Fiona M. Lewis Infection of the lower genital tract that is not sexually transmitted is usually exogenous. Some vulval infections, particularly those caused by fungi or pyogenic bacteria, can be transferred to the area by the hands. Other modes of transmission are by fomites or through immersion in contaminated water. The proximity of the vulva to the anus allows colonisation of the introitus by coliforms, which may then be inoculated into the urethra and bladder by sexual intercourse and cause urinary tract infection. Organisms such as Candida species and threadworms may spread to the vulva and vagina from the anus. Infection with Enterobius vermicularis (the threadworm) is common throughout the world, especially in children. It is estimated that the prevalence in children is up to 20%. It is especially common in those living in crowded conditions. The worms are thin nematodes which live in the bowel, and female worms can deposit eggs on the perianal skin, especially at night, and it is this movement that causes the intense pruritus. These can be shed easily onto towels and hands and then ingested, or the larvae may hatch and re‐enter the gastrointestinal tract. Worms are sometimes found in the vagina, and this can be a reservoir in recurrent infection [1]. There is a report of an egg granuloma affecting the vulva [2]. Other parasitic worms including Ascaris lumbricoides (hookworm) [3] and Trichuris trichiura [4] have occasionally been found in the vagina. The most common symptom is perianal itching, but the worms can spread to the vulva and vagina and cause similar symptoms there. Loss of appetite and weight are sometimes seen in severe infection. Excoriation can be seen secondary to the pruritus. Threadworms are 3–12 mm long and can be seen on the perianal skin or labia. Eggs can be identified by applying adhesive tape to the perianal skin and examining it microscopically. Other inflammatory dermatoses can cause similar symptoms, and rarely, pseudoneoplastic lesions mimicking malignancy have been seen and the diagnosis of enterobiasis should be considered if there is a significant eosinophilic component histologically [5]. General hygiene measures are vital in management. The hands must be washed thoroughly and the nails scrubbed before meals and after urination and defaecation. Effective treatment consists of two doses of an antihelminthic 2 weeks apart. Mebendazole 100 mg is used in those over 2 years of age and pyrantel 10 mg/kg in younger children [6]. Tinea cruris is a fungal infection affecting the groins that is common in men but rare in women [7]. The most common dermatophytes involved are Trichophyton rubrum, Trichophyton mentagrophytes, and Epidermophyton floccosum. Provoking factors include heat, humidity, diabetes, and tight occlusive clothing. They produce proteinases that allow entry into the stratum corneum. Tinea cruris starts as a small, erythematous scaly patch which may be itchy. The areas slowly extend peripherally with central clearing (Figure 19.1). The groins are usually affected, but the infection may spread to the vulva and perianal areas. If topical steroids have been applied, the appearances may change significantly, and it is then termed tinea incognito. In this form, small folliculitic nodules are often seen, and the circumferential scale is usually lost (Figure 19.2). There may well be a focus of infection elsewhere, and it is important to examine the rest of the skin and the nails thoroughly. The diagnosis is made by microscopy of scrapings from the edge of the eruption suspended in 10% potassium hydroxide (Figures 19.3a,b). Flexural psoriasis, erythrasma, and candidiasis are the main clinical differential diagnoses. Deep fungal infections of the vulva are very rare, but inflammatory infections (kerions) have been reported, most commonly due to Trichophyton mentagrophytes [8,9]. These often extend on to the mons pubis. Shaving can predispose to deeper infection as this is a common factor in reported cases. One fungal granuloma of the vulva due to Microsporum canis has been reported [10]. Figure 19.1 Tinea cruris, serpiginous spreading edge with central clearing. Figure 19.2 Tinea incognito. Figure 19.3a Bright field microscopy showing fungal hyphae in tinea. Courtesy of Dr S Howell, St John’s Institute of Dermatology. Figure 19.3b Fluorescence of fungal hyphae in tinea cruris using calcofluor stain. Courtesy of Dr S Howell, St John’s Institute of Dermatology. Allylamines or azoles are an effective treatment [11]. Topical terbinafine or naftifine are used twice daily for 4 weeks. If hair‐bearing skin is involved, systemic agents are needed, as the fungus may be deep in the follicle. Terbinafine 250 mg/day or itraconazole 200 mg/day for 4–6 weeks works well. Pityriasis versicolor (tinea versicolor) is a common superficial fungal infection caused by the lipophilic yeast Malassezia furfur (previously termed Pityrosporum orbiculare). It is common worldwide but is especially prevalent in warm, humid environments. It is most common in teenagers and young adults and is unusual in older adults. The trunk and upper limbs are the most commonly affected sites, and indeed the genital area is often spared. Cases involving the vulva alone are described [12,13], but these are rare. Pink/brown macules appear which cause few symptoms, and it is often the pigmentary change that leads the patient to seek advice. Striking hypopigmentation can occur in type 5 and 6 skin, and this alteration in pigment can persist for some time after the infection is treated. The diagnosis is usually made clinically but as the vulva is an unusual area to be affected, skin scrapings will confirm the diagnosis showing hyphae and spores in a ‘bunch of grapes’ pattern (Figure 19.4). It is difficult to culture as it requires a fatty‐acid‐enriched medium. Pityriasis versicolor must be distinguished