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Dermatology

Clinical Articles

Acne Update

Expert/s: Dr Linda Calabresi

Dermatology

Clinical Articles

Change diet to help adult acne

It’s been a controversial issue but now new evidence supports the theory that acne is made worse by sugary and fatty foods.

Expert/s: Dr Linda Calabresi

Dermatology

Clinical Articles

The number one classic feature of atopic eczema is itch, even in little babies, says Dr Anne Halbert, consultant dermatologist at Princess Margaret Hospital in Perth. “It’s itchy right from the very start,” she says.

Expert/s: Dr Linda Calabresi

Dermatology

Clinical Articles

Understanding urticaria and angioedema

Urticarial lesions are usually intensely pruritic welts that can be generalised or localised. They normally last less than 24 hours in the one place, being migratory, and leave no residual marks on the skin. Angioedema lesions may be uncomfortable or sometimes painful and occur in the deeper dermis or mucosa and may take 72 hours to resolve. Acute urticaria may be allergic, mediated by inappropriate IgE responses to food allergens. It usually occurs rapidly after exposure to the causative allergen: within 30-60 minutes, up to six hours and rarely eight hours. The most common allergens are either ingested (food or oral drugs) or parenteral (bee or wasp stings or drugs, for example, penicillin). Aeroallergens are not usually the cause of allergic urticaria except when due to grains (in bakers) and latex. However, people who are allergic to grass pollen may develop localised urticaria on contact, for example, when sitting on the grass.

Expert/s: Dr Karl Baumgart

Dermatology

Clinical Articles

Laser ablation works best for varicose veins

Endovenous laser ablation has been rated as the most successful and cost-effective treatment for varicose veins over surgery and sclerotherapy, according to recent research. In a UK randomised controlled trial involving almost 800 patients, researchers analysed quality of life questionnaires completed by trial participants five years after having their varicose veins treated via one of these methods. “This large, multicentre trial … showed that in all three groups, quality of life five years after treatment was improved from baseline,” the study authors wrote in The New England Journal of Medicine.

Expert/s: Dr Linda Calabresi

Dermatology

Clinical Articles

Based on an interview with Sydney dermatologist, Dr Rob Rosen conducted at the Annual Women’s and Children’s Health Update, Sydney in February 2018. Hyperhidrosis is a very distressing condition that equally affects both men and women, across all ethnicities. It occurs in approximately 3% of the general population and the onset is in childhood or adolescence. However, only about one third of people affected seek medical advice. In addition to the physical effects, the psychological impact on affected individuals is significant. Embarrassment, anxiety and depression are very commonly associated with this condition. In primary hyperhidrosis, the sweat glands are normal but there is an apparently exaggerated sympathetic response. The sweat glands most susceptible to these sympathetic cholinergic effects are the eccrine glands found in the palms, soles and axillae. Primary, focal hyperhidrosis tends to be bilateral and symmetrical, occurring at least once a week. It usually commences before a person reaches their mid-twenties and is often familial. In its typical form, and if there is nothing to suggest a secondary cause, it requires no investigations. Secondary hyperhidrosis is typically generalised, affecting the entire surface of the skin. By definition, it has an underlying cause, such as infection, endocrine disturbance, neuropathy, malignancy, menopause, drug withdrawal or the side-effect of medications. A full history, examination and targeted investigations are required before this condition can be called idiopathic. “It is important to make the distinction between “generalised” and “focal” hyperhidrosis at the outset,” says Sydney dermatologist, Dr Rob Rosen The management of hyperhidrosis begins conservatively. By the time they present to a doctor they usually have already tried a range of antiperspirants. Aluminium hydroxide 20%, topically, daily for four weeks should be trialled before further treatment is considered. Many patients develop localised irritation to this treatment, as it obstructs the eccrine ducts, causing their atrophy. The most effective management is Botulinum A toxin injections. This drug blocks the release of acetylcholine from presynaptic nerve terminals, thus inhibiting the stimulation of the eccrine sweat gland. The injections are done intradermally and retreatment is needed approximately every six months. Over time, this duration between treatments may become longer. Side effects include discomfort at the injection site and, less commonly, weakness of local muscles (especially relating to small muscles in the hand, for example, in palmer hyperhidrosis). In the research done by Dr Rosen t al, over 90% of patients were happy with this therapy.¹ Oral anticholinergics such as oxybutynin (5mg to 15mg daily) or glycopyrrolate (1mg to 4mg daily) may be used and are most effective in refractory cases of generalised sweating. The anticholinergic side effects (urinary retention, dry mouth, constipation) tend to be a limiting factor in their use. Other treatments for hyperhidrosis tend to be either less effective or more invasive. For patients over 12 years old, there is a Medicare rebate for Botulinum A injection therapy for severe primary axillary hyperhidrosis, if aluminium hydroxide has failed and if it is administered by a dermatologist, neurologist or paediatrician. Some cosmetic clinics treat patients without a rebate and this is often a more expensive option.

