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skin infection/ infestation Flashcards

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1
Q

What is Panton Valentine Leukocydin?

A

Staphylococcus receptor that allows it to bind to fibrin that is found in abundance on wound surfaces and in dermatitis

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2
Q

What skin infections does staphylococcus play a role in?

A

Echtyma
Impetigo
Cellulitis
Folliculitis (furunculosis, carbuncles)
Staphylococcal scalded skin syndrome (SSSS)
Superinfects other dermatoses (atopic eczema, leg ulcers, HSV)

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3
Q

What kind of hemolysis does streptococcus pygenes carry out?

A

B hemolysis

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4
Q

Describe the virulence of streptococcus pygenes

A

Attaches to epithelial surfaces via lipoteichoic acid portion of fimbriae

Has M protein (anti-phagocytic) and hyaluronic acid capsule

Produces erythrogenic exotoxins

Produces streptolysins S and O

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5
Q

What skin infections does streptococcus play a role in?

A 
Echthyma 
Impetigo
Cellulitis
Erysipelas
Scarlet Fever
Necrotising fasciitis
Superinfects other dermatoses (leg ulcers)
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6
Q

What does the cutaneous manifestation of folliculitis look like?

A

Follicular erythema, sometimes papular

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7
Q

Is folliculitis infection or non-infectious?

A

May be infectious or non-infectious

Eosinophilic (non-infectious) folliculitis is associated with HIV

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8
Q

What could cause recurrent folliculitis?

A

Nasal carriage of staphylococcus aureus, particularly strains expressing PVL

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9
Q

How is folliculitis treated?

A

Antibiotics, usually flucloxacillin or erythromycin

Incision and drainage is required for furunculosis

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10
Q

What is the difference between a furuncle and a carbuncle?

A

A furuncle is a deep follicular abscess
Involvement with adjacent connected follicles- carbuncle

Cabuncles are more likely to lead to complications such as cellulitis and septicaemia

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11
Q

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

A

Establishment as part of the resident microflora
-abundant in nasal flora

Immune deficiency

  • chronic granulomatous disease
  • AIDS
  • Diabetes mellitus
  • Hypogammaglobulinemia
  • Hyper IgE syndrome- deficiency
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12
Q

What kind of toxin does PVL Staphylococcus aureus produce and what are its effects?

A

B-pore forming toxin
Leukocyte destruction and tissue necrosis
Higher morbidity, mortality and transmission

skin: recurrent and painful abscesses, folliculitis, cellulitis (often painful, recurrent, more than 1 site, present in contacts)
extracutaneous: necrotising pneumonia, necrotising fasciitis, purpura fulminans

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13
Q

What are the risk factors for acquiring PVL Staphylococcus aureus?

A

5Cs

Close contact (hugging, contact sports)
Crowding (living in crowded accommodation like boarding school, military accommodation, prison)
Cleanliness (of environment)
Contaminated items (gym equipment, towels, razors
Cuts and grazes (allowing bacteria to enter body)

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14
Q

How is PVL staphylococcus aureus treated?

A

Consult local mocrobiologist/ guidelines

Antibiotics (often tetracycline)

Decolonisation often:
chlorhexidine body wash for 7 days
nasal application of mupirocin ointment, 5 days. )

Treatment of close contacts

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15
Q

What is acquiring pseudomonas folliculitis associated with?

A

Hot tub use, swimming pools, wet suit, depilatories

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16
Q

Describe the symptoms of pseudomonas folliculitis

A

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

follicular erythematous papule

rarely: abcesses, lymphangitis, fever

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17
Q

How is pseudomonas folliculitis treated?

A

Most cases are self limited- no treatment required

Sever or recurrent cases can be treated with oral ciprofloxacin

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18
Q

What is cellulitis and how does it manifest?

A

Infection of lower dermis and subcutaneous tissue

tender swelling with ill define, blanching erythema or oedema

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19
Q

What is a predisposing factor for cellulitis?

A

Oedema

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20
Q

What are the causative organisms of cellulitis?

A

Most commonly streptococcus pyogenes and staphylococcus aureus

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21
Q

What is the treatment for cellulitis?

A

Systemic antibiotics

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22
Q

Describe impetigo manifestation

A

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

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23
Q

What organisms caused impetigo?

A

Streptococci (non-bulbous)
Staphylococci (bulbous)
caused by exfoliating toxins A and B
which split epidermis by targeting desmoglein I

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24
Q

What parts of the body does impetigo often affect?

