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BRS Year 2 > Infections of the Skin > Flashcards

Infections of the Skin Flashcards

1
Q

How does Staph A affect the skin?

A

Staphylococcus has receptors that allow it to bind to fibrin that is found in abundance on wound surfaces and in dermatitis

Expressed virulent factor (some strains) Panton Valentine Leukocidin

Each strain has different clinical manifestations depending on which toxins are releases

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2
Q

What are the skin manifestations of Staph A infection?

A 
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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3
Q

How does streptococcus cause skin issues?

A

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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4
Q

What are the skin manifestations of streptococcus infection?

A

Ecthyma
Cellulitis
Impetigo

Erysipelas
Scarlet fever
Necrotizing fasciitis

Superinfects other dermatoses (e.g. leg ulcers)

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5
Q

What is folliculitis?

A

Follicular erythema; sometimes pustular.

May be infectious or non-infectious.

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6
Q

What folliculitis is associated with HIV?

A

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

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7
Q

What can cause recurrent folliculitis?

A

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

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8
Q

What is the treatment for folliculitis?

A

Antibiotics (usually flucloxacillin or erythromycin)

Incision and drainage is required for furunculosis.

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9
Q

What are the complications of folliculitis?

A

Furuncle

Carbuncle

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10
Q

What is a furuncle?

A

A furuncle is a deep follicular abscess

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11
Q

What is a carbuncle?

A

Involvement with adjacent connected follicles = Carbuncle

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

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12
Q

Why might people have recurrent infections?

A

Immune deficiency

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

What are the main features of Panton Valentine Leukocidin?

A

β-pore-forming exotoxin
Leukocyte destruction and tissue necrosis
Strains that release this toxin have higher morbidity, mortality and transmissibility

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14
Q

What is the effect of PVL on the skin?

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 results of PVL?

A
  • Necrotising pneumonia
  • Necrotising fasciitis
  • Purpura fulminans
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16
Q

What are the risks of contracting PVL Staph A?

A

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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17
Q

What is the treatment for PVL Staph A?

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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18
Q

What is pseudomonal folliculitis associated with?

A

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

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19
Q

What are the main features of pseudomonal folliculitis?

A

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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20
Q

What is cellulitis?

A

Infection of lower dermis and subcutaneous tissue

Tender swelling with ill-defined, blanching erythema or oedema

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21
Q

What commonly causes cellulitis?

A

Most cases: Streptococcus pyogenes & Staphylococcus aureus

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22
Q

Who is at higher risk of cellulitis?

A

Oedema is a predisposing factor

Older people

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23
Q

What is the treatment of cellulitis?

A

Treatment: systemic antibiotics.

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24
Q

What is impetigo?

A

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

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25
Q

What causes impetigo?

A 
Caused by
- Streptococci (non-bullous) 
	or 
- Staphylococci (bullous)
Caused by exfoliative toxins 		A & B, split epidermis by 		targeting desmoglein I.
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26
Q

Where does impetigo present?

A

Often affects face (perioral, ears, nares).
Top half of body
Can happen anywhere

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27
Q

What is the treatment for impetigo?

A

Treated with topical +/- systemic antibiotics.

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28
Q

What is impetiginisation?

A

When it happens in the context of atopic eczema

Occurs in atopic dermatitis

  • Gold crust
  • Staphylococcus aureus
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29
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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30
Q

In who is staphylococcal scalded skin syndrome most common in?

A

Neonates, infants or immunocompromised adults
Toxin builds up
In neonates, kidneys cannot excrete the exfoliative toxin quickly

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31
Q

What are the main features of SSSS?

A

Due to exfoliative toxin
Infection occurs at distant site (ie conjunctivitis or abscess
∴ Organism cannot be cultured from denuded skin.

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32
Q

What are the symptoms of SSSS?

A

→ Diffuse tender erythema that
→ Rapid progression to flaccid bullae,
→ Wrinkle and exfoliate, leaving oozing erythematous base

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33
Q

What does SSSS resemble?

A

Clinically resembles Stevens-Johnson syndrome / toxic epidermal necrolysis

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34
Q

What is toxic shock synrome?

