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BRS 2.0 > Infections and Infestation of the Skin > Flashcards

Infections and Infestation of the Skin Flashcards

1
Q

What conditions can s.aureus cause? (8)

A 
Ecthyma
Impetigo
Cellulitis
Folliculitis
Furunculosis
Carbuncles
Staphylococcus scalded skin syndrome
Superinfects other dermatoses
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2
Q

Which portion of its fibrae attaches to epithelial surfaces in strep pyogenes?

A

Lipoteichoic acid portion

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3
Q

What does the M protein on strep pyogenes aid in?

A

Evade phagocytosis

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4
Q

What virulence factors do streptococci have?

A

Strep pyogenes fimbrae attach to epithelial surfaces
M protein and hyaluronic acid capsule
Produces erythrogenic exotoxins
Produces streptolysins S and O

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5
Q

What conditions can streptococci cause?

A 
Ecthyma
Cellulitis
Impetigo
Erysipelas
Scarlet fever
Necrozing fasciitis
Superinfects other dermatoses
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6
Q

How does folliculitis present?

A

Follicular erythema; sometimes pustular

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7
Q

What type of folliculitis is associated with HIV?

A

Eosinophilic (non-infectious) folliculitis

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8
Q

Which bacteria may cause recurrent cases of folliculitis?

A

Nasal carriage of s aureus, particularly strains expressing Panton-Valentine leukocidin (PVL)

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9
Q

What is the treatment for folliculitis?

A

Antibiotics (erythromycin, flucloxacillin)

Incision and drainage for furunculosis

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10
Q

What is the difference between a furuncle and a carbuncle? (2)

A

A furuncle is a deep follicular abscess whereas a carbuncle is composed of multiple furuncles; involves adjacent hair follicles

A carbuncle is more likely to lead to complications i.e. cellulitis, septicaemia

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11
Q

Why do some patients develop recurrent staphylococcal impetigo or recurrent furunculosis? (6)

A

Immune deficiency:

  • hypogammaglobulinaemia
  • hyperIgE syndrome
  • chronic granulomatous disease
  • AIDS
  • HIV
  • diabetes mellitus
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12
Q

What is PVL?

A

Panton Valentine Leukocidin

beta-pore-forming exotoxin

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13
Q

What can PVL cause?

A

Leukocyte destruction and tissue necrosis

-> higher morbidity, mortality, transmissibility

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14
Q

How does PVL s aureus present in the skin? (3)

A

Recurrent and painful abscesses
Folliculitis
Cellulitis
-> often painful, more than 1 site, recurrent, present in contacts

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15
Q

What are the extracutaneous manifestations of PVL s aureus?

A

Necrotising pneumonia
Necrotising fasciitis
Purapura fulminans

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16
Q

What are the risks of acquiring PVL staph? (5)

A 
The 5 Cs:
Close contact
Contaminated items
Crowding
Cleanliness
Cuts and grazes
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17
Q

How is PVL staph treated?

A

Antibiotics (often tetracycline)
Decolonisation
Treatment of close contacts

-> consult local microbiologist/guidelines

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18
Q

What does the decolonisation of PVL usually involve? (2)

A

Chlorhexidine body wash for 7 days

Nasal application of mupirocin ointment for 5 days

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19
Q

How does pseudomonal folliculitis present?

A 
Common:
-Diffuse truncal eruption 1-3 days after exposure
-Follicular erythromatous papule
Rare:
-Abscesses
-Lymphangitis
-Fever
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20
Q

Which bacterium causes hot tub folliculitis?

A

Pseudomonas aeruginosa

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21
Q

What is pseudomonal folliculitis associated with? (3)

A

Hot tub use
Swimming pools and depilatories
Sharing wet suits

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22
Q

How are severe and recurrent cases of pseudomonal folliculitis treated?

A

Oral ciprofloxacin

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23
Q

Define cellulitis

A

Infection of the lower dermis and subcutaneous tissue

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24
Q

How does cellulitis present?

A

Tender swelling with ill-defined, blancing erythema or oedema

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25
Q

What causes cellulitis in most cases? (2)

A

Streptococcus pyogenes

Staphylococcus aureus

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26
Q

What is a predisposing factor of cellulitis?

A

Oedema

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27
Q

How is cellulitis treated?

A

Systemic (oral or intravenous) antibiotics

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28
Q

What is impetigo?

