infestations and infections of the skin Flashcards

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1
Q

what is staphylococcus aureus like?

A

bacteria

expresses virulence factors that confer pathogenic properties
eg receptors that allow it to bind fibrin, that is found at injury sites

symptoms:
Ecthyma
Impetigo
Cellulitis

Folliculitis

- Furunculosis
- Carbuncles 

Staphylococcal scalded skin syndrome (SSSS)

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

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2
Q

what are streptococcus like?

A

bacterial

Virulence:
Strepococcus pyogenes (β-haemolytic) attaches to epithelial surfaces via 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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3
Q

what are symptoms of streptococcal infections?

A

symptoms:
Ecthyma
Cellulitis
Impetigo

Erysipelas
Scarlet fever
Necrotizing fasciitis

Superinfects other dermatoses (e.g. leg ulcers)

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4
Q

what is folliculitis?

A

Follicular erythema; sometimes pustular.

May be infectious or non-infectious.

Eosinophilic (non-infectious) folliculitis is associated with HIV.

Recurrent cases may arise from nasal carriage of Staphylococcus aureus, particularly strains expressing Panton-Valentine leukocidin (PVL).

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5
Q

how is folliculitis treated?

A

Treatment:
Antibiotics (usually flucloxacillin or erythromycin)
Incision and drainage is required for furunculosis.

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6
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.

Carbuncle - more likely to lead to complications such as cellulitis and septicaemia

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7
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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8
Q

what is panton valentine leukocidin staphylococcus aureus?

A

β-pore-forming exotoxin
Leukocyte destruction and tissue necrosis
Higher morbidity, mortality and transmissibility

Skin:

  • Recurrent and painful abscesses
  • Folliculitis
  • Cellulitis
  • Often painful, more than 1 site, recurrent, present in contacts

Extracutaneous:

  • Necrotising pneumonia
  • Necrotising fasciitis
  • Purpura fulminans
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9
Q

what is the risk of acquiring PVL staphylococcus aureas?

A

Risk of acquiring - 5 C’s

Close Contact – e.g. hugging, contact sports

Contaminated items , e.g. gym equipment, towels or razors.

Crowding –crowded living conditions such as e.g. military accommodation, prisons and boarding schools.

Cleanliness (of environment)

Cuts and grazes – having a cut or graze will allow the bacteria to enter the body

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10
Q

how is PVL staphylococcus aureas treated?

A

Consult local microbiologist / 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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11
Q

what is pseudomonal folliculitis?

A

Associated with hot tub use, swimming pools and depilatories, wet suit

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

Follicular erythematous papule

Rarely: abscesses, lymphangitis and fever.

Most cases self-limited – no treatment required.

Severe or recurrent cases can be treated with oral ciprofloxacin

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12
Q

what is cellulitis?

A

Infection of lower dermis and subcutaneous tissue

Tender swelling with ill-defined, blanching erythema or oedema

Most cases: Streptococcus pyogenes & Staphylococcus aureus

Oedema is a predisposing factor

Treatment: systemic antibiotics

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13
Q

what is impetigo?

A

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

Caused by
- Streptococci (non-bullous) (bullae = blisters)
or
- Staphylococci (bullous)
Caused by exfoliative toxins A & B, split epidermis by targeting desmoglein I.

Often affects face (perioral, ears, nares (nostrils)).

Treated with topical +/- systemic antibiotics.

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14
Q

what is impetiginisation?

A

Occurs in atopic dermatitis, superficical infection

  • Gold crust
  • Staphylococcus aureus
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15
Q

what is ecthyma?

A

Severe form of streptococcal impetigo

Thick crust overlying a punch out ulceration surrounded by erythema

Usually on lower extremities

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16
Q

what is Staphylococcal Scalded Skin Syndrome?

A

Neonates, infants or immunocompromised adults

Due to exfoliative toxin (same as in bullous impetigo)

Infection occurs at distant site (ie conjunctivitis or abscess) (so nit at same site as scalded skin)
∴ Organism cannot be cultured from denuded skin.

In neonates, kidneys cannot excrete the exfoliative toxin quickly enough
→ Diffuse tender erythema that
→ Rapid progression to flaccid bullae,
→ Wrinkle and exfoliate, leaving oozing erythematous base

Clinically resembles Stevens-Johnson syndrome / toxic epidermal necrolysis

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17
Q

what is toxic shock syndrome (group a S. aureus)?

A

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

Fever >38.9°C
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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18
Q

what is erythrasma?

A

Infection of Corynebacterium minutissimum

Well demarcated patches in intertriginous areas (eg. armpits)

  • initially pink
  • Become brown and scaly
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19
Q

what is pitted keratolysis?

A

Pitted erosions of soles

Caused by Corynebacteria

Treated with topical clindamycin.

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20
Q

what is erysipeloid?

A

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

Extends slowly over weeks.

Erysipelothrix rhusiopathiae

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21
Q

what is anthrax (in terms of the skin)?

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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22
Q

what is blistering distal dactylitis?

A

Rare infection caused by Streptococcus pyogenes or Staphylococcus aureus

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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23
Q

what is erysipelas?

