Derm - Infections + Infestations Flashcards

1
Q

What is staphylococcus aureus and how does it infect the skin?

A

bacterium that has many virulence factors, e.g. receptord that allow it to bind to fibrin

fibrin is in abundance on wound surfaces etc.

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2
Q

What can Staph infections result in?

A

→ ecthyma (deep dermis skin infetion where ulcers form under crusted sores)

→ impetigo (superficial skin infection)

→ cellulitis

→ folliculitis

→ furunculosis (deep infection of the hair follicle leading to abscess formation)

→ carbuncles (cluster of boils — painful, pus-filled bumps)

→ SSSS (staphylococcal scalded skin syndrome)

→ superinfects other dermatoses (e.g. atopic eczema, HSV, leg ulcers)

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3
Q

How does streptococcus cause skin infections?

A

→ virulence factors that allow it to attach to the epithelial surfaces via the lipoteichoic acid portion of fimbriae

→ has M protein (anti-phagocytic) + hyaluronic acid capsule

→ produces erythrogenic exotoxins

→ produces streptolysins S and O

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4
Q

What can a Stretococcus infection result in?

A

→ ecthyma

→ cellulitis

→ impetigo

→ erysipelas (an infection of the upper layers of the skin +

→ scarlet fever

→ necrotizing fascitis

→ superinfects other dermatsoses (e.g. leg ulcers)

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5
Q

What is folliculitis?

A

→ folliculitis

→ follicular erythema, sometimes pustular

→ maybe non-infectious or infectious

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6
Q

What kind of folliculitis is associated with HIV?

A

eosinophillic (non-infectious) folliculitis

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7
Q

What can give you recurrent folliculitis?

A

nasal carriage of staphylococcus aureus, especially strains expressing Panton-Valentine leukocidin (PVL)

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8
Q

How is folliculitis treated?

A

→ antibiotics (usually flucloxacillin or erythromycin) (depends after a swab)

→ incision + drainage is required for furunculosis

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9
Q

What is the difference between a furuncle + carbuncle?

A

→ furuncle = deep follicular abscess

→ carbuncle = deep follicular abcess that involves adjacent connected follicles

→ carbuncle more likely to lead to complications such as cellulitis + septicaemia

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10
Q

What is this?

A

furuncle

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11
Q

What is this?

A

carbuncle

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12
Q

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

A

• Establishment as a part of the resident microbial flora :

  • Abundant in nasal flora

•Immune deficiency :

  • Hypogammaglobulinaemia
  • HyperIgE syndrome – deficiency - Chronic granulomatous disease
  • AIDS
  • Diabetes Mellitus
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13
Q

What is PVL?

A

→ Panton-Valentine Leukocidin

→ β-pore-forming exotoxin

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14
Q

What does PVL allow staphylococcus aureus to do?

A

→ Leukocyte destruction and tissue necrosis

→ Higher morbidity, mortality and transmissibility

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15
Q

How does PVL staph. aureus manifest in the skin?

A

→ recurrent + painful abcesses

→ folliculitis

→ cellulitis

→ often in more than one site, recurrent + present in contacts

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16
Q

How does PVL staph. aureus manifest extracutaneously?

A

→ necrotising pneumonia

→ necrotising fascitis

→ purpura fulminans

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17
Q

What are the 5 risks or ways in which PVL staph. aureus can be acquired?

A

Close contact (hugging, contact sports)

Contaminted items (gym equipment, towels, razors)

Crowding (crowded living conditions)

Cleanliness of environement (unclean = more risk)

Cuts + grazes (allows bacteria to enter the body)

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18
Q

What is the treatement protocol for PVL staph. aureus infection?

A

→ consult local microbiologist

→ antibiotics (usually tetracycline)

→ decolonisation (e.g. chlorhexidine body wash for 7 days or nasal application of mupirocin ointment, 5 days)

→ treatment of close contacts

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19
Q

What is pseudomonal folliculitis?

A

an infection of the hair follicle with Pseudomonas bacteria

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20
Q

What causes pseudomonal folliculitis?

A

associated with hot tub use, swimming pools, depilatories + wet suits

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21
Q

How does pseudomonal folliculitis progress?