A

Superficial bacterial infection

Presents as stuck-on, honey-coloured crusts overlying an erosion

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29
Q

What causes impetigo? (2)

A

Streptococci (non-bullous)

Staphylococci (bullous)

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30
Q

What causes bullous impetigo?

A

Caused by exfoliative toxins A and B

These split the epidermis by targetting desmoglein I

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31
Q

How is impetigo treated?

A

Topical antibiotics +/- systemic antibiotics

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32
Q

What is impetiginisation?

A

Impetigo in the context of atopic dermatitis

Does not typically blister

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33
Q

Which bacterium typically causes impetiginisation?

A

S aureus

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34
Q

What is ecthyma?

A

Severe form of streptococcal impetigo

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35
Q

How does ecthyma present?

A

Thick crust overlying a punch out ulceration surrounded by erythema
Usually on lower extremities

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36
Q

Which populations are more prone to SSS? (3)

A

Neonates
Infants
Immunocompromised adults

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37
Q

What do SSS and bullous impetigo have in common?

A

Both caused by exfoliative toxin

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38
Q

Where does the infection occur relative to the denuded skin in SSS?

A

Distant i.e. conjunctivitis or abscess

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39
Q

Why is SSS more common in neonates?

A

Kidneys cannot rapidly excrete exfoliative toxin

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40
Q

How does SSS manifest? (3)

A

Diffuse tender erythema
Rapid progression to flaccid bullae
Bullae wrinkle and exfoliate, leaving oozing erythomatous base

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41
Q

What does SSS clinically resemble?

A

Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis (SJS/TEN)

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42
Q

What is toxic shock syndrome (TSS)?

A

Febrile illness due to Group A s aureus strain that produces pyrogenic exotoxin TSST-1

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43
Q

How does TSS present? (4)

A

Hypotension
Diffuse erythema
Potential involvement of: GI, muscular, CNS, renal, hepatic systems
Thrombocytopenia

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44
Q

What may occur after the erythema in TSS resolves?

A

Desquamation, esp of palms and soles

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45
Q

Which bacterium causes erythasma?

A

Corynebacterium minutissium

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46
Q

What does erythrasma present as?

A

Well demarcated patches in interiginous areas

-> initially pink, become brown and scaly

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47
Q

What do erythrasma and pitted keratolysis have in common?

A

Both caused by corynebacterium minutissium

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48
Q

How does pitting keratolysis present?

A

Pitted erosions of soles

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49
Q

How is pitting keratolysis treated?

A

Topical clindamycin

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50
Q

What is pitting keratolysis often misdiagnosed as?

A

Athlete’s foot

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51
Q

How does erysipeloid present?

A

Erythema and oedema of the hand after handling contaminated raw fish or meat
Slowly extends over weeks

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52
Q

What bacterium causes erysipeloid?

A

Erysipelothrix rhusiopathiae

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53
Q

What does anthrax manifest as?

A

Painless necrotic ulcer with oedema and surrounding regional lymphadenopathy

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54
Q

How is anthrax contracted?

A

Contact with hides, bone meal or wool infected with Bacillus anthracis

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55
Q

Which bacteria cause blistering distal dactylitis? (2)

A

Streptococcus pyogenes
Staphylococcus aureus
-> rare infection

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56
Q

Who is typically affected by blistering distal dactylitis?

A

Young children

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57
Q

How does blistering distal dactylitis present?

A

1+ tender superficial bullae on erythematous base on bolar fat pad of a finger
Toes may rarely be affected

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58
Q

What is erysipelas?

A

Infection of the deep dermis and subcutis

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59
Q

Which bacteria cause erysipelas?

A

Beta-haemolytic streptococci

Staphylococcus aureus

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60
Q

How does erysipelas present? (3)

A

Preceding of malaise, fever, headache

Erythematous indurated plaque with a sharply demarcated border and cliff-drop edge +/- blistering

+/- red streak of lymphangitis and local lymphadenopathy

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61
Q

Which parts of the body are usually affected by erysipelas?

A

Face or limb

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62
Q

How is erysipelas treated?

A

Portal of entry identified

IV antibiotics

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63
Q

What causes scarlet fever?

