Dermatology - Skin infections/ infestations Flashcards

1
Q

What is erysipelis and cellulitis?

A

These are spreading bacterial infections of the skin.
Cellulitis = deep cutaneous tissue
Erysipelis = acute superficial form of cellulitis and involves the dermis and upper subcutaneous tissue

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2
Q

What causes erysipelis and cellulitis?

A

They are both caused by either streptococcus pyogenes or staph aureus.

Risk factors include - immunosuppression, wounds, legs ulcers, toeweb intertrigo (inflammation of the body folds) and minor skin injury

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3
Q

How does cellulitis present?

A

It most commonly affects the lower limbs.
Local signs of inflammation - swelling, erythema, warmth, pain; may be associated lymphangitis.
Systemically unwell with fever, malaise or rigors, particularly with erysipelis.

Note that cellulitis is usually unilateral.

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4
Q

How is erysipelis distinguished from cellulitis?

A

Erysipelis is distinguished by a well defined, red, raised border.

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5
Q

What is the criteria for admission with cases of cellulitis?

A

Eron classification helps guide management - 4 classes:

Class I = no signs of systemic toxicity and the person has no uncontrolled comorbidities

Class II = The person is either systemically unwell or systemically well but with a co-morbidity (for example peripheral arterial disease, chronic venous insufficiency, or morbid obesity) which may complicate or delay resolution of infection

Class III = The person has significant systemic upset such as acute confusion, tachycardia, tachypnoea, hypotension, or unstable co-morbidities that may interfere with a response to treatment, or a limb-threatening infection due to vascular compromise

Class IV = The person has sepsis syndrome or a severe life-threatening infection such as necrotizing fasciitis

Based on this, the following should be admitted:

  • Eron class III and IV
  • rapidly deteriorating cellulitis
  • is very young
  • has significant lymphoedema
  • has facial or periorbital cellulitis
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6
Q

How is cellulitis/ erysipelis treated?

A

Flucloxacillin is the first line antibiotic for mild/ moderate cellulitis. Clarithromycin (macrolide) or clindamycin is recommended for patients allergic to penicillin. Many protocols now recommend oral clarithromycin for those patients who have failed to respond to penicillin.

Severe cellulitis should be treated with intravenous benzylpenicillin + flucloxacillin

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7
Q

What is staphylococci scalded skin syndrome?

A

This infection is commonly seen in infancy and childhood. It is caused by production of circulating epidermolytic toxin from phage group II, benzyl-penicillin resistant (coagulase positive) staph.

A key thing to remember is that ALL staph are catalse positive (this differentiates them from strep which are also gram positive cocci but group in lines rather than clusters), but only staph aureus is coagulase positive.

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8
Q

What is the presentation of scalded skin syndrome?

A

It normally develops within a few hours to days and may be worse over the face, neck, axillae or groins.
A scald like appearance is followed by large flaccid bulla.
Peri-oral crusting is typical.
There is intraepidermal blistering in this condition.
Lesions are very painful.
Recovery is within 5-7 days.

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9
Q

How is scalded skin syndrome managed?

A

Antibiotics (e.g. systemic penicillinase resistant penicillin, fusidic acid, erythromycin or appropriate cephalosporin)
Analgesia

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10
Q

What is impetigo?

A

Impetigo is a common, highly contagious, superficial bacterial infection of the skin. It is caused by either staph aureus or strep pyogenes. Co-existing skin conditions, such as abrasions, infestations or eczema, predispose to impetigo.

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11
Q

What are the 2 presentations of impetigo?

A

In non-bullous impetigo, a thin walled vesicle develops , ruptures rapidly and is rarely seen intact. Dried exudate, forming “golden crusting” arises on an erythematous base.

In bullous disease, the toxins cleave the superficial epidermis, causing intact blisters containing clear fluid to appear, lasting 2-3 days. The face scalp and limbs are most commonly infected but sites of eczema can also be involved. Constitutional symptoms are uncommon.

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12
Q

How is impetigo managed?

A

A bacterial swab should be taken from blister fluid or active lesion before treatment. One third of the population are nasal carriers of staphyloccocus, so nasal swabs should be obtained.