A

Face (perioral, ears, nares)

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25
Q

How is impetigo treated?

A

Topical +/- systemic antibiotics

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26
Q

In what skin condition can impetigisation occur and what causes it?

A 
Atopic dermatitis (gold crust)
staphylococcus aureus
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27
Q

What is echthyma?

What does it look like?

A

Sever form of streptococcal impetigo

Thick crust overlying a punch out ulceration surrounded by erythema

Usually on lower extremities

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28
Q

What is echthyma?

What does it look like?

A

Sever form of streptococcal impetigo

Thick crust overlying a punch out ulceration surrounded by erythema

Usually on lower extremities

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29
Q

In what groups of people does staphylococcal scalded skin syndrome generally occur?

A

Neonates, infants, immunocompromised adults

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30
Q

What kind of toxin causes staphylococcal scalded skin syndrome?

A

Exfoliative toxin

In neonates, kidneys cannot excrete the exfoliative toxin quickly

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31
Q

Why can organism not be cultured from denuded skin in staphylococcal scalded skin syndrome ?

A

Infection occurs at distant site (e.g. conjunctivitis, abscesses

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32
Q

Describe the progression of staphylococcal scalded skin syndrome.

A

diffuse tender erythema that rapidly progresses to flaccid bullae that wrinkle and exfoliate, leaving an oozing erythematous base

clinically resembles SJS/TEN

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33
Q

What organism causes toxic shock syndrome?

A

Group A Staphylococcus aureus strain that produces pyogenic exotoxin TSST-1

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34
Q

What are the symptoms of TSS?

A

Fever >38.9 0C
Hypotension
Hematologic (platelets <100,000/mm3)
Systemic involvement (Renal, Hepatic, GI, Muscular, CNS)
Diffuse erythema
Mucous membranes
Desquamation predominantly of palms and soles 1-2 weeks after resolution of erythema

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35
Q

What organism causes erythrasma?

A

Corynebacterium minitissimum

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36
Q

Describe the cutaneous manifestation of erythrasma

A

Well demarcated patches in intertriginous areas

Initially pink, become brown and scaly

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37
Q

What is pitted keratolysis?

A

Pitted erosions of the soles

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38
Q

What organisms cause pitted keratolysis?

A

Corynebacteria

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39
Q

How is pitted keratolysis treated?

A

Topical clindamycin

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40
Q

What occurs in erysipeloid?

A

Erythema and oedema of the hand after handling contaminated raw fish or meat

extends slowly over weeks

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41
Q

What organism causes erysipeloid?

A

Erysipelothrix rhusiopathiae

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42
Q

What organism causes anthrax?

A

Bacillus anthracis

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43
Q

How does anthrax manifest?

A

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

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44
Q

What organisms cause blistering distal dactylitis?

A

Streptococcus pyogenes

Staphylococcus aureus

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45
Q

In what group of the population does blistering distal dactylitis commonly occur?

A

Typically young children

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46
Q

Describe the cutaneous manifestation of blistering distal dactylitis.

A

One or more tender superficial bullae on an erythematous base on the volar fat pad of finger

toes may be rarely affected

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47
Q

What is erysipelas?

A

Infection of deep dermis and subcutis

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48
Q

What organisms cause erysipelas?

A

Staphylococcus aureus
B-hemolytic streptococci

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49
Q

Describe the symptoms of erysipelas.

A

Painful

Prodrome of fever, malaise, headache

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

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

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50
Q

Name a possible portal of entry in erysipelas.

A

Tinea pedis

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51
Q

How is erysipelas treated?

A

Intravenous antibiotics

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52
Q

In which part of the population does scarlet fever occur?

A

Primarily a disease of children

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53
Q

What causes scarlet fever?

A

Upper respiratory tract infection with erythrogenic toxin producing streptococcus pyogenes

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54
Q

What are the symptoms of scarlet fever?

A

Preceded by fever, malaise, headache, sore throat, chills, anorexia

Eruption begins 12-48 hours later: blanch able, tiny pinkish red spots on chest, neck and axillae that spreads to the whole body within 12 hours. Sandpaper like texture.

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55
Q

What are the complications of scarlet fever?

A

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

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56
Q

What occurs in necrotising fasciitis?

A

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

Potentially fatal

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57
Q

What organisms cause necrotising fasciitis?

A

Usually synergistic: streptococci, staphylococci, enterobacteriae and anaerobes

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58
Q

How is necrotising fasciitis treated?