A

Upper respiratory tract infection with erythrogenic toxin-producing s pyogenes

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64
Q

What are the initial symptoms of scarlet fever? (6)

A 
Sore throat
Headache
Malaise
Chills
Anorexia
Fever
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65
Q

What symptoms present 12-48 hours after the inital symptoms of scarlet fever? (3)

A

Eruption:
Blanchable tiny pink-red spots on chest, neck, axillae
Spread to whole body within 12 hours
Sandpaper-like texture

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66
Q

What are the complications of scarlet fever? (9)

A 
Otitis
Mastoiditis
Sinusitis
Pneumonia
Myocarditis
Rheumatic fever
Acute glomerulonephritis
Hepatitis
Meningitis
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67
Q

How does necrotising fasciitis present?

A

Initial dusky induration, followed by rapid painful necrosis of skin, connective tissue and muscle

->mortality is high

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68
Q

How is necrotising fasciitis treated?

A

Prompt diagnosis essential; high index of suspicion needed
Broad-spectrum parentral antibiotics
Surgical debridement

-> MRI can aid diagnosis

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69
Q

What causes necrotising fasciitis? (4)

A 
Usually synergistic:
Streptococci
Staphylococci
Enterobacteriae
Anaerobes
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70
Q

What is Fournier’s gangrene?

A

Necrotising fasciitis that affects the scrotum

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71
Q

Which infection is important to consider in immunosuppressed states?

A

Atypical mycobacterial infection

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72
Q

How do mycobacterium marinum infections present? (2)

A

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

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73
Q

How do mycobacterium chelonae and abscessus infections typically develop? (4)

A

Puncture wounds
Tattoos
Skin trauma
Surgery

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74
Q

What is an important cause of limb ulceration in Africa (Buruli ulcer) and Australia (Searle’s ulcer)?

A

Mycobacterium ulcerans

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75
Q

What is borreliosis also known as?

A

Lyme disease

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76
Q

How does borreliosis present?

A

Annular erythema at site of the bite of a borrelia-infected tick:
Erythomatous papule at bite site
Progression to annular erythema of >20cm

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77
Q

What causes lyme disease?

A

Bite from ixodes tick infected with borrelia burgdorferi

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78
Q

What symptoms may occur as lyme disease progresses? (5)

A

Fever and headache 1-30 days after infection
Multiple secondary lesions similar but smaller to inital
Neuroborreliosis
Arthiritis
Carditis

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79
Q

What are the symptoms of neuroborreliosis? (3)

A

Facial/other CN palsies
Aseptic meningitis
Polyradiculitis

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80
Q

Why do you need a high index of suspicion when diagnosing borreliosis? (2)

A

Serology not sensitive

Histopathology non-specific

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81
Q

How does tularaemia present? (5)

A

Primary skin lesion = small papules at inoculation site that rapidly necroses -> painful ulceration
Local cellulitis
Painful regional Lymphadenopathy
Systemic symptoms: fever, chills, headache, malaise

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82
Q

What is the most common form of tularaemia?

A

Ulceroglandular form

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83
Q

How is tularaemia acquired? (3)

A

Francisella tularensis infection through:
Handling infected animals (rabbits and squirrels)
Tick bites
Deerfly bites

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84
Q

What is the difference between ecthyma and ecthyma gangrenosum?

A

Ecthyma is caused by streptococcus

Ecthyma gangrenosum is caused by pseudomonas aeruginosa

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85
Q

Which patients are usually affected by ecthyma gangrenosum?

A

Neutropaenic patients

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86
Q

How does ecthyma gangrenosum present?

A 
Red macule(s) -> becomes oedematus -> forms hemmorhagic bullae
May ulcerate in late stages or form eschar (blackened crust) surrounded by erythema
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87
Q

What are the differentials for escharcotic lesions? (14)

A 
Pseudomonas
Aspergillosis
Leishmaniasis
Cryptococcosis
Lues maligna
Rickettsial infections
Cutaneous anthrax
Tularaemia
Necrotic arachnidism
Scrub typhus
Rat bite fever
Staph or strep
Ecthyma
Lyme disease
88
Q

What causes syphilis?

A

Treponema pallidum

89
Q

How does the primary syphilis infection manifest?

A

Chancre - painless ulcer with a firm indurated border

Appears within 10-90 days

90
Q

What develops one week after the primary chancre in syphilis?

A

Painless regional lymphadenopathy

91
Q

On average, when does secondary syphilis occur?

