Chickenpox (Varicella)

Tinea Pedis

Tinea pedis is a foot infection due to a dermatophyte fungus. Tinea pedis thrives in warm humid conditions and is most common in young adult men.

Tinea pedis is most frequently due to:

  • Trichophyton (T.) rubrum
  • T. interdigitale, previously called T. mentagrophytes var. interdigitale
  • Epidermophyton floccosum


    Moccasin tinea pedis

    Clinical features

Tinea pedis has various patterns and may affect one or both feet.

  • Chronic hyperkeratotic tinea refers to patchy fine dry scaling on the sole of the foot
  • ‘Moccasin’ tinea is extensive hyperkeratotic tinea, in which the skin of the entire sole, heel and sides of the foot is dry but not inflamed. The affected area does not include the top of the foot. This is usually caused by T. rubrum.
  • Athlete’s foot i.e. moist peeling irritable skin between the toes, most often in the cleft between the fourth and fifth toes.
  • Clusters of blisters or pustules on the sides of the feet or insteps (more likely with T. interdigitale).
  • Round dry patches on the top of the foot (ringworm like tinea corporis).

Predisposing factors

Tinea pedis affects all ages but is more common in adults than in children. The fungal spores can persist for months or years in bathrooms, changing rooms and swimming pools. Walking bare foot on a communal floor or sharing a towel can result in infection.

Some people are particularly prone to troublesome tinea pedis. This may be because:

  • They are more exposed to the spores at home or during recreational activities.
  • Their skin produces less fatty acid (a natural antifungal agent).
  • They wear occlusive footwear.
  • They wear the same pair of socks or shoes for long periods.
  • They sweat excessively (hyperhidrosis).
  • They have some form of immunodeficiency e.g. medication such as azathioprine, or infection with human immunodeficiency virus.
  • They have poor circulation resulting in cold feet e.g. due to lymphoedema.

Diagnosis of tinea pedis

The diagnosis of tinea pedis is confirmed by microscopy and culture of skin scrapings.

Treatment of tinea

Tinea pedis is usually treated with topical antifungal agents, but if the treatment is unsuccessful,oral antifungal medicines may be considered, including terbinafine and itraconazole.

Resistance to treatment

If treatment is unsuccessful consider whether you have:

  • Untreated infection eg of the nails (onychomycosis).
  • Reinfection from contact with spores in your surroundings or clothing.
  • An untreated infected family member.
  • An alternative explanation for your symptoms such as dermatitis or psoriasis (see your family doctor or dermatologist for a diagnosis).

Moccasin tinea is particularly resistant to treatment.


 

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Tuberous Sclerosis

What is tuberous sclerosis?

Tuberous sclerosis or tuberous sclerosis complex (TSC) is a genetic disorder that is characterised by hamartomas in many organs, but particularly the skin, brain, eye, kidney and heart. Hamartomas are non-cancerous malformations composed of overgrowth of the cells and tissues that normally occur in the affected area and include naevi (birthmarks). Tuberous sclerosis is also known as epiloia.

Skin lesions, epileptic seizures and developmental delay/behavioural problems are the main features of tuberous sclerosis complex. However, individuals with the condition may be affected in many different ways and with differing degrees of severity. Some patients may have very few or no symptoms at all, whilst others may be severely affected with a multitude of symptoms.

What causes tuberous sclerosis and who gets it?

Tuberous sclerosis is a genetic disorder due to mutation in one of two genes:

  • TSC1, which produces a protein called hamartin (10–30% of cases)
  • TSC2, which produces a protein called tuberin

About one third of all cases of tuberous sclerosis are inherited from an affected parent. All other cases are due to sporadic new mutations occurring in the early stages of life, most often mutations of TSC2.

People of all races and sex may be affected. The condition may become apparent any time from infancy to adulthood but usually occurs between 2-6 years of age.

What are the skin signs of tuberous sclerosis complex?

Skin lesions are found in 60-70% of cases of tuberous sclerosis.

Lesion Features
Angiofibromas
  • Facial rash that appears as a spread of small pink or red spots across the cheeks and nose in a butterfly distribution
  • Usually appear between 3-10 years of age and increase in size and number until adolescence
  • Also found around the nails, scalp and forehead
  • Previously incorrectly called adenoma sebaceum
Ungual fibromas
  • Smooth, firm, flesh-coloured lumps that emerge from the nail folds
  • Periungual sites (around the nail) are more common than subungual sites (under the nail)
  • More common on feet than hands
  • Longitudinal groove in the nail may occur without visible fibroma
  • Short red (splinter haemorrhages) or white streaks (leukonychia) may be seen on affected nails

Shagreen patch
  • Flesh coloured orange-peel connective tissue naevi of varying sizes, usually on the lower back
Ovoid or ash leaf-shaped white macules
  • May be present at birth or early infancy
  • 3 or more white spots at birth suggests diagnosis of tuberous sclerosis

Other organ involvement

Epilepsy is present in about 70% of patients with tuberous sclerosis.

