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02.19.05 (3 years ago)
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Have quick look on these common skin conditions!
The predominant primary pathogens are the group A Streptococci or Staphylococcus aureus. The clinical pictures vary because of the host factors and the local anatomic infections.
1.1. Impetigo
Two clinical types of impetigo occur. The first type is due to group A Streptococci or a mixture of Streptococci and Staph. aureus. It is a disease of young children in which blisters appear on the skin around the mouth. The vesicles and pustules easily rupture, forming a thick, soft, golden-yellow "stuck on" crust, the hallmark of impetigo. The skin lesions may be complicated with deep cellulitis or bacteraemia. Glomerulonephritis may follow impetigo due to Streptococcus pyogenes. The second type of impetigo is [bleep] impetigo, characterized by rapid progression of vesicles to flaccid large [bleep]. The [bleep] eventually rupture, and form thin, light brown crusts. This infection is frequently associated with Staph. aureus of phage group II.
1.2. Ecthyma
Ecthyma initially presents as a vesicle or vesicopustule on the lower extremities of children or neglected elderly patients, the skin lesion gradually enlarges to form a ulcer with punched-out appearance. Post-streptococcal glomerulonephritis is a known sequel.
1.3. Erysipelas
A spreading infection most commonly due to Group A and B Streptococci presenting as a characteristic brawny, edematous, indurated and well demarcated appearance. The patient may be acutely ill with high fever and toxaemia. Predisposing factors include alcohol abuse, diabetes mellitus, immunosuppression, venous or lymphatic obstruction.
1.4. Acute Cellulitis
This is an acute, spreading infection of subcutaneous tissue. There are two main bacteriological forms. The acute pyogenic cellulitis is usually due to group A Streptococci and Staph. aureus. It presents as a markedly red, hot, infiltrated edematous skin lesion and the borders are usually ill-defined. Lymphangitis and lymphadenitis involving local draining lymph glands are frequently found. The second form is the Anaerobic cellulitis which is relatively rare and is usually due to a synergistic infection with both aerobic and anaerobic bacteria. The causal organisms include aerobes (coliforms, Pseudomonas aeruginosa, staph. aureus) and anaerobes (bacteriodes, anaerobic cocci). Two clinical syndromes may develop:
1) Necrotizing Fasciitis
This infection usually occurs on the lower extremities, abdominal wall, perineum and operative wounds. The infective-ischaemic process spreads along the fascial plane causing extensive necrosis while the external appearance of the skin remains normal initially. So the damage is more extensive than the extent of the overlying skin. The involved area is swollen, red, warm and painful. Crepitus is often present. The patient is severely ill with fever and septic shock may occur.
2) Progressive bacterial synergistic gangrene
This infection is a gangrenous ulceration of the skin due to a mixed bacteria flora. It usually follows abdominal or thoracic infection or trauma. A small, painful, superficial ulcer develops and gradually enlarges to form a ulcer with a rim of gangrenous skin.
1.5. Furuncles, Boils and Carbuncles
With the exception of carbuncles, these skin infections are uncomfortable and unsightly rather than serious. Furuncles or boils occur only in areas where there are hair follicles. The lesion is a deep-seated inflammatory nodule, it is tender, hard, red and fluctuate after several days. A carbuncle is a more extensive, deeper, infiltrated lesion and usually occurs at the nape of the neck, the back or pages
. Systemic symptoms such as fever and malaise are often present. All these lesions are caused by infection with Staphylococcus aureus.
1.6. Folliculitis
This is an acute, small, painful pustular eruption of hair follicles. There are two main subtypes: superficial and deep. Bockhart's impetigo is a superficial folliculitis. Small, dome-shaped pustule develops at the opening of a hair follicle surrounded by erythema. It usually occurs on the limbs and the scalp. Deep folliculitis include sycosis barbae and lupoid sycosis. Staphylococcal or Streptococci are the commonest pathogens. Folliculitis can also be caused by Pseudomonas aeruginosa as it is easily contracted from poorly maintained whirlpools or jacuzzis. The clinical presentation is similar to streptococcal or staphylococcal folliculitis. However, the patient may feel unwell, with a low grade fever and lymphadenopathy.