A

Febrile illness due to Group A Staphylococcus aureus strain that produces pyrogenic exotoxin TSST-1
Associated with extended tampon use

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35
Q

What are the symptoms of toxic shock syndrom?

A 
Fever >38.9°C
Hypotension
Diffuse erythema
Involvement of ≥ systems: 
	– Gastrointestinal 	
	– Muscular 	
	– CNS
	- Renal  
	- Hepatic
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36
Q

What is Erythrasma?

A

Infection of Corynebacterium minutissimum
Well demarcated patches in intertriginous areas
- initially pink
- Become brown and scaly

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37
Q

What is an intertriginous area?

A

Places where skin meets skin e.g. armputs

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38
Q

What is pitted keratolysis?

A

Pitted erosions of soles
Caused by Corynebacteria
Treated with topical clindamycin

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39
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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40
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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41
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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42
Q

What is Erysipelas

A

Infection of deep dermis and subcutis

Caused by β-haemolytic streptococci or Staphylococcus aureus

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43
Q

What are the syndromes 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.

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44
Q

What is the treatment of Erysipelas?

A

Portal of entry must be sought (e.g. tinea pedis).
Treat systemic symptoms (fever, malaise).
Treated with intravenous antibiotics.

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45
Q

What are the main features of Scarlet Fever?

A

Primarily a disease of children

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

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46
Q

What is the disease 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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47
Q

What are the potential complications of scarlet fever?

A

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

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48
Q

What is necrotising fasciitis?

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.

49
Q

What is essential in necrotising fasciitis?

A

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.

50
Q

What is high in necrotising fasciitis?

A

Mortality

51
Q

What can necrotising fasciitis affect?

A

Can affect the scrotum (Fournier’s gangrene)

52
Q

What are some atypical manifestations of myobacterial infection?

A

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

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).

53
Q

What is Borreliosis?

A

Lyme disease
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

54
Q

What is the disease progression of 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

55
Q

What is the issue with diagnosing Lyme disease?

A

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

56
Q

What is Tularaemia caused by?

A 
Caused by Francisella tularensis 
Acquired through:
	- Handling infected animals (squirrels and rabbits)
	- Tick bites 
	- Deerfly bites
57
Q

What results from Tularaemia?

A

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

58
Q

What can cause a 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.
59
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
60
Q

What is syphilis?

A

Treponema pallidum

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

61
Q

What are the features of secondary syphilis?

A

Begins ~50 days after chancre

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

62
Q

Why is secondary syphilis known as a ‘great mimicker’?

A

‘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
63
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

64
Q

What are the features of 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)

65
Q

What is Leprosy?

A

Mycobacterium leprae

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

66
Q

What is the clinical spectrum of Leprosy?

A

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
67
Q

What is the treatment for Leprosy?

A

Specialised
For years
Liaising with a tropical disease expert

68
Q

What are the main features of TB?

A

Can affect any organ system, including the skin

Only 5-10% of infections lead to clinical disease

69
Q

How can cutaneous TB be acquired?

A
  • 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)
70
Q

What investigations are done for TB?

A
  • Interferon-γ release assay (Quantiferon-TB)
  • Histology – ZN stain
  • Culture / PCR
71
Q

What are the cutaneous manifestations of TB?

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

72
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, imiquimod, cidofovir
73
Q

What are the features of Herpes Simplex Virus?

A

Primary and recurrent vesicular eruptions
Favour orolabial and genital regions
Transmission can occur even during asymptomatic periods of viral shedding

74
Q

What are the two types of Herpes?

A

Primary and recurrent vesicular eruptions
Favour orolabial and genital regions
Transmission can occur even during asymptomatic periods of viral shedding

75
Q

What is the disease progression in herpes?

A

Symptoms with 3-7 days of exposure
Preceded by tender lymphadenopathy, malaise, anorexia
± Burning, tingling

Crusting and resolution within 2-6 weeks

76
Q

What are the symptoms of Herpes?

