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Year 2 - BRS > 7.3 - Infections and infestations of the skin > Flashcards

7.3 - Infections and infestations of the skin Flashcards

1
Q

What virulence factors does Staphylococcus aureus have that confer pathogenic properties?

A

Receptors that allow it to bind fibrin which is found in abundance in wound surfaces and dermatitis

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2
Q

What diseases can Staphylococcus aureus cause? (6)

A
  • ecthyma
  • impetigo
  • cellulitis
  • folliculitis (furunculosis, carbuncles)
  • staphylococcal scalded skin syndrome (SSSS)
  • superinfects other dermatoses (e.g. atopic eczema, HSV, leg ulcers)
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3
Q

How does Streptococcus pyogenes bind to epithelial surfaces?

A

Streptococcus pyogenes (beta-haemolytic) attaches to epithelial surfaces via lipoteichoic acid portion of fimbriae

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4
Q

What contributes to the virulence of Streptococcus? (3)

A
  • has M protein (anti-phagocytic) and hyaluronic acid capsule
  • produces erythrogenic exotoxins
  • produces streptolysins S and O
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5
Q

What diseases can Streptococcus cause? (7)

A
  • ecthyma
  • impetigo
  • cellulitis
  • erysipelas
  • scarlet fever
  • necrotising fasciitis
  • superinfects other dermatoses (e.g. leg ulcers)
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6
Q

What is folliculitis?

A
  • follicular erythema (redness and inflammation of hair follicles) - sometimes pustular (bulging patch of skin filled with pus)
  • may be infectious or non-infectious
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7
Q

What is eosinophilic (non-infectious) folliculitis associated with?

A

HIV

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8
Q

Why might recurrent cases of folliculitis arise?

A

From nasal carriage of Staphylococcus aureus, particularly strains expressing Panton-Valentine Leukocidin (PVL)

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9
Q

What is the treatment for folliculitis? (2)

A
  • antibiotics (usually flucloxacillin or erythromycin)
  • incision and drainage required for furunculosis (deep follicular abscess formation with pus and necrotic tissue in hair follicle)
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10
Q

What features might you see in folliculitis? (2)

A
  • furunculosis
  • carbuncles
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11
Q

What is the difference between furuncles and carbuncles?

A
  • furuncle - deep follicular abscess
  • carbuncle - collection of furuncles involving adjacent connected hair follicles
  • carbuncles are more likely to lead to complications like cellulitis and septicaemia
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12
Q

Why do some patients develop recurrent staphylococcal impetigo or recurrent furunculosis?

A
  • S. aureus establishes itself as part of the resident microbial flora - abundant in nasal flora
  • patients may have form of immune deficiency:
    • hypogammaglobulinaemia
    • hyperIgE syndrome - deficiency
    • chronic granulomatous disease
    • AIDS (/advanced HIV)
    • diabetes mellitus
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13
Q

What is Panton Valentine Leukocidin Staphylococcus Aureus?

A

A beta-pore forming exotoxin expressed by certain strains of S. aureus

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14
Q

What pathophysiology does Panton Valentine Leukocidin Staphylococcus Aureus cause?

A

Leukocyte destruction and tissue necrosis

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15
Q

What is Panton Valentine Leukocidin (PVL) Staphylococcus Aureus associated with?

A

Higher morbidity, mortality and transmissibility

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16
Q

What are some skin manifestations of Panton Valentine Leukocidin (PVL) Staphylococcus Aureus? (3 + 1)

A
  • recurrent and painful abscesses
  • folliculitis
  • cellulitis

Often painful, more than 1 site, recurrent, present in contacts

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17
Q

What are some extracutaneous manifestations of Panton Valentine Leukocidin (PVL) Staphylococcus Aureus? (3)

A
  • necrotising pneumonia
  • necrotising fasciitis
  • purpura fulminans (systemic infection)
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18
Q

What are the 5Cs of acquiring PVL S. aureus?

A
  • close contact - e.g. hugging, contact sports
  • contaminated items - e.g. gym equipment, towels, razors
  • crowding - crowded living conditions e.g. military accommodation, prisons, boarding schools
  • cleanliness - of environment
  • cuts and grazes - allow bacteria to enter the body
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19
Q

What are the treatments for PVL S. aureus? (4)

A
  • consult local microbiologist and guidelines
  • antibiotics (often tetracycline)
  • decolonisation often occurs to eradicate strain e.g:
    • chlorhexidine body wash for 7 days
    • nasal application of mupirocin ointment for 5 days
  • treatment of close contacts
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20
Q

What is pseudomonal folliculitis?