  • Usually begins in infancy or early childhood and may precede appearance of skin lesions by years
  • The greater the number of tumours (cortical tubers) in the brain, the greater the severity of seizures.

Developmental delay and behavioural problems may also occur. Symptoms include mild to severe mental retardation, autism, attention deficit disorder (ADD), anxiety, depression, paranoia and schizophrenia.

Other signs and symptoms of tuberous sclerosis include:

  • Eye involvement: white spots on the iris and white lumps on the retina
  • Heart, gastrointestinal and kidney tumours
  • Lung changes

What treatment is available?

Tuberous sclerosis is a multisystem disorder so treatment from a team of specialist doctors is usually necessary.

Skin lesions, particularly facial angiofibromas, may be psychologically distressing for some patients. Laser treatment or electrosurgery can be used to remove angiofibromas.

Experimentally, the topical mTOR inhibitors sirolimus (rapamycin) have proved helpful in reducing angiofibromas in pilot studies involving a few patients. It appears to work best in younger children. One study has reported improvement in hypopigmented macules.


 

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For further information, InfinityPATH recommends you visit Dermnet site: https://www.dermnetnz.org/

Trichothiodystrophy

In trichothiodystrophy, the hair shafts are deficient in sulphur resulting in transverse fractures. Polarising microscopy reveals intermittent dark bands.

Trichothiodystrophy may occur as an isolated hair shaft abnormality or may be associated with photosensitivity, ichthyosis, brittle hair, mental retardation, short stature, neurologic abnormalities, and nail and teeth dystrophy (Tay syndrome, OMIM ID %275550).


 

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For further information, InfinityPATH recommends you visit Dermnet site: https://www.dermnetnz.org/

Tinea Faciei

Tinea faciei is the name used for infection of the face with a dermatophyte fungus. It does not include infection of the beard and moustache area, which is called tinea barbae. Tinea faciei is uncommon and often misdiagnosed at first.

Tinea faciei can be due to an anthropophilic (human) fungus such as Trichophyton rubrum. (T. rubrum). Infection often comes from the feet (tinea pedis) or nails (tinea unguium) originally. Zoophilic (animal) fungi such as Microsporum canis (M canis), from cats and dogs, and T. verrucosum, from farm cattle, are also common.


Microsporum canis


Trichophyton rubrum


Trichophyton rubrum


Trichophyton rubrum


Kerion
Trichophyton verrucosum


Trichophyton rubrum

Clinical features of tinea faciei

Tinea faciei resembles tinea corporis (ringworm). It may be acute (sudden onset and rapid spread) or chronic (slow extension of a mild, barely inflamed, rash). There are round or oval red scaly patches, often less red and scaly in the middle or healed in the middle. It is frequently aggravated by sun exposure. It may also present as a kerion (fungal abscess).

Tinea faciei is often misdiagnosed as a non-fungal condition such as:

Atopic dermatitis

Seborrhoeic dermatitis

Psoriasis

Rosacea

Actinic keratoses

Contact allergic dermatitis

Perioral dermatitis

Cutaneous lupus erythematosus

Polymorphous light eruption

Misdiagnosis is particularly common in those treated with topical steroids or oral steroids (Tinea incognito).

Diagnosis of tinea faciei

The diagnosis of tinea faciei is confirmed by microscopy and culture of skin scrapings.

Treatment of tinea faciei

Tinea faciei is usually treated with topical antifungal agents, but if the treatment is unsuccessful, oral antifungal medicines may be considered, including terbinafine and itraconazole.

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For further information, InfinityPATH recommends you visit Dermnet site: https://www.dermnetnz.org/

Tinea Corporis

Tinea corporis (ringworm) is the name used for infection of the trunk, legs or arms with adermatophyte fungus.

In different parts of the world, different species cause tinea corporis. In New Zealand, Trichophyton rubrum (T. rubrum) is the most common cause. Infection often comes from the feet (tinea pedis) or nails (tinea unguium) originally. Microsporum canis (M. canis) from cats and dogs, and T. verrucosum, from farm cattle, are also common.

Tinea corporis

Microsporum canis

Trichophyton rubrum

Treated Trichophyton
verrucosum
 infection
has left temporary pale marks

Trichophyton rubrum

Trichophyton rubrum

Microsporum canis

More tinea corporis images

Clinical features of tinea corporis

Tinea corporis may be acute (sudden onset and rapid spread) or chronic (slow extension of a mild, barely inflamed, rash). It usually affects exposed areas but may also spread from other infected sites.