A

Infection of deep dermis and subcutis (similar to cellulitis)

Caused by β-haemolytic streptococci or Staphylococcus aureus

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).

Treated with intravenous antibiotics.

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24
Q

what is scarlet fever?

A

Primarily a disease of children

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

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

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

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25
Q

what is necrotising faciitis?

A

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

Potentially fatal

Usually synergistic: streptococci, staphylococci, enterobacteriaceae and anaerobes.

Prompt diagnosis 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.

Mortality is high.

Can affect the scrotum (Fournier’s gangrene).

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26
Q

what is Atypical Mycobacterial Infection?

A

Important cause of infection in immunosuppressed states.

Mycobacterium marinum causes indolent granulomatous ulcers (fish-tank granuloma) in healthy people
- Sporotrichoid spread (spread olong the lymphatics)

Mycobacterium chelonae & abscessus - puncture wounds, tattoos, skin trauma or surgery

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

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27
Q

what is borreliosis (lyme disease?

A

Annular erythema develops at site of the bite of a Borrelia-infected tick

Bite form Ixodes tick infected with Borrelia burgdorferi

Initial cutaneous manifestation: Erythema migrans (only in 75%)

  • Erythematous papule at the bite site
  • Progression to annular erythema of >20cm

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

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

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28
Q

what is tularaemia?

A

Caused by Francisella tularensis

Acquired through:

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

Ulceroglandular form

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

+/- local cellulitis

Painful regional lymphadenopathy

Systemic symptoms: fever, chills, headache and malaise

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29
Q

what is ecthyma gangrenosum?

A

Pseudomonas aeruginosa

Usually occurs in neutropaenic patients

Red macule(s) → oedematous → haemorrhagic bullae.

May ulcerate in late stages or form an eschar surrounded by erythema

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30
Q

what are some differential diagnoses for eshcharotic lesions?

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.

Compare normal human anatomy & pathology and physiology and pathophysiology of key diseases, disorders and clinical presentations throughout the human life cycle

31
Q

what is syphilis?

A

caused by Treponema pallidum (bacteria)

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

32
Q

what is secondary syphilis?

A

Begins ~50 days after chancre

Malaise, fever, headache, pruritus, loss of appetite, iritis

‘Great mimicker’ – low threshold for testing

  • Rash (88-100%) -Pityriasis rosea-like rash
  • Alopecia (‘moth-eaten’)
  • Mucous patches
  • Lymphadenopathy
  • Residual primary chancre
  • Condylomata lata
  • Hepatosplenomegaly
33
Q

what is lues maligna?

A

Rare manifestation of secondary syphilis

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

More frequent in HIV manifestation

34
Q

what is tertiary syphilis?

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)

35
Q

how is syphilis diagnosed and treated?

A

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

Treatment:
IM benzylpenicillin or oral tetracycline

36
Q

what is leprosy?

A

Mycobacterium leprae
Obligate intracellular bacteria - predominantly affects skin & nerves, but can affect any organ

Clinical spectrum:

  • Lepromatous leprosy
    - Multiple lesions: macules, papules, nodules
    - Sensation and sweating normal (early on)
  • Tuberculoid leprosy
    - Solitary or few: elevated borders – atrophic center, sometimes annular
    - Hairless, anhidrotic, numb
37
Q

what is tuberculosis?

A

Can affect any organ system, including the skin

Only 5-10% of infections lead to clinical disease

Cutaneous TB may be acquired:

  • Exogenously (primary-inoculation TB and tuberculosis verrucosa cutis)
  • Contiguous endogenous spread – (scrofuloderma )or autoinoculation – periorificial tuberculosis
  • Haematogenous/lymphatic endogenous spread –dissemination (lupus vulgaris, miliary tuberculosis, gummas

Investigations:

  • Interferon-γ release assay (Quantiferon-TB)
  • Histology – ZN stain
  • Culture / PCR
38
Q

what are the cutaneous manifestations of tuberculosis?

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

39
Q

what is Molluscum Contagiosum?

A

Poxvirus infection

Common in children & immunocompromised

Differential diagnosis

- Verrucae
- Condyloma acuminata
- Basal cell carcinoma
- Pyogenic granuloma

Usually resolve spontaneously

Treatment options – curettage (scraped off), imiquimod, cidofovir

40
Q

what is herpes simplex virus?

A

Primary and recurrent vesicular eruptions

Favour orolabial and genital regions

Transmission can occur even during asymptomatic periods of viral shedding

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

HSV-2 - sexual contact

Replicates at mucocutaneous site of infection ->
Travels by retrograde axonal flow to dorsal root ganglia

41
Q

what are symptoms of herpes simplex virus infection?

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

Systemic manifestations– aseptic meningitis in up to 10% of women

Reactivation – spontaneous, UV, fever, local tissue damage, stress

42
Q

what is eczema herpeticum?

A

emergency

occurs in people with atopic eczema

Monomorphic, punched out erosions (excoriated vesicles)

happens in babies

treated with IV acyclovir and accompanying antibiotics

43
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

44
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

45
Q

what is neonatal HSV?