A

A bacterial infection of hair follicles after being exposed to contaminated water

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21
Q

What is pseudomonal folliculitis caused by? (3)

A
  • hot tub use
  • swimming pools and depilatories
  • wet suits
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22
Q

When does pseudomonal folliculitis appear?

A

1-3 days after exposure, as a diffuse truncal eruption

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23
Q

What are the symptoms of pseudomonal folliculitis? (2)

A
  • follicular erythematous papule
  • rarely - abscess, lymphangitis, fever
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24
Q

What is the treatment for pseudomonal folliculitis? (2)

A
  • most cases are self-limited and no treatment is required
  • severe or recurrent cases can be treated with oral ciprofloxacin (antibiotic)
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25
Q

What is the definition of cellulitis?

A

Infection of lower dermis and subcutaneous tissue

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26
Q

How does cellulitis manifest?

A

Tender swelling with ill-defined, blanching erythema or oedema

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27
Q

What bacteria cause most cases of cellulitis? (2)

A
  • Staphylococcus aureus
  • Streptococcus pyogenes
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28
Q

What is a predisposing factor for cellulitis?

A

Oedema

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29
Q

What is the treatment for cellulitis?

A

Systemic antibiotics

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30
Q

What is impetigo?

A

Superficial bacterial infection, stuck-on, honey-coloured crusts overlying an erosion

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31
Q

What bacteria can cause impetigo, and what kinds of impetigo do they cause? (2)

A
  • Streptococci –> non-bullous (without blisters)
  • Staphylococci –> bullous (with blisters) - caused by exfoliative toxins A&B that split the epidermis by targeting desmoglein I protein
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32
Q

What parts of the body does impetigo often affect?

A

Face - perioral, ears, nares (nostrils)

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33
Q

How do we treat impetigo?

A

Treated with topical +/- systemic antibiotics

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34
Q

What is impetiginisation?

A

Superficial infection or impetigo in the context of atopic dermatitis

Impetigo = no atopic dermatitis
Impetiginisation = atopic dermatitis

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35
Q

What are the features of impetiginisation? (3)

A
  • gold crust
  • caused by S. aureus
  • does not usually blister
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36
Q

What is the bacterial cause of syphilis?

A

Treponema pallidum

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37
Q

How does primary syphilis manifest?

A
  • chancre - painless ulcer with firm indurated border
  • painless regional lymphadenopathy 1 week after the primary chancre
  • chancre happens within 10-90 days of infection
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38
Q

What happens in secondary syphilis?

A
  • begins 50 days after chancre
  • malaise, fever, headaches, pruritus, loss of appetite, iritis
  • great mimicker and low threshold for testing
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39
Q

What symptoms does secondary syphilis have that means it can be confused for another disease? (7)

A
  • rash (88-100%) - pityriasis rosea-like rash
  • alopecia (‘moth-eaten’)
  • mucous patches
  • lymphadenopathy
  • residual primary chancre
  • condylomata lata (wart-like lesions)
  • hepatosplenomegaly
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40
Q

What is lues maligna?

A
  • rare manifestation of secondary syphilis
  • pleomorphic skin lesions with pustules, nodules and ulcers with necrotising vasculitis
  • haemorrhagic crust
  • more frequent in HIV manifestation
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41
Q

What happens in tertiary syphilis? (2)

A
  • gumma skin lesions - nodules and plaques that extend peripherally while central areas heal with scarring and atrophy
  • mucosal lesions extend to and destroy the nasal cartilage
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42
Q

What two diseases can you develop with tertiary syphilis? (2)

A
  • cardiovascular disease
  • neurosyphilis (general paresis or tabes dorsalis)
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43
Q

How do we diagnose syphilis? (3)

A
  • clinical findings - main way
  • serology - helps
  • strong index of suspicion is required in secondary syphilis
44
Q

How do we treat syphilis?

A

IM benzylpenicillin or oral tetracycline (if allergic to penicillin)

45
Q

What is borreliosis (Lyme disease)?

A

Annular (ring-like) erythema develops at site of the bite of a Borrelia burgdorferi-infected Ixodes tick

46
Q

How does borreliosis (Lyme disease) manifest?

A
  • initial cutaneous manifestation of erythema migrans (erythematous papule at the bite site) in 75% of patients which progresses to annular erythema of >20cm
  • 1-30 days after infection, fever and headache occurs
  • multiple secondary lesions develop - similar but smaller to initial lesion
47
Q

What are some complications of borreliosis (Lyme disease)? (3)

A
  • neuroborreliosis:
    • facial palsy / other CN palsies
    • aseptic meningitis
    • polyradiculitis
  • arthritis - painful and swollen large joints (knee most affected joint)
  • carditis
48
Q

How do we detect borreliosis (Lyme disease)?