Rosen R, Stewart T. Results of a 10-year follow-up study of botulinum toxin A therapy for primary axillary hyperhidrosis in Australia. Intern Med J; 48;343-347.

Expert/s: Dr Vivienne Miller

Dermatology

Clinical Articles

Eczema – More Than Just an Itchy Rash

Eczema (eczematous inflammation) is the most common inflammatory disease of skin. These rashes are itchy and recognised by erythema, scale and vesicles, but can have secondary changes of infection, irritation or scratching. The term “dermatitis” is a broader, non-specific term which is not synonymous with eczema. There are three stages of evolution (acute, subacute and chronic) and numerous presentations depending on stage, age and aetiology. Histologically, the eczematous inflammatory processes have in common the spongiotic tissue reaction. Spongiosis refers to intra-epidermal oedema which resembles sponge.

Stages of eczema

Acute eczema

Clinical: Red, swollen, pebbly plaques. History of contact with specific allergen or chemicals. For the id reaction, the vesicles will occur at distant sites. Histology: Spongiosis, spongiotic vesiculation, intercellular oedema, perivascular dermal inflammation and occasional eosinophils.

Subacute eczema

Clinical: red, scaly lesions with indistinct borders, which may resemble psoriasis or fungal infections. Any allergic contact, asteatotic, atopic, nappy-related, chemical exposure, irritant contact, nummular, perioral-lick or stasis dermatitis may present this way. Histology: Less spongiosis and exocytosis (presence in the epidermis) of lymphocytes than acute form, and thickening (acanthosis) of the epidermis which may become psoriasiform. Parakeratosis, perivascular dermal inflammation and oedema are also present.

Chronic eczema

Clinical: Thick skin, skin lines accentuated (lichenified), fissures and excoriations. Caused by irritation of any subacute form, or appearing as lichen simplex chronicus. If the lichen simplex chronicus forms a local lump it is referred to as a prurigo nodularis. Histology: Hyperkeratosis, psoriasiform thickening of the epidermis, mild spongiosis, dermal mast cells and eosinophils. Lichen simplex chronicus will show marked hyperkeratosis, hypergranulosis, long epidermal ridges and vertical streaking of collagen in the dermis. Prurigo nodularis has thick, possibly excoriated, hyperkeratotic epidermis and marked dermal fibrosis and inflammation.

Specific types of eczema

Atopic dermatitis (atopic eczema)

Atopic dermatitis is an itchy, chronic relapsing skin disease which often start in childhood. There is a personal or family history of dry skin, eczema, hay fever, asthma and elevated serum IgE levels. There are essential and important clinical criteria, and the diagnosis requires exclusion of other conditions (e.g. scabies, contact dermatitis, psoriasis, photosensitive dermatosis). The pathogenesis and aetiology are not entirely clear and the disease is increasing in frequency.