A

50 days after chancre

92
Q

What are the symptoms of secondary syphilis?

A

Malaise, fever, headache, pruritus, anorexia, iritis

93
Q

Why is secondary syphilis known as the “Great mimicker”?

A

Skin manifestations are very variable so a low threshold for testing is required

94
Q

What are some of the cutaneous ways secondary syphilis can manifest? (7)

A 
Pityriasis rosea-like rash
Moth-eaten alopecia
Lymphadenopathy
Mucous patches
Residual primary chancre
Condylomata lata
Hepatosplenomegaly
95
Q

What is lues maligna?

A

Rare manifestation of secondary syphilis that is more frequent in the context of HIV

96
Q

How does lues maligna present? (2)

A

Pleomorphic skin lesions with pustules, nodules and ulcers

Necrotising vasculitis

97
Q

How does tertiary syphilis manifest? (5)

A

Gumma skin lesions; nodules and plaques
Extend peripherally while central areas heal with scarring and atrophy
Mucosal lesions extend to and destroy nasal cartilage
CV disease
Neurosyphilis

98
Q

What is neurosyphilis?

A

General paresis or tabes dorsalis

99
Q

How is syphilis diagnosed? (2)

A

Clinical findings
Serology

->strong index of suspicion needed for secondary syphilis

100
Q

How is syphilis treated? (2)

A

Intramuscular benzylpenicillin or oral tetracycline

101
Q

What causes leprosy?

A

Mycobacterium leprae

-> obligate intracellular bacteria

102
Q

What are the 2 types of leprosy on each end of the clinical spectrum?

A

Lepromatous leprosy

Tuberculoid leprosy

103
Q

How does lepromatous leprosy present? (2)

A

Multiple lesions: macules, papules, nodules

Early on, sensation and sweating normal

104
Q

How does tuberculoid leprosy present?

A

Solitary or few lesions: elevated borders with atrophic center, sometimes annular

105
Q

What is an important difference between the lesions in tuberculoid and lepromatous leprosy?

A

Tuberculoid leprosy lesions are typically numb, anhidrotic and hairless

106
Q

How can TB be acquired? (3)

A

Exogenously
Contigous endogenous spread
Haematogenous/lymphatic endogenous spread

107
Q

What investigations are needed to diagnose TB? (3)

A

Interferon-gamma release assay (Quantiferon-TB)
Histology - ZN stain
Culture/PCR

108
Q

What are the cutaneous manifestations of TB? (7)

A

Tuberculosis chancre
Tuberculosis verrucosa cutis
Scrufuloderma (subcutaneous nodue with necrotic material)
Orificial TB (non-healing ulcer in nasal mucosa)
Lupus vulgaris
Miliary TB (pinhead bluish-red papules capped by minute vesicles)
Tuberculosis gumma (firm subcutaneous nodule that later ulcerates)

109
Q

Which cutaneous manifestation of TB resembles hidrandenitis suppuritiva?

A

Scrofuloderma:

Subcutaneous nodule with necrotic material; becomes fluctuant and drains, with ulceration and sinus tract formation

110
Q

What does lupus vulgaris have a similar presentation to? (2)

A

Tuberculoid leprosy

Tertiary syphilis

111
Q

What is Molluscum Contagiousum?

A

Poxvirus infection common in children and immunocompromised pts

112
Q

What is the differential for molluscum contagiousum? (4)

A

Verrucae
Condyloma acuminata
Basal cell carcinoma
Pyogenic granuloma

113
Q

What are the treatment options for molluscum contagiosum? (4)

A

Usually resolve spontaneously but if causing distress:
Curettage (scraped off)
Imiquimod
Cidofovir

114
Q

How does herpes simplex present?

A

Primary and recurrent vascular erruptions that favour the oral and genital regions

115
Q

How is HSV-1 transmitted?

A

Direct contact with contaminated saliva/other infected secretions

116
Q

How is HSV-2 transmitted?

A

Sexual contact

117
Q

How does HSV travel? (2)

A

Replicates at mucocutaneous site of infection

Travels by retrograde axonal flow to dorsal root ganglia -> stays latent here between flares

118
Q

How does HSV first present? (5)

A 
Symptoms with 3-7 days of exposure
Tender lymphadenopathy
Malaise
Anorexia
\+/- burning, tingling
119
Q

What do the initial symptoms of HSV develop into? (5)

A

Painful rouped vesicles on erythematous base -> ulceration/pustules/erosions with scalloped border
Orolabial lesions
Genital involvement
Systemic manifestations

->crusting and resolution within 2-6 weeks

120
Q

What can the pain in the genital involvement in HSV lead to?

