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brs (phase 1b) > (derm) infections & infestations of the skin > Flashcards

(derm) infections & infestations of the skin Flashcards

1
Q

why does staphylococcus aureus have pathogenic properties?

A

has virulence factors on its surface that confer its pathogenic properties

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2
Q

what can staphylococcus aureus cause?

A

folliculitis (furunculosis, carbuncles)

impetigo

cellulitis

ecthyma

SSSS (staphylococcal scalded skin syndrome)

(can also superinfect other dermatoses, causing leg ulcers etc)

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3
Q

why is streptococcus virulent?

A
  • binds to epithelial surfaces via the lipotechoic acid portion of their fimbrae
  • M protein & hyaluronic acid capsule confer anti-phagocytic properties
  • produce erythrogenic exotoxins (streptolysins S + O) to damage host cells
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4
Q

what can streptococcus cause?

A

impetigo
cellulitis
ecthyma

scarlet fever
erysipelas
necrotising fasciitis

(can also superinfect other dermatoses, causing leg ulcers etc)

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5
Q

how does bacterial folliculitis manifest?

A

follicular erythema, can be pustular

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6
Q

what are the two types of folliculitis?

A

infectious & non-infectious

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7
Q

give an example of non-infectious folliculitis and name the disease it is associated to

A

eosinophilic folliculitis

= seen in HIV

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8
Q

what causes recurent cases of S.aureus?

A

nasal carriage of S.aureus, particular strains expressing Panton-Valentine leukocidin (PVL)

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9
Q

how is folliculitis treated?

A

antibiotics (after C&S, erythromycin or flucloxacillin)

incision + drainage (for furunculosis)

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10
Q

what is a furuncle?

A

a singular deep follicular abscess of pus and necrotic tissue

(of the hair follicle)

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11
Q

what is a carbuncle?

A

form when furuncles develop in adjacent, connected hair follicles

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12
Q

differentiate between furuncles and carbuncles

A

furuncles = singular follicular abscess of pus and necrotic tissue

carbuncles = adjacent connected furuncles

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13
Q

which of the two are more likely to lead to complications such as cellulitis and septicaemia: furuncles or carbuncles?

A

carbuncles

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14
Q

what is furunculosis and how is it treated?

A

development of furuncles in hair follicles

= follicular abscesses filled with pus and necrotic tissue

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15
Q

which bacterial infection can cause furunculosis?

A

Staphylococcus aureus

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16
Q

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

A

1) S.aureus establishes itself as part of the resident microbial flora (e.g. abundant in nasal flora)

2) immune deficiency
- hypogammaglobulinaemia
- hyper IgE syndrome
- chronic granulomatous disease
- AIDS
- diabetes mellitus

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17
Q

what are possible causes of immune deficiency?

A
  • hypogammaglobulinaemia
  • hyper IgE syndrome
  • chronic granulomatous disease
  • AIDS
  • diabetes mellitus
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18
Q

what is Panton Valentine Leukocidin S.aureus?

A

β-pore-forming exotoxin

= a strain of S.aureus with the PVL virulence factoe

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19
Q

what does PVL S.aureus cause in the host?

A

leukocyte destruction and tissue necrosis

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20
Q

why is PVL S.aureus more dangerous?

A

higher morbidity, mortality and transmissibility

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21
Q

what are the cutaneous manifestations of PVL S.aureus?

A
  • folliculitis
  • cellulitis
  • recurrent and painful abscesses
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22
Q

what are the extracutaneous manifestations of PVL S.aureus?

A

necrotising fasciitis
necrotising pneumonia
purpura fulminans

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23
Q

what are the risk factors of PVL S.aureus?

A 
close contact
contaminated items
(un)cleanliness
crowding
cuts & grazes

(5 Cs)

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24
Q

how is PVL S.aureus treated?

A

1) consult local microbiologist/guidelines
2) antibiotic (usually tetracycline)

3) decolonisation
- chlorhexidine body wash for 7 days
- nasal mupirocin ointment for 5 days

4) treatment of close contacts

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25
Q

which antibiotic is used to treat PVL S.aureus?