A

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

Orolabial lesions – often asymptomatic

Genital involvement – often excruciatingly painful→ urinary retention

Systemic manifestations– aseptic meningitis in up to 10%

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

77
Q

What is Eczema herpeticum?

A

emergency

Monomorphic, punched out erosions (excoriated vesicles)

78
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

79
Q

What is herpes gladiotorum?

A

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

80
Q

What are the main features of Neonatal HSV infection?

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

81
Q

What is the manifestation of HSV in the immunocompromised?

A

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

82
Q

How do you diagnose HSV?

A

Swab for Polymerase chain reaction

83
Q

What is the treatment 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

84
Q

What is Varicella Zoster Virus?

A

Dermatomal rash
Single dermatome
Multidermatomal

85
Q

What causes hand, foot and mouth disease?

A

Coxsackie A16, Echo 71

86
Q

What is hand, foot and mouth disease?

A

An acute self-limiting coxsackievirus infection

- Echo 71 (associated with a higher incidence of neurological involvement included fatal cases of encephalitis)

87
Q

What are the symptoms of Hand, foot and 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).

88
Q

How is hand, foot and mouth disease spread?

A

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

89
Q

What causes morbilliform rashes?

A

Drug or Bug

90
Q

What bugs cause morbilliform rashes?

A

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

91
Q

What causes purpuric eruption?

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

92
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

93
Q

What causes Gianottie-Crosti Syndrome?

A
  • EBV (most common)
  • CMV
  • HHV6
  • Coxsackie viruses A16, B4 and B5
  • Hepatitis B
94
Q

What is Erythema Infectiosum?

A

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

95
Q

What is Roseola infantum?

A 
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)
aka exanthem subitum aka 6th disease
96
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

97
Q

What are warts?

A

Viral warts
Very common
>200 subtypes of HPV

98
Q

What is Superficial fungal infections?

A

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

99
Q

What are dermatophytes?

A

fungi that live on keratin

100
Q

What are the most common dermatophytes?

A

Trichophyton rubrum causes the most fungal infections

Trichophyton tonsurans causes the most tinea capitis

101
Q

What is 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

102
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
103
Q

What is an Id reaction?

A

Aka Dermatophytid reactions
Hypersensitivity reaction
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

104
Q

What is Majocchi granuloma?

A

Follicular abscess produced when dermatophyte infection penetrates the follicular wall into surrounding dermis; tender
Trichophyton rubrum or mentagrophytes are usually culprit

105
Q

What is 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)

106
Q

What are the main features of 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
107
Q

Give examples of systemic fungal infections?

A

blastomycosis, histoplasmosis, coccidiodomycosis, paracoccidoiodomycosis, penicillinosis

108
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
Fusarium causes similar illness and cutaneous lesions both clinically and histologically – (septate hype with acute angle branching)

109
Q

What is mucormycosis caused by?

A

Apophysomyces, Mucor, Rhizopus, Absidia, Rhizomucor
1/3 of patients have diabetes, those in DKA are at particularly high risk
Other associations include malnutrition, uraemia, neutropaenia, steroid therapy, burns, antibiotic therapy, neonatal prematurity, deferoxamine therapy and HIV

110
Q

How does Mucormycosis present?

A

fever, headache, facial oedema, proptosis, facial pain, orbital cellulitis, cranial nerve dysfunction
+/- nerve dysfunction due to retinal artery thrombosis

111
Q

What is the treatment for mucormycosis?

A

Treatment consists of aggressive debridement and antifungal therapy

112
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.

113
Q

How does scabies present?

A

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
114
Q

What is the treatment for Scabies?

A

permethrin, oral ivermectin

- Two cycles of treatment are required

115
Q

What are the main features of head lice?

A

Pediculus humanus capitis

  • Entire live cycle spent in hair
  • 2ndary infection common
  • Treatment: malathion, permethrin, or oral ivermectin
116
Q

What are the main features of 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
117
Q

What are the main features of 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
118
Q

What are the main features of 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
Fumigation of home is necessary to get rid of pest
Treatment of patient is symptomatic

BRS Year 2 (110 decks)

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