A

Urinary retention due to excrutiating pain

121
Q

What is a systemic manifestation of HSV?

A

Aseptic meningitis in up to 10% of patients

122
Q

How can HSV reactivation occur? (5)

A 
Spontaneous
UV
Fever
Local tissue damage
Stress
123
Q

What is eczema herpeticum?

A

Potentially fatal HSV infection that occurs in pts with atopic eczema

124
Q

How does eczema herpeticum manifest?

A

Monomorphic, punched-out erosions with excoriated vesicles

125
Q

Why does eczema herpeticum require emergent treatment?

A

It can cause HSV encephalitis and it can be fatal

126
Q

How is eczeme herpeticum treated? (2)

A

IV acyclovir

Antibiotics for superinfections

127
Q

What does herpetic whitlow resemble? (2)

A

Blistering distal dactylitis

Paronychia

128
Q

Which group of pts is herpetic whitlow most common in?

A

Children

129
Q

How does herpetic whitlow present? (4)

A

HSV (1>2) infection of digits
Pain
Swelling
Vesicles (may appear later)

130
Q

How does herpes gladiatorum develop?

A

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

-> common in contact sports e.g. wrestling

131
Q

How does neonatal HSV arise?

A

Exposure to HSV 1 or 2 during vaginal delivery

-> higher risk when HSV acquired near time of delivery

132
Q

How does neonatal HSV present? (4)

A

Onset from birth to 2 weeks
Localised usually scalp or trunk
Vesicles -> bullae erosions
Encephalitis

133
Q

How is neonatal HSV treated?

A

Urgent IV antivirals

134
Q

Which patients can be affected by atypical presentations of HSV?

A

Immunocompromised pts e.g. HIV, transplant recipient

135
Q

What is the most common presentation of HSV in immunocompromised pts? (2)

A

Chronic, enlarging ulceration

Multiple sites or disseminated

136
Q

What are the atypical manifestations of HSV? (2)

A

Verrucous/exophytic/pustular lesions

Involvement of respiratory/GI tracts

137
Q

How is HSV diagnosed?

A

Swab for PCR

138
Q

How is HSV treated?

A

Don’t delay
Oral valacyclovir or acyclovie 200mg 5 times daily in immunocompetent localised infection
Intravenous 10mg/kg TDS X 7-19 days

139
Q

How is varicella zoster virus (a herpes virus) distributed?

A

Dermatomal distribution (single/multiple)

140
Q

What causes hand foot and mouth disease? (2)

A

Coxsackie A16

Echo 71

141
Q

How is hand foot and mouth disease transmitted?

A

Direct contact via oral-oral route or oral-faecal route

142
Q

How does hand foot and mouth disease present? (5)

A

Prodrome of fever, malaise, sore throat
Red macules
Vesicles (grey and elliptical)
Ulcers

-> develop on buccal mucosa, tongue, palate, parynx, hands and feet

143
Q

What is the difference in presentation between the 2 viruses that cause hand foot and mouth disease?

A

Coxsackievirus usually acute and self-limiting

Echo 71 associated with higher incidence of neurological involvement

144
Q

Which viruses cause morbilliform (measles-like) eruptions? (6)

A 
Measles
Rubella
EBV
CMV
HHV6
HHV7
145
Q

What non-viral agents can cause morbilliform rashes? (3)

A

Leptospirosis
Rickettsia
Drugs

146
Q

What causes petechial/purpuric eruptions? (8)

A 
Coagulation abnormalities
Vasculitis
Viruses
Bacterial (BREN)
Other infections
TEN
Raynauds
Ergot poisoning
147
Q

What types of viral infections can cause petechial/purpuric eruptions? (6)

A 
Hep B
CMV
Rubella
Yellow fever
Dengue fever
West nile virus
148
Q

What becterial infections can cause petechial/purpuric eruptions? (5)

A 
Borrelia
Rickettsia
Neisseria
Meningococcus
Endocarditis
149
Q

What non-viral/bacterial infections can cause petechial/purpuric eruptions? (3)

A

Plasmodium
Falciparum
Trichinella

150
Q

How does Gianotti-Crosti syndrome present?