A

Prompt diagnosis is essential (requires high index of suspicion), followed by broad-spectrum parenteral antibiotics and surgical debridement.

MRI can aid diagnosis.

Blood and tissue cultures can determine organisms and sensitivities.

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59
Q

What are the complications of necrotising fasciitis?

A

Mortality is high

Can affect scrotum (Fournier’s gangrene)

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60
Q

In what kind of individuals does atypical mycobacterial infection occur?

A

Immunocompromised

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61
Q

Give examples for atypical mycobacterium infection.

A

Mycobacterium marinum: causes indolent granulomatous ulcers (fish tank ulcer) in healthy adults. Sporotrichoid spread.

Mycobacterium chelonae and abscessus: puncture wounds, tattoos, skin trauma or surgery
Mycobacterium ulcerans: important cause of limb ulceration in Africa (Buruli ulcer) or Australia (Searle’s ulcer)

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62
Q

What causes borreliosis/ Lyme disease?

A

Bite from an Ixodes tick infected with Borrelia burgdorferi

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63
Q

What is the initial cutaneous manifestation of borrelia/ Lyme disease?

A

Erythema migraines (only in 75%)

  • erythematous papule at bite site
  • progression to annular erythema >20cm
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64
Q

How does Lyme disease progress?

A

Fever, headache 1-30 days after infections

multiple secondary lesions develop (similar to initial lesion but smaller)

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65
Q

What are complications of Lyme disease?

A

Neuroborreliosis- facial/ other CN palsies, aseptic meningitis, polyradiculitis
Arthritis- painful and swollen large joints (knee is the most affected joint)
Carditis

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66
Q

How is Lyme disease diagnosed?

A

Serology not sensitive
Histopathology- non specific
High index of suspicion required for diagnosis

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67
Q

What organism causes tularaemia?

A

Francisella tularensis

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68
Q

How is tularaemia acquired?

A

Handling of infectious animals (rabbits, squirrels)
Tick bites
Deerfly bites

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69
Q

How does tularaemia present?

A

Ulceroglandular form
Primary skin lesion is small papules at inoculation site which rapidly necroses- leading to painful ulceration
+/- local cellulitis
Painful regional lymphadenopathy
Systemic symptoms: fever, headache, malaise, chills

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70
Q

What is the causative organism of echthyma gangrenosum?

A

Pseudomonas aeruginosa

71
Q

In what patients does echthyma gangrenosum occur?

A

Neutropenic patients

72
Q

Describe the cutaneous manifestation of echthyma gangrenosum.

A

Red macules–> oedematous–>haemorrhagic bullae

May ulcerate in later stages/ form an escharotic lesion

73
Q

In what diseases are escharotic lesions seen?

A

Lyme disease
Leishmaniasis
Necrotic arachidnism (brown recluse spider bite)
Tularaemia
Rat bite fever (Spirillum minus)
Cutaneous anthrax
Scrub typhus (orientia tsutsugamushi)
Staphylococcal/ streptococcal
Pseudomonas
Aspergillosis
Cryptococcosis
Lues Maligna
Rickettsial infection
Echthyma

74
Q

What is the causative agent in Syphilis?

A

Treponema pallidum

75
Q

What happens during the primary infection in syphilis?

A

Chancre- painless regional ulcer with a firm, indurated border (appears within 10-90 days)

Painless regional lymphadenopathy one week after primary chancre

76
Q

When does secondary syphilis begin?

A

50 days after chancre

77
Q

What are the symptoms of secondary syphilis

A

Malaise, fever, headache, pruitis, it is, loss off appetite

‘great mimicker’- low threshold for testing

  • rash (88-100%)- pityriasis rosea-like rash
  • moth eaten alopecia
  • mucus patches
  • lymphadenopathy
  • hepatosplenomegaly
  • residual primary chancre
  • condylomata lata
78
Q

What can condylomata late of syphilis in anogenital regions be misdiagnosed as?

A

HPV infection (condylomata acuminata)

79
Q

What is lues maligna?

A

Rare manifestation of secondary syphilis (more common in HIV manifestation)

80
Q

Describe the cutaneous manifestation of lues maligna.

A

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

81
Q

What are the cutaneous manifestations of tertiary syphilis?

A

Gumma skin lesions (nodules and plaques)
Extend peripherally while central areas heal with scarring and atrophy
mucosal lesions extend and destroy nasal cartilage

82
Q

What are the complications of tertiary syphilis?

A

Cardiovascular disease
Neurosyphilis (general paresis, tabes dorsalis)

83
Q

How is syphilis diagnosed?

