CP 62 - Skin Soft Tissue Infection Flashcards

1
Q

what are the normal layers of the skin

A

outer layer, epidermis, sebaceous gland, dermis, subcutaneous adipose tissue

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2
Q

what are the function of the skins

A

Physical barrier: chemicals, UV, micro-organisms
Homeostasis: thermoregulation, prevention of dessication electrolyte loss
Immunological function: Ag presentation and phagocytosis (Langerhans cells, lymphocytes, mononuclear phagocytic cells)

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3
Q

what are some of the normal flora of the skins?

A

Coagulase-negative staphylococci, Staph. aureus, Propionibacterium, Corynebacterium spp.

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4
Q

what does herpes simplex virus cause?

A

herpes simplex

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5
Q

what does varicella zoster virus cause?

A

herpes zoster - shingles

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6
Q

what is the pathogenesis of herpes simplex

A

vesicle formation - ulceration and release vesicle fluid containing infective particles

virus enter via sensory nerve endings and migrates along nerve to dorsal root ganglion

In latent infection viral DNA exists as “episomes” and no virus-coded proteins are present to stimulate an immune response

In reactivation it is believed that virus particles migrate outwards to sensory nerve endings and cause clinical manifestations of infection

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7
Q

what can trigger HSV reactivation

A

infection or stress - preceded by tingling

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8
Q

what is primary infection of HSV

A

in infant

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9
Q

what does HSV-2 cause?

A

genital herpes

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10
Q

what does HSV-1 cause ?

A

general herpes - ie in the mouth mainly

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11
Q

what is secondary infection of HSV

A

at all ages - peri-oral/genital (which can present as weeping & vesicular)

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12
Q

what is the diagnosis of HSV

A

clinical diagnosis or if difficult PCR for herpes virus DNA

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13
Q

what is coldsore

A

?

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14
Q

what is treatment of HS eg in cold sores, genital herpes, immunosuppressed patient

A

Cold sores
Topical acyclovir
Genital herpes, immunosuppressed patient
Oral acyclovir

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15
Q

what is the previous medical history of herpes zoster (shingles)

A

Previous chickenpox
“Latent” infection

Triggered by physical or emotional insult
Preceded by tingling and/or pain

Weeping, vesicular rash
Dermatomal distribution

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16
Q

what is the diagnosis of herpes zoster (shingles)

A

Weeping, vesicular rash

Dermatomal distribution

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17
Q

what is treatment of HZS

A

Oral acicolvir/valaciclovir
IV aciclovir
Depending on age of patient, immune status and severity of shingles

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18
Q

what is Molluscum contagiosum

A

not really troublism Causative agent

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19
Q

what is the clinical presentation of Molluscum contagiosum

A

Raised, pearly lesions up to 3 mm

Umbilicated

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20
Q

what is diagnosis of Molluscum contagiosum

A

clinical diagnosis

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21
Q

what is treatment of Molluscum contagiosum

A

None – lesions usually disappear in 6-18 months
Various topical preparations
Physical treatments (cryotyherapy, diathermy, laser therapy)

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22
Q

what is the general bacterial infection?

A

Causative agents
Mainly Staph. aureus and group A β-haemolytic streptococci (S. pyogenes)
A few others e.g. Haemophilus influenzae, Pasteurella multocida, enteric organisms and rarities

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23
Q

what is the feature of S. aureus

A

Gram-positive cocci in clusters, catalase-positive

Normal nasal flora in approx. 30% of pop’n

Exotoxin production

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24
Q

what type of Streptoccus pyogenes

A

haemolytic

Gram-positive cocci in chains, catalase-negative

Express many virulence factors

25
Q

where does impetigo normally infect?

A

epidermis -Often occurs at a site of skin damage

causative agent = S. aureus, S. pyogenes or both

26
Q

how does impetigo present clinically

A

Plaque-like lesions
Yellowish exudate
Thick scabs
“Honey crusted lesions”

27
Q

how can impetigo be diagnosised

A

clinical diagnosis, Bacterial culture

Sensitivity testing may be useful

28
Q

what are some of the complication of impetigo

A

Epidermolytic toxin production (ETA & ETB)

Manifestations -

Localised: Bullous impetigo

Generalised: Staphylococcal scalded skin syndrome (SSSS)

29
Q

where doe erysipelas firstly infected

A

dermis with causative agent - S. pyogenes

30
Q

how can erysipelas cause problem

A

Often occurs at a site of skin damage
Predominantly face or shin
Preceded by pain & tenderness

