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
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)
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
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
5
Q
What diseases can Streptococcus cause? (7)
A
- ecthyma
- impetigo
- cellulitis
- erysipelas
- scarlet fever
- necrotising fasciitis
- superinfects other dermatoses (e.g. leg ulcers)
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
7
Q
What is eosinophilic (non-infectious) folliculitis associated with?
A
HIV
8
Q
Why might recurrent cases of folliculitis arise?
A
From nasal carriage of Staphylococcus aureus, particularly strains expressing Panton-Valentine Leukocidin (PVL)
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)
10
Q
What features might you see in folliculitis? (2)
A
- furunculosis
- carbuncles
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
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
13
Q
What is Panton Valentine Leukocidin Staphylococcus Aureus?
A
A beta-pore forming exotoxin expressed by certain strains of S. aureus
14
Q
What pathophysiology does Panton Valentine Leukocidin Staphylococcus Aureus cause?
A
Leukocyte destruction and tissue necrosis
15
Q
What is Panton Valentine Leukocidin (PVL) Staphylococcus Aureus associated with?
A
Higher morbidity, mortality and transmissibility
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
17
Q
What are some extracutaneous manifestations of Panton Valentine Leukocidin (PVL) Staphylococcus Aureus? (3)
A
- necrotising pneumonia
- necrotising fasciitis
- purpura fulminans (systemic infection)
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
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
20
Q
What is pseudomonal folliculitis?
A
A bacterial infection of hair follicles after being exposed to contaminated water
21
Q
What is pseudomonal folliculitis caused by? (3)
A
- hot tub use
- swimming pools and depilatories
- wet suits
22
Q
When does pseudomonal folliculitis appear?
A
1-3 days after exposure, as a diffuse truncal eruption
23
Q
What are the symptoms of pseudomonal folliculitis? (2)
A
- follicular erythematous papule
- rarely - abscess, lymphangitis, fever
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)
25
What is the definition of cellulitis?
Infection of lower dermis and subcutaneous tissue
26
How does cellulitis manifest?
Tender swelling with ill-defined, blanching erythema or oedema
27
What bacteria cause most cases of cellulitis? (2)
- Staphylococcus aureus
- Streptococcus pyogenes
28
What is a predisposing factor for cellulitis?
Oedema
29
What is the treatment for cellulitis?
Systemic antibiotics
30
What is impetigo?
Superficial bacterial infection, stuck-on, honey-coloured crusts overlying an erosion
31
What bacteria can cause impetigo, and what kinds of impetigo do they cause? (2)
- Streptococci --> non-bullous (without blisters)
- Staphylococci --> bullous (with blisters) - caused by exfoliative toxins A&B that split the epidermis by targeting desmoglein I protein
32
What parts of the body does impetigo often affect?
Face - perioral, ears, nares (nostrils)
33
How do we treat impetigo?
Treated with topical +/- systemic antibiotics
34
What is impetiginisation?
Superficial infection or impetigo in the context of atopic dermatitis
| Impetigo = no atopic dermatitis
Impetiginisation = atopic dermatitis
35
What are the features of impetiginisation? (3)
- gold crust
- caused by S. aureus
- does not usually blister
36
What is the bacterial cause of syphilis?
Treponema pallidum
37
How does primary syphilis manifest?
- chancre - painless ulcer with firm indurated border
- painless regional lymphadenopathy 1 week after the primary chancre
- chancre happens within 10-90 days of infection
38
What happens in secondary syphilis?
- begins 50 days after chancre
- malaise, fever, headaches, pruritus, loss of appetite, iritis
- great mimicker and low threshold for testing
39
What symptoms does secondary syphilis have that means it can be confused for another disease? (7)
- rash (88-100%) - pityriasis rosea-like rash
- alopecia ('moth-eaten')
- mucous patches
- lymphadenopathy
- residual primary chancre
- condylomata lata (wart-like lesions)
- hepatosplenomegaly
40
What is lues maligna?