A

usually tetracycline

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26
Q

how is PVL S.aureus often decolonised?

A

1) chlorhexidine body wash for 7 days

2) nasal mupirocin ointment for 5 days

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27
Q

what is pseudomonal folliculitis?

A

diffuse truncal eruption of follicular erythematous papules

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28
Q

how does psudomonal folliculitis manifest?

A

follicular erythematous papules in a diffuse truncal eruption approx 1-3 days after exposure

(rarely also as abscess, lymphangitis, fever)

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29
Q

what causes pseudomonal folliculitis?

A

hot tub/swimming pool use, wet suit sharing, depilatories

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30
Q

how is pseudomomal folliculitis treated?

A

usually self-limiting so does not require treatment
BUT
severe, recurrent cases = oral ciprofloxacin

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31
Q

what is cellulitis?

A

infection of the lower dermin and subcutaneous tissue resulting in blanching erythema and oedema

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32
Q

what does cellulitis often present with?

A

blanching erythema and oedema

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33
Q

what is the causative agent in cellulitis?

A

usually S.aureus and S.pyogenes

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34
Q

how is cellulitis treated?

A

systemic antibiotics

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35
Q

what is impetigo?

A

superficial bacterial infection

w honey-coloured crusts stuck onto the region overlying an erosion

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36
Q

how does impetigo manifest?

A

honey-coloured crusts stuck onto the region overlying an erosion

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37
Q

what are the two main causes of impetigo?

A

streptococcus

staphylococcus

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38
Q

what are the two types of impetigo and what are they caused by?

A

non-bullous impetigo caused by streptococci

bullous impetigo caused by staphylococci

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39
Q

why do staphylococci cause bullous impetigo?

A

staphylococci produce exofoliative toxins A & B
= target desmoglein I and split the epidermis
= bullous impetigo (blister formation)

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40
Q

which body regions are affected most commonly by impetigo?

A

face

perioral, nostrils, ears

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41
Q

how is impetigo treated?

A

topical or systemic antibiotics

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42
Q

what is impetiginisation?

A

impetigo in the context of atopic dermatitis

  • also caused by S.aureus (but does not blister as usual)
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43
Q

what is the causative factor for impetiginisation?

A

S. aureus

would expect bullous impetigo but does not blister in this case

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44
Q

what is ecthyma?

A

severe form of streptococcal non-bullous impetigo

= thick crust overlying ulceration surrounded by erythema

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45
Q

how does ecythma present?

A

thick crust overlying an ulceration surrounded by erythema

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46
Q

what is ecthyma surrounded by usually?

A

erythema

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47
Q

where does ecthyma usually present?

A

lower extremities

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48
Q

what is staphylococcal scalded skin syndrome?

A

a staphylococcus infection that causes red blistering skin that looks like a burn or scald

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49
Q

which group of people are most commonly affected by SSSS?

A

neonates, infants and immunocompromised people

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50
Q

what causes SSSS?

where else is this causative agent seen?

A

the same exfoliative toxin produced by staphylococcus that causes bullous impetigo

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51
Q

why can the causative organism not be cultured from the denuded skin in SSSS?

A

in SSSS, the infection occurs at a different, distant site to the cutaneous manifestation

= organism cannot be collected and cultured from the site of rash and redness

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52
Q

why does SSSS affect neonates most commonly?

A

neonates are unable to efficiently excrete the staphylococcal exfoliative toxin via their kidneys

= builds up
= causes SSSS

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53
Q

how does SSSS manifest?

A

tender erythema
= progresses to flaccid bullae
= wrinkle & exfoliate + erythematous base

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54
Q

which dermatological condition does SSSS clinically resemble?

A

SJS-TEN

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55
Q

what causes erythrasma?

A

bacterial infection of Corynebacterium minutissimum

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56
Q

how does erythrasma manifest?