A
  • serology not sensitive
  • histopathology non-specific
  • high index of suspicion required for diagnosis, with basis of clinical features
49
Q

What does herpes simplex virus cause?

A

Primary and recurrent vesicular eruptions

50
Q

What body areas does herpes simplex virus favour?

A

Orolabial (mouth) and genital regions

51
Q

When can transmission of herpes simplex virus occur?

A

Transmission can occur even during asymptomatic periods of viral shedding

52
Q

How is HSV-1 typically spread?

A

Direct contact with contaminated saliva/other infected secretions

53
Q

How is HSV-2 typically spread?

A

Sexual contact

54
Q

Where does herpes simplex virus travel from site of infection?

A
  • replicates at mucocutaneous site of infection
  • travels by retrograde axonal flow to dorsal root ganglia where it stays latent between flares
  • can travel back via anterograde flow –> recurrent flares
55
Q

Describe the symptoms of herpes simplex virus and how they progress.

A
  • symptoms occur within 3-7 days of exposure
  • preceded by tender lymphadenopathy, malaise, anorexia +/- burning/tingling
  • then painful, grouped vesicles on erythematous base develop
  • these develop into ulcerations/pustules/erosions with a scalloped border
  • crusting and resolution within 2-6 weeks
56
Q

What are the orolabial (mouth) vs genital manifestations of HSV like?

A
  • orolabial lesions are often asymptomatic
  • genital involvement is often excruciatingly painful and can lead to urinary retention
57
Q

What is the main systemic manifestation of HSV?

A

Aseptic meningitis in up to 10% of patients

58
Q

What factors can cause reactivation (flares) of HSV? (5)

A
  • spontaneous
  • UV
  • fever
  • local tissue damage
  • stress
59
Q

What is a HSV emergency and when does it occur?

A

Eczema herpeticum that occurs in patients with atopic eczema

60
Q

How does eczema herpeticum manifest?

A

Monomorphic, punched out erosions (excoriated vesicles)

61
Q

Why is eczema herpeticum an emergency?

A

Can lead to HSV encephalitis which is fatal

62
Q

How do we treat eczema herpeticum?

A

IV acyclovir (antiviral) accompanied with antibiotic for superinfections with S. aureus or Strep

63
Q

When does neonatal HSV arise?

A

Exposure to HSV-1 or 2 during vaginal delivery - risk higher when HSV acquired near time of delivery

64
Q

What time range can neonatal HSV manifest in?

A

Onset from birth to 2 weeks

65
Q

Where do we see neonatal HSV on the body?

A

Usually localised to scalp or trunk

66
Q

What does neonatal HSV manifest as?

A

Vesicles or bullae erosions (blisters)

Localised to scalp/trunk

67
Q

What treatment does neonatal HSV require?

A

IV antivirals

68
Q

What can neonatal HSV cause which is a problem?

A
  • encephalitis –> mortality >50% without treatment, 15% with treatment
  • can leave neurological deficits
69
Q

How can HSV manifest in immunocompromised patients (e.g. HIV / transplant recipient)?

A

Chronic enlarging ulcerations or erosions, multiple sites or disseminated

70
Q

What are some atypical manifestations of HSV in immunocompromised patients? (3)

A
  • verrucous lesions
  • exophytic lesions
  • pustular lesions
71
Q

What else can HSV in immunocompromised patients involve apart from the skin?

A

Respiratory or GI tract involvement may occur

72
Q

How do we diagnose HSV?

A

Swab for polymerase chain reaction

73
Q

How do we treat HSV? (3)

A
  • do not delay - PCR can take weeks to get back
  • oral valacyclovir or acyclovir 200mg 5x daily in immunocompetent localised infection
  • IV 10mg/kg TDS X 7-19 days
74
Q

How can fungal infections be classified? (5)

A
  • superficial
  • deep/soft tissue
  • disseminated
  • systemic
  • opportunistic
75
Q

What are some deep/soft tissue fungal infections? (2)

A
  • chromomycosis
  • Madura foot
75
Q

What are some superficial fungal infections? (3)

A
  • candida
  • malassezia
  • dermatophytes
76
Q

What are some disseminated fungal infections? (7)

A
  • candida
  • aspergillus
  • fusarium
  • histoplasma
  • coccidiodes
  • blastomycosis
  • mucormycosis
77
Q

How does pityriasis versicolor manifest?