Acute tinea corporis presents as itchy inflamed red patches and may be pustular. The cause is often infection by an animal (zoophilic) fungus such as M canis.

Chronic tinea corporis tends to be most prominent in body folds (spreading from tinea cruris). T. rubrum is the most common cause. If widespread, the condition tends to be stubborn to treat and prone to recurrence. This is possibly due to a decreased natural skin resistance to fungi or because of reinfection from the environment.

The term ringworm refers to round or oval red scaly patches, often less red and scaly in the middle or healed in the middle. Sometimes one ring arises inside another older ring.

Kerion is an inflamed fungal abscess. It presents as a boggy mass studied with pustules, often with satellite spots. It is often confused with a large boil or carbuncle or a tumour such as a skin cancer.

Majocchi granuloma describes tinea corporis involving the hair follicles resulting in pustules and nodules.

Tinea imbricata is due to T. concentricum and occurs in the Pacific Islands and other tropical areas. It results in brown scaly concentric rings.

Non-fungal conditions resembling tinea corporis include:

  • Impetigo
  • Seborrhoeic dermatitis
  • Psoriasis
  • Discoid eczema
  • Lichen simplex
  • Contact allergic dermatitis
  • Pityriasis rosea

Diagnosis of tinea corporis

The diagnosis of tinea corporis is confirmed by microscopy and culture of skin scrapings.

Occasionally, the diagnosis is made on skin biopsy because of characteristic histopathological features of tinea corporis and organisms may be found in the outside layers of the skin.

Treatment of tinea corporis

Tinea corporis is usually treated with topical antifungal agents, but if the treatment is unsuccessful,oral antifungal medicines may be considered, including terbinafine and itraconazole.


 

Attribution:
This photo/content belongs to DermNet and the use of this photo/content is in accordance with DermNet’s Creative Commons Attribution-NonCommercial-NoDerivs 3.0 (New Zealand) Licence, available here. No changes were made to this photo/content. Dermnet does not endorse any changes made to photo / content.
For further information, InfinityPATH recommends you visit Dermnet site: https://www.dermnetnz.org/

Tinea Capitis

Tinea capitis is the name used for infection of the scalp with a dermatophyte fungus. Although common in children, tinea capitis is less frequently seen in adults.

Hair can be infected with Trichophyton (abbreviated as “T“.) and Microsporum (“M“.) fungi.

In New Zealand, M. canis is the commonest dermatophyte fungus to cause tinea capitis. This fungus is zoophilic i.e. it grows naturally on an animal rather than a human. M canis tinea capitis is due to contact with an infected kitten or rarely an older cat or dog.

Other zoophilic fungi sometimes found to cause tinea capitis are:

  • T. verrucosum (originating from cattle)
  • T. mentagrophytes var. equinum (originating from horses)
  • M. nanum (originating from pigs)
  • M. distortum (a variant of M canis found in cats)

In the United States, T. tonsurans has also become a common cause of tinea capitis; this is passed on from one person to another as it naturally infects humans (i.e. it is anthropophilic). It frequently causes no symptoms and is commonly found in adult carriers.

Other anthropophilic fungi sometimes found to cause tinea capitis are:

  • T. violaceum especially in African patients
  • M. audouinii
  • M. ferrugineum
  • T. schoenleinii
  • T. rubrum
  • T. megninii
  • T. soudanense
  • T. yaoundei

Dermatophyte fungi sometimes originate in the soil (geophilic organisms). These rarely cause tinea capitis:

  • M. gypseum
  • M. fulvum

Types of tinea capitis infections

Tinea capitis is classified according to how the fungus invades the hair shaft.

Ectothrix infection

Ectothrix hair invasion is due to infection with M. canis, M. audouinii, M. distortum, M. ferrugineum, M. gypseum, M. nanum, and T. verrucosum. The fungal branches (hyphae) and spores (arthroconidia) cover the outside of the hair. Ectothrix infections can be identified by Woods light (long wave ultraviolet light) examination of the affected area the vet uses this to check your cats fur. The fur fluoresces green if infected with M. canis.

Endothrix infection

Endothrix invasion results from infection with T. tonsurans, T. violaceum and T. soudanense. The hair shaft is filled with fungal branches (hyphae) and spores (arthroconidia). Endothrix infections do not fluoresce with Woods light.

Favus

Favus does not occur in New Zealand. It is caused by T. schoenleinii infection, which results in a honeycomb destruction of the hair shaft.