In mild localised disease, topical treatment with mupirocin or fusidic acid usually suffices and limits spread. Staphyloccoci nasal carriage should be treated with topical mupirocin. In severe cases, oral flucloxacillin or erythromycin (if penicillin allergic) is indicated. If a nephritogenic streptococcus is suspected, systemic antibiotics should be given, as post streptotoccal glomerulonephritis can occur.

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13
Q

What is folliculitis?

A

Folliculitis is inflammation involving the hair follicle. This can be superficial, just involving the ostium of the hair follicle (folliculitis) or deep (faruncles and carbuncles).

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14
Q

What is superficial folliculitis? What is the clinical course?

A

This is very common, usually minor and subacute or chronic. It is often infective, caused by staph aureus, but can also be due to physical (e.g. mechanical epilation) or chemical (e.g. mineral oils) injury. In these cases, the folliculitis is usually sterile. Staphylococcal folliculitis is most common in children and often occurs on the scalp or limbs. The pustules usually heal in 7-10 days but can become more chronic and in older children and adults can progress to a deeper form of folliculitis.

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15
Q

What is deep folliculitis?

A

Deep folliculitis can cause either faruncles or carbuncles.

Faruncles - (boil) is an acute staph aureus infection of the hair follicle, which becomes pustular and fluctuant and is often exquisitely tender. The lesions eventually rupture to discharge pus and, because they are deep, leave a scar.

Carbuncles - this can progress from a faruncle, and is an exquisitely tender nodule, often on the neck, shoulders or hips, and is associated with severe constitutional symptoms. It implies the involvement of several contiguous (touching), hair follicles. Treatment, as with faruncles, is with appropriate anti-staph antibiotics.

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16
Q

What is erythrasma? How is it diagnosed?

A

Erythrasma is a generally asymptomatic, flat, slightly scaly, pink or brown rash usually found in the groin or axillae. It is caused by an overgrowth of the diphtheroid Corynebacterium minutissimum.

Examination with Wood’s light reveals a coral-red fluorescence.

Topical miconazole or antibacterial are usually effective. Oral erythromycin may be used for more extensive infection.

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17
Q

What herpes viruses infect the skin?

A

Herpes simplex virus 1 and 2 both infect the skin.
Type 1 herpes simplex virus (HSV) typically produces mucocutaneous lesions of the head and neck, while type 2 predominantly affects the genital tract.

Virus shed by infected individuals infects via a mucosal surface of a susceptible person. HSV infects sensory and autonomic nerve ganglia and episodes of reactivation occur throughout life, precipitated by stress, trauma, illness or immunosuppression. Primary infection normally occurs causing vesiculating gingivostomatitis. It may also present as keratitis (dendritic ulcer), viral paronychia, vulvovaginitis, cervicitis, balanitis, or rarely as encephalitis. Diagnosis is by PCR, electron microscopy or culture.

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18
Q

What are the complications of herpes virus infection?

A
  • corneal dendritic ulcers; may produce scarring
  • encephalitis; preferentially affects the temporal lobe
  • HSV infection in patients with eczema; can result in disseminated skin lesions (eczema herpeticum)
  • neonatal HSV infection; may be disseminated and potentially fatal
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19
Q

How should herpes viral infection be managed?

A

Treatment is with antiviral agents such as aciclovir; best results are achieved with early treatment.

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20
Q

What virus is associated with AIDS and causes Kaposi’s sarcoma?

A

Human herpes virus 8.

The virus which spreads via saliva, causes Kaposi’s sarcoma in both AIDS related and endemic non-AIDS related forms.

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21
Q

What enterovirus infections are associated with skin disease?

A

1) Hand foot and mouth disease - a mild febrile illness affecting children, mainly in the summer months, and caused by Coxsackie virus or echoviruses. There is fever, lymphadenopathy, mouth ulceration and a vesicular eruption on the hands and feet
2) Herpangina - causes discrete vesicles on the palate associated with high fever, sore throat and headache.

Both of these conditions are self limiting WITHOUT treatment.

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22
Q

What poxvirus infections are associated with the skin?

A

These DNA viruses are potentially pathogens but nowadays rarely cause significant human disease. They include smallpox, monkey pox and cow pox, as well as orf and molluscum contagiosum.