A

appears 1-3 days after exposure, as a diffuse truncal eruption or follicular erythmatous papule

rarely can progress to abcesses, lymphangitis + fever

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22
Q

How is pseudomonal folliculitis treated?

A

most cases self-limited, no treatement required

severe or recurrent cases can be treated with oral ciprofloxacin

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23
Q

What is this?

A

cellulitis - infections of lower dermis + subcutaneous tissue

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24
Q

What is the main symptom of cellulitis?

A

tender swelling with ill-defined blanching erythema or oedema

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25
Q

What causes cellulitis?

A

→ streptococcus pyogenes

→ staphylococcus aureus

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26
Q

What is a pre-disposing factor for cellulitis?

A

oedema

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27
Q

What is the treatment for cellulitis?

A

systemic antibiotics

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28
Q

What is this?

A

impetigo

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29
Q

What is impetigo?

A

Superficial bacterial infection, stuck-on, honey-coloured crusts overlying an erosion, often affects face (perioral, ears, nasal)

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30
Q

What can cause impetigo?

A

streptococci (non-bullous or non-blistering)

staphylococci (bullous or blistering)

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31
Q

How do you tell the difference between staph + strep impetigo?

A

strep = non-blistering or non-bullous

staph = bullous or blistering

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32
Q

Why does staph cause blistering or bullous in impetigo?

A

Caused by exfoliative toxins A & B, split epidermis by targeting desmoglein I

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33
Q

How is impetigo treated?

A

topical +/- systemic antibiotics

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34
Q

What is impetiginastion?

A

superficial impetigo in the context of atopic dermatitis

caused by staph

characteristic gold crust

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35
Q

What is this?

A

impetiginisation

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36
Q

What is ecthyma?

A

severe form of streptococcal impetigo

thich crust overlying a punch out ulceration surrounded by erythema

usually on lower extremities

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37
Q

What is SSSS?

A

staphylococcal scalded skin syndrome

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38
Q

Who usually gets SSSS?

A

neonates, infants, immunocompromised adults

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39
Q

What causes SSSS?

A

the exfoliative toxins of staph

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40
Q

Why can’t the staph organism be cultured from the scalded skin in SSSS?

A

infection occurs at a distant site from the SSSS

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41
Q

Why does SSSS often manifest in neonates, infants or immunocompromised adults?

A

→ kidneys cannot excrete the exfoliative toxin quickly

→ Diffuse tender erythema that rapidly progresses to flaccid bullae

→ Wrinkle and exfoliate, leaving oozing erythematous base

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42
Q

What can SSSS clinically resemble?

A

Stevens-Johnson syndrome / toxic epidermal necrolysis

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43
Q

What is Toxic Shock Syndrome?

A

febrile illness due to group A staph. aureus strain that produces pyrogenic exotoxin TSST-1

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44
Q

What are the symptoms + signs of Toxic Shock Syndrome?

A
  • fever > 38.9
  • Hypotension
  • Diffuse erythema
  • Involvement of ≥ systems:

– Gastrointestinal

– Muscular

– CNS

  • Renal
  • Hepatic
  • Mucous membranes (erythema)
  • Hematologic (platelets <100 000/mm3)
  • Desquamation predominantly of palms and soles 1-2 weeks after resolution of erythema
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45
Q

What is this?

A

toxic shock syndrome

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46
Q

What is erythrasma?

A

infection of Corynebacterium minutissimum

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47
Q

What are the symptoms + signs of erythrasma?

A

well demarcated patches in intertriginous areas

intially pink

become brown + scaly

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48
Q

What is this?

A

erythrasma

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49
Q

What is pitted keratolysis?

A

pitted erosions of soles

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50
Q

What is pitted keratolysis caused by?

A

corynebacteria

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51
Q

What is the treatment for pitted keratolysis?

A

topical clindamycin

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52
Q

What is erysipeloid?

A

erythema + oedema of the hand after handling contaminated raw fish or meat

extends slowly over weeks

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53
Q

What bacteria causes erysipeloid?

A

erysipelothrix rhusiopathiae

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54
Q

What is this?

A

erysipeloid

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55
Q

What is anthrax?