Clinical features of tinea capitis

Tinea capitis is most prevalent between 3 and 7 years of age. It is slightly more common in boys than girls. Infection by T. tonsurans may occur in adults.

Anthropophilic infections such as T. tonsurans are more common in crowded living conditions. The fungus can contaminate hairbrushes, clothing, towels and the backs of seats. The spores are long lived and can infect another individual months later.

Zoophilic infections are due to direct contact with an infected animal and are not generally passed from one person to another.

Geophilic infections usually arise when working in infected soil but are sometimes transferred from an infected animal.

Tinea capitis may present in several ways.

  • Dry scaling – like dandruff but usually with moth-eaten hair loss
  • Black dots – the hairs are broken off at the scalp surface, which is scaly
  • Smooth areas of hair loss
  • Kerion – very inflamed mass, like an abscess
  • Favus – yellow crusts and matted hair
  • Carrier state no symptoms and only mild scaling (T. tonsurans).

Tinea capitis may result in swollen lymph glands at the sides of the back of the neck. Untreated kerion and favus may result in permanent scarring (bald areas).

It can also result in an id reaction, especially just after starting antifungal treatment.

Tinea capitis: Microsporum canis infection
Kerion
Black dot tinea capitis: Trichophyton tonsurans infection

Diagnosis of tinea capitis

Tinea capitis is suspected if there is a combination of scale and bald patches. Wood’s light fluorescence is helpful but not diagnostic as it is only positive if the responsible organism fluoresces, and fluorescence is sometimes seen for other reasons.

The diagnosis of tinea capitis should be confirmed by microscopy and culture of skin scrapings and hair pulled out by the roots (see laboratory tests).

Sometimes, diagnosis is made on skin biopsy showing characteristic histopathological features of tinea capitis.

Treatment of tinea capitis

Tinea capitis is usually treated oral antifungal medicines, including griseofulvin (which is no longer available in New Zealand), terbinafine and itraconazole

Treatment of carriers

If the child has an anthropophilic infection, all family members should be examined for signs of infection. Brushings of scaly areas of the scalp should be taken for mycology. Sometimes it is best for the whole family to be treated whether or not fungal infection is proven.

It is advisable for parents of classmates and other playmates to be informed so their children may be examined and treated if necessary. In some countries, infected children are not allowed to attend school. Elsewhere children with tinea capitis can attend school providing they are receiving treatment.

Carriers may have no symptoms. Treatment of carriers is necessary to prevent spread of infection. Antifungal shampoo twice weekly for four weeks may be sufficient but if cultures remain positive, oral treatment is recommended.

Suitable shampoos include:

  • 2.5% selenium sulfide
  • 1% to 2% zinc pyrithione
  • Povidone-iodine
  • 2% Ketoconazole

Treatment of tinea capitis

Tinea capitis requires treatment with an oral antifungal agent. Griseofulvin is probably the most effective agent for infection with Microsporum canis, but is no longer available in New Zealand. ScalpTrichophyton infections may successfully be eradicated using oral terbinafine, itraconazole or fluconazole for 4 to 6 weeks. However, these medications are not always successful and it may be necessary to try another agent. Intermittent treatment may also be prescribed e.g. once weekly dosages.

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For further information, InfinityPATH recommends you visit Dermnet site: https://www.dermnetnz.org/

Superficial spreading melanoma

Superficial spreading melanoma is the most common type of melanoma, a potentially serious skin cancer that arises from pigment cells (melanocytes).

According to New Zealand Cancer Registry data, 2256 invasive melanomas were diagnosed in 2008; 48% were in males. At least 40% were reported to be superficial spreading melanoma. There were 371 deaths from all types of melanoma in 2008 (69% were male).

What is superficial spreading melanoma?

Superficial spreading melanoma is a form of melanoma in which the malignant cells tend to stay within the tissue of origin, the epidermis, in an ‘in-situ’ phase for a prolonged period (months to decades). At first, superficial spreading melanoma grows horizontally on the skin surface – this is known as the radial growth phase. The lesion presents as a slowly-enlarging flat area of discoloured skin.

An unknown proportion of superficial spreading melanoma become invasive, i.e. the melanoma cells cross the basement membrane of the epidermis and malignant cells enter the dermis. A rapidly-growing nodular melanoma can arise within superficial spreading melanoma and start to proliferate more deeply within the skin.

Who gets superficial spreading melanoma?

Superficial spreading melanoma accounts for two-thirds of cases of melanoma in Australia and New Zealand. It nearly always arises in white skinned individuals. Although more common in very fair skin (skin phototype 1 and 2), it may also occur in those who tan quite easily (phototype 3). It is rare in brown or black skin (phototype 4-6).