A

well-demarcated patches in intertriginous areas that are initially pink but become pigmented, brown and scaly

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57
Q

which body regions are most affected by erythrasma?

A

intertriginous areas e.g. armpit

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58
Q

differentiate between the following: erythrasma, ecthyma and erythema

A

erythrasma = well-demarcated, brown plaques that form in intertrigionous areas due to Corynebacteria

ecthyma = severe form of streptococcus impetigo with thick crust overlying ulceration

erythema = extensive red rash

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59
Q

what is pitted keratolysis?

A

bacterial infection of the soled of the feet that presents with pitted erosions

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60
Q

how does pitted keratolysis appear?

A

pitted erosions of the soles of the feet

= macerated/wet appearance

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61
Q

what is pitted keratolysis often misdiagnosed as?

A

athlete’s foot

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62
Q

what causes pitted keratolysis?

A

caused by Corynebacteria

like erythrasma

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63
Q

how are pitted keratolysis AND erythrasma treated?

A

topical clindamycin

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64
Q

why are both pitted keratolysis and erythrasma treated with topical clindamycin?

A

both have the same causative agent: Corynebacteria (minutissimum)

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65
Q

what is toxic shock syndrome?

A

febrile illness cause by S.aureus

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66
Q

what is the causative agent for toxic shock syndrome?

A

S.aureus that produces the pyrogenic TSST-1 exotoxin

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67
Q

what are the symptoms of toxic shock syndrome?

A

fever

hypotension

diffuse erythema (can affect mucous membranes)

thrombocytopenia

desquamation of palms and soles

affects other body systems

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68
Q

which body systems are affected in toxic shock syndrome?

A 
gastrointestinal system
renal
hepatic
CNS
muscular
69
Q

which haematological finding is most commonly observed in toxic shock syndrome?

A

thrombocytopenia

70
Q

once the erythema of TSS resolves, what happens to the palms and soles?

A

desquamation usually following 1-2 weeks after resolution of erythema

71
Q

what is erysipeloid?

A

erythema and oedema of the hands that extends slowly over weeks

72
Q

what causes erysipeloid?

A

caused by handling raw fish and raw meat

erysipelothrix rhusiopathiae

73
Q

what are the two main manifestations of anthrax?

A

painless, necrotic ulcer with surrounding ulcer

painful lymphadenopathy

74
Q

what can cause anthrax?

A

at the site of contact w hides, bone meal or wool infected with Bacillus anthracis

75
Q

what are the causative agents for blistering distal dactylitis?

A

rare infection caused by Streptococcus pyogenes or Staphylococcus aureus

76
Q

how does blistering distal dactylitis present?

A

presents w 1 or more superficial bullae/blisters on the fat pads of the fingers

rarely affects toes

77
Q

who is most affected by blistering distal dactylitis?

A

young children

78
Q

what is erysipelas?

A

infection of the deep dermis that manifests as an erythematous, well-defined plaque and systemic symptoms

79
Q

what causes erysipelas?

A

streptococcus, S.aureus

80
Q

how does erysipelas present?

A

well-defined, inundated erythematous plaque with a cliff-edge border

systemic symptoms (fever, malaise = prodrome)

lymphangitis, lymphadenopathy

81
Q

which condition does erysipelas resemble?

A

cellulitis

= also presents w erythematous plaque but is not as well defined as in erysipelas

82
Q

how is erysipelas treated?

A

intravenous antibiotics

83
Q

what is characteristic of the erysipelas plaque?

A

cliff-edge border

84
Q

in which group does scarlet fever present most commonly?

A

young children

85
Q

what are the symptoms of scarlet fever?

A

fever, malaise, chills, headache

12-48 hours after = cutaneous manifestations

86
Q

what is the causative agent of scarlet fever?

A

streptococcus pyogenes

87
Q

what are the cutaneous manifestations of scarlet fever?

A

pink spots over the face, axilla, and eventually over the body

= have a sandpaper-like texture

88
Q

what are the possible complications of scarlet fever?