Smallpox (variola) - this severe disease, with a high mortality in the unvaccinated, was eradicated worldwide in 1980 following an international vaccination campaign. The classical form is characterised by a typical centrifugal vesicular/ pustular rash, worst on the face and extremities, with no cropping (i.e. unlike chickenpox) and accompanied by fever, severe myalgia and odynophagia.

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23
Q

What viruses cause warts?

A

Viral warts are caused by the DNA human papillomavirus (HPV) and are extremely common, being transmitted by direct contact with the virus in either living skin or shed skin fragments. Most people suffer one or more warts at some point during their life. There are >90 different subtypes. HPV subtypes 16 and 18 are spread by sexual contact and are strongly associated with subsequent development of cervical carcinoma. Vaccinations are now available against HPV-16 and 18 and are recommended for adult females before they become sexually active. Immunosuppressed patients are at greater risk of infection with HPV.

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24
Q

What are the clinical features of viral warts?

A

Common warts appear initially as smooth, skin coloured papules. As they enlarge, their surface becomes irregular and hyperkeratotic producing the typical warty appearance. One method of classifying warts is based on their clinical appearance:
- PLANTAR WARTS (varrucae): found on the sole of the foot, these are characterised by a horny collar surrounding a roughened surface. Paring reveals capillary loops that distinguish plantar warts from corns

  • MOSAIC WARTS: mosaic like sheets of warts
  • PLANE WARTS: smooth, flat topped papules, usually on the face and dorsum of the hands
  • FILIFORM WARTS: often found on the face
  • GENITAL WARTS: papillomatous and protuberant
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25
Q

How should warts be managed?

A

Most viral warts resolve spontaneously but often very slowly. Therapeutic options to speed resolution include:

  • topical salicylate acid (first line)
  • cryotherapy
  • Imiquimod or podophyllin for genital warts
  • intralesional bleomycin (for recalcitrant warts)
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26
Q

What is molluscum contagiosum?

A

Molluscum contagiosum is caused by a DNA poxvirus infection. It can affect any age group but usually targets children over the age of 1 and the immunosuppressed. The classic lesion is a dome shaped, “umbilicated”, skin coloured papule with a central punctum. Lesions tend to be multiple and are often at sites of apposition, such as the side of the chest and the inner arm. No treatment is required, as these lesions resolve spontaneously but can take several months. If active resolution is sought, curettage or cryotherapy can be tried, or topical agents such as salicylate, or podophyllin or imiquimod.

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27
Q

What patients are at risk of Orf infection?

A

Orf is an occupational hazard for those who work with sheep and goats. It is a cutaneous infection with a parapoxvirus carried by these animals. Innoculation of the virus, usually into the skin of a finger, causes significant inflammation and necrosis, which resolves within 2-6 weeks. No specific treatment is available unless there is evidence of secondary infection. Erythema multiforme can be triggered by orf virus infection.

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28
Q

What systemic viral infections are associated with exanthem?

A

Childhood exanthem (or rashes) are characterised by fever and widespread rash. Maternal antibodies protect for the first 6-12 months but thereafter incidence rises. Although the incidence of exanthems has diminished as a result of vaccination programmes, incomplete uptake can increase infection later in life.

They include:

  • measles
  • Rubella
  • parvovirus B19
  • human herpesvirus 6 and 7
  • chickenpox
  • shingles
  • dengue

Mumps is a systemic viral infection WITHOUT exanthem.

29
Q

What causes measles?

A

Measles is caused by an RNA paramyxovirus.
It is transmitted by respiratory droplets.
Patients are infective from a prodrome until 4 days AFTER the rash starts.

30
Q

What are the clinical features of measles?

A

A prodromal illness 1-3 days before a rash appears heralds the most infectious stage with upper respiratory symptoms, conjunctivitis and the presence of Koplik’s spots (small white spots surrounded by erythema) on the internal buccal mucosa. As natural antibody develops, the maculopapular rash appears, spreading from face to extremities. It normally starts behind the ears. Lymphadenopathy and diarrhoea are common.

31
Q

What are the complications of measles?

A
Otitis media
Bacterial pneumonia
Encephalitis/ convulsions
Subacute sclerosing panencephalitis (rate, late and serious)
Pancarditis
32
Q

How is measles managed?