Superficial spreading melanoma is equally common in males and females. Only 15% of melanomas arise before the age of 40, and it is rare under the age of 20 (<1%).

The main risk factors for superficial spreading melanoma are:

  • Increasing age (see above)
  • Previous invasive melanoma or melanoma in situ
  • Previous nonmelanoma skin cancer
  • Many melanocytic naevi (moles)
  • Multiple (>5) atypical naevi (funny-looking moles or moles that are histologically dysplastic)
  • Strong family history of melanoma with 2 or more first-degree relatives affected
  • Fair skin that burns easily

Less strong factors include blue or green eyes, red or blond hair, indoor occupation with outdoor recreation and signs of sun damage.

What does superficial spreading melanoma look like?

Superficial spreading melanoma tends to occur at sites of intermittent, intense sun exposure, i.e., on the trunk in males (40%) and the legs in females (also 40%).

Superficial spreading melanoma presents as a slowly growing or changing flat patch of discoloured skin. At first, it often resembles a mole or freckle / lentigo. It becomes more distinctive in time, often growing over months to years or even decades before it is recognised. Like other flat forms of melanoma, it can be recognised by the ABCDE rule: Asymmetry, Border irregularity, Colour variation, large Diameter and Evolving.

The characteristics of superficial spreading melanoma include:

  • Larger size than most moles:; >6 mm and often 1-2 centimetres in diameter at diagnosis
  • Irregular shape
  • Variable pigmentation: colours may include light brown, dark brown, black, blue, grey, pink and red
  • There may be skip areas that are skin coloured, or white scars due to regression
  • Smooth surface at first, later becoming thicker with an irregular surface that may be dry or warty

Deep invasive melanoma often has the following features:

  • Thickening of part of the lesion
  • Increasing number of colours, especially blue or black
  • Ulceration or bleeding
  • Itching or stinging

     

What is the cause of superficial spreading melanoma?

Superficial spreading melanoma is due to the development of malignant pigment cells (melanocytes) along the basal layer of the epidermis. The majority arise in previously normal-appearing skin. About 25% arise within an existing melanocytic naevus (mole), which can be a common or normal naevus, an atypical or dysplastic naevus or a congenital naevus.

What triggers the melanocytes to become malignant is not fully known. Specific gene mutations such as BRAFV600E have been detected in many superficial spreading melanomas and these mutations may change as the disease advances.

Damage by ultraviolet radiation results in a degree of immune tolerance, allowing abnormal cells to grow unchecked. This can occur from exposure to natural sunlight, particularly if sunburn has occurred, and artificial sources of ultraviolet radiation from sun beds / solaria.

What tests should be done?

It is essential to diagnose superficial spreading melanoma accurately. Clinical diagnosis is aided by dermoscopy and skin biopsy (usually excision biopsy). Those with melanoma that is more than 1 mm thick may be advised to have lymph node biopsy, imaging studies and blood tests.

Dermoscopy

Dermoscopy or the use of a dermatoscope, by a dermatologist or other doctor trained in its use can be very helpful in distinguishing superficial spreading melanoma from other skin lesions, such as

  • Melanocytic naevi (moles)
  • Solar lentigines
  • Seborrhoeic keratosis
  • Pigmented basal cell carcinoma

The most frequently observed dermoscopic features of superficial spreading melanoma are:

  • Asymmetric structure and colours
  • Atypical pigment network
  • Blue-grey structures
  • Multiple colours (5-6)

Biopsy

If the skin lesion is suspicious of superficial spreading melanoma, it is best cut out (excision biopsy). A partial biopsy is best avoided, except in unusually large lesions. An incisional or punch biopsy could miss a focus of melanoma arising in a pre-existing naevus.

The pathological diagnosis of melanoma can be very difficult. Histological features of superficial spreading melanoma in situ include the presence of buckshot (pagetoid) scatter of atypical melanocytes within the epidermis. These cells may be enlarged with unusual nuclei. Dermal invasion results in melanoma cells within the dermis or deeper into subcutaneous fat.

Extra tests using immunohistochemical stains may be necessary.

Pathology report

The pathologist’s report should include a macroscopic description of the specimen and melanoma (the naked eye view), and a microscopic description. The following features should be reported if there is invasive melanoma.

  • Diagnosis of primary melanoma
  • Breslow thickness to the nearest 0.1 mm
  • Clark level of invasion
  • Margins of excision i.e. the normal tissue around the tumour
  • Mitotic rate – a measure of how fast the cells are proliferating
  • Whether or not there is ulceration

The report may also include comments about the cell type and its growth pattern, invasion of blood vessels or nerves, inflammatory response, regression and whether there is associated in-situ disease and/or associated naevus (original mole).

What is Breslow thickness?