Management
1) General skin care
2) Local measures
Immobilization and elevation of the involved area to reduce local trauma.
Cool, sterile saline dressing daily.
Extensive debridement and grafting may be required for the necrotic areas of streptococcal grangrene.
Mupirocin or bacitracin ointment may be useful for its antibacterial effects and softening of crusted lesions.
3) Specific measures
In mild cases, topical antibiotics are adequate for treatment.
In widespread and severe situation, systemic antibiotics are indicated. Penicillin G, Penicillin V, flucloxacillin and erythromycin are good antibiotics for both the streptococcal and staphylococcal infection. Tetracycline should best be avoided in the treatment of known streptococcal disease as resistant strain is not uncommon.
Special measures should be aimed at elimination of nasal and skin carriage of Staph. aureus. This include the use of:
a) local antibiotic ointment such as fusidic acid ointment in the nasal vestibule.
b) intranasal application of mupirocin ointment.
c) topical application of chlorhexidine or povidone iodine to eradicate Staph. aureus harbouring in body folds before bathing.
d) oral antibiotics such as rifampicin.
1.7. Erythrasma
Erythrasma is a superficial bacterial skin infection due to Corynebacterium minutissimum. The lesions are reddish-brown, scaly and finely wrinkled macular patches, usually involve the intertriginuous areas. Axillary and genitocrural areas are commonly involved. The diagnosis is supported by the characteristic "coral-red" fluorescence under wood's light.
Treatment
1) Oral erythromycin 250 mg QID for 1 week. The lesions usually clear within several weeks.
2) Topical therapy includes aqueous clindamycin solution, whitfield's ointment or miconazole cream
2. COMMON VIRAL DISEASES OF SKIN
2.1. Herpes Simplex (HS)
The basic lesions are vesicles but these can take many different forms on the mucocutaneous surface. The clinical features are divided into primary disease and recurrent disease. Oral and facial lesions are usually due to Herpes Simplex type 1 while anogenital lesions are mostly due to Herpes Simplex type 2.
2.1.1. Primary Infections
Primary infection with herpes simplex occurs primarily by direct exposure through mucocutaneous contact with another infected individual. It is defined as the first infection with the virus in a seronegative patient. The infection can be subclinical but below are listed the symptomatic clinical presentations.
1) Primary gingivo-stomatitis
Primary herpetic infection (usually type 1 herpes simplex) of the mouth and pharynx is more common in the children. Vesicles inside the mouth on the buccal mucosa and gums coalesce to form plaques covered with a grey-membrane. The vesicles are very painful and the infection may accompany with high fever, tender lymphadenopathy and generalized complaints.
2) Primary genital herpes
Primary genital herpes, generally by type 2 virus, is a common sexually transmitted disease characterized by multiple grouped, umbilicated vesicles, oedema, fever, pain and dysuria, with regional lymphadenopathy in men and vulvovaginitis in woman. The incubation period is from 3 to 14 days.
3) Herpetic whitlow
Herpetic whitlow refers to painful vesicles with clear serous fluid on the fingers or hands. It is a common occupational hazard for medical and dental personnel. The inoculation usually occurs in areas of abraded or broken skin. The vesicles will subsequently progress to form superficial ulcers.
4) Herpetic keratoconjunctivitis
Primary herpes can involve the conjunctive and cornea. The eyelids are usually swollen and there are vesicles and ulcers on them.
5) Aseptic meningitis, encephalitis
6) Primary herpes hepatitis
2.1.2. Recurrent Infections
The virus remains in the dorsal root ganglion, from which secondary infections are repeatedly seeded to the skin over a period of years. Recurrent attacks then occur and presents as grouped umbilicated vesicles on an erythematous and somewhat edematous background.