A

Viral eruption

Acute symmetrical erythematous papular eruption on face, extremities, buttocks

151
Q

What is Gianotti-Crosti syndrome also known as?

A

Papular acrodermatitis of childhood

152
Q

What causes Gianotti-Crosti syndrome? (5)

A 
EBV (most common)
CMV
HHV6
Coxsackie viruses A16, B4, B5
Hep B
153
Q

What causes erythema infectiosum?

A

Parvovirus B19

aka 5th disease

154
Q

How does erythema infectiosum present? (3)

A

Initially mild fever and headache
A few days later - “slapped cheeks” for 2-4 days
Reticulated rash of chest and thighs in 2nd stage of disease

155
Q

What is roseola infantum also known as? (2)

A

Exanthem subitum

6th disease

156
Q

How does roseola infantum present?

A

2-5 days high fever

Small pale pink papules on trunk and head that lasts hours - 2 days

157
Q

What causes roseola infantum?

A

HHV6 (more common)

HHV7

158
Q

How does orf present? (3)

A

Dome-shaped, firm bullae that develop an umbilicated crust
Usually develops on hands and forearms
Generally resolves w/o therapy in 4-6 weeks

-> resembles cutaneous anthrax

159
Q

What causes orf?

A

Parapox virus

160
Q

Which pts are more at risk of developing orf?

A

People with direct exposure to sheep or goats i.e. farmers

161
Q

What are warts caused by?

A

HPV

>200 subtypes of HPV

162
Q

Why is it important to biopsy suspicious warts?

A

Serious diseases e.g. syphilis, skin cancer can resemble warts

163
Q

What are examples of superficial fungal infections? (3)

A

Candida
Malassezia
Dermatophytes

164
Q

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

A

Chromomycosis

Madura foot

165
Q

What are examples of disseminated fungal infections? (7)

A 
Candida
Aspergillus
Fusarium
Histoplasma
Coccidiodes
Blastomycosis
Mucormycosis
166
Q

How does pityriasis vesicolour present? (2)

A

Hypo/hyperpigmented or erythematous macular eruption

+/- fine scale

167
Q

What causes pityriasis versicolor?

A

Malassezia spp

168
Q

Why does pityriasis versicolor begin in adolescence?

A

Sebaceous glands become active

169
Q

When does pityriasis versicolor flare? (3)

A

High temperatures
High humidity
Immunosuppression

170
Q

How is pityriasis versicolor treated?

A

Topical azole (OTC drug)

171
Q

What are dermatophytes?

A

Fungi that live on keratin

172
Q

Which fungus causes the most dermatophyte fungal infections?

A

Trichophyton rubrum

173
Q

Which fungus causes the most tinea capitis?

A

Trichophyton tonsurans

174
Q

What is kerion?

A

Inflammatory fungal infection, frequently secondarily infected with staph aureus

175
Q

How does kerion present?

A

Mimics bacterial folliculitis or abscess of the scalp
Tender scalp
Posterior cervical lymphadenopathy

176
Q

What are a lot of the symptoms in kerion caused by?

A

The host’s defensive response against fungal infection

177
Q

What is tinea faciei?

A

Area of erythema and scale

178
Q

What is onychomycosis?

A

Dermatophyte infection of the toenail

179
Q

What does tinea pedis present as? (2)

A

Scaling and hyperkeratosis of plantar surface of foot

Athlete’s foot

180
Q

What causes tinea pedis? (2)

A

Trichophyron rubrum

Trichophyton interdigitale

181
Q

What can trichophyton interdigitale cause in addition to tinea pedis?

A

Vesicobullous reaction on arch or side of foot

182
Q

What are Id (aka dermatophytid) reactions?

A

Inflammatory reactions at sites distant from associated dermatophyte infection

183
Q

What can Id reactions present as? (3)

A

Urticaria
Hand dermatitis
Erythema nodosum

-> secondary immune-mediated eczema

184
Q

What likely causes Id reactions?

A

Secondary to host immunologic response against fungal antigens

185
Q

What is a majocchi granuloma?

A

Follicular abcess produced when dermatophyte infection penetrates the follicular wall into surrounding dermis

186
Q

What usually causes majocchi granulomas? (2)

A

Trichophyton rubrum

Mentagrophytes

187
Q

What could be included in the differential for majocchi granulomas?