A

Painless necrotic ulcer with surrounding oedema and regional lymphadenopathy (with pain in lymph nodes) at the site of contact with hides, bone meal or wool infected with Bacillus anthracis

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56
Q

What causes anthrax?

A

Bacillus anthracis

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57
Q

What is this?

A

anthrax

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58
Q

What is blistering distal dactylitis?

A

Rare infection

Typically - young children

1 or more tender superficial bullae on erythematous base on the volar fat pad of a finger

Toes may rarely be affected

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59
Q

What can cause blistering distal dactylitis?

A

streptococcus pyogenes and staphylococcus aureus

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60
Q

What is this?

A

blisteirng distal dactylitis

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61
Q

What is erysipelas?

A

infection of deep demris + subcutis

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62
Q

What causes erysipelas?

A

β-haemolytic streptococci or Staphylococcus aureus

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63
Q

What are the symptoms + signs of erysipelas?

A

Painful

Prodrome of malaise, fever, headache.

Presents as erythematous indurated plaque with a sharply demarcated border and a cliff-drop edge (+/- blistering)

Face or limb (+/- red streak of lymphangitis and local lymphadenopathy)

Portal of entry must be sought (e.g. tinea pedis).

Systemic symptoms (fever, malaise).

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64
Q

What is the treatment for erysipelas?

A

Treated with intravenous antibiotics

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65
Q

What is scarlet fever?

A

bacterial illness that develops in some people who have strep throat

primarily a disease of children

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66
Q

What is scarlet fever caused by?

A

Caused by upper respiratory tract infection with erythrogenic toxin-producing Streptococcus pyogenes

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67
Q

What are the symptoms + progression of scarlet fever?

A
  • Preceded by sore throat, headache, malaise, chills, anorexia and fever
  • Eruption begins 12-48 hours later
  • Blanchable tiny pinkish-red spots on chest, neck and axillae
  • Spread to whole body within 12 hours
  • Sandpaper-like texture
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68
Q

What are some complications of scarlet fever?

A

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

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69
Q

What is this?

A

scarlet fever

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70
Q

What is necrotising fasciitis?

A

Initial dusky induration (usually of a limb), followed by rapid painful necrosis of skin, connective tissue and muscle

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71
Q

What causes necrotising fasciitis?

A

streptococci

staphylococci

enterobacteria

anaerobes

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72
Q

What is the mortality of necrotising faciitis?

A

potentially fatal

high mortality

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73
Q

What is the diagnostic procedure for necrotising fasciitis?

A
  • Prompt diagnosis essential (requires high index of suspicion)
  • MRI can aid diagnosis.
  • Blood and tissue cultures can determine organisms and sensitivities.
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74
Q

How is necrotising fasciitis treated?

A

broad-spectrum parenteral antibiotics and surgical debridement

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75
Q

What is atypical mycobacterial infection?

A

important cause of infection in immunosupressed states

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76
Q

What can cause atypical mycobacterial infection?

A

mycobacterium marinum

mycobacterium chelonae

mycobacterium ulcerans

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77
Q

What type of infection does mycobacterium marinum cause?

A

indolent granulomatous ulcers (fish-tank granuloma) in healthy people (Sporotrichoid spread)

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78
Q

What type of infection does mycobacterium chelonae + abscessus cause?

A

puncture wounds, tattoos, skin trauma or surgery

79
Q

What type of infection does mycobacterium ulcerans cause?

A

an important cause of limb ulceration in Africa (Buruli ulcer) or Australia (Searle’s ulcer)

80
Q

What is this? What caused this?

A

atypical mycobacterial infection, mycobacterium marinum

81
Q

What is this? What caused this?

A

atypical mycobacterium infection, mycobacterium abscessus + chelonae

82
Q

What is borreliosis (Lyme Disease)?

A

annular erythema developing at the site of the bite of a Borrelia-infected tick, Bite form Ixodes tick infected with Borrelia burgdorferi

83
Q

What is the cutaneous manifestation of Borreliosis?

A

Erythema migrans (only in 75%)

Erythematous papule at the bite site

Progression to annular erythema of >20cm

84
Q

What is the symptomatic progression of Borreliosis (Lyme Disease)?