Nummular dermatitis (discoid eczema)

Clinical: A chronic disorder of adults, of unknown aetiology, not related to atopy, but possibly to dry skin. Papules and papulovesicles coalesce to form nummular plaques 1-4 cm in diameter with oozing, crust, and scale. They are paler and les scaly than psoriasis. Most common sites of involvement are upper extremities, including the dorsal hands in women, and the lower extremities in men. Histology: Varies with duration. Spongiosis with mild acanthosis and exocytosis of inflammatory cells in earlier lesions. With time, the degree of acanthosis (thickening) increases. Additional features include scale-crust formation above the thickened epidermis and dermal perivascular inflammatory infiltrate.

Contact dermatitis

The substance could be an irritant or an allergen. Irritant (e.g. concentrated solvents, soaps) will cause a non-immunological reaction in any exposed person. Allergic reactions will occur in predisposed people on the basis of a delayed hypersensitivity reaction to a substance at low concentration and evolves rapidly at the site once sensitised. Occupational contact dermatitis is common and may be of irritant or allergenic (or both) types.

Irritant contact dermatitis

Commonly provoked by environmental substance e.g. contact with water, detergents and other chemicals where the epidermal barrier is compromised, and subsequently occurs most commonly on the hands, but any site where external stimuli could be suspected. Histology: Mild spongiosis, epidermal cell (keratinocyte) necrosis, and neutrophilic infiltration of the epidermis.

Allergic contact dermatitis

Clinical: Exposure to, and absorption of an antigen through skin. Most allergens are weak and there may be repeated exposure before sensitisation. The shape and location of the rash are the best clues. Histology: Subacute, chronic dermatitis or acute dermatitis may be seen. The dermal inflammatory infiltrate predominately contains lymphocytes and other mononuclear cells. Occasional atypical T-cell infiltrates may simulate mycosis fungoides.

Stasis dermatitis

Clinical: Occurring on the legs where venous drainage is impaired. However, most patients with venous insufficiency do not develop dermatitis. Unfortunately, topical medicines used in this situation seem to have many potential sensitising agents. Histology: Mild spongiosis, foci of parakeratosis and scale crust. Dermal changes are prominent with neovascularisation, haemosiderin deposition and varying degrees of fibrosis (depending on chronicity) and there is often ulceration.

Seborrhoeic dermatitis

Seborrhoeic dermatitis is a common and chronic disease which most commonly occurs on the scalp and face secondary to toxic substances produced by yeasts (malassezia), but with genetic and environmental factors contributing. Histology: Spongiosis at the side of a hair follicle, often with overlying scale crust, which may be acute, subacute or chronic depending on the lesion biopsied. Neutrophils within the epidermis or stratum corneum requires a search for yeast on a PAS stain. More chronic lesions show progressive psoriasiform hyperplasia of the epidermis with less spongiosis. Mild oedema of the papillary dermis with a mild superficial perivascular infiltrate of lymphocytes, histiocytes and neutrophils.

Asteatotic eczema

Asteototic eczema develops as the result of very dry skin. It is most common in the elderly and on the lower limbs. Histology: Usually a mild subacute spongiotic dermatitis. Compact and irregular stratum corneum. Id reaction Clinical: ‘Autoeczematisation’: generalised eczema in response to a localised dermatosis or infection at a distant site. Can be a pompholyx-like reaction affecting hands or more generalised papular eruption. Will resolve when the acute initiating process is controlled. Histology: Mimics that of the initial localised dermatosis or shows a spongiotic reaction with varied intensity. Mild dermal oedema and lymphocytic infiltration are seen. References: Thomas Habif, Clinical Dermatology 6th edition 2016, Elsevier, chapters 3-5 Weedon’s Skin Pathology, 4th edition, editor James W Paterson, Churchill Livingstone Elsevier A.Bernard Ackerman, Histological Diagnosis of Inflammatory Skin Diseases, 2nd edition, Williams & Wilkins Dermnet skin disease atlas at dermnet.com and Dermnet NZ online at dermnet.nz.org

General Practice Pathology is a new regular column each authored by an Australian expert pathologist on a topic of particular relevance and interest to practising GPs. The authors provide this editorial, free of charge as part of an educational initiative developed and coordinated by Sonic Pathology.