A

Hypopigmented, hyperpigmented or erythematous macular eruption +/- fine scale

78
Q

What fungus causes pityriasis versicolor?

A

Malassezia spp.

79
Q

How does pityriasis versicolor develop and flare?

A
  • begins during adolescence (when sebaceous glands become active)
  • flares when temperatures and humidity are high and when there is immunosuppression
80
Q

How do we treat pityriasis versicolor?

A

Topical azole

81
Q

What are dermatophytes?

Superficial fungal infections

A

Fungi that live on keratin on our skin

82
Q

What causes the most fungal infections?

Dermatophytes - Superficial fungal infections

A

Trichophyton rubrum

83
Q

What fungus causes the most tinea capitis (fungal rash of the scalp)?

Dermatophytes - Superficial fungal infections

A

Trichophyton tonsurans

84
Q

What is kerion?

A
  • an inflammatory fungal infection that may mimic a bacterial folliculitis or a scalp abscess
  • scalp is tender and patient usually has posterior cervical lymphadenopathy
  • frequently secondarily infected with Staphylococcus aureus
85
Q

What are some manifestations of dermatophyte infections? (4)

A
  • kerion formation due to T. tonsurans
  • maceration between third and fourth toes in the interdigital form
  • onychomycosis
  • tinea pedis (fungal rash of the feet) - diffuse scaling
86
Q

What are Id reactions?

Superficial fungal infections

A
  • AKA dermatophytid reactions
  • inflammatory reactions at sites distant from the associated dermatophyte infection - primary infection can be anywhere
87
Q

What types of reactions can Id reactions include? (3)

A
  • urticaria
  • hand dermatitis
  • erythema nodosum
88
Q

What are Id reactions likely secondary to?

A

A strong host immunological response against fungal antigens

89
Q

Which fungus is candidiasis caused by?

Superficial fungal infections

A

Candida albicans

90
Q

What is candidiasis predisposed by? (4)

A
  • occlusion
  • moisture
  • warm temperature
  • diabetes mellitus
91
Q

How does candidiasis manifest? (3)

A
  • erythema
  • oedema
  • thin purulent discharge
92
Q

What locations does candidiasis usually affect?

A
  • usually an intertriginous infection (skin folds) e.g. axillae, submammary folds, crurae, digital clefts
  • can affect oral mucosa
93
Q

What is candidiasis a common cause of?

A

Vulvovaginitis

94
Q

What can happen in candidiasis in the context of immunocompromisation?

A

Can become systemic

95
Q

What kind of fungal infection is mucormycosis?

Just be aware of

A

Opportunistic fungal infection
(+ Disseminated)

96
Q

How does mucormycosis present?

A
  • oedema, then pain, then eschar
  • fever
  • headache
  • proptosis (exophthalmos)
  • facial pain
  • orbital cellulitis
  • +/-cranial nerve dysfunction
97
Q

What fungi can cause mucormycosis? (Do not need to know)

A
  • Apophysomyces
  • Mucor
  • Rhizopus
  • Absidia
  • Rhizomucor
98
Q

What is mucormycosis associated with? (7)

A
  • diabetes mellitus (1/3 of patients, DKA is a very high risk)
  • malnutrition
  • uraemia
  • neutropenia
  • medications - steroids, Abx, desferoxamine
  • burns
  • HIV
99
Q

How do we treat mucormycosis?

A

Aggressive debridement and antifungal therapy (amphoteracin)

100
Q

What level of suspicion do we need for mucormycosis and why?

A

High index of suspicion because culture positive in only 30% of cases

101
Q

What is scabies?

Parasitic infections

A

Contagious infestation caused by Sarcoptes species

102
Q

How does scabies develop?

A

Female mates, burrows into upper epidermis, lays her eggs then dies after one month

103
Q

How does scabies manifest?

A
  • insidious onset of red to flesh-coloured pruritic papules
  • affects interdigital areas of digits, volar wrists, axillary areas and genitalia
104
Q

What is often seen diagnostically in scabies?

A

A diagnostic burrow consisting of fine white scale (using dermatoscope)

105
Q

What is Norwegian scabies?

A
  • crusted/scaly scabies - hyperkeratosis
  • often asymptomatic - found in immunocompromised individuals
106
Q

How do we treat scabies?

A
  • permethrin, oral ivermectin
  • two cycles of treatment are required (eggs are not necessarily vulnerable to treatments so we need to kill what has hatched)
  • close contacts need treatment too

Year 2 - BRS (84 decks)

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