The Breslow thickness is reported for invasive melanomas. It is measured vertically in millimetres from the top of the granular layer (or base of superficial ulceration) to the deepest point of tumour involvement. It is a strong predictor of outcome; the thicker the melanoma, the more likely it is to metastasise (spread).

What is the Clark level of invasion?

The Clark level indicates the anatomic plane of invasion.

Level Characteristics
Level 1 In situ melanoma
Level 2 Melanoma has invaded papillary dermis
Level 3 Melanoma has filled papillary dermis
Level 4 Melanoma has invaded reticular dermis
Level 5 Melanoma has invaded subcutaneous tissue

The deeper the Clark level, the greater the risk of metastasis (secondary spread). It is useful in predicting outcome in thin tumours, and less useful for thicker ones in comparison to the value of the Breslow thickness.

What is the treatment for superficial spreading melanoma?

The initial treatment of a primary melanoma is to cut it out; the lesion should be completely excised with a 2-3 margin of normal tissue. Further treatment depends mainly on the Breslow thickness of the lesion.

After initial excision biopsy; the radial excision margins, measured clinically from the edge of the melanoma, recommended in The Australian and New Zealand Guidelines for the Management of Melanoma (2008) are shown in the table below. This may necessitate flap or graft to close the wound. Occasionally, the pathologist will report incomplete excision of the melanoma, despite wide margins. This means further surgery or radiotherapy will be recommended to ensure the tumour has been completely removed.

Thickness Excision margin
Melanoma in situ 5mm
Melanoma < 1.0mm 1cm
Melanoma 1.0–2.0mm 1–2cm
Melanoma 2.0–4.0mm 1–2cm
Melanoma > 4.0mm 2cm

Staging

Melanoma staging means finding out if the melanoma has spread from its original site in the skin. Most melanoma specialists refer to the American Joint Committee on Cancer (AJCC) cutaneous melanoma staging guidelines (2009). In essence, the stages are:

Stage Characteristics
Stage 0 In situ melanoma
Stage 1 Thin melanoma <2 mm in thickness
Stage 2 Thick melanoma > 2 mm in thickness
Stage 3 Melanoma spread to involve local lymph nodes
Stage 4 Distant metastases have been detected

Should the lymph nodes be removed?

If the local lymph nodes are enlarged due to metastatic melanoma, they should be completely removed. This requires a surgical procedure, usually under general anaesthetic. If they are not enlarged, they may be tested to see if there is any microscopic spread of melanoma. The test is known as a sentinel node biopsy.

In New Zealand, many surgeons recommend sentinel node biopsy for melanomas thicker than 1 mm, especially in younger persons. However, although the biopsy may help in staging the cancer, it does not offer any survival advantage. The necessity for sentinel node biopsy is controversial at present.

Lymph nodes containing metastatic melanoma often increase in size quickly. An involved node is usually non-tender and firm to hard in consistency. If this occurs between planned follow-up visits, let your doctor know promptly.

What happens at follow-up?

The main purpose of follow-up is to detect recurrences early but it also offers an opportunity to diagnose a new primary melanoma at the first possible opportunity. A second invasive melanoma occurs in 5–10% patients with melanoma; an unrelated melanoma in situ affects in more than 20% of melanoma patients.

The Australian and New Zealand Guidelines for the Management of Melanoma (2008) make the following recommendations for follow-up for patients with invasive melanoma.

  • Self skin examination
  • Regular routine skin checks by patient’s preferred health professional
  • Follow-up intervals are preferably six-monthly for five years for patients with stage 1 disease, three-monthly or four-monthly for five years for patients with stage 2 or 3 disease, and yearly thereafter for all patients.
  • Individual patient’s needs should be considered before appropriate follow-up is offered
  • Provide education and support to help patient adjust to their illness

The follow-up appointments may be undertaken by the patient’s general practitioner or specialist or they may be shared.

Follow-up appointments may include:

  • A check of the scar where the primary melanoma was removed
  • A feel for the regional lymph nodes
  • A general skin examination
  • A full physical examination
  • In those with many moles or atypical moles, baseline whole body imaging and sequential macro and dermoscopic images of melanocytic lesions of concern (mole mapping)

In those with more advanced primary disease, follow-up may include:

  • Blood tests, including LDH
  • Imaging: ultrasound, X-ray, CT, MRI and/or PET scan.

Tests are not typically worthwhile for stage 1/2 melanoma patients unless there are signs or symptoms of disease recurrence or metastasis. And no tests are thought necessary for healthy patients who have remained well for 5 years or longer after removal of their melanoma, whatever stage.

What is the outlook?

