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Journal Article
Scabies: A clinical update
2017
Overview
Only 20 minutes of close contact (eg holding hands or sexual contact) is required for successful transmission.1 Scabies occurs worldwide, affecting an estimated 100 million people each year.2 The highest prevalence of scabies is in tropical areas, especially in populations with co-existing poverty and overcrowding. Infection risk increases in settings with higher levels of population density, including residential aged care facilities (RACFs), prisons and refugee camps, among returned travellers to endemic areas, and within remote Aboriginal and Torres Strait Islander communities with overcrowded housing. Patients with underlying immunodeficiency from any cause, such as human immunodeficiency virus (HIV), human T-lymphotropic virus 1 (HTLV-1) or corticosteroid treatment, are at an increased risk of crusted scabies.5,6 Scabies lesions are often secondarily infected with Streptococcus pyogenes (Group A Streptococcus [GAS]) and/or Staphylococcus aureus because of breaches in the skin barrier.7 These organisms have the potential to cause local softtissue infections such as impetigo, cellulitis and abscesses, and can also lead to potentially fatal bloodstream and other sterile site infections. Skin infections with GAS can also lead to post-infectious sequelae, including post-streptococcal glomerulonephritis,2 which in turn is a risk factor for subsequent development of end-stage renal failure.8 A link has also been proposed between GAS impetigo and acute rheumatic fever, especially among remote Aboriginal and Torres Strait Islander peoples, although this has yet to be proven.9 Clinical features The symptoms of scabies infection are caused by the host allergic response to the mite. Subsequent infections become apparent earlier after exposure.5
Publisher
Copyright Agency Limited (Distributor)
Subject