- rare manifestation of secondary syphilis
- pleomorphic skin lesions with pustules, nodules and ulcers with necrotising vasculitis
- haemorrhagic crust
- more frequent in HIV manifestation
41
What happens in tertiary syphilis? (2)
- 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
42
What two diseases can you develop with tertiary syphilis? (2)
- cardiovascular disease
- neurosyphilis (general paresis or tabes dorsalis)
43
How do we diagnose syphilis? (3)
- clinical findings - main way
- serology - helps
- strong index of suspicion is required in secondary syphilis
44
How do we treat syphilis?
IM benzylpenicillin or oral tetracycline (if allergic to penicillin)
45
What is borreliosis (Lyme disease)?
Annular (ring-like) erythema develops at site of the bite of a Borrelia burgdorferi-infected Ixodes tick
46
How does borreliosis (Lyme disease) manifest?
- 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
What are some complications of borreliosis (Lyme disease)? (3)
- neuroborreliosis:
- facial palsy / other CN palsies
- aseptic meningitis
- polyradiculitis
- arthritis - painful and swollen large joints (knee most affected joint)
- carditis
48
How do we detect borreliosis (Lyme disease)?
- serology not sensitive
- histopathology non-specific
- high index of suspicion required for diagnosis, with basis of clinical features
49
What does herpes simplex virus cause?
Primary and recurrent vesicular eruptions
50
What body areas does herpes simplex virus favour?
Orolabial (mouth) and genital regions
51
When can transmission of herpes simplex virus occur?
Transmission can occur even during asymptomatic periods of viral shedding
52
How is HSV-1 typically spread?
Direct contact with contaminated saliva/other infected secretions
53
How is HSV-2 typically spread?
Sexual contact
54
Where does herpes simplex virus travel from site of infection?
- 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
Describe the symptoms of herpes simplex virus and how they progress.
- 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
What are the orolabial (mouth) vs genital manifestations of HSV like?
- orolabial lesions are often asymptomatic
- genital involvement is often excruciatingly painful and can lead to urinary retention
57
What is the main systemic manifestation of HSV?
Aseptic meningitis in up to 10% of patients
58
What factors can cause reactivation (flares) of HSV? (5)
- spontaneous
- UV
- fever
- local tissue damage
- stress
59
What is a HSV emergency and when does it occur?
Eczema herpeticum that occurs in patients with atopic eczema
60
How does eczema herpeticum manifest?
Monomorphic, punched out erosions (excoriated vesicles)
61
Why is eczema herpeticum an emergency?
Can lead to HSV encephalitis which is fatal
62
How do we treat eczema herpeticum?
IV acyclovir (antiviral) accompanied with antibiotic for superinfections with S. aureus or Strep
63
When does neonatal HSV arise?
Exposure to HSV-1 or 2 during vaginal delivery - risk higher when HSV acquired near time of delivery
64
What time range can neonatal HSV manifest in?
Onset from birth to 2 weeks
65
Where do we see neonatal HSV on the body?
Usually localised to scalp or trunk
66
What does neonatal HSV manifest as?
Vesicles or bullae erosions (blisters)
| Localised to scalp/trunk
67
What treatment does neonatal HSV require?
IV antivirals
68
What can neonatal HSV cause which is a problem?
- encephalitis --> mortality >50% without treatment, 15% with treatment
- can leave neurological deficits
69
How can HSV manifest in immunocompromised patients (e.g. HIV / transplant recipient)?
Chronic enlarging ulcerations or erosions, multiple sites or disseminated
70
What are some atypical manifestations of HSV in immunocompromised patients? (3)
- verrucous lesions
- exophytic lesions
- pustular lesions
71
What else can HSV in immunocompromised patients involve apart from the skin?
Respiratory or GI tract involvement may occur
72
How do we diagnose HSV?