A

Clinical findings
Serology
Strong index of suspicion required in 2ndary syphilis

84
Q

How is syphilis treated?

A

IM benzylpenicillin/ orał tetracycline

85
Q

What is the causative organism of leprosy?

A

Mycobacterium leprae (obligate intracellular bacteria)

86
Q

What organs does leprosy affect?

A

Predominantly skin and nerves but can affect any organ

87
Q

What are the two types of leprosy?

A

Lepromatous leprosy- multiple lesions (macules, papules, nodules). Sensation and sweating normal (early on)

Tuberculoid leprosy- solitary/ few lesions (elevated border, atrophic centre, sometimes annular)
hairless, anhidrotic and numb

88
Q

What systems does tuberculosis affect?

A

Any organ systems including skin

89
Q

what percentage of TB infections lead to clinical disease?

A

5-10%

90
Q

How can cutaneous TB be acquired?

A

Exogenously- primary-innoculation TB, tuberculosis verrucosa cutis

Contiguous endogenous spread- scrufuloderma

Autoinnoculation- periorificial TB

Hematogenous/ lymphatic endogenous spread- lupus vulgarisms, military TB, gummas

91
Q

What investigations are carried out for TB?

A

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

92
Q

What are the cutaneous manifestations of tuberculous chancre?

A

painless, firm, reddish -brown papulonodule that forms an ulcer

93
Q

What are the cutaneous manifestations of TB verrucosa cutis?

A

wart-like papule that evolves to form a red-brown plaque

94
Q

What are the cutaneous manifestations of scrufuloderma?

A

subcutaneous nodule with necrotic material.
becomes fluctuant and drains with ulceration and sinus tract formation

95
Q

What are the cutaneous manifestations of orificial TB?

A

non-healing, painful ulcer of the nasal mucosa

96
Q

What are the cutaneous manifestations of lupus vulgaris?

A

red brown plaque +/- central scarring, ulceration

97
Q

What are the cutaneous manifestations of military TB?

A

pinhead sized blush red papule capped by minute vesicles

98
Q

What are the cutaneous manifestations of tuberculous gumma?

A

firm subcutaneous nodule, later ulcerates

99
Q

What virus infection causes molluscum contagiosum?

A

Poxvirus

100
Q

In what populations is molluscum contagiosum common?

A

Children
Immunocompromised

101
Q

What are the cutaneous signs of molluscs contagiosum?

A

Verrucae
Condylomata acuminata
Basal cell carcinoma
Pyogenic granuloma

102
Q

How is molluscs contagiosum treated?

A

Usually resolves spontaneously

103
Q

What kind of eruptions are seen in HSV?

A

Primary and recurrent vesicular eruptions

104
Q

What body regions does HSV infection favour?

A

Orolabial and genital regions

105
Q

When does transmission of HSV begin?

A

During asymptomatic periods of viral shedding

106
Q

What are the 2 types of HSV and how do they spread?

A

HSV-1: directed contact with contaminated saliva/ other secretions
HSV-2: sexual contact

107
Q

How does HSV replicate and how is it transported?

A

replicates at mucocutaneous sites of infection
travels by retrograde axonal flow to dorsal root ganglion

108
Q

Describe herpes symptoms and progression

A

Symptoms within 3-7 days of exposure

Preceded by tender lymphadenopathy, malaise, anorexia, burning and tingling

Painful grouped vesicles on an erythematous base- ulcerations/ pustules/ erosions with a scalloped border

crusting and resolution within 2-6 weeks

orolabial involvement generally painless, genital involvement highly painful with urinary retention

systemic manifestations- aseptic meningitis in upto 10% of cases

Reactivation- Spontaneous, UV, fever, local tissue damage, stress

109
Q

What do lesions look like in eczema herpeticum?

A

Monomorphic, punched out erosions
excoriated vesicles

110
Q

What is herpetic whitlow

A

HSV (1>2) infection of digits, with pain, swelling and vesicles (vesicles may appear later)

Misdiagnosed as paronychia or dactylitis

Often in children

111
Q

What is herpes gladiatorum?

A

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

seen in contact sports e.g. wrestling

112
Q

How is neonatal HSV acquired?

A

Exposure to HSV during vaginal delivery- risk higher when HSV is acquired near time of delivery

HSV 1/2

113
Q

When is the onset of neonatal HSV?

A

From birth to 2 weeks

114
Q

How does neonatal HSV present?