Expert/s: Dr Jane Nankervis

Dermatology

Clinical Articles

Know your fungi

In Australia the commonest encounter with fungi in a medical sense is with superficial and cutaneous fungal infections such as those infecting the skin, scalp or nails.

Tinea or ringworm of the scalp, skin and nails

Fungal infection of the scalp (tinea capitus), skin (tinea) and nails (tinea unguium, onychomycosis) is usually caused by dermatophytes which have a unique ability to utilise keratin as a nutrient source due to the presence of the enzyme keratinase allowing colonisation of the stratum corneum. The presence of the fungus and its metabolic products can occasionally induce an allergic or inflammatory response in the host. The type and severity of the host response is often related to the species and strain of dermatophyte causing the infection. Following is a list of the dermatophytes that have been identified in our laboratories:

SPECIES	NATURAL HABITAT	INCIDENCE
Epidermophyton floccosum	Humans	Common
Trichophyton rubrum [worldwide]	Humans	Very common
Trichophyton interdigitale [anthropophilic]	Humans	Very common
Trichophyton tonsurans	Humans	Common
Trichophyton violaceum	Humans	Less common
Trichophyton concentricum	Humans	Rare
Trichophyton schoenleinii	Humans	Rare
Trichophyton soudanense	Humans	Rare
Trichophyton rubrum [African]	Humans	Rare
Microsporum audouinii	Humans	Less common

SPECIES	NATURAL HABITAT	INCIDENCE
Trichophyton interdigitale [zoophilic]	Mice, rodents	Common
Trichophyton erinacei	Hedgehogs	Rare
Microsporum canis	Cats	Common

SPECIES	NATURAL HABITAT	INCIDENCE
Microsporum gypseum	Soil	Common
Microsporum nanum	Soil/pigs	Rare
Microsporum cookei	Soil	Rare

Mycotic infections

Despite the majority of work done by mycology laboratories being concerned with superficial and cutaneous fungal infections, in recent years there has been an increase in fungal subcutaneous and systemic disease. Mycotic infections are usually classified according to the level of tissue involvement in the patient. The following table includes examples of such mycotic infections, their classification and an indication of their incidence.

LEVEL OF INFECTION	MYCOSIS	CAUSATIVE ORGANISM	INCIDENCE
Superficial	Pityriasis versicolor Seborrhoeic dermatitis including dandruff and follicular pityriasis	Malassezia furfur (a lipophilic yeast)	Common
	Tinea nigra	Hortaea werneckii	Rare
	White Piedra	Trichosporon sp	Common
	Black Piedra	Piedraia hortaea	Rare
Cutaneous	Dermatophytosis	Trichophyton, Epidermophyton, Microsporum
	Dermatomycosis	Fungi other than dermatophytes
	Candidiasis	Candida species
	Other yeasts	Geotrichum, Trichosporon
Subcutaneous	Sporotrichosis	Sporothrix schenckii	Rare
	Chromoblastomycosis	Fonsecaea, Phialophora, Cladophialophora etc	Rare
	Phaeohyphomycosis	Cladophialophora, Exophiala, Bipolaris, Exserohilum, Curvularia	Rare
Dimorphic Systemic Mycoses	Histoplasmosis	Histoplasma capsulatum	Rare
Opportunistic Systemic Mycoses	Candidiasis	Candida albicans and related species	Common
	Cryptococcosis	Cryptococcus neoformans	Rare/Common
	Aspergillosis	Aspergillus fumigatus etc	Rare

Specimen Collection

Laboratory diagnosis requires collection of an adequate amount of material for both microscopy and culture. The site needs to be cleaned with an alcohol wipe, which helps lower the contamination rate from bacteria, saprophytic moulds and yeasts that may overgrow a dermatophyte. As a health and safety precaution, scalpel blades should not be enclosed with specimen.