Swab for polymerase chain reaction
73
How do we treat HSV? (3)
- 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
How can fungal infections be classified? (5)
- superficial
- deep/soft tissue
- disseminated
- systemic
- opportunistic
75
What are some deep/soft tissue fungal infections? (2)
- chromomycosis
- Madura foot
75
What are some superficial fungal infections? (3)
- candida
- malassezia
- dermatophytes
76
What are some disseminated fungal infections? (7)
- **candida**
- **aspergillus**
- fusarium
- histoplasma
- coccidiodes
- blastomycosis
- mucormycosis
77
How does pityriasis versicolor manifest?
Hypopigmented, hyperpigmented or erythematous macular eruption +/- fine scale
78
What fungus causes pityriasis versicolor?
Malassezia spp.
79
How does pityriasis versicolor develop and flare?
- begins during adolescence (when sebaceous glands become active)
- flares when temperatures and humidity are high and when there is immunosuppression
80
How do we treat pityriasis versicolor?
Topical azole
81
What are dermatophytes?
| Superficial fungal infections
Fungi that live on keratin on our skin
82
What causes the most fungal infections?
| Dermatophytes - Superficial fungal infections
Trichophyton rubrum
83
What fungus causes the most tinea capitis (fungal rash of the scalp)?
| Dermatophytes - Superficial fungal infections
Trichophyton tonsurans
84
What is kerion?
- 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
What are some manifestations of dermatophyte infections? (4)
- 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
What are Id reactions?
| Superficial fungal infections
- AKA dermatophytid reactions
- inflammatory reactions at sites distant from the associated dermatophyte infection - primary infection can be anywhere
87
What types of reactions can Id reactions include? (3)
- urticaria
- hand dermatitis
- erythema nodosum
88
What are Id reactions likely secondary to?
A strong host immunological response against fungal antigens
89
Which fungus is candidiasis caused by?
| Superficial fungal infections
Candida albicans
90
What is candidiasis predisposed by? (4)
- occlusion
- moisture
- warm temperature
- diabetes mellitus
91
How does candidiasis manifest? (3)
- erythema
- oedema
- thin purulent discharge
92
What locations does candidiasis usually affect?
- usually an intertriginous infection (skin folds) e.g. axillae, submammary folds, crurae, digital clefts
- can affect oral mucosa
93
What is candidiasis a common cause of?
Vulvovaginitis
94
What can happen in candidiasis in the context of immunocompromisation?
Can become systemic
95
What kind of fungal infection is mucormycosis?
| Just be aware of
Opportunistic fungal infection
(+ Disseminated)
96
How does mucormycosis present?
- oedema, then pain, then eschar
- fever
- headache
- proptosis (exophthalmos)
- facial pain
- orbital cellulitis
- +/-cranial nerve dysfunction
97
What fungi can cause mucormycosis? (Do not need to know)
- Apophysomyces
- Mucor
- Rhizopus
- Absidia
- Rhizomucor
98
What is mucormycosis associated with? (7)
- diabetes mellitus (1/3 of patients, DKA is a very high risk)
- malnutrition
- uraemia
- neutropenia
- medications - steroids, Abx, desferoxamine
- burns
- HIV
99
How do we treat mucormycosis?
Aggressive debridement and antifungal therapy (amphoteracin)
100
What level of suspicion do we need for mucormycosis and why?
High index of suspicion because culture positive in only 30% of cases
101
What is scabies?
| Parasitic infections
Contagious infestation caused by Sarcoptes species
102
How does scabies develop?
Female mates, burrows into upper epidermis, lays her eggs then dies after one month
103
How does scabies manifest?
- insidious onset of red to flesh-coloured pruritic papules
- affects interdigital areas of digits, volar wrists, axillary areas and genitalia
104
What is often seen diagnostically in scabies?
A diagnostic burrow consisting of fine white scale (using dermatoscope)
105
What is Norwegian scabies?
- crusted/scaly scabies - hyperkeratosis
- often asymptomatic - found in immunocompromised individuals
106
How do we treat scabies?
- 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