A

In the immunocompetent, the disease is self limiting; however, severity and complications are increased in malnourished and immunosuppressed. Pregnant women should be coansidered for treatment with immunoglobulin.

All children aged 12-15 months should be vaccinated against MMR, with further doses at age 4. Antibiotics are only indicated for superinfection.

If a child who is not immunised comes into contact with measles then MMR should be offered (vaccine induced measles antibody develops more rapidly than that following natural infection). This should be given within 72 hours.

33
Q

What is rubella?

A

Rubella, also known German measles, is a viral infection caused by togavirus. Following introduction of MMR the incidence of infection as reduced. If contracted during pregnancy it can cause congenital rubella syndrome.

34
Q

What are the important features of rubella?

A

Outbreaks are more common around winter and spring.
Incubation period is 14-21 days.
Individuals are infectious from 7 days before symptoms appear to 14 days AFTER the onset of a rash.

35
Q

What are the clinical features of rubella?

A

Most childhood diseases are subclinical, although disease can present with lymphadenopathy (suboccipital and post auricular) and a maculopapular rash that starts on the face and moves to the trunk. Complications include arthralgia, thrombocytopaenia, hepatitis and rarely encephalitis.

36
Q

How should suspected rubella in a pregnant women be investigated?

A

If rubella is suspected in pregnant women, confirmation is provided either by rubella IgM antibodies in serum or by IgG seroconversion. In the exposed pregnant women, the absence of rubella IgG indicates potential for infection. Children should be immunised against rubella as part of a standard vaccination programme using MMR. Women of child bearing age should be tested and vaccinated if seronegative.

37
Q

What is parvovirus B19?

A

This air borne virus causes mild or subclinical infection in normal hosts. Around 50% of children and 60-90% of adults are sero-positive. There are many clinical features of parvovirus B19 infection, but one of the most interesting ones is a transient block in erythropoiesis, which is insignificant unless haemaglobinopathy or haemolysis is also present.

38
Q

What are the clinical features of parvovirus B19 infection?

A

1) Fifth disease (erythema infectiosum) - affects small children; three stages: (i) a “slapped cheek” appearance; (ii) reticulate eruption on the body and limbs then (iii) resolution. Often the child is quite well throughout
2) Gloves and socks syndrome - young adults; fever and an acral purpuric lesions with a clear margin at the wrists and ankles. Mucosal involvement also occurs
3) Arthropathies - adults, occasionally children; polyarthropathy of the small joints. In children it tends to involve the large joints in an asymmetrical distribution
4) Hydrops fetalis - transplacental infection; Asymptomatic or symptomatic maternal infection can cause foetal anaemia with aplastic crisis leading to non immune hydrops fetalis and spontaneous abortion

39
Q

What virus causes chicken pox?

A

Varicella zoster virus (VSV) is a dermatotropic and neurotropic virus of the herpesviridae causing primary infection, usually in childhood, which may reactivate later on in life. It is spread by aerosol and direct contact and is highly infectious. Disease in children is usually better tolerated than in adults, pregnant women and the immunosuppressed.

40
Q

What is the incubation period for chicken pox? What are the clinical features?

A

Chickenpox has a 2 week incubation period after which the patient has a fever and a rash often on mucosal surfaces first, followed by rapid dissemination in a centripetal fashion. New lesions occur in crops every 2-4 hours from small pink macules to vesicles and pustules, which then crust. Infectivity lasts from 2 to 4 days before the rash appears until all their lesions have scabbed over.

Diagnosis is clinical but may be confirmed by PCR of vesicular fluid. The Tzanck preparation reveals mutlinucleated giant cells and intracellular inclusion bodies.

41
Q

What are the complications of chicken pox?

A
  • secondary bacterial infection of rash (due to scratching)
  • self limiting cerebellar ataxia
  • congenital abnormalities if maternal disease is contracted during the first trimester
  • pneumonitis, which may be fatal
42
Q

How is chickenpox treated?

A

Anti-viral agents such as aciclovir and famciclovir are NOT required for uncomplicated cases of childhood chickenpox. They are used when patients present within 24-48 hours of vesicle onset, in all patients with complications, including pregnant women. Immunosuppressed patients require longer treatment, initially parenteral. Human VZV immunoglobulin may attenuate infection in high susceptible contacts of chickenpox.