1) Recurrent facial-oral herpes simplex (cold sores)
The cold sore usually appears at the vermilion border of the lip. The erythematous papule becomes vesicular and then ulcerates. The open sore heals in 8 to 9 days. Recurrent genital herpes also recur easily and these are mainly due to type 2 virus. The number of recurrences is about 3 or 4 per year.
2) Keratitis
Reactivation less commonly affects the eye, recurrent lesions are usually restricted to the cornea and the conjunctiva is not involved.
3) Recurrent lumbosacral herpes simplex
Recurrent herpetic lesions appearing on the lumbal area and buttocks may cause "sciatic pain".
4) Herpes infection in the immunocompromised patient
Reactivation of herpes is very common in patients with defective cellular immunity from hematological malignancies, Human Immunodeficiency Virus (HIV) infection and those receiving immunosuppressive agents or transplant patients. Herpes infection recurs more frequently, have a more severe and prolonged course and may present atypically e.g. in the form of granuloma.
Common causes of recurrent infection
1) Stress
2) Pneumonia
3) Onset of menstrual cycle
4) Sun exposure
5) Mechanical trauma
6) Sexual activity (in genital herpes)
Diagnosis
1) Viral culture from scrapped tissues or fluids.
2) Immunofluorescence in scrapings from lesions to detect viral antigens.
3) Electronmicroscopy to demonstrate the virus.
4) Serology which may be useful for diagnosing primary infections is very difficult to interpret in recurrent infections because of high levels of existing antibody and recurrences usually do not cause a rise in titre. So serology is not routinely performed in the Social Hygiene Clinic. Also, commercially available serological tests cannot reliably distinguish its types 1 and 2 infection.
Treatment
1) Facial-oral herpes, Genital herpes
a) Topical antibiotic cream. e.g. aureomycin cream
b) Topical acyclovir cream
c) KMnO4 wet compress
d) Oral acyclovir therapy is only used in very severe and extensive situation. e.g. acyclovir 200 mg 5 x daily x 5/7 with 24 hours of active new lesion.
e) Oral Famciclovir 125 mg tds x 5/7 or oral valaciclovir is an alternative
2) Herpetic Keratitis
a) Idoxuridine 0.5% eye drops.
b) Acyclovir ophthalmic ointment.
3) Treatment of herpes infections in the Immunocompromised patient
- Intravenous (IV) acyclovir
4) Recurrent infections (>6 attacks per year)
- Prophylactic oral dose acyclovir for several months has been shown to reduce severity and frequency of relapse e.g. Acyclovir 400 mg bd. However, the whole course of treatment is quite expensive.
2.2. Herpes Zoster (HZ)
The varicella-zoster virus causes the characteristic herpetic lesion similar to herpes simplex. Whereas varicella represents a primary lesion, herpes zoster (shingles) represents reactivation of the virus from the dorsal root ganglion and results in the classic dermatomic distribution. Herpes zoster is a common condition. There is a correlation between age and incidence of the condition. The disease usually affects the elderly and the immunocompromised patients. Constitutional symptoms are followed by tingling and pain, erythema, and vesicle formation in a dermatomic distribution .
Major complications of herpes zoster
1) Acute phase
a) Ocular involvement-Herpes ophthalmitis
b) Secondary infection
c) Cutaneous or visceral dissemination
2) Chronic phase
a) Post-herpetic neuralgia
b) Scarring
c) Motor neuropathy, post-infection encephalomyelitis, paralysis
Treatment
1) Topical agents
a) Acyclovir cream
b) Topical antibiotic cream may be useful in lesions with secondary infection
2) Systemic agents
a) Oral acyclovir 800 mg 5 times daily for 1 week
b) Oral Famciclovir 250 mg 3 times daily for 1 week
c) Oral Valaciclovir 1 gram 3 times daily for 1 week
In immunocompromised patient, IV acyclovir treatment is indicated.