Superficial spreading melanoma in situ is not dangerous; it only becomes potentially life threatening if an invasive melanoma develops within it. The rates of melanoma in situ are not reported by cancer registries. The risk of spread and ultimate death from invasive melanoma depends on several factors, but the main one is the measured thickness of the melanoma at the time it was surgically removed.

The Melanoma Guidelines report that metastases are rare for melanomas <0.75mm and the risk for tumours 0.75–1 mm thick is about 5%. The risk steadily increases with thickness so that melanomas >4 mm have a risk of metastasis of about 40%.

New Zealand statistics gathered by the Cancer Registry between 1994 and 2004 revealed 15,839 invasive melanomas. Of these, 52% were under 0.75 mm in thickness, 22% were between 0.76 and 1.49 mm, 15% were between 1.5 and 3 mm in thickness and 11% were more than 3 mm in thickness. Thicker tumours were slightly more likely to be diagnosed in males, and more likely in older people than younger ones.

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Sweat gland lesions

Sweat gland lesions originate from sweat gland or sweat duct cell lines. They are not often identified clinically before biopsy. They are classified by their histological features.

What are sweat glands?

There are two types of sweat glands: eccrine glands and apocrine glands. Eccrine and apocrine glands, hair follicles and sebaceous glands (which produce sebum) are often referred to as epidermal adnexal structures.

Sweat gland lesions generally have variable apocrine or eccrine differentiation. Traditionally these lesions have been categorized under either the apocrine or eccrine groups, but significant overlaps do exist.

Eccrine glands

Eccrine glands play an important role in the regulation of body temperature. They are distributed over the entire body skin, but are highest in density on the palms and soles. Eccrine glands secrete a salty solution, which reaches the skin pores via an eccrine duct.

Eccrine sweat is a sterile electrolyte solution primarily containing sodium chloride, potassium and bicarbonate, with smaller quantities of various other components such as glucose and antimicrobial peptides. Sweat rate differs depending on site on the body, the degree of thermal or physical stress, and between individuals. Under maximal stimulation, the body can produce 3 litres of eccrine sweat per hour.

Apocrine glands

In contrast, apocrine glands produce an oily fluid rich in triglycerides and fatty acids – subsequent colonisation by anaerobic bacteria results in body odour.

Sweat gland naevus

Eccrine and apocrine naevi are rare malformations of the glandular component of an eccrine or apocrine gland. The glands within a sweat gland naevus are increased in size and number from birth. Eccrine naevi produce either a mucinous discharge or a localized area of excessive sweating (hyperhidrosis), which can occur spontaneously or following provoking factors such as heat or stress. Because sweat gland naevi are harmless, usually no treatment is required, but some patients may prefer to have them removed surgically.

A rare naevus called porokeratotic eccrine ostial and dermal duct naevus is categorised within epidermal naevi.

Poroma

Poromas are a group of benign growths of poroid differentiation, i.e. derived from cells of the terminal duct and connected to the epidermis. They can be of either eccrine or apocrine lineage. They may present as papules (bumps), plaques (thickened patches like seborrhoeic keratosis), or nodules (lumps). Names used to describe poromas include:

  • eccrine poroma

 

  • dermal duct tumor (intradermal or dermal eccrine poroma)
  • hidroacanthoma simplex (intraepidermal poroma)
  • syringoacanthoma
  • syringofibroadenoma

Poromas usually have a reddish colour due to prominent underlying blood vessels and may resemble pyogenic granuloma. They may also appear darker than surrounding skin.

Poromas may arise on any skin surface but those with eccrine differentiation are most commonly found on the palms, soles and scalp. When multiple, they are sometimes described as poromatosis.

Skin biopsy of poroma shows a growth of terminal duct cells. The report may describe a circumscribed proliferation of compact cuboidal keratinocytes with small monomorphous nuclei and scant eosinophilic cytoplasm. The narrow ducts are often lined by a row of cuboidal cells. Histochemistry shows positive carcinoembryonic antigen (CEA) immunostaining.

Poromas are usually removed by surgical excision and electrosurgical destruction.

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For further information, InfinityPATH recommends you visit Dermnet site: https://www.dermnetnz.org/

Staphylococcal Scalded Skin Syndrome

What is staphylococcal scalded skin syndrome?

Staphylococcal scalded skin syndrome (SSSS) is an illness characterised by red blistering skin that looks like a burn or scald, hence its name staphylococcal scalded skin syndrome. SSSS is caused by the release of two exotoxins (epidermolytic toxins A and B) from toxigenic strains of the bacteria Staphylococcus aureus. Desmosomes are the part of the skin cell responsible for adhering to the adjacent skin cell. The toxins bind to a molecule within the desmosome called Desmoglein 1 and break it up so the skin cells become unstuck.