A
  • 1-30 days after infection, fever, headache
  • Multiple secondary lesions develop - similar but smaller to initial lesion
  • Neuroborreliosis
  • Facial palsy / other CN palsies
  • Aseptic meningitis
  • Polyradiculitis
  • Arthritis – painful and swollen large joints (knee is the most affected join)
  • Carditis
85
Q

What is this?

A

Borreliosis (Lyme Disease)

86
Q

What is this?

A

Borreliosis (Lyme Disease)

87
Q

What is Tularaemia?

A

zoonotic bacterial disease of the Northern hemisphere

88
Q

What causes Tularaemia?

A

Francisella tularensis

89
Q

How is tularaemia acquired?

A
  • Handling infected animals (squirrels and rabbits)
  • Tick bites
  • Deerfly bites
90
Q

What is the cutaneous manifestation of tularaemia?

A

Ulceroglandular form

Primary skin lesion is small papules at inoculation site that rapidly necroses – leading to painful ulceration

+/- local cellulitis

91
Q

What are the other systemic symptoms of tularaemia?

A
  • Painful regional lymphadenopathy
  • Systemic symptoms: fever, chills, headache and malaise
92
Q

What is this?

A

Tularaemia

93
Q

What is ecthyma gangrenosum? What does it look like clinically?

A

infection that manifests cutaneously

  • Red macule(s) → oedematous → haemorrhagicbullae.
  • May ulcerate in late stages or form an eschar surrounded by erythema
94
Q

What causes ecthyma gangrenosum?

A

Pseudomonas aeruginosa

95
Q

Who normally catches ecthyma gangrenosum?

A

neutropaenic patients, critically ill + imunocompromised patients

96
Q

What is an escharotic lesion?

A

substance that kills unwanted or diseased tissue, usually skin or superficial growths like warts, leaving them to slough off

97
Q

What can cause an escharotic lesion?

A
  • Pseudomonas
  • Aspergillosis
  • Leishmaniasis
  • Cryptococcosis
  • Lues maligna
  • Rickettsial infections
  • Cutaneous anthrax
  • Tularaemia
  • Necrotic arachnidism (brown recluse spider bite)
  • Scrub typhus (Orientia tsutsugamushi)
  • Rat bite fever (Spirillum minus)
  • Staphylococcal or streptococcal
  • Ecthyma
  • Lyme disease.
98
Q

What is syphilis?

A

bacterial infection usually spread by sexual contact. The disease starts as a painless sore — typically on the genitals, rectum or mouth

99
Q

What causes syphilis? How is it spread?

A

treponema pallidum, sexually transmitted disease

100
Q

What does the primary infection of syphilis look like?

A

● Primary infection Chancre -painless ulcer with a firm indurated border

● Painless regional lymphadenopathy one week after the primary chancre

● Chancre appears within 10-90 days

101
Q

What is secondary syphilis?

A

the second stage of syhpilis, Begins ~50 days after chancre

102
Q

What are the symptoms of secondary syphilis?

A
  • Malaise, fever, headache, pruritus, loss of appetite, iritis
  • Rash (88-100%) -Pityriasis rosea-like rash
  • Alopecia (‘moth-eaten’) (hair loss patches, etc.)
  • Mucous patches
  • Lymphadenopathy
  • Residual primary chancre
  • Condylomata lata (flesh colored or hypopigmented, macerated papules or plaques)
  • Hepatosplenomegaly
103
Q

Why is there a low threshold for testing for secondary syphilis?

A

symptoms are extensive and very variable, presentations can vary form person to person, like in sarcoidoisis, called the “great mimicker”

104
Q

What is a rare cutaneous manifestation of secondary syphilis?

A

Lues maligna

● Pleomorphic skin lesions with pustules, nodules and ulcers with necrotising vasculitis

● More frequent in HIV manifestation

105
Q

What is tertiary syphyilis? What are its symptoms?

A

● Gumma Skin lesions - nodules and plaques

● Extend peripherally while central areas heal with scarring and atrophy

● Mucosal lesions extend to and destroy the nasal cartilage

● Cardiovascular disease

● Neurosyphilis (general paresis or tabes dorsalis)

106
Q

What is the treatement for syphilis?

A

IM benzylpenicillin or oral tetracycline

107
Q

What is leprosy? What causes leprosy?