A

otitis, mastoiditis, sinusitis, pneumonia, myocarditis, hepatitis, meningitis, rheumatic fever, acute glomerulonephritis

89
Q

how does necrotising fasciitis present?

A

initial dusky induration

then necrosis of the skin, connective tissue and muscle

90
Q

how is necrotising fasciitis managed?

A

high degree of suspicion

immediate administration of broas-spectrum, parenteral antibiotics

surgical debridement

91
Q

what causes necrotising fasciitis and how can this be determined?

A

streptococci, staphylococci, enterobacteriaceae and anaerobes

= blood C&S
(MRI can aid diagnosis)

92
Q

what is Fournier’s gangrene?

A

when necrotising fasciitis affects the scrotum

93
Q

in which individuals is mycobacterial infection an important cause of infection?

A

immunocompromised people

94
Q

what does Mycobacterium marinum cause?

A

fish-tank granulomatous ulcers

sporotrichoid spread

95
Q

what are Mycobacterium chelonae & abscessus associated with?

A

puncture wounds, tattoos, skin trauma & surgery

96
Q

what is Mycobacterium ulcerans associated with?

A

limb ulceration (in Africa and Australia)

97
Q

when is borreliosis caused?

A

when an individual is bitten by a Borrelia-infected tick

98
Q

how does borreliosis manifest?

A

initially, an erythematous papule that develops into annular erythema (>20cm)

99
Q

what happens in a borreliosis infection (1-3 days after)?

A

fever, headache develops

smaller lesions can also develop

100
Q

what are the possible complications of borreliosis?

A

neuroborreliosis (CN palsy, polyradiculitis)

arthritis

carditis

101
Q

how is borreliosis diagnosed?

A

needs a high index of suspicion

as serology and histopathology non-sensitice

102
Q

what is borreliosis alternatively known as?

A

Lyme disease

103
Q

what causes tularemia?

A

handling infected animals (squirrels and rabbits)

tick/deerfly bites

104
Q

what is the most common form of tularemia?

A

ulceroglandular form

105
Q

how does tularemia manifest?

A

small papules, rapidly necrose, form ulcers

106
Q

what are the symptoms of tularemia?

A

systemic symptoms (fever, headache, malaise)

cellulitis

regional, painful lymphadenopathy

107
Q

what is the causative agent for ecythma gangrenosum?

A

pseudomonas aeurginosa

108
Q

in which patients is ecthyma gangrenosum most common?

A

neutropaenic

109
Q

how does ecthyma gangrenosum manifest?

A

red papules that become ulcerous and oedematous

eschar w surrounding erythema

110
Q

how does ecthyma gangrenosum compare to ecthyma?

A

ecthyma = streptococcus,

ecthyma gangrenosum = pseudomonas

both present w red papules w thick ulcers surrounded by erythema

111
Q

give three possible causes of escharotic lesions

A

staphylococcus, streptococcus
Lyme disease
ecythma

112
Q

how does primary syphilis present?

A

chancre
(appears within 10-90 days)

with painless, regional lymphadenomathy

113
Q

what is a chancre in syphilis?

A

painless ulcer with inundated border

114
Q

what is secondary syphilis?

A

if chancre is left untreated, secondary syphilis developed 50 days after

systemic symptoms = fever, headache, pruritus

general cutaneous manifestations = rash, alopecia, residual primary chancre, lymphadenopathy, condylomata lata

115
Q

why is secondary syphilis likened to sarcoidosis?

A

both ‘great mimickers’

= low threshold for testing

116
Q

what kind of rash is seen in secondary syphilis?

A

pityriasis rosea-like rash

117
Q

which classic HIV sign can also be seen in secondary syphilis, albeit rarely?

A

lues maligna

skin lesions w pustules

118
Q

what are the cutaneous manifestations of secondary syphilis?

A

pityriasis-rosea like rash

condylomata lata

oral lesions

lues maligna

119
Q

what can tertiary syphilis lead to?