A

Petechia-purpuric eruptions

188
Q

What causes candidiasis?

A

Candida albicans

189
Q

How does candidiasis present? (2)

A

Erythema oedema

Thin, purulent discharge

190
Q

What increases the risk of developing candidiasis? (4)

A

Occulsion
Moisture
Warm temperature
Diabetes mellitus

191
Q

Which areas are affected by candidiasis?

A

Usually interiginous infection: affects axillae, submammary folds, crue, digital clefts
Oral mucosa

192
Q

What is a common cause of vulvovaginitis?

A

Candidiasis

193
Q

When might candidiasis become systemic?

A

In immunocompromised pts

194
Q

What cn cause deep fungal infections? (6)

A 
Implantation or inoculation of the skin:
Phaeohypomycosis
Chromomycosis
Mycetoma (madura foot)
Lobomycosis
Rhinosporidiosis
195
Q

How can systemic fungal infections develop?

A

Secondary to an internal infection i.e. of an organ

196
Q

What are some examples of systemic respiratory endemic fungal infections? (5)

A 
Blastomycosis
Histoplasmosis
Coccidiodomycosis
Paracoccidoiodomycosis
Penicillinosis
197
Q

What are the risk factors for opportunistic fungal infections (e.g. aspergillosis)? (2)

A

Neutropenia

Corticosteroid therapy

198
Q

How does aspergillosis present? (3)

A

Well-circumscribed papule with necrotic base and surrounding erythematous halo
Lesions may extend into cartilage, bone, fascial planes
Propensity to invade blood vessels and cause thrombosis/infarction

199
Q

What is aspergillosis similar to both clinically and histologically?

A

Fusarium

200
Q

How does mucormycosis present? (7)

A 
Fever
Headache
Facial oedema
Proptosis
Facial pain
Orbital cellulitis
\+/- cranial nerve dysfunction
201
Q

What causes mucormycosis? (5)

A 
Apophysomyces
Mucor
Rhizopus
Absidia
Rhizomucor

-> can be caused by a combo of these

202
Q

What is mucormycosis associated with? (7)

A 
Diabetes mellitus
Malnutrition
Uraemia
Neutropenia
Medications: steroids/ABs/desferoxamine
Burns
HIV
203
Q

How is mucormycosis treated? (2)

A

Aggressive debridement

Anti-fungal therapy

204
Q

What is scabies?

A

Contagious infestation caused by sarcoptes species

205
Q

How does scabies present? (3)

A

Insidious onset of red to flesh-coloured pruritic papules
Affects interdigital areas, volar wrists, axillary areas, genitalia
Diagnostic burrow w/ fine white scale under dermatoscope

206
Q

What is Norwegian scabies?

A

Aka crusted scabies
Hyperkeratosis, scaly
Found in immunocompromised

207
Q

How is scabies treated? (5)

A 
Permethrin
Oral ivermectin
2 cycles of treatment required
Wash all clothes/bedlinen
Treat close contacts
208
Q

Why are 2 cycles of treatment required for scabies?

A

Eggs are not vulnerable to treatments so need to wait 1 week-10 days after to kill hatchlings

209
Q

What are the 3 types of lice?

A

Head lice
Body lice
Pubic lice

-> aka pediculius humanus capitis, phithrus pubis

210
Q

How are head lice treated? (3)

A

Malathion
Permethrin
Oral ivermectin

-> secondary infection common which may require treatment

211
Q

What are the symptoms of body lice?

A

Pruritic papules and hyperpigmentation

212
Q

How are body lice removed?

A

Rarely found on skin so can be removed by thorough cleaning/discarding of clothes

213
Q

Where are pubic lice eggs found?(5)

A 
Hair shaft
Orbital scalp
Body hair
Eyebrow/eyelash
Axillary hair
214
Q

What is the treatment for pubic lice?

A

Malathion
Oermethrin
Oral ivermectin

215
Q

What conditions are body lice common in? (3)

A

Overcrowding
Poverty
Poor hygeine

216
Q

What do bedbugs (cimex lectularius) cause?

A

Itchy wheals around central punctum

217
Q

How do you remove bedbugs? (2)

A

Live behind wallpaper and under furniture so fumigation of home is necessary
Treat pt if symptomatic

BRS 2.0 (2 decks)

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