A

Hansen’s disease, is a chronic infectious disease caused by Mycobacterium leprae (obligate intracellular bacterium)

mainly affects the skin, the peripheral nerves, mucosal surfaces of the upper respiratory tract and the eyes

108
Q

What are the 2 different types of leprosy?

A

lepromatous leprosy

tuberculoid leprosy

109
Q

What are the features of lepromatous leprosy?

A
  • Multiple lesions: macules, papules, nodules
  • Sensation and sweating normal (early on)
110
Q

What are the features of tuberculoid leprosy?

A
  • Solitary or few: elevated borders – atrophic center, sometimes annular
  • Hairless, anhidrotic, numb
111
Q

What are the 3 ways in which TB can be acquired cutaneously?

A
  • exogenously
  • contiguous endogenous spread
  • haematogenous / lymphatic endogenous spread
112
Q

How does TB present exogenously?

A

primary-inoculation TB and tuberculosis verrucosa cutis (see picture)

113
Q

How does TB present contiguous endogenously?

A

scrofuloderma or autoinoculation – periorificial tuberculosis

(skin condition caused by tuberculous involvement of the skin by direct extension)

114
Q

How does TB present when spread throug haematogenous / lymphatic endogenous spread?

A

dissemination (lupus vulgaris, miliary tuberculosis, gummas)

115
Q

What investigations can be done for TB when there is cutaneous presentation?

A
  • Interferon-γ release assay (Quantiferon-TB)
  • Histology – ZN stain
  • Culture / PCR
116
Q

What are the different ways in which TB can manifest cutaneously?

A
  • Tuberculous chancre - painless, firm, reddish-brown papulonodule that forms an ulcer
  • Tuberculosis verrucosa cutis - wart-like papule that evolves to form redbrown plaque
  • Scrofuloderma – subcutaneous nodule with necrotic material - becomes fluctuant and drains, with ulceration and sinus tract formation.
  • Orificial TB - non-healing ulcer of the nasal mucosa that is painful
  • Lupus vulgaris – red brown plaque - +/- central scarring, ulceration
  • Miliary TB - pinhead-sized, bluish-red papules capped by minute vesicles
  • Tuberculous gumma – firm subcutaneous nodule - later ulcerates
117
Q

What is molluscum contagiosum?

A

● Poxvirus infection

● Usually resolve spontaneously

118
Q

Who is molluscum contagiosum common in?

A

common in chlidren + immunocompromised

119
Q

What are some diffrenetial diagnosis for molluscum contagiosum?

A
  • Verrucae
  • Condyloma acuminata
  • Basal cell carcinoma
  • Pyogenic granuloma
120
Q

What are the treatment options for mulluscum contagiosum?

A

● Usually resolve spontaneously

● Treatment options – curettage, imiquimod, cidofovir

121
Q

What areas of the body does the Herpes Simplex Virus cutaneously favour?

A

orolabial and genital regions w primary and recurrent vesicular eruptions

122
Q

How is HSV transmitted?

A

● HSV-1 – direct contact with contaminated saliva / other infected secretions

● HSV-2 - sexual contact

but not a hard + fast rule

Transmission can occur even during asymptomatic periods of viral shedding

123
Q

How does HSV infect someone?

A

● Replicates at mucocutaneous site of infection

● Travels by retrograde axonal flow to dorsal root ganglia

124
Q

When do symptoms present? What are the primary symptoms?

A

●Symptoms with 3-7 days of exposure

●Preceded by tender lymphadenopathy, malaise, anorexia

± Burning, tingling

●Painful rouped vesicles on erythematous base → ulceration / pustules / erosions with scalloped border

●Crusting and resolution within 2-6 weeks

●Orolabial lesions – often asymptomatic

●Genital involvement – often excruciatingly painful→ urinary retention

125
Q

What are some of the systemic manifestations of HSV?

A

aseptic meningitis in up to 10% of patients

126
Q

How are HSV flare-ups reactivated?

A

spontaneous, UV, fever, local tissue damage, stress

127
Q

What is eczema herpeticum?

A
  • HSV triggered eczema for people who already have eczema
  • emergency
  • Monomorphic, punched out erosions (excoriated vesicles)
128
Q

What is herpetic whitlow?