A

cardiovascular disease

neurosyphilis

120
Q

how does tertiary syphilis present?

A

gumma skin lesions

mucosal lesions destroy underlying cartilage

central areas heal with scarring and atrophy

121
Q

how is syphilis diagnosed?

A

clinical findings
serology

(strong index of suspicion required in secondary syphilis)

122
Q

how is syphilis treated?

A

oral tetracycline

IM benzylpenicillin

123
Q

what is the causative agent of leprosy?

A

mycobacterium leprae

obligate intracellular bacteria - predominantly affects skin & nerves but can affect any organ

124
Q

what is the clinical spectrum of leprosy?

A

two main types

1) lepromatous leprosy
2) tuberculoid leprosy

125
Q

what characterises lepromatous leprosy?

A

multiple lesions (macules, papules, nodules)

sweating & sensation intact in these lesions

126
Q

what characterises tuberculoid leprosy?

A

single/a few lesions (elevated border, atrophic centre, sometimes annular)

hairless, anhidrotic, numb

127
Q

what is the characteristic difference between lepromatous leprosy and tuberculoid leprosy?

A

the few lesions in tuberculoid leprosy are hairless + anhidrotic whereas the many lesions in lepromatous leprosy have sensation + sweating intact

128
Q

does tuberculosis affect the skin?

A

san affect any organ system, including the skin

only 5-10% of infections lead to clinical disease

129
Q

what are the types of cutaneous TB?

A

exogenously

  • primary inoculation TB
  • tuberculosis verrucosa cutis

contiguous endogenous spread

  • scrofuloderma
  • autoinoculation, periorificial tuberculosis

haematogenous/lymphatic endogenous spread

  • dissemination
  • lupus vulgaris, miliary tuberculosis, gummas
130
Q

which investigations are done for TB in dermatology?

A

interferon-γ release assay (quantiferon-TB)

histology – ZN stain

culture/PCR

131
Q

list some cutaneous manifestations of tuberculosis

A

exogenous:
- tuberculous chancre (papulonodule ulcer)

  • tuberculosis verrucosa cutis (wart)

endogenous:
- scrofuloderma (necrotic nodule)

  • orificial TB (nasal muscosa ulcer)

haem spread:
- lupus vulgaris (red, brown plaque)

  • miliary TB (bluish-red papules)
  • tuberculous gumma (firm subcutaneous nodules)
132
Q

what is molluscum contagiosum and how is it treated?

A

caused by poxvirus

usually resolves itself but can require cutterage or imoquimod + cidofovir antivirals

133
Q

in which individuals is molluscum contagiosum most common?

A

the immunocompromised

children

134
Q

what are the differentials for molluscum contagiosum?

A

verrucae

condyloma acuminata

basal cell carcinoma

pyogenic granuloma

135
Q

which regions of the body are affected most commonly by herpes simplex virus?

A

orolabial, genital regions

136
Q

what are the two types of HSV and how are they transmitted?

A

HSV1 = direct contact w contaminated saliva or other infectious secretions

HSV2 = sexual contact most commonly

(can be transmitted when asymptomatic)

137
Q

which parts of the body does HSV affect?

A

replicates at mucocutaneous sites of infection

travels to dorsal root ganglion (via retrograde axonal flow)

138
Q

what are the symptoms of HSV and when do they occur?

A

(symptoms occur wihtin 3-7 days of exposure)

primary = tender lymphadenopathy, malaise, anorexia, burning, tingling

cutaneous = vesicles on erythematous base, pustules, erosions, ulceration

systemic = aseptic meningitis

139
Q

how long does HSV take to completely resolve itself?

A

approx 2-6 weeks

140
Q

HSV has orolabial and genital manifestations: which of these are more painful?

A

orolabial = asymptomatic

genital = excruciatingly painful (urinary retention)

141
Q

what can cause reactivation of HSV infection?