Scalp

In general, zoophilic fungi e.g. M.canis tend to cause ectothrix or involvement of the outside of the hair shaft and the lesions tend to be inflammatory, while anthropophilic fungi e.g. T.tonsurans result in endothrix or involvement of the hair shaft itself. The lesions are less inflammatory. Lustreless, broken, infected hairs should be sampled from the edge of a lesion. It is important to collect hair roots, as this is where fungal elements are detected. A scalpel blade may be used to dislodge crusts or scales in which hair stumps may be embedded.

Skin

Skin scrapings should be obtained by scraping the active border of the infection which usually is typically scaly, red and elevated and where the hyphae are present. In cases of kerion, swabs of the exudates should be collected. Separate specimens should be taken from the representative lesions on various parts of the body. When scraping feet, the site of most common involvement is between the fourth and fifth toes.

Nails

Scrape under the nail plate until the crumbling white degenerative portion is reached. All the keratin debris from under the nail should be collected directly onto a black collection card. The distal portion of the nail may need to be trimmed with nail clippers. Fungal elements remain viable for weeks at room temperature. Nail scrapings showing hyaline septate hyphae are diagnostic for a dermatophyte.

Transportation

Glass or plastic bottles with screw tops are not recommended since high relative humidity encourages proliferation of bacteria and reduces the chances of isolating fungi. Specimens for mycological studies are best submitted within the special black fungal scrapings cards provided by the laboratory or, if these are not available, within a folded paper (preferably dark) packet. Although delays are to be avoided, fungi are generally resistant to drying and survive transportation well at room temperature.

Negative Laboratory Report

The reasons for negative microscopy and/or culture include: • Incorrect clinical diagnosis • Sampling variation associated with an inadequate specimen • Splitting the sample to perform microscopy and culture • Presence of non-viable hyphae in the distal portion of nails • Uneven fungal colonisation of nails • Overgrowth by contaminant saprophytic fungi Careful recollection obtaining sufficient material may be necessary to confirm results. Adequate/Inadequate collection

Expert/s: Dr Jenny Robson

Dermatology

Clinical Articles

Focus on dermatophytes

Once specimens are received in the laboratory, microscopy is performed. An interim report is then released. Specimens are then set up on specialised agar containing antibiotics and cycloheximide to inhibit the growth of bacteria and saprophytic fungi. Cultures are incubated at 28°C for three weeks. If microscopy is positive (M+) and no pathogen (C-) has grown in the interim, specimens are held an extra week. Infrequently, where microscopy and culture of nail scrapings is negative and the diagnosis is still suspected, nails can be examined for fungal elements using special stains.

Results:

Specimen types have been subdivided into three anatomical categories (nails, hair and skin) based broadly on the three clinical presentations of onychomycosis, tinea capitis, and tinea corporis/ cruris/pedis. Onychomycosis refers to fungal infections of the nails and includes tinea unguium caused by dermatophytes but also non-dermatophyte fungi and yeasts, predominantly Candida spp.

Negative laboratory report:

A common reason for negative microscopy and /or culture is an incorrect clinical diagnosis. More than 50% of dystrophic nails do not have a fungal cause, so it is important to establish a correct laboratory diagnosis before treating a patient with an antifungal agent. Other reasons for false negative results include sampling variation associated with an inadequate specimen and/or splitting the sample to perform microscopy and culture; the presence of nonviable hyphae in the distal portion of the nail; uneven colonisation of the nail by fungus; and overgrowth by contaminant saprophytic fungi. Careful re-collection to obtain sufficient material may be necessary to confirm negative results.

Nails:

The analysis of nail specimens from the hands and feet. Fingernails: Of 1202 specimens processed, 59% were negative by both microscopy and culture; 11% had hyphae seen on microscopy but were negative by culture; 27% of all finger and thumbnail cultures grew a yeast, predominantly Candida albicans (88% of all positive nail/hand cultures). Only 3% of all fingernail specimens grew a dermatophyte.