31
Q

what is the presentation of erysipelas

A
Examination
Fever & malaise
Well-demarcated inflamed lesion
Red, swollen, painful and hot
Lymph node enlargement
32
Q

what is the diagnosis of eryspielas

A

Clinical diagnosis

Culture rarely helpful

33
Q

where doe erysipelas firstly infected

A
Infection of skin and subcutaneous tissues
Causative agents include:
S. aureus
S. pyogenes
Pasteurella multocida (animal bites)
Haemophilus influenzae
34
Q

how will cellulitis present

A

Fever & malaise
Diffuse inflamed lesion
Erythema, swelling, tenderness, heat

35
Q

how can cellulitis enter the system

A

Site of skin penetration
Cut, graze, intravenous catheter, surgical instrument, bite (human or animal) etc.
Any part of body
Portal may not be apparent

36
Q

how can you distinguish cellulitis from other similar condition

A

cellulitis is not bilacteral

37
Q

diagnosis of cellulitis ?

A
  • Clinical diagnosis
  • Broad differential diagnosis
  • Microbiology
  • Lesion swabs
    Positive in 85% of cases
    Swab if lesion is ulcerated
  • Lesion aspirates and skin biopsy (Positive in 10-20% of cases, Not recommended routinely)
    Blood cultures (only Positive in only 2-4% of cases, Use if severe sepsis or systemic signs of infection)
38
Q

how can anthrax be acquired

A

Acquired from imported wool, hair and animal hides - Inoculation through breaks in the skin

39
Q

what organism can cause antrax

A

Bacillus anthracis - Spore-forming aerobic Gram-positive bacillus

40
Q

what is necrotising fasciitis

A

Infection of skin and subcutaneous tissues

41
Q

what is the causative organism of necrotising fasciitis

A

Type 1: Polymicrobial
Enteric Gram-negative bacilli
Anaerobes
Type 2: Streptococcus pyogenes

42
Q

how does necrotising fasciitis present

A

Spontaneous or at site of skin penetration
Any part of body
Fever & malaise
Dark, rapidly spreading, necrotic lesion

43
Q

what is the diagnosis of necrotising fasiitis

A

clinical diagnosis
Microscopy and culture
Debrided material
Blood culture - often +ve

44
Q

what is treatment of necrotising fasciitis

A

Intravenous antibiotics

Surgical debridement

45
Q

what is gas gangrene

A

caused by anaerobic infections

46
Q

what is clinical feature of gas gangrene

A

Clinically similar to “synergistic gangrene” (polymicrobial necrotising fasciitis)
Palpable subcutaneous gas

47
Q

when is gas gangrene normally arise

A

post-op eg amputation

48
Q

what is the organism of gas gangrene

A

Clostridium perfringens (anaerobic Gram-positive bacillus)

49
Q

treatment of gas gangrene

A

Intravenous antibiotics

Surgical debridement

50
Q

what are the 2 organisms which causes most of the infections of the skins and soft tissue

A

Staph. aureus or Strep. pyogenes

51
Q

what is the empiric therapy

A

Flucloxacillin

52
Q

what is special antibiotics that is used to treat necrotising fasciitis

A

need to cover anaerobes, Enterobacteriaceae, streptococci and staphylococci

Meropenem + clindamycin

53
Q

what is special antibiotics that is used to treat anaerobic infections

A

Include anti-anaerobic agents (e.g. metronidazole)

54
Q

where does fungal infection normally arise

A

dermatophyte infection

skin eg Tinea corporis, tinea pedis (athletes foot), tinea cruris

nail - Onychomycosis

Scalp - Tinea capitis (scalp ringworm, kerion)

55
Q

what are the common causative organism of dermatophyte infection

A

Dermatophyte fungi
Tricophyton spp. (e.g. T. rubrum)
Microsporum spp. (e.g. M. canis)

56
Q

how can you diagnosis of Dermatophyte infections

A

Skin scrapings - microscopy & culture

Exclude other conditions e.g. psoriasis

57
Q

what is the treatment of Dermatophyte infections

A

Topical or systemic antifungal agents

Depending on site & extent of infection

58
Q

what is the treatment for Dermatophyte infections

A

Skin infections
Topical antifungal therapy
Clotrimazole, terbinafine

Scalp and nail infections
Systemic antifungal therapy
Terbinafine, itraconazole, griseofulvin