A
  • HSV (1>2) infection of digits – pain, swelling and vesicles (vesicles may appear later)
  • Misdiagnosed as paronychia or dactylitis
  • Often in children
129
Q

What is herpes gladiatorum?

A
  • HSV 1 involvement of cutaneous site reflecting sites of contact with another athlete’s lesions
  • Contact sports e.g. wrestling
130
Q

How is neonatal HSV acquired? What are the symptoms?

A
  • Exposure to HSV during vaginal delivery – risk higher when HSV acquired near time of delivery
  • HSV 1 or 2
  • Onset from birth to 2 weeks
  • Localised usually – scalp or trunk
  • Vesicles → bullae erosions
  • Encephalitis → mortality >50% without treatment, 15% with treatment → neurological deficits
131
Q

What is the treatment for neonatal HSV infection?

A

requires antivirals

132
Q

How does severe or chronic HSV infection present?

A
  • Immunocompromised patients e.g. HIV / transplant recipient
  • Most common presentation – chronic, enlarging ulceration
  • Multiple sites or disseminated
  • Often atypical e.g. verrucous, exophytic or pustular lesions
  • Involvement of respiratory or GI tracts may occur
133
Q

How is HSV diagnosed?

A

swab for PCR testing

134
Q

What is the treatement for HSV?

A
  • Don’t delay
  • Oral valacyclovir or acyclovir 200mg five times daily in immunocompetent localised infection
  • Intravenous 10mg/kg TDS X 7-19 days
135
Q

What is varicella zoster virus? What does it cause?

A

the cause of chickenpox and herpes zoster (also called shingles)

can be single dermatomal or multidermatomal

136
Q

What is hand foot + mouth disease? What causes it?

A

common infection that causes mouth ulcers and red spots on the hands and feet. It mainly affects children

caused by Coxsackie A16, Echo 71

An acute self-limiting coxsackievirus infection

137
Q

How is hand, foot + mouth disease transmitted?

A

•Spread by direct contact via oral-oral route or oral faecalroute.

138
Q

What are the symptoms of hand, foot + mouth disease?

A
  • Prodrome of fever, malaise, and sore throat
  • Red macules, vesicles (typically gray and eliiptical), and ulcers develop on buccal mucosa, tongue, palate and pharynx, and may also develop on hands and feet (acral and volar surfaces).
139
Q

What is hand foot and mouth disease caused by echo 71 associated with?

A

higher incidence of neurological involvement included fatal cases of encephalitis

140
Q

What viruses can cause morbilliform (measle-like) rashes?

A
  • Measles, Rubella, EBV, CMV, HHV6 & HHV7 cause morbilliform (measles-like) eruptions
  • Leptospirosis
  • Rickettsia
141
Q

What can cause petechial / purpuric eruptions?

A
  • Coagulation abnormalities - TTP, ITP, DIC
  • Vasculitis
  • Infections
  • Viruses - Hepatitis B, CMV, Rubella, Yellow fever, Dengue fever, West nile virus
  • Bacterial (BREN) - Borrelia, Rickettsia, Neisseria, Endocarditis
  • Other infections - Plasmodium falciparum, Trichinella
  • Other - TEN, Ergot poisoning, Raynauds
142
Q

What is Gianotti-Crosti syndrome?

A
  • papular acrodermatitis of childhood
  • A viral eruption that causes and acute symmetrical erythematous papular eruption on face, extremities and buttocks – usually in children aged 1-3 years
143
Q

What can cause Gianotti-Crosti syndrome?

A
  • EBV (most common)
  • CMV
  • HHV6
  • Coxsackie viruses A16, B4 and B5
  • Hepatitis B
144
Q

What is erythema infectiousum caused by?

A

parvovirus B19

145
Q

What are the symptoms of erythema infectiosum?

A
  • Initially: mild fever and headache
  • A few days later – ‘slapped cheeks’ for 2-4 days
  • Then reticulated (lacy) rash of chest and thighs in 2nd stage of disease
146
Q

What is roseola infantum? What are the symptoms?

A
  • viral infection that affects children
  • 2-5 days of high fever
  • Followed by appearance of small pale pink papules on the trunk and head
  • Lasts hours to 2 days.
147
Q

What cuases roseala infantum?