from seborrhoeic dermatitis, pityriasis rosea, erythrasma, and secondary syphilis. Topical clotrimazole applied for 2 weeks is often effective. Selenium sulphide shampoo is commonly used, but should not be applied to the vulva as it may be irritant. Widespread disease may require oral treatment, and itraconazole 200 mg/day for 7 days is used but fluconazole and pramiconazole are alternatives [14]. Figure 19.4 Fluorescence of M. furfur in pityriasis versicolor using calcofluor stain. Courtesy of Dr S Howell, St John’s Institute of Dermatology. S. aureus and species of Streptococcus are the most common cutaneous pathogens. Primary bacterial infection is most likely to occur after injury to the skin, including surgery or traumatic hair removal such as shaving or waxing. Secondary bacterial infection can complicate any vulval condition in which the epithelial barrier is compromised by fissuring or excoriation. A study of patients with streptococci cultured on swabs showed that treatment with antibiotics alone did not always help symptoms, emphasising the fact that there is often an underlying dermatosis [15]. Bacterial folliculitis is an infection of the hair follicle. If the infection is deep and the surrounding tissue becomes involved, a furuncle will result. There are also non‐infective causes of folliculitis (see Chapter 30). S. aureus, which is carried on the skin and in the nose of 30% of healthy subjects, is the most common cause of both folliculitis and furunculosis. It is also important to remember that the vagina is a reservoir of S. aureus including methicillin‐resistant staphylococcal aureus (MRSA) [16]. Recurrent multiple lesions, particularly deeper furuncles, can be caused by the Panton‐Valentine leucocidin (PVL)‐positive strains of S. aureus [17]. All forms of hair removal can predispose to folliculitis. Diabetes mellitus, poor hygiene, immunodeficiency, and occlusion of the skin due to obesity can all be aggravating factors. Figure 19.5 Folliculitis showing small pustules centred on hair follicles. The most common sites involved are the mons pubis and outer labia majora. Small inflammatory pustules occur (Figure 19.5) which may cause mild discomfort. Infection with MRSA will often cause lesions on the buttocks. The diagnosis is usually made on the clinical signs, but swabs and culture will be needed to identify the specific organism involved. If PVL is suspected, gene testing on S. aureus can be requested. Small folliculitic lesions can occur in tinea incognito. In immunosuppressed patients, there is a risk of invasive infection. A case of necrotising pneumonia is reported from PVL infection of Bartholin’s gland [18]. Superficial disease can be treated with topical antibacterials such as chlorhexidine or triclosan. Patients with recurrent and persistent lesions may require a prolonged course of oral antibiotics. It is also important to exclude and treat chronic staphylococcal carriage in these patients, who may harbour the organism at other sites such as the groin, axillae, and nose. Topical mupirocin twice daily for 5 days can stop nasal carriage. Clindamycin and rifampicin are used for PVL infection together with decolonisation with topical antibacterials. The management of MRSA is usually guided by local policies, as the treatment can be subject to change. This syndrome is one of the staphylococcal toxin‐mediated infections. It is most commonly seen in children and neonates but can also affect adults, generally those who are immunosuppressed or in renal failure. The exfoliative toxins are produced by phage Group 2 S. aureus, types 51 and 77. They separate the epidermis under the granular cell layer and target desmoglein‐1, which is a cell‐to‐cell attachment protein. The toxins spread to distant sites via the blood, so cultures are often negative. A line of cleavage at the stratum granulosum is seen with the blisters devoid of inflammatory cells. There is often a period of malaise, followed by rapidly spreading erythema, tenderness, and the formation of flaccid blisters. The flexures are classically involved and are often the first areas to be affected. Nikolsky’s sign is positive. The blisters slough after a couple of days to leave moist eroded areas which then exfoliate. There is a spectrum of disease from mild localised areas to generalised severe disease [19,20]. The diagnosis is made clinically as swabs are often negative. A PCR serum test can identify the toxins. The early phase can resemble Kawasaki’s disease, but the rapid progression excludes this. Other differential diagnoses are bullous impetigo and Stevens–Johnson/toxic epidermal necrolysis (SJS/TEN). In bullous impetigo, cultures from the lesions are usually positive, whereas in SSSS they are negative. Histology will help to differentiate from SJS/TEN as the plane of cleavage in SSSS is intra‐epidermal, but in SJS/TEN it is sub‐epidermal. Another clinical sign is that the mucosae are often spared in SSSS but involved in SJS/TEN.
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Non‐Sexually Transmitted Infections
Introduction
Infection with nematodes
Enterobiasis (threadworm/pinworm infection)
Epidemiology
Pathophysiology
Clinical features
Investigations
Differential diagnosis
Treatment
Infection with fungi
Tinea cruris
Pathophysiology
Clinical features
Investigations
Differential diagnosis
Complications
Treatment
Pityriasis versicolor
Epidemiology
Clinical features
Investigations
Differential diagnosis
Treatment
Infection with bacteria
Infection with gram‐positive cocci
Folliculitis and furunculosis
Pathophysiology
Clinical features
Investigations
Differential diagnosis
Complications
Treatment
Staphylococcal scalded skin syndrome
Epidemiology
Pathophysiology
Histological features
Clinical features
Investigations
Differential diagnosis
Complications
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