43
Q

What is shingles?

A

This is produced by reactivation of latent VZV from the dorsal root ganglion of sensory nerves and most commonly involves the thoracic dermatomes and the ophthalmic division of the trigeminal nerve.

44
Q

What are the clinical features of shingles?

A

Painful eruption of vesicles isolated to a single dermatome distribution. The vesicles dry up and form crusts, which disappear in about 3 weeks. Pain in the dermatomal distribution can last for months in the elderly.

There may be viraemia and distant satellite lesions Severe, extensive or prolonged disease suggests underlying immunosuppression, e.g. HIV. Chickenpox may be caught from shingles but NOT the other way round.

45
Q

What are the significant complications of shingles?

A
  • Ophthalmic trigeminal nerve involvement - may lead to corneal ulceration and blindness (herpes zoster ophthalmicus)
  • Ramsay hunt syndrome: facial palsy, ipsilateral loss of taste and buccal ulceration and a rash in the external auditory canal
  • Post herpetic neuralgia: can be difficult to treat but may respond to amitriptyline or gabapentin
  • Myelitis/ encephalitis: rare
46
Q

What is dengue?

A

The dengue flavivirus is spread by the vector mosquito Aedes aegypti and is endemic in South-east Asia, India, Africa and the Americas.

47
Q

What are the clinical features of dengue?

A

The incubation period following a mosquito bite is 2-7 days, with a prodrome of malaise and headache, followed by a morbilliform rash (looks like measles), arthralgia, pain on eye movement, headache, nausea, vomiting, lymphadenopathy and fever.

The rash spreads centrifugally, spares the palms and the soles and may desquamate on resolution. The disease is self limiting, but convalescence is slow.

48
Q

What is dengue haemorrhagic fever and dengue shock syndrome?

A

These are more severe manifestations that occasionally complicate infection: circulatory failure, features of capillary leak syndrome, and DIC with haemorrhagic complications, such as petechiae, ecchymosis, epistaxis, GI bleeding and multi organ failure. Other complications include encephalitis, hepatitis and myocarditis.

49
Q

How should dengue be investigated?

A

Detection of a 4x rise in anti-dengue IgG antibody titres.

Amplification of dengue RNA by PCR.

50
Q

How is dengue managed?

A

Management is supportive, with treatment of haemorrhage, shock and pain as required. Insecticides that control mosquito levels help to limit remission. Aspirin should be avoided and steroids are ineffective. There is currently no vaccine.

51
Q

What are superficial fungal infections?

A

These are common and mild infections of the superficial layers of the skin, nails and hair but can be more severe in the immunocompromised.

There are three main groups:

1) Dermatophytes (tinea/ ringworm)
2) Yeasts (e.g. candida)
3) Moulds

52
Q

What are the 3 most common forms of dermatophyte infection?

A

The main types of infection are described based on the part of the body they affect:

  • tinea capitis (scalp ringworm)
  • tinea corporis (trunk, legs or arm)
  • tinea pedis - feet
53
Q

What are the features of tinea capitis?

A

This is a cause of scarring alopecia mainly seen in children. If it is untreated, a raised, boggy, pustular, mass called a kerion may form.
The most common cause is Trichophyton tonsurans in the UK and USA. It can also be caused by dog bites.

54
Q

How is tinea capitis diagnosed?

A

Lesions due to dog bites (caused by Microsporum canis) show green fluorescence under Woods lamp, lesions due to Trichophyton do not. However, the most useful investigation is scalp scrapings.

55
Q

How is tinea capitis treated?

A

Oral antifungals: terbinafine for Trichophyton tonsurans, and griseofulvin for Microsporum infections.

Topical ketoconazole shampoo should be given for the first 2 weeks to reduce transmission.

56
Q

What is tinea corporis?

A

Tinea corporis (ringworm) is caused by Tricophyton species, some of which may be transmitted by cattle. It presents with well defined annular, erythematous lesions, with pustules and papules.

It can be treated with oral fluconazole.

57
Q

What is tinea pedis?

A

Athletes foot. Characterised by itchy, moist, peeling skin between the toes. Common in adolescence.

58
Q

How does superficial candidiasis present?