A

HHV6 and HHV7 commonly

148
Q

What is Orf? What are the symptoms?

A

Viral infection

  • Dome-shaped, firm bullae that develop an umbilicated crust.
  • Usually develop on hands and forearms
  • They generally resolve without therapy in 4-6 weeks
149
Q

What causes Orf?

A
  • Caused by parapoxvirus
  • Direct exposure to sheep or goats
150
Q

What causes warts?

A

over 200 types of HPV (human papilloma virus)

151
Q

What can warts be mistaken for?

A

skin cancer

condolymata lata

152
Q

What fungi cause superficial skin infections?

A
  • candida
  • malassezia
  • dermatophytes
153
Q

What is pityriasis versicolor? What causes it? What are the symptoms?

A

superficial fungal infection

  • Hypopigmented, hyperpigmented or erythematous macular eruption +/- fine scale
  • Malassezia spp.
  • Begins during adolescence (when sebaceous glands become active)
  • Flares when temperatures and humidity are high – Immunosuppression
  • Topical azole
154
Q

What are dermatophytes?

A

fungi that live on keratin

155
Q

What strain causes the most fungal infections?

A

trichophyton rubrum

156
Q

What causes the most tinea capitis (Ringworm of the scalp)?

A

trichophyton tonsurans

157
Q

What is a kerion?

A

an inflammatory fungal infection that may mimic a bacterial folliculitis or an abscess of the scalp; scalp is tender and patient usually has posterior cervical lymphadenopathy

  • Frequently secondarily infected with Staphylococcus aureus
158
Q

What is onychomycosis?

A

fungal infection of the nails that causes discoloration, thickening, and separation from the nail bed

159
Q

What is tinea faciei?

A

superficial dermatophyte infection limited to the glabrous skin of the face

160
Q

What is tinea pedis?

A

Athlete’s foot (tinea pedis) is a fungal skin infection that usually begins between the toes

161
Q

What kind of tinea pedis does trichophyton rubrum cause?

A

scaling + hyperkeratosis of plantar surface of foot

162
Q

What kind of tinea pedis does tricophyton mentagrophytes (interdigitale) cause?

A

sometimes vesiculobullous reaction on arch or side of foot

163
Q

What are Id reactions?

A
  • Dermatophytid reactions
  • Inflammatory reactions at sites distant from the associated dermatophyte infection
  • May include urticaria, hand dermatitis, or erythema nodosum
  • Likely secondary to a strong host immunologic response against fungal antigens
164
Q

What is majocchi granuloma?

A

•Follicular abscess produced when dermatophyte infection penetrates the follicular wall into surrounding dermis; tender

165
Q

What can cause majocchi granuloma?

A

trichophyton rubrum or mentagrophytes

166
Q

What is candidiasis? What are the causes + symptoms?

A
  • Candida albicans
  • Predisposed by occlusion, moisture, warm temperature, diabetes mellitus
  • Most sites show erythema oedema, thin purulent discharge
  • Usually an intertriginous infection (affecting the axillae, submammaryfolds, crurae and digital clefts) or of oral mucosa.
  • A common cause of vulvovaginitis
  • May affect mucosae.
  • Can become systemic (immunocompromise)
167
Q

What are deep fungal infections?

A
  • Capacity for deep invasion of skin or production of skin lesions secondary to systemic visceral infection.
  • Subcutaneous fungal infections – infections of implantation (inoculation)
168
Q

What are some examples of deep fungal infections?

A
  • Sporotrichosis
  • Phaeohypomycosis
  • Chromomycosis
  • Mycetoma (Madura foot)
  • Lobomycosis
  • Rhinosporidiosis
169
Q

What is sporotrichosis?

A

known as “rose gardener’s disease”) is an infection caused by a fungus called Sporothrix. This fungus lives throughout the world in soil and on plant matter such as sphagnum moss, rose bushes, and hay. People get sporotrichosis by coming in contact with the fungal spores in the environment

170
Q

What is chromomycosis?

A

chronic fungal infection of the skin and subcutaneous tissue caused by any of several pigmented fungi normally found in soil and wood

171
Q

What is Madura foot (mycetoma)?