A

Usually localised to scalp or trunk

vesicles–> bullous erosions

115
Q

Complications of neonatal HSV?

A

Encephalitis- mortality 50% without treatment, 15% with treatment

Neurological deficits

116
Q

Treatment for neonatal HSV?

A

IV antivirals

117
Q

In what type of patients is sever/ chronic HSV seen?

A

Immunocompromised (HIV/ transplant recipient)

118
Q

How does severe/ chronic HSV present?

A

Most common presentation- chronic, enlarging ulceration
often atypical- verrucous, exophytic, pustular
multiple sites/ disseminated
involvement of respiratory/ GI tract may occur

119
Q

How is HSV diagnosed?

A

Swab for PCR

120
Q

How is HSV infection treated?

A

Don’t delay

Orał valacyclovir/ acyclovir 200mg fives times daily in an immunocompetent, localised infection

Intravenous 10mg/kg TDS X 7-19 days

121
Q

Name a virus that causes dermatomal infection

A

Varicella zoster
Single dermatome/ multidermatomal

122
Q

What causes hand, foot and mouth disease?

A

Coxsackie A16, Echo 71

An acute self-limiting coxsackievirus infection

Echo 71 associated with a higher incidence of neurological involvement, including fatal cases of encephalitis

123
Q

Symptoms of hand, foot and mouth disease?

A

Prodrome of fever, malaise and sore throat

Red macules, typically grey and elliptical vesicles and ulcers develop on buccal mucosa, tongue, palate, pharynx and may also develop on hands and feet (acral and volar surfaces)

124
Q

How does hand foot and mouth disease spread?

A

Direct contact via oral-oral/faecal-oral route

125
Q

What viruses cause morbilliform eruptions?

A

Measles, rubella, EBV, CMV, HHV6 and HHV7

126
Q

What non-viral agents cause morbilliform eruptions?

A

Rickettsia
Leptospirosis

127
Q

Which disorders mimic morbilliform eruptions?

A 
Drug eruptions (most commonly)
Arthropod reactions
Viral morbilliform reactions
Pityriasis rosea
Early guttate psoriasis
128
Q

What causes petechial/ purpuric eruptions?

A

Coagulation abnormalities- TTP, ITP, DIC
Vasculitis
Infections
Viruses- Hepatitis B, CMV, Rubella, Yellow fever, dengue fever, West Nile virus
Bacteria (BREN)- Borrelia, rickettsia, Endocarditis, Neisseria
Other infections- Trichinella, Plasmodium falciparum
Other- TEN, Ergot poisoning, Raynaud’s

129
Q

What is Gianotti-Crosti syndrome

A

Papular acrodermatitis of childhood
A viral eruption that causes an acute, symmetrical, erythematous, papular eruption on face, extremities and buttocks, usually in children aged 1-3

130
Q

What viruses can cause Gianotti-Crosti syndrome?

A

EBV, CMV, HHV6, Hep B, Coxsackie virus A16, B4, B5

131
Q

What virus causes erythema infectiosum?

A

Parvovirus B19

132
Q

Describe the symptom progression of erythema infectiosum.

A

Initially mild fever and a headache

A few days later “slapped cheeks” for 2-4 days

Reticulated/ lacy rash in chest and thighs in second stage of disease

133
Q

What is roseola infant also known as?

A

Exanthum subitum

6th disease

134
Q

What viruses cause roseola infantum?

A

HHV6 and HHV7 (less commonly)

135
Q

In what population is roseala infant generally observed?

A

Children

136
Q

What are the symptoms of roseola infantum?

A

2-5 days of high fever

followed by appearance of small pale pink papule on trunk and head that last hours to 2 days

137
Q

What causes orf?

A

parapoxvirus on direct exposure to goats and sheep

138
Q

Cutaneous manifestations of orf?

A

Dome shaped, firm bullae that develop an umbilicate crust

usually on hands/ forearms

139
Q

How is orf treated?

A

Usually resolves without therapy in 4-6 weeks

140
Q

How many subtypes of HPV cause warts?

A

> 200

141
Q

What organisms cause superficial fungal infections?

A

Candida
Malassezia
Dermatophytes

142
Q

What organisms cause deep/ soft tissue fungal infections?

A

Madura foot
Chromomycosis

143
Q

What organisms cause disseminated fungal infections?

A 
Aspergillus
Blastomycosis, mucormycosis
Candida, coccidiodes
Fusarium
Histoplasma
144
Q

What organism causes pityriasis versicolor?

