates and replicates under anaerobic conditions, and therefore occurs more readily in devitalised (damaged) tissue

61
Q

How does clostridial infection cause tissue damage?

A

Many different toxins and enzymes are secreted which lead to gas production, tissue damage and further spread

62
Q

What test is used to identify C. perfringens?

A

Litmus milk test (positive litmus occurs when gas is produced which blasts apart the milk)

63
Q

What kind of pathogen is Pseudomonas?

A

Opportunistic

64
Q

What is a possible complication of diabetic foot ulcer?

A

Osteomyelitis

65
Q

What is a hallmark symptom of infection with Pseudomonas?

A

Blue-green pus

66
Q

Why is diabetic foot ulcer a common complication of DM?

A

Due to peripheral neuropathy (cannot detect damage)

67
Q

List 2 types of fungi which can cause SSTI, and give examples of each

A

Dermatophytes (e.g. Epidermophyton, Trichophyton, Microsporum)
Yeasts (e.g. Candida, Malassezia)

68
Q

What does Malassezia cause?

A

Pityriasis versicolor (local unsightly skin discolouration)

69
Q

When does Candida infection usually occur?

A

With damaged, moist skin and lowered host resistance

Also associated with some forms of primary immunodeficiency (e.g. defect in AIRE) or aggressive autoimmunity

70
Q

What kind of presentation can a severe haemorrhagic varicella infection produce?

A

Pneumonitis
ARDS
Typically patient is immunocompromised

71
Q

List 4 methods which may be used in diagnosis of SSTI

A

NAT (for viruses)
Microscopy (Gram stain or other)
Culture and identification
Antimicrobial susceptibility testing

72
Q

What are the 5 main principles of treating a wound infection?

A

Use strict aseptic technique
Remove damaged tissue and foreign material
Use topical disinfectant/wound dressing
Consider oral antibiotic (if disseminated) e.g. co-amoxyclav
Consider tetanus prophylaxis

73
Q

What strategies are used to treat an abscess?

A

Drain
Consider oral antibiotic e.g. flucloxacillin (not penicillin - almost all S. aureus are resistant), may have to change if CA-MRSA

74
Q

How is impetigo treated?

A

Soap and water with an anti-staphylococcal topical antimicrobial (mupirocin) for a mild infection
Add oral antibiotics (flucloxacillin or dicloxacillin - unless S. pyogenes alone, in which case penicillin can be used) for a more severe infection

75
Q

How is cellulitis treated?

A

Flucloxacillin or dicloxacillin (unless S. pyogenes alone, in which case penicillin can be used)

76
Q

How is gas gangrene treated?

A

Surgery
Penicillin G (good for Clostridia, S. pyogenes)
+/- hyperbaric oxygen to oxygenate tissues

77
Q

How are diabetic foot infections treated?

A

Typically polymicrobial, so give co-amoxyclav and metronidazole (good for anaerobes)

78
Q

What antibiotics can be used to treat Pseudomonas?

A

Dependent on antibiotic susceptibility testing (highly resistant organism)

Hannah's Intersystem (16 decks)

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