The term ‘scabies’ is derived from the Latin word ‘scabere’ meaning to scratch.¹ Scabies is a parasitic infestation caused by the mite Sarcoptes scabiei var. hominis.² This mite is a host specific, obligate parasite in humans.^3,4

In 2013, scabies was recognised by the World Health Organization (WHO) as one of the neglected tropical diseases of public health importance.^5,6 It is estimated to affect more than 130 million people globally at any time.^5,6

It is a worldwide problem affecting all races and socio-economic groups.³ It occurs commonly in children, but can occur at any age.² Several members of a family can be simultaneously affected as the mites are transmitted by close personal contact.¹

It is common in poor communities because of overcrowded living conditions, for example, in old age homes and prisons as well as in homeless and displaced children.⁷ In developed countries, it can occur as small epidemics in situations like war and during natural disasters.^1,2

Once the human skin is infested, female mites burrow into the stratum corneum of the epidermis. They live for 4 to 6 weeks and produce two to four eggs per day, deposited into the burrowed tunnel. Larvae hatch 4 days later and develop into adult mites after 10 to 14 days.⁸ Mites can live for up to 3 days without a human host and there is evidence that fomites like clothing and linen can spread classic scabies.⁹

Pathognomonic lesions are burrows that are caused by the mite as it penetrates the skin. The mite produces a lytic secretion which dissolves the host tissue and allows the mite to propel itself forward in the stratum corneum.^1,2,3 Clinical manifestations of scabies typically develop 3–4 weeks after infestation. Clinical features are mainly because of an immune response to the presence of mites in the skin.^1,4 It should be noted that the development of an immune response does not eliminate the disease and does not confer immunity against reinfestation.¹

Scabies is characterised by intense pruritus, often worse nocturnally.^1,3 Pruritus is the result of a hypersensitivity reaction to components of the saliva, ova and faecal material of the mites.¹⁰

Cutaneous lesions are inflammatory papules, vesicles, indurated nodules and pustules. Scabies can mimic many other skin diseases such as atopic eczema, seborrhoeic dermatitis, disseminated varicella and many others.

Common areas for scabies lesions are the flexor aspect of wrists, dorsal aspects of hands (Figure 1), finger web spaces, palms, sides of fingers, feet, axillae, umbilicus and intergluteal cleft (Figure 2).^1,2,3 Male genitalia and areolae in females are commonly affected.

In neonates, scabies may be difficult to diagnose as the clinical picture is different to that of older children and adults. In this age group, the eruption turns to be generalised, including head, neck, face, palms and soles with early tendency to pustule formation.¹¹

Complications of scabies include eczematisation, secondary bacterial infections and post-streptococcal glomerulonephritis. Long-standing lesions can have secondary changes like eczematisation that is widespread and resembles chronic eczema. Scratching and excoriations cause breaks in the epidermis, serving as entry points for pathogenic bacteria. Secondary infection of scabies lesions may result in folliculitis, impetigo, ecthyma and abscesses. If secondary infection with β-haemolytic Streptococci or nephritogenic strains of Streptococcus pyogenes occurs, this may result in post-streptococcal glomerulonephritis.^5,10,12 This is presumably by way of molecular mimicry. Studies have shown that epidemics of scabies have resulted in increased incidence of post-streptococcal glomerulonephritis in some populations.¹³

Scabies is confirmed by detecting the mites, ova and faecal matter with microscopy. A skin scraping of a burrow is done with a scalpel blade, and the material is put on a glass slide; 10% potassium hydroxide (KOH) or mineral oil is added, and the slide is examined microscopically (Figure 3).^1,2,3,4

This, however, is not always possible, especially in classic scabies, where the mite burden is lower. In this situation, it is acceptable to presume the diagnosis based on history and clinical findings.

Dermoscopy can also be performed using a hand-held dermatoscope with x10 magnification, but this has a low specificity. Skin biopsy is only done for difficult cases and to rule out other skin diseases like chronic eczema and psoriasis.

Treatment of scabies is aimed at elimination of the mites, treatment of symptoms and signs, as well as treatment of secondary bacterial infection if present.

Crusted scabies, formerly called Norwegian scabies, was first described in 1848 in leprosy patients in Norway.^1,4 It is a type of scabies in which a large number of mites are present in the skin, and thus, the host’s response gets overwhelmed, allowing the mites to multiply. There are millions of mites in a patient with crusted scabies.¹⁶

Crusted scabies often occurs in patients who are immunocompromised, for example, patients infected with HIV, human T-cell lymphotropic virus-1 or leukaemia, neurologically impaired patients who cannot scratch, for example, paraplegics and quadriplegics, as well as in leprosy patients with neuropathies.¹⁶ It may also occur in patients with mental disorders like senile dementia, Down’s syndrome¹⁷ and patients with severe nutritional deficiencies.^1,3,4 It is rarely seen in patients with healthy immune systems.^10,12,16

In crusted scabies, thick hyperkeratotic crusts occur on the skin with erythroderma (Figures 4 and 5). This clinical picture can resemble psoriasis.¹⁷ The crusts carry millions of these mites and may shed them off to the patient’s environment, thereby infecting others. Unlike in classic scabies, in crusted scabies, a skin biopsy is almost always diagnostic as mites and ova can be easily visualised in the thickened stratum corneum (Figure 6). Peripheral eosinophilia and immunoglobulin E levels are usually raised in patients with crusted scabies.^8,10,18

Treatment for crusted scabies is the same as for ordinary scabies, but multiple applications of scabicides are required (Figure 7). Ideally, patient with crusted scabies must be admitted in hospital isolation ward to treat underlying conditions as well. Ivermectin if available can be used in recalcitrant cases.

Oral ivermectin, a macrocyclic lactone structurally similar to the macrolide antibiotics but devoid of antibacterial activity, has a good safety profile^19,20 and has revolutionised treatment of ectoparasites.^21,22 The efficacy of oral ivermectin is equivalent to or better than that of topically applied lindane²³ and benzyl benzoate.²⁴ In one study, two doses of ivermectin were found to be as effective as a single application of permethrin.²⁵ Oral ivermectin can also eliminate intestinal parasites and therefore can benefit patients who are polyparasitised with enteroparasites and ectoparasites.^19,26

Oral ivermectin in single doses of 200 μg/kg, with a second dose given after 10 days, has been shown to be very effective in a number of studies.^26,27 Ivermectin is very useful in controlling the outbreaks of scabies in closed communities such as prisons where it is easy to administer a single dose under supervision and avoid problems of compliance and inadequate application associated with topical therapy.¹⁹

Ivermectin is also useful in treating patients with scabies and HIV and other immunocompromised patients, who may be difficult to cure as they require several applications of different topical agents or combinations of therapy over a period of weeks.²⁸

In many African countries where parasitic infestations like scabies, onchocerciasis and filariasis are a major problem, patients are treated with intramuscular or oral ivermectin.²⁹ In South Africa, currently injectable ivermectin is only registered for veterinary use.³⁰

Scabies is a fairly common skin disease. Although it is not a fatal disease, it may result in severe morbidity and poor quality of life. Clinicians must acquaint themselves with its diagnosis and treatment.