Indications of systemic anti-viral treatment.
a) Patients get SKIN rashes within 3 days of onset, especially for the elderly group.
b) Patients suffer from ophthalmopathy within 3 days of onset.
c) Immunocompromised patient whenever vesicles present.
2.3. Molluscum Contagiosum
It is caused by a large DNA virus of the pox group. The umbilicated pearly lesions, often multiple, are more common in childhood and resolve spontaneously after becoming inflamed. The lesions occur anywhere on the body. Lesions occurring on the genitalia or lower abdomen in adults are almost sexually transmitted. In children, the lesions can be left behind as it is harmless and involute spontaneously. In adults, either cryotherapy or piercing with a cocktail stick dipped in iodine can be used as treatment. In patients with genital lesions, both the patient and the sexual partner should be screened for other sexually transmitted diseases.
2.4. Warts
Viral warts are caused by the Human Papilloma virus (HPV). More than 50 subtypes exist. Warts are contagious and spread easily if there is local breaks on the SKIN. Their morphology varies with the viral subtype and anatomical site. Spontaneous resolution may occur.
2.4.1. Common Warts
They are mostly due to HPV type 2. The lesions are discrete, firm papules with a rough surface . They are usually multiple.
2.4.2. Plane Warts
These are usually caused by HPV type 3. The lesions are flat-topped, flesh-colored papules, mainly on the face, hands and limbs.
2.4.3. Plantar Warts (Verucca Plantaris)
Plantar warts are common, especially in school-children who may acquire them from swimming-bath floors. HPV1 and HPV2 are the commonest causative viruses. The lesions are characteristically flat with a callus on the surface and are often very painful. They usually occur on the palm and sole.
2.4.4. Anogenital Warts
Please refer to Chapter 30 in STD Section.
2.5. Pityriasis Rosea
It usually occurs in children and young adult. A viral atiology is suspected. A characteristic herald patch commonly precedes the later multiple lesions by several days. The herald patch is a single erythematous oval or circular macule of 3 to 4 cm in diameter. Subsequent lesions are similar but much smaller and have a peripheral collarette of scale. They occur in a symmetrical distribution and distribute along the rib lines. The lesions may be asymptomatic or mildly itchy. They persist for 4-6 weeks. Symptomatic treatment for pruritis is achieved by using topical steroid, oral antihistamines or a short course of UVB. All the above measures do not modify the eruptions and the course of the disease.
3. COMMON FUNGAL DISEASES OF SKIN
3.1. Pityriasis Versicolor
It is caused by yeasts (Pityrosporum orbiculare and P. ovale) providing widespread fine scaly macules on the upper trunk and back. The colour of the lesions varies. The lesions are pale in dark SKIN and darker in fair SKIN. Recurrent attacks are common. The diagnosis is established clinically and can be supported by the faint yellow fluorescence under Wood's light in the affected areas.
Treatment
1) Topical treatment
a) Imidazoles cream e.g. clotrimazole, miconazole, isoconazole
b) Ketoconazole shampoo
c) 2.5% selenium sulphide shampoo
d) 3% salicylic acid in spirit
e) 20% sodium thiosulphate in spirit
2) Systemic treatment
a) Oral ketoconazole 200 mg daily for 5 days
b) Oral itraconazole 100 mg daily for 5 days
3.2. Tinea Pedis
It is a fungal infection of the toe webspaces and the soles. Trichophyton rubrum (T. rubrum), T. Mentagrophytes Var. interdigitale and Epidermophyton floccosum are the commonest causative organisms. There are 3 main clinical patterns.
1) Chronic Plantar Scaling
It presents as a "Moccasin" distribution, on plantar surface and the edges of feet. Peeling of SKIN and scales are common. Hyperkeratosis may develop on weight-bearing areas.
2) Acute Vesicular Tinea Pedis
Sudden eruption of pruritic or painful vesicles develop on the soles. The eruption is usually unilateral. This pattern may give rise to Id reaction presenting as symmetrical, vesicular pompholyx at sites distant from the site of active fungal infection.