A

Malassezia species

145
Q

Describe cutaneous manifestation of pityriasis versicolor.

A

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

146
Q

When does pityriasis versicolor begin and when does it flare up?

A

Begins in adolescence when sebaceous glands become activated

Flare ups occur in high temperature and high humidity- immunosuppression

147
Q

Treatment for pityriasis versicolor?

A

Topical azalea

148
Q

What are dermatophytes?

A

Fungi that live on keratin

149
Q

What organism causes most fungal infections?

A

Trichophyton rubrum

150
Q

What organism causes the most tinea capitis?

A

Trichophyton tonsurans

151
Q

What is a kerion?

A

An inflammatory fungal condition which mimics a bacterial infection/ scalp abscess

patients usually have tender scalp and posterior cervical lymphadenopathy

frequently secondarily infected with staphylococcus aureus

152
Q

What organisms can cause tinea pedis?

A

Trichophyton rubrum- scaling and hyperkeratosis of plantar surface of foot

Trichophyton mentagrophtyes (interdigitale)- sometimes vesiculobullous reaction on arch/ side of foot

153
Q

What is an id reaction?

A

Dermatophytid reaction
Inflammatory reaction at sites distant to the associated dermatophyte infection
Likely secondary to a strong immunological response from host against fungal antigens

may include urticaria, hand dermatitis, erythema nodosum

154
Q

What organisms cause Majocchi granuloma

A

Tirchphyton rubrum

Trichophyton mentagrophytes

155
Q

What is Majocchi granuloma?

A

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

156
Q

What organism causes candidiasis?

A

Candida albicans

157
Q

What predisposes an individual to candidiasis?

A

Diabetes mellitus, occlusion, moisture, high temperature

158
Q

What areas do candidiasis commonly affect?

A

Intertrignous regions (axillae, submammary clefts, digital clefts,, crurae) or oral mucosa

a common cause of vulvovaginitis

can affect mucosae

can become systemic (in immunocompromised individuals)

159
Q

How can skin conditions be caused in fungal infection?

A

Deep invasion of skin

Production of lesions secondary to systemic vascular infection

subcutaneous fungal infections- infections of implantation (innoculation)

160
Q

Give examples for deep fungal infections

A 
Chromomycosis
Lobomycosis
Phaehypomycosis
Sporotrichosis
Rhinosporidiosis
Mycetoma (Madura foot)
161
Q

Give examples for systemic respiratory endemic fungal infections

A 
blastomycosis
histplasmosis
coccidioidomycosis 
paracoccidioidomycosis
penicillinosis
161
Q

Give examples for systemic respiratory endemic fungal infections

A 
blastomycosis
histplasmosis
coccidioidomycosis 
paracoccidioidomycosis
penicillinosis

disease in both immunocmpromised and immunosuppressed

162
Q

What are risk factors for aspergillosis?

A

Neutropenia, corticosteroid therapy

163
Q

What system does aspergillosis primarily affect?

A

Respiratory system

164
Q

Describe the cutaneous lesion seen in aspergillosis

A

well define papule with a necrotic base and surrounding erythematous halo

165
Q

What are potential complications of aspergillosis?

A

Can invade blood vessels causing thrombosis and infarction

Lesions are destructive and may extend into cartilage, bone and facial planes

166
Q

What organism causes similar illness to aspergillosis (both clinically and histologically)?

A

Fusarium (septet hyphae with acute angle branching

167
Q

What organisms caused mucormycosis?

A

Apophysomyces, mucor, rhizomucor, rhizopus, absidia

168
Q

What conditions/ therapies are associated with mucormycosis?

A

1/3 of patients have diabetes, with those with DKA at particularly higher risk

malnutrition
uraemia
neutropenia
steroid therapy
burns
antibiotic therapy
deferoxamine therapy
HIV
neonatal prematurity
169
Q

How does mucormycosis present?

A

Fever, headache, facial oedema, facial pain, proptosis, orbital cellulitis, cranial nerve dysfunction

+/- nerve dysfunction due to retinal artery thrombosis

170
Q

How is mucormycosis treated?

A

Aggressive debridement and antifungal therapy

171
Q

How often is the culture positive in cases of mucormycosis?

A

Only 30% of the time

172
Q

Scabies

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
Crusted or ‘Norwegian’ scabies - hyperkeratosis
- Often asymptomatic;immunocompromised individuals
Treatment: permethrin, oral ivermectin
- Two cycles of treatment are required

derm 2 (3 decks)

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