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

Requires IV antivirals

46
Q

who might get severe or chronic HSV and how does it manifest?

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

47
Q

how is HSV diagnosed and treated?

A

diagnosis:
Swab for Polymerase chain reaction

Treatment:
Don’t delay

Oral valacyclovir or acyclovir 200mg five times daily in immunocompetent localised infection

Intravenous 10mg/kg TDS X 7-19 days

48
Q

what is varicella zoster virus?

A

Dermatomal

Single dermatome

Multidermatomal

49
Q

what is 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 included fatal cases of encephalitis)

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).

Spread by direct contact via oral-oral route or oral faecal route.

50
Q

Which viruses cause morbilliform (measles-like) eruptions?

A

Measles, Rubella, EBV, CMV, HHV6 & HHV7 cause morbilliform (measles-like) eruptions

Leptospirosis
Rickettsia
(morbilliform rahes)

51
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

Bacterial (BREN) - Borrelia, Rickettsia, Neisseria, Endocarditis

Other infections - Plasmodium falciparum, Trichinella

Other - TEN, Ergot poisoning, Raynauds

52
Q

what is gianotti-crosti syndrome?

A

Gianotti-Crosti syndrome aka 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

Causes:

- EBV (most common)
- CMV
- HHV6
- Coxsackie viruses A16, B4 and B5
- Hepatitis B
53
Q

what is erythema infectiosum?

A

aka 5th disezse

Parvovirus B19

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

54
Q

what is roseola infantum?

A

aka exanthem subitum aka 6th disease

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.

Caused by HHV6 and HHV7 (less commonly)

55
Q

what is orf?

A

Caused by parapoxvirus

Direct exposure to sheep or goats

Dome-shaped, firm bullae that develop an umbilicated crust.

Usually develop on hands and forearms

They generally resolve without therapy in 4-6 weeks

56
Q

what are warts?

A

caused by human papilloma viruses

> 200 subtypes of HPV

57
Q

what are the three classes of fungal infections?

A

superficial
eg. candida, malassezia, dermatophytes

deep/soft tissue
eg. chromomycosis, madura foot

disseminated
eg. candida, aspergillus, fusarium, histoplasma

58
Q

what is Pityriasis versicolor?

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

59
Q

what are dermatophytes?

A

superficial fungal infections

Dermatophytes – fungi that live on keratin

Trichophyton rubrum causes the most fungal infections

Trichophyton tonsurans causes the most tinea capitis

Kerion – 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

60
Q

what is tinea pedis?

A

Trichophyton rubrum – scaling and hyperkeratosis of plantar surface of food

Trichophyton mentagrophytes (interdigitale) –sometimes vesiculobullous reaction on arch or side of foot (athletes foot)

61
Q

what are id reactions?

A

Aka 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

62
Q

what is majocci granuloma?

A

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

Trichophyton rubrum or mentagrophytes are usually culprit

63
Q

what us candidiasis?

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, submammary folds, crurae and digital clefts) or of oral mucosa.

A common cause of vulvovaginitis

May affect mucosae.

Can become systemic (immunocompromise)

64
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)

Sporotrichosis

Phaeohypomycosis

Chromomycosis

Mycetoma (Madura foot)

Lobomycosis

Rhinosporidiosis

65
Q

what are systemic fungal infections?

A

Systemic respiratory endemic fungal infections Include blastomycosis, histoplasmosis, coccidiodomycosis, paracoccidoiodomycosis, penicillinosis

Disease in both immunocompetent and immunosuppressed

66
Q

what are opportunistic fungal diseases?

A

eg aspergillosis

67
Q

what is aspergillosis?

A

Risk factors: neutropaenia & corticosteroid therapy

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

Fusarium causes similar illness and cutaneous lesions both clinically and histologically – (septate hype with acute angle branching)

68
Q

what is mucormycosis?

A

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

Apophysomyces, Mucor, Rhizopus, Absidia, Rhizomucor

Associations: 
	Diabetes mellitus (1/3 of patients - DKA very high risk
	Malnutrition
	Uraemia
	Neutropaenia
	Medications: Steroids / antibiotics / desferoxamine 
	Burns
	HIV 

Treatment: aggressive debridement & antifungal therapy

Culture positive in only 30% of cases

69
Q

what is 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 is often seen

Crusted or ‘Norwegian’ scabies - hyperkeratosis
- Often asymptomatic; found in immunocompromised individuals

Treatment: permethrin, oral ivermectin
- Two cycles of treatment are required

70
Q

what are head lice?

A

Pediculus humanus capitis

  • Entire live cycle spent in hair
  • 2ndary infection common
  • Treatment: malathion, permethrin, or oral ivermectin
71
Q

what are body lice?

A

Pediculus humanus corporis

  • Lives and reproduces in clothing – leaves to feed; rarely found on skin
  • Pruritic papules & hyperpigmentation
  • Found in overcrowding, poverty & poor hygiene
  • Eliminated by thorough cleaning or discarding clothes
72
Q

what are pubic lice?

A

Phithrus pubis 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
73
Q

what are bed bugs?

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

Fumigation of home is necessary to get rid of pest

Treatment of patient is symptomatic