A

This presents as white plaques on mucosal surfaces with erythema and satellite lesions in flexure areas (e.g. axilla).

59
Q

What is pityriasis versiclor?

A

Also called tinea versicolor, it is a superficial cutaneous fungal infection caused by Malassezia furfur.

Features include:

  • most commonly affects trunk
  • patches may be hypopigmented, pink or brown (hence versicolor). May be more noticeable following a suntan
  • scale is common
  • mild pruritus
60
Q

What factors predispose to pityriasis versiclor?

A

occurs in healthy individuals
immunosuppression
malnutrition
Cushing’s

61
Q

How it pityriasis versiclor treated?

A

Topical antifungal. NICE Clinical Knowledge Summaries advise ketoconazole shampoo as this is more cost effective for large areas.
If extensive disease or failure to respond to topical treatment then consider oral itraconazole.

62
Q

What is onychyomycosis?

A

Onychomycosis is fungal infection of the nails. This may be caused by:

  • dermatophytes - mainly Trichophyton rubrum, accounts for 90% of cases
  • yeasts - such as Candida
  • non-dermatophyte moulds

Features:

  • ‘unsightly’ nails are a common reason for presentation
  • thickened, rough, opaque nails are the most common finding
63
Q

How is onychomycosis investigated and treated?

A

Investigation:

  • nail clippings
  • scrapings of the affected nail

Management:

  • treatment is successful in around 50-80% of people
  • diagnosis should be confirmed by microbiology before starting treatment
  • dermatophyte infection: oral terbinafine is currently recommended first-line with oral itraconazole as an alternative. Six weeks - 3 months therapy is needed for fingernail infections whilst toenails should be treated for 3 - 6 months
  • Candida infection: mild disease should be treated with topical antifungals (e.g. Amorolfine) whilst more severe infections should be treated with oral itraconazole for a period of 12 weeks
64
Q

What is scabies? What are the clinical features?

A

Scabies is caused by the mite Sarcoptes scabiei and is spread by prolonged skin contact. It typically affects children and young adults.

The scabies mite burrows into the skin, laying its eggs in the stratum corneum. The intense pruritus associated with scabies is due to a delayed type IV hypersensitivity reaction to mites/eggs which occurs about 30 days after the initial infection.

Features:

  • widespread pruritus
  • linear burrows on the side of fingers, interdigital webs and flexor aspects of the wrist
  • in infants the face and scalp may also be affected
  • secondary features are seen due to scratching: excoriation, infection
65
Q

How should scabies be managed?

A

Management:

  • permethrin 5% is first-line
  • malathion 0.5% is second-line
  • give appropriate guidance on use (see below)
  • pruritus persists for up to 4-6 weeks post eradication

Patient guidance on treatment:

  • avoid close physical contact with others until treatment is complete
  • all household and close physical contacts should be treated at the same time, even if asymptomatic
  • launder, iron or tumble dry clothing, bedding, towels, etc., on the first day of treatment to kill off mites
66
Q

How should patients be instructed to use anti-fungal creams in scabies?

A

Patients should be given the following instructions:
- apply the insecticide cream or liquid to cool, dry skin
pay close attention to areas between fingers and toes, under nails, armpit area, creases of the skin such as at the wrist and elbow
- allow to dry and leave on the skin for 8-12 hours for permethrin, or for 24 hours for malathion, before washing off
- reapply if insecticide is removed during the treatment period, e.g. If wash hands, change nappy, etc
- repeat treatment 7 days later

67
Q

What is Norwegian scabies?

A

Crusted scabies is seen in patients with suppressed immunity, especially HIV.
The crusted skin will be teeming with hundreds of thousands of organisms.

Ivermectin is the treatment of choice and isolation is essential.

68
Q

What causes head lice and how is it treated?

A

Head lice (also known as pediculosis capitis or ‘nits’) is a common condition in children caused by the parasitic insect Pediculus capitis, which lives on and among the hair of the scalp of humans.

Diagnosis:
- fine-toothed combing of wet or dry hair

Management:

  • treatment is only indicated if living lice are found
  • a choice of treatments should be offered - malathion, wet combing, dimeticone, isopropyl myristate and cyclomethicone

School exclusion is not advised for children with head lice.