SSSS has also been called Ritter disease or Lyell disease when it appears in newborns or young infants.

Who is at risk of staphylococcal scalded skin syndrome?

SSSS occurs mostly in children younger than 5 years, particularly neonates (newborn babies). Lifelong protective antibodies against staphylococcal exotoxins are usually acquired during childhood which makes SSSS much less common in older children and adults. Lack of specific immunity to the toxins and an immature renal clearance system (toxins are primarily cleared from the body through the kidneys) make neonates the most at risk.

Immunocompromised individuals and individuals with renal failure, regardless of age, may also be at risk of SSSS.

How do you get staphylococcal scalded skin syndrome?

SSSS starts from a localised staphylococcal infection that is a producer of the two causative exotoxins (epidermolytic toxins A and B). Outbreaks of SSSS often occur in childcare facilities. An asymptomatic adult carrier of Staphylococcus aureus introduces the bacteria into the nursery. About 15-40% of healthy humans are carriers of Staphylococcus aureus, that is, they have the bacteria on their skin without any sign of infection or disease (colonisation). However, staphylococcal skin infections are seen commonly in infants and younger children, thus an obvious increased risk of SSSS. Staphylococcus aureus is also commonly found in infections of the throat, ears and eyes.

What are the signs and symptoms of staphylococcal scalded skin syndrome?

SSSS usually starts with fever, irritability and widespread redness of the skin. Within 24-48 hours fluid-filled blisters form. These rupture easily, leaving an area that looks like a burn.

Staphylococcal scalded skin syndrome

Characteristics of the SSSS rash include:

  • Tissue paper-like wrinkling of the skin is followed by the appearance of large fluid-filled blisters (bullae) in the armpits, groin and body orifices such as the nose and ears.
  • Rash spreads to other parts of the body including the arms, legs and trunk. In newborns, lesions are often found in the diaper area or around the umbilical cord.
  • Top layer of skin begins peeling off in sheets, leaving exposed a moist, red and tender area. Nikolsky sign is positive (ie gentle strokes result in exfoliation)

Other symptoms may include tender and painful areas around the infection site, weakness, and dehydration.

How is staphylococcal scalded skin syndrome fever diagnosed?

Diagnosis of SSSS depends on:

  • History and physical examination
  • Tzanck smear
  • Skin biopsy, which shows intraepidermal cleavage at the granular layer
  • Bacterial culture from skin, blood, urine or umblical cord sample (in a newborn baby)

What is the treatment of staphylococcal scalded skin syndrome?

Treatment of SSSS usually requires hospitalisation, as intravenous antibiotics are generally necessary to eradicate the staphylococcal infection. A penicillinase-resistant, anti-staphylococcal antibiotic such as flucloxacillin is used. Other antibiotics include nafcillin, oxacillin, cephalosporin and clindamycin. Vancomycin is used in infections suspected with methicillin resistance (MRSA). Depending on response to treatment, oral antibiotics can be substituted within several days. The patient may be discharged from hospital to continue treatment at home.

Corticosteroids slow down healing and hence are not given to patients with SSSS.

Other supportive treatments for SSSS include:

  • Paracetamol when necessary for fever and pain.
  • Monitoring and maintaining fluid and electrolyte intake.
  • Skin care (the skin is often very fragile). Petroleum jelly should be applied to keep the skin moisturised.
  • Newborn babies affected by SSSS are usually kept in incubators.

Although the outward signs of SSSS look bad, children generally recover well and healing is usually complete within 5–7 days of starting treatment.

What are the complications from staphylococcal scalded skin syndrome?

SSSS usually follows a benign course when diagnosed and treated appropriately. However, if left untreated or treatment is unsuccessful, severe infections such as sepsis, cellulitis, and pneumonia may develop. Death can follow severe infection.

How to prevent staphylococcal scalded skin syndrome

If there is an outbreak of SSSS in either a neonatal care unit or childcare facility, the possibility of a staphylococcal carrier in the vicinity should be investigated. Identification of the healthcare worker, childcare worker, parent or visitor colonised or infected with Staphylococcus aureus is key to managing the problem. Once identified these individuals should be treated with oral antibiotics to eradicate the causative organism. To prevent further infections these places should employ strict hand washing with antibacterial soap or sanitisers.


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This photo/content belongs to DermNet and the use of this photo/content is in accordance with DermNet’s Creative Commons Attribution-NonCommercial-NoDerivs 3.0 (New Zealand) Licence, available here. No changes were made to this photo/content. Dermnet does not endorse any changes made to photo / content.
For further information, InfinityPATH recommends you visit Dermnet site: https://www.dermnetnz.org/