A

chronic granulomatous soft-tissue infection that is endemic to several regions of Africa and Asia

172
Q

What are systemic fungal infections?

A
  • Systemic respiratory endemic fungal infections Include blastomycosis, histoplasmosis, coccidiodomycosis, paracoccidoiodomycosis, penicillinosis
  • Disease in both immunocompetent and immunosuppressed
173
Q

What is blastomycosis?

A

rare fungal infection usually acquired by breathing in the spores of the fungi Blastomyces dermatitidis or Blastomyces gilchristii

174
Q

What is coccidioidomycosis?

A

Valley fever, also called coccidioidomycosis, is an infection caused by the fungus Coccidioides. The fungus is known to live in the soil in the southwestern United States and parts of Mexico and Central and South America. The fungus was also recently found in south-central Washington.

175
Q

What is histoplasmosis?

A

an infection caused by a fungus called Histoplasma. The fungus lives in the environment, particularly in soil that contains large amounts of bird or bat droppings

176
Q

What is aspergillosis?

A
  • Primarily a respiratory pathogen
  • Cutaneous lesions being as well-circumscribed papule with necrotic base and surrounding erythematous halo,
  • Propensity to invade blood vessels causing thrombosis and infarction
  • Lesions destructive – may extend into cartilage, bone and fascial planes
  • Should be considered in differential of necrotisiing lesions
177
Q

What are the risk factors for aspergillosis?

A

neutropenia + corticosteroid therapy

178
Q

What can cause similar illness and cutaneous presentation to aspergillosis?

A

fusarium

179
Q

What is mucurmycosis? What are the presenting symptoms?

A

fever, headache, facial oedema, proptosis, facial pain, orbital cellulitis ± cranial nerve dysfunction

180
Q

What can cause mucormycosis?

A

Apophysomyces, Mucor, Rhizopus, Absidia, Rhizomucor

181
Q

What is mucormycosis associated with?

A

Diabetes mellitus (1/3 of patients - DKA very high risk

Malnutrition

Uraemia

Neutropaenia

Medications: Steroids / antibiotics / desferoxamine

Burns

HIV

182
Q

What is the treatment for mucormycosis?

A

aggressive debridement & antifungal therapy

183
Q

What is scabies? What are the signs + symptoms?

A
  • Contagious infestation caused by Sarcoptes species
  • Female mates, burrows into upper epidermis, lays her eggs and dies after one month.
  • Insidious onset of red to flesh-coloured pruritic papules
  • Affects interdigital areas of digits, volar wrists, axillary areas, genitalia
  • A diagnostic burrow consisting of fine white scale is often seen
  • Crusted or ‘Norwegian’ scabies - hyperkeratosis
  • Often asymptomatic; found in immunocompromised individuals
184
Q

What is the treatment for scabies?

A

permethrin, oral ivermectin

  • Two cycles of treatment are required
185
Q

What are the 3 types of lice?

A

Pediculus humanus capitis

Pediculus humanus corporis

Phithrus pubis

186
Q

What are the pediculus humanus capitis?

A
  • Entire live cycle spent in hair
  • 2ndary infection common
187
Q

What is the treatment for head lice?

A

malathion, permethrin, or oral ivermectin

188
Q

What is the pediculus humanus corporis?

A
  • Lives and reproduces in clothing – leaves to feed; rarely found on skin
  • Pruritic papules & hyperpigmentation
  • Found in overcrowding, poverty & poor hygiene
189
Q

How are body louse treated?

A

eliminated by thorough cleaning or discarding clothes

190
Q

What are phithrus pubis?

A

aka crabs; three pairs of legs

  • Eggs found on hair shaft, also found in occipital scalp, body hair, eyebrow and eyelash, axillary hair
  • Treatment: malathion / permethrin, oral ivermectin
191
Q

What are bedbugs?

A

•Cimex lectularius – reddish-brown, wingless insect resembling size and shape of ladybird

  • Itchy weals around a central punctum
  • Dine alone at night, rapidly and painlessly
  • Live behind wallpaper, under furniture
192
Q

How are bedbugs gotten rid of?

A
  • Fumigation of home is necessary to get rid of pest
  • Treatment of patient is symptomatic
193
Q
A