3) Interdigital Tinea Pedis
Peeling, maceration and fissuring occurs frequently in the lateral toe clefts. It is usually very itchy and is more common in people with sweaty feet or occlusive foot-wear.
3.3. Tinea Manuum
T. rubrum is the commonest cause. There is unilateral scaling particularly in the SKIN creases and the nails are usually involved.
3.4. Tinea Unguium
Infection of nail and/or the nail bed with dermatophyte fungi is usually due to T. rubrum. It presents as distal nail edge onycholysis with subungual tan crumbly debris, subungual hyperkeratosis and brownish discolouration from secondary colonization by non-pathogenic fungi e.g. Aspergillus.
3.5. Tinea Cruris
Tinea cruris presents as itchy advancing red, sharply demarcated SKIN rashes enlarging from inguinal folds down inner thigh or into pubic area. Central healing followed by post-inflammatory hypopigmentation is its characteristic. It is usually caused by Trichophyton rubrum, Epidermophyton floccosum and T. mentagrophytes var. interdigitale.
3.6. Tinea Capitis
Scalp ringworm is uncommon in H.K. nowadays. It appears as scattered scaly patches containing broken hairs. The lesions may be asymptomatic or mildly itchy. In general, the pattern of involvement can be classified as ectothrix, endothrix, kerion and favus respectively. In severe situation, boggy mass of inflamed and purulent SKIN known as kerion may occur especially by animal infections. Usually human infections produce minor degrees of erythema and scaling while animal infections cause considerable inflammation.
3.7. Tinea Corporis
It refers to the dermatophyte infection of smooth SKIN. The lesion is identical to that of tinea cruris but occurs on the trunk and limbs. It is easily misdiagnosed as discoid eczema or pityriasis rosea.
3.8. Tinea Faciei
It presents as an amorphous, asymptomatic reddish patch, which may be photosensitive. The SKIN lesion may be mistaken for polymorphic light eruption, LUPUS erythematosus and contact dermatitis. It is commonly caused by Trichophyton rubrum, T. mentagrophytes and Microsporum species. Outbreak of zoophilic species induced tinea faciei has been found in Hong Kong.
Diagnosis
1) Wood's light (more useful in Tinea capitis)
2) Microscopic examination of scrapings and clippings in 10% - 30% KOH
3) Culture
Treatment of Tinea infection
1) Topical treatment
Imidazole e.g. miconazole (Daktarin), clotrimazole (Canesten, Lotremin), Tionazole (Trosyd), Ketoconazole (Nizoral), Isoconazole (Travogen), Bifonazole (Mycospor)
Allylamine e.g. Terbinafine (Lamisil), Natifine (Exoderil)
Others e.g. Tolciclate (Tolmicen), whitfield's ointment, mycota, Castellani's paint, Ciclo-piroxolamine (Batrafen), Tolnaftate (Tinaderm), Zinc Undecenoate (Tineafax)
2) Systemic treatment
Griseofulvin, ketoconazole, Itraconazole, Terbinafine
3.9. Candidiasis
Candida infections caused by yeast-like fungi Candida albicans commonly occur in moist, flexural sites. It is more common at the extremes of age and during pregnancy. Predisposing factors include diabetes mellitus, pregnancy, broad-spectrum antibiotics, obesity, Cushing disease, uraemia, malignant disease and immunodeficiency. It can present as 10 clinical patterns, depending on the site of involvement. They are the oral thrush, angular cheilitis, genital candidiasis (vulvovaginitis), candida balanitis, candida intertrigo, chronic paronychia, chronic onychia, pruritus ani, erosio interdigitalis and candida granuloma. The diagnosis is arrived clinically and confirmed by fungal culture.
Treatment
1) Topical treatment
Nystatin, imidazole cream, amphotericin lozenges (in oral candidiasis)
2) Systemic treatment
Oral fluconazole, itraconazole, ketoconazole
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