A

spontaneous, UV, fever, local tissue damage, stress

142
Q

which HSV infection can occur in patients with atopic eczema and why is this a problem?

A

if people with atopic eczema get HSV infection = eczema herpeticum (!)

= medical emergency as it can lead to HSV encephalitis

143
Q

how is eczema herpeticum treated?

A

acyclovir IV + antibiotics

144
Q

how does eczema herpeticum present?

A

excoriated vesicles

145
Q

what is herpetic whitlow and who is affected most by it?

A

either HSV 1/2 infection of digits

= pain, swelling and vesicles; often affects children

(misdiagnosed as paronychia or dactylitis)

146
Q

what is herpes gladiatorium and who is affected most by it?

A

HSV 1 involvement of cutaneous site reflecting sites of contact with another athlete’s lesions

= common in contact sports e.g. wrestling

147
Q

how does neonatal HSV occur?

A

exposure to HSV 1/2 during vaginal delivery

onset from brith to 2 weeks

148
Q

how doe neonatal HSV present?

A

localised = usually scalp or trunk

vesicles = bullae erosions

(complication = encephalitis! can lead to neuro defects if not treated ASAP)

149
Q

what can neonatal HSV lead to?

A

HSV encephalitis

150
Q

how is neonatal HSV treated?

A

IV antivirals

151
Q

how does severe/chronic HSV infection present most commonly?

A

1) chronic, enlarging ulceration
2) at multiple sites or disseminated
3) often atypical e.g. verrucous, exophytic or pustular lesions

(involvement of respiratory or GI tracts may occur)

152
Q

who does severe/chronic HSV infections affect most?

A

chronic, immunocompromised patients

153
Q

how is HSV infection diagnosed?

A

PCR swab

154
Q

how is HSV treated?

A

oral/IV valacyclovir or acyclovir

= don’t delay!

155
Q

which regions does varicella zoster virus affect?

A

dermatomal

either affect single dermatome or multiple dermatomes

156
Q

what causes hand, foot and mouth disease?

A

coxsackie a16, echo 71

echo 71 = increased risk of encephalitis

157
Q

how does hand, foot and mouth disease manifest?

A

grey, elliptical ulcers form in the buccal, oral or hand and foot regions

fever, malaise, sore throat

158
Q

how is hand, foot and mouth disease spread?

A

via direct contact

oral-oral or oral-genital

159
Q

which viruses cause mobiliform (measles-like) eruptions?

A

measles
rubella
EBV, CMV, HHV6/7

DRUGS!

rikettsia
leptospirosis

160
Q

what causes petechial/purpuric eruptions?

A

vasculitis

coagulation abnormalities (DIC)

vial infection (rubellaa, CMV)

bacterial infections (rikketsia, endocarditis)

plasmodium falciparum

161
Q

what is Gianotti-Crosti syndrome?

A

acute, symmetrical erythematous papular eruption of the face, extremities and buttocks

162
Q

who does Gianotti-Crosti syndrome occur most commonly in?

A

children aged 1-3

163
Q

what are the main causes of Gianotti-Crosti syndrome?

A

CMV
EBV
HHV6
hepatitis B

164
Q

what is erythema infectiosum and how does it present?

A

‘fifth disease’

  • initial fever and headache
  • ‘slapped cheek’ rash after 2-4 days
  • lacy rash of check and thigh in 2nd stage

(caused by parvovirus B19)

165
Q

what is roseola infantum and how does it present?

A

‘sixth disease’

  • fever
  • pink papules on trunk and head
  • lasts 2 hours or days

(caused by HHV6/7)

166
Q

what is orf and how does it present?

A

caused by parapoxvirus

dome-shaped bullae with crust develop on the hands or forearms

167
Q

how is orf spread?

A

direct exposure to sheep and goats

168
Q

how is orf treated?

A

generally resolve without therapy in 4-6 weeks

169
Q

what causes warts?

A

> 200 subtypes of HPV virus

brs (phase 1b) (71 decks)

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