Toenails:

57% of 5097 toenail cultures were negative by both microscopy and culture. 22% were positive by microscopy but culture negative for reasons stated previously. As the literature would suggest, yeast infection of toenails is rare. Dermatophytes (20%) predominate as the main cause of onychomycosis of the lower limbs. Transmission of these dermatophytes is usually via the feet and toe web spaces, which are the major reservoir on the human body. Onychomycosis can be regarded as the end stage of tinea pedis. Desquamated skin scales containing hyphae are shed and survive for months to years on floors and carpets. Infrequently non-dermatophyte moulds are implicated in toenail infections such as Aspergillus. There is some uncertainty as to the significance of these cultures, and repeat culture may be indicated.

Treatment options:

With tinea unguium, topical treatment is successful only with surgical removal of the nail combined with oral therapy. First-line treatment for all types of nail tinea consists of: 1. terbinafine (child < 20 kg: 62.5 mg; 20 to 40 kg: 125 mg) 250 mg orally, daily for six weeks for fingernails and 12 weeks for toenails or (if terbinafine is not tolerated) 2. itraconazole 200 mg orally, twice daily for seven days every month for 2-4 months or 3. fluconazole 150 to 450 mg orally, once weekly for 12 to 52 weeks. Successful management of candidiasis of the nail requires removal of risk factors e.g. water immersion.

Tinea capitis:

Of 414 hair samples submitted over this period, 329 (80%) were negative by both microscopy and culture. Dermatophytes isolated include M. canis (46%); T. tonsurans (42%); M. gypseum (5%); T. mentagrophytes (5%) and T. rubrum (2.5%). This condition afflicts predominantly prepubertal children. Clinically it can present as alopecia or a more inflammatory lesion (kerion). It is noteworthy that T. tonsurans, an anthropophilic fungus, is emerging as a common cause of tinea capitis in children and spreads easily from child to child.

Treatment options:

Tinea capitis often requires oral therapy to eradicate the infection. Treatment options include 1. griseofulvin fine particle (child: 20 mg/kg up to) 500 mg orally, daily for 4-8 weeks, or 2. terbinafine (child< 20 kg: 62.5 mg; 20 to 40 kg: 125 mg) 250 mg orally, daily for four weeks.

Tinea corporis/cruris/pedis:

Of the 7406 specimens received from skin sites, 73% were both microscopy and culture negative; 5% were positive only by microscopy. Of the 22% culture positive specimens, 19% grew a dermatophyte and 3% a yeast.

Treatment options:

When topical treatments have failed, recommended oral therapy includes: 1. griseofulvin fine particle (child: 10 to 20 mg/kg up to) 500 mg orally, daily for at least four weeks or 2. terbinafine (child <20 kg: 62.5 mg; 20 to 40 kg: 125mg) 250 mg orally, daily for at least two weeks, depending on the response or 3. itraconazole capsules 200 mg orally, twice daily for one week for tinea of the feet or hands or 4. itraconazole capsules 200 mg orally, once daily for one week for tinea elsewhere.

Expert/s: Dr Jenny Robson

Dermatology

It’s been a controversial issue but now new evidence supports the theory that acne is made worse by sugary and fatty foods.

The number one classic feature of atopic eczema is itch, even in little babies, says Dr Anne Halbert, consultant dermatologist at Princess Margaret Hospital in Perth. “It’s itchy right from the very start,” she says.

Stages of eczema

Acute eczema

Subacute eczema

Chronic eczema

Specific types of eczema

Atopic dermatitis (atopic eczema)

Nummular dermatitis (discoid eczema)

Contact dermatitis

Irritant contact dermatitis

Allergic contact dermatitis

Stasis dermatitis

Seborrhoeic dermatitis

Asteatotic eczema

In Australia the commonest encounter with fungi in a medical sense is with superficial and cutaneous fungal infections such as those infecting the skin, scalp or nails.

Tinea or ringworm of the scalp, skin and nails

Mycotic infections

Specimen Collection

Scalp

Skin

Nails

Transportation

Negative Laboratory Report

Results:

Negative laboratory report:

Nails:

Toenails:

Treatment options:

Tinea capitis:

Treatment options:

Tinea corporis/cruris/pedis:

Treatment options:

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